The effects of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 during myocardial ischemia/reperfusion in a model of rats with depression.

PubMed

Wang, Yiming; Zhang, Hongming; Chai, Fangxian; Liu, Xingde; Berk, Michael

2014-12-04

Major depressive disorder (MDD) is an independent risk factor for coronary heart disease (CHD), and influences the occurrence and prognosis of cardiovascular events. Although there is evidence that antidepressants may be cardioprotective after acute myocardial infarction (AMI) comorbid with MDD, the operative pathophysiological mechanisms remain unclear. Our aim was therefore to explore the molecular mechanisms of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 in a rat model of depression during myocardial ischemia/reperfusion (I/R). Rats were divided randomly into 3 groups (n = 8): D group (depression), DI/R group (depression with myocardial I/R) and escitalopram + DI/R group. The rats in all three groups underwent the same chronic mild stress and separation for 21 days, at the same time, in the escitalopram + DI/R group, rats were administered escitalopram by gavage (10 mg/kg/day). Ligation of the rat's left anterior descending branch was done in the myocardial I/R model. Following which behavioral tests were done. The size of the myocardial infarction was detected using 1.5% TTC dye. The Tunel method was used to detect apoptotic myocardial cells, and both the Rt-PCR method and immunohistochemical techniques were used to detect the expression of Bcl-2 and Bax. Compared with the D and DI/R groups, rats in Escitalopram + DI/R group showed significantly increased movements and sucrose consumption (P < .01). Compared with the DI/R group, the myocardial infarct size in the escitalopram + DI/R group was significantly decreased (P < .01). Compared with the D group, there were significantly increased apoptotic myocardial cells in the DI/R and escitalopram + DI/R groups (P < .01); however compared with the DI/R group, apoptotic myocardial cell numbers in the escitalopram + DI/R group were significantly decreased (P < .01). Compared with the DI/R group, there was a down-regulated Bax:Bcl-2 ratio in the escitalopram + DI/R group (P < .01). These results suggest that in patients with AMI comorbid with MDD, there is an increase in pro-apoptotic pathways that is reversed by escitalopram. This suggests that clinically escitalopram may have a direct cardioprotective after acute myocardial infarction.

Influence of renal impairment on myocardial function in outpatients with systolic heart failure: an echocardiographic and cardiac biomarker study.

PubMed

Bosselmann, Helle; Tonder, Niels; Sölétormos, György; Rossing, Kasper; Iversen, Kasper; Goetze, Jens P; Gustafsson, Finn; Schou, Morten

2014-12-20

Renal dysfunction (RD) is associated with poor outcome in systolic heart failure (HF). Left ventricular ejection fraction (LVEF) is not depressed to a greater extent in patients with RD compared to patients with normal renal function, but it is relatively unknown whether other measures of myocardial function are impaired by RD. The objective of the present study is to evaluate whether RD in systolic HF is associated with excessive impairment of myocardial function, evaluated by strain analysis and cardiac biomarkers. Patients with LVEF <0.45% were enrolled from an outpatient HF clinic. The patients underwent advanced echocardiography. Glomerular filtration rate was estimated by the CKD-EPI equation (eGFR) and patients grouped by eGFR: eGFR group-I, ≥ 90 ml/min/1.73 m(2); eGFR group-II, 60-89 ml/min/1.73 m(2); and eGFR group-III, ≤ 59 ml/min/1.73 m(2). Multivariate regression models were developed to evaluate the associations between eGFR groups, echocardiographic measures and cardiac biomarkers. A total of 149 patients participated in the study. Median age was 69 years, 26% were female; LVEF was 33%. Patients with a low eGFR were older (P < 0.001), but there were no differences in frequency of atrial fibrillation, hypertension, diabetes and ischemic heart disease between eGFR groups (P > 0.05 for all). RD was associated with impaired global longitudinal strain (P = 0.018), increased E/e' (P = 0.032), larger left atria (P = 0.038) and increased levels of proANP (P < 0.001), NT-proBNP (P < 0.001) and troponin I (P = 0.019) after adjustment for traditional confounders. Echocardiographic measures and biomarkers reflecting different aspects of myocardial function are impaired in systolic HF patients with RD and the increased mortality risk in these patients may partly be explained by a depressed cardiac function. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

The Psycho-cardiac Coupling, Myocardial Remodeling, and Neuroendocrine Factor Levels: The Psychosomatics of Major Depressive Disorder.

PubMed

Syeda, Javeria N; Rutkofsky, Ian H; Muhammad, Adnan S; Balla Abdalla, Tarig H; Saghir, Zahid

2018-04-11

The association of major depressive disorder (MDD) with myocardial infarction (MI) and vice versa is not unknown. Depression, along with many other systemic factors like atherosclerosis, obesity, diabetes and vascular dysfunction, contributes to the development of adverse cardiac events in the future and, has always been a topic of interest in the fields of cardiology and psychosomatics. We wrote this review article to elaborate this relationship in detail. This article suggests that the individuals with type D personality who already had cardiovascular disease had undergone more serious myocardial damage. In addition, we elucidated the effects of depression on sympathetic activity and remodeling of myocardium after MI. The alterations in the neuroendocrine factors, which included the changes in levels of Serotonin (5-HT), Norepinephrine and Corticosterone, also geared towards the changes associated with depression-induced myocardial injury. However, we need more studies in the near future to further dig into this association process. Therefore, we recommend more research to explore the relationship of psychological factors and adverse cardiac outcomes.

Correlation between cardiac remodelling, function, and myocardial contractility in rat hearts 5 weeks after myocardial infarction.

PubMed

Gosselin, H; Qi, X; Rouleau, J L

1998-01-01

Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest that reduced myocardial contractility contributes to this ventricular dysfunction, in vivo studies indicate that at rest, cardiac output is normal or near normal, suggesting that contractility of the remaining viable myocardium of the ventricular wall is preserved. However, this has never been verified. To explore this further, 100 rats with various-sized myocardial infarctions had ventricular function assessed by Langendorff preparation or by isolated papillary muscle studies 5 weeks after infarction. Morphologic studies were also done. Rats with large infarctions (54%) had marked ventricular dilatation (dilatation index from 0.23 to 0.75, p < 0.01) and papillary muscle dysfunction (total tension from 6.7 to 3.2 g/mm2, p < 0.01) but only moderate left ventricular dysfunction (maximum developed tension from 206 to 151 mmHg (1 mmHg = 133.3 Pa), p < 0.01), a decrease less than one would expect with an infarct size of 54%. The contractility of the remaining viable myocardium of the ventricle was also moderately depressed (peak systolic midwall stress 91 to 60 mmHg, p < 0.01). Rats with moderate infarctions (32%) had less marked but still moderate ventricular dilatation (dilatation index 0.37, p < 0.001) and moderate papillary muscle dysfunction (total tension 4.2 g/mm2, p < 0.01). However, their decrease in ventricular function was only mild (maximum developed pressure 178 mmHg, p < 0.01) and less than one would expect with an infarct size of 32%. The remaining viable myocardium of the ventricular wall appeared to have normal contractility (peak systolic midwall stress = 86 mmHg, ns). We conclude that in this postinfarction model, in large myocardial infarctions, a loss of contractility of the remaining viable myocardium of the ventricular wall occurs as early as 5 weeks after infarction and that papillary muscle studies slightly overestimate the degree of ventricular dysfunction. In moderate infarctions, the remaining viable myocardium of the ventricular wall has preserved contractility while papillary muscle function is depressed. In this relatively early postinfarction phase, ventricular remodelling appears to help maintain left ventricular function in both moderate and large infarctions.

Reduction of myocardial blood flow reserve in idiopathic dilated cardiomyopathy without overt heart failure and its relation with functional indices: an echo-Doppler and positron emission tomography study.

PubMed

Morales, Maria-Aurora; Neglia, Danilo; L'Abbate, Antonio

2008-08-01

Myocardial blood flow during pharmacological vasodilatation is depressed in patients with idiopathic dilated cardiomyopathy even the in absence of overt heart failure; the extent of myocardial blood flow abnormalities is not predictable by left ventricular ejection fraction (LVEF) and diastolic dimensions. To assess whether myocardial blood flow impairment in idiopathic dilated cardiomyopathy without overt heart failure can be related to Doppler-derived dP/dt and to echocardiographically determined left ventricular end systolic stress - which is linked to myocardial blood flow reserve in advanced disease. Twenty-six patients, New York Heart Association Class I-II, (LVEF 37.4 +/- 1.4%, left ventricular diastolic dimensions 62.6 +/- 0.9 mm) underwent resting/dipyridamole [13N]NH3 flow positron emission tomography and an ultrasonic study. Regional myocardial blood flow values (ml/min per g) were computed from positron emission tomography data in 13 left ventricular (LV) myocardial regions and averaged to provide mean myocardial blood flow and myocardial blood flow reserve, defined as dipyridamole/resting mean myocardial blood flow ratio. Resting myocardial blood flow was 0.686 +/- 0.045, dipyridamole myocardial blood flow 1.39 +/- 0.15 and myocardial blood flow reserve 2.12 +/- 0.2, lower than in controls (P < 0.01). The ratio dP/dt was directly related to dipyridamole myocardial blood flow and myocardial blood flow reserve (r = 0.552 and 0.703, P < 0.005 and P < 0.0001); no relation was found between myocardial blood flow and LVEF left ventricular diastolic dimensions, and left ventricular end systolic stress. In idiopathic dilated cardiomyopathy patients without overt heart failure, the extent of myocardial blood flow reserve impairment is related to dP/dt but not to more classical indices of left ventricular function.

Progressive epicardial coronary blood flow reduction fails to produce ST-segment depression at normal heart rates.

PubMed

de Chantal, Marilyn; Diodati, Jean G; Nasmith, James B; Amyot, Robert; LeBlanc, A Robert; Schampaert, Erick; Pharand, Chantal

2006-12-01

ST-segment depression is commonly seen in patients with acute coronary syndromes. Most authors have attributed it to transient reductions in coronary blood flow due to nonocclusive thrombus formation on a disrupted atherosclerotic plaque and dynamic focal vasospasm at the site of coronary artery stenosis. However, ST-segment depression was never reproduced in classic animal models of coronary stenosis without the presence of tachycardia. We hypothesized that ST-segment depression occurring during acute coronary syndromes is not entirely explained by changes in epicardial coronary artery resistance and thus evaluated the effect of a slow, progressive epicardial coronary artery occlusion on the ECG and regional myocardial blood flow in anesthetized pigs. Slow, progressive occlusion over 72 min (SD 27) of the left anterior descending coronary artery in 20 anesthetized pigs led to a 90% decrease in coronary blood flow and the development of ST-segment elevation associated with homogeneous and transmural myocardial blood flow reductions, confirmed by microspheres and myocardial contrast echocardiography. ST-segment depression was not observed in any ECG lead before the development of ST-segment elevation. At normal heart rates, progressive epicardial stenosis of a coronary artery results in myocardial ischemia associated with homogeneous, transmural reduction in regional myocardial blood flow and ST-segment elevation, without preceding ST-segment depression. Thus, in coronary syndromes with ST-segment depression and predominant subendocardial ischemia, factors other than mere increases in epicardial coronary resistance must be invoked to explain the heterogeneous parietal distribution of flow and associated ECG changes.

Regional heterogeneity in cardiac sympathetic innervation in acute myocardial infarction: relationship with myocardial oedema on magnetic resonance.

PubMed

Gimelli, Alessia; Masci, Pier Giorgio; Liga, Riccardo; Grigoratos, Chrysanthos; Pasanisi, Emilio Maria; Lombardi, Massimo; Marzullo, Paolo

2014-09-01

To assess the relationships between myocardial structure and function on cardiac magnetic resonance (CMR) imaging and sympathetic tone on (123)I-metaiodobenzylguanidine ((123)I-MIBG) scintigraphy early after myocardial infarction (MI). Ten patients underwent (123)I-MIBG and (99m)Tc-tetrofosmin rest cadmium zinc telluride scintigraphy 4 ± 1 days after MI. The segmental left ventricular (LV) relative radiotracer uptake of both (99m)Tc-tetrofosmin and early (123)I-MIBG was calculated. The day after scintigraphy, on CMR imaging, the extent of ischaemia-related oedema and of myocardial fibrosis (late gadolinium enhancement, LGE) was assessed. Accordingly, the extent of oedema and LGE was evaluated for each segment and segmental wall thickening determined. Based on LGE distribution, LV segments were categorized as "infarcted" (56 segments), "adjacent" (66 segments) or "remote" (48 segments). Infarcted segments showed a more depressed systolic wall thickening and greater extent of oedema than adjacent segments (p < 0.001) and remote segments (p < 0.001). Interestingly, while uptake of (99m)Tc-tetrofosmin was significantly depressed only in infarcted segments (p < 0.001 vs. both adjacent and remote segments), uptake of (123)I-MIBG was impaired not only in infarcted segments (p < 0.001 vs. remote) but also in adjacent segments (p = 0.024 vs. remote segments). At the regional level, after correction for (99m)Tc-tetrofosmin and LGE distribution, segmental (123)I-MIBG uptake (p < 0.001) remained an independent predictor of ischaemia-related oedema. After acute MI the regional impairment of sympathetic tone extends beyond the area of altered myocardial perfusion and is associated with myocardial oedema.

Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanisms of action.

PubMed Central

Mannheimer, C; Eliasson, T; Andersson, B; Bergh, C H; Augustinsson, L E; Emanuelsson, H; Waagstein, F

1993-01-01

OBJECTIVE--To investigate the effects of spinal cord stimulation on myocardial ischaemia, coronary blood flow, and myocardial oxygen consumption in angina pectoris induced by atrial pacing. DESIGN--The heart was paced to angina during a control phase and treatment with spinal cord stimulation. Blood samples were drawn from a peripheral artery and the coronary sinus. SETTING--Multidisciplinary pain centre, department of medicine, Ostra Hospital, and Wallenberg Research Laboratory, Sahlgrenska Hospital, Gothenburg, Sweden. SUBJECTS--Twenty patients with intractable angina pectoris, all with a spinal cord stimulator implanted before the study. RESULTS--Spinal cord stimulation increased patients' tolerance to pacing (p < 0.001). At the pacing rate comparable to that producing angina during the control recording, myocardial lactate production during control session turned into extraction (p = 0.003) and, on the electrocardiogram, ST segment depression decreased, time to ST depression increased, and time to recovery from ST depression decreased (p = 0.01; p < 0.05, and p < 0.05, respectively). Spinal cord stimulation also reduced coronary sinus blood flow (p = 0.01) and myocardial oxygen consumption (p = 0.02). At the maximum pacing rate during treatment, all patients experienced anginal pain. Myocardial lactate extraction reverted to production (p < 0.01) and the magnitude and duration of ST segment depression increased to the same values as during control pacing, indicating that myocardial ischaemia during treatment with spinal cord stimulation gives rise to anginal pain. CONCLUSIONS--Spinal cord stimulation has an anti-anginal and anti-ischaemic effect in severe coronary artery disease. These effects seem to be secondary to a decrease in myocardial oxygen consumption. Furthermore, myocardial ischemia during treatment gives rise to anginal pain. Thus, spinal cord stimulation does not deprive the patient of a warning signal. PMID:8400930

Depression and prognosis following hospital admission because of acute myocardial infarction

PubMed Central

Lauzon, Claude; Beck, Christine A.; Huynh, Thao; Dion, Danielle; Racine, Normand; Carignan, Suzanne; Diodati, Jean G.; Charbonneau, François; Dupuis, Robert; Pilote, Louise

2003-01-01

Background Whether there is an association between depression at the time of acute myocardial infarction and subsequent risk of cardiac complications and death remains controversial. Most studies of this risk factor have been limited to patients of single institutions, and this might account for the varying results. We prospectively evaluated patients admitted to 5 tertiary care and 5 community hospitals and followed them for 1 year to measure the prevalence and prognostic impact of depressive symptoms after acute myocardial infarction. Methods Patients were recruited for the study by trained nurse interviewers who had documented acute myocardial infarction within 2–3 days of admission. The nurses collected information from the medical records and asked study subjects to complete the Beck Depression Inventory questionnaire during their stay in hospital and using a mailed questionnaire 30 days, 6 months and 1 year later. We obtained information on vital status for patients lost to follow-up from a central death registry. Results Of the 587 study subjects, 550 (94%) completed the Beck Depression Inventory at baseline and 191 (35%) had a score of 10 or more, indicating at least mild depression. Rates of depression did not vary over the follow-up period and were similar among patients admitted to tertiary care or community hospitals. Depressed patients were more likely to undergo catheterization (57% v. 47%, 95% confidence interval [CI] around the difference 0.1%–19.6%) and were more likely to undergo percutaneous coronary intervention (32% v. 24%, 95% CI around the difference 0.1%–16.2%) within 30 days of first admission to hospital. Patients with depression on admission had higher rates of a composite of cardiac complications, including recurrent ischemia, infarction or congestive heart failure during their first stay in hospital or readmission for angina, recurrent acute myocardial infarction, congestive heart failure or arrhythmia (adjusted hazard ratio 1.4, 95% CI 1.05–1.86), compared with patients who were not depressed on admission. After 1 year, death rates were higher among patients who were depressed at admission (30 patients, 16%) compared with nondepressed patients (28 patients, 8%), although the difference was not statistically significant (hazard ratio 1.3, 95% CI 0.59–3.05). Interpretation Depressive symptoms are common after acute myocardial infarction and are associated with a slight increase in risk of in-hospital catheterization and angiography and readmission because of cardiac complications. Death was infrequent, with no statistically significant difference between the 2 groups. PMID:12615746

Does overprotection cause cardiac invalidism after acute myocardial infarction?

PubMed

Riegel, B J; Dracup, K A

1992-01-01

To determine if overprotection on the part of the patient's family and friends contributes to the development of cardiac invalidism after acute myocardial infarction. Longitudinal survey. Nine hospitals in the southwestern United States. One hundred eleven patients who had experienced a first acute myocardial infarction. Subjects were predominantly male, older-aged, married, caucasian, and in functional class I. Eighty-one patients characterized themselves as being overprotected (i.e., receiving more social support from family and friends than desired), and 28 reported receiving inadequate support. Only two patients reported receiving as much support as they desired. Self-esteem, emotional distress, health perceptions, interpersonal dependency, return to work. Overprotected patients experienced less anxiety, depression, anger, confusion, more vigor, and higher self-esteem than inadequately supported patients 1 month after myocardial infarction (p < 0.05). Inadequately supported patients were more dependent 4 months after the event. Overprotection on the part of family and friends may facilitate psychosocial adjustment in the early months after an acute myocardial infarction rather than lead to cardiac invalidism.

Treatment of depression after myocardial infarction and the effects on cardiac prognosis and quality of life: rationale and outline of the Myocardial INfarction and Depression-Intervention Trial (MIND-IT).

PubMed

van den Brink, Rob H S; van Melle, Joost P; Honig, Adriaan; Schene, Aart H; Crijns, Harry J G M; Lambert, Frank P G; Ormel, Johan

2002-08-01

Patients with a depressive disorder after myocardial infarction (MI) have a significantly increased risk of major cardiac events. The Myocardial INfarction and Depression-Intervention Trial (MIND-IT) investigates whether antidepressive treatment can improve the cardiac prognosis for these patients. The rationale and outline of the study are described. In this multicenter randomized clinical trial, 2140 patients admitted for MI are screened for depressive symptoms with a questionnaire 0, 3, 6, 9, and 12 months after MI. Patients with symptoms undergo a standardized psychiatric interview. Those with a post-MI depressive episode are randomized to intervention (ie, antidepressive treatment; n = 190) or care-as-usual (CAU; n = 130). In the intervention arm, the research diagnosis is to be confirmed by a psychiatrist. First-choice treatment consists of placebo-controlled treatment with mirtazapine. In case of refusal or nonresponse, alternative open treatment with citalopram is offered. In the CAU arm, the patient is not informed about the research diagnosis. Psychiatric treatment outside the study is recorded, but no treatment is offered. Both arms are followed for end points (cardiac death or hospital admission for MI, unstable angina, heart failure, or ventricular tachyarrhythmia) during an average period of 27 months. Analysis is on an intention-to-treat basis. The MIND-IT study will show whether treatment of post-MI depression can improve cardiac prognosis.

Endogenous sulfur dioxide aggravates myocardial injury in isolated rat heart with ischemia and reperfusion.

PubMed

Zhang, Suqing; Du, Junbao; Jin, Hongfang; Li, Wei; Liang, Yinfang; Geng, Bin; Li, Shukui; Zhang, Chunyu; Tang, Chaoshu

2009-02-27

Ischemia-reperfusion (I/R) injury is an important clinical problem. This article investigated the role of sulfur dioxide (SO2) in the regulation of cardiac function and in the pathogenesis of cardiac I/R injury in isolated rat heart. Rat hearts isolated on a Langendorff apparatus were divided into control, I/R, I/R+SO2, and I/R+hydroxamate groups. Hydroxamate is an inhibitor of SO2 synthetase. I/R treatment was ischemia for 2 hr in hypothermic solution (4 degrees C), then reperfusion/rewarming (37 degrees C) for 60 min. Cardiac function was monitored by MacLab analog to a digital converter. Determination of sulfite content involved reverse-phase high performance liquid chromatography with fluorescence detection. Myoglobin content of coronary perfusate was determined at 410 nm. Myocardial malondialdehyde (MDA) was determined by thiobarbituric acid method, and conjugated diene (CD) was extracted by chloroform. 5,50-Dithiobis-2-nitrobenzoic acid was used to determine glutathione (GSH). The results showed that I/R treatment obviously increased myocardial sulfite content, and sulfite content of myocardium was negatively correlated with the recovery rate of left-ventricle developed pressure and positively correlated with the leakage of myoglobin. In postreperfusion, myocardial function recovery was decreased by SO2. During reperfusion, myocardium-released enzymes, MDA and CD level were increased but myocardial GSH content was depressed with the treatment of SO2 donor. Incubation of myocardial tissue with SO2 significantly increased MDA and CD generation. Endogenous SO2 might be involved in the pathogenesis of myocardial I/R injury, and its mechanism might be associated with an increase in lipid peroxide level and a decrease in GSH generation.

The impact of exercise-only-based rehabilitation on depression and anxiety in patients after myocardial infarction.

PubMed

Korzeniowska-Kubacka, Iwona; Bilińska, Maria; Piotrowska, Dorota; Stepnowska, Monika; Piotrowicz, Ryszard

2017-06-01

The aim of the study was to assess the effectiveness of exercise training on depression, anxiety, physical capacity and sympatho-vagal balance in patients after myocardial infarction and compare differences between men and women. Thirty-two men aged 56.3±7.6 years and 30 women aged 59.2±8.1 years following myocardial infarction underwent an 8-week training programme consisting of 24 interval trainings on cycloergometer, three times a week. Before and after completing the training programme, patients underwent: depression intensity assessment with the Beck depression inventory; anxiety assessment with the state-trait anxiety inventory; a symptom-limited exercise test during which were analysed: maximal workload, duration, double product. In women the initial depression intensity was higher than in men, and decreased significantly after the training programme (14.8±8.7 vs. 10.5±8.8; P<0.01). The anxiety manifestation for state anxiety in women was higher than in men and decreased significantly after the training programme (45.7±9.7 vs. 40.8±0.3; P<0.01). Of note, no depression and anxiety manifestation was found in men. Physical capacity improved significantly after the training programme in all groups, and separately in men and in women. Moreover, an 8-week training programme favourably modified the parasympathetic tone. Participating in the exercise training programme contributed beneficially to a decrease in depression and anxiety manifestations in women post-myocardial infarction. Neither depression nor anxiety changed significantly in men. The impact of exercise training on physical capacity and autonomic balance was beneficial and comparable between men and women.

Effect of Low Perceived Social Support on Health Outcomes in Young Patients With Acute Myocardial Infarction: Results From the VIRGO (Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients) Study

PubMed Central

Bucholz, Emily M.; Strait, Kelly M.; Dreyer, Rachel P.; Geda, Mary; Spatz, Erica S.; Bueno, Hector; Lichtman, Judith H.; D'Onofrio, Gail; Spertus, John A.; Krumholz, Harlan M.

2014-01-01

Background Social support is an important predictor of health outcomes after acute myocardial infarction (AMI), but social support varies by sex and age. Differences in social support could account for sex differences in outcomes of young patients with AMI. Methods and Results Data from the Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO) study, an observational study of AMI patients aged ≤55 years in the United States and Spain, were used for this study. Patients were categorized as having low versus moderate/high perceived social support using the ENRICHD Social Support Inventory. Outcomes included health status (Short Form‐12 physical and mental component scores), depressive symptoms (Patient Health Questionnaire), and angina‐related quality of life (Seattle Angina Questionnaire) evaluated at baseline and 12 months. Among 3432 patients, 21.2% were classified as having low social support. Men and women had comparable levels of social support at baseline. On average, patients with low social support reported lower functional status and quality of life and more depressive symptoms at baseline and 12 months post‐AMI. After multivariable adjustment, including baseline health status, low social support was associated with lower mental functioning, lower quality of life, and more depressive symptoms at 12 months (all P<0.001). The relationship between low social support and worse physical functioning was nonsignificant after adjustment (P=0.6). No interactions were observed between social support, sex, or country. Conclusion Lower social support is associated with worse health status and more depressive symptoms 12 months after AMI in both young men and women. Sex did not modify the effect of social support. PMID:25271209

Depressive symptoms, functional measures and long-term outcomes of high-risk ST-elevated myocardial infarction patients treated by primary angioplasty.

PubMed

Compostella, Leonida; Lorenzi, Sonia; Russo, Nicola; Setzu, Tiziana; Compostella, Caterina; Vettore, Elia; Isabella, Giambattista; Tarantini, Giuseppe; Iliceto, Sabino; Bellotto, Fabio

2017-02-01

The presence of major depressive symptoms is usually considered a negative long-term prognostic factor after an acute myocardial infarction (AMI); however, most of the supporting research was conducted before the era of immediate reperfusion by percutaneous coronary intervention. The aims of this study are to evaluate if depression still retains long-term prognostic significance in our era of immediate coronary reperfusion, and to study possible correlations with clinical parameters of physical performance. In 184 patients with recent ST-elevated AMI (STEMI), treated by immediate reperfusion, moderate or severe depressive symptoms (evaluated by Beck Depression Inventory version I) were present in 10 % of cases. Physical performance was evaluated by two 6-min walk tests and by a symptom-limited cardiopulmonary exercise test: somatic/affective (but not cognitive/affective) symptoms of depression and perceived quality of life (evaluated by the EuroQoL questionnaire) are worse in patients with lower levels of physical performance. Follow-up was performed after a median of 29 months by means of telephone interviews; 32 major adverse cardiovascular events (MACE) occurred. The presence of three vessels disease and low left ventricle ejection fraction are correlated with a greater incidence of MACE; only somatic/affective (but not cognitive/affective) symptoms of depression correlate with long-term outcomes. In patients with recent STEMI treated by immediate reperfusion, somatic/affective but not cognitive/affective symptoms of depression show prognostic value on long-term MACE. Depression symptoms are not predictors "per se" of adverse prognosis, but seem to express an underlying worse cardiac efficiency, clinically reflected by poorer physical performance.

[Myocardial imaging in acute myocardial infarction using beta-methyl-p-(123I)-iodophenylpentadecanoic acid: comparison with 201Tl imaging and wall motion].

PubMed

Naruse, H; Itano, M; Kondo, T; Kogame, T; Yamamoto, J; Morita, M; Kawamoto, H; Fukutake, N; Ohyanagi, M; Iwasaki, T

1992-01-01

Myocardial imaging using beta-methyl-p-(123I)-iodophenylpentadecanoic acid (BMIPP) was performed in 11 patients with acute myocardial infarction. The left ventricular images were divided into 12 segments, and myocardial imagings with BMIPP were compared with coronary angiography (CAG), thallium-201 myocardial scintigraphy (TL) and wall motion obtained by two-dimensional echocardiography (WM). When the culprit lesion was at the proximal point of the left anterior descending artery (LAD), all segments showed depressed uptake. In 3 cases with single vessel disease of the LAD, inferior wall of the basis showed reduced uptake of BMIPP despite the location of the culprit lesion. In cases with discordant uptake between the two tracers, BMIPP frequently showed more severely depressed uptake than TL in the subacute phase, although the uptake of BMIPP correlated with that of TL (tau = 0.82, p less than 0.001). In such cases, the discordance was related to the improvement in WM from the acute phase to the convalescent phase. BMIPP uptake correlated with WM in the subacute phase (tau = 0.50, p less than 0.001). BMIPP showed more severely depressed uptake while WM showed mild asynergy in most cases in which discordance was found between the BMIPP and WM findings. However, there was no correlation between the change in WM from the acute to subacute phases, or the uptakes of BMIPP and TL alone. We concluded that the myocardial condition can be evaluated in detail in acute myocardial infarction by comparing the findings of BMIPP with those of TL and WM.

The long-term risk of recognized and unrecognized myocardial infarction for depression in older men.

PubMed

Jovanova, O; Luik, A I; Leening, M J G; Noordam, R; Aarts, N; Hofman, A; Franco, O H; Dehghan, A; Tiemeier, H

2016-07-01

The association between myocardial infarction (MI) and depression is well described. Yet, the underlying mechanisms are unclear and the contribution of psychological factors is uncertain. We aimed to determine the risk of recognized (RMI) and unrecognized (UMI) myocardial infections on depression, as both have a similar impact on cardiovascular health but differ in psychological epiphenomena. Participants of the Rotterdam Study, 1823 men aged ⩾55 years, were followed for the occurrence of depression. RMI and UMI were ascertained using electrocardiography and medical history at baseline. We determined the strength of the association of RMI and UMI with mortality, and we studied the relationship of RMI and UMI with depressive symptoms and the occurrence of major depression. The risk of mortality was similar in men with RMI [adjusted hazard ratio (aHR) 1.71, 95% confidence interval (CI) 1.45-2.03] and UMI (aHR 1.58, 95% CI 1.27-1.97). Men with RMI had on average [unstandardized regression coefficient (B) 1.14, 95% CI 0.07-2.21] higher scores for depressive symptoms. By contrast, we found no clear association between UMI and depressive symptoms (B 0.55, 95% CI -0.51 to 1.62) in men. Analysis including occurrence of major depression as the outcome were consistent with the pattern of association. The discrepant association of RMI and UMI with mortality compared to depression suggests that the psychological burden of having experienced an MI contributes to the long-term risk of depression.

Fractal analysis of heart rate dynamics as a predictor of mortality in patients with depressed left ventricular function after acute myocardial infarction. TRACE Investigators. TRAndolapril Cardiac Evaluation

NASA Technical Reports Server (NTRS)

Makikallio, T. H.; Hoiber, S.; Kober, L.; Torp-Pedersen, C.; Peng, C. K.; Goldberger, A. L.; Huikuri, H. V.

1999-01-01

A number of new methods have been recently developed to quantify complex heart rate (HR) dynamics based on nonlinear and fractal analysis, but their value in risk stratification has not been evaluated. This study was designed to determine whether selected new dynamic analysis methods of HR variability predict mortality in patients with depressed left ventricular (LV) function after acute myocardial infarction (AMI). Traditional time- and frequency-domain HR variability indexes along with short-term fractal-like correlation properties of RR intervals (exponent alpha) and power-law scaling (exponent beta) were studied in 159 patients with depressed LV function (ejection fraction <35%) after an AMI. By the end of 4-year follow-up, 72 patients (45%) had died and 87 (55%) were still alive. Short-term scaling exponent alpha (1.07 +/- 0.26 vs 0.90 +/- 0.26, p <0.001) and power-law slope beta (-1.35 +/- 0.23 vs -1.44 +/- 0.25, p <0.05) differed between survivors and those who died, but none of the traditional HR variability measures differed between these groups. Among all analyzed variables, reduced scaling exponent alpha (<0.85) was the best univariable predictor of mortality (relative risk 3.17, 95% confidence interval 1.96 to 5.15, p <0.0001), with positive and negative predictive accuracies of 65% and 86%, respectively. In the multivariable Cox proportional hazards analysis, mortality was independently predicted by the reduced exponent alpha (p <0.001) after adjustment for several clinical variables and LV function. A short-term fractal-like scaling exponent was the most powerful HR variability index in predicting mortality in patients with depressed LV function. Reduction in fractal correlation properties implies more random short-term HR dynamics in patients with increased risk of death after AMI.

Modulation of sarcoplasmic reticulum Ca(2+)-release channels by caffeine, Ca2+, and Mg2+ in skinned myocardial fibers of fetal and adult rats.

PubMed

Su, J Y; Chang, Y I

1993-05-01

Ryanodine causes depression of the caffeine-induced tension transient (ryanodine depression) in skinned muscle fibers, because it blocks the sarcoplasmic reticulum (SR) Ca(2+)-release channels [Su, J. Y. (1988) Pflügers Arch 411:132-136, 371-377; (1992) Pflügers Arch 421:1-6]. This study was performed to examine the sensitivity of SR Ca(2+)-release channels to ryanodine in fetal compared to adult myocardium and to investigate the influence of Ca2+, caffeine, and Mg2+ on ryanodine depression in skinned fibers. Ryanodine (0.3 nM-1 microM) caused a dose-dependent depression in skinned myocardial fibers of the rat, and the fetal fibers (IC50 approximately 74 nM) were 26-fold less sensitive than those of the adult (IC50 approximately 2.9 nM). The depression induced by 0.1 microM or 1 microM ryanodine was a function of [caffeine], or [Ca2+] (pCa < 6.0), which was potentiated by caffeine, and an inverse function of [Mg2+]. At pCa > 8.0 plus 25 mM caffeine, a 20% ryanodine depression was observed in both the fetal and adult fibers, indicating independence from Ca2+. Ryanodine depression in skinned fibers of the fetus was less affected than that seen in the adult by pCai, [caffeine]i, or 25 mM caffeine plus pCai or plus pMgi (IC50 approximately pCa 4.5 versus 5.1; caffeine 12.7 mM versus 2 mM; pCa 6.7 versus 7.3; and pMg 3.9 versus 3.3 respectively). The results show that the SR Ca(2+)-release channel in both fetal and adult myocardium is modulated by Ca2+, caffeine, and Mg2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Overexpression of Hsp20 Prevents Endotoxin-Induced Myocardial Dysfunction and Apoptosis via Inhibition of NF-κB Activation

PubMed Central

Wang, Xiaohong; Zingarelli, Basilia; Connor, Michael O’; Zhang, Pengyuan; Adeyemo, Adeola; Kranias, Evangelia G.; Wang, Yigang; Fan, Guo-Chang

2009-01-01

The occurrence of cardiovascular dysfunction in sepsis is associated with a significantly increased mortality rate of 70% to 90% compared with 20% in septic patients without cardiovascular impairment. Thus, rectification or blockade of myocardial depressant factors should partly ameliorate sepsis progression. Heat shock protein 20 (Hsp20) has been shown to enhance myocardial contractile function and protect against doxorubicin-induced cardiotoxicity. To investigate the possible role of Hsp20 in sepsis-mediated cardiac injury, we first examined the expression profiles of five major Hsps in response to lipopolysaccharide (LPS) challenge, and observed that only the expression of Hsp20 was downregulated in LPS-treated myocardium, suggesting that this decrease might be one of mechanisms contributing to LPS-induced cardiovascular defects. Further studies using loss-of-function and gain-of function approaches in adult rat cardiomyocytes verified that reduced Hsp20 levels were indeed correlated with the impaired contractile function. In fact, overexpression of Hsp20 significantly enhanced cardiomyocyte contractility upon LPS treatment. Moreover, after administration of LPS (25μg/g) in vivo, Hsp20 transgenic mice (10-fold overexpression) displayed: 1) an improvement in myocardial function; 2) reduced the degree of cardiac apoptosis; and 3) decreased NF-κB activity, accompanied with reduced myocardial cytokines IL-1β and TNF-α production, compared to the LPS-treated non-transgenic littermate controls. Thus, the increases in Hsp20 levels can protect against LPS-induced cardiac apoptosis and dysfunction, associated with inhibition of NF-κB activity, suggesting that Hsp20 may be a new therapeutic agent for the treatment of sepsis. PMID:19501592

Heart rate variability measurement and clinical depression in acute coronary syndrome patients: narrative review of recent literature

PubMed Central

Harris, Patricia RE; Sommargren, Claire E; Stein, Phyllis K; Fung, Gordon L; Drew, Barbara J

2014-01-01

Aim We aimed to explore links between heart rate variability (HRV) and clinical depression in patients with acute coronary syndrome (ACS), through a review of recent clinical research literature. Background Patients with ACS are at risk for both cardiac autonomic dysfunction and clinical depression. Both conditions can negatively impact the ability to recover from an acute physiological insult, such as unstable angina or myocardial infarction, increasing the risk for adverse cardiovascular outcomes. HRV is recognized as a reflection of autonomic function. Methods A narrative review was undertaken to evaluate state-of-the-art clinical research, using the PubMed database, January 2013. The search terms “heart rate variability” and “depression” were used in conjunction with “acute coronary syndrome”, “unstable angina”, or “myocardial infarction” to find clinical studies published within the past 10 years related to HRV and clinical depression, in patients with an ACS episode. Studies were included if HRV measurement and depression screening were undertaken during an ACS hospitalization or within 2 months of hospital discharge. Results Nine clinical studies met the inclusion criteria. The studies’ results indicate that there may be a relationship between abnormal HRV and clinical depression when assessed early after an ACS event, offering the possibility that these risk factors play a modest role in patient outcomes. Conclusion While a definitive conclusion about the relevance of HRV and clinical depression measurement in ACS patients would be premature, the literature suggests that these measures may provide additional information in risk assessment. Potential avenues for further research are proposed. PMID:25071372

Learned Helplessness and Depressive Symptoms Following Myocardial Infarction.

PubMed

Smallheer, Benjamin A; Vollman, Michael; Dietrich, Mary S

2018-06-01

Psychosocial factors are known to impact depressive symptoms across clinical populations. Learned helplessness has the potential of affecting depressive symptoms following acute myocardial infarction (AMI), though little is known about this relationship. The purpose of this study was to examine the relationship between learned helplessness and depressive symptoms in patients following an AMI. Using a descriptive cross-sectional design, participants with a diagnosed AMI within the past 12 months were recruited. Standardized instruments and measures were used to evaluate learned helplessness and depressive symptoms. A statistically significant direct relationship was found between learned helplessness and depressive symptoms, suggesting that individuals with higher self-reported levels of learned helplessness also reported more depressive symptoms. These results indicate learned helplessness is associated with depressive symptoms in individuals following an AMI. In developing post-AMI treatment plans, health care staff should focus on psychologic points of intervention to the same extent as physiologic interventions.

Physical activity after myocardial infarction: is it related to mental health?

PubMed

Rius-Ottenheim, Nathaly; Geleijnse, Johanna M; Kromhout, Daan; van der Mast, Roos C; Zitman, Frans G; Giltay, Erik J

2013-06-01

Physical inactivity and poor mental wellbeing are associated with poorer prognoses in patients with cardiovascular disease. We aimed to analyse the cross-sectional and prospective associations between physical activity and mental wellbeing in patients with a history of myocardial infarction. Longitudinal, observational study. We investigated 600 older subjects with a history of myocardial infarction (age range 60-80 years) who participated in the Alpha Omega Trial (AOT). They were tested twice at baseline and at 40 months follow-up for physical activity - with the Physical Activity Scale for the Elderly (PASE); depressive symptoms - with the Geriatric Depression Scale (GDS-15); and dispositional optimism - with the Life Orientation Test (LOT-R). Linear (multilevel) and logistic regression analyses were used to examine cross-sectional and longitudinal associations. Physical activity was cross-sectionally associated with depressive symptoms (adjusted beta = -0.143; p = 0.001), but not with dispositional optimism (adjusted beta = 0.074; p = 0.07). We found a synchrony of change between physical activity and depressive symptoms (adjusted beta = -0.155; p < 0.001), but not with dispositional optimism (adjusted beta = 0.049; p = 0.24). Baseline physical activity did not predict depressive symptoms at 40 months follow-up. Concordant inverse associations were observed for (changes) in physical activity and depressive symptoms. Physical activity did not predict depressive symptoms or low optimism.

Broken heart: depression in cardiovascular disease

PubMed Central

Krishnan, K. Ranga R.

2003-01-01

Heart disease and depression are among the most common diseases seen in developed countries. The relation-ship between heart disease and depression has been the subject of both popular interest and scientific research. Sadness is often portrayed as a feeling of heaviness in the chest or as a “broken heart.” Interestingly as we learn more about the expression of emotions, it appears that these perceptions may simply be the language representation of somatic feelings. Large, prospective, longitudinal studies that have examined the relationship between depression and development of coronary artery disease (CAD) have shown that depression is a risk factor for the development of CAD. Depression also increases mortality in patients with stable CAD or myocardial infarction compared with patients without depression. The recent Sertraline AntiDepressant HeARt attack Trial (SADHART) has shown that selective serotonin reuptake inhibitors like sertraline can be safely used in patients with depression following myocardial infarction. There is also intriguing evidence that treating depression with antidepressants may improve outcomes, including mortality. PMID:22034195

T-Wave Abnormality as Electrocardiographic Signature of Myocardial Edema in Non-ST-Elevation Acute Coronary Syndromes.

PubMed

Cardona, Andrea; Zareba, Karolina M; Nagaraja, Haikady N; Schaal, Stephen F; Simonetti, Orlando P; Ambrosio, Giuseppe; Raman, Subha V

2018-01-26

T-wave abnormalities are common during the acute phase of non-ST-segment elevation acute coronary syndromes, but mechanisms underlying their occurrence are unclear. We hypothesized that T-wave abnormalities in the presentation of non-ST-segment elevation acute coronary syndromes correspond to the presence of myocardial edema. Secondary analysis of a previously enrolled prospective cohort of patients presenting with non-ST-segment elevation acute coronary syndromes was conducted. Twelve-lead electrocardiography (ECG) and cardiac magnetic resonance with T2-weighted imaging were acquired before invasive coronary angiography. ECGs were classified dichotomously (ie, ischemic versus normal/nonischemic) and nominally according to patterns of presentation: no ST- or T-wave abnormalities, isolated T-wave abnormality, isolated ST depression, ST depression+T-wave abnormality. Myocardial edema was determined by expert review of T2-weighted images. Of 86 subjects (65% male, 59.4 years), 36 showed normal/nonischemic ECG, 25 isolated T-wave abnormalities, 11 isolated ST depression, and 14 ST depression+T-wave abnormality. Of 30 edema-negative subjects, 24 (80%) had normal/nonischemic ECGs. Isolated T-wave abnormality was significantly more prevalent in edema-positive versus edema-negative subjects (41.1% versus 6.7%, P =0.001). By multivariate analysis, an ischemic ECG showed a strong association with myocardial edema (odds ratio 12.23, 95% confidence interval 3.65-40.94, P <0.0001). Among individual ECG profiles, isolated T-wave abnormality was the single strongest predictor of myocardial edema (odds ratio 23.84, 95% confidence interval 4.30-132, P <0.0001). Isolated T-wave abnormality was highly specific (93%) but insensitive (43%) for detecting myocardial edema. T-wave abnormalities in the setting of non-ST-segment elevation acute coronary syndromes are related to the presence of myocardial edema. High specificity of this ECG alteration identifies a change in ischemic myocardium associated with worse outcomes that is potentially reversible. © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

Superior Effects of High-Intensity Interval Training Compared to Conventional Therapy on Cardiovascular and Psychological Aspects in Myocardial Infarction

PubMed Central

2018-01-01

Objective To evaluate the effect of high-intensity interval training (HIIT) on psychological symptoms, activity states, and cardiovascular functions in patients with myocardial infarction (MI) of low and moderate risk stratification. Methods This prospective study randomly allocated 44 patients with MI to 18 sessions of HIIT or conventional moderate-intensity continuous training (MICT). Outcome measures were assessed at baseline and after 18 sessions. Results Post-exercise cardiovascular and functional states, maximal oxygen uptake (VO2max), metabolic equivalents (METs), 6-Minute Walking Test (6MWT), and Korean Activity Scale/Index (KASI) scores were significantly improved in the HIIT group compared to those in the MICT group after 18 exercise sessions. In particular, VO2max was significantly (p<0.005) improved in the HIIT group (7.58 mL/kg/min) compared to that in the MICT group (2.42 mL/kg/min). In addition, post-exercise psychological states (i.e., scores of Fatigue Severity Scale [FSS] and depression items of the Hospital Anxiety and Depression Scale [HADS_D]) were significantly improved in the HIIT group compared to those in the MICT group after 18 exercise sessions. HADS-D was improved by 1.89 in the HIIT group compared to decrement of 0.47 in the MICT group. FSS was improved by 6.38 in the HIIT group compared to decrement of 0.77 in the MICT group (p<0.005). Conclusion This study demonstrates that HIIT can improve cardiac function, psychological, and activity states in low and moderate risk MI patients. Compared to conventional MICT, HIIT can improve cardiovascular functions, activity states, depression, and fatigue more effectively. PMID:29560335

Superior Effects of High-Intensity Interval Training Compared to Conventional Therapy on Cardiovascular and Psychological Aspects in Myocardial Infarction.

PubMed

Choi, Ha-Yoon; Han, Hee-Jun; Choi, Ji-Won; Jung, Han-Young; Joa, Kyung-Lim

2018-02-01

To evaluate the effect of high-intensity interval training (HIIT) on psychological symptoms, activity states, and cardiovascular functions in patients with myocardial infarction (MI) of low and moderate risk stratification. This prospective study randomly allocated 44 patients with MI to 18 sessions of HIIT or conventional moderate-intensity continuous training (MICT). Outcome measures were assessed at baseline and after 18 sessions. Post-exercise cardiovascular and functional states, maximal oxygen uptake (VO 2max ), metabolic equivalents (METs), 6-Minute Walking Test (6MWT), and Korean Activity Scale/Index (KASI) scores were significantly improved in the HIIT group compared to those in the MICT group after 18 exercise sessions. In particular, VO 2max was significantly (p<0.005) improved in the HIIT group (7.58 mL/kg/min) compared to that in the MICT group (2.42 mL/kg/min). In addition, post-exercise psychological states (i.e., scores of Fatigue Severity Scale [FSS] and depression items of the Hospital Anxiety and Depression Scale [HADS_D]) were significantly improved in the HIIT group compared to those in the MICT group after 18 exercise sessions. HADS-D was improved by 1.89 in the HIIT group compared to decrement of 0.47 in the MICT group. FSS was improved by 6.38 in the HIIT group compared to decrement of 0.77 in the MICT group (p<0.005). This study demonstrates that HIIT can improve cardiac function, psychological, and activity states in low and moderate risk MI patients. Compared to conventional MICT, HIIT can improve cardiovascular functions, activity states, depression, and fatigue more effectively.

Dependence of Ca outflow and depression of frog myocardium contraction on ryodipine concentration.

PubMed

Narusevicius, E; Gendviliene, V; Macianskiene, R; Hmelj-Dunai, G; Velena, A; Duburs, G

1988-02-01

The effect of ryodipine on calcium outflow from tissues, on contraction force, the duration of action potentials and the relaxation phase time-constant in the contraction cycles of myocardial strips was studied using frog heart preparations. It was found that calcium outflow (delta Ca) as a function on ryodipine concentration can be represented as: (formula; see text) A linear correlation exists between Ca2+, contraction blocking and the shortening of the action potential in the presence of various ryodipine concentrations. Ryodipine (10(-5) mol/l) decreased the relaxation time-constant by about 20% as compared to controls. It was concluded that calcium outflow from myocardial tissues in response to ryodipine is due to blockade of calcium entry into the cells and their output through the Na+--Ca2+ exchange system. Frog heart myocardial contractions are essentially under the control of calcium entry through sarcolemmal calcium channels.

The effect of N-acetylcysteine on cardiac contractility to dobutamine in rats with streptozotocin-induced diabetes.

PubMed

Cheng, Xing; Xia, Zhengyuan; Leo, Joyce M; Pang, Catherine C Y

2005-09-05

We examined if myocardial depression at the acute phase of diabetes (3 weeks after injection of streptozotocin, 60 mg/kg i.v.) is due to activation of inducible nitric oxide synthase and production of peroxynitrite, and if treatment with N-acetylcysteine (1.2 g/day/kg for 3 weeks, antioxidant) improves cardiac function. Four groups of rats were used: control, N-acetylcysteine-treated control, diabetic and N-acetylcysteine-treated diabetic. Pentobarbital-anaesthetized diabetic rats, relative to the controls, had reduced left ventricular contractility to dobutamine (1-57 microg/min/kg). The diabetic rats also had increased myocardial levels of thiobarbituric acid reactive substances, immunostaining of inducible nitric oxide synthase and nitrotyrosine, and similar baseline 15-F2t-isoprostane. N-acetylcysteine did not affect responses in the control rats; but increased cardiac contractility to dobutamine, reduced myocardial immunostaining of inducible nitric oxide synthase and nitrotyrosine and level of 15-F2t-isoprostane, and increased cardiac contractility to dobutamine in the diabetic rats. Antioxidant supplementation in diabetes reduces oxidative stress and improves cardiac function.

Perception of stress, depression, hypertension and myocardial infarction as predictors of adherence to hypertension drug treatment.

PubMed

Ljubotina, Aleksandar; Mićović, Vladimir; Kapović, Miljenko; Ljubotina, Maja; Popović, Branislava; Materljan, Eris

2014-12-01

This survey was performed to determine the relationship between the adherence to hypertension drug treatment and the perception of stress, depression, hypertension, and myocardial infarction. 300 patients with uncomplicated hyperten- sion from Rijeka, Croatia, were included (131 women, 169 men, mean age 53.5 years). Adherence to hypertension drug treatment as criterion, and the perception of stress, depression hypertension and myocardial infarction as prediclors were determined by self-assessment. Collected data were analysed using factor analysis, regression analysis, Kolmogorov-Smirnov test, chi2-test and t-test. The statistical significance was set at a probability rate of less than 5% (p < 0.05). 45.09% of women (p=0.479), and 64.08% of men (p = 0.032) were motivated to take antihypertensives. 55.79% of women (p = 0.382) and 64.78% of men (p = 0.028) had sufficient knowledge about drug treatment of hypertension. The positive predictors of motivation for taking antihypertensives were physiological disturbances and perceived potency of hypertension and the negative were perceived helplessness in stress control and negative thoughts and emotions. The positive predictors of knowledge about taking antihypertensives were perceived helplessness in stress control, perceived potency of hypertension and myocardial infarction and the negative predictors were perceived self-efficacy in stress control, physiological disturbances and evaluation of hypertension. Both the motivation as well as the knowledge about taking antihypertensives should be improved, especially in women. The perception of stress, depression, hypertension and myocardial infarction can be used to predict adherence to hypertension drug treatment.

Illness representation after acute myocardial infarction: impact on in-hospital recovery.

PubMed

Cherrington, Candace C; Moser, Debra K; Lennie, Terry A; Kennedy, Carol W

2004-03-01

Despite significant progress in the treatment of coronary artery disease, myocardial infarction is still the leading cause of death in the United States. As suggested by Leventhal's Self-Regulation Model of Illness, the continued high morbidity and mortality may be due to a failure to address the role of psychosocial factors such as illness representation, depression, and anxiety in recovery. To determine the relationship between illness representation of myocardial infarction and the occurrence of in-hospital complications and if anxiety and depression mediate this relationship. A prospective correlational design was used to measure illness representation, depression, and anxiety 24 to 48 hours after admission for myocardial infarction in 49 patients and the frequency of complications during the acute event. Logistic regression was used to determine the likelihood of experiencing a complication. When demographic and clinical variables were controlled for, the more negative the representation of illness, the greater were the odds of experiencing a complication (chi2 = 16.9, df = 6, P =.01). The odds of experiencing a complication increased 5.1% for each 1 unit increase in the score on the Illness Preparation Questionnaire (B = 0.05, Wald = 4.442, Exp(B) = 1.051, 95% CI = 1.003-1.1010). Neither anxiety (chi2 = 3.0, df = 1, P =. 09) nor depression (chi2 = 2.5, df = 1, P = .11) were significant predictors of the occurrence of complications. In these patients, illness representation was predictive of the likelihood of experiencing a complication. Thus, illness representation appears to be an important psychosocial factor in acute recovery from myocardial infarction.

Diabetic cardiomyopathy is associated with defective myocellular copper regulation and both defects are rectified by divalent copper chelation

PubMed Central

2014-01-01

Background Heart disease is the leading cause of death in diabetic patients, and defective copper metabolism may play important roles in the pathogenesis of diabetic cardiomyopathy (DCM). The present study sought to determine how myocardial copper status and key copper-proteins might become impaired by diabetes, and how they respond to treatment with the Cu (II)-selective chelator triethylenetetramine (TETA) in DCM. Methods Experiments were performed in Wistar rats with streptozotocin (STZ)-induced diabetes with or without TETA treatment. Cardiac function was analyzed in isolated-perfused working hearts, and myocardial total copper content measured by particle-induced x-ray emission spectroscopy (PIXE) coupled with Rutherford backscattering spectrometry (RBS). Quantitative expression (mRNA and protein) and/or activity of key proteins that mediate LV-tissue-copper binding and transport, were analyzed by combined RT-qPCR, western blotting, immunofluorescence microscopy, and enzyme activity assays. Statistical analysis was performed using Student’s t-tests or ANOVA and p-values of < 0.05 have been considered significant. Results Left-ventricular (LV) copper levels and function were severely depressed in rats following 16-weeks’ diabetes, but both were unexpectedly normalized 8-weeks after treatment with TETA was instituted. Localized myocardial copper deficiency was accompanied by decreased expression and increased polymerization of the copper-responsive transition-metal-binding metallothionein proteins (MT1/MT2), consistent with impaired anti-oxidant defences and elevated susceptibility to pro-oxidant stress. Levels of the high-affinity copper transporter-1 (CTR1) were depressed in diabetes, consistent with impaired membrane copper uptake, and were not modified by TETA which, contrastingly, renormalized myocardial copper and increased levels and cell-membrane localization of the low-affinity copper transporter-2 (CTR2). Diabetes also lowered indexes of intracellular (IC) copper delivery via the copper chaperone for superoxide dismutase (CCS) to its target cuproenzyme, superoxide dismutase-1 (SOD1): this pathway was rectified by TETA treatment, which normalized SOD1 activity with consequent bolstering of anti-oxidant defenses. Furthermore, diabetes depressed levels of additional intracellular copper-transporting proteins, including antioxidant-protein-1 (ATOX1) and copper-transporting-ATPase-2 (ATP7B), whereas TETA elevated copper-transporting-ATPase-1 (ATP7A). Conclusions Myocardial copper deficiency and defective cellular copper transport/trafficking are revealed as key molecular defects underlying LV impairment in diabetes, and TETA-mediated restoration of copper regulation provides a potential new class of therapeutic molecules for DCM. PMID:24927960

Prognostic value of depressed midwall systolic function in cardiac light-chain amyloidosis.

PubMed

Perlini, Stefano; Salinaro, Francesco; Musca, Francesco; Mussinelli, Roberta; Boldrini, Michele; Raimondi, Ambra; Milani, Paolo; Foli, Andrea; Cappelli, Francesco; Perfetto, Federico; Palladini, Giovanni; Rapezzi, Claudio; Merlini, Giampaolo

2014-05-01

Cardiac amyloidosis represents an archetypal form of restrictive heart disease, characterized by profound diastolic dysfunction. As ejection fraction is preserved until the late stage of the disease, the majority of patients do fulfill the definition of diastolic heart failure, that is, heart failure with preserved ejection fraction (HFpEF). In another clinical model of HFpEF, that is, pressure-overload hypertrophy, depressed midwall fractional shortening (mFS) has been shown to be a powerful prognostic factor. To assess the potential prognostic role of mFS in cardiac light-chain amyloidosis with preserved ejection fraction, we enrolled 221 consecutive untreated patients, in whom a first diagnosis of cardiac light-chain amyloidosis was concluded between 2008 and 2010. HFpEF was present in 181 patients. Patients in whom cardiac involvement was excluded served as controls (n = 121). Prognosis was assessed after a median follow-up of 561 days. When compared with light-chain amyloidosis patients without myocardial involvement, cardiac light-chain amyloidosis was characterized by increased wall thickness (P <0.001), reduced end-diastolic left ventricular volumes (P <0.001), and diastolic dysfunction (P <0.001). In patients with preserved ejection fraction, mFS was markedly depressed [10.6% (8.7-13.5) vs. 17.8% (15.9-19.5) P <0.001]. At multivariable analysis, mFS, troponin I, and NT-pro-brain natriuretic peptide were the only significant prognostic determinants (P <0.001), whereas other indices of diastolic (E/E' ratio, transmitral and pulmonary vein flow velocities) and systolic function (tissue Doppler systolic indices, ejection fraction), or the presence/absence of congestive heart failure did not enter the model. In cardiac light-chain amyloidosis with normal ejection fraction, depressed circumferential mFS, a marker of myocardial contractile dysfunction, is a powerful predictor of survival.

What is the predictive value of ST segment depression in inferior leads in first acute anterior myocardial infarction?

PubMed

Hayıroğlu, Mert İlker; Keskin, Muhammed; Uzun, Ahmet Okan; Türkkan, Ceyhan; Tekkeşin, Ahmet İlker; Kozan, Ömer

Electrical phenomenon and remote myocardial ischemia are the main factors of ST segment depression in inferior leads in acute anterior myocardial infarction (AAMI). We investigated the prognostic value of the sum of ST segment depression amplitudes in inferior leads in patients with first AAMI treated with primary percutaneous coronary intervention. (PPCI). In this prospective analysis, we evaluated the in-hospital prognostic impact of the sum of ST segment depression in inferior leads on 206 patients with first AAMI. Patients were stratified by tertiles of the sum of admission ST segment depression in inferior leads. Clinical outcomes were compared between those tertiles. Univariate analysis revealed higher rate of in-hospital death for patients with ST segment depression in inferior leads in tertile 3, as compared to patients in tertile 1 (OR 9.8, 95% CI 1.5-78.2, p<0.001). After adjustment for baseline variables, ST segment depression in inferior leads in tertile 3 was associated with 5.7-fold hazard of in-hospital death (OR: 5.7, 95% CI 1.2-35.1, p<0.001). Spearman rank correlation test revealed correlation between the sum of ST segment depression amplitude in inferior leads and the sum of ST segment elevation amplitude in V1-6, L1 and aVL. Multivessel disease and additional RCA stenosis were also detected more often in tertile 3. The sum of ST segment depression amplitude in inferior leads of admission ECG in patients with first AAMI treated with PPCI provide an independent prognostic marker of in-hospital outcomes. Our data suggest the sum of ST segment depression amplitude to be a simple, feasible and clinically applicable tool for rapid risk stratification in patients with first AAMI. Copyright © 2017 Elsevier Inc. All rights reserved.

Enhanced platelet/endothelial activation in depressed patients with acute coronary syndromes: evidence from recent clinical trials.

PubMed

Serebruany, Victor L; Glassman, Alexander H; Malinin, Alex I; Sane, David C; Finkel, Mitchell S; Krishnan, Ranga R; Atar, Dan; Lekht, Vladimir; O'Connor, Christopher M

2003-09-01

Platelets play a key role in the progression of acute coronary syndromes (ACS). Clinical depression alone is also associated with enhanced platelet activation. The purpose of this study was to compare concentrations of established biomarkers of enhanced platelet/endothelial activation in clinically depressed versus non-depressed patients enrolled in recent clinical trials for ACS. Two hundred and eighty-one baseline plasma samples from patients with acute myocardial infarction (ASSENT-2; n = 41), with ACS (PRONTO; n = 126) and with clinical depression plus previous acute coronary syndrome within 6 months (SADHART; n = 64), and from normal healthy controls (n = 50) were analyzed. Blood was drawn before applying any therapeutic strategies including interventions, thrombolytics, infusions, and selective serotonin re-uptake inhibitors. Platelet factor 4, beta-thromboglobulin, platelet/endothelial cell adhesion molecule-1, P-selectin, thromboxane, prostacyclin, vascular cell adhesion molecule-1, and E-selectin were measured by enzyme-linked immunosorbent assay by a single core laboratory. Patients with ACS exhibited a higher degree of platelet activation than controls independently of the presence of depression. Plasma levels of P-selectin, thromboxane, prostacyclin, and vascular cell adhesion molecule-1 were the highest in the acute myocardial infarction group when compared with ACS despite the presence or absence of clinical depression. Surprisingly, patients with ACS and depression exhibited the highest levels of platelet factor 4, beta-thromboglobulin, and platelet/endothelial cell adhesion molecule-1 when compared with myocardial infarction or angina patients without clinical depression. E-selectin plasma level was constantly elevated compared with controls but did not differ among the groups dependent on the incidence of depression. The depressed plus ACS group had higher plasma levels of all biomarkers compared with the non-depressed patients. Retrospective analysis of the data from several clinical trials reveals that clinical depression is associated with enhanced activation of platelet/endothelial biomarkers even above the level expected in ACS. These findings may contribute to the unfavorable outcome associated with clinical depression in patients with ACS.

Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy.

PubMed

Ross, J

1985-04-01

In the management of patients with valvular heart disease, an understanding of the effects of altered loading conditions on the left ventricle is important in reaching a proper decision concerning the timing of corrective operation. In acquired valvular aortic stenosis, concentric hypertrophy generally maintains left ventricular chamber size and ejection fraction within normal limits, but in late stage disease function can deteriorate as preload reserve is lost and aortic stenosis progresses. In this setting, even when the ejection fraction is markedly reduced (less than 25%), it can improve to normal after aortic valve replacement, suggesting that afterload mismatch rather than irreversibly depressed myocardial contractility was responsible for left ventricular failure. Therefore, patients with severe aortic stenosis and symptoms should not be denied operation because of impaired cardiac function. In chronic severe aortic and mitral regurgitation, operation is generally recommended when symptoms are present, but whether to recommend operation to prevent irreversible myocardial damage in patients with few or no symptoms has remained controversial. In aortic regurgitation, left ventricular function generally improves postoperatively, even if it is moderately impaired preoperatively, indicating correction of afterload mismatch. Most such patients can be carefully followed by echocardiography. However, in some patients, severe left ventricular dysfunction fails to improve postoperatively. Therefore, when echocardiographic studies in the patient with severe aortic regurgitation show an ejection fraction of less than 40% (fractional shortening less than 25%) plus enlarging left ventricular end-diastolic diameter (approaching 38 mm/m2 body surface area) and end-systolic diameter (approaching 50 mm or 26 mm/m2), confirmation of these findings by cardiac catheterization and consideration of operation are advisable even in patients with minimal symptoms. In chronic mitral regurgitation, maintenance of a normal ejection fraction can mask depressed myocardial contractility. Pre- and postoperative studies in such patients have shown a poor clinical result after mitral valve replacement, associated with a sharp decrease in the ejection fraction after operation. This response appears to reflect unmasking of decreased myocardial contractility by mitral valve replacement, with ejection of the total stroke volume into the high impedance of the aorta (afterload mismatch produced by operation).(ABSTRACT TRUNCATED AT 400 WORDS)

Amiodarone. Haemodynamic profile during intravenous administration and effect on pacing-induced ischaemia in man.

PubMed

Remme, W J; van Hoogenhuyze, D C; Kruyssen, D A; Krauss, X H; Storm, C J

1985-03-01

The haemodynamic changes during intravenous amiodarone administration in laboratory animals and human studies are reviewed and compared with the results from our investigations. While the results of previous human studies have been rather variable, our investigations suggest that the cardiovascular changes following intravenous amiodarone include an early and usually short reduction of systemic and coronary vascular resistance, which may be partially due to the vasodilating properties of the solvent, polysorbate 80. As a result, a decrease in afterload and cardiac work and increases in cardiac output and coronary blood flow occur. Contrary to the observations in the animal experiments, heart rate increases in man, presumably as a result of the relatively greater fall in afterload which occurs. However, in spite of this increase in heart rate, contractility is reduced at the end of amiodarone administration and remains depressed after the infusion, resulting in a significant increase in left ventricular filling pressure. Neither myocardial oxygen demand nor consumption change during amiodarone administration. Although the intrinsic negative inotropic effects of amiodarone warrant a cautious approach in patients with left ventricular dysfunction, worsening of heart failure or the occurrence of myocardial ischaemia has been reported in only very few cases so far. In contrast, the drug was demonstrated to protect against pacing-induced myocardial ischaemia, in patients with both normal and depressed left ventricular function. These anti-ischaemic properties of amiodarone were investigated in a second study using a double pacing stress test protocol. Overall myocardial oxygen consumption did not change during pacing after amiodarone, but it clearly reduced (regional) myocardial ischaemia, as demonstrated by a reduction of ST-segment changes and anginal pain, and in particular by the absence of myocardial lactate production during pacing after amiodarone. These anti-ischaemic properties are mainly based on a reduction of myocardial oxygen demand, rather than on an improvement in coronary flow. It is concluded then, that amiodarone has significant haemodynamic effects as manifested by an early reduction in vascular resistance and a late negative inotropic effect. Although vasodilatation of short duration caused by its solvent, polysorbate 80, also occurs, the overall cardiovascular changes are caused by the direct, intrinsic haemodynamic effects of amiodarone alone. The important anti-ischaemic properties of amiodarone appear to result primarily from these cardiovascular actions and the inherent reduction in myocardial oxygen demand.

Comorbid depression and anxiety symptoms as predictors of cardiovascular events: results from the NHLBI-sponsored Women's Ischemia Syndrome Evaluation (WISE) study.

PubMed

Rutledge, Thomas; Linke, Sarah E; Krantz, David S; Johnson, B Delia; Bittner, Vera; Eastwood, Jo-Ann; Eteiba, Wafia; Pepine, Carl J; Vaccarino, Viola; Francis, Jennifer; Vido, Diane A; Merz, C Noel Bairey

2009-11-01

To study the independent and interactive effects of depression and anxiety symptoms as predictors of cardiovascular disease (CVD) events in a sample of women with suspected myocardial ischemia. Symptoms of depression and anxiety overlap strongly and are independent predictors of CVD events. Although these symptoms commonly co-occur in medical patients, little is known about combined effects of depression and anxiety on CVD risk. A total of 489 women completed a baseline protocol including coronary angiogram, CVD risk factor assessment, and questionnaire-based measures of depression and anxiety symptoms, using the Beck Depression Inventory (BDI) and State Trait Anxiety Inventory (STAI), respectively. Participants were followed for a median 5.9 years to track the prevalence of CVD events (stroke, myocardial infarction, heart failure, and CVD-related mortality). We tested the BDI x STAI interaction effect in addition to the BDI and STAI main effects. Seventy-five women (15.3% of sample) experienced a CVD event, of which 18 were deaths attributed to cardiovascular causes. Results using Cox regression indicated a significant BDI x STAI interaction effect in the prediction of CVD events (p = .02) after covariate adjustment. Simple effect analyses indicated that depression scores were significant predictors of CVD events among women with low anxiety scores (hazard ratio [HR] = 2.3 [in standard deviation units]; 95% Confidence Interval [CI] = 1.3-3.9; p = .005) but not among women with higher levels of anxiety (HR = 0.99; 95% CI = 0.70-1.4; p = .95). Among women with suspected myocardial ischemia, the value of depression symptoms for predicting CVD events varied by the severity of comorbid anxiety. These results suggest that the clinical utility of depression measures may be improved by using them in combination with measures of anxiety.

[Evaluation of myocardial ischemia using Holter monitoring].

PubMed

Kodama, Y

1995-07-01

To establish the diagnostic criteria for myocardial ischemia, Holter monitoring and coronary angiography were performed on 46 cases (24 males (51.8 +/- 9.3 years), 22 females (47.5 +/- 10.5 years)). These patients were retrospectively selected from about 12000 patients who had the Holter monitorings from 1980 to 1993. The criteria for the entry were 1) reliable trend recordings of heart rate and 2) reliable recording of ST trend with accurate 1 mV calibration. The coronary stenosis greater than 75% in diameter was considered to be significant. Results were as follows: 1) ST trend pattern was classified into typical type, atypical type and box type. There were no significant differences in the incidence of typical and atypical types between ischemic and nonischemic groups, 2) Diagnostic accuracy of the criteria for myocardial ischemia, that is, the horizontal or downsloping ST segment depression with 0.1 mV at the point of 80 msec from the J point lasting for 1 minute, was higher in male than in female: the sensitivity was 93.3% and the specificity was 55.6% for men respectively, whereas the sensitivity was 66.7% and the specificity was 37.5% for women respectively, 3) Diagnostic accuracy of the ST/Heart rate ratio was 80.0% for the sensitivity and 64.7% for the specificity, indicating an improvement of specificity, 4) Maximal ST segment depression was accompanied by pain by 88.8% in true positive group (significant ST segment depression with significant coronary stenosis), whereas that was 28.6% in false positive group (significant ST segment depression without significant coronary stenosis), 5) Comparison of the degree of maximal ST segment depression, duration and frequency between computer and manual measurement showed a good correlation for the degree of maximal ST segment depression, whereas the duration and the frequency showed no significant correlations. The above results suggest that combined evaluation of the ST segment depression criteria (downsloping or horizontal ST segment depression greater than 1 mm at the point of 80 msec from the J point) and the ST/Heart rate criteria (1.4 microV/beats/min) is useful for the diagnosis of myocardial ischemia using Holter monitoring.

Complete regression of myocardial involvement associated with lymphoma following chemotherapy.

PubMed

Vinicki, Juan Pablo; Cianciulli, Tomás F; Farace, Gustavo A; Saccheri, María C; Lax, Jorge A; Kazelian, Lucía R; Wachs, Adolfo

2013-09-26

Cardiac involvement as an initial presentation of malignant lymphoma is a rare occurrence. We describe the case of a 26 year old man who had initially been diagnosed with myocardial infiltration on an echocardiogram, presenting with a testicular mass and unilateral peripheral facial paralysis. On admission, electrocardiograms (ECG) revealed negative T-waves in all leads and ST-segment elevation in the inferior leads. On two-dimensional echocardiography, there was infiltration of the pericardium with mild effusion, infiltrative thickening of the aortic walls, both atria and the interatrial septum and a mildly depressed systolic function of both ventricles. An axillary biopsy was performed and reported as a T-cell lymphoblastic lymphoma (T-LBL). Following the diagnosis and staging, chemotherapy was started. Twenty-two days after finishing the first cycle of chemotherapy, the ECG showed regression of T-wave changes in all leads and normalization of the ST-segment elevation in the inferior leads. A follow-up Two-dimensional echocardiography confirmed regression of the myocardial infiltration. This case report illustrates a lymphoma presenting with testicular mass, unilateral peripheral facial paralysis and myocardial involvement, and demonstrates that regression of infiltration can be achieved by intensive chemotherapy treatment. To our knowledge, there are no reported cases of T-LBL presenting as a testicular mass and unilateral peripheral facial paralysis, with complete regression of myocardial involvement.

Depressive Symptoms Effect on Self Care Behavior During the First Month After Myocardial Infarction

PubMed Central

Niakan, Maryam; Paryad, Ezzat; Leili, Ehsan Kazemnezhad; Sheikholeslami, Farzane

2015-01-01

Aim: To determine the effect of severity of depression symptoms on self care behavior in 15th and 30th day after myocardial infarction (MI). Materials and Methods: Gathering data for this cross sectional study was done by Beck depression and self care behavior questionnaires in a heart especial hospital in Rasht in north of Iran. Sample size was 132 after MI patients and data collected from June 2011 to January 2012. Results: Scores of depression symptoms in 15th and 30th day after MI and score of self care behavior in these days had significant difference (P<0.0001). Spearman test showed self care behavior had significant relationship with depression symptoms (P<0.0001). GEE model also showed with control of socio demographic and illness related factors, depression symptoms can decrease self care behavior scores (P<0.001). Conclusion: Severity of depression symptoms increase in 15th to 30th day after MI. This issue can affect on self care behavior. This issue is emphasized on nurses’ notice to plan suitable self care program for these patients. PMID:25946944

Depressive symptoms effect on self care behavior during the first month after myocardial infarction.

PubMed

Niakan, Maryam; Paryad, Ezzat; Kazemnezhad Leili, Ehsan; Sheikholeslami, Farzane

2015-01-26

To determine the effect of severity of depression symptoms on self care behavior in 15th and 30th day after myocardial infarction (MI). Gathering data for this cross sectional study was done by Beck depression and self care behavior questionnaires in a heart especial hospital in Rasht in north of Iran .Sample size was 132 after MI patients and data collected from June 2011 to January 2012. Scores of depression symptoms in 15th and 30th day after MI and score of self care behavior in these days had significant difference (P<0.0001) .Spearman test showed self care behavior had significant relationship with depression symptoms (P<0.0001). GEE model also showed with control of socio demographic and illness related factors, depression symptoms can decrease self care behavior scores (P<0.001). Severity of depression symptoms increase in 15th to 30th day after MI .This issue can affect on self care behavior. This issue is emphasized on nurses' notice to plan suitable self care program for these patients.

Human Myocardium Releases Heat Shock Protein 27 (HSP27) after Global Ischemia: The Proinflammatory Effect of Extracellular HSP27 through Toll-like Receptor (TLR)-2 and TLR4

PubMed Central

Jin, Chunhua; Cleveland, Joseph C; Ao, Lihua; Li, Jilin; Zeng, Qingchun; Fullerton, David A; Meng, Xianzhong

2014-01-01

The myocardial inflammatory response contributes to cardiac functional injury associated with heart surgery obligating global ischemia/reperfusion (I/R). Toll-like receptors (TLRs) play an important role in the mechanism underlying myocardial I/R injury. The aim of this study was to examine the release of small constitutive heat shock proteins (HSPs) from human and mouse myocardium after global ischemia and examine the role of extracellular small HSP in myocardial injury. HSP27 release was assessed by enzyme-linked immunosorbent assay. Anti-HSP27 was applied to evaluate the role of extracellular HSP27 in the postischemic inflammatory response and functional injury in mouse hearts. Isolated hearts and cultured coronary vascular endothelial cells were exposed to recombinant HSP27 to determine its effect on proinflammatory signaling and production of proinflammatory mediators. HSP27 levels were markedly elevated in coronary sinus blood of patients and in coronary effluent of mouse hearts after global ischemia. Neutralizing extracellular HSP27 suppressed myocardial nuclear factor (NF)-κB activation and interleukin (IL)-6 production and improved cardiac function in mouse hearts. Perfusion of HSP27 to mouse hearts induced NF-κB activation and IL-6 production and depressed contractility. Further, recombinant HSP27 induced NF-κB phosphorylation and upregulated monocyte chemoattractant protein (MCP)-1 and intercellular adhesion molecule (ICAM)-1 production in both human and mouse coronary vascular endothelial cells. TLR2 knockout (KO) or TLR4 mutation abolished NF-κB phosphorylation and reduced MCP-1 and ICAM-1 production induced by extracellular HSP27 in endothelial cells. In conclusion, these results show that the myocardium releases HSP27 after global ischemia and that extracellular HSP27 is proinflammatory and contributes to the inflammatory mechanism of myocardial functional injury. Both TLR2 and TLR4 are involved in mediating the proinflammatory effect of extracellular HSP27. PMID:24918749

Human myocardium releases heat shock protein 27 (HSP27) after global ischemia: the proinflammatory effect of extracellular HSP27 through toll-like receptor (TLR)-2 and TLR4.

PubMed

Jin, Chunhua; Cleveland, Joseph C; Ao, Lihua; Li, Jilin; Zeng, Qingchun; Fullerton, David A; Meng, Xianzhong

2014-06-09

The myocardial inflammatory response contributes to cardiac functional injury associated with heart surgery obligating global ischemia/reperfusion (I/R). Toll-like receptors (TLRs) play an important role in the mechanism underlying myocardial I/R injury. The aim of this study was to examine the release of small constitutive heat shock proteins (HSPs) from human and mouse myocardium after global ischemia and examine the role of extracellular small HSP in myocardial injury. HSP27 release was assessed by enzyme-linked immunosorbent assay. Anti-HSP27 was applied to evaluate the role of extracellular HSP27 in the postischemic inflammatory response and functional injury in mouse hearts. Isolated hearts and cultured coronary vascular endothelial cells were exposed to recombinant HSP27 to determine its effect on proinflammatory signaling and production of proinflammatory mediators. HSP27 levels were markedly elevated in coronary sinus blood of patients and in coronary effluent of mouse hearts after global ischemia. Neutralizing extracellular HSP27 suppressed myocardial nuclear factor (NF)-κB activation and interleukin (IL)-6 production and improved cardiac function in mouse hearts. Perfusion of HSP27 to mouse hearts induced NF-κB activation and IL-6 production and depressed contractility. Further, recombinant HSP27 induced NF-κB phosphorylation and upregulated monocyte chemoattractant protein (MCP)-1 and intercellular adhesion molecule (ICAM)-1 production in both human and mouse coronary vascular endothelial cells. TLR2 knockout (KO) or TLR4 mutation abolished NF-κB phosphorylation and reduced MCP-1 and ICAM-1 production induced by extracellular HSP27 in endothelial cells. In conclusion, these results show that the myocardium releases HSP27 after global ischemia and that extracellular HSP27 is proinflammatory and contributes to the inflammatory mechanism of myocardial functional injury. Both TLR2 and TLR4 are involved in mediating the proinflammatory effect of extracellular HSP27.

Correlation of symptom depression levels with mean platelet volume rate on patients of acute coronary syndrome

NASA Astrophysics Data System (ADS)

Hasugian, L.; Hanum, H.; Hanida, W.; Safri, Z.

2018-03-01

Patients with Depression and the acute coronary syndrome (ACS) is rarely detected, although in some studies say that depression can worsen cardiovascularly and increase mortality. From research, Canan F et al found that increasing levels of Mean platelet volume (MPV) as a risk factor for atherosclerosis and MPV was higher in patients with depression compared with patients without depression. In this study used observational methods of measurement of cross-sectional data. Research began in November 2015 - May 2016 against General Hospital inpatients H. Adam Malik Medan. There are 64 patients with a diagnosis of ACS were given quieter Beck Depression Inventory (BDI), then calculated a score of BDI patients and MPV levels were seen when they first entered the hospital before being given treatment. Patients answered quieter on days 3-7 after diagnosis ACS. ACS Patients were divided into 3 groups: acute myocardial infarction with ST elevation, acute myocardial infarction with non-ST elevation and unstable angina pectoris. The level of depression is grouped into not depression, mild depression, moderate depression and severe depression. Statistically significant with p-value<0.05Based on the linear correlation analysis, it was found a positive correlation with r=0.542. And the relationship is statistically significant with p-value 0.000003.

US Army Institute of Surgical Research Annual Research Progress Report for Fiscal Year 1986

DTIC Science & Technology

1987-10-01

Acute myocardial infarctions were seen in four patients and acute pulmonary emboli in four patients. Inhalation injury was identified in 76 patients (38.6...had inhalation injury as a primary or contributing cause of death. Three patients died with acute myocardial infarctions , one with acute phenol...may have been made in patients with complications (sepsis, hypotension, myocardial infarction , aminoglycoside antibiotic therapy, etc.) which depress

Changes in left ventricular function as determined by the multi-wire gamma camera at near presyncopal levels of lower body negative pressure

NASA Technical Reports Server (NTRS)

Pintner, R.; Fortney, S.; Mulvagh, S.; Lacy, J.

1992-01-01

At presyncopal levels of lower body negative pressure (LBNP), we have frequently observed electrocardiographic responses that may be due to changes in cardiac position and/or shape, but could be indicative of altered myocardial function. To further investigate this, we evaluated cardiac function using a nuclear imaging technique in 21 healthy subjects (17 men and 4 women) after 30 minutes of supine rest and near the end of a presyncopal-limited LBNP exposure (LBNP averaged 65 plus or minus 3 mmHg at injection). Cardiac first pass images were obtained with a Multi-Wire Gamma Camera following an intravenous bolus injection of 30-50 millicurries of Tantalum-178. Manual blood pressures and electrocardiograms were obtained throughout the 3 minute graded LBNP protocol. Between rest and injection during LBNP, heart rate increased (P less than 0.01) from 67 plus or minus 3 beats per minute to 99 plus or minus beats per minute, systolic blood pressure decreased (P less than 0.01) from 110 plus or minus 3 mmHg to 107 plus or minus 3 mmHg and left ventricular ejection fraction (EF) decreased (P less than 0.01) from 0.57 plus or minus 0.02 to 0.48 plus or minus 0.02. During LBNP, ST segment depression of at least 0.5 mm occurred in 7 subjects. Subjects with ST depression had greater reductions (P = 0.05) in EF than subjects without ST depression (0.15 plus or minus 0.07 versus 0.005 plus or minus 0.03), but also tolerated greater levels (P less than 0.05) of negative pressure (88 plus or minus mmHg versus 69 plus or minus 5 mmHg). There was a significant relationship between presyncopal LBNP level and EF (R(exp 2) = 0.50, P less than 0.05). Our findings suggest there may be a decrease in systolic myocardial function at high levels of LBNP.

Pets, depression and long term survival in community living patients following myocardial infarction

PubMed Central

Friedmann, Erika; Thomas, Sue A.; Son, Heesook

2011-01-01

Evidence supports the contribution of depression, anxiety, and poor social support to mortality of hospitalized myocardial infarction (MI) patients. The contribution of depression to survival is independent of disease severity. Pet ownership, a non-human form of social support, has also been associated with one year survival of post-MI patients. The current study addresses whether pet ownership contributes independently to long term survival beyond the contributions of depression, anxiety, or low social support in post-MI patients who have already survived at least 6 months. Data from patients (N = 460) enrolled in the “Psychosocial Responses in the Home Automated External Defibrillator Trial (PR-HAT)”were used. Seventeen patients died during a median follow-up of 2.8 years. In Cox proportional hazards regression model that included depression, lack of pet ownership, and the interaction between depression and lack of pet ownership, not owning a pet was the only significant independent predictor of mortality (p = 0.036). The interaction between pet ownership and depression tended to be significant indicating that the effect of pet ownership on survival in this group of people who have supportive spouses/companions living with them may relate to depression. PMID:21857770

Psychobiology of depression/distress in congestive heart failure

PubMed Central

Hassan, Mustafa; Sheps, David S.

2011-01-01

Heart failure affects millions of Americans and new diagnosis rates are expected to almost triple over the next 30 years as our population ages. Affective disorders including clinical depression and anxiety are common in patients with congestive heart failure. Furthermore, the presence of these disorders significantly impacts quality of life, medical outcomes, and healthcare service utilization. In recent years, the literature has attempted to describe potential pathophysiologic mechanisms relating affective disorders and psychosocial stress to heart failure. Several potential mechanisms have been proposed including autonomic nervous system dysfunction, inflammation, cardiac arrhythmias, and altered platelet function. These mechanisms are reviewed in this article. Additional novel mechanisms such as mental stress-induced myocardial ischemia are also discussed. PMID:18368481

Electroconvulsive therapy for depression following acute coronary syndromes: a concern for the anesthesiologist.

PubMed

Pourafkari, Nosratollah; Pourafkari, Leili; Nader, Nader D

2016-06-01

The prevalence of depression in patients with cardiovascular disease is higher than general population and especially following an acute coronary syndrome (ACS), a significant number of patients report a wide spectrum of behavioral and mood changes attributable to clinical depression. Treatment of depression following ACS event is particularly challenging since most of the therapeutic modalities are associated with increasing the systemic sympathetic tone from neurogenic or pharmacologic sources. Increased activity of the adrenergic and catecholamine activity may further deter the myocardial oxygen supply and demand therefore treating depression should be carefully evaluated for its risk benefit ratio. Electroconvulsive therapy (ECT) is recommended for patients with severe depression, in whom behavioral and pharmacologic treatments have failed. Patients who refuse to take medications or present with any psychological emergency such as harming self or others, are also candidates for ECT. ECT is also associated with sudden surges of catecholamines and may cause recurrent myocardial ischemia and fatal dysrhythmias in patients convalescing from an ACS event. Herein, we provide an overview and practical guidelines for management of patients presented for ECT following ACS. Published by Elsevier Inc.

Depressive symptoms and mental stress-induced myocardial ischemia in patients with coronary heart disease.

PubMed

Boyle, Stephen H; Samad, Zainab; Becker, Richard C; Williams, Redford; Kuhn, Cynthia; Ortel, Thomas L; Kuchibhatla, Maragatha; Prybol, Kevin; Rogers, Joseph; O'Connor, Christopher; Velazquez, Eric J; Jiang, Wei

2013-01-01

The aim of this study was to examine the associations between depressive symptoms and mental stress-induced myocardial ischemia (MSIMI) in patients with coronary heart disease (CHD). Adult patients with documented CHD were recruited for baseline mental stress and exercise stress screening testing as a part of the enrollment process of the Responses of Myocardial Ischemia to Escitalopram Treatment trial. Patients were administered the Beck Depression Inventory II and the Center for Epidemiologic Studies Depression Scale. After a 24-48-hour β-blocker withdrawal, participants completed three mental stress tests followed by a treadmill exercise test. Ischemia was defined as a) any development or worsening of any wall motion abnormality and b) reduction of left ventricular ejection fraction at least 8% by transthoracic echocardiography and/or ischemic ST-segment change by electrocardiography during stress testing. MSIMI was considered present when ischemia occurred in at least one mental test. Data were analyzed using logistic regression adjusting for age, sex, and resting left ventricular ejection fraction. One hundred twenty-five (44.2%) of 283 patients were found to have MSIMI, and 93 (32.9%) had ESIMI. Unadjusted analysis showed that Beck Depression Inventory II scores were positively associated with the probability of MSIMI (odds ratio = 0.1.30: 95% confidence interval = 1.06-1.60, p = .013) and number of MSIMI-positive tasks (all p < .005). These associations were still significant after adjustment for covariates (p values <.05). In patients with CHD, depressive symptoms were associated with a higher probability of MSIMI. These observations may enhance our understanding of the mechanisms contributing to the association of depressive symptoms to future cardiovascular events. Trial Registration Clinicaltrials.gov identifier: NCT00574847.

Left ventricular eccentricity index measured with SPECT myocardial perfusion imaging: An additional parameter of adverse cardiac remodeling.

PubMed

Gimelli, Alessia; Liga, Riccardo; Clemente, Alberto; Marras, Gavino; Kusch, Annette; Marzullo, Paolo

2017-01-12

Single-photon emission computed-tomography (SPECT) allows the quantification of LV eccentricity index (EI), a measure of cardiac remodeling. We sought to evaluate the feasibility of EI measurement with SPECT myocardial perfusion imaging and its interactions with relevant LV functional and structural parameters. Four-hundred and fifty-six patients underwent myocardial perfusion imaging on a Cadmium-Zinc-Telluride (CZT) camera. The summed rest, stress, and difference scores were calculated. From rest images, the LV end-diastolic (EDV) and end-systolic volumes, ejection fraction (EF), and peak filling rate (PFR) were calculated. In every patient, the EI, ranging from 0 (sphere) to 1 (line), was computed using a dedicated software (QGS/QPS; Cedars-Sinai Medical Center). Three-hundred and thirty-eight/456 (74%) patients showed a normal EF (>50%), while 26% had LV systolic dysfunction. The EI was computed from CZT images with excellent reproducibility (interclass correlation coefficient: 0.99, 95% CI 0.98-0.99). More impaired EI values correlated with the presence of a more abnormal LV perfusion (P < .001), function (EF and PFR, P < .001), and structure (EDV, P < .001). On multivariate analysis, higher EDV (P < .001) and depressed EF (P = .014) values were independent predictors of abnormal EI. The evaluation of LV eccentricity is feasible on gated CZT images. Abnormal EI associates with significant cardiac structural and functional abnormalities.

Renal impairment and heart failure with preserved ejection fraction early post-myocardial infarction

PubMed Central

Jorapur, Vinod; Lamas, Gervasio A; Sadowski, Zygmunt P; Reynolds, Harmony R; Carvalho, Antonio C; Buller, Christopher E; Rankin, James M; Renkin, Jean; Steg, Philippe Gabriel; White, Harvey D; Vozzi, Carlos; Balcells, Eduardo; Ragosta, Michael; Martin, C Edwin; Srinivas, Vankeepuram S; Wharton III, William W; Abramsky, Staci; Mon, Ana C; Kronsberg, Shari S; Hochman, Judith S

2010-01-01

AIM: To study if impaired renal function is associated with increased risk of peri-infarct heart failure (HF) in patients with preserved ejection fraction (EF). METHODS: Patients with occluded infarct-related arteries (IRAs) between 1 to 28 d after myocardial infarction (MI) were grouped into chronic kidney disease (CKD) stages based on estimated glomerular filtration rate (eGFR). Rates of early post-MI HF were compared among eGFR groups. Logistic regression was used to explore independent predictors of HF. RESULTS: Reduced eGFR was present in 71.1% of 2160 patients, with significant renal impairment (eGFR < 60 mL/min every 1.73 m2) in 14.8%. The prevalence of HF was higher with worsening renal function: 15.5%, 17.8% and 29.4% in patients with CKD stages 1, 2 and 3 or 4, respectively (P < 0.0001), despite a small absolute difference in mean EF across eGFR groups: 48.2 ± 10.0, 47.9 ± 11.3 and 46.2 ± 12.1, respectively (P = 0.02). The prevalence of HF was again higher with worsening renal function among patients with preserved EF: 10.1%, 13.6% and 23.6% (P < 0.0001), but this relationship was not significant among patients with depressed EF: 27.1%, 26.2% and 37.9% (P = 0.071). Moreover, eGFR was an independent correlate of HF in patients with preserved EF (P = 0.003) but not in patients with depressed EF (P = 0.181). CONCLUSION: A significant proportion of post-MI patients with occluded IRAs have impaired renal function. Impaired renal function was associated with an increased rate of early post-MI HF, the association being strongest in patients with preserved EF. These findings have implications for management of peri-infarct HF. PMID:20885993

Complete regression of myocardial involvement associated with lymphoma following chemotherapy

PubMed Central

Vinicki, Juan Pablo; Cianciulli, Tomás F; Farace, Gustavo A; Saccheri, María C; Lax, Jorge A; Kazelian, Lucía R; Wachs, Adolfo

2013-01-01

Cardiac involvement as an initial presentation of malignant lymphoma is a rare occurrence. We describe the case of a 26 year old man who had initially been diagnosed with myocardial infiltration on an echocardiogram, presenting with a testicular mass and unilateral peripheral facial paralysis. On admission, electrocardiograms (ECG) revealed negative T-waves in all leads and ST-segment elevation in the inferior leads. On two-dimensional echocardiography, there was infiltration of the pericardium with mild effusion, infiltrative thickening of the aortic walls, both atria and the interatrial septum and a mildly depressed systolic function of both ventricles. An axillary biopsy was performed and reported as a T-cell lymphoblastic lymphoma (T-LBL). Following the diagnosis and staging, chemotherapy was started. Twenty-two days after finishing the first cycle of chemotherapy, the ECG showed regression of T-wave changes in all leads and normalization of the ST-segment elevation in the inferior leads. A follow-up Two-dimensional echocardiography confirmed regression of the myocardial infiltration. This case report illustrates a lymphoma presenting with testicular mass, unilateral peripheral facial paralysis and myocardial involvement, and demonstrates that regression of infiltration can be achieved by intensive chemotherapy treatment. To our knowledge, there are no reported cases of T-LBL presenting as a testicular mass and unilateral peripheral facial paralysis, with complete regression of myocardial involvement. PMID:24109501

Physical function and independence 1 year after myocardial infarction: observations from the Translational Research Investigating Underlying disparities in recovery from acute Myocardial infarction: Patients' Health status registry.

PubMed

Dodson, John A; Arnold, Suzanne V; Reid, Kimberly J; Gill, Thomas M; Rich, Michael W; Masoudi, Frederick A; Spertus, John A; Krumholz, Harlan M; Alexander, Karen P

2012-05-01

Acute myocardial infarction (AMI) may contribute to health status declines including "independence loss" and "physical function decline." Despite the importance of these outcomes for prognosis and quality of life, their incidence and predictors have not been well described. We studied 2,002 patients with AMI enrolled across 24 sites in the TRIUMPH registry who completed assessments of independence and physical function at the time of AMI and 1 year later. Independence was evaluated by the EuroQol-5D (mobility, self-care, and usual activities), and physical function was assessed with the Short Form-12 physical component score. Declines in ≥1 level on EuroQol-5D and >5 points in PCS were considered clinically significant changes. Hierarchical, multivariable, modified Poisson regression models accounting for within-site variability were used to identify predictors of independence loss and physical function decline. One-year post AMI, 43.0% of patients experienced health status declines: 12.8% independence loss alone, 15.2% physical function decline alone, and 15.0% both. After adjustment, variables that predicted independence loss included female sex, nonwhite race, unmarried status, uninsured status, end-stage renal disease, and depression. Variables that predicted physical function decline were uninsured status, lack of cardiac rehabilitation referral, and absence of pre-AMI angina. Age was not predictive of either outcome after adjustment. >40% of patients experience independence loss or physical function decline 1 year after AMI. These changes are distinct but can occur simultaneously. Although some risk factors are not modifiable, others suggest potential targets for strategies to preserve patients' health status. Copyright © 2012 Mosby, Inc. All rights reserved.

Depression and Anxiety Screens as Predictors of 8-Year Incidence of Myocardial Infarction and Stroke in Primary Care Patients.

PubMed

Stewart, Jesse C; Hawkins, Misty A W; Khambaty, Tasneem; Perkins, Anthony J; Callahan, Christopher M

2016-06-01

Because depression and anxiety are typically studied in isolation, our purpose was to examine the relative importance of these overlapping emotional factors in predicting incident cardiovascular disease (CVD). We examined depression and anxiety screens, and their individual items, as predictors of incident hard CVD events, myocardial infarction, and stroke for 8 years in a diverse sample of 2041 older primary care patients initially free of CVD. At baseline, participants completed self-report depression and anxiety screens. Data regarding CVD events were obtained from an electronic medical record system and the Centers for Medicare and Medicaid Services analytic files. During follow-up, 683 (33%) experienced a CVD event. Cox proportional hazards models-adjusted for demographic and CVD risk factors-revealed that a positive anxiety screen, but not a positive depression screen, was associated with an increased risk of a hard CVD event in separate models (Years 0-3: anxiety hazard ratio [HR] = 1.54, 95% confidence interval [CI] = 1.21-1.96, p < .001; Years 3+: anxiety HR = 0.99, CI = 0.81-1.21), p = .93; depression HR = 1.10, CI = 0.88-1.36, p = .41), as well as when entered into the same model (Years 0-3: anxiety HR = 1.53, CI = 1.20-1.95, p < .001; Years 3+: anxiety HR = 0.99, CI = 0.80-1.21, p = .99; depression HR = 1.03, CI = 0.82-1.29, p = .82). Analyses examining individual items and secondary outcomes showed that the anxiety-CVD association was largely driven by the feeling anxious item and the myocardial infarction outcome. Anxiety, especially feeling anxious, is a unique risk factor for CVD events in older adults, independent of conventional risk factors and depression. Anxiety deserves increased attention as a potential factor relevant to CVD risk stratification and a potential target of CVD primary prevention efforts.

Effect of free fatty acids on myocardial function and metabolism in the ischemic dog heart

PubMed Central

Kjekshus, John K.; Mjøs, Ole D.

1972-01-01

Since elevation of plasma concentrations of free fatty acids (FFA) increases myocardial oxygen consumption without influencing mechanical performance in normal hearts, it was the purpose of this study to determine whether FFA would modify mechanical performance at limited oxygen supply. Left coronary blood flow was reduced by gradual clamping of a shunt from the left carotid artery until moderate ventricular dilatation supervened. Left ventricular systolic pressure (LVSP), its maximal rate of rise (dP/dt) and stroke volume (SV) were unchanged or slightly reduced. The ischemia resulted in a decrease in myocardial oxygen consumption (MVO2) from 9.7±1.1 ml/min to 7.9±0.8 ml/min, and myocardial lactate uptake was reduced or reversed to excretion. Increasing the plasma concentrations of FFA from 359±47 μEq/1 to 3688±520 μEq/1 by intravenous infusion of a triglyceride emulsion and heparin resulted in further ventricular dilatation, accompanied by increased excretion of lactate. The ventricular decompensation and enhancement of anaerobic myocardial metabolism associated with increased uptake of FFA was not related to changes in coronary flow, MVO2, or LVSP. dP/dt and SV were virtually unchanged. Intravenous infusion of glucose/insulin, which lowered plasma concentrations of FFA, reversed ventricular dilatation and lactate excretion. The data support the hypothesis that high concentrations of FFA play a significant role in increasing myocardial oxygen requirement and thereby promote depression of contractility of the hypoxic heart in experimental animals. Images PMID:5032525

Association of Coexisting Diabetes and Depression With Mortality After Myocardial Infarction

PubMed Central

Bot, Mariska; Pouwer, François; Zuidersma, Marij; van Melle, Joost P.; de Jonge, Peter

2012-01-01

OBJECTIVE Diabetes and depression are both linked to an increased mortality risk after myocardial infarction (MI). Population-based studies suggest that having both diabetes and depression results in an increased mortality risk, beyond that of having diabetes or depression alone. The purpose of this study was to examine the joint association of diabetes and depression with mortality in MI patients. RESEARCH DESIGN AND METHODS Data were derived from two multicenter cohort studies in the Netherlands, comprising 2,704 patients who were hospitalized for MI. Depression, defined as a Beck Depression Inventory score ≥10, and diabetes were assessed during hospitalization. Mortality data were retrieved for 2,525 patients (93%). RESULTS During an average follow-up of 6.2 years, 439 patients died. The mortality rate was 14% (226 of 1,673) in patients without diabetes and depression, 23% (49 of 210) in patients with diabetes only, 22% (118 of 544) in patients with depression only, and 47% (46 of 98) in patients with both diabetes and depression. After adjustment for age, sex, smoking, hypertension, left ventricular ejection fraction, prior MI, and Killip class, hazard ratios for all-cause mortality were 1.38 (95% CI 1.00–1.90) for patients with diabetes only, 1.39 (1.10–1.76) for patients with depression only, and as much as 2.90 (2.07–4.07) for patients with both diabetes and depression. CONCLUSIONS We observed an increased mortality risk in post-MI patients with both diabetes and depression, beyond the association with mortality of diabetes and depression alone. PMID:22301118

The Influence of Depression on Utilization of Cardiac Rehabilitation Post-Myocardial Infarction: A Study of 158,991 Medicare Beneficiaries

PubMed Central

Zullo, Melissa D.; Gathright, Emily C.; Dolansky, Mary A.; Josephson, Richard A.; Cheruvu, Vinay K.; Hughes, Joel W.

2016-01-01

Purpose On the basis of several small studies, depression is often considered a barrier to CR enrollment and program completion. The purpose of this research was to examine the association between depression diagnosis and participation in CR in a large sample of Medicare beneficiaries with recent myocardial infarction (MI). Methods This was a retrospective study of Medicare Beneficiaries with an MI during 2008 (n=158,991). CR enrollment was determined by the Carrier and Outpatient files using the Healthcare Common Procedure Coding System #93797 or #93798. Depression diagnosis was obtained from the ICD-9 codes in the MEDPAR, Outpatient, and Carrier Files. The association between depression diagnosis and CR attendance was evaluated using multivariable logistic regression. Results Overall, 14% (n=22,735) of the study population attended CR within 1 year of MI diagnosis. Twenty-eight percent (n=43,827) had a diagnosis of depression with 96% of cases documented prior to enrollment in CR. Twenty-eight percent with a diagnosis of depression compared to 9% without depression attended CR. In adjusted analysis, patients with depression were 3.9 (99% confidence interval: 3.7, 4.2) times more likely to attend CR compared to those without depression. Program completion (≥ 25 sessions) was more common in those with depression (56%) than those without (35%; p < 0.001). Conclusions Diagnosis of depression in Medicare Beneficiaries was strongly associated with attending CR and attending more sessions of CR compared to those without depression. Depression is not a barrier to CR participation after MI in Medicare Beneficiaries. PMID:27755259

Reversal of subcellular remodelling by losartan in heart failure due to myocardial infarction

PubMed Central

Babick, Andrea; Chapman, Donald; Zieroth, Shelley; Elimban, Vijayan; Dhalla, Naranjan S

2012-01-01

This study tested the reversal of subcellular remodelling in heart failure due to myocardial infarction (MI) upon treatment with losartan, an angiotensin II receptor antagonist. Twelve weeks after inducing MI, rats were treated with or without losartan (20 mg/kg; daily) for 8 weeks and assessed for cardiac function, cardiac remodelling, subcellular alterations and plasma catecholamines. Cardiac hypertrophy and lung congestion in 20 weeks MI-induced heart failure were associated with increases in plasma catecholamine levels. Haemodynamic examination revealed depressed cardiac function, whereas echocardiographic analysis showed impaired cardiac performance and marked increases in left ventricle wall thickness and chamber dilatation at 20 weeks of inducing MI. These changes in cardiac function, cardiac remodelling and plasma dopamine levels in heart failure were partially or fully reversed by losartan. Sarcoplasmic reticular (SR) Ca2+-pump activity and protein expression, protein and gene expression for phospholamban, as well as myofibrillar (MF) Ca2+-stimulated ATPase activity and α-myosin heavy chain mRNA levels were depressed, whereas β-myosin heavy chain expression was increased in failing hearts; these alterations were partially reversed by losartan. Although SR Ca2+-release activity and mRNA levels for SR Ca2+-pump were decreased in failing heart, these changes were not reversed upon losartan treatment; no changes in mRNA levels for SR Ca2+-release channels were observed in untreated or treated heart failure. These results suggest that the partial improvement of cardiac performance in heart failure due to MI by losartan treatment is associated with partial reversal of cardiac remodelling as well as partial recovery of SR and MF functions. PMID:22947202

Anisotropic Reinforcement of Acute Anteroapical Infarcts Improves Pump Function

PubMed Central

Fomovsky, Gregory M.; Clark, Samantha A.; Parker, Katherine M.; Ailawadi, Gorav; Holmes, Jeffrey W.

2012-01-01

Background We hypothesize that a therapy that improves LV pump function early after infarction should decrease the need for compensation through sympathetic activation and dilation, thereby reducing the risk of developing heart failure. The mechanical properties of healing myocardial infarcts are an important determinant of left ventricular (LV) function, yet improving function by altering infarct properties has proven unexpectedly difficult. Using a computational model, we recently predicted that stiffening a large anterior infarct anisotropically (in only one direction) would improve LV function, while isotropic stiffening, the focus of previous studies and therapies, would not. The goal of this study was to test the novel strategy of anisotropic infarct reinforcement. Methods and Results We tested the effects of anisotropic infarct reinforcement in 10 open-chest dogs with large anteroapical infarcts that depressed LV pump function. We measured regional mechanics, LV volumes, and cardiac output at a range of preloads at Baseline, 45 minutes after coronary ligation (Ischemia), and 30 minutes later, following surgical reinforcement in the longitudinal direction (Anisotropic). Ischemia shifted the end-systolic pressure-volume relationship (ESPVR) and cardiac output curves rightward, decreasing cardiac output at matched end-diastolic pressure (EDP) by 44%. Anisotropic reinforcement significantly improved systolic function without impairing diastolic function, recovering half the deficit in overall LV function. Conclusions We conclude that anisotropic reinforcement is a promising new approach to improving LV function following a large myocardial infarction. PMID:22665716

Veno-arterial extracorporeal membrane oxygenation for Streptococcus pyogenes toxic shock syndrome in pregnancy.

PubMed

Imaeda, Taro; Nakada, Taka-Aki; Abe, Ryuzo; Tateishi, Yoshihisa; Oda, Shigeto

2016-06-01

Streptococcal toxic shock syndrome (STSS), an invasive Streptococcus pyogenes (Group A streptococcus) infection with hypotension and multiple organ failure, is quite rare in pregnancy but is characterized by rapid disease progression and high fatality rates. We present a case of STSS with infection-induced cardiac dysfunction in a pregnant woman who was treated with veno-arterial extracorporeal membrane oxygenation (VA-ECMO). A 24-year-old multiparous woman in the third trimester had early symptoms of high fever and diarrhea 1 day prior to admission to the hospital emergency department. On admission, she had multiple organ failure including circulatory failure. Due to fetal distress, emergency Cesarean section was carried out and transferred to intensive care units. She had refractory circulatory failure with depressed myocardial contractility with progressive multiple organ failure, despite receiving significant hemodynamic supports including high-dose catecholamine. Thus, VA-ECMO was initiated 18 h after intensive care unit admission. Consequently, ECMO provided extra time to recover from infection and myocardial depression. She was successfully weaned from VA-ECMO on day 7 and was discharged home on day 53. VA-ECMO can be a therapeutic option for refractory circulatory failure with significant myocardial depression in STSS.

Comparative assessment of ECG dynamics in myocardial infarction according to reperfusion therapy approach (primary and facilitated coronary angioplasty) and timing of the procedure.

PubMed

Ryabykina, G V; Sozykin, A V; Dobrovolskaya, S V

2007-07-01

The aim of this study was to compare electrocardiogram (ECG)-12 dynamics depending on the methods of facilitated and primary angioplasty in patients with acute coronary syndrome. The ECG changes in 81 patients - 73 patients with acute myocardial infarction and 8 patients with unstable angina pectoris - were studied. The ECG analysis before reperfusion therapy and after angioplasty included: dynamics of summary elevation (Sigma ST+) and depression (Sigma ST-) of ST segment and changes of summary value of R waves (Sigma R) in 12 leads. The results were estimated with consideration for the length of the period from the beginning of pain syndrome till treatment and topics of the infraction-related artery. According to our data, there was no difference between facilitated and primary transluminal coronary angioplasty in their effect on focal myocardial variation dynamics and the size of peri-infarction zone. A reliable decrease in elevation and depression of ST segment was observed in reperfusion therapy not later than 6 hours after the beginning of pain syndrome. When reperfusion therapy is begun later, dynamics of summary values of ST segment elevation and depression before and after treatment are not reliable.

Smoking Cessation After Acute Myocardial Infarction in Relation to Depression and Personality Factors.

PubMed

Schlyter, Mona; Leosdottir, Margrét; Engström, Gunnar; André-Petersson, Lena; Tydén, Patrik; Östman, Margareta

2016-04-01

Smoking is an important cardiovascular risk factor and smoking cessation should be a primary target in secondary prevention after a myocardial infarction (MI). The purpose of this study was to examine whether personality, coping and depression were related to smoking cessation after an MI. MI patients ≤70 years (n = 323, 73 % men, 58.7 ± 8.3 years), participating in the Secondary Prevention and Compliance following Acute Myocardial Infarction study in Malmö, Sweden, between 2002 and 2005, were interviewed by a psychologist to assess coping strategies and completed Beck Depression and NEO Personality Inventories, in close proximity to the acute event. Correlation between smoking status (current, former and never), personality factors, coping and depression was assessed at baseline and 24 months after the MI using logistic regression and in a multivariate analysis, adjusting for age and sex. Of the participating patients, 46 % were current smokers. Two years after the event, 44 % of these were still smoking. At baseline, current smokers scored higher on the depression and neuroticism scales and had lower agreeableness scores. Patients who continued to smoke after 2 years had higher scores on being confrontational (i.e. confrontative coping style) compared to those who had managed to quit. Patients who continued to smoke had significantly lower agreeableness and were more often living alone. Personality, coping strategies and psychosocial circumstances are associated with smoking cessation rates in patients with MI. Considering personality factors and coping strategies to better individualise smoking cessation programs in MI patients might be of importance.

Particulate Air Pollution as a Risk Factor for ST-segment Depression in Patients with Coronary Artery Disease

PubMed Central

Chuang, Kai Jen; Coull, Brent A.; Zanobetti, Antonella; Suh, Helen; Schwartz, Joel; Stone, Peter H.; Litonjua, Augusto; Speizer, Frank E.; Gold, Diane R.

2009-01-01

Background The association of particulate matter (PM) with cardiovascular morbidity and mortality is well documented. PM-induced ischemia is considered a potential mechanism linking PM to adverse cardiovascular outcomes. Methods and Results In a repeated-measures study including 5,979 observations on 48 patients aged 43–75 years, we investigated associations of ambient pollution with ST-segment level changes averaged over half-hour periods, measured in the modified V5 position by 24-hr Holter electrocardiogram monitoring. Each patient was observed up to 4 times within one year after a percutaneous intervention for myocardial infarction, acute coronary syndrome without infarction, or stable coronary artery disease without acute coronary syndrome. Elevation in fine particles (PM2.5) and black carbon (BC) levels predicted depression of half-hour averaged ST-segment levels. An interquartile increase in the previous 24-h mean BC level was associated with a 1.50-fold increased in risk of ST-segment depression ≥0.1 mm (95% CI: 1.19, 1.89) and a −0.031 mm (95% CI: −0.042, −0.019) decrease in half-hour averaged ST-segment level (continuous outcome). Effects were greatest within the first month after hospitalization, and for patients with myocardial infarction during hospitalization or with diabetes. Conclusions ST-segment depression is associated with increased exposure to PM2.5 and BC in cardiac patients. The risk of pollution-associated ST-segment depression may be greatest in those with myocardial injury in the first month after the cardiac event. PMID:18779445

Functional, morphological and electrocardiographical abnormalities in patients with apical hypertrophic cardiomyopathy and apical aneurysm: correlation with cardiac MR

PubMed Central

Suwa, Kenichiro; Satoh, Hiroshi; Sano, Makoto; Nobuhara, Mamoru; Saitoh, Takeji; Saotome, Masao; Urushida, Tsuyoshi; Katoh, Hideki; Tawarahara, Kei; Ohtani, Hayato; Wakabayashi, Yasushi; Takase, Hiroyuki; Terada, Hajime; Takehara, Yasuo; Sakahara, Harumi; Hayashi, Hideharu

2014-01-01

Objective The prognosis of apical hypertrophic cardiomyopathy (APH) has been benign, but apical myocardial injury has prognostic importance. We studied functional, morphological and electrocardiographical abnormalities in patients with APH and with apical aneurysm and sought to find parameters that relate to apical myocardial injury. Methods Study design: a multicentre trans-sectional study. Patients: 45 patients with APH and 5 with apical aneurysm diagnosed with transthoracic echocardiography (TTE) in the database of Hamamatsu Circulation Forum. Measure: the apical contraction with cine-cardiac MR (CMR), the myocardial fibrotic scar with late gadolinium enhancement (LGE)-CMR, and QRS fragmentation (fQRS) defined when two ECG-leads exhibited RSR’s patterns. Results Cine-CMR revealed 27 patients with normal, 12 with hypokinetic and 11 with dyskinetic apical contraction. TTE misdiagnosed 11 (48%) patients with hypokinetic and dyskinetic contraction as those with normal contraction. Apical LGE was apparent in 10 (83%) and 11 (100%) patients with hypokinetic and dyskinetic contraction, whereas only in 11 patients (41%) with normal contraction (p<0.01). Patients with dyskinetic apical contraction had the lowest left ventricular ejection fraction, the highest prevalence of ventricular tachycardia, and the smallest ST depression and depth of negative T waves. The presence of fQRS was associated with impaired apical contraction and apical LGE (OR=8.32 and 8.61, p<0.05). Conclusions CMR is superior to TTE for analysing abnormalities of the apex in patients with APH and with apical aneurysm. The presence of fQRS can be a promising parameter for the early detection of apical myocardial injury. PMID:25332823

Hibernating myocardium, morphological studies on intraoperatory myocardial biopsies and on chronic ischemia experimental model.

PubMed

Laky, D; Parascan, Liliana

2007-01-01

Hibernating myocardium represent a prolonged but potentially reversible myocardial contractile dysfunction, an incomplete adaptation caused by chronic myocardial ischemia and persisting at least until blood flow restored. The purpose of this study was to investigate the morphological changes and weather relations exist among function, metabolism and structure in left ventricular hibernating myocardium. Material and methods. Experimental study is making on 12 dogs incomplete coronary obstruction during six weeks for morphologic studies of ischemic zones. On 48 patients with coronary stenosis myocardial biopsies was effectuated during aorto-coronarian bypass graft. On 60 patients with valvular disease associated with segmental coronary atherosclerotic obstructions during surgical interventions on a effectuated repeatedly biopsies from ischemic zones. Dyskinetic ischemic areas was identified by angiography, scintigraphy, low dose dobutamine echography to identify the cells viability. On myocardial biopsies various histological, histoenzymological, immunohistochemical and ultrastructural methods were performed. The morphological cardiomyocytic changes can summarized: loss of myofilaments, accumulation of glycogen, small mitochondria with reversible lesions, decrease of smooth reticulum, absence of T tubules, depression of titin in puncted pattern, loss of cardiotonin, disorganization of cytoskeleton, dispersed nuclear heterochromatin, embryofetal dedifferentiation, and persistence of viability. Extracellular matrix is enlarged with early matrix protein such fibronectin, tenascin, fibroblasts. In experimental material the morphological changes present similarities with the human biopsies, but intermixed with postinfarction scar tissue. Redifferentiation of hibernanting cells end remodeling of extracellular matrix is possible after quigle revascularization through aorto-coronary bypass grafts.

Systematic Review and Individual Patient Data Meta-Analysis of Sex Differences in Depression and Prognosis in Persons With Myocardial Infarction: A MINDMAPS Study.

PubMed

Doyle, Frank; McGee, Hannah; Conroy, Ronán; Conradi, Henk Jan; Meijer, Anna; Steeds, Richard; Sato, Hiroshi; Stewart, Donna E; Parakh, Kapil; Carney, Robert; Freedland, Kenneth; Anselmino, Matteo; Pelletier, Roxanne; Bos, Elisabeth H; de Jonge, Peter

2015-05-01

Using combined individual patient data from prospective studies, we explored sex differences in depression and prognosis post-myocardial infarction (MI) and determined whether disease indices could account for found differences. Individual patient data analysis of 10,175 MI patients who completed diagnostic interviews or depression questionnaires from 16 prospective studies from the MINDMAPS study was conducted. Multilevel logistic and Cox regression models were used to determine sex differences in prevalence of depression and sex-specific effects of depression on subsequent outcomes. Combined interview and questionnaire data from observational studies showed that 36% (635/1760) of women and 29% (1575/5526) of men reported elevated levels of depression (age-adjusted odds ratio = 0.68, 95% confidence interval [CI] = 0.60-0.77). The risk for all-cause mortality associated with depression was higher in men (hazard ratio = 1.38, 95% CI = 1.30-1.47) than in women (hazard ratio = 1.22, 95% CI = 1.14-1.31; sex by depression interaction: p < .001). Low left ventricular ejection fraction (LVEF) was associated with higher depression scores in men only (sex by LVEF interaction: B = 0.294, 95% CI = 0.090-0.498), which attenuated the sex difference in the association between depression and prognosis. The prevalence of depression post-MI was higher in women than in men, but the association between depression and cardiac prognosis was worse for men. LVEF was associated with depression in men only and accounted for the increased risk of all-cause mortality in depressed men versus women, suggesting that depression in men post-MI may, in part, reflect cardiovascular disease severity.

Transient abnormal Q waves during exercise electrocardiography

PubMed Central

Alameddine, F F; Zafari, A M

2004-01-01

Myocardial ischaemia during exercise electrocardiography is usually manifested by ST segment depression or elevation. Transient abnormal Q waves are rare, as Q waves indicate an old myocardial infarction. The case of a patient with exercise induced transient abnormal Q waves is reported. The potential mechanisms involved in the development of such an abnormality and its clinical implications are discussed. PMID:14676264

[Effectiveness of various dopamine doses in acute myocardial ischemia complicated by cardiogenic shock (an experimental study)].

PubMed

Kipshidze, N N; Korotkov, A A; Marsagishvili, L A; Prigolashvili, T Sh; Bokhua, M R

1981-06-01

The effect of various doses of dopamine on the values of cardiac contractile and hemodynamic function under conditions of acute two-hour ischemia complicated by cardiogenic shock was studied in 27 experiments on dogs. In a dose of 5 microgram/kg/min dopamine caused an optimum increase in cardiac productive capacity, reduction of peripheral resistance, adequate increase in coronary circulation and decrease in ST segment depression on the ECG. Infusion of 10 microgram/kg/min dopamine usually caused myocardial hyperfunction with an increase in total peripheral resistance and cardiac performance. Maximum dopamine doses (10 microgram/kg/min and more) were effective in the areactive form of cardiogenic shock. In longterm dopamine infusion it is necessary to establish continuous control over the hemodynamic parameters and the ECG to prevent aggravation of ischemia and for stage-by-stage reduction of the drug concentration and determination of the minimum maintenance dose.

Psychometric Evaluation of a Persian Version of the Cardiac Depression Scale in Iranian Patients With Acute Myocardial Infarction.

PubMed

Nia, Hamid Sharif; Sharif, Saeed Pahlevan; Froelicher, Erika Sivarajan; Boyle, Christopher; Goudarzian, Amir Hossein; Yaghoobzadeh, Ameneh; Oskouie, Fatemeh

2018-04-01

The aim of this study was to validate a Persian version of the Cardiac Depression Scale (CDS) in Iranian patients with acute myocardial infarction (AMI). The CDS was forward translated from English into Persian and back-translated to English. Validity was assessed using face, content, and construct validity. Also Cronbach's alpha (α), theta (), and McDonald's omega coefficient were used to evaluate the reliability. Construct validity of the scale showed two factors with eigenvalues greater than one. The Cronbach's α, , McDonald's omega, and construct reliability were greater than .70. The Persian version of the CDS has a two-factor structure (i.e., death anxiety and life satisfaction) and has acceptable reliability and validity. Therefore, the validated instrument can be used in future studies to assess depression in patients with AMI in Iranians.

Effect of Eye Movement Desensitization and Reprocessing (EMDR) on Depression in Patients With Myocardial Infarction (MI)

PubMed Central

Behnammoghadam, Mohammad; Alamdari, Ali Karam; Behnammoghadam, Aziz; Darban, Fatemeh

2015-01-01

Background: Coronary heart disease is the most important cause of death and inability in all communities. Depressive symptoms are frequent among post-myocardial infarction (MI) patients and may cause negative effects on cardiac prognosis. This study was conducted to identify efficacy of EMDR on depression of patients with MI. Methods: This study is a clinical trial. Sixty patients with MI were selected by simple sampling, and were separated randomly into experimental and control groups. To collect data, demographic questionnaire and Beck Depression Questionnaire were used. In experimental group, EMDR therapy were performed in three sessions alternate days for 45–90 minutes, during four months after their MI. Depression level of patients was measured before, and a week after EMDR therapy. Data were analyzed using paired –t- test, t–test, and Chi-square. Results: The mean depression level in experimental group 27.26± 6.41 before intervention, and it was 11.76 ± 3.71 after intervention. Hence, it showed a statistically significant difference (P<0.001). The mean depression level in control group was 24.53 ± 5.81 before intervention, and it was 31.66± 6.09 after intervention, so it showed statistically significant difference (P<0.001). The comparison of mean depression level at post treatment, in both groups showed statistically significant difference (P<0.001). Conclusion: EMDR is an effective, useful, efficient, and non-invasive method for treatment and reducing depression in patients with MI. PMID:26153191

Coronary gas embolism during a dive: a case report.

PubMed

Villela, Alvarez; Weaver, Lindell K; Ritesh, Dhar

2015-01-01

A healthy scuba diver presented with a NSTEMI (non-ST segment elevation myocardial infarction), pneumothorax and pneumomediastinum after diving. A 34-year-old woman with no significant medical history presented to the emergency department after an episode of loss of consciousness and seizure-like activity after an uncontrolled ascent during a dive in a freshwater lake at 5,700 feet of altitude. A chest radiograph showed pneumothorax, pneumomediastinum and pneumopericardium. She had septal infarction as indicated by ECG, and elevated troponin. Echocardiogram revealed a mildly depressed left ventricular ejection fraction (LVEF) with apical akinesis. Coronary angiogram showed normal coronary arteries. Hyperbaric oxygen was not given since evaluation occurred 28 hours after the event: The patient had a pneumothorax, and was neurologically normal. She was discharged on angiotensin-converting enzyme inhibitors (ACE-I) and opioids for chest pain. Cardiac function normalized on transthoracic echocardiogram (TTE) two weeks later, but she continued to complain of chest pain that was treated with dihydropyridine calcium channel blockers. She then developed pericarditis confirmed by CMRI, requiring treatment with non-steroidal anti-inflammatory drugs (NSAIDS), colchicine and steroids. Five months after the accident, she was asymptomatic, with excellent exercise function and normal exercise stress echocardiogram. Reports of myocardial injury caused by arterial gas embolism from diving are rare. This case shows coronary air embolism complicating pulmonary barotrauma and may be the first report of pericarditis complicating myocardial injury after an AGE.

Patterns of ectopy leading to increased risk of fatal or near-fatal cardiac arrhythmia in patients with depressed left ventricular function after an acute myocardial infarction.

PubMed

Lerma, Claudia; Gorelick, Alexander; Ghanem, Raja N; Glass, Leon; Huikuri, Heikki V

2013-09-01

To identify potential new markers for assessing the risk of sudden arrhythmic events based on a method that captures features of premature ventricular complexes (PVCs) in relation to sinus RR intervals in Holter recordings (heartprint). Holter recordings obtained 6 weeks after acute myocardial infarction from 227 patients with reduced ventricular function (left ventricular ejection fraction ≤ 40%) were used to produce heartprints. Measured indices were: PVCs per hour, standard deviation of coupling interval (SDCI), and the number of occurrences of the most prevalent form of PVCs (SNIB). Predictive values, survival analysis, and Cox regression with adjustment for clinical variables were performed based on primary endpoint, defined as an electrocardiogram-documented fatal or near-fatal arrhythmic event, death from any cause, and cardiac death. High ectopy (PVCs per hour ≥10) was a predictor of all endpoints. Repeating forms of PVCs (SNIB ≥ 83) was a predictor of primary endpoint, hazard ratio = 3.5 (1.3-9.5), and all-cause death, hazard ratio = 2.8 (1.1-7.3), but not cardiac death. SDCI ≤ 80 ms was a predictor of all-cause death and cardiac death, but not of primary endpoint. High ectopy, prevalence of repeating forms of PVCs, and low coupling interval variability are potentially useful risk markers of fatal or near-fatal arrhythmias after myocardial infarction.

Myocardial Perfusion and Function Are Distinctly Altered by Sevoflurane Anesthesia in Diet-Induced Prediabetic Rats.

PubMed

van den Brom, Charissa E; Boly, Chantal A; Bulte, Carolien S E; van den Akker, Rob F P; Kwekkeboom, Rick F J; Loer, Stephan A; Boer, Christa; Bouwman, R Arthur

2016-01-01

Preservation of myocardial perfusion during surgery is particularly important in patients with increased risk for perioperative complications, such as diabetes. Volatile anesthetics, like sevoflurane, have cardiodepressive effects and may aggravate cardiovascular complications. We investigated the effect of sevoflurane on myocardial perfusion and function in prediabetic rats. Rats were fed a western diet (WD; n = 18) or control diet (CD; n = 18) for 8 weeks and underwent (contrast) echocardiography to determine perfusion and function during baseline and sevoflurane exposure. Myocardial perfusion was estimated based on the product of microvascular filling velocity and blood volume. WD-feeding resulted in a prediabetic phenotype characterized by obesity, hyperinsulinemia, hyperlipidemia, glucose intolerance, and hyperglycemia. At baseline, WD-feeding impaired myocardial perfusion and systolic function compared to CD-feeding. Exposure of healthy rats to sevoflurane increased the microvascular filling velocity without altering myocardial perfusion but impaired systolic function. In prediabetic rats, sevoflurane did also not affect myocardial perfusion; however, it further impaired systolic function. Diet-induced prediabetes is associated with impaired myocardial perfusion and function in rats. While sevoflurane further impaired systolic function, it did not affect myocardial perfusion in prediabetic rats. Our findings suggest that sevoflurane anesthesia leads to uncoupling of myocardial perfusion and function, irrespective of the metabolic state.

Overexpression of MMP-9 and its inhibitors in blood mononuclear cells after myocardial infarction--is it associated with depressive symptomatology?

PubMed

Jönsson, Simon; Lundberg, Anna K; Jonasson, Lena

2014-01-01

Matrix metalloproteinase (MMP)-9 may play a central role in the development and progression of atherosclerosis. Emerging evidence also indicates an association between MMP-9 and depressive symptomatology. Here, we investigated whether expression of MMP-9 and its inhibitors in blood mononuclear cells and plasma were related to depressive symptoms in patients with a recent myocardial infarction (MI). Blood sampling was performed between 6 and 18 months after MI in 57 patients. Forty-one clinically healthy subjects were included as controls. Gene expression of MMP-9 and its main tissue inhibitors TIMP-1 and -2 were analyzed in freshly isolated or cultured blood mononuclear cells. Corresponding protein levels were assessed in cell supernatants and plasma. In post-MI patients, mRNA levels of MMP-9 and TIMP-1 and -2 were significantly higher than in controls while protein levels in cell supernatants and plasma did not differ between groups. The Center for Epidemiological Studies - Depression (CES-D) scale was used to assess depressive symptomatology. Repeated assessments during the first 18 months after MI showed significantly higher CES-D scores in patients compared with controls. However, there were no relationships between depressive mood and any of the measurements of MMP-9 or TIMPs. Our findings indicate that overexpression of MMP-9 and TIMPs in blood mononuclear cells and elevated depressive symptoms represent two unrelated phenomena after MI.

Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction

PubMed Central

Richart, Adèle; Vilar, Jose; Lemitre, Mathilde; Marck, Pauline; Branchereau, Maxime; Guerin, Coralie; Gautier, Gregory; Blank, Ulrich; Heymes, Christophe; Luche, Elodie; Cousin, Béatrice; Rodewald, Hans-Reimer

2016-01-01

Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in postischemic cardiac remodeling. Because c-Kit mutations affect multiple cell types of both immune and nonimmune origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit–independent MC-deficient (Cpa3Cre/+) mice. In response to MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differentiated into mature MCs. MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractility caused by myofilament Ca2+ desensitization. This effect correlated with increased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C. MC-specific tryptase was identified to regulate PKA activity in cardiomyocytes via protease-activated receptor 2 proteolysis. This work reveals a novel function for cardiac MCs modulating cardiomyocyte contractility via alteration of PKA-regulated force–Ca2+ interactions in response to MI. Identification of this MC-cardiomyocyte cross-talk provides new insights on the cellular and molecular mechanisms regulating the cardiac contractile machinery and a novel platform for therapeutically addressable regulators. PMID:27353089

Physiologic bases for anterior ST segment depression in patients with acute inferior wall myocardial infarction.

PubMed

Mirvis, D M

1988-11-01

Patients with acute inferior myocardial infarction commonly have ST segment depression in the anterior precordial leads. This may reflect either reciprocal changes from the inferior ST elevation or primary ST depression from additional anterior subendocardial ischemia. From a biophysical perspective reciprocal changes should be uniformly anticipated from basic dipole theory. Detection will vary with the size, location, orientation, and electrical intensity of the lesion and with the ECG lead system deployed to register the anterior changes. Alternatively, acute occlusion of the right coronary artery may produce ischemia in the anterior left ventricular wall supplied by a stenotic anterior descending coronary artery. Anterior ischemia may result from the abnormal hemodynamics or the reduced collateral flow produced by acute right coronary artery occlusion. Thus both mechanisms are based on sound physiologic principles. A review of the clinical literature suggests that such patients represent a heterogeneous group. In some instances coexistent anterior ischemia is present, whereas in others the anterior ST depression is the passive reflection of inferior ST elevation augmented in many cases by a large infarct size or more extensive posterobasal or septal involvement.

Minoxidil accelerates heart failure development in rats with ascending aortic constriction.

PubMed

Turcani, M; Jacob, R

1998-06-01

To test the ability of the heart to express characteristic geometric features of concentric and eccentric hypertrophy concurrently, constriction of the ascending aorta was performed in 4-week-old rats. Simultaneously, these rats were treated with an arteriolar dilator minoxidil. An examination 6 weeks after induction of the hemodynamic overload revealed no signs of congestion in systemic or pulmonary circulation in rats with aortic constriction or minoxidil-treated sham-operated rats. The magnitude of hemodynamic overload caused by aortic constriction or minoxidil treatment could be considered as equivalent, because the same enlargement of left ventricular pressure-volume area was necessary to compensate for either pressure or volume overload. Myocardial contractility decreased in rats with aortic constriction, and the compensation was achieved wholly by the marked concentric hypertrophy. Volume overload in minoxidil-treated rats was compensated partially by the eccentric hypertrophy and partially by the increased myocardial contractility. In contrast, increased lung weight and pleural effusion were found in all minoxidil-treated rats with aortic constriction. Unfavorable changes in left ventricular mass and geometry, relatively high chamber stiffness, and depressed ventricular and myocardial function were responsible for the massive pulmonary congestion.

[The investigation into dynamics of depression level and the quality of life in the patients after myocardial infarction under the influence of the program of physical rehabilitation].

PubMed

Belikova, N A; Indyka, S Ya

2016-01-01

The evaluation of the psychological condition of the patients who survived myocardial infarction and its correction taking into consideration the peculiar features of the individual reaction to the disease are the indispensable components of physical rehabilitation. The present article was designed to report the results of the study on the influence of the authors' physical rehabilitation program on the prevalence of depression and the life quality characteristics of the patients treated after myocardial infarction during the follow-up period. The patients of the main group (n=30) were enrolled in the original physical rehabilitation program. Those comprising the group of comparison (n=30) were given a course of rehabilitation in accordance with the scheme that had been recommended by the leading scientists and generally accepted in the Ukraine for the patients recovering after myocardial infarction under conditions of the out-patient clinics, spa and health resort facilities or convalescent centers. The study has demonstrated that the patients of both groups exhibited positive dynamics of their clinical condition (e.g. the decrease in the number of depressed subjects); however, this tendency was more pronounced in the main group where the number of the patients experiencing depression decreased by 61% at the end of the observation period (р<0,05). The analysis of the causes of anxiety associated with this pathology in the individual patients has demonstrated that the main factors responsible for the deterioration of the quality of life were the necessity of treatment, the limitations on the everyday physical activity, and the feeling of emotional tension. Moreover, the positive dynamics of the characteristics being evaluated was documented in the patients of the main group which gives reason to conclude that the program of physical rehabilitation proposed by the authors for the treatment of the patients after myocardial infarction is highly efficient during the follow-up period. Suffice it to say that 23 (76,7%) patients of the main group did not consider their lives as of poor quality by the end of the study period (р<0,01). There were only 18 such patients in the control group (р<0,05). The results of the present study provide a basis for recommending the proposed authors' program of physical rehabilitation for the patients treated after myocardial infarction with the emphasis on the necessity to do special dynamic exercises for the cervical and thoraco-cervical spine segments to be supplemented by the relevant educational program.

Acute Heart Failure Triggered by Coronary Spasm With Transient Left Ventricular Dysfunction.

PubMed

Adachi, Yusuke; Sakakura, Kenichi; Ibe, Tatsuro; Yoshida, Nanae; Wada, Hiroshi; Fujita, Hideo; Momomura, Shin-Ichi

2017-04-06

Coronary spasm is abnormal contraction of an epicardial coronary artery resulting in myocardial ischemia. Coronary spasm induces not only depressed myocardial contractility, but also incomplete myocardial relaxation, which leads to elevated ventricular filling pressure. We herein report the case of a 55-year-old woman who had repeated acute heart failure caused by coronary spasm. Acetylcholine provocation test with simultaneous right heart catheterization was useful for the diagnosis of elevated ventricular filling pressure as well as coronary artery spasm. We should add coronary spasm to a differential diagnosis for repeated acute heart failure.

L-arginine fails to prevent ventricular remodeling and heart failure in the spontaneously hypertensive rat.

PubMed

Brooks, Wesley W; Conrad, Chester H; Robinson, Kathleen G; Colucci, Wilson S; Bing, Oscar H L

2009-02-01

The effects of long-term oral administration of L-arginine, a substrate for nitric oxide (NO) production, on left ventricular (LV) remodeling, myocardial function and the prevention of heart failure (HF) was compared to the angiotensin-converting enzyme (ACE) inhibitor captopril in a rat model of hypertensive HF (aged spontaneously hypertensive rat (SHR)). SHRs and age-matched normotensive Wistar-Kyoto (WKY) rats were assigned to either no treatment, treatment with L-arginine (7.5 g/l in drinking water) or captopril (1 g/l in drinking water) beginning at 14 months of age, a time when SHRs exhibit stable compensated hypertrophy with no hemodynamic impairment; animals were studied at 23 months of age or at the time of HF. In untreated SHR, relative to WKY, there was significant LV hypertrophy, myocardial fibrosis, and isolated LV muscle performance and response to isoproterenol (ISO) were depressed; and, 7 of 10 SHRs developed HF. Captopril administration to six SHRs attenuated hypertrophy and prevented impaired inotropic responsiveness to ISO, contractile dysfunction, fibrosis, increased passive stiffness, and HF. In contrast, L-arginine administration to SHR increased LV hypertrophy and myocardial fibrosis while cardiac performance was depressed; and 7 of 9 SHRs developed HF. In WKY, L-arginine treatment but not captopril resulted in increased LV weight and the contractile response to ISO was blunted. Neither L-arginine nor captopril treatment of WKY changed fibrosis and HF did not occur. These data demonstrate that in contrast to captopril, long-term treatment with L-arginine exacerbates age-related cardiac hypertrophy, fibrosis, and did not prevent contractile dysfunction or the development of HF in aging SHR.

Loss of vagal tone aggravates systemic inflammation and cardiac impairment in endotoxemic rats.

PubMed

Schulte, Astrid; Lichtenstern, Christoph; Henrich, Michael; Weigand, Markus A; Uhle, Florian

2014-05-15

During the course of sepsis, often myocardial depression with hemodynamic impairment occurs. Acetylcholine, the main transmitter of the parasympathetic Nervus vagus, has been shown to be of importance for the transmission of signals within the immune system and also for a variety of other functions throughout the organism. Hypothesizing a potential correlation between this dysfunction and hemodynamic impairment, we wanted to assess the impact of vagal stimulation on myocardial inflammation and function in a rat model of lipopolysaccharide (LPS)-induced septic shock. As the myocardial tissue is (sparsely) innervated by the N. vagus, there might be an important anti-inflammatory effect in the heart, inhibiting proinflammatory gene expression in cardiomyocytes and improving cardiac function. We performed stimulation of the right cervical branch of the N. vagus in vagotomized, endotoxemic (1 mg/kg body weight LPS, intravenously) rats. Hemodynamic parameters were assessed over time using a left ventricular pressure-volume catheter. After the experiments, hearts and blood plasma were collected, and the expression of proinflammatory cytokines was measured using quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. After vagotomy, the inflammatory response was aggravated, measurable by elevated cytokine levels in plasma and ventricular tissue. In concordance, cardiac impairment during septic shock was pronounced in these animals. To reverse both hemodynamic and immunologic effects of diminished vagal tone, even a brief stimulation of the N. vagus was enough during initial LPS infusion. Overall, the N. vagus might play a major role in maintaining hemodynamic stability and cardiac immune homeostasis during septic shock. Copyright © 2014 Elsevier Inc. All rights reserved.

Interactive associations of depression and sleep apnea with adverse clinical outcomes after acute myocardial infarction

PubMed Central

Hayano, Junichiro; Carney, Robert M.; Watanabe, Eiichi; Kawai, Kiyohiro; Kodama, Itsuo; Stein, Phyllis K.; Watkins, Lana L.; Freedland, Kenneth E.; Blumenthal, James A.

2012-01-01

Objective Depression and sleep apnea (SA) are common among patients after acute myocardial infarction (AMI), and both are associated with increased risk for adverse outcomes. We tested the hypothesis that there is an interaction between depression and SA in relation to prognosis in post-AMI patients. Methods Participants were 337 depressed and 379 nondepressed post-AMI patients who participated in a substudy of the Enhancing Recovery in Coronary Heart Disease (ENRICHD) clinical trial. SA was identified from Holter ECG at the entry by an algorithm that detects cyclic variation of heart rate. Results During a median follow-up of 25 months, 43 (6.0%) of patients died and 83 (11.6%) either died or experienced a recurrent AMI. Among 94 patients with both depression and SA, these endpoints occurred in 20 (21.3%) and 25 (26.6%), the prevalence that was 6.9 and 3.9 times higher than predicted probabilities by ENRICHD clinical risk scores (P <.001 for both). In the patients with depression alone, SA alone, or neither, the frequencies did not differ significantly from the predicted probability. Although both depression and SA predicted death and the combined endpoint, we observed depression by SA interactions (P = .03 and .02). SA independently predicted these endpoints in depressed (P <.001 and P = .001), but not in nondepressed patients (P = .73 and .84). Similarly, depression independently predicted these endpoints in SA (P <.001 for both), but not in non-SA patients (P = .61 and .12). Conclusion The combination of depression and SA estimated by CVHR is associated with long-term adverse clinical outcomes after AMI. PMID:23023681

Metformin improves cardiac function in mice with heart failure after myocardial infarction by regulating mitochondrial energy metabolism.

PubMed

Sun, Dan; Yang, Fei

2017-04-29

To investigate whether metformin can improve the cardiac function through improving the mitochondrial function in model of heart failure after myocardial infarction. Male C57/BL6 mice aged about 8 weeks were selected and the anterior descending branch was ligatured to establish the heart failure model after myocardial infarction. The cardiac function was evaluated via ultrasound after 3 days to determine the modeling was successful, and the mice were randomly divided into two groups. Saline group (Saline) received the intragastric administration of normal saline for 4 weeks, and metformin group (Met) received the intragastric administration of metformin for 4 weeks. At the same time, Shame group (Sham) was set up. Changes in cardiac function in mice were detected at 4 weeks after operation. Hearts were taken from mice after 4 weeks, and cell apoptosis in myocardial tissue was detected using TUNEL method; fresh mitochondria were taken and changes in oxygen consumption rate (OCR) and respiratory control rate (RCR) of mitochondria in each group were detected using bio-energy metabolism tester, and change in mitochondrial membrane potential (MMP) of myocardial tissue was detected via JC-1 staining; the expressions and changes in Bcl-2, Bax, Sirt3, PGC-1α and acetylated PGC-1α in myocardial tissue were detected by Western blot. RT-PCR was used to detect mRNA levels in Sirt3 in myocardial tissues. Metformin improved the systolic function of heart failure model rats after myocardial infarction and reduced the apoptosis of myocardial cells after myocardial infarction. Myocardial mitochondrial respiratory function and membrane potential were decreased after myocardial infarction, and metformin treatment significantly improved the mitochondrial respiratory function and mitochondrial membrane potential; Metformin up-regulated the expression of Sirt3 and the activity of PGC-1α in myocardial tissue of heart failure after myocardial infarction. Metformin decreases the acetylation level of PGC-1α through up-regulating Sirt3, mitigates the damage to mitochondrial membrane potential of model of heart failure after myocardial infarction and improves the respiratory function of mitochondria, thus improving the cardiac function of mice. Copyright © 2017. Published by Elsevier Inc.

[Anomalous origin of the left coronary artery from the pulmonary trunk with myocardial infarction and severe left ventricular dysfunction in infancy--assessment of myocardial damage using SPECT studies with 201TlCl and 123I-BMIPP].

PubMed

Miyamoto, T; Horigome, H; Sato, H; Yamada, M; Inai, K; Takeda, T; Ishikawa, N; Hoshino, H; Itai, Y

1996-02-01

A 4-month-old male infant with Bland-White-Garland (BWG) syndrome complicated myocardial infarction was reported. Signs included tachypnea, coughing, and failure to thrive. However, there was no sign of myocardial infarction. A chest radiograph revealed cardiomegaly (CTR = 65%) and electrocardiogram showed abnormal Q waves in I, aVL, V6 leads. Cardiac catheterization and angiography revealed marked dilatation of left ventricle (end-diastolic volume = 384 ml/m2) and extremely depressed ejection fraction (16%), confirming the diagnosis of BWG syndrome. A 201TlCl-myocardial SPECT demonstrated apical defect and hypoperfusion in the anterolateral, inferoposterior walls, whereas 123I-beta-methyl-p-iodophenylpentadecanoic-acid (123I-BMIPP) SPECT showed a wider defect area. SPECT studies with 201TlCl and 123I-BMIPP, are useful to assess myocardial viability more accurately in BWG syndrome.

Psychological symptom profiles in patients with chest pain.

PubMed

Tennant, C; Mihailidou, A; Scott, A; Smith, R; Kellow, J; Jones, M; Hunyor, S; Lorang, M; Hoschl, R

1994-05-01

Five-hundred and thirty-two patients with ischaemic-like chest pain referred for symptom-limited exercise thallium myocardial perfusion studies, were assessed on a range of psychosocial measures. Three groups of patients were identified on the basis of their perfusion studies: (1) normal thallium perfusion; (2) current myocardial ischaemia; and (3) past myocardial infarction (but no current ischaemia). There were no significant psychological differences between these groups on a wide range of measures which included depression, state and trait anxiety, Type A behaviour, personality, suppression of affect, locus of control, alexythymia, and hypochondriasis. Significant differences were identified, however, on measures of anger and coping style. Subjects with no current ischaemia (normal thallium perfusion and those with past myocardial infarction) had higher scores on 'immature coping' and 'anger in', than subjects with current myocardial ischaemia. These findings are discussed in the light of other published research.

The heartbreak of depression: 'Psycho-cardiac' coupling in myocardial infarction.

PubMed

Headrick, John P; Peart, Jason N; Budiono, Boris P; Shum, David H K; Neumann, David L; Stapelberg, Nicolas J C

2017-05-01

Ample evidence identifies strong links between major depressive disorder (MDD) and both risk of ischemic or coronary heart disease (CHD) and resultant morbidity and mortality. The molecular mechanistic bases of these linkages are poorly defined. Systemic factors linked to MDD, including vascular dysfunction, atherosclerosis, obesity and diabetes, together with associated behavioral changes, all elevate CHD risk. Nonetheless, experimental evidence indicates the myocardium is also directly modified in depression, independently of these factors, impairing infarct tolerance and cardioprotection. It may be that MDD effectively breaks the heart's intrinsic defense mechanisms. Four extrinsic processes are implicated in this psycho-cardiac coupling, presenting potential targets for therapeutic intervention if causally involved: sympathetic over-activity vs. vagal under-activity, together with hypothalamic-pituitary-adrenal (HPA) axis and immuno-inflammatory dysfunctions. However, direct evidence of their involvement remains limited, and whether targeting these upstream mediators is effective (or practical) in limiting the cardiac consequences of MDD is unknown. Detailing myocardial phenotype in MDD can also inform approaches to cardioprotection, yet cardiac molecular changes are similarly ill defined. Studies support myocardial sensitization to ischemic insult in models of MDD, including worsened oxidative and nitrosative damage, apoptosis (with altered Bcl-2 family expression) and infarction. Moreover, depression may de-sensitize hearts to protective conditioning stimuli. The mechanistic underpinnings of these changes await delineation. Such information not only advances our fundamental understanding of psychological determinants of health, but also better informs management of the cardiac consequences of MDD and implementing cardioprotection in this cohort. Copyright © 2017 Elsevier Ltd. All rights reserved.

Effects of Insulin Resistance on Myocardial Blood Flow and Arterial Peripheral Circulation in Patients with Polycystic Ovary Syndrome.

PubMed

Aldrighi, José M; Tsutsui, Jeane M; Kowastch, Ingrid; Ribeiro, Alessandra L; Scapinelli, Alessandro; Tamanaha, Sonia; Oliveira, Ricardo M; Mathias, Wilson

2015-08-01

Polycystic ovary syndrome (PCOS) is associated with increased risk for cardiovascular disease. We sought to evaluate the effects of insulin resistance (IR) on myocardial microcirculation and peripheral artery function in patients with PCOS. We studied 55 women (28 with PCOS without IR, 18 with PCOS and IR and 11 normal controls) who underwent laboratorial analysis, high-resolution vascular ultrasound and real time myocardial contrast echocardiography (RTMCE). Intima-media thickness (IMT) and brachial artery flow-mediated dilation (FMD) were evaluated by vascular ultrasound. The replenishment velocity (β), plateau of acoustic intensity (A) and myocardial blood flow reserve (MBFR) were determined by quantitative dipyridamole stress RTMCE. β reserve in group PCOS + IR was lower than control (2.34 ± 0.55 vs. 3.60 ± 0.6; P < 0.001) and than PCOS without IR (2.34 ± 0.55 vs. 3.17 ± 0.65; P < 0.001). MBFR in patients with PCOS without IR did not differ from those of control (4.59 ± 1.59 vs. 5.30 ± 1.64; P = 0.22) or from patients with PCOS + IR (4.59 ± 1.59 vs. 3.70 ± 1.47; P = 0.07). When comparing with control group, patients with PCOS + IR had lower MBFR (5.30 ± 1.64 vs. 3.70 ± 1.47; P = 0.01). No significant differences were found between control, PCOS without IR and PCOS + IR for FMD (0.18 ± 0.05, 0.15 ± 0.04 and 0.13 ± 0.07; P =NS) or IMT (0.48 ± 0.05, 0.47 ± 0.05 and 0.49 ± 0.07; P = NS). Women with PCOS and IR had depressed β and MBFR as demonstrated by quantitative RTMCE, but no alteration in endothelial dysfunction or IMT. PCOS without IR showed isolated depression in β reserve, probably an earlier marker of myocardial flow abnormality. © 2014, Wiley Periodicals, Inc.

Puerarin blocks the signaling transmission mediated by P2X3 in SG and DRG to relieve myocardial ischemic damage.

PubMed

Liu, Shuangmei; Zhang, Chunping; Shi, Qingming; Li, Guilin; Song, Miaomiao; Gao, Yun; Xu, Changshui; Xu, Hong; Fan, Bo; Yu, Shicheng; Zheng, Chaoran; Zhu, Qicheng; Wu, Bing; Peng, Lichao; Xiong, Huangui; Wu, Qin; Liang, Shangdong

2014-02-01

P2X₃ receptors in stellate ganglia (SG) and cervical dorsal root ganglia (DRG) neurons are involved in sympathoexcitatory reflex induced by myocardial ischemic damage. Puerarin, a major active ingredient extracted from the traditional Chinese plant medicine Ge-gen, has been widely used in treatment of myocardial and cerebral ischemia. The present study is aimed to observe the effects of puerarin on the signaling transmission mediated by P2X₃ receptor in SG and DRG after myocardial ischemic damage. Our results showed that systolic blood pressure and heart rate increased, and the expression levels of P2X₃ mRNA and protein in SG and DRG were up-regulated after myocardial ischemic damage. Puerarin reduced systolic blood pressure and heart rate, relieved pain and decreased up-regulated expression of P2X₃ mRNA and protein in SG and DRG after myocardial ischemia. Puerarin inhibited the up-regulated ATP-activated currents in DRG neurons after myocardial ischemia. Thus, puerarin can relieve myocardial ischemic damage through blocking the P2X₃ signaling transmission and then depressed the aggravated sympathoexcitatory reflex. Copyright © 2014 Elsevier Inc. All rights reserved.

A depressed post-menopausal woman.

PubMed

Lutwak, Nancy; Dill, Curt

2012-11-01

Post-menopausal women are at significant risk for coronary artery disease, have increased rates of depression compared to their male counterparts, and often present atypically with coronary insufficiency. The symptoms of depression and coronary ischemia overlap greatly. Complaints like fatigue, body aches, and sleep disturbance reported by a depressed elderly woman may be cardiac related and need to be investigated seriously without physician bias. To ensure that clinicians are cautious when evaluating older women with a history of depression who are presenting with atypical complaints. A 61-year-old woman with history of depression presented to the Emergency Department with multiple complaints atypical for acute coronary syndrome. She had an immediate electrocardiogram and troponin-T Biosite point-of-care test (Biosite Incorporated, San Diego, CA) performed, which were positive for cardiac ischemia and myocardial infarction. The patient underwent immediate cardiac catheterization, which revealed occlusion of the mid left circumflex. After aspiration of thrombus and balloon dilatation of the site, a bare metal stent was deployed, restoring excellent flow. The patient did well medically but her depression worsened after the procedure and continues despite psychiatric intervention. For years there have been gender differences in medical treatment of coronary artery disease, and often women's complaints are not investigated aggressively. Post-menopausal women are at great risk for cardiac ischemia and depression, and their symptoms, which are often atypical, may not be diagnosed as anginal equivalents. In addition, depression is an independent risk factor for cardiovascular disease and, if it occurs after myocardial infarction, may lead to poor quality of life and increased morbidity and mortality. Patients who have had a coronary event must be thoroughly evaluated for signs of depression and receive the necessary treatment. Published by Elsevier Inc.

Psychosocial interventions for patients with coronary heart disease and depression: A systematic review and meta-analysis.

PubMed

Ski, Chantal F; Jelinek, Michael; Jackson, Alun C; Murphy, Barbara M; Thompson, David R

2016-08-01

Depression is common in patients with coronary heart disease, and together these conditions significantly affect health outcomes. Impaired social support is also considered an important predictor of coronary heart disease prognosis and, as there is a complex interplay between social isolation and depression, interventions to address both may be required. This review aimed to assess the effectiveness of psychosocial interventions addressing both depression and social support for people with coronary heart disease and depression. PRISMA guidelines were used to search major health databases to identify randomised controlled trials that evaluated psychosocial interventions compared with usual care in patients with coronary heart disease and depression; the primary outcome was depressive symptoms and secondary outcomes were mortality (all-cause and cardiac), myocardial infarction, revascularisation, anxiety, social support and quality of life. Data, when suitable, were pooled using a random-effects meta-analysis model. Five studies (n=1358 participants) were eligible and included. The psychosocial intervention group had significantly lower levels of depressive symptoms (standardised mean difference (SMD) -0.15, 95% confidence interval (CI) -0.27 to -0.03; P=0.02) and higher levels of social support (SMD 0.17; 95% CI 0.04 to 0.30; P=0.01) but no differences were found for mortality (all-cause and cardiac), myocardial infarction, revascularisation, anxiety or quality of life. Psychosocial interventions for patients with coronary heart disease and depression result in modest reductions in depressive symptoms and improvements in social support. However, caution is warranted in view of the small number of studies included in the review and potential heterogeneity in outcomes and in differences in treatment. © The European Society of Cardiology 2015.

Depression and anxiety as predictors of heart rate variability after myocardial infarction.

PubMed

Martens, E J; Nyklícek, I; Szabó, B M; Kupper, N

2008-03-01

Reduced heart rate variability (HRV) is a prognostic factor for cardiac mortality. Both depression and anxiety have been associated with increased risk for mortality in cardiac patients. Low HRV may act as an intermediary in this association. The present study examined to what extent depression and anxiety differently predict 24-h HRV indices recorded post-myocardial infarction (MI). Ninety-three patients were recruited during hospitalization for MI and assessed on self-reported symptoms of depression and anxiety. Two months post-MI, patients were assessed on clinical diagnoses of lifetime depressive and anxiety disorder. Adequate 24-h ambulatory electrocardiography data were obtained from 82 patients on average 78 days post-MI. In unadjusted analyses, lifetime diagnoses of major depressive disorder was predictive of lower SDNN [standard deviation of all normal-to-normal (NN) intervals; beta=-0.26, p=0.022] and SDANN (standard deviation of all 5-min mean NN intervals; beta=0.25, p=0.023), and lifetime anxiety disorder of lower RMSSD (root mean square of successive differences; beta=-0.23, p=0.039). Depression and anxiety symptoms did not significantly predict HRV. After adjustment for age, sex, cardiac history and multi-vessel disease, lifetime depressive disorder was no longer predictive of HRV. Lifetime anxiety disorder predicted reduced high-frequency spectral power (beta=-0.22, p=0.039) and RMSSD (beta=-0.25, p=0.019), even after additional adjustment of anxiety symptoms. Clinical anxiety, but not depression, negatively influenced parasympathetic modulation of heart rate in post-MI patients. These findings elucidate the physiological mechanisms underlying anxiety as a risk factor for adverse outcomes, but also raise questions about the potential role of HRV as an intermediary between depression and post-MI prognosis.

Treatment of post-myocardial infarction depressive disorder: a randomized, placebo-controlled trial with mirtazapine.

PubMed

Honig, Adriaan; Kuyper, Astrid M G; Schene, Aart H; van Melle, Joost P; de Jonge, Peter; Tulner, Dorien M; Schins, Annique; Crijns, Harry J G M; Kuijpers, Petra M J C; Vossen, Helen; Lousberg, Richel; Ormel, Johan

2007-01-01

To examine the antidepressant efficacy of a dual-acting antidepressant (mirtazapine) in patients with post-myocardial infarction (MI) depressive disorder. Antidepressants used in post MI trials with a randomized, double-blind, placebo-controlled design have been restricted to selective serotonin reuptake inhibitors (SSRIs). Antidepressant effects have been limited. In a prospective multicenter study, 2177 patients with MI were evaluated for depressive disorder during the first year post MI. Ninety-one patients who met the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) criteria for major or minor depressive disorder were randomized to a 24-week, double-blind, placebo-controlled trial. Antidepressant efficacy was tested using last-observation-carried-forward procedure and repeated measurements analysis using the SPPS mixed models approach, with as primary outcome reduction in depressive symptomatology on the 17-item Hamilton-Depression Rating Scale (Ham-D), and secondary outcomes the Beck Depression Inventory (BDI) and depression subscale of the Symptom Check List 90 items (dSCL-90) as well as the Clinical Global Impression (CGI) scale. Using the "last observation carried forward" (LOCF) method, mirtazapine did not show to be superior to placebo on the Ham-D, but did on the BDI, dSCL-90, and CGI scale over the acute treatment phase of 8 weeks (n = 91). Using mixed models analysis over the entire 24 weeks of treatment (n = 40), we did find a significant difference favoring mirtazapine to placebo on the Ham-D, BDI, and CGI, but on the dSCL-90, this difference was not significant. This trial shows efficacy of mirtazapine on primary and secondary depression measures. Mirtazapine seems to be safe in the treatment of post-MI depression.

Depressive symptoms in younger women and men with acute myocardial infarction: insights from the VIRGO study.

PubMed

Smolderen, Kim G; Strait, Kelly M; Dreyer, Rachel P; D'Onofrio, Gail; Zhou, Shengfan; Lichtman, Judith H; Geda, Mary; Bueno, Héctor; Beltrame, John; Safdar, Basmah; Krumholz, Harlan M; Spertus, John A

2015-04-02

Depression was recently recognized as a risk factor for adverse medical outcomes in patients with acute myocardial infarction (AMI). The degree to which depression is present among younger patients with an AMI, the patient profile associated with being a young AMI patient with depressive symptoms, and whether relevant sex differences exist are currently unknown. The Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO) study enrolled 3572 patients with AMI (67.1% women; 2:1 ratio for women to men) between 2008 and 2012 (at 103 hospitals in the United States, 24 in Spain, and 3 in Australia). Information about lifetime history of depression and depressive symptoms experienced over the past 2 weeks (Patient Health Questionnaire; a cutoff score ≥10 was used for depression screening) was collected during index AMI admission. Information on demographics, socioeconomic status, cardiovascular risk, AMI severity, perceived stress (14-item Perceived Stress Scale), and health status (Seattle Angina Questionnaire, EuroQoL 5D) was obtained through interviews and chart abstraction. Nearly half (48%) of the women reported a lifetime history of depression versus 1 in 4 in men (24%; P<0.0001). At the time of admission for AMI, more women than men experienced depressive symptoms (39% versus 22%, P<0.0001; adjusted odds ratio 1.64; 95% CI 1.36 to 1.98). Patients with more depressive symptoms had higher levels of stress and worse quality of life (P<0.001). Depressive symptoms were more prevalent among patients with lower socioeconomic profiles (eg, lower education, uninsured) and with more cardiovascular risk factors (eg, diabetes, smoking). A high rate of lifetime history of depression and depressive symptoms at the time of an AMI was observed among younger women compared with men. Depressive symptoms affected those with more vulnerable socioeconomic and clinical profiles. © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

Perioperative Assessment of Myocardial Deformation

PubMed Central

Duncan, Andra E.; Alfirevic, Andrej; Sessler, Daniel I.; Popovic, Zoran B.; Thomas, James D.

2014-01-01

Evaluation of left ventricular performance improves risk assessment and guides anesthetic decisions. However, the most common echocardiographic measure of myocardial function, the left ventricular ejection fraction (LVEF), has important limitations. LVEF is limited by subjective interpretation which reduces accuracy and reproducibility, and LVEF assesses global function without characterizing regional myocardial abnormalities. An alternative objective echocardiographic measure of myocardial function is thus needed. Myocardial deformation analysis, which performs quantitative assessment of global and regional myocardial function, may be useful for perioperative care of surgical patients. Myocardial deformation analysis evaluates left ventricular mechanics by quantifying strain and strain rate. Strain describes percent change in myocardial length in the longitudinal (from base to apex) and circumferential (encircling the short-axis of the ventricle) direction and change in thickness in the radial direction. Segmental strain describes regional myocardial function. Strain is a negative number when the ventricle shortens longitudinally or circumferentially and is positive with radial thickening. Reference values for normal longitudinal strain from a recent meta-analysis using transthoracic echocardiography are (mean ± SD) −19.7 ± 0.4%, while radial and circumferential strain are 47.3 ± 1.9 and −23.3 ± 0.7%, respectively. The speed of myocardial deformation is also important and is characterized by strain rate. Longitudinal systolic strain rate in healthy subjects averages −1.10 ± 0.16 sec−1. Assessment of myocardial deformation requires consideration of both strain (change in deformation), which correlates with LVEF, and strain rate (speed of deformation), which correlates with rate of rise of left ventricular pressure (dP/dt). Myocardial deformation analysis also evaluates ventricular relaxation, twist, and untwist, providing new and noninvasive methods to assess components of myocardial systolic and diastolic function. Myocardial deformation analysis is based on either Doppler or a non-Doppler technique, called speckle-tracking echocardiography. Myocardial deformation analysis provides quantitative measures of global and regional myocardial function for use in the perioperative care of the surgical patient. For example, coronary graft occlusion after coronary artery bypass grafting is detected by an acute reduction in strain in the affected coronary artery territory. In addition, assessment of left ventricular mechanics detects underlying myocardial pathology before abnormalities become apparent on conventional echocardiography. Certainly, patients with aortic regurgitation demonstrate reduced longitudinal strain before reduction in LVEF occurs, which allows detection of subclinical left ventricular dysfunction and predicts increased risk for heart failure and impaired myocardial function after surgical repair. In this review we describe the principles, techniques, and clinical application of myocardial deformation analysis. PMID:24557101

The Perfect Storm: Concurrent Stress and Depressive Symptoms Increase Risk of Myocardial Infarction or Death

PubMed Central

Alcántara, Carmela; Muntner, Paul; Edmondson, Donald; Safford, Monika M.; Redmond, Nicole; Colantonio, Lisandro D.; Davidson, Karina W.

2015-01-01

Background Depression and stress have each been found to be associated with poor prognosis in coronary heart disease (CHD) patients. A recently offered ‘Psychosocial Perfect Storm’ conceptual model hypothesizes amplified risk will occur in those with concurrent stress and depressive symptoms. We tested this hypothesis in a large sample of U.S. adults with CHD. Methods and Results Participants included 4487 adults with CHD from the REasons for Geographic and Racial Differences in Stroke (REGARDS) study, a prospective cohort study of 30,239 Black and White adults. We conducted Cox proportional hazards regression with the composite outcome of myocardial infarction (MI) or death and adjustment for demographic, clinical, and behavioral factors. Overall, 6.1% reported concurrent high stress and high depressive symptoms at baseline. Over a median 5.95-years of follow-up, 1,337 events occurred. In the first 2.5-years of follow-up, participants with concurrent high stress and high depressive symptoms had increased risk for MI or death (adjusted hazard ratio [HR]=1.48, [95% CI: 1.08–2.02]) relative to those with low stress and low depressive symptoms. Those with low stress and high depressive symptoms (HR=0.92, [95% CI: 0.66–1.28]) or high stress and low depressive symptoms (HR=0.86, [95% CI: 0.57–1.29]) were not at increased risk. The association on MI or death was not significant after the initial 2.5-years of follow-up (HR=0.89, [95% CI: 0.65–1.22]). Conclusions Our results provide initial support for a ‘Psychosocial Perfect Storm’ conceptual model; the confluence of depressive symptoms and stress on medical prognosis in adults with CHD may be particularly destructive in the shorter-term. PMID:25759443

Combined atorvastatin and coenzyme Q10 improve the left ventricular function in isoproterenol-induced heart failure in rat.

PubMed

Garjani, Alireza; Andalib, Sina; Biabani, Sajjad; Soraya, Hamid; Doustar, Yousef; Garjani, Afagh; Maleki-Dizaji, Nasrin

2011-09-01

The effect of atorvastatin on cardiac remodeling, function, and homodynamic parameters in isoproterenol-induced heart failure was evaluated in the present study. A subcutaneous injection of isoproterenol (5mg/kg/day) for 10 days was used for the induction of heart failure. Isoproterenol administration produced intensive myocardial necrosis and fibrosis with a significant decrease in the arterial pressure indices, heart rate, contractility (LVdP/dt(max)) and relaxation (LVdP/dt(min)), but an increase in the left ventricular end-diastolic pressure. Rats were randomly assigned to control, treatment with only atorvastatin, and treatment with atorvastatin plus coenzyme Q10. Histopathological analysis showed a marked attenuation of myocyte necrosis and interstitial fibrosis in all atorvastatin treated groups (P<0.001). A low dose of atorvastatin (5mg/kg/day) significantly improved the left ventricular systolic pressure, contractility and relaxation (P<0.01). On the contrary, a high dose of atorvastatin (20mg/kg/day) worsened the isoproterenol-induced left ventricular dysfunction by a further reduction of LVdP/dt(max) from +2780 ± 94 to +1588 ± 248 (mmHg/s; P<0.01) and LVdP/dt(min) from -2007 ± 190 to -2939 ± 291 (mmHg/s; P<0.05). Co-administration of coenzyme Q10 with atorvastatin reversed the hemodynamic depression and the left ventricular dysfunction to a high level (P<0.001). There was a lower level of LVEDPs in the atorvastatin+coenzyme Q10 treated groups (3 ± 1 and 4 ± 1.4 versus 8 ± 3.5 and 14 ± 3.6 mmHg, respectively), thereby suggesting improvement in the myocardial stiffness by the combined coenzyme Q10 and atorvastatin treatment. The atorvastatin therapy attenuated myocardial necrosis and fibrosis in isoproterenol-induced heart failure. However, a high dose of the drug considerably worsened the left ventricular dysfunction and hemodynamic depression, which was reversed by coenzyme Q10 co-administration. Copyright © 2011 Elsevier B.V. All rights reserved.

First myocardial infarction in patients under 60 years old: the role of exercise tests and symptoms in deciding whom to catheterise.

PubMed Central

Cross, S J; Lee, H S; Kenmure, A; Walton, S; Jennings, K

1993-01-01

OBJECTIVE--To determine the role of exercise tests and assessment of angina in the detection of potentially threatening disease in young patients with infarcts. DESIGN--Elective readmission of patients at a mean (SD) of 60 (30) days after acute myocardial infarction for assessment of angina, treadmill exercise tests, and cardiac catheterisation. SETTING--Cardiology department of a teaching hospital. PATIENTS--186 consecutive survivors, aged under 60 years and discharged from the coronary care unit after a first myocardial infarction. MAIN OUTCOME MEASURES--Coronary arteriography, presence of angina, result of exercise tests, and referral for revascularisation. RESULTS--31% of patients had either two vessel disease (with proximal left anterior descending involvement), three vessel disease, or left main stem disease. 49% of all patients had angina. Of the 173 patients who had an exercise test 34% had 1 mm and 24% had 2 mm of exercise induced ST depression. Thirty percent had no angina and a negative exercise test: after a mean (SD) follow up of 16 (4) months none of this symptom free sub-group had died, had experienced a further myocardial infarction, or had been referred for revascularisation. 79% of patients with either two vessel disease (with proximal left anterior descending involvement), three vessel disease, or left main stem disease had either angina or a 1 mm ST depression during the exercise test. CONCLUSION--Patients without cardiac pain after myocardial infarction and without ST changes during an exercise do not need arteriography. PMID:8260273

Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction.

PubMed

Ngkelo, Anta; Richart, Adèle; Kirk, Jonathan A; Bonnin, Philippe; Vilar, Jose; Lemitre, Mathilde; Marck, Pauline; Branchereau, Maxime; Le Gall, Sylvain; Renault, Nisa; Guerin, Coralie; Ranek, Mark J; Kervadec, Anaïs; Danelli, Luca; Gautier, Gregory; Blank, Ulrich; Launay, Pierre; Camerer, Eric; Bruneval, Patrick; Menasche, Philippe; Heymes, Christophe; Luche, Elodie; Casteilla, Louis; Cousin, Béatrice; Rodewald, Hans-Reimer; Kass, David A; Silvestre, Jean-Sébastien

2016-06-27

Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in postischemic cardiac remodeling. Because c-Kit mutations affect multiple cell types of both immune and nonimmune origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit-independent MC-deficient (Cpa3(Cre/+)) mice. In response to MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differentiated into mature MCs. MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractility caused by myofilament Ca(2+) desensitization. This effect correlated with increased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C. MC-specific tryptase was identified to regulate PKA activity in cardiomyocytes via protease-activated receptor 2 proteolysis. This work reveals a novel function for cardiac MCs modulating cardiomyocyte contractility via alteration of PKA-regulated force-Ca(2+) interactions in response to MI. Identification of this MC-cardiomyocyte cross-talk provides new insights on the cellular and molecular mechanisms regulating the cardiac contractile machinery and a novel platform for therapeutically addressable regulators. ©2016 Ngkelo et al.

Alterations in left ventricular diastolic function in conscious dogs with pacing-induced heart failure

NASA Technical Reports Server (NTRS)

Komamura, K.; Shannon, R. P.; Pasipoularides, A.; Ihara, T.; Lader, A. S.; Patrick, T. A.; Bishop, S. P.; Vatner, S. F.

1992-01-01

We investigated in conscious dogs (a) the effects of heart failure induced by chronic rapid ventricular pacing on the sequence of development of left ventricular (LV) diastolic versus systolic dysfunction and (b) whether the changes were load dependent or secondary to alterations in structure. LV systolic and diastolic dysfunction were evident within 24 h after initiation of pacing and occurred in parallel over 3 wk. LV systolic function was reduced at 3 wk, i.e., peak LV dP/dt fell by -1,327 +/- 105 mmHg/s and ejection fraction by -22 +/- 2%. LV diastolic dysfunction also progressed over 3 wk of pacing, i.e., tau increased by +14.0 +/- 2.8 ms and the myocardial stiffness constant by +6.5 +/- 1.4, whereas LV chamber stiffness did not change. These alterations were associated with increases in LV end-systolic (+28.6 +/- 5.7 g/cm2) and LV end-diastolic stresses (+40.4 +/- 5.3 g/cm2). When stresses and heart rate were matched at the same levels in the control and failure states, the increases in tau and myocardial stiffness were no longer observed, whereas LV systolic function remained depressed. There were no increases in connective tissue content in heart failure. Thus, pacing-induced heart failure in conscious dogs is characterized by major alterations in diastolic function which are reversible with normalization of increased loading condition.

Prophylactic lignocaine and early post-coronary artery occlusion dysrhythmias in anaesthetized greyhounds.

PubMed Central

Marshall, R. J.; Parratt, J. R.

1980-01-01

1. Lignocaine (1 mg kg-1 min-1 infused intravenously for 30 min) greatly reduced the incidence of ventricular ectopic beats that resulted from acute coronary artery ligation in anaesthetized greyhound dogs. However, the incidence of ventricular fibrillation was only slightly reduced by this treatment which caused significant myocardial depression. 2. There is no good evidence from this study that lignocaine is a particularly effective prophylactic in acute myocardial infarction. PMID:7470764

Mitochondrial dysfunction in myocardium obtained from clinically normal dogs, clinically normal anesthetized dogs, and dogs with dilated cardiomyopathy.

PubMed

Sleeper, Meg M; Rosato, Bradley P; Bansal, Seema; Avadhani, Narayan G

2012-11-01

To compare mitochondrial complex I and complex IV activity in myocardial mitochondria of clinically normal dogs, clinically normal dogs exposed to inhalation anesthesia, and dogs affected with dilated cardiomyopathy. Myocardial samples obtained from 21 euthanized dogs (6 clinically normal [control] dogs, 5 clinically normal dogs subjected to inhalation anesthesia with isoflurane prior to euthanasia, 5 dogs with juvenile-onset dilated cardiomyopathy, and 5 dogs with adult-onset dilated cardiomyopathy). Activity of mitochondrial complex I and complex IV was assayed spectrophotometrically in isolated mitochondria from left ventricular tissue obtained from the 4 groups of dogs. Activity of complex I and complex IV was significantly decreased in anesthetized dogs, compared with activities in the control dogs and dogs with juvenile-onset or adult-onset dilated cardiomyopathy. Inhalation anesthesia disrupted the electron transport chain in the dogs, which potentially led to an outburst of reactive oxygen species that caused mitochondrial dysfunction. Inhalation anesthesia depressed mitochondrial function in dogs, similar to results reported in other species. This effect is important to consider when anesthetizing animals with myocardial disease and suggested that antioxidant treatments may be beneficial in some animals. Additionally, this effect should be considered when designing studies in which mitochondrial enzyme activity will be measured. Additional studies that include a larger number of animals are warranted.

B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction.

PubMed

Zouggari, Yasmine; Ait-Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P; Guérin, Coralie; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F; Binder, Christoph J; Danchin, Nicolas; Tedgui, Alain; Tedder, Thomas F; Silvestre, Jean-Sébastien; Mallat, Ziad

2013-10-01

Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6C(hi) monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell-selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction.

B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction

PubMed Central

Zouggari, Yasmine; Ait-Oufella, Hafid; Bonnin, Philippe; Simon, Tabassome; Sage, Andrew P; Guérin, Coralie; Vilar, José; Caligiuri, Giuseppina; Tsiantoulas, Dimitrios; Laurans, Ludivine; Dumeau, Edouard; Kotti, Salma; Bruneval, Patrick; Charo, Israel F; Binder, Christoph J; Danchin, Nicolas; Tedgui, Alain; Tedder, Thomas F; Silvestre, Jean-Sébastien; Mallat, Ziad

2014-01-01

Acute myocardial infarction is a severe ischemic disease responsible for heart failure and sudden death. Here, we show that after acute myocardial infarction in mice, mature B lymphocytes selectively produce Ccl7 and induce Ly6Chi monocyte mobilization and recruitment to the heart, leading to enhanced tissue injury and deterioration of myocardial function. Genetic (Baff receptor deficiency) or antibody-mediated (CD20- or Baff-specific antibody) depletion of mature B lymphocytes impeded Ccl7 production and monocyte mobilization, limited myocardial injury and improved heart function. These effects were recapitulated in mice with B cell–selective Ccl7 deficiency. We also show that high circulating concentrations of CCL7 and BAFF in patients with acute myocardial infarction predict increased risk of death or recurrent myocardial infarction. This work identifies a crucial interaction between mature B lymphocytes and monocytes after acute myocardial ischemia and identifies new therapeutic targets for acute myocardial infarction. PMID:24037091

A comparison of the diagnostic performance of the ST/HR hysteresis with cardiopulmonary stress testing parameters in detecting exercise-induced myocardial ischemia.

PubMed

Zimarino, Marco; Barnabei, Luca; Madonna, Rosalinda; Palmieri, Giuseppe; Radico, Francesco; Tatasciore, Alfonso; Bellisarii, Francesco Iachini; Perrucci, Gianni Mauro; Corazzini, Alessandro; De Caterina, Raffaele

2013-09-30

Because ST segment depression has limited diagnostic performance at exercise electrocardiography (ECG), ST segment depression/heart rate (ST/HR) hysteresis and cardiopulmonary exercise test (CPET)-derived parameters have been proposed as alternatives to diagnose exercise-induced myocardial ischemia. We compared the diagnostic performance of such parameters. We studied 56 subjects (45 men, 11 women, age 59.7 ± 13.6 years) referred for suspected exercise-induced myocardial ischemia with an equivocal ECG exercise test. All subjects serially underwent CPET and a myocardial single-photon emission computerized tomography (SPECT) perfusion imaging (as the gold standard for ischemia). Maximum ST depression at peak exercise (ST-max), the ST/HR hysteresis, ΔVO2/ΔWR b-b1 slope, ΔVO2/ΔWR (aa1-bb1), VO2/HR flattening duration and other CPET parameters were derived in all subjects. On the basis of SPECT, 23 subjects (41%) were considered ischemic and 33 subjects (59%) non-ischemic. ST/HR hysteresis was higher (0.026 mV; 95% CI: 0.003 to 0.049 vs -0.016 mV; 95% CI: -0.031 to -0.001 mV) and ST-max was lower (-0.105 mV; 95% CI: -0.158 to -0.052 vs 0.032 mV; 95% CI: -0.001 to -0.066 mV) in ischemic vs non-ischemic subjects (P=0.004 and P=0.001, respectively). Among CPET parameters, ΔVO2/ΔWR b-b(1) slope was lower (9.4 ± 3.8) and ΔVO2/ΔWR (aa(1)-bb(1)) was higher (2.1 ± 2.6) in ischemic vs non-ischemic subjects (11.4 ± 2.3, P=0.005, and 1.1 ± 1.5, P=0.001, respectively). The ST/HR hysteresis had the highest area under the curve value, better (P<0.05) than any other parameters tested, thus showing the highest overall diagnostic performance. The ST/HR hysteresis is superior to CPET-derived parameters for detecting exercise-induced myocardial ischemia in patients with equivocal ECG exercise test results. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

Non-ST elevation myocardial infarction secondary to carbon monoxide intoxication

PubMed Central

Jankowska, Danuta; Palabindala, Venkataraman; Salim, Sohail Abdul

2017-01-01

ABSTRACT Carbon monoxide poisoning has been documented in literature to cause severe neurological and tissue toxicity within the body. However, cardiotoxicity is often overlooked, but not uncommon. Previous research studies and case reports have revealed a significant relationship between carbon monoxide intoxication and myocardial ischemic events. We report a case of a 48-year-old male, who was exposed to severe smoke inhalation due to a house fire and subsequently developed a non-ST elevation myocardial infarction. Ischemic changes were evident on electrocardiogram, which demonstrated T-wave inversion in lead III and ST-segment depression in leads V4-V6. Elevated cardiac enzymes were also present. After standard treatment for an acute cardiac event, the patient fully recovered. This case demonstrates that myocardial ischemic changes due to carbon monoxide poisoning may be reversible if recognized in early stages and treated appropriately, thus reminding physicians that a proper cardiovascular examination and diagnostic testing should be performed on all patients with carbon monoxide poisoning. Abbreviations: NSTEMI: Non-ST elevation myocardial infarction PMID:28638579

Depression and the Risk of Myocardial Infarction and Coronary Death: A Meta-Analysis of Prospective Cohort Studies.

PubMed

Wu, Qing; Kling, Juliana M

2016-02-01

Findings regarding the association between depression and risk of coronary heart disease are inconsistent. We aimed to assess the association between depression and risk of myocardial infarction (MI) and coronary death through a meta-analysis.We performed an electronic literature search of MEDLINE, EMBASE, PsycINFO, ISI Web of Science, and Scopus databases through August 1, 2015, and manual search of the references of the eligible papers and related review articles. Two investigators independently conducted study selection and data abstraction. Disagreement was resolved by consensus. Confounder-adjusted hazard ratios (HRs) were pooled using a random-effects model. Heterogeneity was evaluated using the Cochran Q statistic and Higgins index. Publication bias was assessed by funnel plot and Egger test. Study quality was appraised with the Newcastle-Ottawa Scale.Among 19 eligible cohort studies including 323,709 participants, 8447 cases of MI and coronary death were reported during follow-up ranging from 4 to 37 years. The pooled adjusted HRs for patients with depression (vs those without) were 1.22 (95% CI, 1.13-1.32) for combined MI and coronary death, 1.31 (95% CI, 1.09-1.57) for MI alone (9 studies), and 1.36 (95% CI, 1.14-1.63) for coronary death alone (8 studies). The increased risk of MI and coronary death associated with depression was consistent using modified inclusion criteria, across most subgroups, and after adjusting for possible publication bias.Depression is associated with a significantly increased risk of MI and coronary death. Effective prevention and treatment of depression may decrease such risk.

Risk of anxiety and depressive disorders in patients with myocardial infarction: A nationwide population-based cohort study.

PubMed

Feng, Hsin-Pei; Chien, Wu-Chien; Cheng, Wei-Tung; Chung, Chi-Hsiang; Cheng, Shu-Meng; Tzeng, Wen-Chii

2016-08-01

Anxiety and depressive symptoms are associated with adverse cardiovascular events after an acute myocardial infarction (MI). However, most studies focusing on anxiety or depression have used rating scales or self-report methods rather than clinical diagnosis. This study aimed to investigate the association between psychiatrist-diagnosed psychiatric disorders and cardiovascular prognosis.We sampled data from the National Health Insurance Research Database; 1396 patients with MI were recruited as the study cohort and 13,960 patients without MI were recruited as the comparison cohort. Cox proportional hazard regression models were used to examine the effect of MI on the risk of anxiety and depressive disorders.During the first 2 years of follow-up, patients with MI exhibited a significantly higher risk of anxiety disorders (adjusted hazard ratio [HR] = 5.06, 95% confidence interval [CI]: 4.61-5.54) and depressive disorders (adjusted HR = 7.23, 95% CI: 4.88-10.88) than those without MI did. Greater risk for anxiety and depressive disorders was observed among women and patients aged 45 to 64 years following an acute MI. Patients with post-MI anxiety had a 9.37-fold (95% CI: 4.45-19.70) higher risk of recurrent MI than those without MI did after adjustment for age, sex, socioeconomic status, and comorbidities.This nationwide population-based cohort study provides evidence that MI increases the risk of anxiety and depressive disorders during the first 2 years post-MI, and post-MI anxiety disorders are associated with a higher risk of recurrent MI.

Risk of anxiety and depressive disorders in patients with myocardial infarction

PubMed Central

Feng, Hsin-Pei; Chien, Wu-Chien; Cheng, Wei-Tung; Chung, Chi-Hsiang; Cheng, Shu-Meng; Tzeng, Wen-Chii

2016-01-01

Abstract Anxiety and depressive symptoms are associated with adverse cardiovascular events after an acute myocardial infarction (MI). However, most studies focusing on anxiety or depression have used rating scales or self-report methods rather than clinical diagnosis. This study aimed to investigate the association between psychiatrist-diagnosed psychiatric disorders and cardiovascular prognosis. We sampled data from the National Health Insurance Research Database; 1396 patients with MI were recruited as the study cohort and 13,960 patients without MI were recruited as the comparison cohort. Cox proportional hazard regression models were used to examine the effect of MI on the risk of anxiety and depressive disorders. During the first 2 years of follow-up, patients with MI exhibited a significantly higher risk of anxiety disorders (adjusted hazard ratio [HR] = 5.06, 95% confidence interval [CI]: 4.61–5.54) and depressive disorders (adjusted HR = 7.23, 95% CI: 4.88–10.88) than those without MI did. Greater risk for anxiety and depressive disorders was observed among women and patients aged 45 to 64 years following an acute MI. Patients with post-MI anxiety had a 9.37-fold (95% CI: 4.45–19.70) higher risk of recurrent MI than those without MI did after adjustment for age, sex, socioeconomic status, and comorbidities. This nationwide population-based cohort study provides evidence that MI increases the risk of anxiety and depressive disorders during the first 2 years post-MI, and post-MI anxiety disorders are associated with a higher risk of recurrent MI. PMID:27559951

Functional parameters but not heart rate variability correlate with long-term outcomes in St-elevation myocardial infarction patients treated by primary angioplasty.

PubMed

Compostella, Leonida; Lakusic, Nenad; Russo, Nicola; Setzu, Tiziana; Compostella, Caterina; Vettore, Elia; Isabella, Giambattista; Tarantini, Giuseppe; Iliceto, Sabino; Bellotto, Fabio

2016-12-01

Depressed heart rate variability (HRV) is usually considered a negative long-term prognostic factor after acute myocardial infarction. Anyway, most of the supporting research was conducted before the era of immediate reperfusion by percutaneous coronary intervention (PCI). Main aim of this study was to evaluate if HRV still retains prognostic significance in our era of immediate PCI. Two weeks after STEMI treated by primary PCI, time-domain HRV was assessed from 24-h Holter recordings in 186 patients: markedly depressed HRV (SDNN <70ms or <50ms) was present in 16% and in 5% of cases, respectively; patients with left ventricle ejection fraction (LVEF) <40% presented more often SDNN values in the lowest quartile. Physical performance was also assessed, by 6-minute walk tests (6MWT) and by cardiopulmonary exercise test (CPET). After >2years from infarction, occurrence of major clinical events (MCE) was investigated. Cases with or without MCE did not differ by initial HRV parameters; Kaplan-Meier events-free survival curves were similar between patients with lowest quartile SDNN and the remaining ones (χ 2 0.981, p=0.322). By the contrary, events-free survival was worse if patients walked shorter distances at 6MWT (χ 2 6.435, p=0.011), developed poorer ventilatory efficiency at CPET (χ 2 10.060, p=0.002), or presented LVEF <40% (χ 2 7.085, p=0.008). In primary-PCI STEMI patients, markedly abnormal HRV was found in a small percentage of cases. HRV seems to have lost its prognostic significance, while parameters indicating LV function (LVEF and physical performance) could allow better prognostication in primary-PCI STEMI patients. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Endothelial function is associated with myocardial diastolic function in women with systemic lupus erythematosus.

PubMed

Chin, Calvin W L; Chin, Chee-Yang; Ng, Marie X R; Le, Thu-Thao; Huang, Fei-Qiong; Fong, Kok-Yong; Thumboo, Julian; Tan, Ru-San

2014-09-01

Endothelial dysfunction is associated with traditional and systemic lupus erythematosus (SLE)-specific risk factors, and early data suggest reversibility of endothelial dysfunction with therapy. The clinical relevance of endothelial function assessment has been limited by the lack of studies, demonstrating its prognostic significance and impact on early myocardial function. Therefore, we aimed to determine the association between endothelial and myocardial diastolic function in SLE women. Women with SLE and no coronary artery disease were prospectively recruited and underwent radionuclide myocardial perfusion imaging (MPI) (Jetstream, Philips, the Netherlands) to exclude subclinical myocardial ischemia. Cardiac and vascular functions were assessed in all patients (Alpha 10, Aloka, Tokyo). Diastolic function was assessed using pulse wave early (E) and late mitral blood inflow and myocardial tissue Doppler (mean of medial and lateral annulus e') velocities. Endothelial function was measured using brachial artery flow-mediated vasodilatation (FMD%). Univariate and multivariate linear regressions were used to assess the association between FMD% and myocardial diastolic function, adjusting for potential confounders. Thirty-eight patients without detectable myocardial ischemia on MPI were studied (mean age 44 ± 10 years; mean disease duration 14 ± 6 years). About 61 % of patients had normal diastolic function (E/e' ≤ 8), and 5 % of patients had definite diastolic dysfunction with E/e' > 13 (mean 7.1 ± 2.9). FMD% was associated with E/e' (regression coefficient β = -0.35; 95 % CI -0.62 to -0.08; p = 0.01) independent of systolic blood pressure, age, and SLICC/ACR Damage Index.

Psychometric Properties of the Persian Version of Death Depression Scale-Revised in Iranian Patients with Acute Myocardial Infarction.

PubMed

Sharif Nia, Hamid; Pahlevan Sharif, Saeed; Lehto, Rebecca H; Allen, Kelly A; Goudarzian, Amir Hossein; Yaghoobzadeh, Ameneh; Soleimani, Mohammad Ali

2017-07-01

Objective: Limited research has examined the psychometric properties of death depression scales in Persian populations with cardiac disease despite the need for valid assessment tools for evaluating depressive symptoms in patients with life-limiting chronic conditions. The present study aimed at evaluating the reliability and validity of the Persian Version of Death Depression Scale - Revised (DDS-R) in Iranian patients who had recent acute myocardial infarction (AMI). Method: This psychometric study was conducted with a convenience sample of 407 patients with AMI diagnosis who completed the Persian version of the DDS-R. The face, content, and construct validity of the scale were ascertained. Internal consistency, test-retest, and construct reliability (CR) were used to assess reliability of the Persian Version of DDS-R. Results: Based on maximum likelihood exploratory factor analysis and consideration of conceptual meaning, a 4-factor solution was identified, explaining 75.89% of the total variance. Goodness-of-fit indices (GFI), Comparative Fit Index (CFI), Normed Fit Index (NFI), Incremental Fit Index (IFI), and Root Mean Square Error of Approximation (RMSEA) in the final DDS-R structure demonstrated the adequacy of the 4-domain structure. The internal consistency, construct reliability, and Intra-class Correlation Coefficients (ICC) were greater than .70. Conclusion: The DDS-R was found to be a valid and reliable assessment tool for evaluating death depression symptoms in Iranian patients with AMI.

Triiodothyronine Facilitates Weaning From Extracorporeal Membrane Oxygenation by Improved Mitochondrial Substrate Utilization

PubMed Central

Files, Matthew D.; Kajimoto, Masaki; O'Kelly Priddy, Colleen M.; Ledee, Dolena R.; Xu, Chun; Des Rosiers, Christine; Isern, Nancy; Portman, Michael A.

2014-01-01

Background Extracorporeal membrane oxygenation (ECMO) provides a bridge to recovery after myocardial injury in infants and children, yet morbidity and mortality remain high. Weaning from the circuit requires adequate cardiac contractile function, which can be impaired by metabolic disturbances induced either by ischemia‐reperfusion and/or by ECMO. We tested the hypothesis that although ECMO partially ameliorates metabolic abnormalities induced by ischemia‐reperfusion, these abnormalities persist or recur with weaning. We also determined if thyroid hormone supplementation (triiodothyronine) during ECMO improves oxidative metabolism and cardiac function. Methods and Results Neonatal piglets underwent transient coronary ischemia to induce cardiac injury then were separated into 4 groups based on loading status. Piglets without coronary ischemia served as controls. We infused into the left coronary artery [2‐13C]pyruvate and [13C6, 15N]l‐leucine to evaluate oxidative metabolism by gas chromatography‐mass spectroscopy and nuclear magnetic resonance methods. ECMO improved survival, increased oxidative substrate contribution through pyruvate dehydrogenase, reduced succinate and fumarate accumulation, and ameliorated ATP depletion induced by ischemia. The functional and metabolic benefit of ECMO was lost with weaning, yet triiodothyronine supplementation during ECMO restored function, increased relative pyruvate dehydrogenase flux, reduced succinate and fumarate, and preserved ATP stores. Conclusions Although ECMO provides metabolic rest by decreasing energy demand, metabolic impairments persist, and are exacerbated with weaning. Treating ECMO‐induced thyroid depression with triiodothyronine improves substrate flux, myocardial oxidative capacity and cardiac contractile function. This translational model suggests that metabolic targeting can improve weaning. PMID:24650924

Triiodothyronine facilitates weaning from extracorporeal membrane oxygenation by improved mitochondrial substrate utilization.

PubMed

Files, Matthew D; Kajimoto, Masaki; O'Kelly Priddy, Colleen M; Ledee, Dolena R; Xu, Chun; Des Rosiers, Christine; Isern, Nancy; Portman, Michael A

2014-03-20

Extracorporeal membrane oxygenation (ECMO) provides a bridge to recovery after myocardial injury in infants and children, yet morbidity and mortality remain high. Weaning from the circuit requires adequate cardiac contractile function, which can be impaired by metabolic disturbances induced either by ischemia-reperfusion and/or by ECMO. We tested the hypothesis that although ECMO partially ameliorates metabolic abnormalities induced by ischemia-reperfusion, these abnormalities persist or recur with weaning. We also determined if thyroid hormone supplementation (triiodothyronine) during ECMO improves oxidative metabolism and cardiac function. Neonatal piglets underwent transient coronary ischemia to induce cardiac injury then were separated into 4 groups based on loading status. Piglets without coronary ischemia served as controls. We infused into the left coronary artery [2-(13)C]pyruvate and [(13)C6, (15)N]l-leucine to evaluate oxidative metabolism by gas chromatography-mass spectroscopy and nuclear magnetic resonance methods. ECMO improved survival, increased oxidative substrate contribution through pyruvate dehydrogenase, reduced succinate and fumarate accumulation, and ameliorated ATP depletion induced by ischemia. The functional and metabolic benefit of ECMO was lost with weaning, yet triiodothyronine supplementation during ECMO restored function, increased relative pyruvate dehydrogenase flux, reduced succinate and fumarate, and preserved ATP stores. Although ECMO provides metabolic rest by decreasing energy demand, metabolic impairments persist, and are exacerbated with weaning. Treating ECMO-induced thyroid depression with triiodothyronine improves substrate flux, myocardial oxidative capacity and cardiac contractile function. This translational model suggests that metabolic targeting can improve weaning.

Association between N-terminal proB-type Natriuretic Peptide and Depressive Symptoms in Patients with Acute Myocardial Infarction

PubMed Central

Ren, Yan; Jia, Jiao; Sa, Jian; Qiu, Li-Xia; Cui, Yue-Hua; Zhang, Yue-An; Yang, Hong; Liu, Gui-Fen

2017-01-01

Background: While depression and certain cardiac biomarkers are associated with acute myocardial infarction (AMI), the relationship between them remains largely unexplored. We examined the association between depressive symptoms and biomarkers in patients with AMI. Methods: We performed a cross-sectional study using data from 103 patients with AMI between March 2013 and September 2014. The levels of depression, N-terminal proB-type natriuretic peptide (NT-proBNP), and troponin I (TnI) were measured at baseline. The patients were divided into two groups: those with depressive symptoms and those without depressive symptoms according to Zung Self-rating Depression Scale (SDS) score. Baseline comparisons between two groups were made using Student's t-test for continuous variables, Chi-square or Fisher's exact test for categorical variables, and Wilcoxon test for variables in skewed distribution. Binomial logistic regression and multivariate linear regression were performed to assess the association between depressive symptoms and biomarkers while adjusting for demographic and clinical variables. Results: Patients with depressive symptoms had significantly higher NT-proBNP levels as compared to patients without depressive symptoms (1135.0 [131.5, 2474.0] vs. 384.0 [133.0, 990.0], Z = −2.470, P = 0.013). Depressive symptoms were associated with higher NT-proBNP levels (odds ratio [OR] = 2.348, 95% CI: 1.344 to 4.103, P = 0.003) and higher body mass index (OR = 1.169, 95% confidence interval [CI]: 1.016 to 1.345, P = 0.029). The total SDS score was associated with the NT-proBNP level (β = 0.327, 95% CI: 1.674 to 6.119, P = 0.001) after multivariable adjustment. In particular, NT-proBNP was associated with three of the depressive dimensions, including core depression (β = 0.299, 95% CI: 0.551 to 2.428, P = 0.002), cognitive depression (β = 0.320, 95% CI: 0.476 to 1.811, P = 0.001), and somatic depression (β = 0.333, 95% CI: 0.240 to 0.847, P = 0.001). Neither the overall depressive symptomatology nor the individual depressive dimensions were associated with TnI levels. Conclusions: Depressive symptoms, especially core depression, cognitive depression, and somatic depression, were related to high NT-proBNP levels in patients with AMI. PMID:28229985

Imaging of Myocardial Fatty Acid Oxidation

PubMed Central

Mather, Kieren J; DeGrado, Tim

2016-01-01

Myocardial fuel selection is a key feature of the health and function of the heart, with clear links between myocardial function and fuel selection and important impacts of fuel selection on ischemia tolerance. Radiopharmaceuticals provide uniquely valuable tools for in vivo, non-invasive assessment of these aspects of cardiac function and metabolism. Here we review the landscape of imaging probes developed to provide noninvasive assessment of myocardial fatty acid oxidation (MFAO). Also, we review the state of current knowledge that myocardial fatty acid imaging has helped establish of static and dynamic fuel selection that characterizes cardiac and cardiometabolic disease and the interplay between fuel selection and various aspects of cardiac function. PMID:26923433

Kawasaki syndrome in an adult: endomyocardial histology and ventricular function during acute and recovery phases of illness.

PubMed

Marcella, J J; Ursell, P C; Goldberger, M; Lovejoy, W; Fenoglio, J J; Weiss, M B

1983-08-01

Kawasaki syndrome, an acute systemic inflammatory illness of unknown origin usually affecting children, may develop into a serious illness complicated by coronary artery aneurysms or myocarditis. This report describes an adult with Kawasaki syndrome studied by right ventricular endomyocardial biopsy and cardiac catheterization during the acute and recovery phases of illness. The initial biopsy specimen showed acute myocarditis and was associated with hemodynamic evidence of biventricular dysfunction, a severely depressed left ventricular ejection fraction and global hypokinesia. With time, there was spontaneous and rapid resolution of the inflammatory cell infiltrate with concurrent return to normal myocardial function. Right ventricular endomyocardial biopsy studies early in the course of the cardiac disease associated with Kawasaki syndrome may correlate with ventricular function and may be useful for monitoring immunosuppressive therapy in patients with this syndrome.

[Treadmill exercise test in patients with coronary artery myocardial bridging].

PubMed

Wan, Jin; Li, Qi-yi; Wang, Guang-yao; Sun, Yi-qiu; Fang, Zhu-yuan; Tang, Shu-hua; Yang, Zong-mei; Zhang, Ya-cheng

2012-07-01

To observe treadmill exercise test (TET) characteristics in patients with myocardial bridging (MB). TET results from January 2003 to December 2010 were retrospectively analyzed in 156 patients with confirmed MB diagnosis. MB patients were divided into smoking group (68 cases) and non-smoking group (88 cases). Coronary angiography results were used to analyze the relations between MB length, myocardial ischemia and exercising duration. (1) MB was documented on two coronary arteries in 2 patients (1%), MB was detected in single artery in 154 patients (99%), of whom 146 cases were located at left anterior descending artery, 8 cases were located at right coronary artery. The degree of narrowing of MB was graded 1 (less than 50%) in 16 patients (10%), grade 2 (50% to 75%) in 108 patients (69%) and grade 3 (greater than 75%) in 32 patients (21%). The length of MB ranged between 4 to 40 mm, MB length was less than 10 mm in 40 patients (26%), between 11 to 20 mm in 48 patients (31%), between 21 to 30 mm in 44 patients (28%), greater than 31 mm in 24 patients (15%). (2) TET positive rate was 41% (64/156) and the TET positive rate was significantly higher in smoking group than in non-smoking group [57% (39/68) vs. 28% (25/88, P < 0.01)]. (3) The length of MB was positively related to the ST-segment depression (r = 0.723, P < 0.01) and negatively related to exercising duration (r = -0.828, P < 0.01). Heart rate was positively related to the ST-segment depression (r = 0.368, P < 0.01). TET may serve as a good test to assess myocardial ischemia in patients with MB. The length of MB is positively related with myocardial ischemia and negatively related with exercising duration. Smoking might increase myocardial ischemic incidence in MB patients, MB patients should be advised to stop smoking.

Action of acetylstrophanthidin on experimental myocardial infarction.

NASA Technical Reports Server (NTRS)

Nola, G. T.; Pope, S. E.; Harrison, D. C.

1972-01-01

An experimental animal model with acute myocardial infarction of a size insufficient to produce profound heart failure or shock was used to study the effects of acute infarction on digitalis tolerance and the hemodynamic changes produced by moderate and large doses of acetylstrophanthidin. With acute myocardial infarction, digitalis toxic arrhythmias could be precipitated with significantly lower doses of digitalis than in animals without myocardial infarction. There was no precise correlation between the size of infarction and the toxic dose of glycoside. Coronary artery ligation produced a stable but relatively depressed circulatory state, as evidenced by lowered cardiac output and stroke volume and elevated systemic vascular resistance and left atrial mean pressure. When digitalis was infused, the following significant changes were observed at nontoxic doses: (1) elevation of aortic and left ventricular pressures; (2) further decline in cardiac output; and (3) decreased left atrial mean pressure.

DOE Office of Scientific and Technical Information (OSTI.GOV)

Kajimoto, Masaki; Ledee, Dolena R.; Xu, Chun

Background: Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. We previously showed that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study was focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. Methods: Nineteen immature piglets (9.1-15.3 kg) were separated into 3 groups with ECMO (6.5 hours) and wean: normal circulation (Group-C);transient coronary occlusion (10 minutes) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon labeled lactate, medium-chain and long-chain FAs were infused as oxidative substrates. Substrate fractional contribution to the citricmore » acid cycle (FC) was analyzed by 13-Carbon nuclear magnetic resonance. Results: ECMO depressed circulating T3 levels to 40% baseline at 4 hours and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [ATP]/[ADP] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR. Conclusions: T3 releases inhibition of lactate oxidation following ischemia-reperfusion injury without impairing FA oxidation. These findings indicate that T3 depression during ECMO is maladaptive, and that restoring levels improves metabolic flux and enhances contractile function during weaning.« less

Associations between positive emotional well-being and stress-induced myocardial ischemia: Well-being scores predict exercise-induced ischemia.

PubMed

Feigal, Jacob P; Boyle, Stephen H; Samad, Zainab; Velazquez, Eric J; Wilson, Jennifer L; Becker, Richard C; Williams, Redford B; Kuhn, Cynthia M; Ortel, Thomas L; Rogers, Joseph G; O'Connor, Christopher M; Jiang, Wei

2017-02-01

Depressive symptoms have been associated with myocardial ischemia induced by mental (MSIMI) and exercise (ESIMI) stress in clinically stable ischemic heart disease (IHD) patients, but the association between positive emotions and inducible ischemia is less well characterized. The objective of this study was to examine the associations between ratings of well-being and stress-induced ischemia. Subjects were adult patients with documented IHD underwent mental and exercise stress testing for the Responses of Myocardial Ischemia to Escitalopram Treatment (REMIT) trial. The General Well-Being Schedule (GWBS), with higher scores reflecting greater subjective well-being, and the Center for Epidemiologic Studies Depression Scale (CES-D) were obtained from the REMIT participants. Echocardiography was used to measure ischemic responses to mental stress and Bruce protocol treadmill exercise testing. Data were analyzed using logistic regression adjusting for age, sex, resting left-ventricular ejection fraction (LVEF), and resting wall motion score index, as well as health-related behaviors. GWBS scores were obtained for 210 individuals, with MSIMI present in 92 (43.8%) and ESIMI present in 64 (30.5%). There was a significant inverse correlation between GWBS-PE (Positive Emotion subscale) scores and probability of ESIMI (OR=0.55 (95%CI 0.36-0.83), p=0.005). This association persisted after additional control for CESD subscales measuring negative and positive emotions and for variables reflecting health-related behaviors. A similar inverse correlation between GWBS-PE and MSIMI was observed, but did not reach statistical significance (OR=0.81 (95%CI 0.54-1.20), p=0.28). This is, to our knowledge, the first study demonstrating that greater levels of self-reported positive emotions are associated with a lower likelihood of ESIMI among patients with known IHD. Our results highlight the important interface functions of the central nervous and cardiovascular systems and underscore areas for future investigation. Copyright © 2016 Elsevier Inc. All rights reserved.

Moderate ethanol administration accentuates cardiomyocyte contractile dysfunction and mitochondrial injury in high fat diet-induced obesity.

PubMed

Yuan, Fang; Lei, Yonghong; Wang, Qiurong; Esberg, Lucy B; Huang, Zaixing; Scott, Glenda I; Li, Xue; Ren, Jun

2015-03-18

Light to moderate drinking confers cardioprotection although it remains unclear with regards to the role of moderate drinking on cardiac function in obesity. This study was designed to examine the impact of moderate ethanol intake on myocardial function in high fat diet intake-induced obesity and the mechanism(s) involved with a focus on mitochondrial integrity. C57BL/6 mice were fed low or high fat diet for 16 weeks prior to ethanol challenge (1g/kg/d for 3 days). Cardiac contractile function, intracellular Ca(2+) homeostasis, myocardial histology, and mitochondrial integrity [aconitase activity and the mitochondrial proteins SOD1, UCP-2 and PPARγ coactivator 1α (PGC-1α)] were assessed 24h after the final ethanol challenge. Fat diet intake compromised cardiomyocyte contractile and intracellular Ca(2+) properties (depressed peak shortening and maximal velocities of shortening/relengthening, prolonged duration of relengthening, dampened intracellular Ca(2+) rise and clearance without affecting duration of shortening). Although moderate ethanol challenge failed to alter cardiomyocyte mechanical property under low fat diet intake, it accentuated high fat diet intake-induced changes in cardiomyocyte contractile function and intracellular Ca(2+) handling. Moderate ethanol challenge failed to affect fat diet intake-induced cardiac hypertrophy as evidenced by H&E staining. High fat diet intake reduced myocardial aconitase activity, downregulated levels of mitochondrial protein UCP-2, PGC-1α, SOD1 and interrupted intracellular Ca(2+) regulatory proteins, the effect of which was augmented by moderate ethanol challenge. Neither high fat diet intake nor moderate ethanol challenge affected protein or mRNA levels as well as phosphorylation of Akt and GSK3β in mouse hearts. Taken together, our data revealed that moderate ethanol challenge accentuated high fat diet-induced cardiac contractile and intracellular Ca(2+) anomalies as well as mitochondrial injury. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Combined milrinone and enteral metoprolol therapy in patients with septic myocardial depression

PubMed Central

Schmittinger, Christian A; Dünser, Martin W; Haller, Maria; Ulmer, Hanno; Luckner, Günter; Torgersen, Christian; Jochberger, Stefan; Hasibeder, Walter R

2008-01-01

Introduction The multifactorial etiology of septic cardiomyopathy is not fully elucidated. Recently, high catecholamine levels have been suggested to contribute to impaired myocardial function. Methods This retrospective analysis summarizes our preliminary clinical experience with the combined use of milrinone and enteral metoprolol therapy in 40 patients with septic shock and cardiac depression. Patients with other causes of shock or cardiac failure, patients with beta-blocker therapy initiated more than 48 hours after shock onset, and patients with pre-existent decompensated congestive heart failure were excluded. In all study patients, beta blockers were initiated only after stabilization of cardiovascular function (17.7 ± 15.5 hours after shock onset or intensive care unit admission) in order to decrease the heart rate to less than 95 beats per minute (bpm). Hemodynamic data and laboratory parameters were extracted from medical charts and documented before and 6, 12, 24, 48, 72, and 96 hours after the first metoprolol dosage. Adverse cardiovascular events were documented. Descriptive statistical methods and a linear mixed-effects model were used for statistical analysis. Results Heart rate control (65 to 95 bpm) was achieved in 97.5% of patients (n = 39) within 12.2 ± 12.4 hours. Heart rate, central venous pressure, and norepinephrine, arginine vasopressin, and milrinone dosages decreased (all P < 0.001). Cardiac index and cardiac power index remained unchanged whereas stroke volume index increased (P = 0.002). In two patients (5%), metoprolol was discontinued because of asymptomatic bradycardia. Norepinephrine and milrinone dosages were increased in nine (22.5%) and six (15%) patients, respectively. pH increased (P < 0.001) whereas arterial lactate (P < 0.001), serum C-reactive protein (P = 0.001), and creatinine (P = 0.02) levels decreased during the observation period. Twenty-eight-day mortality was 33%. Conclusion Low doses of enteral metoprolol in combination with phosphodiesterase inhibitors are feasible in patients with septic shock and cardiac depression but no overt heart failure. Future prospective controlled trials on the use of beta blockers for septic cardiomyopathy and their influence on proinflammatory cytokines are warranted. PMID:18680591

Vitexin exerts cardioprotective effect on chronic myocardial ischemia/reperfusion injury in rats via inhibiting myocardial apoptosis and lipid peroxidation.

PubMed

Che, Xia; Wang, Xin; Zhang, Junyan; Peng, Chengfeng; Zhen, Yilan; Shao, Xu; Zhang, Gongliang; Dong, Liuyi

2016-01-01

The aim of this study was to explore the cardioprotective effect of vitexin on chronic myocardial ischemia/reperfusion injury in rats and potential mechanisms. A chronic myocardial ischemia/reperfusion injury model was established by ligating left anterior descending coronary for 60 minutes, and followed by reperfusion for 14 days. After 2 weeks ischemia/reperfusion, cardiac function was measured to assess myocardial injury. The level of ST segment was recorded in different periods by electrocardiograph. The change of left ventricular function and myocardial reaction degree of fibrosis of heart was investigated by hematoxylin and eosin (HE) staining and Sirius red staining. Endothelium-dependent relaxations due to acetylcholine were observed in isolated rat thoracic aortic ring preparation. The blood samples were collected to measure the levels of MDA, the activities of SOD and NADPH in serum. Epac1, Rap1, Bax and Bcl-2 were examined by using Western Blotting. Vitexin exerted significant protective effect on chronic myocardial ischemia/reperfusion injury, improved obviously left ventricular diastolic function and reduced myocardial reactive fibrosis degree in rats of myocardial ischemia. Medium and high-dose vitexin groups presented a significant decrease in Bax, Epac1 and Rap1 production and increase in Bcl-2 compared to the I/R group. It may be related to preventing myocardial cells from apoptosis, improving myocardial diastolic function and inhibiting lipid peroxidation. Vitexin is a cardioprotective herb, which may be a promising useful complementary and alternative medicine for patients with coronary heart disease.

Small interfering RNA targeting focal adhesion kinase prevents cardiac dysfunction in endotoxemia.

PubMed

Guido, Maria C; Clemente, Carolina F; Moretti, Ana I; Barbeiro, Hermes V; Debbas, Victor; Caldini, Elia G; Franchini, Kleber G; Soriano, Francisco G

2012-01-01

Sepsis and septic shock are associated with cardiac depression. Cardiovascular instability is a major cause of death in patients with sepsis. Focal adhesion kinase (FAK) is a potential mediator of cardiomyocyte responses to oxidative and mechanical stress. Myocardial collagen deposition can affect cardiac compliance and contractility. The aim of the present study was to determine whether the silencing of FAK is protective against endotoxemia-induced alterations of cardiac structure and function. In male Wistar rats, endotoxemia was induced by intraperitoneal injection of lipopolysaccharide (10 mg/kg). Cardiac morphometry and function were studied in vivo by left ventricular catheterization and histology. Intravenous injection of small interfering RNA targeting FAK was used to silence myocardial expression of the kinase. The hearts of lipopolysaccharide-injected rats showed collagen deposition, increased matrix metalloproteinase 2 activity, and myocyte hypertrophy, as well as reduced 24-h +dP/dt and -dP/dt, together with hypotension, increased left ventricular end-diastolic pressure, and elevated levels of FAK (phosphorylated and unphosphorylated). Focal adhesion kinase silencing reduced the expression and activation of the kinase in cardiac tissue, as well as protecting against the increased collagen deposition, greater matrix metalloproteinase 2 activity, and reduced cardiac contractility that occur during endotoxemia. In conclusion, FAK is activated in endotoxemia, playing a role in cardiac remodeling and in the impairment of cardiac function. This kinase represents a potential therapeutic target for the protection of cardiac function in patients with sepsis.

Experimental heart failure causes depression-like behavior together with differential regulation of inflammatory and structural genes in the brain.

PubMed

Frey, Anna; Popp, Sandy; Post, Antonia; Langer, Simon; Lehmann, Marc; Hofmann, Ulrich; Sirén, Anna-Leena; Hommers, Leif; Schmitt, Angelika; Strekalova, Tatyana; Ertl, Georg; Lesch, Klaus-Peter; Frantz, Stefan

2014-01-01

Depression and anxiety are common and independent outcome predictors in patients with chronic heart failure (CHF). However, it is unclear whether CHF causes depression. Thus, we investigated whether mice develop anxiety- and depression-like behavior after induction of ischemic CHF by myocardial infarction (MI). In order to assess depression-like behavior, anhedonia was investigated by repeatedly testing sucrose preference for 8 weeks after coronary artery ligation or sham operation. Mice with large MI and increased left ventricular dimensions on echocardiography (termed CHF mice) showed reduced preference for sucrose, indicating depression-like behavior. 6 weeks after MI, mice were tested for exploratory activity, anxiety-like behavior and cognitive function using the elevated plus maze (EPM), light-dark box (LDB), open field (OF), and object recognition (OR) tests. In the EPM and OF, CHF mice exhibited diminished exploratory behavior and motivation despite similar movement capability. In the OR, CHF mice had reduced preference for novelty and impaired short-term memory. On histology, CHF mice had unaltered overall cerebral morphology. However, analysis of gene expression by RNA-sequencing in prefrontal cortical, hippocampal, and left ventricular tissue revealed changes in genes related to inflammation and cofactors of neuronal signal transduction in CHF mice, with Nr4a1 being dysregulated both in prefrontal cortex and myocardium after MI. After induction of ischemic CHF, mice exhibited anhedonic behavior, decreased exploratory activity and interest in novelty, and cognitive impairment. Thus, ischemic CHF leads to distinct behavioral changes in mice analogous to symptoms observed in humans with CHF and comorbid depression.

Prevalence and predictors of depression and anxiety among survivors of myocardial infarction due to spontaneous coronary artery dissection.

PubMed

Liang, Jackson J; Tweet, Marysia S; Hayes, Sarah E; Gulati, Rajiv; Hayes, Sharonne N

2014-01-01

Depression and anxiety after myocardial infarction (MI) are common and associated with increased morbidity and mortality. The epidemiology and pathophysiology of MI due to spontaneous coronary artery dissection (SCAD) differs substantially from atherosclerotic MI, and rates of mental health comorbidities after SCAD are unknown. We aimed to determine the prevalence and predictors of depression/anxiety in SCAD survivors. In this cross-sectional study, 158 SCAD survivors (97% women; mean age, 45.5 ± 9.3 years) were screened for depression/anxiety via surveys, including the Patient Health Questionnaire Depression Scale (PHQ-9) and Generalized Anxiety Disorder 7-Item Scale (GAD-7), a mean 3.7 ± 4.7 years after SCAD. Comorbidities and environmental, socioeconomic, and clinical cardiovascular characteristics were obtained from the surveys. Since their initial SCAD MI, 51 (33%) patients had received treatment with medications or counseling for depression and 57 (37%) for anxiety. When surveyed, 46 (31.7%) were taking antidepressant or anxiolytic medications. Overall, mean PHQ-9 (4.1) and GAD-7 (4.7) scores suggested borderline mild depression/anxiety (normal range: 0-4). Younger age was associated with higher PHQ-9 (P = .04) and GAD-7 (P = .02) scores. The 19 (12%) patients with peripartum SCAD had higher mean PHQ-9 (6.7 vs 3.7; P < .0005) and GAD-7 (8.1 vs 4.3; P = .003) scores. Patients treated with percutaneous coronary intervention had lower PHQ-9 (1.5; P = .02) and GAD-7 (2.4; P = .004) scores. Symptoms of depression/anxiety are common in patients with MI due to SCAD, particularly younger women and those with peripartum SCAD. The PHQ-9 and GAD-7 assessments may detect depression/anxiety in SCAD survivors who do not self-report these disorders, suggesting a role for routine screening in these patients.

Vital exhaustion and anxiety are related to subjective quality of life in patients with acute myocardial infarct before cardiac rehabilitation.

PubMed

Rafael, Beatrix; Simon, Attila; Drótos, Gergely; Balog, Piroska

2014-10-01

To examine psychological risk factors and somatic factors in patients after myocardial infarction. To study the relationship between somatic and psychological factors, their influence on subjective quality of life (well-being) and also to examine possible gender differences. There has been a growing body of evidence that psychosocial factors are risk factors for incident and recurrent myocardial infarction. Descriptive correlational and cross-sectional survey design. In patients (n = 97, 67 men), the level of depression and anxiety, vital exhaustion, sleep disturbances and well-being were assessed. Left ventricular ejection fraction, left ventricular diastolic diameter, body mass index, metabolic equivalents and the number of diseased vessels were retrieved from medical records. Anxiety, vital exhaustion and sleep disturbances were significantly higher in women than in men. Well-being showed a significant linear correlation with body mass index, anxiety, depression, vital exhaustion and sleep disturbances scores. After adjustment for psychological risk factors and somatic parameters, only vital exhaustion and anxiety correlated significantly with well-being. However, there were gender differences in predictive variables of well-being. Anxiety in men and vital exhaustion in women showed a linear correlation with the subjective quality of life. Our study revealed that only vital exhaustion and anxiety showed a significant correlation with well-being in patients. During cardiac rehabilitation, it is important to detect and treat not only depression but also vital exhaustion and anxiety, because by reducing these psychological conditions, we can improve well-being. © 2014 John Wiley & Sons Ltd.

Patient satisfaction with treatment after acute myocardial infarction: role of psychosocial factors.

PubMed

Barry, Lisa C; Lichtman, Judith H; Spertus, John A; Rumsfeld, John S; Vaccarino, Viola; Jones, Philip G; Plomondon, Mary E; Parashar, Susmita; Krumholz, Harlan M

2007-01-01

To determine if psychosocial status influences treatment satisfaction, a quality-of-care indicator, of patients who were hospitalized for acute myocardial infarction (AMI). Psychosocial variables (social support, dispositional optimism, and depression) were assessed in 1847 AMI patients who completed a 1-month assessment in Prospective Registry Evaluating Myocardial Infarction: Events and Recovery (PREMIER), a multicenter, prospective cohort study. Patients' treatment satisfaction was determined using the Treatment Satisfaction scale of the Seattle Angina Questionnaire. The association between psychosocial variables and treatment satisfaction-adjusted for site, sociodemographics, medical history, clinical presentation, and treatment procedures-was evaluated using a censored normal model. Study participants were primarily white (77.6%) and male (68.8%), with a mean age of 60.6 +/- 12.7 (SD) years. Satisfaction with posthospitalization treatment following AMI increased as social support (Wald chi(2) = 35.02, p < .001) and dispositional optimism (beta = 1.42; 95% CI 0.24, 2.60) increased. Participants with mild (-3.10, 95% CI -5.77, -0.44), moderate (-4.77, 95% CI -8.16, -1.38), moderately severe (-8.49, 95% CI -13.47, -3.52), and severe (-11.65, 95% CI -18.77, -4.53) depression had significantly worse treatment satisfaction compared with the nondepressed participants. Assessing psychosocial variables, such as social support, dispositional optimism, and depression severity before hospital discharge, may indicate who is likely to be more satisfied with posthospitalization cardiac care 1 month following AMI. Without controlling for psychosocial status, treatment satisfaction may be a biased indicator of quality. Future studies should evaluate whether psychosocial intervention after AMI can improve satisfaction.

Catecholamines and myocardial contractile function during hypodynamia and with an altered thyroid hormone balance

NASA Technical Reports Server (NTRS)

Pruss, G. M.; Kuznetsov, V. I.; Zhilinskaya, A. A.

1980-01-01

The dynamics of catecholamine content and myocardial contractile function during hypodynamia were studied in 109 white rats whose motor activity was severely restricted for up to 30 days. During the first five days myocardial catecholamine content, contractile function, and physical load tolerance decreased. Small doses of thyroidin counteracted this tendency. After 15 days, noradrenalin content and other indices approached normal levels and, after 30 days, were the same as control levels, although cardiac functional reserve was decreased. Thyroidin administration after 15 days had no noticeable effect. A detailed table shows changes in 17 indices of myocardial contractile function during hypodynamia.

Posttraumatic stress disorder after myocardial infarction and coronary artery bypass grafting.

PubMed

Singh, Amitoj; Agrawal, Sahil; Gargya, Sanchita; Saluja, Sabir; Kumar, Akshat; Kumar, Abhishek; Kalra, Kartik; Thind, Munveer; Saluja, Sajeev; Stone, Lauren E; Ali, Farhan; Duarte-Chavez, Rodrigo; Marchionni, Christine; Sholevar, Farhad; Shirani, Jamshid; Nanda, Sudip

2017-01-01

Post traumatic stress disorder is a psychiatric disease that is usually precipitated by life threatening stressors. Myocardial infarction, especially in the young can count as one such event. The development of post traumatic stress after a coronary event not only adversely effects psychiatric health, but leads to increased cardiovascular morbidity and mortality. There is increasing evidence that like major depression, post traumatic stress disorder is also a strong coronary risk factor. Early diagnosis and treatment of this disease in patients with acute manifestations of coronary artery disease can improve patient outcomes.

Vitexin exerts cardioprotective effect on chronic myocardial ischemia/reperfusion injury in rats via inhibiting myocardial apoptosis and lipid peroxidation

PubMed Central

Che, Xia; Wang, Xin; Zhang, Junyan; Peng, Chengfeng; Zhen, Yilan; Shao, Xu; Zhang, Gongliang; Dong, Liuyi

2016-01-01

Purpose: The aim of this study was to explore the cardioprotective effect of vitexin on chronic myocardial ischemia/reperfusion injury in rats and potential mechanisms. Methods: A chronic myocardial ischemia/reperfusion injury model was established by ligating left anterior descending coronary for 60 minutes, and followed by reperfusion for 14 days. After 2 weeks ischemia/reperfusion, cardiac function was measured to assess myocardial injury. The level of ST segment was recorded in different periods by electrocardiograph. The change of left ventricular function and myocardial reaction degree of fibrosis of heart was investigated by hematoxylin and eosin (HE) staining and Sirius red staining. Endothelium-dependent relaxations due to acetylcholine were observed in isolated rat thoracic aortic ring preparation. The blood samples were collected to measure the levels of MDA, the activities of SOD and NADPH in serum. Epac1, Rap1, Bax and Bcl-2 were examined by using Western Blotting. Results: Vitexin exerted significant protective effect on chronic myocardial ischemia/reperfusion injury, improved obviously left ventricular diastolic function and reduced myocardial reactive fibrosis degree in rats of myocardial ischemia. Medium and high-dose vitexin groups presented a significant decrease in Bax, Epac1 and Rap1 production and increase in Bcl-2 compared to the I/R group. It may be related to preventing myocardial cells from apoptosis, improving myocardial diastolic function and inhibiting lipid peroxidation. Conclusions: Vitexin is a cardioprotective herb, which may be a promising useful complementary and alternative medicine for patients with coronary heart disease. PMID:27648122

Effects of a 3-year nurse-based case management in aged patients with acute myocardial infarction on rehospitalisation, mortality, risk factors, physical functioning and mental health. a secondary analysis of the randomized controlled KORINNA study.

PubMed

Kirchberger, Inge; Hunger, Matthias; Stollenwerk, Björn; Seidl, Hildegard; Burkhardt, Katrin; Kuch, Bernhard; Meisinger, Christa; Holle, Rolf

2015-01-01

Home-based secondary prevention programs led by nurses have been proposed to facilitate patients' adjustment to acute myocardial infarction (AMI). The objective of this study was to conduct secondary analyses of the three-year follow-up of a nurse-based case management for elderly patients discharged from hospital after an AMI. In a single-centre randomized two-armed parallel group trial of hospitalized patients with AMI ≥65 years, patients hospitalized between September 2008 and May 2010 in the Hospital of Augsburg, Germany, were randomly assigned to case management or usual care. The case-management intervention consisted of a nurse-based follow-up for three years including home visits and telephone calls. Study endpoints were time to first unplanned readmission or death, clinical parameters, functional status, depressive symptoms and malnutrition risk. Persons who assessed three-year outcomes and validated readmission data were blinded. The intention-to-treat approach was applied to the statistical analyses which included Cox Proportional Hazards models. Three hundred forty patients were allocated to receive case-management (n = 168) or usual care (n = 172). During three years, in the intervention group there were 80 first unplanned readmissions and 6 deaths, while the control group had 111first unplanned readmissions and 3 deaths. The intervention did not significantly affect time to first unplanned readmission or death (Hazard Ratio 0.89, 95% confidence interval (CI) 0.67-1.19; p = 0.439), blood pressure, cholesterol level, instrumental activities of daily life (IADL) (only for men), and depressive symptoms. However, patients in the intervention group had a significantly better functional status, as assessed by the HAQ Disability Index, IADL (only for women), and hand grip strength, and better SCREEN-II malnutrition risk scores than patients in the control group. A nurse-based management among elderly patients with AMI did not significantly affect time to unplanned readmissions or death during a three-year follow-up. However, the results indicate that functional status and malnutrition risk can be improved. Current Controlled Trials ISRCTN02893746.

DNA Methylation Analysis of the Angiotensin Converting Enzyme (ACE) Gene in Major Depression

PubMed Central

Zill, Peter; Baghai, Thomas C.; Schüle, Cornelius; Born, Christoph; Früstück, Clemens; Büttner, Andreas; Eisenmenger, Wolfgang; Varallo-Bedarida, Gabriella; Rupprecht, Rainer; Möller, Hans-Jürgen; Bondy, Brigitta

2012-01-01

Background The angiotensin converting enzyme (ACE) has been repeatedly discussed as susceptibility factor for major depression (MD) and the bi-directional relation between MD and cardiovascular disorders (CVD). In this context, functional polymorphisms of the ACE gene have been linked to depression, to antidepressant treatment response, to ACE serum concentrations, as well as to hypertension, myocardial infarction and CVD risk markers. The mostly investigated ACE Ins/Del polymorphism accounts for ∼40%–50% of the ACE serum concentration variance, the remaining half is probably determined by other genetic, environmental or epigenetic factors, but these are poorly understood. Materials and Methods The main aim of the present study was the analysis of the DNA methylation pattern in the regulatory region of the ACE gene in peripheral leukocytes of 81 MD patients and 81 healthy controls. Results We detected intensive DNA methylation within a recently described, functional important region of the ACE gene promoter including hypermethylation in depressed patients (p = 0.008) and a significant inverse correlation between the ACE serum concentration and ACE promoter methylation frequency in the total sample (p = 0.02). Furthermore, a significant inverse correlation between the concentrations of the inflammatory CVD risk markers ICAM-1, E-selectin and P-selectin and the degree of ACE promoter methylation in MD patients could be demonstrated (p = 0.01 - 0.04). Conclusion The results of the present study suggest that aberrations in ACE promoter DNA methylation may be an underlying cause of MD and probably a common pathogenic factor for the bi-directional relationship between MD and cardiovascular disorders. PMID:22808171

Central autonomic network mediates cardiovascular responses to acute inflammation: Relevance to increased cardiovascular risk in depression?

PubMed Central

Harrison, Neil A.; Cooper, Ella; Voon, Valerie; Miles, Ken; Critchley, Hugo D.

2013-01-01

Inflammation is a risk factor for both depression and cardiovascular disease. Depressed mood is also a cardiovascular risk factor. To date, research into mechanisms through which inflammation impacts cardiovascular health rarely takes into account central effects on autonomic cardiovascular control, instead emphasizing direct effects of peripheral inflammatory responses on endothelial reactivity and myocardial function. However, brain responses to inflammation engage neural systems for motivational and homeostatic control and are expressed through depressed mood state and changes in autonomic cardiovascular regulation. Here we combined an inflammatory challenge, known to evoke an acute reduction in mood, with neuroimaging to identify the functional brain substrates underlying potentially detrimental changes in autonomic cardiovascular control. We first demonstrated that alterations in the balance of low to high frequency (LF/HF) changes in heart rate variability (a measure of baroreflex sensitivity) could account for some of the inflammation-evoked changes in diastolic blood pressure, indicating a central (rather than solely local endothelial) origin. Accompanying alterations in regional brain metabolism (measured using 18FDG-PET) were analysed to localise central mechanisms of inflammation-induced changes in cardiovascular state: three discrete regions previously implicated in stressor-evoked blood pressure reactivity, the dorsal anterior and posterior cingulate and pons, strongly mediated the relationship between inflammation and blood pressure. Moreover, activity changes within each region predicted the inflammation-induced shift in LF/HF balance. These data are consistent with a centrally-driven component originating within brain areas supporting stressor evoked blood pressure reactivity. Together our findings highlight mechanisms binding psychological and physiological well-being and their perturbation by peripheral inflammation. PMID:23416033

Protective role of Osthole on myocardial cell apoptosis induced by doxorubicin in rats.

PubMed

Xu, Hongdang; Han, Yu; Zhang, Mengwei; Yan, Min; Gao, Chuanyu

2015-01-01

To explore the effect of Osthole on protecting myocardial cell apoptosis induced by doxorubicin during cardiac failure in rats. Myocardial cells isolated from the newborn SD rats were separated into three groups: cells treated with 1 μmol doxorubicin, cells treated with Osthole at three concentrations of 10, 20, and 40 μmol, cells treated neither with Osthole nor with doxorubicin were the control groups. Consequently, cell apoptosis of myocardial cells in each group was analyzed using TUNEL assay. Also, expressions of oxidase, NADPH, and ROS in myocardial cells were analyzed using different biological methods. Moreover, expressions of cell apoptosis associated proteins were analyzed using Western blotting. Compared with the controls, the results showed that cells received Osthole and doxorubicin treatments performed high percentage of cell apoptosis, suggesting that Osthole could anesis myocardial cell apoptosis induced by doxorubicin (P<0.05). Osthole of 10 μmol depressed the expressions of cell apoptosis associated proteins including Caspase-3 and Cytc, and enhancing expression of Bcl-XL expression (P<0.05). Osthole of 20 μmol significantly decreased the generation of intracellar superoxidase, NADPH, and NADPH activity in myocardial cells treated with doxorubicin (P<0.05). Moreover, Osthole of 20 μmol could significantly increase phosphorylated elF2α level in cells. Our study suggested that Osthole may play a protective role in suppressing myocardial apoptosis induced by doxorubicin through inhibiting NADPH and superoxidase production and downstream phosphorylated elF2α.

Protective role of Osthole on myocardial cell apoptosis induced by doxorubicin in rats

PubMed Central

Xu, Hongdang; Han, Yu; Zhang, Mengwei; Yan, Min; Gao, Chuanyu

2015-01-01

Objective: To explore the effect of Osthole on protecting myocardial cell apoptosis induced by doxorubicin during cardiac failure in rats. Methods: Myocardial cells isolated from the newborn SD rats were separated into three groups: cells treated with 1 μmol doxorubicin, cells treated with Osthole at three concentrations of 10, 20, and 40 μmol, cells treated neither with Osthole nor with doxorubicin were the control groups. Consequently, cell apoptosis of myocardial cells in each group was analyzed using TUNEL assay. Also, expressions of oxidase, NADPH, and ROS in myocardial cells were analyzed using different biological methods. Moreover, expressions of cell apoptosis associated proteins were analyzed using Western blotting. Results: Compared with the controls, the results showed that cells received Osthole and doxorubicin treatments performed high percentage of cell apoptosis, suggesting that Osthole could anesis myocardial cell apoptosis induced by doxorubicin (P<0.05). Osthole of 10 μmol depressed the expressions of cell apoptosis associated proteins including Caspase-3 and Cytc, and enhancing expression of Bcl-XL expression (P<0.05). Osthole of 20 μmol significantly decreased the generation of intracellar superoxidase, NADPH, and NADPH activity in myocardial cells treated with doxorubicin (P<0.05). Moreover, Osthole of 20 μmol could significantly increase phosphorylated elF2α level in cells. Conclusion: Our study suggested that Osthole may play a protective role in suppressing myocardial apoptosis induced by doxorubicin through inhibiting NADPH and superoxidase production and downstream phosphorylated elF2α. PMID:26617794

Effects of oxymatrine on sympathoexcitatory reflex induced by myocardial ischemic signaling mediated by P2X₃ receptors in rat SCG and DRG.

PubMed

Li, Guilin; Liu, Shuangmei; Yang, Yang; Xie, Jinyan; Liu, Jun; Kong, Fanjun; Tu, Guihua; Wu, Raoping; Li, Guodong; Liang, Shangdong

2011-04-05

Sympathoexcitatory reflex is characterized by an increase in blood pressure and sympathetic nerve activity. P2X₃ receptors in SCG neurons are involved in increasing sympathoexcitatory reflex after myocardial ischemic (MI) injury. The present study is aimed to explore the effects of oxymatrine (Oxy) on the transmission of myocardial ischemic signaling mediated by P2X₃ receptors in rat superior cervical ganglia (SCG) and cervical dorsal root ganglia (DRG) in the sympathoexcitatory reflex after myocardial ischemic injury. In this study, the expression levels of P2X₃ immunoreactivity, mRNA and protein were analyzed in SCG and DRG neurons by immunohistochemistry, in situ hybridization and Western blotting. The results show that the myocardial ischemic injury induces the increase of the systolic blood pressure and heart rate and upregulates the expression of P2X₃ receptors in SCG and DRG neurons. Upregulated expression of P2X₃ receptors in SCG and DRG neurons subsequently leads to the aggravated sympathoexcitatory reflex. Oxymatrine reduces the systolic blood pressure and heart rate in myocardial ischemic rats. After myocardial ischemic rats are treated with oxymatrine, the expression levels of P2X₃ immunoreactivity, mRNA and protein are lower than those in myocardial ischemic rats. Oxymatrine may decrease the expression of P2X₃ receptor and depress the aggravated sympathoexcitatory reflex induced by the nociceptive transmission of myocardial ischemic injury via P2X₃ receptors of rat SCG and DRG neurons. Copyright © 2011 Elsevier Inc. All rights reserved.

Cardiovascular magnetic resonance assessment of ventricular function and myocardial scarring before and early after repair of anomalous left coronary artery from the pulmonary artery

PubMed Central

2014-01-01

Background In patients with anomalous left coronary artery from the pulmonary artery (ALCAPA) left ventricular (LV) dilatation and dysfunction evolves due to diminished myocardial perfusion caused by coronary steal phenomenon. Using late gadolinium enhanced cardiovascular magnetic resonance (LGE-CMR) imaging, myocardial scarring has been shown in ALCAPA patients late after repair, however the incidence of scarring before surgery and its impact on postoperative course after surgical repair remained unknown. Methods 8 ALCAPA-patients (mean age 10.0 ± 5.8 months) underwent CMR before and early after (mean 4.9 ± 2.5 months) coronary reimplantation procedures. CMR included functional analysis and LGE for detection of myocardial scars. Results LV dilatation (mean LVEDVI 171 ± 94 ml/m2) and dysfunction (mean LV-EF 22 ± 10 %) was present in all patients and improved significantly after surgery (mean LVEDV 68 ± 42 ml/m2, p = 0.02; mean LV-EF 58 ± 19 %, p < 0.001). Preoperative CMR revealed myocardial scarring in 2 of the 8 patients and did not predict postoperative course. At follow-up CMR, one LGE-positive patient showed delayed recovery of LV function while myocardial scarring was still present in both patients. In two patients new-onset transmural scarring was found, although functional recovery after operation was sufficient. One of them showed a stenosis of the left coronary artery and required resurgery. Conclusions Despite diminished myocardial perfusion and severely compromised LV function, myocardial scarring was preoperatively only infrequently present. Improvement of myocardial function was independent of new-onset scarring while the impact of preoperative scarring still needs to be defined. PMID:24387660

Depression and Heart Diseases: Leading Health Problems.

PubMed

Raič, Matea

2017-12-01

Depression is the most common psychiatric disorder in the world population and the most frequent mental disorder in a primary health care. Unrecognized and untreated depression is associated with a poor outcome of treated chronic diseases which co-exist with depression. Depression and cardiovascular diseases are bidirectional related conditions, risks are for each other, and they often co-exist. Depression is a common disorder in cardiovascular patients with a prevalence of 20% to 45%, which is much more frequent than in the general population. In cardiac patients with acute myocardial infarction, depression occurs three times more often than in the general population. Depression has a direct effect on the pathophysiological changes of various organ systems, changing the values of blood pressure, heart rate, vasomotor tone, vascular resistance, blood viscosity and plasma volume. The potential mechanism for developing heart disease in depressed patients includes hypothalamic-pituitary-adrenal gland dysfunction, increased proinflammatory and prothrombotic factor activity, reduced omega-3 fatty acids, reduced heart rate variability, smoking, physical inactivity, reduced mood, self-esteem and self-efficacy.

Optimism and death: predicting the course and consequences of depression trajectories in response to heart attack.

PubMed

Galatzer-Levy, Isaac R; Bonanno, George A

2014-12-01

The course of depression in relation to myocardial infarction (MI), commonly known as heart attack, and the consequences for mortality are not well characterized. Further, optimism may predict both the effects of MI on depression as well as mortality secondary to MI. In the current study, we utilized a large population-based prospective sample of older adults (N=2,147) to identify heterogeneous trajectories of depression from 6 years prior to their first-reported MI to 4 years after. Findings indicated that individuals were at significantly increased risk for mortality when depression emerged after their first-reported MI, compared with resilient individuals who had no significant post-MI elevation in depression symptomatology. Individuals with chronic depression and those demonstrating pre-event depression followed by recovery after MI were not at increased risk. Further, optimism, measured before MI, prospectively differentiated all depressed individuals from participants who were resilient. © The Author(s) 2014.

IGF-1 Alleviates High Fat Diet-Induced Myocardial Contractile Dysfunction: Role of Insulin Signaling and Mitochondrial Function

PubMed Central

Zhang, Yingmei; Yuan, Ming; Bradley, Katherine M.; Dong, Feng; Anversa, Piero; Ren, Jun

2012-01-01

Obesity is often associated with reduced plasma IGF-1 levels, oxidative stress, mitochondrial damage and cardiac dysfunction. This study was designed to evaluate the impact of IGF-1 on high fat diet-induced oxidative, myocardial, geometric and mitochondrial responses. FVB and cardiomyocyte-specific IGF-1 overexpression transgenic mice were fed a low (10%) or high fat (45%) diet to induce obesity. High fat diet feeding led to glucose intolerance, elevated plasma levels of leptin, interleukin-6, insulin and triglyceride as well as reduced circulating IGF-1 levels. Echocardiography revealed reduced fractional shortening, increased end systolic and diastolic diameter, increased wall thickness, and cardiac hypertrophy in high fat-fed FVB mice. High fat diet promoted ROS generation, apoptosis, protein and mitochondrial damage, reduced ATP content, cardiomyocyte cross-sectional area, contractile and intracellular Ca2+ dysregulation, including depressed peak shortening and maximal velocity of shortening/relengthening, prolonged duration of relengthening, and dampened intracellular Ca2+ rise and clearance. Western blot analysis revealed disrupted phosphorylation of insulin receptor, post-receptor signaling molecules IRS-1 (tyrosine/serine phosphorylation), Akt, GSK3β, Foxo3a, mTOR, as well as downregulated expression of mitochondrial proteins PPARγ coactivator 1α (PGC1α) and UCP-2. Intriguingly, IGF-1 mitigated high fat diet feeding-induced alterations in ROS, protein and mitochondrial damage, ATP content, apoptosis, myocardial contraction, intracellular Ca2+ handling and insulin signaling, but not whole body glucose intolerance and cardiac hypertrophy. Exogenous IGF-1 treatment also alleviated high fat diet-induced cardiac dysfunction. Our data revealed that IGF-1 alleviates high fat diet-induced cardiac dysfunction despite persistent cardiac remodeling, possibly due to preserved cell survival, mitochondrial function and insulin signaling. PMID:22275536

Assessment of mechanical ventricular synchrony in Doberman Pinschers with dilated cardiomyopathy.

PubMed

López-Alvarez, Jordi; Fonfara, Sonja; Pedro, Brigite; Stephenson, Hannah; Cripps, Peter J; Dukes-McEwan, Joanna

2011-09-01

Loss of temporal synchrony of myocardial contraction has been shown to reduce systolic function and be responsible for disease progression in people. The objective of this study is the assessment of inter- and intra ventricular synchrony in healthy Doberman Pinschers and those with dilated cardiomyopathy (DCM) by use of conventional Doppler and tissue velocity imaging. A total of 60 scans from 35 client-owned Doberman Pinschers presented for cardiac evaluation were analysed. Retrospective analysis of data. Using the European Society of Veterinary Cardiology DCM taskforce scoring system, Doberman Pinschers were classified into 4 groups: Control (Group 1; n=12), depressed systolic function other than DCM (Group 2; n=9), preclinical DCM (Group 3; n=8) and symptomatic DCM (Group 4; n=6). The time intervals between the beginning of the QRS complex and the peak velocity of pulmonic flow (Q-P) and the peak aortic flow (Q-Ao) were used to assess global synchrony between both ventricles. The time intervals between the beginning of the QRS complex and the peak myocardial systolic velocity (Q-peak S) and the onset of myocardial systolic velocity (Q-start S) were measured at the base of the right and left ventricular free wall (RVFW and LVFW) and interventricular septum (IVS), and used to determine segmental longitudinal inter- and intra ventricular synchrony. No significant loss of global or segmental longitudinal inter- or intra ventricular synchrony was identified between the groups. Impairment of longitudinal fibre synchrony does not appear to be significantly associated with clinical status of DCM in Doberman Pinschers, although it was identified in certain individuals. Copyright © 2011 Elsevier B.V. All rights reserved.

Contractility and Ventricular Systolic Stiffening in Hypertensive Heart Disease: Insights into the Pathogenesis of Heart Failure with Preserved Ejection Fraction

PubMed Central

Borlaug, Barry A.; Lam, Carolyn S.P.; Roger, Véronique L.; Rodeheffer, Richard J.; Redfield, Margaret M.

2009-01-01

Objectives: 1) Compare left ventricular (LV) systolic stiffness and contractility in normal subjects, hypertensives without heart failure, and patients with heart failure and preserved ejection fraction (HFpEF); and 2) Determine whether LV systolic stiffness or myocardial contractility are associated with mortality in HFpEF. Background: Arterial load is increased in hypertension and is matched by increased end-systolic LV stiffness (ventricular-arterial coupling). Increased end-systolic LV stiffness may be mediated by enhanced myocardial contractility or processes which increase passive myocardial stiffness. Methods: Healthy controls (n=617), hypertensives (No HF, n=719) and patients with HFpEF (n=244, 96% hypertensive) underwent echo-Doppler characterization of arterial (Ea) and LV end-systolic (Ees) stiffness (elastance), ventricular-arterial coupling (Ea/Ees ratio), chamber-level and myocardial contractility (stress-corrected midwall shortening). Results: Ea and Ees were similarly elevated in hypertensives with or without HFpEF compared with controls, but ventricular-arterial coupling was similar across groups. In hypertensives, elevated Ees was associated with enhanced chamber-level and myocardial contractility, while in HFpEF, chamber and myocardial contractility were depressed compared with both hypertensives and controls. Group differences persisted after adjusting for geometry. In HFpEF, impaired myocardial contractility (but not Ees) was associated with increased age-adjusted mortality. Conclusions: While arterial load is elevated and matched by increased LV systolic stiffness in hypertension with or without HFpEF, the mechanisms of systolic LV stiffening differ substantially. These data suggest that myocardial contractility increases to match arterial load in asymptomatic hypertensive heart disease, but that progression to HFpEF may be mediated by processes which simultaneously impair myocardial contractility and increase passive myocardial stiffness. PMID:19628115

Correlations among Psychological Resilience, Self-Efficacy, and Negative Emotion in Acute Myocardial Infarction Patients after Percutaneous Coronary Intervention.

PubMed

Liu, Neng; Liu, Shaohui; Yu, Nan; Peng, Yunhua; Wen, Yumei; Tang, Jie; Kong, Lingyu

2018-01-01

We investigated the influencing factors of the psychological resilience and self-efficacy of acute myocardial infarction (AMI) patients after percutaneous coronary intervention (PCI) and the relationships of psychological resilience and self-efficacy with negative emotion. Eighty-eight participants were enrolled. Psychological resilience, self-efficacy, and negative emotion were assessed with the Psychological Resilience Scale, Self-Efficacy Scale, Zung Self-Rating Anxiety Scale (SAS), and Zung Self-Rating Depression Scale (SDS), respectively. Furthermore, the relationships of psychological resilience and self-efficacy with negative emotion were investigated. The average scores of psychological resilience, self-efficacy, anxiety, and depression were 70.08 ± 13.26, 21.56 ± 9.66, 53.68 ± 13.10, and 56.12 ± 12.37, respectively. The incidences of anxiety and depression were 23.90% (21/88) and 28.40% (25/88), respectively. The psychological resilience and self-efficacy scores of AMI patients after PCI varied significantly with age and economic status. SAS scores and SDS scores were significantly negatively correlated with psychological resilience and self-efficacy. Negative emotions in AMI patients after PCI are closely related to psychological resilience and self-efficacy. Therefore, anxiety and depression could be alleviated by improving the psychological resilience and self-efficacy of patients undergoing PCI, thus improving patients' quality of life.

Treatment of depression and anxiety with internet-based cognitive behavior therapy in patients with a recent myocardial infarction (U-CARE Heart): study protocol for a randomized controlled trial.

PubMed

Norlund, Fredrika; Olsson, Erik M G; Burell, Gunilla; Wallin, Emma; Held, Claes

2015-04-11

Major depression and depressive symptoms are common in patients with a recent myocardial infarction (MI), and depression is associated with adverse cardiovascular outcomes. Anxiety post-MI is less studied, but occurs commonly in patients with heart disease, and is also considered a risk factor for recurrence of cardiac events. Cognitive behavior therapy (CBT) is an established therapy for depression and anxiety disorders. To the best of our knowledge, there have not been any studies to determine if internet-based CBT (iCBT) can reduce the symptoms of depression and anxiety in patients with a recent MI. The main aim of the U-CARE Heart trial is to evaluate an iCBT intervention for patients with a recent MI. This is a randomized, controlled, prospective study with a multicenter design. A total of 500 participants will be randomized at a 1:1 ratio, around two months after an acute MI, to either iCBT or to a control group. Both groups will receive an optimal standard of care according to guidelines. The intervention consists of a self-help program delivered via the internet with individual online support from a psychologist. Treatment duration is 14 weeks. The primary outcome is change in patients' self-rated anxiety and depression symptoms from baseline to end of treatment. An internal pilot study was conducted indicating sufficient levels of study acceptability and engagement in treatment. The present study is designed to evaluate an iCBT intervention targeting symptoms of depression and anxiety in a post-MI population. If effective, iCBT has several advantages, and will potentially be implemented as an easily accessible treatment option added to modern standard of care. This trial was registered with Clinicaltrials.gov (identifier: NCT01504191 ) on 19 December 2011.

Use of beta blockers in postinfarct prophylaxis: aspects on quality of life.

PubMed

Hjalmarson, A C

1987-07-01

The value of beta blockade after myocardial infarction is extremely well documented. Close to 50 randomized trials have been performed, involving about 40,000 patients with short- or long-term follow-up. Over 20,000 patients have been included in more than 20 placebo-controlled trials with a follow-up period of 3 months or more. In long-term follow-up studies, about 1 to 2 weeks to 1 year after myocardial infarction, mortality was reduced by 21% and reinfarction by 24% (about 20,000 patients in 24 trials). The trial medication was withdrawn in about 20% in both placebo and beta-blocker groups in the major trials. In addition to reduction of mortality and reinfarction rate, benefits have clearly been demonstrated on severity of chest pain, arrhythmias, and other thromboatherosclerotic complications, as well as on readmissions. Significantly more patients experienced congestive heart failure, hypotension, bradycardia, and cold hands with beta-blocker treatment, whereas no clear-cut difference was found for atrioventricular block, bronchial constriction, and intermittent claudication. Some studies have reported more tiredness, depression, and gastrointestinal disturbances. In the Stockholm metoprolol trial, analyses on quality of life have been performed. In this trial, 3 years of metoprolol treatment after myocardial infarction resulted in a prolongation of both survival and time spent completely asymptomatic, as well as in an optimal functional state. Furthermore, less time was spent disabled after serious atherosclerotic complications. Long-term beta blockade after myocardial infarction reduces mortality and morbidity but causes adverse reactions in some patients. With proper selection of patients and type and dosage of beta blocker, survival without atherosclerotic complications and side effects can be prolonged.

[ECG and ST-elevation myocardial infarction in multivessel coronary disease].

PubMed

Slavich, Gianaugusto; Spedicato, Leonardo; Poli, Stefano; Sappa, Roberta; Piccoli, Gianluca

2010-12-01

Percutaneous coronary intervention is the first-line treatment for ST-elevation myocardial infarction. In the setting of multivessel disease, concomitant reperfusion of all obstructed vessels is controversial, notably when the culprit vessel cannot be easily identified. We describe two cases with acute inferior-posterior myocardial infarction (ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads). In the first case, angiography revealed severe three-vessel disease and the culprit vessel could not be identified. Following standard pharmacological therapy, the clinical picture and the ECG pattern improved, so that coronary revascularization was postponed. In the second case, angiography showed two-vessel disease with total occlusion of the right coronary and left circumflex arteries, which was treated with coronary angioplasty and drug-eluting stent implantation on the right coronary artery. In patients who undergo coronary angioplasty immediately, careful reading of the ECG can be a reliable tool for the identification of the culprit vessel in ST-elevation myocardial infarction associated with multivessel disease, allowing to choose the appropriate reperfusion strategy.

Epicardial infarct repair with bioinductive extracellular matrix promotes vasculogenesis and myocardial recovery.

PubMed

Mewhort, Holly E M; Turnbull, Jeannine D; Satriano, Alessandro; Chow, Kelvin; Flewitt, Jacqueline A; Andrei, Adin-Cristian; Guzzardi, David G; Svystonyuk, Daniyil A; White, James A; Fedak, Paul W M

2016-05-01

Infarcted myocardium can remodel after successful reperfusion, resulting in left ventricular dilation and heart failure. Epicardial infarct repair (EIR) using a bioinductive extracellular matrix (ECM) biomaterial is a novel surgical approach to promote endogenous myocardial repair and functional recovery after myocardial infarction. Using a pre-clinical porcine model of coronary ischemia-reperfusion, we assessed the effects of EIR on regional functional recovery, safety, and possible mechanisms of benefit. An ECM biomaterial (CorMatrix ECM) was applied to the epicardium after 75 minutes of coronary ischemia in a porcine model. Following ischemia-reperfusion injury, animals were randomly assigned in 2:1 fashion to EIR (n = 8) or sham treatment (n = 4). Serial cardiac magnetic resonance imaging was performed on normal (n = 4) and study animals at baseline (1 week) and 6 weeks after treatment. Myocardial function and tissue characteristics were assessed. Functional myocardial recovery was significantly increased by EIR compared with sham treatment (change in regional myocardial contraction at 6 weeks, 28.6 ± 14.0% vs 4.2 ± 13.5% wall thickening, p < 0.05). Animals receiving EIR had reduced adhesions compared with animals receiving sham treatment (1.44 ± 0.51 vs 3.08 ± 0.89, p < 0.05). Myocardial fibrosis was not increased, and EIR did not cause myocardial constriction, as left ventricular compliance by passive pressure distention at matched volumes was similar between groups (13.9 ± 4.0 mm Hg in EIR group vs 16.0 ± 5.2 mm Hg in sham group, p = 0.61). Animals receiving EIR showed evidence of vasculogenesis in the region of functional recovery. In addition to the beneficial effects of successful reperfusion, EIR using a bioinductive ECM enhances myocardial repair and functional recovery. Clinical translation of EIR early after myocardial infarction as an adjunct to surgical revascularization may be warranted in the future. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

Depressive Symptoms and Mental Stress Induced Myocardial Ischemia in Patients with Coronary Heart Disease

PubMed Central

Boyle, Stephen; Samad, Zainab; Becker, Richard C.; Williams, Redford; Kuhn, Cynthia; Ortel, Thomas L.; Kuchibhatla, Maragatha; Prybol, Kevin; Rogers, Joseph; O’Connor, Christopher; Velazquez, Eric J.; Jiang, Wei

2015-01-01

Objectives The primary focus of this study was to examine associations between depressive symptoms and mental stress induced myocardial ischemia (MSIMI) in patients with coronary heart disease (CHD). Methods Adult patients with documented CHD were recruited for baseline mental stress and exercise stress screening testing as a part of the enrollment process of the REMIT trial. Patients were administered the Beck Depression Inventory II (BDI-II) and the Center for Epidemiologic Studies Depression Scale (CESD). Following a 24-48-hour Beta-blocker withdrawal, consented patients completed three mental stress tests followed by a treadmill exercise test. Ischemia was defined as 1) any development or worsening of any wall motion abnormality (WMA), 2) reduction of left ventricular ejection fraction (LVEF) ≥ 8% by transthoracic echocardiography, and/or ischemic ST-segment change by electrocardiography during stress testing. MSIMI was considered present when ischemia occurred in at least one mental test. Data were analyzed using logistic regression adjusting for age, gender, and resting left ventricular ejection fraction. Results One hundred twenty five (44.2 %) of 283 patients were found to have MSIMI and 93 (32.9%) had ESIMI. Unadjusted analysis showed that BDI-II scores were positively associated with the probability of MSIMI (OR = .1.30: 95% CI 1.06 – 1.60, p = .013) and number of MSIMI positive tasks (all p < .005). These associations were still significant after adjustment for covariates (ps ≤ .05). Conclusions In CHD patients, depressive symptoms were associated with a higher probability of MSIMI. These observations may enhance our understanding of the mechanisms contributing to the association of depressive symptoms to future cardiovascular events. PMID:24163385

Detection and monitoring of cardiotoxicity-what does modern cardiology offer?

PubMed

Jurcut, Ruxandra; Wildiers, Hans; Ganame, Javier; D'hooge, Jan; Paridaens, Robert; Voigt, Jens-Uwe

2008-05-01

With new anticancer therapies, many patients can have a long life expectancy. Treatment-related comorbidities become an issue for cancer survivors. Cardiac toxicity remains an important side effect of anticancer therapies. Myocardial dysfunction can become apparent early or long after end of therapy and may be irreversible. Detection of cardiac injury is crucial since it may facilitate early therapeutic measures. Traditionally, chemotherapy-induced cardiotoxicity has been detected by measuring changes in left ventricular ejection fraction. This parameter is, however, insensitive to subtle changes in myocardial function as they occur in early cardiotoxicity. This review will discuss conventional and modern cardiologic approaches of assessing myocardial function. It will focus on Doppler myocardial imaging, a method which allows to sensitively measure myocardial function parameters like myocardial velocity, deformation (strain), or deformation rate (strain rate) and which has been shown to reliably detect early abnormalities in both regional and global myocardial function in an early stage. Other newer echocardiographic function estimators are based on automated border detection algorithms and ultrasonic integrated backscatter analysis. A further technique to be discussed is dobutamine stress echocardiography. The use of new biomarkers like B-type natriuretic peptide and troponin and less often used imaging techniques like magnetic resonance imaging and computed tomography will also be mentioned.

Sevoflurane postconditioning improves myocardial mitochondrial respiratory function and reduces myocardial ischemia-reperfusion injury by up-regulating HIF-1

PubMed Central

Yang, Long; Xie, Peng; Wu, Jianjiang; Yu, Jin; Yu, Tian; Wang, Haiying; Wang, Jiang; Xia, Zhengyuan; Zheng, Hong

2016-01-01

Background: Sevoflurane postconditioning (SPostC) can exert myocardial protective effects similar to ischemic preconditioning. However, the exact myocardial protection mechanism by SPostC is unclear. Studies indicate that hypoxia-inducible factor-1 (HIF-1) maintains cellular respiration homeostasis by regulating mitochondrial respiratory chain enzyme activity under hypoxic conditions. This study investigated whether SPostC could regulate the expression of myocardial HIF-1α and to improve mitochondrial respiratory function, thereby relieving myocardial ischemia-reperfusion injury in rats. Methods: The myocardial ischemia-reperfusion rat model was established using the Langendorff isolated heart perfusion apparatus. Additionally, postconditioning was performed using sevoflurane alone or in combination with the HIF-1α inhibitor 2-methoxyestradiol (2ME2). The changes in hemodynamic parameters, HIF-1α protein expression levels, mitochondrial respiratory function and enzyme activity, mitochondrial reactive oxygen species (ROS) production rates, and mitochondrial ultrastructure were measured or observed. Results: Compared to the ischemia-reperfusion (I/R) group, HIF-1α expression in the SPostC group was significantly up-regulated. Additionally, cardiac function indicators, mitochondrial state 3 respiratory rate, respiratory control ratio (RCR), cytochrome C oxidase (CcO), NADH oxidase (NADHO), and succinate oxidase (SUCO) activities, mitochondrial ROS production rate, and mitochondrial ultrastructure were significantly better than those in the I/R group. However, these advantages were completely reversed by the HIF-1α specific inhibitor 2ME2 (P<0.05). Conclusion: The myocardial protective function of SPostC might be associated with the improvement of mitochondrial respiratory function after up-regulation of HIF-1α expression. PMID:27830025

Sevoflurane postconditioning improves myocardial mitochondrial respiratory function and reduces myocardial ischemia-reperfusion injury by up-regulating HIF-1.

PubMed

Yang, Long; Xie, Peng; Wu, Jianjiang; Yu, Jin; Yu, Tian; Wang, Haiying; Wang, Jiang; Xia, Zhengyuan; Zheng, Hong

2016-01-01

Sevoflurane postconditioning (SPostC) can exert myocardial protective effects similar to ischemic preconditioning. However, the exact myocardial protection mechanism by SPostC is unclear. Studies indicate that hypoxia-inducible factor-1 (HIF-1) maintains cellular respiration homeostasis by regulating mitochondrial respiratory chain enzyme activity under hypoxic conditions. This study investigated whether SPostC could regulate the expression of myocardial HIF-1α and to improve mitochondrial respiratory function, thereby relieving myocardial ischemia-reperfusion injury in rats. The myocardial ischemia-reperfusion rat model was established using the Langendorff isolated heart perfusion apparatus. Additionally, postconditioning was performed using sevoflurane alone or in combination with the HIF-1α inhibitor 2-methoxyestradiol (2ME2). The changes in hemodynamic parameters, HIF-1α protein expression levels, mitochondrial respiratory function and enzyme activity, mitochondrial reactive oxygen species (ROS) production rates, and mitochondrial ultrastructure were measured or observed. Compared to the ischemia-reperfusion (I/R) group, HIF-1α expression in the SPostC group was significantly up-regulated. Additionally, cardiac function indicators, mitochondrial state 3 respiratory rate, respiratory control ratio (RCR), cytochrome C oxidase (C c O), NADH oxidase (NADHO), and succinate oxidase (SUCO) activities, mitochondrial ROS production rate, and mitochondrial ultrastructure were significantly better than those in the I/R group. However, these advantages were completely reversed by the HIF-1α specific inhibitor 2ME2 ( P <0.05). The myocardial protective function of SPostC might be associated with the improvement of mitochondrial respiratory function after up-regulation of HIF-1α expression.

Symptom-limited exercise testing causes sustained diastolic dysfunction in patients with coronary disease and low effort tolerance.

PubMed

Fragasso, G; Benti, R; Sciammarella, M; Rossetti, E; Savi, A; Gerundini, P; Chierchia, S L

1991-05-01

Exercise stress testing is routinely used for the noninvasive assessment of coronary artery disease and is considered a safe procedure. However, the provocation of severe ischemia might potentially cause delayed recovery of myocardial function. To investigate the possibility that maximal exercise testing could induce prolonged impairment of left ventricular function, 15 patients with angiographically proved coronary disease and 9 age-matched control subjects with atypical chest pain and normal coronary arteries were studied. Radionuclide ventriculography was performed at rest, at peak exercise, during recovery and 2 and 7 days after exercise. Ejection fraction, peak filling and peak emptying rates and left ventricular wall motion were analyzed. All control subjects had a normal exercise test at maximal work loads and improved left ventricular function on exercise. Patients developed 1 mm ST depression at 217 +/- 161 s at a work load of 70 +/- 30 W and a rate-pressure product of 18,530 +/- 4,465 mm Hg x beats/min. Although exercise was discontinued when angina or equivalent symptoms occurred, in all patients diagnostic ST depression (greater than or equal to 1 mm) developed much earlier than symptoms. Predictably, at peak exercise patients showed a decrease in ejection fraction and peak emptying and filling rates. Ejection fraction and peak emptying rate normalized within the recovery period, whereas peak filling rate remained depressed throughout recovery (p less than 0.002) and was still reduced 2 days after exercise (p less than 0.02). In conclusion, in patients with severe impairement of coronary flow reserve, maximal exercise may cause sustained impairement of diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Intra-renal delivery of mesenchymal stem cells attenuates myocardial injury after reversal of hypertension in porcine renovascular disease.

PubMed

Eirin, Alfonso; Zhu, Xiang-Yang; Ferguson, Christopher M; Riester, Scott M; van Wijnen, Andre J; Lerman, Amir; Lerman, Lilach O

2015-01-19

Percutaneous transluminal renal angioplasty (PTRA) fails to fully improve cardiac injury and dysfunction in patients with renovascular hypertension (RVH). Mesenchymal stem cells (MSCs) restore renal function, but their potential for attenuating cardiac injury after reversal of RVH has not been explored. We hypothesized that replenishment of MSCs during PTRA would improve cardiac function and oxygenation, and decrease myocardial injury in porcine RVH. Pigs were studied after 16 weeks of RVH, RVH treated 4 weeks earlier with PTRA with or without adjunct intra-renal delivery of MSC (10^6 cells), and controls. Cardiac structure, function (fast-computed tomography (CT)), and myocardial oxygenation (Blood-Oxygen-Level-Dependent- magnetic resonance imaging) were assessed in-vivo. Myocardial microvascular density (micro-CT) and myocardial injury were evaluated ex-vivo. Kidney venous and systemic blood levels of inflammatory markers were measured and their renal release calculated. PTRA normalized blood pressure, yet stenotic-kidney glomerular filtration rate, similarly blunted in RVH and RVH + PTRA, normalized only in PTRA + MSC-treated pigs. PTRA attenuated left ventricular remodeling, whereas myocardial oxygenation, subendocardial microvascular density, and diastolic function remained decreased in RVH + PTRA, but normalized in RVH + PTRA-MSC. Circulating isoprostane levels and renal release of inflammatory cytokines increased in RVH and RVH + PTRA, but normalized in RVH + PTRA-MSC, as did myocardial oxidative stress, inflammation, collagen deposition, and fibrosis. Intra-renal MSC delivery during PTRA preserved stenotic-kidney function, reduced systemic oxidative stress and inflammation, and thereby improved cardiac function, oxygenation, and myocardial injury four weeks after revascularization, suggesting a therapeutic potential for adjunctive MSC delivery to preserve cardiac function and structure after reversal of experimental RVH.

Triiodothyronine activates lactate oxidation without impairing fatty acid oxidation and improves weaning from extracorporeal membrane oxygenation.

PubMed

Kajimoto, Masaki; Ledee, Dolena R; Xu, Chun; Kajimoto, Hidemi; Isern, Nancy G; Portman, Michael A

2014-01-01

Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. It has previously been shown that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. METHODS AND RESULTS: Nineteen immature piglets (9.1-15.3 kg) were separated into 3 groups with ECMO (6.5 h) and wean: normal circulation (Group-C); transient coronary occlusion (10 min) for ischemia-reperfusion (IR) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon ((13)C)-labeled lactate, medium-chain and long-chain FAs, was infused as oxidative substrates. Substrate fractional contribution (FC) to the citric acid cycle was analyzed by(13)C-nuclear magnetic resonance. ECMO depressed circulating T3 levels to 40% of the baseline at 4 h and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [adenosine triphosphate]/[adenosine diphosphate] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR. T3 releases inhibition of lactate oxidation following IR injury without impairing FA oxidation. These findings indicate that T3 depression during ECMO is maladaptive, and that restoring levels improves metabolic flux and enhances contractile function during weaning.

A new methodological approach to assess cardiac work by pressure-volume and stress-length relations in patients with aortic valve stenosis and dilated cardiomyopathy.

PubMed

Alter, P; Rupp, H; Rominger, M B; Klose, K J; Maisch, B

2008-01-01

In experimental animals, cardiac work is derived from pressure-volume area and analyzed further using stress-length relations. Lack of methods for determining accurately myocardial mass has until now prevented the use of stress-length relations in patients. We hypothesized, therefore, that not only pressure-volume loops but also stress-length diagrams can be derived from cardiac volume and cardiac mass as assessed by cardiac magnetic resonance imaging (CMR) and invasively measured pressure. Left ventricular (LV) volume and myocardial mass were assessed in seven patients with aortic valve stenosis (AS), eight with dilated cardiomyopathy (DCM), and eight controls using electrocardiogram (ECG)-gated CMR. LV pressure was measured invasively. Pressure-volume curves were calculated based on ECG triggering. Stroke work was assessed as area within the pressure-volume loop. LV wall stress was calculated using a thick-wall sphere model. Similarly, stress-length loops were calculated to quantify stress-length-based work. Taking the LV geometry into account, the normalization with regard to ventricular circumference resulted in "myocardial work." Patients with AS (valve area 0.73+/-0.18 cm(2)) exhibited an increased LV myocardial mass when compared with controls (P<0.05). LV wall stress was increased in DCM but not in AS. Stroke work of AS was unchanged when compared with controls (0.539+/-0.272 vs 0.621+/-0.138 Nm, not significant), whereas DCM exhibited a significant depression (0.367+/-0.157 Nm, P<0.05). Myocardial work was significantly reduced in both AS and DCM when compared with controls (129.8+/-69.6, 200.6+/-80.1, 332.2+/-89.6 Nm/m(2), P<0.05), also after normalization (7.40+/-5.07, 6.27+/-3.20, 14.6+/-4.07 Nm/m(2), P<0.001). It is feasible to obtain LV pressure-volume and stress-length diagrams in patients based on the present novel methodological approach of using CMR and invasive pressure measurement. Myocardial work was reduced in patients with DCM and noteworthy also in AS, while stroke work was reduced in DCM only. Most likely, deterioration of myocardial work is crucial for the prognosis. It is suggested to include these basic physiological procedures in the clinical assessment of the pump function of the heart.

Initiation of Beta-Blocker Therapy and Depression After Acute Myocardial Infarction

PubMed Central

Ranchord, Anil M.; Spertus, John A.; Buchanan, Donna M.; Gosch, Kensey L.; Chan, Paul S.

2016-01-01

Introduction Although beta (β)-blockers reduce mortality after acute myocardial infarction (AMI), early reports linking β-blocker use with subsequent depression have potentially limited their use in vulnerable patients. We sought to provide empirical evidence to support or refute this concern by examining the association between β-blocker initiation and change in depressive symptoms in AMI patients. Methods Using data from 2 US multi-center, prospective registries of AMI patients, we examined 1-, 6-, and 12-month changes in depressive symptoms after the index hospitalization among patients who were β-blocker naïve on admission. Depressive symptoms were assessed using the validated 8-item Patient Health Questionnaire (PHQ-8), which rates depressive symptoms from 0 to 24, with higher scores indicating more depressive symptoms. A propensity-matched repeated measures linear regression model was used to compare change in depressive symptoms among patients who were and were not initiated on a β-blocker after AMI. Results Of 3470 AMI patients who were β-blocker naïve on admission, 3190 (91.9%) were initiated on a β-blocker and 280 (8.1%) were not. Baseline PHQ-8 scores were higher in patients not initiated on a β-blocker (mean 5.78 ± 5.45 vs. 4.88 ± 5.11, P=0.005). PHQ-8 scores were progressively lower at 1, 6 and 12 months in both the β-blocker (mean decrease at 12 months, 1.16; p<0.0001) and no β-blocker groups (mean decrease, 1.71; p<0.0001). After propensity matching 201 untreated patients with 567 treated patients, initiation of β-blocker therapy was not associated with a difference in mean change in PHQ-8 scores at 1, 6 or 12 months after AMI (absolute mean difference with β-blocker initiation at 12 months of 0.08, 95% CI: −0.81 to 0.96, P=0.86). Conclusions Initiation of β-blocker therapy after AMI was not associated with an increase in depressive symptoms. Restricting β-blocker use because of concerns about depression appears unwarranted and may lead to under-treatment of AMI patients. PMID:26995368

Essential Hypotension and Allostasis Registry

ClinicalTrials.gov

2018-03-30

Blood Pressure; Depression; Panic Attack; Fibromyalgia; POTS; Inappropriate Sinus Tachycardia; Coronary Heart Disease; Acute Coronary Syndrome (ACS); Acute Myocardial Infarction (AMI); Cerebrovascular Disease (CVD); Transient Ischemic Attack (TIA); Atrial Fibrillation; Diabetes Mellitus; Cancer; Systolic Heart Failure; Diastolic Heart Failure; Chronic Fatigue Syndrome; Syncope; Vasovagal Syncope

Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury.

PubMed

McDonough, Kathleen H; Virag, Jitka Ismail

2006-01-01

Sepsis, bacteremia and inflammation cause myocardial depression. The mechanism of the dysfunction is not clearly established partly because dysfunction can be elicited by many different mechanisms which can all manifest in disruption of myocardial mechanical function. In addition the models of sepsis and bacteremia and inflammation may vary drastically in the sequence of the coordinated immune response to the inflammatory or septic stimulus. Patterns of cytokine expression can vary as can other responses of the immune system. Patterns of neurohumoral activation in response to the stress of sepsis or bacteremia or inflammation can also vary in both magnitude of response and temporal sequence of response. Stress induced activation of the sympathetic nervous system and humoral responses to stress have a wide range of intensity that can be elicited. The fairly uniform response of the myocardium indicating cardiac dysfunction is surprisingly constant. Systolic performance, as measured by stroke volume or cardiac output and pressure work as estimated by ventricular pressure, are impaired when myocardial contraction is compromised. At times, diastolic function, assessed by ventricular relaxation and filling, is impaired. In addition to the dysfunction that occurs, there is a longer term response of the myocardium to sepsis, and this response is similar to that which is elicited in the heart by multiple brief ischemia/reperfusion episodes and by numerous pharmacological agents as well as heat stress and modified forms of lipopolysaccharide. The myocardium develops protection after an initial stress such that during a second stress, the myocardium does not exhibit as much damage as does a non-protected heart. Many agents can induce this protection which has been termed preconditioning. Both early preconditioning (protection that is measurable min to hours after the initial stimulus) and late preconditioning (protection that is measurable hours to days after the initial trigger or stimulus) are effective in protecting the heart from prolonged ischemia and reperfusion injury. Understanding the mechanisms of sepsis/bacteremia induced dysfunction and protection and if the dysfunction and protection are the products of the same intracellular pathways is important in protecting the heart from failing to perform adequately during severe sepsis and/or septic shock and for understanding the multitude of mechanism by which the myocardium maintains reserve capacity.

Experimental heart failure causes depression-like behavior together with differential regulation of inflammatory and structural genes in the brain

PubMed Central

Frey, Anna; Popp, Sandy; Post, Antonia; Langer, Simon; Lehmann, Marc; Hofmann, Ulrich; Sirén, Anna-Leena; Hommers, Leif; Schmitt, Angelika; Strekalova, Tatyana; Ertl, Georg; Lesch, Klaus-Peter; Frantz, Stefan

2014-01-01

Background: Depression and anxiety are common and independent outcome predictors in patients with chronic heart failure (CHF). However, it is unclear whether CHF causes depression. Thus, we investigated whether mice develop anxiety- and depression-like behavior after induction of ischemic CHF by myocardial infarction (MI). Methods and Results: In order to assess depression-like behavior, anhedonia was investigated by repeatedly testing sucrose preference for 8 weeks after coronary artery ligation or sham operation. Mice with large MI and increased left ventricular dimensions on echocardiography (termed CHF mice) showed reduced preference for sucrose, indicating depression-like behavior. 6 weeks after MI, mice were tested for exploratory activity, anxiety-like behavior and cognitive function using the elevated plus maze (EPM), light-dark box (LDB), open field (OF), and object recognition (OR) tests. In the EPM and OF, CHF mice exhibited diminished exploratory behavior and motivation despite similar movement capability. In the OR, CHF mice had reduced preference for novelty and impaired short-term memory. On histology, CHF mice had unaltered overall cerebral morphology. However, analysis of gene expression by RNA-sequencing in prefrontal cortical, hippocampal, and left ventricular tissue revealed changes in genes related to inflammation and cofactors of neuronal signal transduction in CHF mice, with Nr4a1 being dysregulated both in prefrontal cortex and myocardium after MI. Conclusions: After induction of ischemic CHF, mice exhibited anhedonic behavior, decreased exploratory activity and interest in novelty, and cognitive impairment. Thus, ischemic CHF leads to distinct behavioral changes in mice analogous to symptoms observed in humans with CHF and comorbid depression. PMID:25400562

Hemodynamic effects of aerosol propellants. I. Cardiac depression in the dog.

PubMed

Simaan, J A; Aviado, D M

1975-11-01

The inhalation of fluorocarbons caused a depression of myocardial contractility, aortic hypotension, a decrease in cardiac output and an increase in pulmonary vascular resistance. The minimal concentrations that elicited these changes are as follows: 1% trichlorofluoromethane (FC11); 2.5% dichlorotetrafluoroethane (FC114); and 10% dichlorodifluoromethane (FC12). Inhalation of 20% octafluorocyclobutane (FC318) and difluoroethane (FC152a) did not influence these hemodynamic parameters. As in previous comparisons, the most widely used aerosol propellants are potentially cardiotoxic in the anesthetized dog.

Coronary microvascular dysfunction equivalent to left main coronary artery disease.

PubMed

Panç, Cafer; Kocaağa, Mehmet; Erdoğan, Onur; Sarıkaya, Remzi; Umman, Sabahattin

2017-04-01

Coronary microvascular dysfunction, also known as cardiac syndrome X, is a clinical syndrome presenting with typical angina and evidence of myocardial ischemia in the absence of flow-limiting stenosis on coronary angiography. Of patients undergoing coronary angiography due to suspected myocardial ischemia, 50% are found to have normal or near-normal coronary arteries. Described in this case report is a patient who developed hypotension and ST segment depressions during treadmill exercise test. Left main coronary artery or multivessel disease was suspected. Coronary angiography was normal, but coronary flow reserve measurement revealed severe microvascular dysfunction.

Controversies in cardiovascular care: silent myocardial ischemia

NASA Technical Reports Server (NTRS)

Hollenberg, N. K.

1987-01-01

The objective evidence of silent myocardial ischemia--ischemia in the absence of classical chest pain--includes ST-segment shifts (usually depression), momentary left ventricular failure, and perfusion defects on scintigraphic studies. Assessment of angina patients with 24-hour ambulatory monitoring may uncover episodes of silent ischemia, the existence of which may give important information regarding prognosis and may help structure a more effective therapeutic regimen. The emerging recognition of silent ischemia as a significant clinical entity may eventually result in an expansion of current therapy--not only to ameliorate chest pain, but to minimize or eliminate ischemia in the absence of chest pain.

Impact of impaired coronary flow reserve and insulin resistance on myocardial energy metabolism in patients with syndrome X.

PubMed

Bøtker, H E; Sonne, H S; Bagger, J P; Nielsen, T T

1997-06-15

To evaluate the role of a decreased coronary flow reserve in the genesis of angina pectoris in patients with syndrome X, we studied myocardial hemodynamics and metabolism at rest, during pace stress, and in the recovery period after pacing in 18 consecutive patients with syndrome X and in 10 control subjects. By means of positron emission tomography or the intracoronary flow-wire method, patients were subclassified as having microvascular angina (MA, n = 8) when coronary flow reserve was reduced (<2.5) or no microvascular angina (non-MA, n = 10) when coronary flow reserve was preserved (> or =2.5). At rest, coronary sinus blood flow was increased in MA patients. During pace stress, coronary sinus blood flow increased by 39 +/- 6% in MA patients versus 67 +/- 12% in non-MA patients and 69 +/- 7% in controls (p <0.05). Patients with non-MA revealed fasting hyperinsulinemia, increased arterial concentration of free fatty acids, and a similar tendency for beta-hydroxybutyrate. Oxygen extraction and carbon dioxide release did not differ between groups. Net myocardial lactate release was not observed in any patient during pace stress and myocardial energy metabolism was preserved in all patients with syndrome X. During pacing, myocardial uptake of free fatty acids and beta-hydroxybutyrate was increased in non-MA patients. Myocardial uptake of free fatty acids correlated positively and myocardial glucose and lactate uptake correlated inversely with arterial concentrations of free fatty acids in all subjects. Metabolic evidence of myocardial ischemia is uncommon in patients with syndrome X, irrespective of a globally reduced coronary flow reserve. Although patients with syndrome X can be subclassified according to presence of a microvascular or a metabolic disorder, angina pectoris and ST-segment depressions coexist with a preserved global myocardial energy efficiency in all patients.

Importance of compensatory heart rate increase during myocardial ischemia to preserve appropriate oxygen kinetics.

PubMed

Yoshida, Sadamitsu; Adachi, Hitoshi; Murata, Makoto; Tomono, Junichi; Oshima, Shigeru; Kurabayashi, Masahiko

2017-09-01

Myocardial ischemia induces cardiac dysfunction, resulting in insufficient oxygen supply to peripheral tissues and mismatched energy production during exercise. To relieve the insufficient oxygen supply, heart rate (HR) response is augmented; however, beta-adrenergic receptor blockers (BB) restrict HR response. Although BB are essential drugs for angina pectoris, the effect of BB on exercise tolerance in patients with angina has not been studied. The aim of this study was to clarify the importance of HR augmentation to preserve exercise tolerance in patients with angina pectoris. Forty-two subjects who underwent cardiopulmonary exercise testing (CPX) to detect myocardial ischemia were enrolled. CPX was performed until exhaustion or onset of significant myocardial ischemia using a ramp protocol. Subjects were assigned to three groups (Group A: with ST depression during CPX with significant coronary stenosis and taking BB; Group B: with ST depression and not taking BB; Group C: without ST depression and not taking BB). HR response to exercise was evaluated during the following two periods: below and above ischemic threshold (IT). In Group C, it was evaluated during the first 2min and the last 2min of a ramp exercise. No significant differences were observed among the three groups with regard to patients' basic characteristics. Below IT, there were no differences in oxygen pulse/watt (O 2 pulse increasing rate), HR/watt (ΔHR/ΔWR), and ΔV˙O 2 /ΔWR. Above IT, O 2 pulse increasing rate was greater in Group A than in Group B. ΔHR/ΔWR was smaller in Group A than in Group B. ΔV˙O 2 /ΔWR became smaller in Group A than in Group B. There was no difference in anaerobic threshold, and peak V˙O 2 was smaller in Group A than in Group B. Restriction of HR response by a BB is shown to be one of the important factors in diminished exercise tolerance. Copyright © 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Myxedema coma with cardiac tamponade and severe cardiomyopathy.

PubMed

Majid-Moosa, Abdulla; Schussler, Jeffrey M; Mora, Adan

2015-10-01

Myxedema coma is an infrequent but potentially fatal complication of hypothyroidism. We present a rare case of previously undiagnosed hypothyroidism presenting in cardiogenic shock from pericardial tamponade and depressed myocardial contractility in myxedema coma. Here, we focus on cardiovascular complications associated with the condition.

The Na+/H+ exchange inhibitor cariporide is washed out of the myocardium by crystalloid cardioplegia.

PubMed

Bechtel, J F M; Eichler, W; Toerber, K; Weidtmann, B; Hernandez, M; Klotz, K F; Sievers, H H; Bartels, C

2006-08-01

Inhibition of the Na (+)/H (+) exchanger (NHE) is cardioprotective, but dosage and timing of NHE-inhibitors are critical for their efficacy. We studied the effect of a new dosing regime of the NHE-inhibitor cariporide on myocardial function and damage after cardioplegic arrest (CPA) and determined its myocardial and serum concentrations. 3 pigs received a bolus of 180 mg cariporide intravenously (i. v.) and were sacrificed shortly thereafter to allow measurement of the myocardial concentrations of cariporide. Subsequently, 10 pigs were randomized to receive either i. v. cariporide (bolus followed by an infusion of 40 mg/h) or placebo. Cardiopulmonary bypass was initiated, and the heart was arrested for 60 minutes by infusion of St. Thomas Hospital solution. Left ventricular (LV) function was studied using microsonometry. Myocardial damage was assessed by troponin T. Serum concentrations of cariporide were measured throughout the study, and myocardial concentrations were measured before the end of CPA and 180 minutes thereafter. Cariporide was present in all myocardial specimens (median: 1.4 ng/mg) studied previously. In the main study, LV function or myocardial damage did not differ significantly between the groups at any time point. Stable serum cariporide concentrations were achieved (3.4 +/- 0.5 microg/ml). Cariporide was detectable in only one of the myocardial biopsies obtained before the end of CPA, but 180 minutes thereafter, the myocardial cariporide concentration was 2.5 +/- 0.3 ng/mg. We observed no effect of i. v. cariporide on LV function or myocardial damage after cardioplegic arrest. Our data suggest that cariporide is washed out of the myocardium by repeated application of crystalloid cardioplegia. Thus, the mode of delivery also appears to be critical for cardioprotection with NHE-inhibitors.

[Assessment of myocardial perfusion and left ventricular function with 99mTc-PPN 1011].

PubMed

Kumita, S; Mizumura, S; Oishi, T; Kumazaki, T; Sano, J; Yamazaki, Y; Munakata, K

1993-04-01

First-pass radionuclide angiography (FPRNA) was performed with the new myocardial perfusion agent 99mTc-1,2,bis[bis(2-ethoxyethyl)phosphino] ethane (99mTc-PPN 1011) on stress and at rest. One hour after that, myocardial perfusion was counted by 99mTc-PPN 1011 SPECT. Left ventricular ejection fraction (LVEF) obtained by FPRNA correlated with that by multigated image with 99mTc-HSAD (r = 0.94, n = 11). The reduction of left ventricular function under the exercise (delta LVEF) and the increase of severity score (delta Severity score) have a good relation (r = 0.88) in 7 patients with prior myocardial infarction. Thus 99mTc-PPN 1011 appears to be an ideal radiopharmaceutical for evaluation of ventricular function and myocardial perfusion.

Vasospasm of atherosclerotic coronary arteries precipitates acute ischemic myocardial damage in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits.

PubMed

Shiomi, Masashi; Ishida, Tatsuro; Kobayashi, Tsutomu; Nitta, Norihisa; Sonoda, Akinaga; Yamada, Satoshi; Koike, Tomonari; Kuniyoshi, Nobue; Murata, Kiyoshi; Hirata, Ken-ichi; Ito, Takashi; Libby, Peter

2013-11-01

This study tested the hypothesis that vasospasm can trigger coronary plaque injury and acute ischemic myocardial damage. Myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits received an intravenous bolus of ergonovine maleate (0.45 µmol/kg) during intravenous infusion of norepinephrine (12 nmol/kg per minute) to provoke coronary spasm in vivo. After this treatment, coronary angiography demonstrated vasospasm, and the ECG showed ischemic abnormalities (ST depression/elevation and T-wave inversion) in 77% of animals (23/30). These changes normalized after nitroglycerin injection. In rabbits that demonstrated these ECG findings for >20 minutes, echocardiograms showed left ventricular wall motion abnormality. Serum levels of heart-type fatty acid-binding protein, cardiac troponin-I, and myoglobin increased markedly 4 hours after spasm provocation. In coronary lesions of myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits with provoked coronary spasm, we observed intimal injury in 60.9% in the form of endothelial cell protrusions (39.1%), denudation (30.4%), and macrophage extravasation (56.5%). Plaque disruption with luminal thrombus, however, was only seen in 2 of 23 animals (8.7%), and mural microthrombus was rarely observed (4.3%). These observations show that provocation of vasospasm in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits associates with subsequent ischemic myocardial damage. Although treatment with spasmogens altered aspects of plaque morphology, for example, endothelial protrusion and macrophage emigration, thrombosis was rare in these animals with chronic atherosclerotic disease.

Future cardiac events in patients with ischemic ECG changes during adenosine infusion as a myocardial stress agent and normal cardiac scan.

PubMed

Amer, Hamid; Niaz, Khalid; Hatazawa, Jun; Gasmelseed, Ahmed; Samiri, Hussain Al; Al Othman, Maram; Hammad, Mai Al

2017-11-01

We sought to determine the prognostic importance of adenosine-induced ischemic ECG changes in patients with normal single-photon emission computed tomography myocardial perfusion images (MPI). We carried out a retrospective analysis of 765 patients undergoing adenosine MPI between January 2013 and January 2015. Patients with baseline ECG abnormalities and/or abnormal scan were excluded. Overall, 67 (8.7%) patients had ischemic ECG changes during adenosine infusion in the form of ST depression of 1 mm or more. Of these, 29 [43% (3.8% of all patients)] had normal MPI (positive ECG group). An age-matched and sex-matched group of 108 patients with normal MPI without ECG changes served as control participants (negative ECG group). During a mean follow-up duration of 33.3±6.1 months, patients in the positive ECG group did not have significantly more adverse cardiac events than those in the negative ECG group. One (0.9%) patient in the negative ECG group had a nonfatal myocardial infarction (0.7% annual event rate after a negative MPI). Also in this group, two (1.8%) patients admitted with a diagnosis of CAD where they have been ruled out by angiography. A fourth case in this, in the negative ECG group, was admitted because of heart failure that proved to be secondary to a pulmonary cause and not CAD. A case only in the positive ECG group was admitted as a CAD that was ruled out by coronary angiography. Patients with normal myocardial perfusion scintigraphy in whom ST-segment depression develops during adenosine stress test appear to have no increased risk for future cardiac events compared with similar patients without ECG evidence of ischemia.

Comparison of myocardial ischemia during intense mental stress using flight simulation in airline pilots with coronary artery disease to that produced with conventional mental and treadmill exercise stress testing.

PubMed

Doorey, Andrew; Denenberg, Barry; Sagar, Vidya; Hanna, Tracy; Newman, Jack; Stone, Peter H

2011-09-01

Mental stress increases cardiovascular morbidity and mortality. Although laboratory mental stress often causes less myocardial ischemia than exercise stress (ES), it is unclear whether mental stress is intrinsically different or differences are due to less hemodynamic stress with mental stress. We sought to evaluate the hemodynamic and ischemic response to intense realistic mental stress created by modern flight simulators and compare this response to that of exercise treadmill testing and conventional laboratory mental stress (CMS) testing in pilots with coronary disease. Sixteen airline pilots with angiographically documented coronary disease and documented myocardial ischemia during ES were studied using maximal treadmill ES, CMS, and aviation mental stress (AMS) testing. AMS testing was done in a sophisticated simulator using multiple system failures as stressors. Treadmill ES testing resulted in the highest heart rate, but AMS caused a higher blood pressure response than CMS. Maximal rate-pressure product was not significantly different between ES and AMS (25,646 vs 23,347, p = 0.08), although these were higher than CMS (16,336, p <0.0001). Despite similar hemodynamic stress induced by ES and AMS, AMS resulted in significantly less ST-segment depression and nuclear ischemia than ES. Differences in induction of ischemia by mental stress compared to ES do not appear to be due to the creation of less hemodynamic stress. In conclusion, even with equivalent hemodynamic stress, intense realistic mental stress induced by flight simulators results in significantly less myocardial ischemia than ES as measured by ST-segment depression and nuclear ischemia. Copyright © 2011 Elsevier Inc. All rights reserved.

[Nuclear cardiology with new radiopharmaceuticals].

PubMed

Bunko, H

1994-08-01

In the field of nuclear cardiology, 99mTc labeled myocardial perfusion agents such as MIBI, Tetrofosmin and Teboroxime, 111In-antimyosin for imaging of myocardial necrosis, 123I-betamethyl-iodophenylpentadecanoic acid (BMIPP) for imaging of myocardial fatty acid metabolism and 123I-metaiodobenzylguanidine (MIBG) for imaging of myocardial adrenergic function are introduced recently in Japan. Improved image quality and simultaneous evaluation of myocardial perfusion, function and wall motion can be obtained with use of 99mTc labeled myocardial perfusion agents. 111In-antimyosin enables specific imaging of myocardial necrosis which leads to the use for wide variety of heart diseases. Discrepancy of the myocardial perfusion and metabolism in case of stunned myocardium or cardiomyopathy can be evaluated by 123I-BMIPP in conjunction with perfusion agent. Recently wide variety of diseases which may have cardiac adrenergic abnormality are targeted for 123I-MIBG imaging. These new radiopharmaceuticals are expected to be powerful tool for evaluation of the pathophysiology including severity and prognosis and evaluation of the etiology of the various heart diseases.

The Prevalence of Insomnia on School Principals and Superintendents in Missouri

ERIC Educational Resources Information Center

Williams, Regina Johnson

2017-01-01

Chronic insomnia can lead to depression, anxiety, cognitive difficulties, workplace absenteeism, underperformance, and high employee turnover as well as medical issues such as Alzheimer's, hypertension, myocardial infarction, obesity, and diabetes. Researchers have argued that healthful sleep is the most important factor in predicting longevity…

Imaging and Modeling of Myocardial Metabolism

PubMed Central

Jamshidi, Neema; Karimi, Afshin; Birgersdotter-Green, Ulrika; Hoh, Carl

2010-01-01

Current imaging methods have focused on evaluation of myocardial anatomy and function. However, since myocardial metabolism and function are interrelated, metabolic myocardial imaging techniques, such as positron emission tomography, single photon emission tomography, and magnetic resonance spectroscopy present novel opportunities for probing myocardial pathology and developing new therapeutic approaches. Potential clinical applications of metabolic imaging include hypertensive and ischemic heart disease, heart failure, cardiac transplantation, as well as cardiomyopathies. Furthermore, response to therapeutic intervention can be monitored using metabolic imaging. Analysis of metabolic data in the past has been limited, focusing primarily on isolated metabolites. Models of myocardial metabolism, however, such as the oxygen transport and cellular energetics model and constraint-based metabolic network modeling, offer opportunities for evaluation interactions between greater numbers of metabolites in the heart. In this review, the roles of metabolic myocardial imaging and analysis of metabolic data using modeling methods for expanding our understanding of cardiac pathology are discussed. PMID:20559785

Fropofol decreases force development in cardiac muscle.

PubMed

Ren, Xianfeng; Schmidt, William; Huang, Yiyuan; Lu, Haisong; Liu, Wenjie; Bu, Weiming; Eckenhoff, Roderic; Cammarato, Anthony; Gao, Wei Dong

2018-03-09

Supranormal contractile properties are frequently associated with cardiac diseases. Anesthetic agents, including propofol, can depress myocardial contraction. We tested the hypothesis that fropofol, a propofol derivative, reduces force development in cardiac muscles via inhibition of cross-bridge cycling and may therefore have therapeutic potential. Force and intracellular Ca 2+ ([Ca 2+ ] i ) transients of rat trabecular muscles were determined. Myofilament ATPase, actin-activated myosin ATPase, and velocity of actin filaments propelled by myosin were also measured. Fropofol dose dependently decreased force without altering [Ca 2+ ] i in normal and pressure-induced hypertrophied-hypercontractile muscles. Similarly, fropofol depressed maximum Ca 2+ -activated force ( F max ) and increased the [Ca 2+ ] i required for 50% activation at steady-state (Ca 50 ) without affecting the Hill coefficient in both intact and skinned cardiac fibers. The drug also depressed cardiac myofibrillar and actin-activated myosin ATPase activity. In vitro actin sliding velocity was significantly reduced when fropofol was introduced during rigor binding of cross-bridges. The data suggest that the depressing effects of fropofol on cardiac contractility are likely to be related to direct targeting of actomyosin interactions. From a clinical standpoint, these findings are particularly significant, given that fropofol is a nonanesthetic small molecule that decreases myocardial contractility specifically and thus may be useful in the treatment of hypercontractile cardiac disorders.-Ren, X., Schmidt, W., Huang, Y., Lu, H., Liu, W., Bu, W., Eckenhoff, R., Cammarato, A., Gao, W. D. Fropofol decreases force development in cardiac muscle.

Social inequality in morbidity, framed within the current economic crisis in Spain.

PubMed

Zapata Moya, A R; Buffel, V; Navarro Yáñez, C J; Bracke, P

2015-11-14

Inspired by the 'Fundamental Cause Theory (FCT)' we explore social inequalities in preventable versus relatively less-preventable illnesses in Spain. The focus is on the education-health gradient, as education is one of the most important components of an individual's socioeconomic status (SES). Framed in the context of the recent economic crisis, we investigate the education gradient in depression, diabetes, and myocardial infarction (relatively highly preventable illnesses) and malignant tumors (less preventable), and whether this educational gradient varies across the regional-economic context and changes therein. We use data from three waves of the Spanish National Health Survey (2003-2004, 2006-2007, and 2011-2012), and from the 2009-2010 wave of the European Health Survey in Spain, which results in a repeated cross-sectional design. Logistic multilevel regressions are performed with depression, diabetes, myocardial infarction, and malignant tumors as dependent variables. The multilevel design has three levels (the individual, period-regional, and regional level), which allows us to estimate both longitudinal and cross-sectional macro effects. The regional-economic context and changes therein are assessed using the real GDP growth rate and the low work intensity indicator. Education gradients in more-preventable illness are observed, while this is far less the case in our less-preventable disease group. Regional economic conditions seem to have a direct impact on depression among Spanish men (y-stand. OR = 1.04 [95 % CI: 1.01-1.07]). Diabetes is associated with cross-regional differences in low work intensity among men (y-stand. OR = 1.02 [95 % CI: 1.00-1.05]) and women (y-stand. OR = 1.04 [95 % CI: 1.01-1.06]). Economic contraction increases the likelihood of having diabetes among men (y-stand. OR = 1.04 [95 % CI: 1.01-1.06]), and smaller decreases in the real GDP growth rate are associated with lower likelihood of myocardial infarction among women (y-stand. OR = 0.83 [95 % CI: 0.69-1.00]). Finally, there are interesting associations between the macroeconomic changes across the crisis period and the likelihood of suffering from myocardial infarction among lower educated groups, and the likelihood of having depression and diabetes among less-educated women. Our findings partially support the predictions of the FCT for Spain. The crisis effects on health emerge especially in the case of our more-preventable illnesses and among lower educated groups. Health inequalities in Spain could increase rapidly in the coming years due to the differential effects of recession on socioeconomic groups.

Caffeoylquinic Acid Derivatives Extract of Erigeron multiradiatus Alleviated Acute Myocardial Ischemia Reperfusion Injury in Rats through Inhibiting NF-KappaB and JNK Activations

PubMed Central

Liu, Yuan; Ren, Xuecong; Wang, Kaishun; Zhang, Hao

2016-01-01

Erigeron multiradiatus (Lindl.) Benth. has been used in Tibet folk medicine to treat various inflammatory diseases. The aim of this study was to investigate antimyocardial ischemia and reperfusion (I/R) injury effect of caffeoylquinic acids derivatives of E. multiradiatus (AE) in vivo and to explain underling mechanism. AE was prepared using the whole plant of E. multiradiatus and contents of 6 caffeoylquinic acids determined through HPLC analysis. Myocardial I/R was induced by left anterior descending coronary artery occlusion for 30 minutes followed by 24 hours of reperfusion in rats. AE administration (10, 20, and 40 mg/kg) inhibited I/R-induced injury as indicated by decreasing myocardial infarct size, reducing of CK and LDH activities, and preventing ST-segment depression in dose-dependent manner. AE decreased cardiac tissue levels of proinflammatory factors TNF-α and IL-6 and attenuated leukocytes infiltration. AE was further demonstrated to significantly inhibit I-κB degradation, nuclear translocation of p-65 and phosphorylation of JNK. Our results suggested that cardioprotective effect of AE could be due to suppressing myocardial inflammatory response and blocking NF-κB and JNK activation pathway. Thus, caffeoylquinic acids might be the active compounds in E. multiradiatus on myocardial ischemia and be a potential natural drug for treating myocardial I/R injury. PMID:27516722

Myocardial perfusion imaging with thallium-201: correlation with coronary arteriography and electrocardiography

PubMed Central

Sternberg, Leonard; Wald, Robert W.; Feiglin, David H.I.; Morch, John E.

1978-01-01

Myocardial perfusion imaging with thallium-201 and electrocardiography with the subject at rest and undergoing submaximal treadmill exercise were performed in 19 men and 3 women. Selective coronary arteriography and left ventriculography showed that 7 had normal coronary arteries and 15 had coronary artery disease. The 11 persons with electrocardiographic evidence of an old myocardial infarct (q waves) had a perfusion defect at rest in the area of the infarct and a segmental abnormality of wall motion apparent on the left ventriculogram corresponding to the perfusion defect. Myocardial perfusion imaging and electrocardiography were equally sensitive in detecting coronary artery disease in exercising individuals: perfusion defects were noted in 7 of the 15 persons with coronary artery disease, and diagnostic ST-segment depression was present in 8 of the 15. Combination of the results of the two tests with exercise permitted the identification of 11 of the 15 persons and improved the sensitivity. Combination of the results of rest and exercise imaging and electrocardiography permitted the identification of 94% of the patients with coronary artery disease. Myocardial perfusion imaging with 201TI in the subject at rest is a sensitive indicator of previous myocardial infarction. Imaging after the subject has exercised is a useful adjunct to conventional exercise electrocardiography, especially in those whose exercise electrocardiogram is non-interpretable. ImagesFIG. 1FIG. 2FIG. 3FIG. 4FIG. 5 PMID:630487

Low-Level Laser Application in the Early Myocardial Infarction Stage Has No Beneficial Role in Heart Failure.

PubMed

Manchini, Martha T; Antônio, Ednei L; Silva Junior, José Antônio; de Carvalho, Paulo de Tarso C; Albertini, Regiane; Pereira, Fernando C; Feliciano, Regiane; Montemor, Jairo; Vieira, Stella S; Grandinetti, Vanessa; Yoshizaki, Amanda; Chaves, Marcio; da Silva, Móises P; de Lima, Rafael do Nascimento; Bocalini, Danilo S; de Melo, Bruno L; Tucci, Paulo J F; Serra, Andrey J

2017-01-01

Low-level laser therapy (LLLT) has been targeted as a promising approach that can mitigate post-infarction cardiac remodeling. There is some interesting evidence showing that the beneficial role of the LLLT could persist long-term even after the end of the application, but it remains to be systematically evaluated. Therefore, the present study aimed to test the hypothesis that LLLT beneficial effects in the early post-infarction cardiac remodeling could remain in overt heart failure even with the disruption of irradiations. Female Wistar rats were subjected to the coronary occlusion to induce myocardial infarction or Sham operation. A single LLLT application was carried out after 60 s and 3 days post-coronary occlusion, respectively. Echocardiography was performed 3 days and at the end of the experiment (5 weeks) to evaluate cardiac function. After the last echocardiographic examination, LV hemodynamic evaluation was performed at baseline and on sudden afterload increases. Compared with the Sham group, infarcted rats showed increased systolic and diastolic internal diameter as well as a depressed shortening fraction of LV. The only benefit of the LLLT was a higher shortening fraction after 3 days of infarction. However, treated-LLLT rats show a lower shortening fraction in the 5th week of study when compared with Sham and non-irradiated rats. A worsening of cardiac function was confirmed in the hemodynamic analysis as evidenced by the higher LV end-diastolic pressure and lower +dP/dt and -dP/dt with five weeks of study. Cardiac functional reserve was also impaired by infarction as evidenced by an attenuated response of stroke work index and cardiac output to a sudden afterload stress, without LLLT repercussions. No significant differences were found in the myocardial expression of Akt 1 /VEGF pathway. Collectively, these findings illustrate that LLLT improves LV systolic function in the early post-infarction cardiac remodeling. However, this beneficial effect may be dependent on the maintenance of phototherapy. Long-term studies with LLLT application are needed to establish whether these effects ultimately translate into improved cardiac remodeling.

Prediction of myocardial functional recovery by noninvasive evaluation of Basal and hyperemic coronary flow in patients with previous myocardial infarction.

PubMed

Djordjevic-Dikic, Ana; Beleslin, Branko; Stepanovic, Jelena; Giga, Vojislav; Tesic, Milorad; Dobric, Milan; Stojkovic, Sinisa; Nedeljkovic, Milan; Vukcevic, Vladan; Dikic, Nenad; Petrasinovic, Zorica; Nedeljkovic, Ivana; Tomasevic, Miloje; Vujisic-Tesic, Bosiljka; Ostojic, Miodrag

2011-05-01

The aim of this study was to evaluate the relation of basal and hyperemic coronary flow with myocardial functional improvement in patients with previous myocardial infarction undergoing elective percutaneous coronary intervention (PCI). Coronary flow was measured using transthoracic Doppler echocardiography in 50 patients (41 men; mean age, 53 ± 8 years) with previous myocardial infarction before, 24 hours, and 3 months after elective PCI. Diastolic deceleration time (DDT) was measured from the peak diastolic velocity to the point of intercept of initial decay slope with baseline. Coronary flow reserve (CFR) was calculated as the ratio of hyperemic to basal peak diastolic flow velocities. In comparison with patients without improvements in left ventricular function, patients with recovered left ventricular function had longer DDTs before angioplasty (841 ± 286 vs. 435 ± 80 msec, P < .001). CFR was significantly higher in recovered compared with nonrecovered patients (2.60 ± 0.70 vs. 2.16 ± 0.34, P = .034) 24 hours after PCI. Global and regional wall motion scores before PCI, end-diastolic and end-systolic volumes, and CFR 24 hours after PCI and DDT before PCI were univariate predictors of left ventricular functional recovery. By multivariate analysis, DDT and regional wall motion score before PCI were independent predictors of left ventricular recovery in the follow-up period (P = .003 and P = .007, respectively). In patients with previous myocardial infarction undergoing elective PCI, evaluation of basal coronary flow pattern and measurement of DDT before angioplasty may predict functional improvement of myocardium in the follow-up period and could be useful quantitative parameters in the evaluation of potential improvement in myocardial function. Copyright © 2011 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.

Adverse effects of doping with anabolic androgenic steroids (AAS) in competitive athletics, recreational sports and bodybuilding.

PubMed

Vorona, Elena; Nieschlag, Eberhard

2018-02-19

Despite the fact that sports organizations and legislators have introduced various mechanisms to discourage athletes from using performance and appearance enhancing substances a high percentage of athletes admits to their unabated application. In competitive athletics, bodybuilding and in recreational sports anabolic androgenic steroids (AAS) continue to be the substances most abused. This review summarizes the side effects of AAS abuse on organs and system functions in both sexes. High doses of AAS cause a significant increase of erythrocytes und haemoglobin concentration, which may lead to thromboembolism, intracardiac thrombosis and stroke. Long-term AAS abusers have a higher incidence of arrhythmias, atherosclerosis, concentric left-ventricular myocardial hypertrophy with impaired diastolic function and also sudden cardiac death. Changes of liver function and structure, up to hepatocellular carcinoma, have been described, mainly in cases of chronic misuse of 17α-alkylated AAS. Sleeplessness, increased irritability, depressive mood status are often observed in AAS abuse. In former AAS abusers depression, anxiety and melancholy may persist for many years. Due to negative feedback in the regulation of the hypothalamic-pituitary-gonadal axis AAS can cause reversible suppression of spermatogenesis up to azoospermia. In women the changes most often caused by AAS abuse are hirsutism, irreversible deepening of voice, dysmenorrhoea, secondary amenorrhoea with anovulation and infertility. AAS abuse notwithstanding, under clinical conditions testosterone remains the most important hormone for substitution therapy of male hypogonadism.

Cardiorespiratory fitness modifies the relationship between myocardial function and cerebral blood flow in older adults.

PubMed

Johnson, Nathan F; Gold, Brian T; Bailey, Alison L; Clasey, Jody L; Hakun, Jonathan G; White, Matthew; Long, Doug E; Powell, David K

2016-05-01

A growing body of evidence indicates that cardiorespiratory fitness attenuates some age-related cerebral declines. However, little is known about the role that myocardial function plays in this relationship. Brain regions with high resting metabolic rates, such as the default mode network (DMN), may be especially vulnerable to age-related declines in myocardial functions affecting cerebral blood flow (CBF). This study explored the relationship between a measure of myocardial mechanics, global longitudinal strain (GLS), and CBF to the DMN. In addition, we explored how cardiorespiratory affects this relationship. Participants were 30 older adults between the ages of 59 and 69 (mean age=63.73years, SD=2.8). Results indicated that superior cardiorespiratory fitness and myocardial mechanics were positively associated with DMN CBF. Moreover, results of a mediation analysis revealed that the relationship between GLS and DMN CBF was accounted for by individual differences in fitness. Findings suggest that benefits of healthy heart function to brain function are modified by fitness. Copyright © 2015 Elsevier Inc. All rights reserved.

Transient ST segment depression during Holter monitoring: how to avoid false positive findings.

PubMed

Völler, H; Andresen, D; Brüggemann, T; Jereczek, M; Becker, B; Schröder, R

1992-09-01

To increase the specificity of 24-hour Holter monitoring in detecting transient myocardial ischemia, we separated genuine ST deviations from those dependent on artifacts by adding a detailed shape analysis of real-time printouts to the usual criteria of significant ST segment depression. We screened 116 apparently healthy subjects; 31 had to be excluded, because of pathologic findings in preliminary examinations. The remaining 85 (49 women and 36 men; mean age, 43.1 years) underwent Holter monitoring for assessment of the extent, frequency, and duration of episodes of horizontal and descending ST segment depression of at least 0.1 mV that persisted for at least 60 msec after the J point and that were at least 1 minute apart. On the basis of these criteria, six subjects (7.1%) showed 24 episodes of horizontal or descending ST segment depression with a mean of 0.2 mV (range, 0.15 to 0.25 mV), a frequency of four episodes per 24 hours (one to nine), and a duration of 12.2 minutes (range 3-range 41 minutes). Supplementary criteria--e.g., sudden onset of ST segment depression, identical orientation of PQ and ST segments, or simultaneous increase in R and P wave amplitude--made it possible to identify ST changes caused by artifacts in four volunteers. In only two subjects (2.4%) could true silent ischemia not be differentiated from false positive results. Thus consideration of only the extent, frequency, and duration of episodes does not permit a differentiation between true silent ischemia and false positive results. A supplementary shape analysis increases the specificity of ST segment analysis in detecting transient myocardial ischemia during 24-hour Holter monitoring.

The effect of patient anxiety and depression on motion during myocardial perfusion SPECT imaging.

PubMed

Lyra, Vassiliki; Kallergi, Maria; Rizos, Emmanouil; Lamprakopoulos, Georgios; Chatziioannou, Sofia N

2016-08-22

Patient motion during myocardial perfusion SPECT imaging (MPI) may be triggered by a patient's physical and/or psychological discomfort. The aim of this study was to investigate the impact of state anxiety (patient's reaction to exam-related stress), trait anxiety (patient's personality characteristic) and depression on patient motion during MPI. All patients that underwent MPI in our department in a six-month period were prospectively enrolled. One hundred eighty-three patients (45 females; 138 males) filled in the State-Trait Anxiety Inventory (STAI) and the Beck Depression Inventory (BDI), along with a short questionnaire regarding their age, height and weight, level of education in years, occupation, and marital status. Cardiovascular and other co-morbidity factors were also evaluated. Through inspection of raw data on cinematic display, the presence or absence of patient motion was registered and classified into mild, moderate and severe, for both phases involved in image acquisition. The correlation of patient motion in the stress and delay phases of MPI and each of the other variables was investigated and the corresponding Pearson's coefficients of association were calculated. The anxiety-motion (r = 0.43, P < 0.0001) and depression-motion (r = 0.32, P < 0.0001) correlation results were moderately strong and statistically significant for the female but not the male patients. All the other variables did not demonstrate any association with motion in MPI, except a weak correlation between age and motion in females (r = 0.23, P < 0.001). The relationship between anxiety-motion and depression-motion identified in female patients represents the first supporting evidence of psychological discomfort as predisposing factor for patient motion during MPI.

Long-Term Preservation of Left Ventricular Systolic Function in Patients With Refractory Angina Pectoris and Inducible Myocardial Ischemia on Optimal Medical Therapy.

PubMed

Slavich, Massimo; Maranta, Francesco; Fumero, Andrea; Godino, Cosmo; Giannini, Francesco; Oppizzi, Michele; Colombo, Antonio; Fragasso, Gabriele; Margonato, Alberto

2016-05-15

Refractory angina pectoris (RAP) represents a clinical condition characterized by frequent episodes of chest pain despite therapy optimization. According to myocardial stunning and myocardial hibernation definitions, RAP should represent the ideal condition for systolic dysfunction development. We aim to investigate the evolution of left ventricular (LV) function in patients with RAP. A retrospective study which encompasses 144 patients with RAP referred to our institution from 1999 to December 2014 was performed. Of them, 88 met the inclusion criteria, and LV function was assessed by echocardiography. All of them had persistent angina episodes on top of optimal medical therapy and evidence of significant inducible myocardial ischemia and no further revascularization options. Nitrates consumption rate, time of angina duration, and the number of angina attacks were evaluated. In the whole population, ejection fraction (EF) was 44% ± 2. EF was significantly lower in patients with previous myocardial infarction (41% ± 1.5 vs 51% ± 1.8, p <0.0001). The duration time and the number of angina attacks did not correlate with EF in the whole population and in patients without previous myocardial infarction. In patients with previous myocardial infarction, the number of anginal attacks did not correlate with EF, but EF appeared higher in patients with angina duration >5 years (<5 years EF 37% ± 1 [n = 26]; >5 years 44% ± 2 [n = 44]; p 0.02). Long-term LV function in patients with RAP is generally preserved. A previous history of myocardial infarction is the only determinant in the development of systolic dysfunction. In conclusion, frequent angina attacks and a long-term history of angina are not apparently associated to worse LV function. Copyright © 2016 Elsevier Inc. All rights reserved.

Myocardial perfusion and left ventricular function indices assessed by gated myocardial perfusion SPECT in methamphetamine abusers.

PubMed

Dadpour, Bita; Dabbagh Kakhki, Vahid R; Afshari, Reza; Dorri-Giv, Masoumeh; Mohajeri, Seyed A R; Ghahremani, Somayeh

2016-12-01

Methamphetamine (MA) is associated with alterations of cardiac structure and function, although it is less known. In this study, we assessed possible abnormality in myocardial perfusion and left ventricular function using gated myocardial perfusion SPECT. Fifteen patients with MA abuse, on the basis of Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) MA dependency determined by Structured Clinical Interview for DSM-IV, underwent 2-day dipyridamole stress/rest Tc-sestamibi gated myocardial perfusion SPECT. An average daily dose of MA use was 0.91±1.1 (0.2-4) g. The duration of MA use was 3.4±2.1 (1-7) years. In visual and semiquantitative analyses, all patients had normal gated myocardial perfusion SPECT, with no perfusion defects. In all gated SPECT images, there was no abnormality in left ventricular wall motion and thickening. All summed stress scores and summed rest scores were below 3. Calculated left ventricular functional indices including the end-diastolic volume, end-systolic volume, and left ventricular ejection fraction were normal. Many cardiac findings because of MA mentioned in previous reports are less likely because of significant epicardial coronary artery stenosis.

A Deep Learning Approach to Examine Ischemic ST Changes in Ambulatory ECG Recordings.

PubMed

Xiao, Ran; Xu, Yuan; Pelter, Michele M; Mortara, David W; Hu, Xiao

2018-01-01

Patients with suspected acute coronary syndrome (ACS) are at risk of transient myocardial ischemia (TMI), which could lead to serious morbidity or even mortality. Early detection of myocardial ischemia can reduce damage to heart tissues and improve patient condition. Significant ST change in the electrocardiogram (ECG) is an important marker for detecting myocardial ischemia during the rule-out phase of potential ACS. However, current ECG monitoring software is vastly underused due to excessive false alarms. The present study aims to tackle this problem by combining a novel image-based approach with deep learning techniques to improve the detection accuracy of significant ST depression change. The obtained convolutional neural network (CNN) model yields an average area under the curve (AUC) at 89.6% from an independent testing set. At selected optimal cutoff thresholds, the proposed model yields a mean sensitivity at 84.4% while maintaining specificity at 84.9%.

[Stress and myocardial infarction].

PubMed

Csef, H; Hefner, J

2005-03-31

Most people throughout the world die from the consequences of cardiovascular disease. Stress and psychosocial burdens have, in the past, been underestimated with regard to the importance of their impact on the development and course of such diseases. In the INTERHEART study, psychosocial burdens occupy third place among the risk factors for developing acute myocardial infarction. The relevance of these factors is underscored by more recent studies, also with regard to the prognosis in already manifest CAH. The causes of mental stresses may be intrapsychic problems (e.g. depression). The roots may, however, also be found in the private sphere or at the workplace. On the basis of specific history-taking, relevant risk constellations can be identified for a comparatively low expenditure of time. Specific therapeutic approaches aimed at reducing and coping with stress may, in future, help prevent diseases of the heart and lower the risk of contracting a myocardial infarction.

Triiodothyronine Activates Lactate Oxidation Without Impairing Fatty Acid Oxidation and Improves Weaning From Extracorporeal Membrane Oxygenation

PubMed Central

Kajimoto, Masaki; Ledee, Dolena R.; Xu, Chun; Kajimoto, Hidemi; Isern, Nancy G.; Portman, Michael A.

2017-01-01

Background Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. It has previously been shown that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. Methods and Results Nineteen immature piglets (9.1–15.3 kg) were separated into 3 groups with ECMO (6.5 h) and wean: normal circulation (Group-C); transient coronary occlusion (10 min) for ischemia-reperfusion (IR) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon (13C)-labeled lactate, medium-chain and long-chain FAs, was infused as oxidative substrates. Substrate fractional contribution (FC) to the citric acid cycle was analyzed by 13C-nuclear magnetic resonance. ECMO depressed circulating T3 levels to 40% of the baseline at 4 h and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [adenosine triphosphate]/[adenosine diphosphate] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR. Conclusions T3 releases inhibition of lactate oxidation following IR injury without impairing FA oxidation. These findings indicate that T3 depression during ECMO is maladaptive, and that restoring levels improves metabolic flux and enhances contractile function during weaning. PMID:25421230

Evaluation of effect of atorvastatin on left ventricular systolic function in rats with myocardial infarction via 2D-STI technique.

PubMed

Hua, Yan; Xie, Manying; Yin, Jiabao; Wang, Yu; Gan, Ling; Sang, Ming; Sun, Xiaodong; Li, Mingyang; Liu, Shanjun; Xu, Jinzhi

2018-05-01

This report aims to evaluate the effect of atorvastatin (Ator) on left ventricular systolic function in myocardial infarction (MI) rats. Forty healthy adult Sprague-Dawley rats were randomly divided into four groups: Ator group, MI group, sham-operation group and normal group. The left anterior descending coronary arteries were ligated to establish the MI model; after modeling, the Ator group was treated with Ator for 4 consecutive weeks. The echocardiographic detection was performed; the left ventricular myocardial systolic peak velocities, strain and strain rates were analyzed using the 2D-STI technique. After 4 weeks, myocardial tissues were taken from all rats and received the pathological examination. Left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) in Ator group and MI group were increased after operation, but left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were decreased; myocardial function were decreased significantly (p<0.05). After Ator treatment, myocardial function at the 3rd and 4th week after operation increased significantly (p<0.05). After Ator treatment, LVEDD and LVESD decreased while LVEF and LVFS increased in Ator group at the 3rd and 4th week after operation compared with MI group (p<0.05). At the 4th week after operation, LVEDD and LVESD in Ator group were decreased compared with those at the 1st and 2nd week after operation, but LVEF and LVFS were increased compared with those at the 1st, 2nd and 3rd week after operation (p<0.05). Pathological examination showed that necrosis and fibrosis of myocardial cells and inflammatory reaction were obvious in MI group. The inflammatory reaction of myocardial cells and myocardial fibrosis were lighter in Ator group. Ator can effectively improve the left ventricular systolic function in MI rats, which could be related to the reduction of response to inflammation and fibrosis.

Pericardial application as a new route for implanting stem-cell cardiospheres to treat myocardial infarction.

PubMed

Zhang, Jianhua; Wu, Zheng; Fan, Zepei; Qin, Zixi; Wang, Yingwei; Chen, Jiayuan; Wu, Maoxiong; Chen, Yangxin; Wu, Changhao; Wang, Jingfeng

2018-06-01

Cardiospheres (CSps) are a promising new form of cardiac stem cells with advantage over other stem cells for myocardial regeneration, but direct implantation of CSps by conventional routes has been limited due to potential embolism. We have implanted CSps into the pericardial cavity and systematically demonstrated its efficacy regarding myocardial infarction. Stem cell potency and cell viability can be optimized in vitro prior to implantation by pre-conditioning CSps with pericardial fluid and hydrogel packing. Transplantation of optimized CSps into the pericardial cavity improved cardiac function and alleviated myocardial fibrosis, increased myocardial cell survival and promoted angiogenesis. Mechanistically, CSps are able to directly differentiate into cardiomyocytes in vivo and promote regeneration of myocardial cells and blood vessels through a paracrine effect with released growth factors as potential paracrine mediators. These findings establish a new strategy for therapeutic myocardial regeneration to treat myocardial infarction. Cardiospheres (CSps) are a new form of cardiac stem cells with an advantage over other stem cells for myocardial regeneration. However, direct implantation of CSps by conventional routes to treat myocardial infarction has been limited due to potential embolism. We have implanted CSps into the pericardial cavity and systematically assessed its efficacy on myocardial infarction. Preconditioning with pericardial fluid enhanced the activity of CSps and matrix hydrogel prolonged their viability. This shows that pretransplant optimization of stem cell potency and maintenance of cell viability can be achieved with CSps. Transplantation of optimized CSps into the pericardial cavity improved cardiac function and alleviated myocardial fibrosis in the non-infarcted area, and increased myocardial cell survival and promoted angiogenesis in the infarcted area. Mechanistically, CSps were able to directly differentiate into cardiomyocytes in vivo and promoted regeneration of myocardial cells and blood vessels in the infarcted area through a paracrine effect with released growth factors in pericardial cavity serving as possible paracrine mediators. This is the first demonstration of direct pericardial administration of pre-optimized CSps, and its effectiveness on myocardial infarction by functional and morphological outcomes with distinct mechanisms. These findings establish a new strategy for therapeutic myocardial regeneration to treat myocardial infarction. © 2018 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.

Illness consequences after myocardial infarction: problems with physical functioning and return to work.

PubMed

Brink, Eva; Brändström, Yvonne; Cliffordsson, Christina; Herlitz, Johan; Karlson, Björn W

2008-12-01

This paper is a report of a study to explore health problems, physical and mental functioning, and physical activity in working-age patients after myocardial infarction, in order to assess the possible effects of these factors on return to work. A diagnosis of myocardial infarction may discourage patients from continuing an active working life. Enabling myocardial infarction patients to return to work has benefits for both individuals and society. A convenience sample was recruited of 88 patients,

Apathy and depressive symptoms in older people and incident myocardial infarction, stroke, and mortality: a systematic review and meta-analysis of individual participant data.

PubMed

Eurelings, Lisa Sm; van Dalen, Jan Willem; Ter Riet, Gerben; Moll van Charante, Eric P; Richard, Edo; van Gool, Willem A

2018-01-01

Previous findings suggest that apathy symptoms independently of depressive symptoms measured using the Geriatric Depression Scale (GDS) are associated with cardiovascular disease (CVD) in older individuals. To study whether apathy and depressive symptoms in older people are associated with future CVD, stroke, and mortality using individual patient-data meta-analysis. Medline, Embase, and PsycInfo databases up to September 3, 2013, were systematically searched without language restrictions. We sought prospective studies with older (mean age ≥65 years) community-dwelling populations in which the GDS was employed and subsequent stroke and/or CVD were recorded to provide individual participant data. Apathy symptoms were defined as the three apathy-related subitems of the GDS, with depressive symptoms the remaining items. We used myocardial infarction (MI), stroke, and all-cause mortality as main outcomes. Analyses were adjusted for age, sex, and MI/stroke history. An adaptation of the Newcastle-Ottawa scale was used to evaluate bias. Hazard ratios were calculated using one-stage random-effect Cox regression models. Of the 52 eligible studies, 21 (40.4%) were included, comprising 47,625 older people (mean age [standard deviation] 74 [7.4] years), over a median follow-up of 8.8 years. Participants with apathy symptoms had a 21% higher risk of MI (95% confidence interval [CI] 1.08-1.36), a 37% higher risk of stroke (95% CI 1.18-1.59), and a 47% higher risk of all-cause mortality (95% CI 1.38-1.56). Participants with depressive symptoms had a comparably higher risk of stroke (HR 1.36, 95% CI 1.18-1.56) and all-cause mortality (HR 1.44, 95% CI 1.35-1.53), but not of MI (HR 1.08, 95% CI 0.91-1.29). Associations for isolated apathy and isolated depressive symptoms were comparable. Sensitivity analyses according to risk of bias yielded similar results. Our findings stress the clinical importance of recognizing apathy independently of depressive symptoms, and could help physicians identify persons at increased risk of vascular disease.

Prevalence of silent myocardial ischaemia during exercise stress testing. Its relation to effort tolerance and myocardial perfusion abnormalities.

PubMed

Fragasso, G; Sciammarella, M G; Rossetti, E E; Xuereb, R G; Xuereb, M; Bonetti, F; Carandente, O M; Margonato, A; Chierchia, S L

1992-07-01

The number of underperfused myocardial segments, the extent of coronary artery disease and the severity of impairment of coronary flow reserve were compared in 147 consecutive patients exhibiting painful or painless ischaemic ST segment depression on exercise testing. Of 147 patients, only 61 (41%) experienced angina (group 1) whilst 86 (59%) did not (group 2). In the two groups coronary disease was comparable for both extent and distribution, and neither the location of transient perfusion defects nor their relation to areas of old myocardial necrosis appeared to influence the presence or absence of chest pain. However, exercise duration, exercise time and rate-pressure product at the beginning of ischaemia were lower in group 1. Furthermore, a greater proportion of asymptomatic patients had only one ischaemic segment on 99mTc-MIBI perfusion scintigraphy. We conclude that: (1) in patients with effort angina and coronary disease, the incidence of electrocardiographic silent ischaemic events induced by exercise is similar to that observed in studies based on continuous ECG monitoring. (2) Exertional angina is more frequently associated with greater ischaemic areas and with more severe degrees of impairment of residual coronary flow reserve. (3) The presence of an old myocardial infarction does not appear to influence the incidence of ischaemic cardiac pain.

Effects of Concurrent Depressive Symptoms and Perceived Stress on Cardiovascular Risk in Low- and High-Income Participants: Findings From the Reasons for Geographical and Racial Differences in Stroke (REGARDS) Study.

PubMed

Sumner, Jennifer A; Khodneva, Yulia; Muntner, Paul; Redmond, Nicole; Lewis, Marquita W; Davidson, Karina W; Edmondson, Donald; Richman, Joshua; Safford, Monika M

2016-10-10

Psychosocial risk for cardiovascular disease (CVD) may be especially deleterious in persons with low socioeconomic status. Most work has focused on psychosocial factors individually, but emerging research suggests that the confluence of psychosocial risk may be particularly harmful. Using data from the Reasons for Geographical and Racial Differences in Stroke (REGARDS) study, we examined associations among depressive symptoms and stress, alone and in combination, and incident CVD and all-cause mortality as a function of socioeconomic status. At baseline, 22 658 participants without a history of CVD (58.8% female, 41.7% black, mean age 63.9±9.3 years) reported on depressive symptoms, stress, annual household income, and education. Participants were classified into 1 of 3 psychosocial risk groups at baseline: (1) neither depressive symptoms nor stress, (2) either depressive symptoms or stress, or (3) both depressive symptoms and stress. Cox proportional hazards models were used to predict physician-adjudicated incident total CVD events (nonfatal myocardial infarction, nonfatal stroke, and cardiovascular death) and all-cause mortality over a median of 7.0 years (interquartile range 5.4-8.3 years) of follow-up. In fully adjusted models, participants with both depressive symptoms and stress had the greatest elevation in risk of developing total CVD (hazard ratio 1.48, 95% CI 1.21-1.81) and all-cause mortality (hazard ratio 1.33, 95% CI 1.13-1.56) but only for those with low income (<$35 000) and not high (≥$35 000) income. This pattern of results was not observed in models stratified by education. Findings suggest that screening for a combination of elevated depressive symptoms and stress in low-income persons may help identify those at increased risk of incident CVD and mortality. © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

Effects of glutamine treatment on myocardial damage and cardiac function in rats after severe burn injury.

PubMed

Yan, Hong; Zhang, Yong; Lv, Shang-jun; Wang, Lin; Liang, Guang-ping; Wan, Qian-xue; Peng, Xi

2012-01-01

Treatment with glutamine has been shown to reduce myocardial damage associated with ischemia/reperfusion injury. However, the cardioprotective effect of glutamine specifically after burn injury remains unclear. The present study explores the ability of glutamine to protect against myocardial damage in rats that have been severely burned. Seventy-two Wistar rats were randomly divided into three groups: normal controls (C), burned controls (B) and a glutamine-treated group (G). Groups B and G were subjected to full thickness burns comprising 30% of total body surface area. Group G was administered 1.5 g/ (kg•d) glutamine and group B was given the same dose of alanine via intragastric administration for 3 days. Levels of serum creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST) and blood lactic acid were measured, as well as myocardial ATP and glutathione (GSH) contents. Cardiac function indices and histopathological changes were analyzed at 12, 24, 48 and 72 post-burn hours. In both burned groups, levels of serum CK, LDH, AST and blood lactic acid increased significantly, while myocardial ATP and GSH contents decreased. Compared with group B, CK, LDH, and AST levels were lower and blood lactic acid, myocardial ATP and GSH levels were higher in group G. Moreover, cardiac contractile function inhibition and myocardial histopathological damage were significantly reduced in group G compared to B. Taken together, these results show that glutamine supplementation protects myocardial structure and function after burn injury by improving energy metabolism and by promoted the synthesis of ATP and GSH in cardiac myocytes.

Effects of glutamine treatment on myocardial damage and cardiac function in rats after severe burn injury

PubMed Central

Yan, Hong; Zhang, Yong; Lv, Shang-jun; Wang, Lin; Liang, Guang-ping; Wan, Qian-xue; Peng, Xi

2012-01-01

Treatment with glutamine has been shown to reduce myocardial damage associated with ischemia/reperfusion injury. However, the cardioprotective effect of glutamine specifically after burn injury remains unclear. The present study explores the ability of glutamine to protect against myocardial damage in rats that have been severely burned. Seventy-two Wistar rats were randomly divided into three groups: normal controls (C), burned controls (B) and a glutamine-treated group (G). Groups B and G were subjected to full thickness burns comprising 30% of total body surface area. Group G was administered 1.5 g/ (kg•d) glutamine and group B was given the same dose of alanine via intragastric administration for 3 days. Levels of serum creatine kinase (CK), lactate dehydrogenase (LDH), aspartate transaminase (AST) and blood lactic acid were measured, as well as myocardial ATP and glutathione (GSH) contents. Cardiac function indices and histopathological changes were analyzed at 12, 24, 48 and 72 post-burn hours. In both burned groups, levels of serum CK, LDH, AST and blood lactic acid increased significantly, while myocardial ATP and GSH contents decreased. Compared with group B, CK, LDH, and AST levels were lower and blood lactic acid, myocardial ATP and GSH levels were higher in group G. Moreover, cardiac contractile function inhibition and myocardial histopathological damage were significantly reduced in group G compared to B. Taken together, these results show that glutamine supplementation protects myocardial structure and function after burn injury by improving energy metabolism and by promotedthe synthesis of ATP and GSH in cardiac myocytes. PMID:22977661

Effect of cold air inhalation and isometric exercise on coronary blood flow and myocardial function in humans

PubMed Central

Muller, Matthew D.; Gao, Zhaohui; Drew, Rachel C.; Herr, Michael D.; Leuenberger, Urs A.

2011-01-01

The effects of cold air inhalation and isometric exercise on coronary blood flow are currently unknown, despite the fact that both cold air and acute exertion trigger angina in clinical populations. In this study, we used transthoracic Doppler echocardiography to measure coronary blood flow velocity (CBV; left anterior descending coronary artery) and myocardial function during cold air inhalation and handgrip exercise. Ten young healthy subjects underwent the following protocols: 5 min of inhaling cold air (cold air protocol), 5 min of inhaling thermoneutral air (sham protocol), 2 min of isometric handgrip at 30% of maximal voluntary contraction (grip protocol), and 5 min of isometric handgrip at 30% maximal voluntary contraction while breathing cold air (cold + grip protocol). Heart rate, blood pressure, inspired air temperature, CBV, myocardial function (tissue Doppler imaging), O2 saturation, and pulmonary function were measured. The rate-pressure product (RPP) was used as an index of myocardial O2 demand, whereas CBV was used as an index of myocardial O2 supply. Compared with the sham protocol, the cold air protocol caused a significantly higher RPP, but there was a significant reduction in CBV. The cold + grip protocol caused a significantly greater increase in RPP compared with the grip protocol (P = 0.045), but the increase in CBV was significantly less (P = 0.039). However, myocardial function was not impaired during the cold + grip protocol relative to the grip protocol alone. Collectively, these data indicate that there is a supply-demand mismatch in the coronary vascular bed when cold ambient air is breathed during acute exertion but myocardial function is preserved, suggesting an adequate redistribution of blood flow. PMID:21940852

Assessment of myocardial viability using 123I-labeled iodophenylpentadecanoic acid at sustained low flow or after acute infarction and reperfusion.

PubMed

Yang, J Y; Ruiz, M; Calnon, D A; Watson, D D; Beller, G A; Glover, D K

1999-05-01

123I-labeled iodophenylpentadecanoic acid (IPPA) is a synthetic fatty acid that may be useful for determination of myocardial viability. We investigated the uptake and clearance kinetics of this tracer in canine models of ischemia and infarction. In protocol 1, 185 MBq (5 mCi) 123I-IPPA were injected intravenously in 19 dogs with 50% left anterior descending artery (LAD) flow reduction. In 9 dogs, 201TI was coinjected. In protocol 2, 5 dogs underwent LAD occlusion for 3 h, and 123I-IPPA was injected 60 min after reperfusion. All dogs had flow measured by microspheres, regional systolic thickening by ultrasonic crystals and measurements of postmortem risk area and infarct size. Tracer activities were quantified by gamma well counting and by serial imaging. In protocol 1 dogs with sustained low flow (50% +/- 4%) and absence of systolic thickening (-3.2% +/- 1%), 123I-IPPA defect magnitude (LAD/left circumflex artery [LCX] count ratios) decreased from 0.65 +/- 0.02 to 0.74 +/- 0.02 at 30 min and to 0.84 +/- 0.03 at 2 h (P < 0.01), indicative of rest redistribution. Final transmural 123I-IPPA LAD/LCX activity ratio (0.99 +/- 0.05) was significantly greater than the flow ratio (0.53 +/- 0.04) at injection, confirming complete rest redistribution. The final 123I-IPPA activity ratio was significantly greater than the 201TI ratio over the 2-h period (P < 0.01). In protocol 2 dogs that underwent 3 h of total LAD occlusion and reflow (infarct size = 51% +/- 13% of risk area), viability was overestimated with 123I-IPPA, because uptake averaged 64% of normal in the central necrotic region, where flow averaged < 10% of normal. These findings suggest that serial 123I-IPPA imaging may be useful for assessing myocardial viability under conditions of sustained low flow and myocardial asynergy, such as appears to exist in patients with chronic coronary artery disease and depressed left ventricular function. In contrast, 123I-IPPA given early after reperfusion following prolonged coronary occlusion overestimates the degree of viability and therefore may not provide useful information pertaining to the degree of myocardial salvage after reflow in the setting of acute myocardial infarction.

Sepiapterin reduces postischemic injury in the rat heart.

PubMed

Tiefenbacher, Christiane P; Lee, Ching-Hua; Kapitza, Jolanthe; Dietz, Volker; Niroomand, Feraydoon

2003-10-01

A reduced availability of tetrahydrobiopterin (BH4), an essential cofactor for NO-synthesis, is causally involved in the development of endothelial dysfunction associated with ischemia/reperfusion. We, therefore, investigated the effect of sepiapterin, a substrate for BH4 synthesis, on postischemic injury in myocardial infarction and myocardial stunning. In rats, myocardial stunning was induced by repetitive ischemia (5 x 10-min ligature of the left coronary artery, 5 x 20-min reperfusion) and myocardial infarction by 50-min ligature and 60-min reperfusion. Myocardial blood flow was determined by H2-clearance, regional myocardial function by pulsed Doppler and infarct size by tetrazolium staining. Myeloperoxidase (MPO) activity was measured as a marker of neutrophil extravasation. cGMP was determined in rat serum as an indicator of increased NO synthesis. In animals treated with sepiapterin, regional myocardial function was significantly improved in both myocardial stunning and infarction and infarct size was significantly reduced. MPO activity decreased with sepiapterin treatment in both models. The systemic level of cGMP was reduced both following myocardial stunning and myocardial infarction in the control group. Pretreatment with sepiapterin induced a significant increase of cGMP level at the end of the protocol in both models. Substitution of sepiapterin reduces postischemic injury both in myocardial stunning and infarction apparently by ameliorating the availability of NO, thereby attenuating the activation of neutrophils in ischemia/reperfusion.

Depressed left ventricular performance. Response to volume infusion in patients with sepsis and septic shock

DOE Office of Scientific and Technical Information (OSTI.GOV)

Ognibene, F.P.; Parker, M.M.; Natanson, C.

Volume infusion, to increase preload and to enhance ventricular performance, is accepted as initial management of septic shock. Recent evidence has demonstrated depressed myocardial function in human septic shock. We analyzed left ventricular performance during volume infusion using serial data from simultaneously obtained pulmonary artery catheter hemodynamic measurements and radionuclide cineangiography. Critically ill control subjects (n = 14), patients with sepsis but without shock (n = 21), and patients with septic shock (n = 21) had prevolume infusion hemodynamic measurements determined and received statistically similar volumes of fluid resulting in similar increases in pulmonary capillary wedge pressure. There was amore » strong trend (p = 0.004) toward less of a change in left ventricular stroke work index (LVSWI) after volume infusion in patients with sepsis and septic shock compared with control subjects. The LVSWI response after volume infusion was significantly less in patients with septic shock when compared with critically ill control subjects (p less than 0.05). These data demonstrate significantly altered ventricular performance, as measured by LVSWI, in response to volume infusion in patients with septic shock.« less

Does nurse-based case management for aged myocardial infarction patients improve risk factors, physical functioning and mental health? The KORINNA trial.

PubMed

Hunger, Matthias; Kirchberger, Inge; Holle, Rolf; Seidl, Hildegard; Kuch, Bernhard; Wende, Rupert; Meisinger, Christine

2015-04-01

Older patients with acute myocardial infarction (MI) are often lacking optimal support to continue rehabilitation after discharge from hospital. The objective of the study was to examine whether a home-based case management programme led by nurses can improve atherogenic risk factors, physical functioning, and mental health in the first year following discharge. The KORINNA study is a randomized two-armed parallel group trial including 329 patients (aged 65-92 years) from the Augsburg Hospital in southern Germany. The intervention consisted of an individualized follow-up programme with a duration of 1 year, including home visits and telephone calls. The control group received usual care. Secondary outcome measures included clinical parameters (blood pressure, lipid parameters), functional status measures, cognitive status, depressive symptoms, and nutrition risk. At 1-year follow up, patients in the intervention group (n = 116) had significantly better low-density lipoprotein cholesterol levels (-8.4 mg/dl, 95% CI -16.4 to -0.4), hand grip strength (+2.53 kg, 95% CI 0.56 to 4.50), and SCREEN-II nutrition risk scores (+2.03, 95% CI 0.58 to 3.48) than patients in the control group (n = 136). The intervention group also had better mean scores with regard to self-reported disability, activities in daily living, and mental health, but differences were not always significant and meaningful. The results of the KORINNA study indicate that nurse-based case management can improve blood lipid levels, functional status, and nutrition risk of aged patients with MI. © The European Society of Cardiology 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.

Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients: a losartan intervention for endpoint reduction in hypertension (LIFE) cardiovascular magnetic resonance and echocardiographic substudy.

PubMed

Biederman, Robert W W; Doyle, Mark; Young, Alistair A; Devereux, Richard B; Kortright, Eduardo; Perry, Gilbert; Bella, Jonathan N; Oparil, Suzanne; Calhoun, David; Pohost, Gerald M; Dell'Italia, Louis J

2008-08-01

Concentric hypertensive left ventricular (LV) hypertrophy is presumed to be a symmetrical process. Using MRI-derived intramyocardial strain, we sought to determine whether segmental deformation was also symmetrical, as suggested by echocardiography. High echocardiographic LV relative wall thickness in hypertensive LV hypertrophy allows preserved endocardial excursion despite depressed LV midwall shortening (MWS). Depressed MWS is an adverse prognostic indicator, but whether this is related to global or regional myocardial depression is unknown. We prospectively compared MWS derived from linear echocardiographic dimensions with MR strain(in) in septal and posterior locations in 27 subjects with ECG LV hypertrophy in the Losartan Intervention for Endpoint Reduction in Hypertension Study. Although MRI-derived mass was higher in patients than in normal control subjects (124.0+/-38.6 versus 60.5+/-13.2g/m(2); P<0.001), fractional shortening (30+/-5% versus 33+/-3%) and end-systolic stress (175+/-22 versus 146+/-28 g/cm(2)) did not differ between groups. However, mean MR(in) was decreased in patients versus normal control subjects (13.9+/-6.8% versus 22.4+/-3.5%), as was echo MWS (13.4+/-2.8% versus 18.2+/-1.4%; both P<0.001). For patients versus normal control subjects, posterior wall(in) was not different (17.8+/-7.1% versus 21.6+/-4.0%), whereas septal(in) was markedly depressed (10.1+/-6.6% versus 23.2+/-3.4%; P<0.001). Although global MWS by echocardiography or MRI is depressed in hypertensive LV hypertrophy, MRI tissue tagging demonstrates substantial regional intramyocardial strain(in) heterogeneity, with most severely depressed strain patterns in the septum. Although posterior wall 2D principal strain was inversely related to radius of curvature, septal strain was not, suggesting that factors other than afterload are responsible for pronounced myocardial strain heterogeneity in concentric hypertrophy.

Impact of enzyme replacement therapy on cardiac morphology and function and late enhancement in Fabry's cardiomyopathy.

PubMed

Beer, Meinrad; Weidemann, Frank; Breunig, Frank; Knoll, Anita; Koeppe, Sabrina; Machann, Wolfram; Hahn, Dietbert; Wanner, Christoph; Strotmann, Jörg; Sandstede, Jörn

2006-05-15

The present study evaluated the evolution of cardiac morphology, function, and late enhancement as a noninvasive marker of myocardial fibrosis, and their inter-relation during enzyme replacement therapy in patients with Fabry's disease using magnetic resonance imaging and color Doppler myocardial imaging. Late enhancement, which was present in up to 50% of patients, was associated with increased left ventricular mass, the failure of a significant regression of hypertrophy during enzyme replacement therapy, and worse segmental myocardial function. Late enhancement may predict the effect of enzyme replacement therapy on left ventricular mass and cardiac function.

Norepinephrine turnover in heart and spleen of 7-, 22-, and 34 C-acclimated hamsters

NASA Technical Reports Server (NTRS)

Jones, S. B.; Musacchia, X. J.

1976-01-01

The relationship of norepinephrine (NE) concentration and endogenous turnover rates in both myocardial and spleen tissues in the golden hamster is examined as a function of chronic exposure to either high or low ambient temperatures. Changes in myocardial and spleen NE turnover values are discussed in terms of functional alterations in sympathetic nerve activity and the importance of such changes in temperature acclimation. It is found that acclimation of hamsters to 7 C for 7-10 weeks results in decreased myocardial NE concentration and an apparent increase in myocardial NE turnover. In contrast, exposure to 34 C for 6-8 weeks results in increased myocardial NE concentration and an apparent decrease in NE turnover in both myocardial and spleen tissues. The implication of altered NE synthesis is that sympathetic nerve activity is reduced with heat acclimation and is enhanced with cold acclimation.

Nuclear cardiac

DOE Office of Scientific and Technical Information (OSTI.GOV)

Slutsky, R.; Ashburn, W.L.

1982-01-01

The relationship between nuclear medicine and cardiology has continued to produce a surfeit of interesting, illuminating, and important reports involving the analysis of cardiac function, perfusion, and metabolism. To simplify the presentation, this review is broken down into three major subheadings: analysis of myocardial perfusion; imaging of the recent myocardial infarction; and the evaluation of myocardial function. There appears to be an increasingly important relationship between cardiology, particularly cardiac physiology, and nuclear imaging techniques. (KRM)

Injectable Microsphere Gel Progressively Improves Global Ventricular Function, Regional Contractile Strain, and Mitral Regurgitation after Myocardial Infarction

PubMed Central

McGarvey, Jeremy R; Kondo, Norihiro; Witschey, Walter RT; Takebe, Manabu; Aoki, Chikashi; Burdick, Jason A.; Spinale, Francis G; Gorman, Joseph H; Pilla, James J; Gorman, Robert C

2014-01-01

Background There is continued need for therapies which reverse or abate the remodeling process following myocardial infarction (MI). In this study, we evaluate the longitudinal effects of calcium hydroxyapatite microsphere gel on regional strain, global ventricular function, and mitral regurgitation (MR) in a porcine MI model. Methods Twenty five Yorkshire swine were enrolled. Five were dedicated weight-matched controls. Twenty underwent posterolateral infarction by direct ligation of the circumflex artery and its branches. Infarcted animals were randomly divided into four groups: one week treatment, one week control, four week treatment, and four week control. Following infarction, animals received either twenty 150μl calcium hydroxyapatite gel or saline injections within the infarct. At their respective timepoints, echocardiograms, cardiac MRI, and tissue were collected for evaluation of MR, regional and global left ventricular function, wall thickness, and collagen content. Results Global and regional LV function were depressed in all infarcted subjects at one week compared to healthy controls. By four weeks post-infarction, global function had significantly improved in the calcium hydroxyapatite group compared to infarcted controls (EF 48.5±1.9% vs. 38.0±1.7%, p<0.01). Similarly, regional borderzone radial contractile strain (16.3±1.5% vs. 11.2±1.5%, p=0.04), MR grade (0.4±0.2 vs. 1.2±0.2, p=0.04), and infarct thickness (7.8±0.5mm vs. 4.5±0.2mm, p<0.01) were improved at this timepoint in the treatment group compared to infarct controls. Conclusions Calcium hydroxyapatite injection following MI progressively improves global LV function, borderzone function, and mitral regurgitation. Using novel biomaterials to augment infarct material properties is viable alternative in the current management of heart failure. PMID:25524397

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status.

PubMed

Léger, Thibault; Charrier, Alice; Moreau, Clarisse; Hininger-Favier, Isabelle; Mourmoura, Evangelia; Rigaudière, Jean-Paul; Pitois, Elodie; Bouvier, Damien; Sapin, Vincent; Pereira, Bruno; Azarnoush, Kasra; Demaison, Luc

2017-07-01

If it is sustained for several days, sepsis can trigger severe abnormalities of cardiac function which leads to death in 50% of cases. This probably occurs through activation of toll-like receptor-9 by bacterial lipopolysaccharides and overproduction of proinflammatory cytokines such as TNF- α and IL-1 β In contrast, early sepsis is characterized by the development of tachycardia. This study aimed at determining the early changes in the cardiac function during sepsis and at finding the mechanism responsible for the observed changes. Sixty male Wistar rats were randomly assigned to two groups, the first one being made septic by cecal ligation and puncture (sepsis group) and the second one being subjected to the same surgery without cecal ligation and puncture (sham-operated group). The cardiac function was assessed in vivo and ex vivo in standard conditions. Several parameters involved in the oxidative stress and inflammation were determined in the plasma and heart. As evidenced by the plasma level of TNF- α and gene expression of IL-1 β and TNF- α in the heart, inflammation was developed in the sepsis group. The cardiac function was also slightly stimulated by sepsis in the in vivo and ex vivo situations. This was associated with unchanged levels of oxidative stress, but several parameters indicated a lower cardiac production of reactive oxygen species in the septic group. In conclusion, despite the development of inflammation, early sepsis did not increase reactive oxygen species production and did not reduce myocardial function. The depressant effect of TNF- α and IL-1 β on the cardiac function is known to occur at very high concentrations. The influence of low- to moderate-grade inflammation on the myocardial mechanical behavior must thus be revisited. © 2017 French National Institute of Agronomical Research (INRA). Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

Reciprocal ST-Segment Changes in Myocardial Infarction: Ischemia at Distance Versus Mirror Reflection of ST-Elevation.

PubMed

Vaidya, Gaurang Nandkishor; Antoine, Steve; Imam, Syed Haider; Kozman, Hani; Smulyan, Harold; Villarreal, Daniel

2018-02-01

Reciprocal ST-depression in the electrocardiograms (ECGs) of patients with ST-elevation myocardial infarction (STEMI) results from either true ischemia at a distance via collateral circulation diverting blood to the infarcted region or an electrical phenomenon that results from a mirror reflection of ST-elevation. We aimed to identify the role of reciprocal ECG changes in predicting collateral circulation to the infarcted area determined angiographically. In a retrospective study, ECG and angiography of 53 STEMI patients admitted to SUNY Upstate Medical University in 2014 were reviewed independently by experts blinded to the results of ECG and coronary angiography. Reciprocal changes (RC) in ECG were present in 41 patients (77%) and on angiography, 14 patients (26%) exhibited collateral vessels to the ischemic areas. No correlation was found between the presence of RC and collateral circulation (P = 0.384), or between the depth of reciprocal ST-depression and the degree of the collateral circulation (P = 0.195). However, 84% of patients without collaterals exhibited resolution of RC after successful percutaneous coronary intervention (PCI) (P = 0.036), suggesting that the ST depressions that resolved after reperfusion were directly caused by the culprit vessel. Patients without RC presented late after symptom onset (9.25 versus 3.83 hours, P = 0.004), also suggesting time related resolution. RC had no relation to or predictive value for collaterals on angiography. Among late presenting patients, RC were less frequent. Thus, reciprocal ST-depression may represent subendocardial ischemia from the primary coronary event or simply an electrical phenomenon, rather than ischemia at distance from impaired collateral circulation. Published by Elsevier Inc.

Smoking-associated factors in myocardial infarction and unstable angina: do gender differences exist?

PubMed

Perez, Glória Heloise; Nicolau, José Carlos; Romano, Bellkiss Wilma; Laranjeira, Ronaldo

2007-06-01

The aim of this study was to investigate demographic and psychological characteristics associated with smoking in patients with acute coronary syndrome (myocardial infarction or unstable angina). Interviews were conducted with 348 consecutive hospitalized patients with acute coronary syndrome and included questions about demographic characteristics, coffee consumption, heart disease risk perception, economic status, alcohol consumption, depression, anxiety, and stress. Female group multivariate analysis showed that smoking in females was significantly and negatively associated with age, heart disease risk perception, and positively associated with coffee consumption. Male group multivariate analysis showed that for males, smoking was significantly and negatively associated with age, heart disease risk perception, and positively associated with coffee and alcohol consumption. Unlike studies conducted with non-heart disease patients, our results do not show an association between smoking and depression. Compared with nonsmokers, smokers with acute coronary syndrome are younger, more likely to drink coffee, and less likely to perceive smoking as a heart disease risk. Male smokers are also more likely to drink alcohol, indicating that they use more psycho-stimulants than do nonsmoking men and women who smoke.

Relationship Between Blood Pressure Values, Depressive Symptoms, and Cardiovascular Outcomes in Patients With Cardiometabolic Disease.

PubMed

Jani, Bhautesh Dinesh; Cavanagh, Jonathan; Barry, Sarah J E; Der, Geoff; Sattar, Naveed; Mair, Frances S

2016-10-01

The authors studied the joint effect of blood pressure (BP) and depression on the risk of major adverse cardiovascular outcome in patients with existing cardiometabolic disease. A cohort of 35,537 patients with coronary heart disease, diabetes, or stroke underwent depression screening and BP measurement recorded concurrently. The authors used Cox's proportional hazards to calculate risk of major adverse cardiovascular event (MACE; myocardial infarction/heart failure/stroke or cardiovascular death) over 4 years associated with baseline BP and depression. A total of 11% (3939) had experienced a MACE within 4 years. Patients with very high systolic BP (160-240 mm Hg; hazard ratio, 1.28) and depression (hazard ratio, 1.22) at baseline had significantly higher adjusted risk. Depression had a significant interaction with systolic BP in risk prediction (P=.03). Patients with a combination of high systolic BP and depression at baseline had 83% higher adjusted risk of MACE, as compared with patients with reference systolic BP without depression. Patients with cardiometabolic disease and comorbid depression may benefit from closer monitoring of systolic BP. © 2016 The Authors. The Journal of Clinical Hypertension Published by Wiley Periodicals, Inc.

Prophylactic Catheter Ablation for the Prevention of Defibrillator Therapy

PubMed Central

Reddy, Vivek Y.; Reynolds, Matthew R.; Neuzil, Petr; Richardson, Allison W.; Taborsky, Milos; Jongnarangsin, Krit; Kralovec, Stepan; Sediva, Lucie; Ruskin, Jeremy N.; Josephson, Mark E.

2008-01-01

BACKGROUND For patients who have a ventricular tachyarrhythmic event, implantable cardioverter–defibrillators (ICDs) are a mainstay of therapy to prevent sudden death. However, ICD shocks are painful, can result in clinical depression, and do not offer complete protection against death from arrhythmia. We designed this randomized trial to examine whether prophylactic radiofrequency catheter ablation of arrhythmogenic ventricular tissue would reduce the incidence of ICD therapy. METHODS Eligible patients with a history of a myocardial infarction underwent defibrillator implantation for spontaneous ventricular tachycardia or fibrillation. The patients did not receive antiarrhythmic drugs. Patients were randomly assigned to defibrillator implantation alone or defibrillator implantation with adjunctive catheter ablation (64 patients in each group). Ablation was performed with the use of a substrate-based approach in which the myocardial scar is mapped and ablated while the heart remains predominantly in sinus rhythm. The primary end point was survival free from any appropriate ICD therapy. RESULTS The mortality rate 30 days after ablation was zero, and there were no significant changes in ventricular function or functional class during the mean (±SD) follow-up period of 22.5±5.5 months. Twenty-one patients assigned to defibrillator implantation alone (33%) and eight patients assigned to defibrillator implantation plus ablation (12%) received appropriate ICD therapy (antitachycardia pacing or shocks) (hazard ratio in the ablation group, 0.35; 95% confidence interval, 0.15 to 0.78, P = 0.007). Among these patients, 20 in the control group (31%) and 6 in the ablation group (9%) received shocks (P = 0.003). Mortality was not increased in the group assigned to ablation as compared with the control group (9% vs. 17%, P = 0.29). CONCLUSIONS In this randomized trial, prophylactic substrate-based catheter ablation reduced the incidence of ICD therapy in patients with a history of myocardial infarction who received ICDs for the secondary prevention of sudden death. (Current Controlled Trials number, ISRCTN62488166.) PMID:18160685

Both Selenium Deficiency and Modest Selenium Supplementation Lead to Myocardial Fibrosis in Mice via Effects on Redox-Methylation Balance

PubMed Central

Metes-Kosik, Nicole; Luptak, Ivan; DiBello, Patricia M.; Handy, Diane E.; Tang, Shiow-Shih; Zhi, Hui; Qin, Fuzhong; Jacobsen, Donald W.; Loscalzo, Joseph; Joseph, Jacob

2013-01-01

Scope Selenium has complex effects in vivo on multiple homeostatic mechanisms such as redox balance, methylation balance, and epigenesis, via its interaction with the methionine-homocysteine cycle. In this study, we examined the hypothesis that selenium status would modulate both redox and methylation balance and thereby modulate myocardial structure and function. Methods and Results We examined the effects of selenium deficient (<0.025 mg/kg), control (0.15 mg/kg), and selenium supplemented (0.5 mg/kg) diets on myocardial histology, biochemistry and function in adult C57/BL6 mice. Selenium deficiency led to reactive myocardial fibrosis and systolic dysfunction accompanied by increased myocardial oxidant stress. Selenium supplementation significantly reduced methylation potential, DNA methyltransferase activity and DNA methylation. In mice fed the supplemented diet, inspite of lower oxidant stress, myocardial matrix gene expression was significantly altered resulting in reactive myocardial fibrosis and diastolic dysfunction in the absence of myocardial hypertrophy. Conclusions Our results indicate that both selenium deficiency and modest selenium supplementation leads to a similar phenotype of abnormal myocardial matrix remodeling and dysfunction in the normal heart. The crucial role selenium plays in maintaining the balance between redox and methylation pathways needs to be taken into account while optimizing selenium status for prevention and treatment of heart failure. PMID:23097236

Positron Emission Tomography of the Heart

DOE R&D Accomplishments Database

Schelbert, H. R.; Phelps, M. E.; Kuhl, D. E.

1979-01-01

Positron emission computed tomography (PCT) represents an important new tool for the noninvasive evaluation and, more importantly, quantification of myocardial performance. Most currently available techniques permit assessment of only one aspect of cardiac function, i.e., myocardial perfusion by gamma scintillation camera imaging with Thallium-201 or left ventricular function by echocardiography or radionuclide angiocardiography. With PCT it may become possible to study all three major segments of myocardial performance, i.e., regional blood flow, mechanical function and, most importantly, myocardial metabolism. Each of these segments can either be evaluated separately or in combination. This report briefly describes the principles and technological advantages of the imaging device, reviews currently available radioactive tracers and how they can be employed for the assessment of flow, function and metabolism; and, lastly, discusses possible applications of PCT for the study of cardiac physiology or its potential role in the diagnosis of cardiac disease.

Relationship of myocardial hibernation, scar, and angiographic collateral flow in ischemic cardiomyopathy with coronary chronic total occlusion.

PubMed

Wang, Li; Lu, Min-Jie; Feng, Lei; Wang, Juan; Fang, Wei; He, Zuo-Xiang; Dou, Ke-Fei; Zhao, Shi-Hua; Yang, Min-Fu

2018-03-07

The relationship between myocardial viability and angiographic collateral flow is not fully elucidated in ischemic cardiomyopathy (ICM) with coronary artery chronic total occlusion (CTO). We aimed to clarify the relationship between myocardial hibernation, myocardial scar, and angiographic collateral flow in these patients. Seventy-one consecutive ICM patients with 122 CTOs and 652 dysfunctional segments within CTO territories were retrospectively analyzed. Myocardial hibernation (perfusion-metabolism mismatch) and the extent of 18 F-fluorodeoxyglucose (FDG) abnormalities were assessed using 99m Tc-sestamibi and 18 F-FDG imaging. Myocardial scar was evaluated by late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) imaging. Collateral flow observed on coronary angiography was assessed using Rentrop classification. In these patients, neither the extent nor frequency of myocardial hibernation or scar was related to the status of collateral flow. Moreover, the matching rate in determining myocardial viability was poor between any 2 imaging indices. The extent of 18 F-FDG abnormalities was linearly related to the extent of LGE rather than myocardial hibernation. Of note, nearly one-third (30.4%) of segments with transmural scar still had hibernating tissue. Hibernation and non-transmural scar had higher sensitivity (63.0% and 66.7%) than collateral flow (37.0%) in predicting global functional improvement. Angiographic collateral cannot accurately predict myocardial viability, and has lower sensitivity in prediction of functional improvement in CTO territories in ICM patients. Hence, assessment of myocardial viability with non-invasive imaging modalities is of importance. Moreover, due to the lack of correlation between myocardial hibernation and scar, these two indices are complementary but not interchangeable.

Ectopic fat depots and left ventricular function in nondiabetic men with nonalcoholic fatty liver disease.

PubMed

Granér, Marit; Nyman, Kristofer; Siren, Reijo; Pentikäinen, Markku O; Lundbom, Jesper; Hakkarainen, Antti; Lauerma, Kirsi; Lundbom, Nina; Nieminen, Markku S; Taskinen, Marja-Riitta

2015-01-01

Nonalcoholic fatty liver disease has emerged as a novel cardiovascular risk factor. The aim of the study was to assess the effect of different ectopic fat depots on left ventricular (LV) function in subjects with nonalcoholic fatty liver disease. Myocardial and hepatic triglyceride contents were measured with 1.5 T magnetic resonance spectroscopy and LV function, visceral adipose tissue (VAT) and subcutaneous adipose tissue, epicardial and pericardial fat by MRI in 75 nondiabetic men. Subjects were stratified by hepatic triglyceride content into low, moderate, and high liver fat groups. Myocardial triglyceride, epicardial and pericardial fat, VAT, and subcutaneous adipose tissue increased stepwise from low to high liver fat group. Parameters of LV diastolic function showed a stepwise decrease over tertiles of liver fat and VAT, and they were inversely correlated with hepatic triglyceride, VAT, and VAT/subcutaneous adipose tissue ratio. In multivariable analyses, hepatic triglyceride and VAT were independent predictors of LV diastolic function, whereas myocardial triglyceride was not associated with measures of diastolic function. Myocardial triglyceride, epicardial and pericardial fat increased with increasing amount of liver fat and VAT. Hepatic steatosis and VAT associated with significant changes in LV structure and function. The association of LV diastolic function with hepatic triglyceride and VAT may be because of toxic systemic effects. The effects of myocardial triglyceride on LV structure and function seem to be more complex than previously thought and merit further study. © 2014 American Heart Association, Inc.

Effect of granulocyte colony stimulating EPC on cardiac function and myocardial energy expenditure in patients with heart failure after myocardial infarction.

PubMed

Zhao, Zilin; Luo, Jianchun; Ma, Lixian; Luo, Xia; Huang, Liangyan

2015-01-01

To study the changes of cardiac function and myocardial energy expenditure following treatment with granulocyte colony stimulating factor (G-CSF) in patients with heart failure after myocardial infarction. Thirty-eight patients with heart failure after myocardial infarction were randomized into G-CSF treatment group and control group. All the patients received conventional treatment (medication and interventional therapy), and the patients in treatment group were given additional G-CSF (600 μg/day) for 7 consecutive days. The plasma level of brain-type natriuretic peptide (BNP) and the number of endothelial progenitor cells (EPC) in the peripheral blood were detected before and at 7 days and 4 months after the treatment. The cardiac functions (LVEF, FS, LVIDs, PWTs, EDV, SV, ET) was evaluated by ultrasonic imaging before and at 2 weeks and 4 months after the treatment. The MEE and circumferential end-systolic wall stress (cESS) were calculated by correlation formula. The number of EPC was significantly higher in the treatment group than in the control group after the treatment especially at 7 days (P<0.01). In both groups, BNP level was lowered significantly after the treatment to recover the normal level (P<0.01). The cardiac functions and myocardial energy expenditure were improved in all the patients at 2 weeks and 4 months after the treatment, and the improvement was more obvious in the treatment group (P<0.05), especially in terms of the MEE and cESS was significantly lowered in the treatment group than in the control group after the treatment at 2 weeks (P<0.01), the LVEF and FS was significantly increased in the treatment group than in the control group after the treatment at 4 months (P<0.01). EPC mobilization by G-CSF can effectively improve the cardiac functions, lessen ventricular remodeling and reduce myocardial energy expenditure in patients with heart failure after myocardial infarction.

Atrial electromechanical delay and diastolic dysfunction in primary Sjögren syndrome.

PubMed

Akyel, Ahmet; Tavil, Yusuf; Tufan, Abdurrahman; Yayla, Cagri; Kaya, Arif; Tezcan, Mehme Engin; Ozturk, Mehmet Akif; Boyaci, Bulent

2012-10-06

In this study we aimed to investigate myocardial function and atrial electromechanical properties by conventional and tissue doppler echocardiography in patients with primary Sjögren syndrome. Forty patients with Sjögren syndrome (SS) and 25 age- and sex-matched healthy volunteers were enrolled in the study. Using transthoracic echocardiography, myocardial performance index and atrial electromechanical properties were measured. Basal characteristics were similar between two groups. Myocardial performance index values were disturbed in patients with Sjögren syndrome (0.41 vs. 0.32, p < 0.01). There was significant intraatrial (16.4±6.4, 5.0±4.5, p < 0.01) and interatrial (30.6±10.1, 15.4±5.9, p < 0.01) electromechanical delay in this patient group. Myocardial function is disturbed and there is significant atrial electromechanical delay in patients with primary SS. This study is the first to show altered myocardial function and atrial electromechanical properties in primary SS.

Initial shunt type at the Norwood operation impacts myocardial function in hypoplastic left heart syndrome.

PubMed

Ruotsalainen, Hanna K; Pihkala, Jaana; Salminen, Jukka; Hornberger, Lisa K; Sairanen, Heikki; Ojala, Tiina

2017-08-01

We investigated the impact of initial shunt type, a Blalock-Taussig (BT) shunt versus a right ventricle to pulmonary artery conduit (RV-PA) on myocardial function at different stages of surgical palliation in patients with hypoplastic left heart syndrome (HLHS). A population-based cohort of 63 Finnish children with HLHS (BT n  = 23, RV-PA n  = 40) born between 2003 and 2010 were studied retrospectively by echocardiography prior to Stages 1, 2 and 3 palliation and 0.5-3 years after Stage 3. For comparison of systolic myocardial function, we evaluated the RV fractional area change (FAC), strain, strain rate and mechanical synchrony from the apical 4-chamber view by velocity vector imaging. There were no intergroup differences in demographics during the study period. At baseline, no intergroup differences were detected in RV systolic myocardial function. Before Stage 2, RV FAC was higher ( P  = 0.03) in the RV-PA conduit group. At Stage 3, an increase in all systolic myocardial functional parameters was observed in the BT shunt group. After Stage 3, the BT shunt group had better RV systolic function. In multiple regression analysis, the shunt type and the stage of palliation had an impact on myocardial function. Although patients with HLHS initially palliated with a BT shunt demonstrate lower RV FAC after Stage I, RV FAC improves after Stage 2 with better systolic performance after Stage 3 compared with those initially palliated with an RV-PA conduit. © The Author 2017. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.

Recent Advances in Cardiovascular Magnetic Resonance Techniques and Applications

PubMed Central

Salerno, Michael; Sharif, Behzad; Arheden, Håkan; Kumar, Andreas; Axel, Leon; Li, Debiao; Neubauer, Stefan

2018-01-01

Cardiovascular magnetic resonance imaging has become the gold standard for evaluating myocardial function, volumes, and scarring. Additionally, cardiovascular magnetic resonance imaging is unique in its comprehensive tissue characterization, including assessment of myocardial edema, myocardial siderosis, myocardial perfusion, and diffuse myocardial fibrosis. Cardiovascular magnetic resonance imaging has become an indispensable tool in the evaluation of congenital heart disease, heart failure, cardiac masses, pericardial disease, and coronary artery disease. This review will highlight some recent novel cardiovascular magnetic resonance imaging techniques, concepts, and applications. PMID:28611116

Protective effect of N-acetylcysteine activated carbon release microcapsule on myocardial ischemia-reperfusion injury in rats

PubMed Central

Cai, Zhaobin; Shi, Tingting; Zhuang, Rangxiao; Fang, Hongying; Jiang, Xiaojie; Shao, Yidan; Zhou, Hongping

2018-01-01

With the development of science and technology, and development of artery bypass, methods such as cardiopulmonary cerebral resuscitation have been practiced in recent years. Despite this, some methods fail to promote or recover the function of tissues and organs, and in some cases, may aggravate dysfunction and structural damage to tissues. The latter is typical of ischemia-reperfusion (IR) injury. Lipid peroxidation mediated by free radicals is an important process of myocardial IR injury. Myocardial IR has been demonstrated to induce the formation of large numbers of free radicals in rats, which promotes the peroxidation of lipids within unsaturated fatty acids in the myocardial cell membrane. Markers of lipid peroxidation include malondialdehyde, superoxide dismutase and lactic dehydrogenase. Recent studies have demonstrated that N-acetylcysteine (NAC) is able to dilate blood vessels, prevent oxidative damage, improve immunity, inhibit apoptosis and the inflammatory response and promote glutathione synthesis in cells. NAC also improves the systolic function of myocardial cells and cardiac function, prevents myocardial apoptosis, protects ventricular remodeling and vascular remodeling, reduces opiomelanocortin levels in the serum and increases the content of nitric oxide in the serum, thus improving vascular endothelial function. Therefore, NAC has potent pharmacological activity; however, the relatively fast metabolism of NAC, along with its large clinical dose and low bioavailability, limit its applications. The present study combined NAC with medicinal activated carbons, and prepared N-acetylcysteine activated carbon sustained-release microcapsules (ACNACs) to overcome the limitations of NAC. It was demonstrated that ACNACs exerted greater effective protective effects than NAC alone on myocardial IR injury in rats. PMID:29434769

Systemic pretreatment with dimethyloxalylglycine increases myocardial HIF-1α and VEGF production and improves functional recovery after acute ischemia/reperfusion.

PubMed

Poynter, Jeffrey A; Manukyan, Mariuxi C; Wang, Yue; Brewster, Benjamin D; Herrmann, Jeremy L; Weil, Brent R; Abarbanell, Aaron M; Meldrum, Daniel R

2011-08-01

Stem cells protect the heart from ischemic damage in part by the release of cytoprotective growth factors, particularly vascular endothelial growth factor (VEGF). Production of VEGF is regulated in part by levels of the transcription factor hypoxia inducible factor 1-α (HIF-1α). Dimethyloxalylglycine (DMOG) prevents the deactivation of HIF-1α and increases VEGF production. However, the effects of systemic DMOG treatment on myocardial tolerance for ischemia are unknown. We hypothesized that systemic pretreatment with DMOG would improve myocardial ischemic tolerance. To study this hypothesis, adult male rats were randomly given an intraperitoneal injection of DMOG (40 mg/kg in 1 mL saline, n = 5) or saline (1 mL, n = 6) 24 h before cardiectomy and isolated heart perfusion. All hearts were subjected to 15 min equilibration, 25 min ischemia and 40 min reperfusion. Myocardial function was continuously monitored. Following reperfusion, myocardial homogenates were analyzed for HIF-1α and VEGF production. We observed that hearts in the DMOG group exhibited greater recovery of left ventricular developed pressure LVDP, +dP/dt and -dP/dt. Myocardial HIF-1α and VEGF levels were increased by DMOG therapy. In conclusion, systemic pretreatment with DMOG augments post-ischemic myocardial functional recovery through increased HIF-1α levels and greater VEGF production. Copyright © 2011 Mosby, Inc. All rights reserved.

Experimental myocardial infarction

PubMed Central

Kumar, Raj; Joison, Julio; Gilmour, David P.; Molokhia, Farouk A.; Pegg, C. A. S.; Hood, William B.

1971-01-01

The hemodynamic effects of tachycardia induced by atrial pacing were investigated in left ventricular failure of acute and healing experimental myocardial infarction in 20 intact, conscious dogs. Myocardial infarction was produced by gradual inflation of a balloon cuff device implanted around the left anterior descending coronary artery 10-15 days prior to the study. 1 hr after acute myocardial infarction, atrial pacing at a rate of 180 beats/min decreased left ventricular end-diastolic pressure from 19 to 8 mm Hg and left atrial pressure from 17 to 12 mm Hg, without change in cardiac output. In the healing phase of myocardial infarction 1 wk later, atrial pacing decreased left ventricular end-diastolic pressure from 17 to 9 mm Hg and increased the cardiac output by 37%. This was accompanied by evidence of peripheral vasodilation. In two dogs with healing anterior wall myocardial infarction, left ventricular failure was enhanced by partial occlusion of the circumflex coronary artery. Both the dogs developed pulmonary edema. Pacing improved left ventricular performance and relieved pulmonary edema in both animals. In six animals propranolol was given after acute infarction, and left ventricular function deteriorated further. However the pacing-induced augmentation of cardiac function was unaltered and, hence, is not mediated by sympathetics. The results show that the spontaneous heart rate in left ventricular failure of experimental canine myocardial infarction may be less than optimal and that maximal cardiac function may be achieved at higher heart rates. Images PMID:4395910

Different Sequences of Fractionated Low-Dose Proton and Single Iron-Radiation-Induced Divergent Biological Responses in the Heart.

PubMed

Sasi, Sharath P; Yan, Xinhua; Zuriaga-Herrero, Marian; Gee, Hannah; Lee, Juyong; Mehrzad, Raman; Song, Jin; Onufrak, Jillian; Morgan, James; Enderling, Heiko; Walsh, Kenneth; Kishore, Raj; Goukassian, David A

2017-08-01

Deep-space travel presents risks of exposure to ionizing radiation composed of a spectrum of low-fluence protons ( 1 H) and high-charge and energy (HZE) iron nuclei (e.g., 56 Fe). When exposed to galactic cosmic rays, each cell in the body may be traversed by 1 H every 3-4 days and HZE nuclei every 3-4 months. The effects of low-dose sequential fractionated 1 H or HZE on the heart are unknown. In this animal model of simulated ionizing radiation, middle-aged (8-9 months old) male C57BL/6NT mice were exposed to radiation as follows: group 1, nonirradiated controls; group 2, three fractionated doses of 17 cGy 1 H every other day ( 1 H × 3); group 3, three fractionated doses of 17 cGy 1 H every other day followed by a single low dose of 15 cGy 56 Fe two days after the final 1 H dose ( 1 H × 3 + 56 Fe); and group 4, a single low dose of 15 cGy 56 Fe followed (after 2 days) by three fractionated doses of 17 cGy 1 H every other day ( 56 Fe + 1 H × 3). A subgroup of mice from each group underwent myocardial infarction (MI) surgery at 28 days postirradiation. Cardiac structure and function were assessed in all animals at days 7, 14 and 28 after MI surgery was performed. Compared to the control animals, the treatments that groups 2 and 3 received did not induce negative effects on cardiac function or structure. However, compared to all other groups, the animals in group 4, showed depressed left ventricular (LV) functions at 1 month with concomitant enhancement in cardiac fibrosis and induction of cardiac hypertrophy signaling at 3 months. In the irradiated and MI surgery groups compared to the control group, the treatments received by groups 2 and 4 did not induce negative effects at 1 month postirradiation and MI surgery. However, in group 3 after MI surgery, there was a 24% increase in mortality, significant decreases in LV function and a 35% increase in post-infarction size. These changes were associated with significant decreases in the angiogenic and cell survival signaling pathways. These data suggest that fractionated doses of radiation induces cellular and molecular changes that result in depressed heart functions both under basal conditions and particularly after myocardial infarction.

Sequential evaluation of coronary flow patterns after primary angioplasty in acute anterior ST-elevation myocardial infarction predicts recovery of left ventricular systolic function.

PubMed

Sharif, Dawod; Sharif-Rasslan, Amal; Makhoul, Nabeel; Shefer, Arie; Hassan, Amin; Rosenschein, Uri

2014-05-01

Function of the microcirculation after primary percutaneous coronary intervention (PCI) is dynamic and contributes to unpredictability of recovery of left ventricular (LV) systolic function. This study was conducted to evaluate sequential Doppler velocity parameters of the left anterior descending coronary artery (LAD) in predicting recovery of global and regional LV systolic function. Thirty-five consecutive patients, 24 males, age 59 ± 12 years, with acute anterior ST-elevation myocardial infarction (STEMI) who had primary PCI were studied. Thrombolysis in myocardial infarction (TIMI) and myocardial blush grades were evaluated. Transthoracic echocardiographic (TTE) studies, evaluation of left ventricular ejection fraction (LVEF), LAD territory wall-motion score index (WMSI), and sampling of LAD Doppler velocities up to 6 hours post-PCI, 48 hours postprocedure, and predischarge were performed. Thrombolysis in myocardial infarction grade before PCI averaged 0.86 ± 1.19 and post-PCI 2.89 ± 0.32, P < 0.05. Myocardial blush grade before PCI was 0.41 ± 0.98 and after PCI 2.22 ± 0.93, P < 0.05. Diastolic velocity deceleration time (DDT) in the LAD early after PCI was less than 600 ms in 16 subjects. Immediately after PCI, in subjects with DDT > 600 ms, LVEF was 38.5 ± 6% and predischarge 49.2 ± 8.7%, P = 9.77 × 10−5 and LAD-WMSI decreased from 2 ± 0.38 to 1.4 ± 0.48, P = 0.000163. In subjects with DDT < 600 ms LAD-WMSI did not change significantly. Early and minimal LAD-DDT correlated with improvement in LV systolic function, r = 0.6, whereas post-PCI blush grade had lower correlation with LVEF, r = 0.39. Global and regional LV systolic function after PCI in acute anterior MI can be predicted by LAD-DDT better than by post-PCI myocardial blush.

Novel cardiovascular magnetic resonance oxygenation approaches in understanding pathophysiology of cardiac diseases.

PubMed

Sree Raman, Karthigesh; Nucifora, Gaetano; Selvanayagam, Joseph B

2018-05-01

Cardiovascular magnetic resonance imaging (CMR) permits accurate phenotyping of many cardiac diseases. CMR's inherent advantages are its non-invasive nature, lack of ionizing radiation and high accuracy and reproducibility. Furthermore, it is able to assess many aspects of cardiac anatomy, structure and function. Specifically, it can characterize myocardial tissue, myocardial function, myocardial mass, myocardial blood flow/perfusion, irreversible and reversible injury, all with a high degree of accuracy and reproducibility. Hence, CMR is a powerful tool in clinical and pre-clinical research. In recent years there have been novel advances in CMR myocardial tissue characterization. Oxygenation-sensitive CMR (OS-CMR) is a novel non-invasive, contrast independent technique that permits direct quantification of myocardial tissue oxygenation, both at rest and during stress. In this review, we will address the principles of the OS-CMR technique, its recent advances and summarize the studies in the effects of oxygenation on cardiac diseases. © 2018 John Wiley & Sons Australia, Ltd.

Spontaneous coronary artery dissection as a cause of myocardial infarction

PubMed Central

Aksakal, Aytekin; Arslan, Uğur; Yaman, Mehmet; Urumdaş, Mehmet; Ateş, Ahmet Hakan

2014-01-01

Spontaneous coronary artery dissection (SCAD) is a rare disease that is usually seen in young women in left descending coronary artery and result in events like sudden cardiac death and acute myocardial infarction. A 70-year-old man was admitted to the emergency department with chest pain which started 1 h ago during a relative’s funeral. The initial electrocardiography demonstrated 2 mm ST-segment depression in leads V1-V3 and the patient underwent emergent coronary angiography. SCAD simultaneously in two different coronary arteries [left anterior descending (LAD) artery and left circumflex (LCx)] artery was detected and SCAD in LCx artery was causing total occlusion which resulted in acute myocardial infarction. Successful stenting was performed thereafter for both lesions. In addition to the existence of SCAD simultaneously in two different coronary arteries, the presence of muscular bridge and SCAD together at the same site of the LAD artery was another interesting point which made us report this case. PMID:25548620

Hydrogen peroxide changes in ischemic and reperfused heart. Cytochemistry and biochemical and X-ray microanalysis.

PubMed Central

Slezak, J.; Tribulova, N.; Pristacova, J.; Uhrik, B.; Thomas, T.; Khaper, N.; Kaul, N.; Singal, P. K.

1995-01-01

Active oxygen species including hydrogen peroxide (H2O2) play a major role in ischemia-reperfusion injury. In the present study, changes in myocardial H2O2 content as well as its subcellular distribution were examined in rat hearts subjected to ischemia-reperfusion. Isolated perfused rat hearts were made globally ischemic for 20 or 30 minutes and were reperfused for different durations. H2O2 content in these hearts was studied biochemically and changes were correlated with the recovery of function. These hearts were also analyzed for subcellular distribution of H2O2. Optimal conditions of tissue processing as well as incubation medium were established for reacting cerium chloride with H2O2 to form cerium perhydroxide, an insoluble electron-dense product. The chemical composition of these deposits was confirmed by x-ray micro-analysis. Global ischemia caused complete contractile failure in minutes and after 30 minutes of ischemia, these was a > 250% increase in the myocardial H2O2 content. Depressed contractile function recovery in the early phase of reperfusion was accompanied by approximately a 600% increase in the myocardial H2O2 content. Brief pre-fixation with low concentrations of glutaraldehyde, inhibition of alkaline phosphatase, glutathione peroxidase, and catalase, post-fixation but no post-osmication, and no counterstaining yielded the best cytochemical definition of H2O2. In normal hearts, extremely small amounts of cerium hydroperoxide precipitates were located on the endothelial cells. X-ray microanalysis confirmed the presence of cerium in the reaction product. Ischemia resulted in a stronger reaction, particularly on the sarcolemma as well as abluminal side of the endothelial cells; and upon reperfusion, cerium precipitate reaction at these sites was more intense. In the reperfused hearts, the reaction product also appeared within mitochondria between the cristae as well as on the myofibrils, but Z-lines were devoid of any precipitate. The data support a significant increase in myocardial H2O2 during both the phase of ischemia and the first few minutes of reperfusion. A stronger reaction on the sarcolemma and abluminal side of endothelial cells may also indicate enhanced H2O2 accumulation as well as vulnerability of these sites to oxidative stress injury. Images Figure 1 Figure 2 Figure 4 Figure 5 Figure 6 Figure 7 Figure 8 Figure 9 Figure 10 PMID:7677188

Tissue Engineering Strategies for Myocardial Regeneration: Acellular Versus Cellular Scaffolds?

PubMed

Domenech, Maribella; Polo-Corrales, Lilliana; Ramirez-Vick, Jaime E; Freytes, Donald O

2016-12-01

Heart disease remains one of the leading causes of death in industrialized nations with myocardial infarction (MI) contributing to at least one fifth of the reported deaths. The hypoxic environment eventually leads to cellular death and scar tissue formation. The scar tissue that forms is not mechanically functional and often leads to myocardial remodeling and eventual heart failure. Tissue engineering and regenerative medicine principles provide an alternative approach to restoring myocardial function by designing constructs that will restore the mechanical function of the heart. In this review, we will describe the cellular events that take place after an MI and describe current treatments. We will also describe how biomaterials, alone or in combination with a cellular component, have been used to engineer suitable myocardium replacement constructs and how new advanced culture systems will be required to achieve clinical success.

Both selenium deficiency and modest selenium supplementation lead to myocardial fibrosis in mice via effects on redox-methylation balance.

PubMed

Metes-Kosik, Nicole; Luptak, Ivan; Dibello, Patricia M; Handy, Diane E; Tang, Shiow-Shih; Zhi, Hui; Qin, Fuzhong; Jacobsen, Donald W; Loscalzo, Joseph; Joseph, Jacob

2012-12-01

Selenium has complex effects in vivo on multiple homeostatic mechanisms such as redox balance, methylation balance, and epigenesis, via its interaction with the methionine-homocysteine cycle. In this study, we examined the hypothesis that selenium status would modulate both redox and methylation balance and thereby modulate myocardial structure and function. We examined the effects of selenium-deficient (<0.025 mg/kg), control (0.15 mg/kg), and selenium-supplemented (0.5 mg/kg) diets on myocardial histology, biochemistry and function in adult C57/BL6 mice. Selenium deficiency led to reactive myocardial fibrosis and systolic dysfunction accompanied by increased myocardial oxidant stress. Selenium supplementation significantly reduced methylation potential, DNA methyltransferase activity and DNA methylation. In mice fed the supplemented diet, inspite of lower oxidant stress, myocardial matrix gene expression was significantly altered resulting in reactive myocardial fibrosis and diastolic dysfunction in the absence of myocardial hypertrophy. Our results indicate that both selenium deficiency and modest selenium supplementation leads to a similar phenotype of abnormal myocardial matrix remodeling and dysfunction in the normal heart. The crucial role selenium plays in maintaining the balance between redox and methylation pathways needs to be taken into account while optimizing selenium status for prevention and treatment of heart failure. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Tissue Inhibitor of Matrix Metalloproteinase-1 Promotes Myocardial Fibrosis by Mediating CD63-Integrin β1 Interaction.

PubMed

Takawale, Abhijit; Zhang, Pu; Patel, Vaibhav B; Wang, Xiuhua; Oudit, Gavin; Kassiri, Zamaneh

2017-06-01

Myocardial fibrosis is excess accumulation of the extracellular matrix fibrillar collagens. Fibrosis is a key feature of various cardiomyopathies and compromises cardiac systolic and diastolic performance. TIMP1 (tissue inhibitor of metalloproteinase-1) is consistently upregulated in myocardial fibrosis and is used as a marker of fibrosis. However, it remains to be determined whether TIMP1 promotes tissue fibrosis by inhibiting extracellular matrix degradation by matrix metalloproteinases or via an matrix metalloproteinase-independent pathway. We examined the function of TIMP1 in myocardial fibrosis using Timp1 -deficient mice and 2 in vivo models of myocardial fibrosis (angiotensin II infusion and cardiac pressure overload), in vitro analysis of adult cardiac fibroblasts, and fibrotic myocardium from patients with dilated cardiomyopathy (DCM). Timp1 deficiency significantly reduced myocardial fibrosis in both in vivo models of cardiomyopathy. We identified a novel mechanism for TIMP1 action whereby, independent from its matrix metalloproteinase-inhibitory function, it mediates an association between CD63 (cell surface receptor for TIMP1) and integrin β1 on cardiac fibroblasts, initiates activation and nuclear translocation of Smad2/3 and β-catenin, leading to de novo collagen synthesis. This mechanism was consistently observed in vivo, in cultured cardiac fibroblasts, and in human fibrotic myocardium. In addition, after long-term pressure overload, Timp1 deficiency persistently reduced myocardial fibrosis and ameliorated diastolic dysfunction. This study defines a novel matrix metalloproteinase-independent function of TIMP1 in promoting myocardial fibrosis. As such targeting TIMP1 could prove to be a valuable approach in developing antifibrosis therapies. © 2017 American Heart Association, Inc.

DOE Office of Scientific and Technical Information (OSTI.GOV)

Hartmann, A.; Frenkel, J.; Hopf, R.

Amyloidosis is a systemic disease frequently involving the myocardium and leading to functional disturbances of the heart. Amyloidosis can mimic other cardiac diseases. A conclusive clinical diagnosis of cardiac involvement can only be made by a combination of different diagnostic methods. In 7 patients with myocardial amyloidosis we used a combined first-pass and static scintigraphy with technetium-99 m-pyrophosphate. There was only insignificant myocardial uptake of the tracer. The first-pass studies however revealed reduced systolic function in 4/7 patients and impaired diastolic function in 6/7 patients. Therefore, although cardiac amyloid could not be demonstrated in the static scintigraphy due to amyloidmore » fibril amount and composition, myocardial functional abnormalities were seen in the first-pass study.« less

Transmyocardial drilling revascularization combined with heparinized bFGF-incorporating stent activates resident cardiac stem cells via SDF-1/CXCR4 axis

DOE Office of Scientific and Technical Information (OSTI.GOV)

Zhang, Guang-Wei; Wen, Ti; Gu, Tian-Xiang, E-mail: cmugtx@sina.com

Objective: To investigate whether transmyocardial drilling revascularization combined with heparinized basic fibroblast growth factor (bFGF)-incorporating degradable stent implantation (TMDRSI) can promote myocardial regeneration after acute myocardial infarction (AMI). Methods: A model of AMI was generated by ligating the mid-third of left anterior descending artery (LAD) of miniswine. After 6 h, the animals were divided into none-treatment (control) group (n = 6) and TMDRSI group (n = 6). For TMDRSI group, two channels with 3.5 mm in diameter were established by a self-made drill in the AMI region, into which a stent was implanted. Expression of stromal cell-derived factor-1{sub {alpha}} (SDF-1{submore » {alpha}}) and CXC chemokine receptor 4 (CXCR4), cardiac stem cell (CSC)-mediated myocardial regeneration, myocardial apoptosis, myocardial viability, and cardiac function were assessed at various time-points. Results: Six weeks after the operation, CSCs were found to have differentiated into cardiomyocytes to repair the infarcted myocardium, and all above indices showed much improvement in the TMDRSI group compared with the control group (P < 0.001). Conclusions: The new method has shown to be capable of promoting CSCs proliferation and differentiation into cardiomyocytes through activating the SDF-1/CXCR4 axis, while inhibiting myocardial apoptosis, thereby enhancing myocardial regeneration following AMI and improving cardiac function. This may provide a new strategy for myocardial regeneration following AMI. -- Highlights: Black-Right-Pointing-Pointer The effects of TMDR and bFGF-stent on myocardial regeneration were studied in a pig model of AMI. Black-Right-Pointing-Pointer TMDR and bFGF-stent implantation activated CSCs via the SDF-1/CXCR4 axis. Black-Right-Pointing-Pointer CSC-mediated myocardial regeneration improved cardiac function. Black-Right-Pointing-Pointer It may be a new therapeutic strategy for AMI.« less

Scaling of Myocardial Mass to Flow and Morphometry of Coronary Arteries

PubMed Central

Choy, Jenny Susana; Kassab, Ghassan S.

2009-01-01

There is no doubt that scaling relations exist between myocardial mass and morphometry of coronary vasculature. The purpose of this study is to quantify several morphological (diameter, length, and volume) and functional (flow) parameters of the coronary arterial tree in relation to myocardial mass. Eight normal porcine hearts of 117-244 g (mean of 177.5±32.7) were used in this study. Various coronary sub-trees of the Left Anterior Descending (LAD), Right Coronary (RCA) and Left Circumflex (LCX) arteries were perfused at pressure of 100 mmHg with different colors of a polymer (Microfil) in order to obtain rubber casts of arterial trees corresponding to different regions of myocardial mass. Volume, diameter and cumulative length of coronary arteries were reconstructed from casts to analyze their relationship to the perfused myocardial mass. Volumetric flow was measured in relationship with perfused myocardial mass. Our results show that arterial volume is linearly related to regional myocardial mass, whereas the sum of coronary arterial branch lengths, vessel diameters and volumetric flow show an approximately 3/4, 3/8 and 3/4 power-law relationship, respectively, in relation to myocardial mass. These scaling laws suggest fundamental design principles underlying the structure-function relationship of the coronary arterial tree that may facilitate diagnosis and management of diffuse coronary artery disease. PMID:18323461

Scaling of myocardial mass to flow and morphometry of coronary arteries.

PubMed

Choy, Jenny Susana; Kassab, Ghassan S

2008-05-01

There is no doubt that scaling relations exist between myocardial mass and morphometry of coronary vasculature. The purpose of this study is to quantify several morphological (diameter, length, and volume) and functional (flow) parameters of the coronary arterial tree in relation to myocardial mass. Eight normal porcine hearts of 117-244 g (mean of 177.5 +/- 32.7) were used in this study. Various coronary subtrees of the left anterior descending, right coronary, and left circumflex arteries were perfused at pressure of 100 mmHg with different colors of a polymer (Microfil) to obtain rubber casts of arterial trees corresponding to different regions of myocardial mass. Volume, diameter, and cumulative length of coronary arteries were reconstructed from casts to analyze their relationship to the perfused myocardial mass. Volumetric flow was measured in relationship with perfused myocardial mass. Our results show that arterial volume is linearly related to regional myocardial mass, whereas the sum of coronary arterial branch lengths, vessel diameters, and volumetric flow show an approximately 3/4, 3/8, and 3/4 power-law relationship, respectively, in relation to myocardial mass. These scaling laws suggest fundamental design principles underlying the structure-function relationship of the coronary arterial tree that may facilitate diagnosis and management of diffuse coronary artery disease.

Cardioprotective Properties of Aerobic and Resistance Training Against Myocardial Infarction.

PubMed

Barboza, C A; Souza, G I H; Oliveira, J C M F; Silva, L M; Mostarda, C T; Dourado, P M M; Oyama, L M; Lira, F S; Irigoyen, M C; Rodrigues, B

2016-06-01

We evaluated the effects of aerobic and resistance exercise training on ventricular morphometry and function, physical capacity, autonomic function, as well as on ventricular inflammatory status in trained rats prior to myocardial infarction. Male Wistar rats were divided into the following groups: sedentary+Sham, sedentary+myocardial infarction, aerobic trained+myocardial infarction, and resistance trained+myocardial infarction. Sham and myocardial infarction were performed after training periods. In the days following the surgeries, evaluations were performed. Aerobic training prevents aerobic (to a greater extent) and resistance capacity impairments, ventricular dysfunction, baroreflex sensitivity and autonomic disorders (vagal tonus decrease and sympathetic tonus increase) triggered by myocardial infarction. Resistance training was able to prevent negative changes to aerobic and resistance capacity (to a greater extent) but not to ventricular dysfunction, and it prevented cardiovascular sympathetic increments. Additionally, both types of training reduced left ventricle inflammatory cytokine concentration. Our results suggest that aerobic and, for the first time, dynamic resistance training were able to reduce sympathetic tonus to the heart and vessels, as well as preventing the increase in pro-inflammatory cytokine concentrations in the left ventricle of trained groups. These data emphasizes the positive effects of aerobic and dynamic resistance training on the prevention of the negative changes triggered by myocardial infarction. © Georg Thieme Verlag KG Stuttgart · New York.

Postinfarct intramyocardial injection of mesenchymal stem cells pretreated with TGF-α improves acute myocardial function

PubMed Central

Herrmann, Jeremy L.; Abarbanell, Aaron M.; Weil, Brent R.; Wang, Yue; Poynter, Jeffrey A.; Manukyan, Mariuxi C.

2010-01-01

Stem cell-based therapies offer promising potential for myocardial infarction (MI), but endogenous molecules released in response to injury likely impair posttransplantation stem cell function. Stem cell-mediated cardioprotection occurs in part via paracrine effects, and transforming growth factor-α (TGF-α) has been shown to enhance paracrine function. However, it is unknown whether pretreating stem cells with TGF-α increases stem cell-mediated cardioprotection after acute MI. Mesenchymal stem cells (MSCs) were treated with TGF-α (250 ng/ml) for 24 h. Adult male Sprague-Dawley rat hearts were isolated and perfused using the Langendorff method. MI was induced by ligating the left anterior descending coronary artery. Postligation (30 min), vehicle or 1 × 106 MSCs with or without pretreatment were injected in the infarct border zones, and the hearts were perfused for an additional 60 min. Left ventricular function was continuously measured, and infarct size was assessed with Evans blue dye and 2,3,5-triphenyltetrazolium chloride staining. Myocardial production of interleukin (IL)-1β and IL-6 and caspase 3 activation was also measured. Left ventricular function decreased significantly following coronary artery ligation but improved following injection of untreated MSCs and to a greater extent after injection of pretreated MSCs. In addition, the infarct area, myocardial caspase 3 activation, and IL-6 production were lowest in hearts injected with pretreated cells. Intramyocardial injection of TGF-α-pretreated MSCs after acute MI is associated with increased myocardial function and decreased myocardial injury. This strategy may be useful for optimizing the therapeutic efficacy of stem cells for the treatment of acute MI. PMID:20484699

Myocardial contusion in patients with blunt chest trauma as evaluated by thallium 201 myocardial scintigraphy

DOE Office of Scientific and Technical Information (OSTI.GOV)

Bodin, L.; Rouby, J.J.; Viars, P.

1988-07-01

Fifty five patients suffering from blunt chest trauma were studied to assess the diagnosis of myocardial contusion using thallium 201 myocardial scintigraphy. Thirty-eight patients had consistent scintigraphic defects and were considered to have a myocardial contusion. All patients with scintigraphic defects had paroxysmal arrhythmias and/or ECG abnormalities. Of 38 patients, 32 had localized ST-T segment abnormalities; 29, ST-T segment abnormalities suggesting involvement of the same cardiac area as scintigraphic defects; 21, echocardiographic abnormalities. Sixteen patients had segmental hypokinesia involving the same cardiac area as the scintigraphic defects. Fifteen patients had clinical signs suggestive of myocardial contusion and scintigraphic defects. Almostmore » 70 percent of patients with blunt chest trauma had scintigraphic defects related to areas of myocardial contusion. When thallium 201 myocardial scintigraphy directly showed myocardial lesion, two-dimensional echocardiography and standard ECG detected related functional consequences of cardiac trauma.« less

[Effects of Chinese herbal compound for supplementing qi and activating blood circulation on actin, Cx43 expressions and gap junctional intercellular communication functions of myocardial cells in patients with Coxsackie virus B 3 viral myocarditis].

PubMed

Zhang, Ming-xue; He, Wei; Gu, Ping

2010-08-01

To observe the effect of Chinese herbal compound for supplementing qi and activating blood circulation (CHC) on the gap junctional intercellular communication (GJIC) function of myocardial cells in patients with Coxsackie virus B 3 (CVB3) viral myocarditis. Expressions of actin and connexin43 (Cx43) in myocardial cells of patients arranged in three groups (the normal control group, the viral infected group and the CHC treated group) were detected by immunohistochemical method; the fluorescence photobleaching recovery rate of cells was detected by laser scanning confocal microscope. As compared with the viral infected group, the expressions of actin and Cx43 were increased and the GJIC function was improved in the CHC treated group. CHC could antagonize viral injury on skeleton protein, and repair the structure of gap junction channel to improve the GJIC function of myocardial cells after being attacked by CVB3.

Stress, depression, and cardiovascular dysregulation: A review of neurobiological mechanisms and the integration of research from preclinical disease models

PubMed Central

Grippo, Angela J.; Johnson, Alan Kim

2008-01-01

A bidirectional association between mood disorders such as depression, and cardiovascular diseases such as myocardial infarction and congestive heart failure, has been described; however, the precise neurobiological mechanisms that underlie these associations have not been fully elucidated. This review is focused on the neurobiological processes and mediators that are common to both mood and cardiovascular disorders, with an emphasis on the role of exogenous stressors in addition to: (a) neuroendocrine and neurohumoral changes involving dysfunction of the hypothalamic-pituitary-adrenal axis and activation of the renin-angiotensin-aldosterone system, (b) immune alterations including activation of pro-inflammatory cytokines, (c) autonomic and cardiovascular dysregulation including increased sympathetic drive, withdrawal of parasympathetic tone, cardiac rate and rhythm disturbances, and altered baroreceptor reflex function, (d) central neurotransmitter system dysfunction including dopamine, norepinephrine and serotonin, and (e) behavioral changes including fatigue and physical inactivity. We also focus specifically on experimental investigations with preclinical disease models, conducted to elucidate the neurobiological mechanisms underlying the link between mood disorders and cardiovascular disease. These include: (a) the chronic mild stress model of depression, (b) a model of congestive heart failure, a model of cardiovascular deconditioning, (d) pharmacological manipulations of body fluid and sodium balance, and (e) pharmacological manipulations of the central serotonergic system. In combination with the extensive literature describing findings from human research, the investigation of mechanisms underlying mood and cardiovascular regulation using animal models will enhance our understanding of the association of depression and cardiovascular disease, and can promote the development of better treatments and interventions for individuals with these co-morbid conditions. PMID:19116888

The effects of compound danshen dripping pills and human umbilical cord blood mononuclear cell transplant after acute myocardial infarction.

PubMed

Jun, Yi; Chunju, Yuan; Qi, Ai; Liuxia, Deng; Guolong, Yu

2014-04-01

The low frequency of survival of stem cells implanted in the myocardium after acute myocardial infarction may be caused by inflammation and oxidative stress in the myocardial microenvironment. We evaluated the effects of a traditional Chinese medicine, Compound Danshen Dripping Pills, on the cardiac microenvironment and cardiac function when used alone or in combination with human umbilical cord blood mononuclear cell transplant after acute myocardial infarction. After surgically induced acute myocardial infarction, rabbits were treated with Compound Danshen Dripping Pills alone or in combination with human umbilical cord blood mononuclear cell transplant. Evaluation included histology, measurement of left ventricular ejection fraction and fractional shortening, leukocyte count, count of green fluorescent protein positive cells, superoxide dismutase activity, and malondialdehyde content. Combination treatment with Compound Danshen Dripping Pills and human umbilical cord blood mononuclear cell transplant significantly increased the survival of implanted cells, inhibited cardiac cell apoptosis, decreased oxidative stress, decreased the inflammatory response, and improved cardiac function. Rabbits treated with either Compound Danshen Dripping Pills or human umbilical cord blood mononuclear cells alone had improvement in these effects compared with untreated control rabbits. Combination therapy with Compound Danshen Dripping Pills and human umbilical cord blood mononuclear cells may improve cardiac function and morphology after acute myocardial infarction.

Major Depression and Coronary Flow Reserve Detected by Positron Emission Tomography

PubMed Central

Vaccarino, Viola; Votaw, John; Faber, Tracy; Veledar, Emir; Murrah, Nancy V.; Jones, Linda R.; Zhao, Jinying; Su, Shaoyong; Goldberg, Jack; Raggi, J. Paolo; Quyyumi, Arshed A.; Sheps, David S.; Bremner, J. Douglas

2010-01-01

Background Major depressive disorder (MDD) is associated with coronary heart disease (CHD), but the mechanisms are unclear. The presence of MDD may increase CHD risk by affecting microvascular circulation. It is also plausible that genetic factors influencing MDD may overlap with those for CHD. We sought to examine the relationship between MDD and coronary flow reserve (CFR), the ratio of maximum flow during stress to flow at rest measured in milliliters per minute per gram of tissue. Methods We examined 289 male middle-aged twins, including 106 twins (53 twin pairs) discordant for a lifetime history of MDD and 183 control twins (unrelated to any twins in the experimental group) without MDD. To calculate CFR, we used positron emission tomography with nitrogen 13 (13N) ammonia to evaluate myocardial blood flow at rest and after adenosine stress. A standard perfusion defect score was also used to assess myocardial ischemia. Results There was no difference in myocardial ischemia between twins with and without MDD. Among the dizygotic twin pairs discordant for MDD, the CFR was 14% lower in the twins with MDD than in their brothers without MDD (2.36 vs 2.74) (P=.03). This association was not present in the monozygotic discordant pairs who were genetically matched (2.86 vs 2.64) (P = .19). The zygosity-MDD interaction after adjustment was significant (P=.006). The CFR in the dizygotic twins with MDD was also lower than in the control twins. Conclusions Our results provide evidence for a shared genetic pathway between MDD and microvascular dysfunction. Common pathophysiologic processes may link MDD and early atherosclerosis. PMID:19822823

Gualou Xiebai Decoction, a Traditional Chinese Medicine, Prevents Cardiac Reperfusion Injury of Hyperlipidemia Rat via Energy Modulation.

PubMed

Yan, Lu-Lu; Zhang, Wei-Yang; Wei, Xiao-Hong; Yan, Li; Pan, Chun-Shui; Yu, Yang; Fan, Jing-Yu; Liu, Yu-Ying; Zhou, Hua; Han, Jing-Yan; Yao, Xin-Sheng

2018-01-01

Background: Gualou Xiebai Decoction (GLXB) is a classic prescription of Chinese medicine used for the treatment of cardiac problems. The present study was designed to explore the effect and mechanism of GLXB on ischemia/reperfusion (I/R) induced disorders in myocardial structure and function, focusing on the regulation of energy metabolism and the RhoA/ROCK pathway. Methods: After hyperlipidemic rat model was established by oral administration of high fat diet, the rats were treated with GLXB for 6 weeks and subjected to 30 min occlusion of the left anterior descending coronary artery (LADCA) followed by 90 min reperfusion to elicit I/R challenge. Myocardial infarct size was assessed by Evans blue-TTC staining. Myocardial blood flow (MBF) and cardiac function were evaluated. Enzyme-linked immunosorbent assay was performed to examine the content of ATP, ADP, AMP, CK, CK-MB, LDH, cTnT, cTnI, and IL-6. Double staining of F-actin and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling was conducted to assess myocardial apoptosis. Expressions of ATP synthase subunit δ (ATP 5D), and RhoA and ROCK were determined by Western blotting. Results: Administration with GLXB at high dose for 6 weeks protected heart against I/R-induced MBF decrease, myocardial infarction and apoptosis, ameliorated I/R-caused impairment of cardiac function and myocardial structure, restored the decrease in the ratio of ADP/ATP and AMP/ATP, and the expression of ATP 5D with inhibiting the expression of RhoA and ROCK. Conclusions: Treatment with GLXB effectively protects myocardial structure and function from I/R challenge, possibly via regulating energy metabolism involving inactivation of RhoA/ROCK signaling pathway.

Cobalt Chloride Upregulates Impaired HIF-1α Expression to Restore Sevoflurane Post-conditioning-Dependent Myocardial Protection in Diabetic Rats.

PubMed

Wu, Jianjiang; Yang, Long; Xie, Peng; Yu, Jin; Yu, Tian; Wang, Haiying; Maimaitili, Yiliyaer; Wang, Jiang; Ma, Haiping; Yang, Yining; Zheng, Hong

2017-01-01

Previous studies from our group have demonstrated that sevoflurane post-conditioning (SPC) protects against myocardial ischemia reperfusion injury via elevating the intranuclear expression of hypoxia inducible factor-1 alpha (HIF-1α). However, diabetic SPC is associated with decreased myocardial protection and disruption of the HIF-1 signaling pathway. Previous studies have demonstrated that cobalt chloride (CoCl 2 ) can upregulate HIF-1α expression under diabetic conditions, but whether myocardial protection by SPC can be restored afterward remains unclear. We established a rat model of type 2 diabetes and a Langendorff isolated heart model of ischemia-reperfusion injury. Prior to reperfusion, 2.4% sevoflurane was used as a post-conditioning treatment. The diabetic rats were treated with CoCl 2 24 h before the experiment. At the end of reperfusion, tests were performed to assess myocardial function, infarct size, mitochondrial morphology, nitric oxide (NO), Mitochondrial reactive oxygen species (ROS), mitochondrial respiratory function and enzyme activity, HIF-1α, vascular endothelial growth factor (VEGF) and endothelial NO synthase (eNOS) protein levels. In addition, myocardial protection by SPC was monitored after the blood glucose levels were lowered by insulin. The diabetic state was associated with deficient SPC protection and decreased HIF-1α expression. After treating the diabetic rats with CoCl 2 , SPC significantly upregulated the expression of HIF-1α, VEGF and eNOS, which markedly improved cardiac function, NO, mitochondrial respiratory function, and enzyme activity and decreased the infarction areas and ROS. In addition, these effects were not influenced by blood glucose levels. This study proved that CoCl 2 activates the HIF-1α signaling pathway, which restores SPC-dependent myocardial protection under diabetic conditions, and the protective effects of SPC were independent of blood glucose levels.

[The relationship between depression, anxiety and heart disease - a psychosomatic challenge].

PubMed

Kapfhammer, Hans-Peter

2011-12-01

Depressive and cardiological disorders present a major comorbidity. Their manifold interrelations may be best analysed within a biopsychosocial model of disease. A systematic research was done on empirical studies published during the last 15 years and dealing with epidemiological, etiopathogenetic and therapeutic dimensions of the comorbidity of depression, anxiety and heart disease. From an epidemiological perspective recurrent depressions are associated with a significantly increased risk of coronary heart disease. Depressive disorders play a major role in triggering critical cardiac events, e.g. myocardial infarction. The prevalence rates of depressive disorders in various cardiological conditions are significantly higher than the frequencies that can be expected in healthy general population. Depression shows a negative impact on the somatic morbidity and mortality during the further course of illness. Anxiety and posttraumatic stress disorders seem to be interrelated with cardiological conditions in quite a similar way, probably contributing even more negatively to critical and lethal cardiological events than depression. From an etiopathogenetic perspective some clusters of depressive symptoms seem to be linked to cardiotoxicity more closely than other, vital exhaustion, anhedonia, and hopelessness probably mediating a special risk. In any case, postmyocardial infarct depression that proves treatment-resistent indicates a negative prognosis of the prevailing cardiological condition. On a level of psychological and psychosocial constructs type-A personality, anger/hostility, type-D personality, and alexithymia have been explored regarding its proper pathogenetic role. Psychological and psychopathological variables have to be set into a context of psychosocial stressors on the one hand, and have to be simultaneously analysed with various underlying psycho- and neurobiological variables on the other. Above all, HPA- and sympathicomedullary dysfunctions, reduced heart rate variability, altered functions of thrombocytes, and increased proinflammatory processes have to be recognized as significantly contributing to the pathophysiology both of depression and of heart condition. Neurobiological aspects of anxiety and posttraumatic stress disorders must be interlinked with these underpinnings of depression. Differential effects on critical cardiological events must be supposed. From a therapeutic perspective several RCTs demonstrate that SSRIs may safely and efficiently treat depressive disorders in cardiological conditions, and may even improve the general somatic prognosis. Cognitive-behavioural psychotherapies have been empirically validated in treating depression and anxiety with cardiological patients. So far, however, a differential indication of psychopharmacological versus psychotherapeutic approaches has not been proved yet. Depression and anxiety disorders in patients with heart disease paradigmatically define a psychosomatic-somatopsychic challenge to any health delivery system. A psychosomatic perspective may best be practised within a Consultation-Liaison psychiatric service that cooperates continuously and closely with cardiological departments and experts.

VALSARTAN REGULATES MYOCARDIAL AUTOPHAGY AND MITOCHONDRIAL TURNOVER IN EXPERIMENTAL HYPERTENSION

PubMed Central

Zhang, Xin; Li, Zi-Lun; Crane, John A.; Jordan, Kyra L.; Pawar, Aditya S.; Textor, Stephen C.; Lerman, Amir; Lerman, Lilach O.

2014-01-01

Renovascular hypertension alters cardiac structure and function. Autophagy is activated during left ventricular hypertrophy and linked to adverse cardiac function. The Angiotensin II receptor blocker Valsartan lowers blood pressure and is cardioprotective, but whether it modulates autophagy in the myocardium is unclear. We hypothesized that Valsartan would alleviate autophagy and improve left ventricular myocardial mitochondrial turnover in swine renovascular hypertension. Domestic pigs were randomized to control, unilateral renovascular hypertension, and renovascular hypertension treated with Valsartan (320 mg/day) or conventional triple therapy (Reserpine+hydralazine+hydrochlorothiazide) for 4 weeks post 6-weeks of renovascular hypertension (n=7 each group). Left ventricular remodeling, function and myocardial oxygenation and microcirculation were assessed by multi-detector computer tomography, blood-oxygen-level-dependent magnetic resonance imaging and microcomputer tomography. Myocardial autophagy, markers for mitochondrial degradation and biogenesis, and mitochondrial respiratory-chain proteins were examined ex vivo. Renovascular hypertension induced left ventricular hypertrophy and myocardial hypoxia, enhanced cellular autophagy and mitochondrial degradation, and suppressed mitochondrial biogenesis. Valsartan and triple therapy similarly decreased blood pressure, but Valsartan solely alleviated left ventricular hypertrophy, ameliorated myocardial autophagy and mitophagy, and increased mitochondrial biogenesis. In contrast, triple therapy only slightly attenuated autophagy and preserved mitochondrial proteins, but elicited no improvement in mitophagy. These data suggest a novel potential role of Valsartan in modulating myocardial autophagy and mitochondrial turnover in renovascular hypertension-induced hypertensive heart disease, which may possibly bolster cardiac repair via a blood pressure-independent manner. PMID:24752430

Myocardial aging as a T-cell–mediated phenomenon

PubMed Central

Ramos, Gustavo Campos; van den Berg, Anne; Nunes-Silva, Vânia; Weirather, Johannes; Peters, Laura; Burkard, Matthias; Friedrich, Mike; Pinnecker, Jürgen; Abeßer, Marco; Heinze, Katrin G.; Schuh, Kai; Beyersdorf, Niklas; Kerkau, Thomas; Demengeot, Jocelyne; Frantz, Stefan; Hofmann, Ulrich

2017-01-01

In recent years, the myocardium has been rediscovered under the lenses of immunology, and lymphocytes have been implicated in the pathogenesis of cardiomyopathies with different etiologies. Aging is an important risk factor for heart diseases, and it also has impact on the immune system. Thus, we sought to determine whether immunological activity would influence myocardial structure and function in elderly mice. Morphological, functional, and molecular analyses revealed that the age-related myocardial impairment occurs in parallel with shifts in the composition of tissue-resident leukocytes and with an accumulation of activated CD4+ Foxp3− (forkhead box P3) IFN-γ+ T cells in the heart-draining lymph nodes. A comprehensive characterization of different aged immune-deficient mouse strains revealed that T cells significantly contribute to age-related myocardial inflammation and functional decline. Upon adoptive cell transfer, the T cells isolated from the mediastinal lymph node (med-LN) of aged animals exhibited increased cardiotropism, compared with cells purified from young donors or from other irrelevant sites. Nevertheless, these cells caused rather mild effects on cardiac functionality, indicating that myocardial aging might stem from a combination of intrinsic and extrinsic (immunological) factors. Taken together, the data herein presented indicate that heart-directed immune responses may spontaneously arise in the elderly, even in the absence of a clear tissue damage or concomitant infection. These observations might shed new light on the emerging role of T cells in myocardial diseases, which primarily affect the elderly population. PMID:28255084

Calpain inhibition preserves myocardial structure and function following myocardial infarction.

PubMed

Mani, Santhosh K; Balasubramanian, Sundaravadivel; Zavadzkas, Juozas A; Jeffords, Laura B; Rivers, William T; Zile, Michael R; Mukherjee, Rupak; Spinale, Francis G; Kuppuswamy, Dhandapani

2009-11-01

Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca(2+)-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated (n = 6) and untreated (n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 + or - 2% pre-MI to 30 + or - 4% with MI only vs. 41 + or - 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 + or - 2 microl pre-MI to 73 + or - 4 microl with MI only vs. 55 + or - 4 microl with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain- and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients.

Stabilization of mitochondrial membrane potential prevents doxorubicin-induced cardiotoxicity in isolated rat heart

DOE Office of Scientific and Technical Information (OSTI.GOV)

Montaigne, David; Marechal, Xavier; Baccouch, Riadh

2010-05-01

The present study was undertaken to examine the effects of doxorubicin on left ventricular function and cellular energy state in intact isolated hearts, and, to test whether inhibition of mitochondrial membrane potential dissipation would prevent doxorubicin-induced mitochondrial and myocardial dysfunction. Myocardial contractile performance and mitochondrial respiration were evaluated by left ventricular tension and its first derivatives and cardiac fiber respirometry, respectively. NADH levels, mitochondrial membrane potential and glucose uptake were monitored non-invasively via epicardial imaging of the left ventricular wall of Langendorff-perfused rat hearts. Heart performance was reduced in a time-dependent manner in isolated rat hearts perfused with Krebs-Henseleit solutionmore » containing 1 muM doxorubicin. Compared with controls, doxorubicin induced acute myocardial dysfunction (dF/dt{sub max} of 105 +- 8 mN/s in control hearts vs. 49 +- 7 mN/s in doxorubicin-treated hearts; *p < 0.05). In cardiac fibers prepared from perfused hearts, doxorubicin induced depression of mitochondrial respiration (respiratory control ratio of 4.0 +- 0.2 in control hearts vs. 2.2 +- 0.2 in doxorubicin-treated hearts; *p < 0.05) and cytochrome c oxidase kinetic activity (24 +- 1 muM cytochrome c/min/mg in control hearts vs. 14 +- 3 muM cytochrome c/min/mg in doxorubicin-treated hearts; *p < 0.05). Acute cardiotoxicity induced by doxorubicin was accompanied by NADH redox state, mitochondrial membrane potential, and glucose uptake reduction. Inhibition of mitochondrial permeability transition pore opening by cyclosporine A largely prevented mitochondrial membrane potential dissipation, cardiac energy state and dysfunction. These results suggest that in intact hearts an impairment of mitochondrial metabolism is involved in the development of doxorubicin cardiotoxicity.« less

Myocardial oedema in acute myocarditis detected by echocardiographic 2D myocardial deformation analysis.

PubMed

Løgstrup, B B; Nielsen, J M; Kim, W Y; Poulsen, S H

2016-09-01

The clinical diagnosis of acute myocarditis is based on symptoms, electrocardiography, elevated myocardial necrosis biomarkers, and echocardiography. Often, conventional echocardiography reveals no obvious changes in global cardiac function and therefore has limited diagnostic value. Myocardial deformation imaging by echocardiography is an evolving method used to characterize quantitatively longitudinal systolic function, which may be affected in acute myocarditis. The aim of our study was to assess the utility of echocardiographic deformation imaging of the left ventricle in patients with diagnosed acute myocarditis in whom cardiovascular magnetic resonance (CMR) evaluation was performed. We included 28 consecutive patients (mean age 32 ± 13 years) with CMR-verified diagnosis of acute myocarditis according to the Lake Louise criteria. Cardiac function was evaluated by a comprehensive assessment of left ventricular (LV) function, including 2D speckle-tracking echocardiography. We found no significant correlation between the peak values of cardiac enzymes and the amount of myocardial oedema assessed by CMR (troponin: r= 0.3; P = 0.05 and CK-MB: r = 0.1; P = 0.3). We found a larger amount of myocardial oedema in the basal part of the left ventricle [American Heart Association (AHA) segments 1-6] in inferolateral and inferior segments, compared with the anterior, anterolateral, anteroseptal, and inferoseptal segments. In the mid LV segments (AHA segments 7-12), this was more pronounced in the anterior, anterolateral, and inferolateral segments. Among conventional echocardiographic parameters, LV function was not found to correlate with the amount of myocardial oedema of the left ventricle. In contrast, we found the wall motion score index to be significantly correlated with the amount of myocardial oedema, but this correlation was only present in patients with an extensive amount of oedema (>11% of the total left ventricle). Global longitudinal systolic myocardial strain correlated significantly with the amount of oedema (r = 0.65; P < 0.001). We found that both the epicardial longitudinal and the endocardial longitudinal systolic strains were significantly correlated with oedema (r = 0.55; P = 0.003 and r = 0.54; P < 0.001). In patients with acute myocarditis, 2D speckle-tracking echocardiography was a useful tool in the diagnostic process of acute myocarditis. Global longitudinal strain adds important information that can support clinical and conventional echocardiographic evaluation, especially in patients with preserved LV ejection fraction in relation to the diagnosis and degree of myocardial dysfunction. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.

Functional Cardiac Magnetic Resonance Imaging (MRI) in the Assessment of Myocardial Viability and Perfusion

PubMed Central

2003-01-01

Executive Summary Objective The objective of this health technology policy assessment was to determine the effectiveness safety and cost-effectiveness of using functional cardiac magnetic resonance imaging (MRI) for the assessment of myocardial viability and perfusion in patients with coronary artery disease and left ventricular dysfunction. Results Functional MRI has become increasingly investigated as a noninvasive method for assessing myocardial viability and perfusion. Most patients in the published literature have mild to moderate impaired LV function. It is possible that the severity of LV dysfunction may be an important factor that can alter the diagnostic accuracy of imaging techniques. There is some evidence of comparable or better performance of functional cardiac MRI for the assessment of myocardial viability and perfusion compared with other imaging techniques. However limitations to most of the studies included: Functional cardiac MRI studies that assess myocardial viability and perfusion have had small sample sizes. Some studies assessed myocardial viability/perfusion in patients who had already undergone revascularization, or excluded patients with a prior MI (Schwitter et al., 2001). Lack of explicit detail of patient recruitment. Patients with LVEF >35%. Interstudy variability in post MI imaging time(including acute or chronic MI), when patients with a prior MI were included. Poor interobserver agreement (kappa statistic) in the interpretation of the results. Traditionally, 0.80 is considered “good”. Cardiac MRI measurement of myocardial perfusion to as an adjunct tool to help diagnose CAD (prior to a definitive coronary angiography) has also been examined in some studies, with methodological limitations, yielding comparable results. Many studies examining myocardial viability and perfusion report on the accuracy of imaging methods with limited data on long-term patient outcome and management. Kim et al. (2000) revealed that the transmural extent of hyperenhancement was significantly related to the likelihood of improvement in contractility after revascularization. However, the LVEF in the patient population was 43% prior to revascularization. It is important to know whether the technique has the same degree of accuracy in patients who have more severe LV dysfunction and who would most benefit from an assessment of myocardial viability. “Substantial” viability used as a measure of a patient’s ability to recover after revascularization has not been definitively reported (how much viability is enough?). Patients with severe LV dysfunction are more likely to have mixtures of surviving myocardium, including normal, infarcted, stunned and hibernating myocardium (Cowley et al., 1999). This may lead to a lack of homogeneity of response to testing and to revascularization and contribute to inter- and intra-study differences. There is a need for a large prospective study with adequate follow-up time for patients with CAD and LV dysfunction (LVEF<35%) comparing MRI and an alternate imaging technique. There is some evidence that MRI has comparable sensitivity, specificity and accuracy to PET for determining myocardial viability. However, there is a lack of evidence comparing the accuracy of these two techniques to predict LV function recovery. In addition, some studies refer to PET as the gold standard for the assessment of myocardial viability. Therefore, PET may be an ideal noninvasive imaging comparator to MRI for a prospective study with follow-up. To date, there is a lack of cost-effectiveness analyses (or any economic analyses) of functional cardiac MRI versus an alternate noninvasive imaging method for the assessment of myocardial viability/perfusion. Conclusion There is some evidence that the accuracy of functional cardiac MRI compares favourably with alternate imaging techniques for the assessment of myocardial viability and perfusion. There is insufficient evidence whether functional cardiac MRI can better select which patients [who have CAD and severe LV dysfunction (LVEF <35%)] may benefit from revascularization compared with an alternate noninvasive imaging technology. There is insufficient evidence whether functional cardiac MRI can better select which patients should proceed to invasive coronary angiography for the definitive diagnosis of CAD, compared with an alternate noninvasive imaging technology. There is a need for a large prospective (potentially multicentre) study with adequate follow-up time for patients with CAD and LV dysfunction (LVEF<35%) comparing MRI and PET. Since longer follow-up time may be associated with restenosis or graft occlusion, it has been suggested to have serial measurements after revascularization (Cowley et al., 1999). PMID:23074446

Cpg-ODN, a TLR9 Agonist, Aggravates Myocardial Ischemia/Reperfusion Injury by Activation of TLR9-P38 MAPK Signaling.

PubMed

Xie, Liang; He, Songqing; Kong, Na; Zhu, Ying; Tang, Yi; Li, Jianhua; Liu, Zhengbing; Liu, Jing; Gong, Jianbin

2018-06-19

Toll-like receptors (TLRs) have been implicated in myocardial ischemia/ reperfusion (I/R) injury. We examined the effect of CpG-oligodeoxynucleotide (ODN) on myocardial I/R injury. Male Sprague-Dawley rats were treated with either CpG-ODN or control ODN 1 h prior to myocardial ischemia (30 min) followed by reperfusion. Rats treated with phosphate-buffered saline (PBS) served as I/R controls (n = 8/group). Infarct size was determined by 2,3,5-triphenyltetrazolium chloride and Evans blue straining. Cardiac function was examined by echocardiography before and up to 14 days after myocardial I/R. CpG-ODN administration significantly increased infarct size and reduced cardiac function and survival rate after myocardial I/R, compared to the PBS-treated I/R group. Control-ODN did not alter I/R-induced myocardial infarct size, cardiac dysfunction, and survival rate. Additionally, CpG-ODN promoted I/R-induced myocardial apoptosis and cleaved caspase-3 levels in the myocardium. CpG-ODN increased TLR9 activation and p38 phosphorylation in the myocardium. In vitro data also suggested that CpG-ODN treatment induced TLR9 activation and p38 phosphorylation. Importantly, p38 mitogen-activated protein kinase (MAPK) inhibition abolished CpG-ODN-induced cardiac injury. CpG-ODN, the TLR9 ligand, accelerates myocardial I/R injury. The mechanisms involve activation of the TLR9-p38 MAPK signaling pathway. © 2018 The Author(s). Published by S. Karger AG, Basel.

Adenosine triphosphate postconditioning is associated with better preserved global and regional cardiac function during myocardial ischemia and reperfusion: a speckle tracking imaging-based echocardiologic study.

PubMed

Ren, Min; Liu, Yujie; Zhao, Huiya; Dong, Shixia; Jiang, Zhonghui; Li, Keting; Tian, Jiawei

2016-10-01

Effects of ischemic postconditioning (IPostC) and adenosine triphosphate (ATP)-mediated pharmacologic postconditioning (ATP-PPostC) on cardiac function were evaluated by speckle tracking imaging (STI)-based echocardiography. A myocardial I/R model was induced in rabbits by reversible ligation of the left ventricular branch of coronary artery. Rabbits were randomized into three groups: ischemia and reperfusion (IR) (no further intervention), IPostC, and ATP-PPostC groups. Cardiac function was evaluated by conventional and STI-based echocardiography. Myocardial necrosis, apoptosis, and myocardial mRNAs of apoptosis-related proteins (Bcl-2 and Bax) were evaluated. Speckle tracking imaging (STI)-based echocardiography revealed that IPostC and ATP-PPostC were associated with better preserved global and regional cardiac function, as indicated by significantly increased GLSrsys, GLSrd, GLSsys, SrLsys, SrLd, and SLsys in both groups (all P<.5). Subsequent pathologic studies indicate that the percentage of necrotic myocardium and permillage of apoptotic cells were significantly lower in the IPostC and ATP-PPostC groups than in the IR group (all P<.05). Moreover, both IPostC and ATP-PPostC were associated with increased Bcl-2 mRNA levels and reduced Bax mRNA levels. IPostC and ATP-PPostC may exert cardioprotective functions by better preservation of cardiac function during the I/R process and at least partly via attenuation of myocardial apoptosis. © 2016 John Wiley & Sons Ltd.

Myocardial regeneration potential of adipose tissue-derived stem cells

DOE Office of Scientific and Technical Information (OSTI.GOV)

Bai, Xiaowen, E-mail: baixw01@yahoo.com; Alt, Eckhard, E-mail: ealt@mdanderson.org

Research highlights: {yields} Various tissue resident stem cells are receiving tremendous attention from basic scientists and clinicians and hold great promise for myocardial regeneration. {yields} For practical reasons, human adipose tissue-derived stem cells are attractive stem cells for future clinical application in repairing damaged myocardium. {yields} This review summarizes the characteristics of cultured and freshly isolated stem cells obtained from adipose tissue, their myocardial regeneration potential and the, underlying mechanisms, and safety issues. -- Abstract: Various tissue resident stem cells are receiving attention from basic scientists and clinicians as they hold promise for myocardial regeneration. For practical reasons, adipose tissue-derivedmore » stem cells (ASCs) are attractive cells for clinical application in repairing damaged myocardium based on the following advantages: abundant adipose tissue in most patients and easy accessibility with minimally invasive lipoaspiration procedure. Several recent studies have demonstrated that both cultured and freshly isolated ASCs could improve cardiac function in animal model of myocardial infarction. The mechanisms underlying the beneficial effect of ASCs on myocardial regeneration are not fully understood. Growing evidence indicates that transplantation of ASCs improve cardiac function via the differentiation into cardiomyocytes and vascular cells, and through paracrine pathways. Paracrine factors secreted by injected ASCs enhance angiogenesis, reduce cell apoptosis rates, and promote neuron sprouts in damaged myocardium. In addition, Injection of ASCs increases electrical stability of the injured heart. Furthermore, there are no reported cases of arrhythmia or tumorigenesis in any studies regarding myocardial regeneration with ASCs. This review summarizes the characteristics of both cultured and freshly isolated stem cells obtained from adipose tissue, their myocardial regeneration potential, and the underlying mechanisms for beneficial effect on cardiac function, and safety issues.« less

Erythropoietin alleviates post-resuscitation myocardial dysfunction in rats potentially through increasing the expression of angiotensin II receptor type 2 in myocardial tissues

PubMed Central

Zhou, Hourong; Huang, Jia; Zhu, Li; Cao, Yu

2018-01-01

Activation of renin-angiotensin system (RAS) is one of the pathological mechanisms associated with myocardial ischemia-reperfusion injury following resuscitation. The present study aimed to determine whether erythropoietin (EPO) improves post-resuscitation myocardial dysfunction and how it affects the renin-angiotensin system. Sprague-Dawley rats were randomly divided into sham, vehicle, epinephrine (EP), EPO and EP + EPO groups. Excluding the sham group, all groups underwent cardiopulmonary resuscitation (CPR) 4 min after asphyxia-induced cardiac arrest (CA). EP and/or EPO was administrated by intravenous injection when CPR began. The results demonstrated that the vehicle group exhibited lower mean arterial pressure, left ventricular systolic pressure, maximal ascending rate of left ventricular pressure during left ventricular isovolumic contraction and maximal descending rate of left ventricular pressure during left ventricular isovolumic relaxation (+LVdP/dt max and -LVdP/dt max, respectively), and higher left ventricular end-diastolic pressure, compared with the sham group following return of spontaneous circulation (ROSC). Few significant differences were observed concerning the myocardial function between the vehicle and EP groups; however, compared with the vehicle group, EPO reversed myocardial function indices following ROSC, excluding-LVdP/dt max. Serum renin and angiotensin (Ang) II levels were measured by ELISA. The serum levels of renin and Ang II were significantly increased in the vehicle group compared with the sham group, which was also observed for the myocardial expression of renin and Ang II receptor type 1 (AT1R), as determined by reverse transcription-quantitative polymerase chain reaction and western blotting. EPO alone did not significantly reduce the high serum levels of renin and Ang II post-resuscitation, but changed the protein levels of renin and AT1R expression in myocardial tissues. However, EPO enhanced the myocardial expression of Ang II receptor type 2 (AT2R) following ROSC. In conclusion, the present study confirmed that CA resuscitation activated the renin-Ang II-AT1R signaling pathway, which may contribute to myocardial dysfunction in rats. The present study confirmed that EPO treatment is beneficial for protecting cardiac function post-resuscitation, and the roles of EPO in alleviating post-resuscitation myocardial dysfunction may potentially be associated with enhanced myocardial expression of AT2R. PMID:29393490

Myocardial metabolism during exposure to carbon monoxide in the conscious dog.

NASA Technical Reports Server (NTRS)

Adams, J. D.; Erickson, H. H.; Stone, H. L.

1973-01-01

Investigation of the relationship between coronary flow, heart rate, left ventricular function, and myocardial oxygen consumption at increasing levels of carboxyhemoglobin in conscious dogs. The results demonstrate a linear increase in coronary flow and heart rate as the carboxyhemoglobin increases up to 20%. Myocardial oxygen consumption declined during the same period.

Cardiac CT for myocardial ischaemia detection and characterization--comparative analysis.

PubMed

Bucher, A M; De Cecco, C N; Schoepf, U J; Wang, R; Meinel, F G; Binukrishnan, S R; Spearman, J V; Vogl, T J; Ruzsics, B

2014-11-01

The assessment of patients presenting with symptoms of myocardial ischaemia remains one of the most common and challenging clinical scenarios faced by physicians. Current imaging modalities are capable of three-dimensional, functional and anatomical views of the heart and as such offer a unique contribution to understanding and managing the pathology involved. Evidence has accumulated that visual anatomical coronary evaluation does not adequately predict haemodynamic relevance and should be complemented by physiological evaluation, highlighting the importance of functional assessment. Technical advances in CT technology over the past decade have progressively moved cardiac CT imaging into the clinical workflow. In addition to anatomical evaluation, cardiac CT is capable of providing myocardial perfusion parameters. A variety of CT techniques can be used to assess the myocardial perfusion. The single energy first-pass CT and dual energy first-pass CT allow static assessment of myocardial blood pool. Dynamic cardiac CT imaging allows quantification of myocardial perfusion through time-resolved attenuation data. CT-based myocardial perfusion imaging (MPI) is showing promising diagnostic accuracy compared with the current reference modalities. The aim of this review is to present currently available myocardial perfusion techniques with a focus on CT imaging in light of recent clinical investigations. This article provides a comprehensive overview of currently available CT approaches of static and dynamic MPI and presents the results of corresponding clinical trials.

Assessment of myocardial viability: comparison of echocardiography versus cardiac magnetic resonance imaging in the current era.

PubMed

Tomlinson, David R; Becher, Harald; Selvanayagam, Joseph B

2008-06-01

Detecting viable myocardium, whether hibernating or stunned, is of clinical significance in patients with coronary artery disease and left ventricular dysfunction. Echocardiographic assessments of myocardial thickening and endocardial excursion during dobutamine infusion provide a highly specific marker for myocardial viability, but with relatively less sensitivity. The additional modalities of myocardial contrast echocardiography and tissue Doppler have recently been proposed to provide further, quantitative measures of myocardial viability assessment. Cardiac magnetic resonance (CMR) has become popular for the assessment of myocardial viability as it can assess cardiac function, volumes, myocardial scar, and perfusion with high-spatial resolution. Both 'delayed enhancement' CMR and dobutamine stress CMR have important roles in the assessment of patients with ischaemic cardiomyopathy. This article reviews the recent advances in both echocardiography and CMR for the clinical assessment of myocardial viability. It attempts to provide a pragmatic approach toward the patient-specific assessment of this important clinical problem.

Functional Testing Underlying Coronary Revascularisation

ClinicalTrials.gov

2016-10-04

Multivessel Coronary Artery Disease; Vessel Disease; Stable Angina; Unstable Angina or Stabilized Non-ST Elevated Myocardial Infarction; Patients With ST-elevated Myocardial Infarction; Revascularization of Culprit Coronary Artery

Long-term benefit of early pre-reperfusion metoprolol administration in patients with acute myocardial infarction: results from the METOCARD-CNIC trial (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction).

PubMed

Pizarro, Gonzalo; Fernández-Friera, Leticia; Fuster, Valentin; Fernández-Jiménez, Rodrigo; García-Ruiz, José M; García-Álvarez, Ana; Mateos, Alonso; Barreiro, María V; Escalera, Noemí; Rodriguez, Maite D; de Miguel, Antonio; García-Lunar, Inés; Parra-Fuertes, Juan J; Sánchez-González, Javier; Pardillos, Luis; Nieto, Beatriz; Jiménez, Adriana; Abejón, Raquel; Bastante, Teresa; Martínez de Vega, Vicente; Cabrera, José A; López-Melgar, Beatriz; Guzman, Gabriela; García-Prieto, Jaime; Mirelis, Jesús G; Zamorano, José Luis; Albarrán, Agustín; Goicolea, Javier; Escaned, Javier; Pocock, Stuart; Iñiguez, Andrés; Fernández-Ortiz, Antonio; Sánchez-Brunete, Vicente; Macaya, Carlos; Ibanez, Borja

2014-06-10

The goal of this trial was to study the long-term effects of intravenous (IV) metoprolol administration before reperfusion on left ventricular (LV) function and clinical events. Early IV metoprolol during ST-segment elevation myocardial infarction (STEMI) has been shown to reduce infarct size when used in conjunction with primary percutaneous coronary intervention (pPCI). The METOCARD-CNIC (Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction) trial recruited 270 patients with Killip class ≤II anterior STEMI presenting early after symptom onset (<6 h) and randomized them to pre-reperfusion IV metoprolol or control group. Long-term magnetic resonance imaging (MRI) was performed on 202 patients (101 per group) 6 months after STEMI. Patients had a minimal 12-month clinical follow-up. Left ventricular ejection fraction (LVEF) at the 6 months MRI was higher after IV metoprolol (48.7 ± 9.9% vs. 45.0 ± 11.7% in control subjects; adjusted treatment effect 3.49%; 95% confidence interval [CI]: 0.44% to 6.55%; p = 0.025). The occurrence of severely depressed LVEF (≤35%) at 6 months was significantly lower in patients treated with IV metoprolol (11% vs. 27%, p = 0.006). The proportion of patients fulfilling Class I indications for an implantable cardioverter-defibrillator (ICD) was significantly lower in the IV metoprolol group (7% vs. 20%, p = 0.012). At a median follow-up of 2 years, occurrence of the pre-specified composite of death, heart failure admission, reinfarction, and malignant arrhythmias was 10.8% in the IV metoprolol group versus 18.3% in the control group, adjusted hazard ratio (HR): 0.55; 95% CI: 0.26 to 1.04; p = 0.065. Heart failure admission was significantly lower in the IV metoprolol group (HR: 0.32; 95% CI: 0.015 to 0.95; p = 0.046). In patients with anterior Killip class ≤II STEMI undergoing pPCI, early IV metoprolol before reperfusion resulted in higher long-term LVEF, reduced incidence of severe LV systolic dysfunction and ICD indications, and fewer heart failure admissions. (Effect of METOprolol in CARDioproteCtioN During an Acute Myocardial InfarCtion. The METOCARD-CNIC Trial; NCT01311700). Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Myocardial infarction during anaphylaxis in a young healthy male with normal coronary arteries- is epinephrine the culprit?

PubMed

Jayamali, W D; Herath, H M M T B; Kulathunga, Aruna

2017-09-04

Anaphylaxis is an acute, potentially fatal medical emergency. Myocardial injury or infarction in the setting of an anaphylaxis can be due the anaphylaxis itself, when it is known as Kounis syndrome or it can also be due to the effect of epinephrine treatment. Epinephrine is considered as the cornerstone in management of anaphylaxis. Myocardial infarction secondary to therapeutic doses of adrenaline is a rare occurrence and only a few cases have been reported in literature. The mechanism of myocardial injury was considered to be due to coronary vasospasm secondary to epinephrine as the coronary angiograms were normal on these occasions. A 21-year- old previously healthy male got admitted to the local hospital with an urticarial rash and difficulty in breathing, one hour after ingestion of prawns for which he was known to be allergic. He was treated with 0.5 ml of intramuscular adrenaline (1:1000) which was administered to the lateral side of the thigh, following which he developed palpitations and tightening type central chest pain. Electrocardiogram showed ST segment depressions in leads III, aVF and V1 to V5 and he was transferred to a tertiary care hospital. The second electrocardiogram, done 2 h later, showed resolution of ST segment depressions but new T inversions in leads I and aVL. Troponin I was elevated with a titer of 2.15 ng/ml. He was treated with sublingual GTN in the emergency treatment unit and the symptoms resolved. Transthoracic 2D echocardiogram and stress testing with treadmill was normal and CT coronary angiogram revealed normal coronary arteries. Here we present a case of a young healthy adult with no significant risk factors for coronary artery disease who developed myocardial infarction following intramuscular administration of therapeutic dose of adrenalin for an anaphylactic reaction. The postulated mechanism is most likely an alpha receptor mediated coronary vascular spasm. However the use of adrenaline in the setting of life threatening anaphylaxis is life saving and the benefits far outweigh the risks of adverse effects. Therefore the purpose of reporting this case is not to discourage the use of adrenaline in anaphylaxis but to make aware of this potential adverse effect which can occur in the acute setting.

Associations of preexisting depression and anxiety with hospitalization in patients with cardiovascular disease.

PubMed

Chamberlain, Alanna M; Vickers, Kristin S; Colligan, Robert C; Weston, Susan A; Rummans, Teresa A; Roger, Véronique L

2011-11-01

To determine the risk of hospitalization and death in relation to preexisting depression and anxiety among patients with cardiovascular disease (CVD). The cohort consisted of 799 Olmsted County, MN, residents diagnosed with CVD (myocardial infarction or heart failure) from January 1, 1979, to December 31, 2009, who completed a Minnesota Multiphasic Personality Inventory (MMPI) prior to their event. The MMPI was used to identify depression and anxiety, and participants were followed up for hospitalizations and death during an average of 6.2 years. Depression and anxiety were identified in 282 (35%) and 210 (26%) participants, respectively. After adjustment, depression and anxiety were independently associated with a 28% (95% confidence interval [CI], 8%-51%) and 26% (95% CI, 3%-53%) increased risk of being hospitalized, respectively. Depression also conferred an increased risk of all-cause mortality of similar magnitude, whereas the hazard ratio for anxiety was not statistically significant. The combined occurrence of depression and anxiety led to a 35% (95% CI, 8%-71%) increase in the risk of hospitalizations. Among patients with CVD, both preexisting depression and anxiety, occurring on average 17 years before the CVD event, independently predict hospitalizations. In addition, the 2 conditions may act synergistically on increasing health care utilization in patients with CVD.

Cardiac-Specific Overexpression of Catalase Attenuates Lipopolysaccharide-Induced Myocardial Contractile Dysfunction: Role of Autophagy

PubMed Central

Turdi, Subat; Han, Xuefeng; Huff, Anna F.; Roe, Nathan D.; Hu, Nan; Gao, Feng; Ren, Jun

2012-01-01

Lipopolysaccharide (LPS) from Gram-negative bacteria is a major initiator of sepsis, leading to cardiovascular collapse. Accumulating evidence has indicated a role of reactive oxygen species (ROS) in cardiovascular complication in sepsis. This study was designed to examine the effect of cardiac-specific overexpression of catalase in LPS-induced cardiac contractile dysfunction and the underlying mechanism(s) with a focus on autophagy. Catalase transgenic and wild-type FVB mice were challenged with LPS (6 mg/kg) and cardiac function was evaluated. Levels of oxidative stress, autophagy, apoptosis and protein damage were examined using fluorescence microscopy, Western blot, TUNEL assay, caspase-3 activity and carbonyl formation. Kaplan-Meier curve was constructed for survival following LPS treatment. Our results revealed a lower mortality in catalase mice compared with FVB mice following LPS challenge. LPS injection led to depressed cardiac contractile capacity as evidenced by echocardiography and cardiomyocyte contractile function, the effect of which was ablated by catalase overexpression. LPS treatment induced elevated TNF-α level, autophagy, apoptosis (TUNEL, caspase-3 activation, cleaved caspase-3), production of ROS and O2−, and protein carbonyl formation, the effects of which were significantly attenuated by catalase overexpression. Electron microscopy revealed focal myocardial damage characterized by mitochondrial injury following LPS treatment, which was less severe in catalase mice. Interestingly, LPS-induced cardiomyocyte contractile dysfunction was prevented by antioxidant NAC and the autophagy inhibitor 3-methyladenine. Taken together, our data revealed that catalase protects against LPS-induced cardiac dysfunction and mortality, which may be associated with inhibition of oxidative stress and autophagy. PMID:22902401

Diet compounds, glycemic index and obesity-related cardiac effects.

PubMed

Diniz, Yeda S; Burneiko, Regina M; Seiva, Fabio R F; Almeida, Flávia Q A; Galhardi, Cristiano Machado; Filho, José Luiz V B Novelli; Mani, Fernanda; Novelli, Ethel L B

2008-02-20

Diet compounds may influence obesity-related cardiac oxidative stress and metabolic sifting. Carbohydrate-rich diet may be disadvantageous from fat-rich diet to cardiac tissue and glycemic index rather than lipid profile may predict the obesity-related cardiac effects. Male Wistar rats were divided into three groups (n=8/group): (C) receiving standard chow (3.0 kcal/g); (CRD) receiving carbohydrate-rich diet (4.0 kcal/g), and (FRD) receiving fat-rich diet (4.0 kcal/g). Rats were sacrificed after the oral glucose tolerance test (OGTT) at 60 days of dietary treatments. Lipid profile and oxidative stress parameters were determined in serum. Myocardial samples were used to determine oxidative stress, metabolic enzymes, glycogen and triacylglycerol. FRD rats showed higher final body weight and body mass index than CRD and C. Serum cholesterol and low-density lipoprotein were higher in FRD than in CRD, while triacylglycerol and oxidized low-density lipoprotein cholesterol were higher in CRD than in FRD. CRD rats had the highest myocardial lipid hydroperoxide and diminished superoxide dismutase and catalase activities. Myocardial glycogen was lower and triacylglycerol was higher in CRD than in C and FRD rats. Although FRD rats had depressed myocardial-reducing power, no significant changes were observed in myocardial energy metabolism. Myocardial beta-hydroxyacyl coenzyme-A dehydrogenase and citrate synthase, as well as the enhanced lactate dehydrogenase/citrate synthase ratio indicated that fatty acid degradation was decreased in CRD rats. Glycemic index was positively correlated with obesity-related cardiac effects. Isoenergetic carbohydrate-rich and fat-rich diets induced different degree of obesity and differently affected lipid profile. Carbohydrate-rich diet was deleterious relative to fat-rich diet in the heart enhancing lipoperoxidation and shifting the metabolic pathway for energy production. Glycemic index rather than dyslipidemic profile may predict the obesity effects on cardiac tissue.

Toll-like receptor 3 plays a role in myocardial infarction and ischemia/reperfusion injury.

PubMed

Lu, Chen; Ren, Danyang; Wang, Xiaohui; Ha, Tuanzhu; Liu, Li; Lee, Eric J; Hu, Jing; Kalbfleisch, John; Gao, Xiang; Kao, Race; Williams, David; Li, Chuanfu

2014-01-01

Innate immune and inflammatory responses mediated by Toll like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. This study examined the role of TLR3 in myocardial injury induced by two models, namely, myocardial infarction (MI) and I/R. First, we examined the role of TLR3 in MI. TLR3 deficient (TLR3(-/-)) and wild type (WT) mice were subjected to MI induced by permanent ligation of the left anterior descending (LAD) coronary artery for 21days. Cardiac function was measured by echocardiography. Next, we examined whether TLR3 contributes to myocardial I/R injury. TLR3(-/-) and WT mice were subjected to myocardial ischemia (45min) followed by reperfusion for up to 3days. Cardiac function and myocardial infarct size were examined. We also examined the effect of TLR3 deficiency on I/R-induced myocardial apoptosis and inflammatory cytokine production. TLR3(-/-) mice showed significant attenuation of cardiac dysfunction after MI or I/R. Myocardial infarct size and myocardial apoptosis induced by I/R injury were significantly attenuated in TLR3(-/-) mice. TLR3 deficiency increases B-cell lymphoma 2 (BCL2) levels and attenuates I/R-increased Fas, Fas ligand or CD95L (FasL), Fas-Associated protein with Death Domain (FADD), Bax and Bak levels in the myocardium. TLR3 deficiency also attenuates I/R-induced myocardial nuclear factor KappaB (NF-κB) binding activity, Tumor necrosis factor alpha (TNF-α) and Interleukin-1 beta (IL-1β) production as well as I/R-induced infiltration of neutrophils and macrophages into the myocardium. TLR3 plays an important role in myocardial injury induced by MI or I/R. The mechanisms involve activation of apoptotic signaling and NF-κB binding activity. Modulation of TLR3 may be an effective approach for ameliorating heart injury in heart attack patients. © 2013.

Losartan treatment attenuates tumor-induced myocardial dysfunction

PubMed Central

Stevens, Sarah CW; Velten, Markus; Youtz, Dane J.; Clark, Yvonne; Jing, Runfeng; Reiser, Peter J.; Bicer, Sabahattin; Devine, Raymond; McCarthy, Donna O.; Wold, Loren E.

2015-01-01

Fatigue and muscle wasting are common symptoms experienced by cancer patients. Data from animal models demonstrate that angiotensin is involved in tumor-induced muscle wasting, and that tumor growth can independently affect myocardial function, which could contribute to fatigue in cancer patients. In clinical studies, inhibitors of angiotensin converting enzyme (ACE) can prevent the development of chemotherapy-induced cardiovascular dysfunction, suggesting a mechanistic role for the renin-angiotensin-aldosterone system (RAAS). In the present study, we investigated whether an angiotensin (AT)1-receptor antagonist could prevent the development of tumor-associated myocardial dysfunction. Methods and Results: Colon26 adenocarcinoma (c26) cells were implanted into female CD2F1 mice at 8 weeks of age. Simultaneously, mice were administered Losartan (10 mg/kg) daily via their drinking water. In vivo echocardiography, blood pressure, in vitro cardiomyocyte function, cell proliferation assays, and measures of systemic inflammation and myocardial protein degradation were performed 19 days following tumor cell injection. Losartan treatment prevented tumor-induced loss of muscle mass and in vitro c26 cell proliferation, decreased tumor weight, and attenuated myocardial expression of interleukin-6. Furthermore, Losartan treatment mitigated tumor-associated alterations in calcium signaling in cardiomyocytes, which was associated with improved myocyte contraction velocity, systolic function, and blood pressures in the hearts of tumor-bearing mice. Conclusions: These data suggest that Losartan may mitigate tumor-induced myocardial dysfunction and inflammation. PMID:25988231

Losartan treatment attenuates tumor-induced myocardial dysfunction.

PubMed

Stevens, Sarah C W; Velten, Markus; Youtz, Dane J; Clark, Yvonne; Jing, Runfeng; Reiser, Peter J; Bicer, Sabahattin; Devine, Raymond D; McCarthy, Donna O; Wold, Loren E

2015-08-01

Fatigue and muscle wasting are common symptoms experienced by cancer patients. Data from animal models demonstrate that angiotensin is involved in tumor-induced muscle wasting, and that tumor growth can independently affect myocardial function, which could contribute to fatigue in cancer patients. In clinical studies, inhibitors of angiotensin converting enzyme (ACE) can prevent the development of chemotherapy-induced cardiovascular dysfunction, suggesting a mechanistic role for the renin-angiotensin-aldosterone system (RAAS). In the present study, we investigated whether an angiotensin (AT) 1-receptor antagonist could prevent the development of tumor-associated myocardial dysfunction. Colon26 adenocarcinoma (c26) cells were implanted into female CD2F1 mice at 8weeks of age. Simultaneously, mice were administered Losartan (10mg/kg) daily via their drinking water. In vivo echocardiography, blood pressure, in vitro cardiomyocyte function, cell proliferation assays, and measures of systemic inflammation and myocardial protein degradation were performed 19days following tumor cell injection. Losartan treatment prevented tumor-induced loss of muscle mass and in vitro c26 cell proliferation, decreased tumor weight, and attenuated myocardial expression of interleukin-6. Furthermore, Losartan treatment mitigated tumor-associated alterations in calcium signaling in cardiomyocytes, which was associated with improved myocyte contraction velocity, systolic function, and blood pressures in the hearts of tumor-bearing mice. These data suggest that Losartan may mitigate tumor-induced myocardial dysfunction and inflammation. Copyright © 2015 Elsevier Ltd. All rights reserved.

Pyridostigmine ameliorates cardiac remodeling induced by myocardial infarction via inhibition of the transforming growth factor-β1/TGF-β1-activated kinase pathway.

PubMed

Lu, Yi; Liu, Jin-Jun; Bi, Xue-Yuan; Yu, Xiao-Jiang; Kong, Shan-Shan; Qin, Fang-Fang; Zhou, Jun; Zang, Wei-Jin

2014-05-01

Autonomic imbalance characterized by sympathetic predominance coinciding with diminished vagal activity is an independent risk factor in cardiovascular diseases. Several studies show that vagus nerve stimulation exerted beneficial effects on cardiac function and survival. In this study, we investigated the vagomimetic effect of pyridostigmine on left ventricular (LV) remodeling in rats after myocardial infarction. After myocardial infarction, surviving rats were treated with or without pyridostigmine (31 mg·kg⁻¹·d⁻¹) for 2 weeks, and hemodynamic parameters were measured. LV tissue was used to assess infarct size and interstitial fibrosis by Masson's trichrome and 0.1% picrosirius red staining. Protein expression of heart tissues was used to assess the efficacy of the treatment. Pyridostigmine markedly reduced myocardial infarct size and improved cardiac diastolic function. These improvements were accompanied with a significant decrease in matrix metalloproteinase-2 expression and collagen deposition. Additionally, pyridostigmine inhibited both transforming growth factor-β1 (TGF-β1) and TGF-β1-activated kinase expression in hearts postmyocardial infarction. Thus, pyridostigmine reduces collagen deposition, attenuates cardiac fibrosis, and improves LV diastolic function after myocardial infarction via TGF-β1/TGF-β1-activated kinase pathway inhibition.

Effects of glycyl-glutamine dipeptide supplementation on myocardial damage and cardiac function in rats after severe burn injury

PubMed Central

Zhang, Yong; Yan, Hong; Lv, Shang-Gun; Wang, Lin; Liang, Guang-Ping; Wan, Qian-Xue; Peng, Xi

2013-01-01

Glutamine decreases myocardial damage in ischemia/reperfusion injury. However, the cardioprotective effect of glutamine after burn injury remains unclear. Present study was to explore the protective effect of glycyl-glutamine dipeptide on myocardial damage in severe burn rats. Seventy-two Wistar rats were randomly divided into three groups: normal control (C), burned control (B) and glycyl-glutamine dipeptide-treated (GG) groups. B and GG groups were inflicted with 30% total body surface area of full thickness burn. The GG group was given 1.5 g/kg glycyl-glutamine dipeptide per day and the B group was given the same dose of alanine via intraperitoneal injection for 3 days. The serum CK, LDH, AST, and, blood lactic acid levels, as well as the myocardium ATP and GSH contents, were measured. The indices of cardiac contractile function and histopathological change were analyzed at 12, 24, 48, and 72 post-burn hours (PBH). The serum CK, LDH, AST and blood lactic acid levels increased, and the myocardium ATP and GSH content decreased in both burned groups. Compared with B group, the CK, LDH, AST and blood lactic acid levels reduced, myocardium ATP and GSH content increased in GG group. Moreover, the inhibition of cardiac contractile function and myocardial histopathological damage were reduced significantly in GG group. We conclude that myocardial histological structure and function were damaged significantly after burn injury, glycyl-glutamine dipeptide supplementation is beneficial to myocardial preservation by improving cardiocyte energy metabolism, increasing ATP and glutathione synthesis. PMID:23638213

Association of ST segment depression >5 min after exercise testing with severity of coronary artery disease.

PubMed

Shaikh, Ayaz Hussain; Hanif, Bashir; Siddiqui, Adeel M; Shahab, Hunaina; Qazi, Hammad Ali; Mujtaba, Iqbal

2010-04-01

To determine the association of prolonged ST segment depression after an exercise test with severity of coronary artery disease. A cross sectional study of 100 consecutive patients referred to the cardiology laboratory for stress myocardial perfusion imaging (MPI) conducted between April-August 2008. All selected patients were monitored until their ST segment depression was recovered to baseline. ST segment recovery time was categorized into less and more than 5 minutes. Subsequent gated SPECT-MPI was performed and stratified according to severity of perfusion defect. Association was determined between post exercise ST segment depression recovery time (<5 minutes and >5 minutes) and severity of perfusion defect on MPI. The mean age of the patients was 57.12 +/- 9.0 years. The results showed statistically insignificant association (p > 0.05) between ST segment recovery time of <5 minutes and >5 minutes with low, intermediate or high risk MPI. Our findings suggest that the commonly used cut-off levels used in literature for prolonged, post exercise ST segment depression (>5 minutes into recovery phase) does not correlate with severity of ischaemia based on MPI results.

Metaiodobenzylguanidine (/sup 131/I) scintigraphy detects impaired myocardial sympathetic neuronal transport function of canine mechanical-overload heart failure

DOE Office of Scientific and Technical Information (OSTI.GOV)

Rabinovitch, M.A.; Rose, C.P.; Rouleau, J.L.

1987-12-01

In heart failure secondary to chronic mechanical overload, cardiac sympathetic neurons demonstrate depressed catecholamine synthetic and transport function. To assess the potential of sympathetic neuronal imaging for detection of depressed transport function, serial scintigrams were acquired after the intravenous administration of metaiodobenzylguanidine (/sup 131/I) to 13 normal dogs, 3 autotransplanted (denervated) dogs, 5 dogs with left ventricular failure, and 5 dogs with compensated left ventricular hypertrophy due to a surgical arteriovenous shunt. Nine dogs were killed at 14 hours postinjection for determination of metaiodobenzylguanidine (/sup 131/I) and endogenous norepinephrine content in left atrium, left ventricle, liver, and spleen. By 4more » hours postinjection, autotransplanted dogs had a 39% reduction in mean left ventricular tracer accumulation, reflecting an absent intraneuronal tracer pool. Failure dogs demonstrated an accelerated early mean left ventricular tracer efflux rate (26.0%/hour versus 13.7%/hour in normals), reflecting a disproportionately increased extraneuronal tracer pool. They also showed reduced late left ventricular and left atrial concentrations of tracer, consistent with a reduced intraneuronal tracer pool. By contrast, compensated hypertrophy dogs demonstrated a normal early mean left ventricular tracer efflux rate (16.4%/hour) and essentially normal late left ventricular and left atrial concentrations of tracer. Metaiodobenzylguanidine (/sup 131/I) scintigraphic findings reflect the integrity of the cardiac sympathetic neuronal transport system in canine mechanical-overload heart failure. Metaiodobenzylguanidine (/sup 123/I) scintigraphy should be explored as a means of early detection of mechanical-overload heart failure in patients.« less

Estrogen modulation of the ethanol-evoked myocardial oxidative stress and dysfunction via DAPK3/Akt/ERK activation in male rats

DOE Office of Scientific and Technical Information (OSTI.GOV)

El-Mas, Mahmoud M., E-mail: mahelm@hotmail.com; Abdel-Rahman, Abdel A., E-mail: abdelrahmana@ecu.edu

Evidence suggests that male rats are protected against the hypotensive and myocardial depressant effects of ethanol compared with females. We investigated whether E{sub 2} modifies the myocardial and oxidative effects of ethanol in male rats. Conscious male rats received ethanol (0.5, 1 or 1.5 g/kg i.v.) 30-min after E{sub 2} (1 μg/kg i.v.) or its vehicle (saline), and hearts were collected at the conclusion of hemodynamic measurements for ex vivo molecular studies. Ethanol had no effect in vehicle-treated rats, but it caused dose-related reductions in LV developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of rise in LV pressure (dP/dt{sub max})more » and systolic (SBP) and diastolic (DBP) blood pressures in E{sub 2}-pretreated rats. These effects were associated with elevated (i) indices of reactive oxygen species (ROS), (ii) malondialdehyde (MDA) protein adducts, and (iii) phosphorylated death-associated protein kinase-3 (DAPK3), Akt, and extracellular signal-regulated kinases (ERK1/2). Enhanced myocardial anti-oxidant enzymes (heme oxygenase-1, catalase and aldehyde dehydrogenase 2) activities were also demonstrated. In conclusion, E{sub 2} promotes ethanol-evoked myocardial oxidative stress and dysfunction in male rats. The present findings highlight the risk of developing myocardial dysfunction in men who consume alcohol while receiving E{sub 2} for specific medical conditions. - Highlights: • Ethanol lowers blood pressure and causes LV dysfunction in E{sub 2}-treated rats. • E{sub 2}/ethanol aggravates cardiac oxidative state via of DAPK3/Akt/ERK activation. • E{sub 2}/ethanol causes a feedback increase in cardiac HO-1, catalase and ALDH2. • Alcohol might increase risk of myocardial dysfunction in men treated with E{sub 2}.« less

Is there an association between depression and cardiovascular mortality or sudden death?

PubMed

Alboni, Paolo; Favaron, Elisa; Paparella, Nelly; Sciammarella, Massimo; Pedaci, Mario

2008-04-01

The results of many studies and recent meta-analyses strongly suggest that depression is a risk factor for total and cardiovascular mortality, both in the general population and in patients with known heart disease. By contrast, the association between depression and sudden death or cardiac arrest has received little attention. This issue has been investigated in three recent studies; two were carried out in the general population and showed depression to be a independent risk factor for sudden death. The other study was carried out in patients with acute myocardial infarction (AMI); the adjusted relative risk (RR) of sudden death was significantly increased in depressed patients but, after adjustment for dyspnea/fatigue (a common symptom for heart disease and depression), the RR was no longer statistically significant. However, when the cognitive-affective depressive symptoms were examined separately from the somatic ones (dyspnea/fatigue, etc.), there was a clear trend for an association between cognitive-affective symptoms and sudden death. Because a risk factor can be defined as 'independent' only in a multivariate analysis in which variables are dichotomized, the presence of common symptoms between heart disease and depression represents a very difficult problem. However, taken together, the results of studies carried out in the general population and in patients with AMI strongly suggest that depression is a significant risk factor for sudden death.

[The brain and cytokines - the mutual origin of depression, obesity and cardiovascular diseases?].

PubMed

Ufnal, Marcin; Wolynczyk-Gmaj, Dorota

2011-04-19

Accumulating evidence points to a pivotal role of the brain in the regulation of the circulatory system and energy balance. It has also been found that common civilization diseases such as depression, obesity, hypertension, myocardial infarction or heart failure are accompanied by an increase in concentration of inflammatory mediators in the blood, cerebrospinal fluid and various tissues. Recent studies have revealed that inflammatory mediators that are synthesized peripherally or in the brain may affect the nervous regulation of animal body systems. For example, it has been found that non-specific pro-inflammatory stimuli as well as treatment with several cytokines may cause depressive behavior, disturbances in energy balance and alterations in the circulatory system. On the other hand, knockout of genes for pro-inflammatory cytokines or administration of anti-inflammatory mediators may normalize the pathological changes. In the present manuscript we will review studies that imply the common neuroinflammatory pathogenesis of cardiovascular diseases, depression and energy balance disorders.

TGF-β improves myocardial function and prevents apoptosis induced by anoxia-reoxygenation, through the reduction of endoplasmic reticulum stress.

PubMed

Wang, Yufeng; Zong, Ligeng; Wang, Xiaolei

2016-01-01

Transforming growth factor-β (TGF-β) is known for its role in ventricular remodeling, inflammatory response, cell survival, and apoptosis. However, its role in improving myocardial function in rat hearts subjected to ischemia-reperfusion (I/R) and protecting against apoptosis induced in cardiomyocytes by anoxia-reoxygenation (A/R) has not been elucidated. This study investigated the protective effects and molecular mechanisms of TGF-β on myocardial function and cardiomyocyte apoptosis. We used TUNEL staining, we tested cell viability, and we measured mitochondrial membrane potential and levels of mitochondrial ROS after 6 h of simulated anoxia together with various durations of simulated reoxygenation in H9c2 cells. We further observed the contractile function in rat hearts after they were subjected to 30 min global ischemia and 180 min reperfusion. Pretreatment with TGF-β markedly inhibited apoptosis in H9c2 cells, as evidenced by increased cell viability and decreased numbers of TUNEL-positive cells, maintained mitochondrial membrane potential, and diminished mitochondrial production of reactive oxygen species (ROS). These changes were associated with the inhibition of endoplasmic reticulum (ER) stress-dependent markers of apoptosis (GRP78, CHOP, caspase-12, and JNK), and the modulation of the expression of Bcl2/Bax. Furthermore, TGF-β improved I/R-induced myocardial contractile dysfunction. All of these protective effects were concentration-dependent. Our results show that TGF-β prevents A/R-induced apoptosis of cardiomyocytes and improves myocardial function in rat hearts injured by I/R.

Personality, disease severity, and the risk of long-term cardiac events in patients with a decreased ejection fraction after myocardial infarction.

PubMed

Denollet, J; Brutsaert, D L

1998-01-20

Patients with myocardial infarction (MI) with a decreased left ventricular ejection fraction (LVEF) have a poor prognosis, but the role of emotional stress in prognosis is not known. We hypothesized that emotional stress in these patients (1) is unrelated to the severity of cardiac disorder, (2) predicts cardiac events, and (3) is a function of basic personality traits. Eighty-seven patients with MI (age, 41 to 69 years) with an LVEF of < or =50% underwent psychological assessment at baseline. Patients and their families were contacted after 6 to 10 years (mean, 7.9 years); cardiac events were defined as cardiac death or nonfatal MI. Emotional distress was unrelated to the severity of cardiac disorder. At follow-up, 21 patients had experienced a cardiac event (13 fatal events). These events were related to LVEF of < or =30%, poor exercise tolerance, previous MI, anxiety, anger, and depression (all P< or =.02). Patients with a distressed personality (type D; ie, the tendency to suppress negative emotions) were more likely to experience an event over time compared with non-type D patients (P=.00005). Cox proportional hazards analysis yielded LVEF of < or =30% (relative risk, 3.0; 95% confidence interval, 1.2 to 7.7; P=.02) and type D (relative risk, 4.7; 95% confidence interval, 1.9 to 11.8; P=.001) as independent predictors. Anxiety, anger, and depression did not add to the predictive power of type D; these negative emotions were highly correlated and reflected the personality domain of negative affectivity. Personality influences the clinical course of patients with a decreased LVEF. Emotional distress in these patients is unrelated to disease severity but reflects individual differences in personality. Clinical trials should take a broad view of the target of intervention; assessment of LVEF and personality may identify patients at risk.

Human cardiomyocyte calcium handling and transverse tubules in mid-stage of post-myocardial-infarction heart failure.

PubMed

Høydal, Morten Andre; Kirkeby-Garstad, Idar; Karevold, Asbjørn; Wiseth, Rune; Haaverstad, Rune; Wahba, Alexander; Stølen, Tomas L; Contu, Riccardo; Condorelli, Gianluigi; Ellingsen, Øyvind; Smith, Godfrey L; Kemi, Ole J; Wisløff, Ulrik

2018-06-01

Cellular processes in the heart rely mainly on studies from experimental animal models or explanted hearts from patients with terminal end-stage heart failure (HF). To address this limitation, we provide data on excitation contraction coupling, cardiomyocyte contraction and relaxation, and Ca 2+ handling in post-myocardial-infarction (MI) patients at mid-stage of HF. Nine MI patients and eight control patients without MI (non-MI) were included. Biopsies were taken from the left ventricular myocardium and processed for further measurements with epifluorescence and confocal microscopy. Cardiomyocyte function was progressively impaired in MI cardiomyocytes compared with non-MI cardiomyocytes when increasing electrical stimulation towards frequencies that simulate heart rates during physical activity (2 Hz); at 3 Hz, we observed almost total breakdown of function in MI. Concurrently, we observed impaired Ca 2+ handling with more spontaneous Ca 2+ release events, increased diastolic Ca 2+ , lower Ca 2+ amplitude, and prolonged time to diastolic Ca 2+ removal in MI (P < 0.01). Significantly reduced transverse-tubule density (-35%, P < 0.01) and sarcoplasmic reticulum Ca 2+ adenosine triphosphatase 2a (SERCA2a) function (-26%, P < 0.01) in MI cardiomyocytes may explain the findings. Reduced protein phosphorylation of phospholamban (PLB) serine-16 and threonine-17 in MI provides further mechanisms to the reduced function. Depressed cardiomyocyte contraction and relaxation were associated with impaired intracellular Ca 2+ handling due to impaired SERCA2a activity caused by a combination of alteration in the PLB/SERCA2a ratio and chronic dephosphorylation of PLB as well as loss of transverse tubules, which disrupts normal intracellular Ca 2+ homeostasis and handling. This is the first study that presents these mechanisms from viable and intact cardiomyocytes isolated from the left ventricle of human hearts at mid-stage of post-MI HF. © 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.

Decreased coronary vasodilatory capacity in hypertrophic cardiomyopathy determined by split-dose thallium-dipyridamole myocardial scintigraphy

DOE Office of Scientific and Technical Information (OSTI.GOV)

Koga, Y.; Yamaguchi, R.; Ogata, M.

1990-05-01

Split-dose thallium-dipyridamole myocardial scintigraphy was performed in patients with nonobstructive hypertrophic cardiomyopathy (HC) who had angiographically normal coronary arteries. The dipyridamole-induced increases in thallium-201 uptake, calculated to evaluate coronary vasodilatory capacity, were significantly lower in 30 patients with HC than in 13 control subjects (177 +/- 58 vs 281 +/- 46%) and the reductions were observed in both the septal and lateral segments. The reductions of the septal segment in HC patients were significantly greater than those in 10 hypertensive patients with comparable degrees of septal hypertrophy. Of patients with HC, 16 had increases in thallium uptake well below themore » normal range. Compared with those having normal increases, these patients had significantly lower exercise duration (11 vs 15 minutes), with 33% having ST depression develop at a workload less than or equal to 80 watts. These data indicate that approximately one-half of patients with HC have impaired coronary vasodilatory capacity that could be an important pathophysiologic abnormality of HC resulting in the development of myocardial ischemia and the impairment of cardiac performance during exercise.« less

Post-traumatic stress disorder and incidence of coronary heart disease: a twin study.

PubMed

Vaccarino, Viola; Goldberg, Jack; Rooks, Cherie; Shah, Amit J; Veledar, Emir; Faber, Tracy L; Votaw, John R; Forsberg, Christopher W; Bremner, J Douglas

2013-09-10

The aim of this study was to determine whether post-traumatic stress disorder (PTSD) is associated with coronary heart disease (CHD) using a prospective twin study design and objective measures of CHD. It has long been hypothesized that PTSD increases the risk of CHD, but empirical evidence using objective measures is limited. We conducted a prospective study of middle-aged male twins from the Vietnam Era Twin Registry. Among twin pairs without self-reported CHD at baseline, we selected pairs discordant for a lifetime history of PTSD, pairs discordant for a lifetime history of major depression, and pairs without either condition. All underwent a clinic visit after a median follow-up of 13 years. Outcomes included clinical events (myocardial infarction, other hospitalizations for CHD and coronary revascularization) and quantitative measures of myocardial perfusion by [(13)N] ammonia positron emission tomography, including a stress total severity score and coronary flow reserve. A total of 562 twins (281 pairs) with a mean age of 42.6 years at baseline were included in this study. The incidence of CHD was more than double in twins with PTSD (22.6%) than in those without PTSD (8.9%; p < 0.001). The association remained robust after adjusting for lifestyle factors, other risk factors for CHD, and major depression (odds ratio: 2.2; 95% confidence interval: 1.2 to 4.1). Stress total severity score was significantly higher (+95%, p = 0.001) and coronary flow reserve was lower (-0.21, p = 0.02) in twins with PTSD than in those without PTSD, denoting worse myocardial perfusion. Associations were only mildly attenuated in 117 twin pairs discordant for PTSD. Among Vietnam-era veterans, PTSD is a risk factor for CHD. Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Myocardial viability assessed with fluorodeoxyglucose and PET in patients with Q wave myocardial infarction receiving thrombolysis: relationship to coronary anatomy and ventricular function.

PubMed

Fragasso, G; Chierchia, S L; Rossetti, E; Sciammarella, M G; Conversano, A; Lucignani, G; Landoni, C; Calori, G; Margonato, A; Fazio, F

1997-03-01

In previously thrombolysed patients, we analysed residual myocardial viability using the PET-FDG technique and correlated its presence and extent to the angiographic appearance of the infarct-related vessel and left ventricular function. Thirty-six patients who had undergone intravenous thromboloysis for acute myocardial infarction 4.8 +/- 7.2 months previously were studied. Coronary angiography, left ventriculography, and assessment of myocardial perfusion and metabolism were all performed within 1 week. All patients exhibited perfusion defects consistent with the clinically identified myocardial infarction site. Residual viability, as assessed by the PET-FDG technique, was present in 53% of cases. The infarct-related coronary artery was patent in 19 (53%) patients (TIMI grade 3, 79%); of the remaining 17 with occluded infarct-related arteries, 11 had collaterals to the infarct area. Significant FDG uptake was observed in 63% of patients with a patent infarct-related artery and in 41% of those with an occluded infarct-related artery. The same study protocol was adopted in a control group of 30 patients with myocardial infarction who did not receive thrombolysis. The number of infarct-related patent vessels was significantly lower in these patients (30 vs 53%) (TIMI grade 3, 56%), but the overall percentage of PET viability was again 53%. Qualitative analysis of the regional perfusion pattern showed that the magnitude and severity of the perfusion defect was similar in the two groups, regardless of the presence or absence of FDG uptake. Global left ventricular function was also similar in the two groups. However, regional wall motion was significantly better in the thrombolysed patients with a patent infarct-related artery than in those who had not received thrombolysis and whose culprit vessel was also patent. In conclusion, the results of our study support the notion that early recanalization of the infarct-related artery is critical for preserving left ventricular function. Although the number of patent infarct-related coronary arteries is greater and left ventricular function is better in successfully thrombolysed patients, the regional metabolic pattern does not apparently correlate with the patency of the infarct-related artery. This suggests that, in "chronic' myocardial infarction, residual tissue viability as assessed by fluorodeoxyglucose uptake does not necessarily correlate with coronary recanalization.

Extracellular Vesicle Injection Improves Myocardial Function and Increases Angiogenesis in a Swine Model of Chronic Ischemia.

PubMed

Potz, Brittany A; Scrimgeour, Laura A; Pavlov, Vasile I; Sodha, Neel R; Abid, M Ruhul; Sellke, Frank W

2018-06-12

Mesenchymal stem cell-derived extracellular vesicles (EVs) are believed to be cardioprotective in myocardial infarct. The objective of this study was to examine the effects of human mesenchymal cell-derived EV injection on cardiac function, myocardial blood flow, and vessel density in the setting of chronic myocardial ischemia. Twenty-three Yorkshire swine underwent placement of an ameroid constrictor on their left circumflex artery. Two weeks later, the animals were split into 2 groups: the control group (CON; n=7) and the EV myocardial injection group (MVM; n=10). The MVM group underwent myocardial injection of 50 μg of EVs in 2 mL 0.9% saline into the ischemic myocardium. Five weeks later, the pigs underwent a harvest procedure, and the left ventricular myocardium was analyzed. Absolute blood flow and the ischemic/nonischemic myocardial perfusion ratio were increased in the ischemic myocardium in the MVM group compared with the CON group. Pigs in the MVM group had increased capillary and arteriolar density in the ischemic myocardial tissue compared with CON pigs. There was an increase in expression of the phospho-mitogen-activated protein kinase/mitogen-activated protein kinase ratio, the phospho-endothelial nitric oxide synthase/endothelial nitric oxide synthase ratio, and total protein kinase B in the MVM group compared with CON. There was an increase in cardiac output and stroke volume in the MVM group compared with CON. In the setting of chronic myocardial ischemia, myocardial injection of human mesenchymal cell-derived EVs increases blood flow to ischemic myocardial tissue by induction of capillary and arteriolar growth via activation of the protein kinase B/endothelial nitric oxide synthase and mitogen-activated protein kinase signaling pathways resulting in increased cardiac output and stroke volume. © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

Decrease of Total Antioxidative Capacity in Developed Low Cardiac Output Syndrome

PubMed Central

Kunt, Alper Sami; Andac, Mehmet Halit

2012-01-01

Background. It has been known that cardiac surgery induces an oxidative stress. The persistent oxidative stress during reperfusion may lead to depressed myocardial function resulting in low cardiac output syndrome (LCOS) necessitating inotropic or intra-aortic balloon counterpulsation support. Total antioxidant capacity (TAC) is a measurement of oxidative stress in tissues. The purpose of this study was to examine the TAC differences during coronary artery bypass graft (CABG) operation in patients who have developed LCOS and who have not. Material and Methods. Seventy-nine patients were enrolled in the study. Central venous blood samples were obtained immediately before surgery, during operation, and at the end of surgery to assess TAC. Clinical data regarding patient demographics and operative outcomes were prospectively collected and entered into our clinical database. Results. LCOS developed in 8 patients (10.12%). The TAC has decreased sharply in the LCOS patients compared with those who did not develop LCOS (P < 0.001) during operation. In addition, the receiver operating characteristic (ROC) area was 0.879. Conclusion. TAC has decreased during operation in a significant proportion of patients undergoing isolated CABG, and this is more prominent and serious and might be an independent variable in patients who have developed LCOS. This may be related to intraoperative misadventure or inadequate myocardial antioxidative protection. Routine measurement of the TAC during operation may provide information for assessment of the LCOS development. PMID:23251720

Cobalt Chloride Upregulates Impaired HIF-1α Expression to Restore Sevoflurane Post-conditioning-Dependent Myocardial Protection in Diabetic Rats

PubMed Central

Wu, Jianjiang; Yang, Long; Xie, Peng; Yu, Jin; Yu, Tian; Wang, Haiying; Maimaitili, Yiliyaer; Wang, Jiang; Ma, Haiping; Yang, Yining; Zheng, Hong

2017-01-01

Previous studies from our group have demonstrated that sevoflurane post-conditioning (SPC) protects against myocardial ischemia reperfusion injury via elevating the intranuclear expression of hypoxia inducible factor-1 alpha (HIF-1α). However, diabetic SPC is associated with decreased myocardial protection and disruption of the HIF-1 signaling pathway. Previous studies have demonstrated that cobalt chloride (CoCl2) can upregulate HIF-1α expression under diabetic conditions, but whether myocardial protection by SPC can be restored afterward remains unclear. We established a rat model of type 2 diabetes and a Langendorff isolated heart model of ischemia-reperfusion injury. Prior to reperfusion, 2.4% sevoflurane was used as a post-conditioning treatment. The diabetic rats were treated with CoCl2 24 h before the experiment. At the end of reperfusion, tests were performed to assess myocardial function, infarct size, mitochondrial morphology, nitric oxide (NO), Mitochondrial reactive oxygen species (ROS), mitochondrial respiratory function and enzyme activity, HIF-1α, vascular endothelial growth factor (VEGF) and endothelial NO synthase (eNOS) protein levels. In addition, myocardial protection by SPC was monitored after the blood glucose levels were lowered by insulin. The diabetic state was associated with deficient SPC protection and decreased HIF-1α expression. After treating the diabetic rats with CoCl2, SPC significantly upregulated the expression of HIF-1α, VEGF and eNOS, which markedly improved cardiac function, NO, mitochondrial respiratory function, and enzyme activity and decreased the infarction areas and ROS. In addition, these effects were not influenced by blood glucose levels. This study proved that CoCl2activates the HIF-1α signaling pathway, which restores SPC-dependent myocardial protection under diabetic conditions, and the protective effects of SPC were independent of blood glucose levels. PMID:28659817

Differences between Slovak and Dutch patients scheduled for coronary artery bypass graft surgery regarding clinical and psychosocial predictors of physical and mental health-related quality of life.

PubMed

El-Baz, Noha; Ondusova, Daniela; Studencan, Martin; Rosenberger, Jaroslav; Reijneveld, Sijmen A; van Dijk, Jitse P; Middel, Berrie

2018-04-01

Differences in health-related quality of life in coronary artery disease patients and associated factors between patients of central and western European descent are rarely investigated. We aim to test differences between Dutch and Slovak health-related quality of life, whether nationality predicted health-related quality of life and if standardised beta weights of health-related quality of life determinants differ across countries. An observational multicentre study at university cardiac centres in the Netherlands and Slovakia. In 226 coronary artery disease patients, health-related quality of life was measured by the Short Form Health Survey 36, anxiety and depression were measured using the Hospital Anxiety and Depression Scale, and type D personality was assessed with the 14-item Type D Scale. Multivariate analysis was used to explore the effect of patient characteristics on the physical and mental component summaries. Estimates of each predictor's beta value of the physical and mental component summaries in the Slovak and Dutch patient sample were separately calculated using the Cummings criterion for comparison of two independent betas. Stronger predictors of physical health-related quality of life in Slovak patients were educational level, current smoking, poor functional status, history of diabetes and amount of social support. In Dutch patients, only more symptoms of depression was a stronger predictor ( P<0.05). Regarding Slovak mental health-related quality of life, stronger predictors were educational level, current smoking and amount of social support. Female gender, history of myocardial infarction and more symptoms of depression were stronger predictors in Dutch patients ( P<0.05). Descent and differences between both populations in determinants of health-related quality of life should be considered while planning care, follow-up, health education and rehabilitation.

One-year follow-up of myocardial perfusion and function evaluated by gated SPECT MIBI in patients with earlier myocardial infarction and chronic total occlusion.

PubMed

Pavlovic, Smiljana V; Sobic-Saranovic, Dragana P; Beleslin, Branko D; Ostojic, Miodrag C; Nedeljkovic, Milan A; Giga, Vojislav L; Petrasinovic, Zorica R; Artiko, Vera M; Todorovic-Tirnanic, Mila V; Obradovic, Vladimir B

2009-01-01

Optimal treatment for chronic total occlusion (CTO) in the infarct-related coronary artery is not clear. Our aim was to assess myocardial perfusion, left ventricular ejection fraction (EF), and left ventricular size using gated single-photon emission computed tomography (SPECT) myocardial perfusion imaging with 99mTc-methoxy-isobutyl-isonitrile in patients with CTO before and 1 year after recanalization. Thirty patients with earlier myocardial infarction and at least one CTO underwent percutaneous coronary intervention (PCI) as well as nitrate-enhanced gated SPECT myocardial perfusion and dobutamine stress echocardiography before and 11 +/- 1 months after recanalization. They were divided into three groups based on the outcome of the follow-up angiography: (i) successful recanalization with no evidence of in-stent restenosis (n=13); (ii) successful recanalization with in-stent restenosis (n=7) and (iii) unsuccessful recanalization (n=10). Overall success of recanalization for CTO was 74%. In group 1, myocardial viability was preserved in 11 of 13 (85%) patients at baseline. Gated SPECT at 1 year showed a significant decrease in perfusion abnormalities (29 +/- 12 to 23 +/- 14%, P < 0.05) and left ventricular end-diastolic volume (EDV) (168 +/- 47 to 151 +/- 47 ml, P < 0.05). Improvement in EF (51 +/- 11 to 54 +/- 13%, P > 0.05) and reduction in left ventricular end-systolic volume (ESV) (84 +/- 37 to 77 +/- 40 ml, P > 0.05) did not reach the level of significance. Myocardial viability was preserved in only two of seven patients (28%) in group 2. Neither mean perfusion abnormalities (37 +/- 24 to 35 +/- 22%, P > 0.05) nor global left ventricular parameters (EF 41 +/- 15 vs. 42 +/- 19%, EDV 298 +/- 33 vs. 299 +/- 57 mL, ESV 197 +/- 12 vs. 195 +/- 32 ml; P > 0.05) changed at the follow-up. In group 3, myocardial viability was preserved in seven of 10 patients (70%) at baseline, but no significant changes in perfusion (40 +/- 18 vs. 41 +/- 19%, P > 0.05) and left ventricular function (EF 42 +/- 17 vs. 44 +/- 14%, EDV 228 +/- 101 vs. 227 +/- 81 ml, ESV 143 +/- 87 vs. 146 +/- 8 ml; P > 0.05) were seen at the follow-up. Myocardial perfusion and EDV may significantly improve 1 year after PCI provided recanalization of CTO was successful. Our preliminary findings suggest that successful recanalization of CTO may have favorable outcome on left ventricular perfusion and function, particularly in patients with viable myocardium before PCI. The gated SPECT myocardial perfusion imaging with 99mTc-methoxy-isobutyl-isonitrile may be useful for monitoring long-term functional outcome of PCI in patients with CTO.

Assessment of left ventricular myocardial deformation by cardiac MRI strain imaging reveals myocardial dysfunction in patients with primary cardiac tumors.

PubMed

Chen, Jing; Yang, Zhi-Gang; Xu, Hua-Yan; Shi, Ke; Guo, Ying-Kun

2018-02-15

To assess left ventricular myocardial deformation in patients with primary cardiac tumors. MRI was retrospectively performed in 61 patients, including 31 patients with primary cardiac tumors and 30 matched normal controls. Left ventricular strain and function parameters were then assessed by MRI-tissue tracking. Differences between the tumor group and controls, left and right heart tumor groups, left ventricular wall tumor and non-left ventricular wall tumor groups, and tumors with and without LV enlargement groups were assessed. Finally, the correlations among tumor diameter, myocardial strain, and LV function were analyzed. Left ventricular myocardial strain was milder for tumor group than for normal group. Peak circumferential strain (PCS) and its diastolic strain rate, longitudinal strains (PLS) and its diastolic strain rates, and peak radial systolic and diastolic velocities of the right heart tumor group were lower than those of the left heart tumor group (all p<0.050), but the peak radial systolic strain rate of the former was higher than that of the latter (p=0.017). The corresponding strains were lower in the left ventricular wall tumor groups than in the non-left ventricular wall tumor group (p<0.050). Peak radial systolic velocities were generally higher for tumors with LV enlargement than for tumors without LV enlargement (p<0.050). Peak radial strain, PCS, and PLS showed important correlations with the left ventricular ejection fraction (all p<0.050). MRI-tissue tracking is capable of quantitatively assessing left ventricular myocardial strain to reveal sub-clinical abnormalities of myocardial contractile function. Copyright © 2017 Elsevier B.V. All rights reserved.

Nuclear medicine in the management of patients with heart failure: guidance from an expert panel of the International Atomic Energy Agency (IAEA).

PubMed

Peix, Amalia; Mesquita, Claudio Tinoco; Paez, Diana; Pereira, Carlos Cunha; Felix, Renata; Gutierrez, Claudia; Jaimovich, Rodrigo; Ianni, Barbara Maria; Soares, Jose; Olaya, Pastor; Rodriguez, Ma Victoria; Flotats, Albert; Giubbini, Raffaele; Travin, Mark; Garcia, Ernest V

2014-08-01

Heart failure is increasing worldwide at epidemic proportions, resulting in considerable disability, mortality, and increase in healthcare costs. Gated myocardial perfusion single photon emission computed tomography or PET imaging is the most prominent imaging modality capable of providing information on global and regional ventricular function, the presence of intraventricular synchronism, myocardial perfusion, and viability on the same test. In addition, I-mIBG scintigraphy is the only imaging technique approved by various regulatory agencies able to provide information regarding the adrenergic function of the heart. Therefore, both myocardial perfusion and adrenergic imaging are useful tools in the workup and management of heart failure patients. This guide is intended to reinforce the information on the use of nuclear cardiology techniques for the assessment of heart failure and associated myocardial disease.

52 Genetic Loci Influencing Myocardial Mass

PubMed Central

van der Harst, Pim; van Setten, Jessica; Verweij, Niek; Vogler, Georg; Franke, Lude; Maurano, Matthew T.; Wang, Xinchen; Leach, Irene Mateo; Eijgelsheim, Mark; Sotoodehnia, Nona; Hayward, Caroline; Sorice, Rossella; Meirelles, Osorio; Lyytikäinen, Leo-Pekka; Polašek, Ozren; Tanaka, Toshiko; Arking, Dan E.; Ulivi, Sheila; Trompet, Stella; Müller-Nurasyid, Martina; Smith, Albert V.; Dörr, Marcus; Kerr, Kathleen F.; Magnani, Jared W.; Fabiola Del Greco, M.; Zhang, Weihua; Nolte, Ilja M.; Silva, Claudia T.; Padmanabhan, Sandosh; Tragante, Vinicius; Esko, Tõnu; Abecasis, Gonçalo R.; Adriaens, Michiel E.; Andersen, Karl; Barnett, Phil; Bis, Joshua C.; Bodmer, Rolf; Buckley, Brendan M.; Campbell, Harry; Cannon, Megan V.; Chakravarti, Aravinda; Chen, Lin Y.; Delitala, Alessandro; Devereux, Richard B.; Doevendans, Pieter A.; Dominiczak, Anna F.; Ferrucci, Luigi; Ford, Ian; Gieger, Christian; Harris, Tamara B.; Haugen, Eric; Heinig, Matthias; Hernandez, Dena G.; Hillege, Hans L.; Hirschhorn, Joel N.; Hofman, Albert; Hubner, Norbert; Hwang, Shih-Jen; Iorio, Annamaria; Kähönen, Mika; Kellis, Manolis; Kolcic, Ivana; Kooner, Ishminder K.; Kooner, Jaspal S.; Kors, Jan A.; Lakatta, Edward G.; Lage, Kasper; Launer, Lenore J.; Levy, Daniel; Lundby, Alicia; Macfarlane, Peter W.; May, Dalit; Meitinger, Thomas; Metspalu, Andres; Nappo, Stefania; Naitza, Silvia; Neph, Shane; Nord, Alex S.; Nutile, Teresa; Okin, Peter M.; Olsen, Jesper V.; Oostra, Ben A.; Penninger, Josef M.; Pennacchio, Len A.; Pers, Tune H.; Perz, Siegfried; Peters, Annette; Pinto, Yigal M.; Pfeufer, Arne; Pilia, Maria Grazia; Pramstaller, Peter P.; Prins, Bram P.; Raitakari, Olli T.; Raychaudhuri, Soumya; Rice, Ken M.; Rossin, Elizabeth J.; Rotter, Jerome I.; Schafer, Sebastian; Schlessinger, David; Schmidt, Carsten O.; Sehmi, Jobanpreet; Silljé, Herman H.W.; Sinagra, Gianfranco; Sinner, Moritz F.; Slowikowski, Kamil; Soliman, Elsayed Z.; Spector, Timothy D.; Spiering, Wilko; Stamatoyannopoulos, John A.; Stolk, Ronald P.; Strauch, Konstantin; Tan, Sian-Tsung; Tarasov, Kirill V.; Trinh, Bosco; Uitterlinden, Andre G.; van den Boogaard, Malou; van Duijn, Cornelia M.; van Gilst, Wiek H.; Viikari, Jorma S.; Visscher, Peter M.; Vitart, Veronique; Völker, Uwe; Waldenberger, Melanie; Weichenberger, Christian X.; Westra, Harm-Jan; Wijmenga, Cisca; Wolffenbuttel, Bruce H.; Yang, Jian; Bezzina, Connie R.; Munroe, Patricia B.; Snieder, Harold; Wright, Alan F.; Rudan, Igor; Boyer, Laurie A.; Asselbergs, Folkert W.; van Veldhuisen, Dirk J.; Stricker, Bruno H.; Psaty, Bruce M.; Ciullo, Marina; Sanna, Serena; Lehtimäki, Terho; Wilson, James F.; Bandinelli, Stefania; Alonso, Alvaro; Gasparini, Paolo; Jukema, J. Wouter; Kääb, Stefan; Gudnason, Vilmundur; Felix, Stephan B.; Heckbert, Susan R.; de Boer, Rudolf A.; Newton-Cheh, Christopher; Hicks, Andrew A.; Chambers, John C.; Jamshidi, Yalda; Visel, Axel; Christoffels, Vincent M.; Isaacs, Aaron; Samani, Nilesh J.; de Bakker, Paul I.W.

2017-01-01

BACKGROUND Myocardial mass is a key determinant of cardiac muscle function and hypertrophy. Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude and duration of the QRS complex on the electrocardiogram (ECG). Abnormal QRS amplitude or duration reflect changes in myocardial mass and conduction, and are associated with increased risk of heart failure and death. OBJECTIVES This meta-analysis sought to gain insights into the genetic determinants of myocardial mass. METHODS We carried out a genome-wide association meta-analysis of 4 QRS traits in up to 73,518 individuals of European ancestry, followed by extensive biological and functional assessment. RESULTS We identified 52 genomic loci, of which 32 are novel, that are reliably associated with 1 or more QRS phenotypes at p < 1 × 10−8. These loci are enriched in regions of open chromatin, histone modifications, and transcription factor binding, suggesting that they represent regions of the genome that are actively transcribed in the human heart. Pathway analyses provided evidence that these loci play a role in cardiac hypertrophy. We further highlighted 67 candidate genes at the identified loci that are preferentially expressed in cardiac tissue and associated with cardiac abnormalities in Drosophila melanogaster and Mus musculus. We validated the regulatory function of a novel variant in the SCN5A/SCN10A locus in vitro and in vivo. CONCLUSIONS Taken together, our findings provide new insights into genes and biological pathways controlling myocardial mass and may help identify novel therapeutic targets. PMID:27659466

Prevalence and Prognostic Value of Depression and Anxiety in Patients with Diabetic Foot Ulcers and Possibilities of their Treatment.

PubMed

Udovichenko, Oleg V; Maximova, N V; Amosova, M V; Yunilaynen, O A; Berseneva, E A; Starostina, E G

2017-01-01

Depression and anxiety can potentially influence treatment results of diabetic complications. Of our study was to explore: (1) prevalence of these disorders in patients with diabetic foot ulcers (DFU); (2) possible risk factors of depression and anxiety; (3) possible links between ulcer treatment results and depression/anxiety status. 285 outpatients with diabetes and foot or leg ulcers were tested for depression and anxiety with self-report scales: CES-D and the anxiety subscale from HADS. Ulcer treatment results, incidence of new ulcers and number of hospital admissions were assessed after 1.5 years of follow-up. Depression was detected in 110 patients (39%), anxiety in 103 (36%). Females had depression and anxiety more often than males (48% and 46% vs. 27% and 25% respectively). A combined score based on diabetes duration, insulin treatment, history of myocardial infarction, history of foot ulcers and recent foot surgery was higher in patients with than without depression (3.0 vs. 2.0, p=0.02). Every of these or other potential risk factors alone was not associated with depression or anxiety. Patients with depression did not demonstrate poorer prognosis except higher mortality in subgroup of severely depressed patients without ulcer history. For anxiety we got similar results as its presence strongly correlated with depression. The overall prevalence of depression and anxiety in DFU patients is compatible with other diabetic populations. Various parameters of ulcer severity and duration did not influence the probability of depression and anxiety occurrence. Depression in general was not associated with poorer ulcer treatment results. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Pattern of myocardial 99mTc-HMDP uptake and impact on myocardial function in patients with transthyretin cardiac amyloidosis.

PubMed

Pradel, Sarah; Brun, Stéphanie; Victor, Gérard; Pascal, Pierre; Fournier, Pauline; Ribes, David; Lavie-Badie, Yoan; Galinier, Michel; Carrié, Didier; Berry, Isabelle; Lairez, Olivier

2018-06-07

The purpose of the study was to describe the pattern of 99m Tc-labeled phosphate agents myocardial uptake by scintigraphy and explore its impact on left ventricular (LV) functions in transthyretin cardiac amyloidosis (TTR-CA). Fifty patients with TTR-CA underwent 99m Tc- hydroxymethylene-diphosphonate ( 99m Tc-HMDP) scintigraphy and echocardiography with measure of LV thickness, longitudinal strain (LS), systolic and diastolic functions. Cardiac retention by scintigraphy was assessed by visual scoring and the heart/whole body (H/WB) ratio was calculated by dividing counts in the heart by counts in late whole-body images. The mean population age was 79 ± 10 years. Mean H/WB ratio was 12 ± 7. Myocardial 99m Tc-HMDP uptake on segments 5, 6, 7, 8, 11, 12, 13, 14, 16, and 17 was correlated with H/WB ratio. Mean LVEF and global LS were 51 ± 10% and - 10 ± 3%, respectively. H/WB ratio was correlated with global LS (R = 0.408, P = .003), Ea (R = - 0.566, P < .001) and mean left ventricular wall thickness (R = 0.476, P < .001) but not with LVEF (R = - 0.109, P = .453). Segmental myocardial uptake was slightly correlated with segmental LS (R = 0.152, P < .001). H/WB ratio was not correlated with NT-proBNP levels (R = 0.219, P = .148) neither E/Ea ratio (R = 0.204, P = .184). These findings show the relationship between bone tracer myocardial uptake and LV functions in patients with TTR cardiac amyloidosis.

Hypercholesterolemia and Myocardial function evaluated via Tissue Doppler Imaging

PubMed Central

2009-01-01

Objective To establish a link between hypercholesterolemia and myocardial dysfunction. Background Heart failure is a complex disease involving changes in systolic and diastolic function. Newer echocardiographic imaging modalities may be able to detect discreet changes in myocardial function associated with hypercholesterolemia. Therefore we sought to establish a link between hypercholesterolemia and myocardial dysfunction with tissue Doppler imaging (TDI). Methods Twenty-seven rabbits were studied: 7 were fed normal chow (group 1) and 20 a high cholesterol diet (10 with ezetimibe, 1 mg/kg/day; group 2 and 10 without, group 3). Echocardiographic images were obtained under general anesthesia. Serum cholesterol levels were obtained at baseline, 3 and 6 months and myocardial cholesterol levels measured following euthanasia. Results Doppler measurements, including E/A, E'/A' and S' were significantly lower in group 3 compared to both groups 1 and 2 but no significant differences were noted in chamber sizes or ejection fraction among the groups. Average serum cholesterol was higher in group 3 compared to groups 1 and 2 respectively (495 ± 305 mg/dl vs. 114 ± 95 mg/dl and 87 ± 37 mg/dl; p < 0.01). Myocardial cholesterol content was also higher in group 3 compared to group 2 (0.10 ± 0.04 vs. 0.06 mg/dl ± 0.02; p = 0.05). There was significant correlation between S', E'/A', E/E' and serum cholesterol (r2 = 0.17 p = 0.04, r2 = 0.37 p = 0.001 and r2 = 0.24 p = 0.01). Conclusion Cholesterol load in the serum and myocardium was significantly associated with decreased systolic and diastolic function by TDI. Moreover, lipid lowering was protective. PMID:19943937

[Effects of hypoxic acclimatization on myocardial sarcoplasmic reticulum ATPase and 45Ca2+ uptake in rats].

PubMed

Long, Chao-liang; Zhang, Yan-fang; Yin, Zhao-yun; Wang, Hai

2005-08-01

To study the effect of acute hypoxia and hypoxic acclimatization on myocardial function of rats. Eighteen male Wistar rats were randomly divided into three groups: normoxic control, acute hypoxia and intermittent hypoxic acclimatization group (n=6). After being exposed to hypoxia (8000 m) for 4 h before and after intermittent hypoxic acclimatization (3000 m and 5000 m, 14 d respectively, 4 h/d), the rats were decapitated and then myocardial sarcoplasmic reticulum (SR) were derived from cardiac muscles. Activities of Na+, K(+)-ATPase, Ca2+, Mg2(+)-ATPase in SR, phosphorylation of phospholamban (PLB) and the ability of 45Ca2+ uptake in SR were observed in all these three groups. 1) Hypoxia had no effects on the activity of Na+, K(+)-ATPase in rats myocardial SR of rats. 2) Compared with normoxic control rats, the activity of Ca2+, Mg2(+)-ATPase in myocardial SR of rats after acute hypoxia was reduced significantly (P<0.01). After intermittent hypoxic acclimatization, its activity increased significantly as compared with that of acute hypoxic rats (P<0.01). 3) The phosphorylation of PLB in acute hypoxic rats was reduced significantly compared with normoxic control rats. After intermittent hypoxic acclimatization, its phosphorylation was increased significantly compared with that of acute hypoxic rats. It suggests that hypoxic acclimatization could alleviate the inhibition of calcium pump. 4) The ability of 45Ca2+ uptake of SR in acute hypoxic rats was decreased significantly. After hypoxic acclimatization, its ability was strengthened significantly. These results suggest that the increased function of myocardial SR calcium pump, the strengthened phosphorylation of PLB to alleviate the inhibition of calcium pump and the increased function of Ca2+ transport in SR are the mechanisms of hypoxic acclimatization protecting cardiac functions from injury induced by severe hypoxia.

[Effect and mechanism of total flavonoids of bugloss on rats with myocardial ischemia and reperfusion injury].

PubMed

Xu, Xiao-Na; Niu, Zi-Ran; Wang, Shou-Bao; Chen, Yu-Cai; Gao, Li; Fang, Lian-Hu; Du, Guan-Hua

2014-06-01

This study is to investigate the effect of total flavonoids of Uygur medicine bugloss (BTF) on rats with myocardial ischemia/reperfusion injury, and to explore the mechanisms by which it acts. Left anterior descending (LAD) coronary artery in rats was occluded for 30 min followed by 4 h reperfusion. Meanwhile, BTF dissolved in saline was administered intraperitoneally at dosage of 10, 30 and 50 mg x kg(-1). Electrocardiograph, infarction index, serum myocardial enzymes and heart function were determined to evaluate the effect of BTF. Some other observations were carried out to explore whether inhibiting inflammation and apoptosis is involved in the mechanisms underlying BTF. Our results showed that in ischemia/reperfusion injured rats BTF could dose-dependently reduce myocardial infarction index and myocardial enzyme leakage, and enhance heart function, indicating that it possesses significant cardio protection. ELISA analysis showed that BTF could decrease the content of myocardial inflammatory cytokines such as IL-1beta, IL-6 and TNF-alpha. Western-blotting confirmed that BTF could increase the expression of anti-apoptotic protein Bcl-2 and reduce the expression of proapoptosis protein Bax. Further more, the phosphorylation level of PI3K and Akt was upregulated by BTF treatment. BTF can protect rat against myocardial ischemia/reperfusion injury. Anti-inflammation and inhibition of apoptosis through upregulating PI3K/Akt signal pathway may contribute to the protective effect of BTF.

Eotaxin/CCL11 levels correlate with myocardial fibrosis and mast cell density in native and transplanted rat hearts.

PubMed

Zweifel, M; Matozan, K; Dahinden, C; Schaffner, T; Mohacsi, P

2010-09-01

Myocardial fibrosis contributes to hemodynamic and cardiac functional alterations commonly observed posttransplantation. Cardiac mast cells (MC) have been linked to fibrosis in posttransplantation hearts. Eotaxin, which has been shown to be involved in fibrogenesis, has been demonstrated to be increased in production in cardiac macrophages. The aim of our study was to correlate myocardial fibrosis during heart transplant rejection in the rat with eotaxin/chemokine [c-c motif] ligand 11 (CCL11) expression, and with various subtypes of infiltrating cardiac MC, namely connective-type MC (CTMC) and mucosa-type MC (MMC). We used tissues from 2 previous studies of ongoing acute rejection in allogeneic Brown-Norway to Lewis rat and an isogeneic Brown-Norway to Brown-Norway heterotopic heart transplantation models under cyclosporin/prednisolone immunosuppression. Collagen fibrils were stained with Masson's trichrome with myocardial fibrosis expressed as percent fibrotic area per total section area. Eotaxin/CCL11 previously measured in heart tissue using enzyme-linked immunosorbent assay (ELISA) was correlated with the extent of myocardial fibrosis. We compared values from native hearts (n = 4) as well as transplants on days 5, 16, and 28 (n = 4 in each group). The area of myocardial fibrosis was significantly increased in the allogeneic compared with the isogeneic group at day 16 (38% vs 21%) and at day 28 (49% vs 22%) after transplantation. Myocardial fibrosis correlated significantly with eotaxin/CCL11 concentrations and the density of MMC, but not with CTMC in heart tissue. Eotaxin-triggered MC infiltration of the heart may contribute to myocardial fibrosis after transplantation. Targeting eotaxin/CCL11 with monoclonal antibodies, such as bertilimumab, could reduce MC infiltration, possibly resulting in decreased myocardial fibrosis and improved contractile function after heart transplantation. 2010 Elsevier Inc. All rights reserved.

School burnout: increased sympathetic vasomotor tone and attenuated ambulatory diurnal blood pressure variability in young adult women.

PubMed

May, Ross W; Sanchez-Gonzalez, Marcos A; Fincham, Frank D

2015-01-01

Two studies examined autonomic and cardiovascular functioning that may link school burnout to cardiovascular risk factors in young healthy adult females. Study 1 (N = 136) investigated whether school burnout was related to resting values of blood pressure (BP) and blood pressure variability (BPV) through laboratory beat-to-beat BP assessment. Study 2 (N = 94) examined the link between school burnout and diurnal BPV through ambulatory BP monitoring. Controlling for anxiety and depressive symptomatology, school burnout demonstrated strong positive relationships with indices of cardiac sympathovagal tone, sympathetic vasomotor tone, inefficient myocardial oxygen consumption, increased 24-h ambulatory heart rate and BP, blunted BP diurnal variability, and increased arterial stiffness. These studies establish cardiovascular biomarkers of school burnout and suggest that even in a seemingly healthy sample school burnout may predispose females to increased cardiovascular risk. Several future lines of research are outlined.

Depression, anxiety, and the cardiovascular system: the psychiatrist's perspective.

PubMed

Roose, S P

2001-01-01

It is becoming clear that the comorbidity of depression and cardiovascular disease does not occur by chance but rather is an inevitable consequence of the relationship between the conditions. Depression in patients with cardiovascular disease is a significant risk factor for developing symptomatic and fatal ischemic heart disease. Moreover, depressed patients have a higher than expected rate of sudden cardiovascular death. Therefore, appropriate treatment of patients with depression and cardiovascular disease cannot be restricted to considerations of either depression or cardiovascular disease in isolation. The tricyclic antidepressants (TCAs) have various effects on the cardiovascular system, including Type IA antiarrhythmic activity that has been associated with an increased risk of mortality in post-myocardial infarction patients. The selective serotonin reuptake inhibitors (SSRIs) are not associated with adverse cardiac effects. The SSRI paroxetine was compared with a therapeutic level of the TCA nortriptyline in a randomized, controlled study and demonstrated a benign cardiovascular profile, while the TCA induced a significantly higher rate of serious adverse cardiovascular events. On the basis of this favorable cardiovascular profile, the SSRIs should therefore be the preferred choice for the treatment of most patients with comorbid depression and cardiovascular disease. Investigation of putative pathophysiologic mechanisms linking depression and cardiovascular mortality, such as the role of platelet activation, will form the basis for further investigation of antidepressant treatments in order to establish if the antidepressants have a beneficial effect on the prognosis of cardiovascular diseases.

[Myocardial viability: update in nuclear cardiology].

PubMed

Vallejo, Enrique

2007-01-01

Evaluation of myocardial viability with the aid of radionuclides, is a technique that offers reliable, reproducible information, with an attractive cost-benefit relationship, in the study of the myocardial viability, integrating cardiac molecular, metabolic, and functional aspects. Nowadays, coronary risk stratification in post-myocardial infarction patients pretends to locate them as low-, intermediate, and high risk-subjects that can suffer cardiovascular complications in the very near future. Low-risk patients are characterized by a cardiac-related mortality below 1%, whereas high-risk mortality is greater than 3%. Because of clinical complications following a myocardial infarction are observed during the first month of evolution, clinical guidelines suggest to evaluate the cardiovascular risk before hospital discharge.

Evaluation of left ventricular function using electrocardiographically gated myocardial SPECT with (123)I-labeled fatty acid analog.

PubMed

Nanasato, M; Ando, A; Isobe, S; Nonokawa, M; Hirayama, H; Tsuboi, N; Ito, T; Hirai, M; Yokota, M; Saito, H

2001-12-01

Electrocardiographically (ECG) gated myocardial SPECT with (99m)Tc-tetrofosmin has been used widely to assess left ventricular (LV) function. However, the accuracy of variables using ECG gated myocardial SPECT with beta-methyl-p-(123)I-iodophenylpentadecanoic acid (BMIPP) has not been well defined. Thirty-six patients (29 men, 7 women; mean age, 61.6 +/- 15.6 y) with ischemic heart disease underwent ECG gated myocardial SPECT with (123)I-BMIPP and with (99m)Tc-tetrofosmin and left ventriculography (LVG) within 1 wk. LV ejection fraction (LVEF), LV end-diastolic volume (LVEDV), and LV end-systolic volume (LVESV) were determined on gated SPECT using commercially available software for automatic data analysis. These volume-related items on LVG were calculated with an area-length method and were estimated by 2 independent observers to evaluate interobserver validity. The regional wall motion with these methods was assessed visually. LVEF was 41.1% +/- 12.5% on gated SPECT with (123)I-BMIPP, 44.5% +/- 13.1% on gated SPECT with (99m)Tc-tetrofosmin, and 46.0% +/- 12.7% on LVG. Global LV function and regional wall motion between both gated SPECT procedures had excellent correlation (LVEF, r = 0.943; LVEDV, r = 0.934; LVESV, r = 0.952; regional wall motion, kappa = 0.92). However, the correlations of global LV function and regional wall motion between each gated SPECT and LVG were significantly lower. Gated SPECT with (123)I-BMIPP showed the same interobserver validity as gated SPECT with (99m)Tc-tetrofosmin. Gated SPECT with (123)I-BMIPP provides high accuracy with regard to LV function and is sufficiently applicable for use in clinical SPECT. This technique can simultaneously reveal myocardial fatty acid metabolism and LV function, which may be useful to evaluate various cardiac diseases.

Differences between Human and Rodent Plasmacytoid Dendritic Cells May Explain the Pathogenic Disparity of Hantavirus Infection

DTIC Science & Technology

2016-06-01

cause two acute febrile diseases in humans: hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardio-pulmonary syndrome (HCPS). The purpose...of Biochemistry, School of Medicine, University of Nevada, Reno, NV, USA Hantavirus pulmonary syndrome (HPS) is an acute zoonotic disease transmitted...bling acute respiratory distress syndrome (10). Rapidly progress- ing pulmonary edema, myocardial depression, and hypovolemia are the leading cause of

Acute pancreatitis: a multisystem disease.

PubMed

Agarwal, N; Pitchumoni, C S

1993-06-01

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.

Acute Stress Disorder Symptoms Predict All-Cause Mortality Among Myocardial Infarction Patients: a 15-Year Longitudinal Study.

PubMed

Ginzburg, Karni; Kutz, Ilan; Koifman, Bella; Roth, Arie; Kriwisky, Michael; David, Daniel; Bleich, Avi

2016-04-01

Studies have recognized myocardial infarction (MI) as a risk for acute stress disorder (ASD), manifested in dissociative, intrusive, avoidant, and hyperarousal symptoms during hospitalization. This study examined the prognostic role of ASD symptoms in predicting all-cause mortality in MI patients over a period of 15 years. One hundred and ninety-three MI patients filled out questionnaires assessing ASD symptoms during hospitalization. Risk factors and cardiac prognostic measures were collected from patients' hospital records. All-cause mortality was longitudinally assessed, with an endpoint of 15 years after the MI. Of the participants, 21.8 % died during the follow-up period. The decedents had reported higher levels of ASD symptoms during hospitalization than had the survivors, but this effect became nonsignificant when adjusting for age, sex, education, left ventricular ejection fraction, and depression. A series of analyses conducted on each of the ASD symptom clusters separately indicated that-after adjusting for age, sex, education, left ventricular ejection fraction, and depression-dissociative symptoms significantly predicted all-cause mortality, indicating that the higher the level of in-hospital dissociative symptoms, the shorter the MI patients' survival time. These findings suggest that in-hospital dissociative symptoms should be considered in the risk stratification of MI patients.

Measurement of myocardial blood flow by cardiovascular magnetic resonance perfusion: comparison of distributed parameter and Fermi models with single and dual bolus.

PubMed

Papanastasiou, Giorgos; Williams, Michelle C; Kershaw, Lucy E; Dweck, Marc R; Alam, Shirjel; Mirsadraee, Saeed; Connell, Martin; Gray, Calum; MacGillivray, Tom; Newby, David E; Semple, Scott Ik

2015-02-17

Mathematical modeling of cardiovascular magnetic resonance perfusion data allows absolute quantification of myocardial blood flow. Saturation of left ventricle signal during standard contrast administration can compromise the input function used when applying these models. This saturation effect is evident during application of standard Fermi models in single bolus perfusion data. Dual bolus injection protocols have been suggested to eliminate saturation but are much less practical in the clinical setting. The distributed parameter model can also be used for absolute quantification but has not been applied in patients with coronary artery disease. We assessed whether distributed parameter modeling might be less dependent on arterial input function saturation than Fermi modeling in healthy volunteers. We validated the accuracy of each model in detecting reduced myocardial blood flow in stenotic vessels versus gold-standard invasive methods. Eight healthy subjects were scanned using a dual bolus cardiac perfusion protocol at 3T. We performed both single and dual bolus analysis of these data using the distributed parameter and Fermi models. For the dual bolus analysis, a scaled pre-bolus arterial input function was used. In single bolus analysis, the arterial input function was extracted from the main bolus. We also performed analysis using both models of single bolus data obtained from five patients with coronary artery disease and findings were compared against independent invasive coronary angiography and fractional flow reserve. Statistical significance was defined as two-sided P value < 0.05. Fermi models overestimated myocardial blood flow in healthy volunteers due to arterial input function saturation in single bolus analysis compared to dual bolus analysis (P < 0.05). No difference was observed in these volunteers when applying distributed parameter-myocardial blood flow between single and dual bolus analysis. In patients, distributed parameter modeling was able to detect reduced myocardial blood flow at stress (<2.5 mL/min/mL of tissue) in all 12 stenotic vessels compared to only 9 for Fermi modeling. Comparison of single bolus versus dual bolus values suggests that distributed parameter modeling is less dependent on arterial input function saturation than Fermi modeling. Distributed parameter modeling showed excellent accuracy in detecting reduced myocardial blood flow in all stenotic vessels.

Use of wave intensity analysis of carotid arteries in identifying and monitoring left ventricular systolic function dynamics in rabbits.

PubMed

Zhang, Hui; Zheng, Rongqin; Qian, Xiaoxian; Zhang, Chengxi; Hao, Baoshun; Huang, Zeping; Wu, Tao

2014-03-01

Wave intensity analysis (WIA) of the carotid artery was conducted to determine the changes that occur in left ventricular systolic function after administration of doxorubicin in rabbits. Each randomly selected rabbit was subject to routine ultrasound, WIA of the carotid artery, cardiac catheterization and pathologic examination every week and was followed for 16 wk. The first positive peak (WI1) of the carotid artery revealed that left ventricular systolic dysfunction occurred earlier than conventional indexes of heart function. WI1 was highly, positively correlated with the maximum rate of rise in left ventricular pressure in cardiac catheterization (r = 0.94, p < 0.01) and moderately negatively correlated with the apoptosis index of myocardial cells, an indicator of myocardial damage (r = -0.69, p < 0.01). Ultrasound WIA of the carotid artery sensitively reflects early myocardial damage and cardiac function, and the result is highly consistent with cardiac catheterization findings and the apoptosis index of myocardial cells. Copyright © 2014 World Federation for Ultrasound in Medicine & Biology. Published by Elsevier Inc. All rights reserved.

Intravenously Delivered Mesenchymal Stem Cells: Systemic Anti-Inflammatory Effects Improve Left Ventricular Dysfunction in Acute Myocardial Infarction and Ischemic Cardiomyopathy.

PubMed

Luger, Dror; Lipinski, Michael J; Westman, Peter C; Glover, David K; Dimastromatteo, Julien; Frias, Juan C; Albelda, M Teresa; Sikora, Sergey; Kharazi, Alex; Vertelov, Grigory; Waksman, Ron; Epstein, Stephen E

2017-05-12

Virtually all mesenchymal stem cell (MSC) studies assume that therapeutic effects accrue from local myocardial effects of engrafted MSCs. Because few intravenously administered MSCs engraft in the myocardium, studies have mainly utilized direct myocardial delivery. We adopted a different paradigm. To test whether intravenously administered MSCs reduce left ventricular (LV) dysfunction both post-acute myocardial infarction and in ischemic cardiomyopathy and that these effects are caused, at least partly, by systemic anti-inflammatory activities. Mice underwent 45 minutes of left anterior descending artery occlusion. Human MSCs, grown chronically at 5% O 2 , were administered intravenously. LV function was assessed by serial echocardiography, 2,3,5-triphenyltetrazolium chloride staining determined infarct size, and fluorescence-activated cell sorting assessed cell composition. Fluorescent and radiolabeled MSCs (1×10 6 ) were injected 24 hours post-myocardial infarction and homed to regions of myocardial injury; however, the myocardium contained only a small proportion of total MSCs. Mice received 2×10 6 MSCs or saline intravenously 24 hours post-myocardial infarction (n=16 per group). At day 21, we harvested blood and spleens for fluorescence-activated cell sorting and hearts for 2,3,5-triphenyltetrazolium chloride staining. Adverse LV remodeling and deteriorating LV ejection fraction occurred in control mice with large infarcts (≥25% LV). Intravenous MSCs eliminated the progressive deterioration in LV end-diastolic volume and LV end-systolic volume. MSCs significantly decreased natural killer cells in the heart and spleen and neutrophils in the heart. Specific natural killer cell depletion 24 hours pre-acute myocardial infarction significantly improved infarct size, LV ejection fraction, and adverse LV remodeling, changes associated with decreased neutrophils in the heart. In an ischemic cardiomyopathy model, mice 4 weeks post-myocardial infarction were randomized to tail-vein injection of 2×10 6 MSCs, with injection repeated at week 3 (n=16) versus PBS control (n=16). MSCs significantly increased LV ejection fraction and decreased LV end-systolic volume. Intravenously administered MSCs for acute myocardial infarction attenuate the progressive deterioration in LV function and adverse remodeling in mice with large infarcts, and in ischemic cardiomyopathy, they improve LV function, effects apparently modulated in part by systemic anti-inflammatory activities. © 2017 American Heart Association, Inc.

Myocardial 2D strain echocardiography and cardiac biomarkers in children during and shortly after anthracycline therapy for acute lymphoblastic leukaemia (ALL): a prospective study.

PubMed

Mavinkurve-Groothuis, Annelies M C; Marcus, Karen A; Pourier, Milanthy; Loonen, Jacqueline; Feuth, Ton; Hoogerbrugge, Peter M; de Korte, Chris L; Kapusta, Livia

2013-06-01

The aim of this study was to investigate myocardial 2D strain echocardiography and cardiac biomarkers in the assessment of cardiac function in children with acute lymphoblastic leukaemia (ALL) during and shortly after treatment with anthracyclines. Cardiac function of 60 children with ALL was prospectively studied with measurements of cardiac troponin T (cTnT) and N-terminal-pro-brain natriuretic peptide (NT-pro-BNP) and conventional and myocardial 2D strain echocardiography before start (T = 0), after 3 months (T = 1), and after 1 year (T = 2), and were compared with 60 healthy age-matched controls. None of the patients showed clinical signs of cardiac failure or abnormal fractional shortening. Cardiac function decreased significantly during treatment and was significantly decreased compared with normal controls. Cardiac troponin T levels were abnormal in 11% of the patients at T = 1 and were significantly related to increased time to global peak systolic longitudinal strain at T = 2 (P = 0.003). N-terminal-pro-brain natriuretic peptide levels were abnormal in 13% of patients at T = 1 and in 20% at T = 2, absolute values increased throughout treatment in 59%. Predictors for abnormal NT-pro-BNP at T = 2 were abnormal NT-pro-BNP at T = 0 and T = 1, for abnormal myocardial 2D strain parameters at T = 2 cumulative anthracycline dose and z-score of the diastolic left ventricular internal diameter at baseline. Children with newly diagnosed ALL showed decline of systolic and diastolic function during treatment with anthracyclines using cardiac biomarkers and myocardial 2D strain echocardiography. N-terminal-pro-brain natriuretic peptide levels were not related to echocardiographic strain parameters and cTnT was not a predictor for abnormal strain at T = 2.Therefore, the combination of cardiac biomarkers and myocardial 2D strain echocardiography is important in the assessment of cardiac function of children with ALL treated with anthracyclines.

The value of fractional and coronary flow reserve in predicting myocardial recovery in patients with previous myocardial infarction.

PubMed

Beleslin, Branko; Ostojic, Miodrag; Djordjevic-Dikic, Ana; Vukcevic, Vladan; Stojkovic, Sinisa; Nedeljkovic, Milan; Stankovic, Goran; Orlic, Dejan; Milic, Natasa; Stepanovic, Jelena; Giga, Vojislav; Saponjski, Jovica

2008-11-01

The aim of the study was to evaluate the relation between fractional flow reserve (FFR) and simultaneously evaluated coronary flow reserve by thermodilution (CFRthermo), with the improvement of left ventricular (LV) function in patients with previous myocardial infarction (MI) undergoing percutaneous coronary intervention (PCI). Study population consisted of 46 patients (mean age 53 +/- 7 years; 36 male) with previous MI and significant coronary stenosis undergoing PCI of infarct-related coronary artery. In all patients, we evaluated FFR and CFRthermo by single pressure/thermo wire during maximal hyperaemia before and immediately after PCI. We performed echocardiographic assessment of LV ejection fraction before and 6 months after PCI. Dobutamine stress echocardiography test was also performed before PCI. LV functional improvement was observed in 33/46 (72%) of patients. In patients with LV functional recovery in comparison with patients with no recovery, there was a significant difference in FFR before PCI (0.56 +/- 0.14 vs. 0.70 +/- 0.07, P < 0.001), improvement of FFR (0.35 +/- 0.14 vs. 0.21 +/- 0.07, P < 0.001), improvement of CFRthermo (1.3 +/- 0.6 vs. 0.5 +/- 0.3, P < 0.001), and CFRthermo after PCI (2.6 +/- 0.7 vs. 2.0 +/- 0.4, P < 0.001). When only parameters evaluated before PCI were taken into account, FFR before angioplasty (P = 0.001) and dobutamine-assessed viability (P = 0.006) were the most significant multivariate predictors of myocardial recovery. When all significant univariate parameters were evaluated, the most significant independent predictors for improvement in myocardial function were the improvement of CFRthermo during angioplasty (P < 0.001) and FFR before angioplasty (P = 0.002). Simultaneous evaluation of FFR and CFRthermo provide significant complementary data on the improvement in myocardial function in patients with previous MI. However, the evaluation of FFR before angioplasty identifies viable myocardium that may recover following revascularization and may be used as an alternative to non-invasive testing.

Early Left and Right Ventricular Response to Aortic Valve Replacement.

PubMed

Duncan, Andra E; Sarwar, Sheryar; Kateby Kashy, Babak; Sonny, Abraham; Sale, Shiva; Alfirevic, Andrej; Yang, Dongsheng; Thomas, James D; Gillinov, Marc; Sessler, Daniel I

2017-02-01

The immediate effect of aortic valve replacement (AVR) for aortic stenosis on perioperative myocardial function is unclear. Left ventricular (LV) function may be impaired by cardioplegia-induced myocardial arrest and ischemia-reperfusion injury, especially in patients with LV hypertrophy. Alternatively, LV function may improve when afterload is reduced after AVR. The right ventricle (RV), however, experiences cardioplegic arrest without benefiting from improved loading conditions. Which of these effects on myocardial function dominate in patients undergoing AVR for aortic stenosis has not been thoroughly explored. Our primary objective is thus to characterize the effect of intraoperative events on LV function during AVR using echocardiographic measures of myocardial deformation. Second, we evaluated RV function. In this supplementary analysis of 100 patients enrolled in a clinical trial (NCT01187329), 97 patients underwent AVR for aortic stenosis. Of these patients, 95 had a standardized intraoperative transesophageal echocardiographic examination of systolic and diastolic function performed before surgical incision and repeated after chest closure. Echocardiographic images were analyzed off-line for global longitudinal myocardial strain and strain rate using 2D speckle-tracking echocardiography. Myocardial deformation assessed at the beginning of surgery was compared with the end of surgery using paired t tests corrected for multiple comparisons. LV volumes and arterial blood pressure decreased, and heart rate increased at the end of surgery. Echocardiographic images were acceptable for analysis in 72 patients for LV strain, 67 for LV strain rate, and 54 for RV strain and strain rate. In 72 patients with LV strain images, 9 patients required epinephrine, 22 required norepinephrine, and 2 required both at the end of surgery. LV strain did not change at the end of surgery compared with the beginning of surgery (difference: 0.7 [97.6% confidence interval, -0.2 to 1.5]%; P = 0.07), whereas LV systolic strain rate improved (became more negative) (-0.3 [-0.4 to -0.2] s; P < 0.001). In contrast, RV systolic strain worsened (became less negative) at the end of surgery (difference: 4.6 [3.1 to 6.0]%; P < 0.001) although RV systolic strain rate was unchanged (0.0 [97.6% confidence interval, -0.1 to 0.1]; P = 0.83). LV function improved after replacement of a stenotic aortic valve demonstrated by improved longitudinal strain rate. In contrast, RV function, assessed by longitudinal strain, was reduced.

Epicardial FSTL1 reconstitution regenerates the adult mammalian heart.

PubMed

Wei, Ke; Serpooshan, Vahid; Hurtado, Cecilia; Diez-Cuñado, Marta; Zhao, Mingming; Maruyama, Sonomi; Zhu, Wenhong; Fajardo, Giovanni; Noseda, Michela; Nakamura, Kazuto; Tian, Xueying; Liu, Qiaozhen; Wang, Andrew; Matsuura, Yuka; Bushway, Paul; Cai, Wenqing; Savchenko, Alex; Mahmoudi, Morteza; Schneider, Michael D; van den Hoff, Maurice J B; Butte, Manish J; Yang, Phillip C; Walsh, Kenneth; Zhou, Bin; Bernstein, Daniel; Mercola, Mark; Ruiz-Lozano, Pilar

2015-09-24

The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans.

Cortistatin Improves Cardiac Function After Acute Myocardial Infarction in Rats by Suppressing Myocardial Apoptosis and Endoplasmic Reticulum Stress.

PubMed

Shi, Zhi-Yu; Liu, Yue; Dong, Li; Zhang, Bo; Zhao, Meng; Liu, Wen-Xiu; Zhang, Xin; Yin, Xin-Hua

2016-04-18

The endoplasmic reticulum (ER) stress-induced apoptotic pathway is associated with the development of acute myocardial infarction (AMI). Cortistatin (CST) is a novel bioactive peptide that inhibits apoptosis-related injury. Therefore, we investigated the cardioprotective effects and potential mechanisms of CST in a rat model of AMI. Male Wistar rats were randomly divided into sham, AMI, and AMI + CST groups. Cardiac function and the degree of infarction were evaluated by echocardiography, cardiac troponin I activity, and 2,3,5-triphenyl-2H-tetrazolium chloride staining after 7 days. The expression of CST, ER stress markers, and apoptotic markers was examined using immunohistochemistry and Western blotting. Compared to the AMI group, the AMI + CST group exhibited markedly better cardiac function and a lower degree of infarction. Electron microscopy and terminal deoxynucleotidyl transferase dUTP nick end labeling confirmed that myocardial apoptosis occurred after AMI. Cortistatin treatment reduced the expression of caspase 3, cleaved caspase 3, and Bax (proapoptotic proteins) and promoted the expression of Bcl-2 (antiapoptotic protein). In addition, the reduced expression of glucose-regulated protein 94 (GRP94), glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding proteins homologous protein, and caspase 12 indicated that ER stress and the apoptotic pathway associated with ER stress were suppressed. Exogenous CST has a notable cardioprotective effect after AMI in a rat model in that it improves cardiac function by suppressing ER stress and myocardial apoptosis. © The Author(s) 2016.

Biventricular assist device for scombroid poisoning with refractory myocardial dysfunction: a bridge to recovery.

PubMed

Grinda, Jean-Michel; Bellenfant, Florence; Brivet, François Gilles; Carel, Yvan; Deloche, Alain

2004-09-01

We report the usefulness of biventricular mechanical circulatory support in a 36-yr-old woman with refractory myocardial dysfunction resulting from scombroid poisoning. Case report. Medical and surgical university care units. A previously healthy 36-yr-old woman with severe myocardial dysfunction unresponsive to epinephrine (1.3 microg/kg/min) and dobutamine (18 microg/kg/min) after the ingestion of cooked fresh tuna. Implantation at day 3 of a biventricular assist device consisting of two paracorporeal pneumatic pumps set at 70 beats/min to reach an output of 5.6 L/min during 8 days. The biventricular mechanical circulatory assist device allowed weaning of the inotropic drugs, maintenance of end-organ function, and support of the patient until myocardial recovery. The patient was successfully explanted 11 days after ingestion. Cardiac function had totally recovered, but a stroke was noted. At 3-yrs follow-up, there was no cardiac or neurologic sequela. This report describes severe myocardial dysfunction secondary to scombroid poisoning and demonstrates the usefulness of a mechanical circulatory assist device as a bridge to recovery.

[Oxygen-transporting function of the blood circulation system in sevoflurane anesthesia during myocardial revascularization under extracorporeal circulation].

PubMed

Skopets, A A; Lomivorotov, V V; Karakhalis, N B; Makarov, A A; Duman'ian, E S; Lomivorotova, L V

2009-01-01

The purpose of the study was to evaluate the efficiency of oxygen-transporting function of the circulatory system under sevoflurane anesthesia during myocardial revascularization operations under extracorporeal circulation. Twenty-five patients with coronary heart disease were examined. Mean blood pressure, heart rate, cardiac index, total peripheral vascular resistance index, pulmonary pressure, pulmonary wedge pressure, and central venous pressure were measured. Arterial and mixed venous blood oxygen levels, oxygen delivery and consumption index, arteriovenous oxygen difference, and glucose and lactate concentrations were calculated. The study has demonstrated that sevoflurane is an effective and safe anesthetic for myocardial revascularization operations in patients with coronary heart disease. The use of sevoflurane contributes to steady-state oxygen-transporting function of the circulatory system at all surgical stages.

Relationship of biomarkers of extracellular matrix with myocardial function in Type 2 diabetes mellitus.

PubMed

Liu, Ju-Hua; Chen, Yan; Zhen, Zhe; Ho, Lai-Ming; Tsang, Anita; Yuen, Michele; Lam, Karen; Tse, Hung-Fat; Yiu, Kai-Hang

2017-07-01

The study evaluated the relationship of extracellular matrix and renin angiotensin system with myocardial dysfunction in Type 2 diabetes mellitus. All patients underwent resting and exercise echocardiography, including conventional parameters, E/E' ratio, global longitudinal strain and diastolic function reserve index. Plasma matrix metalloproteinase-1, TIMP-1, amino-terminal propeptide of type I and type III procollagen and renin angiotensin system activity were measured. As patients with diastolic dysfunction had a higher plasma level of TIMP-1 and propeptide of type III procollagen than those with no diastolic dysfunction. After multivariate adjustment, TIMP-1 associated with E/E' (both at rest and stress) and diastolic function reserve index. TIMP-1 is independently associated with myocardial diastolic dysfunction in patients with Type 2 diabetes mellitus.

The role of a structured exercise training program on cardiac structure and function after acute myocardial infarction: study protocol for a randomized controlled trial.

PubMed

Fontes-Carvalho, Ricardo; Sampaio, Francisco; Teixeira, Madalena; Gama, Vasco; Leite-Moreira, Adelino F

2015-03-12

Exercise training is effective in improving functional capacity and quality of life in patients with coronary artery disease, but its effects on left ventricular systolic and diastolic function are controversial. Diastolic dysfunction is a major determinant of adverse outcome after myocardial infarction and, contrary to systolic function, no therapy or intervention has proved to significantly improve diastolic function. Data from animal studies and from patients with diastolic heart failure has suggested that exercise training can have a positive effect on diastolic function parameters. This trial aims to evaluate if a structured exercise training program can improve resting left ventricular diastolic and systolic function in patients who have had an acute myocardial infarction. This is a phase II, prospective, randomized, open-label, blinded-endpoint trial that will include at least 96 consecutive patients who have had an acute myocardial infarction one month previously. Patients will be randomized (1:1) to an exercise training program or a control group, receiving standard of care. At enrolment, and at the end of the follow-up period, patients will be submitted to an echocardiography (with detailed assessment of diastolic and systolic function using recent consensus guidelines), cardiopulmonary exercise testing, an anthropometric assessment, blood testing, and clinical evaluation. Patients randomized to the intervention group will be submitted to an eight-week outpatient exercise program, combining endurance and resistance training, for three sessions per week. The primary endpoint will be the change in lateral E' velocity immediately after the eight-week exercise training program. Secondary endpoints will include other echocardiographic parameters of left ventricular diastolic and systolic function, cardiac structure, metabolic and inflammation biomarkers (high-sensitivity C-reactive protein and pro-BNP), functional capacity (peak oxygen consumption and anaerobic threshold) and anthropometric measurements. New strategies that can improve left ventricular diastolic function are clinically needed. This will be the first trial to evaluate, in patients who have had an acute myocardial infarction, the effects of a structured program of exercise training on diastolic and systolic function, assessed by novel echocardiographic parameters. Registered with ClinicalTrials.gov (reference: NCT02224495 ) on 21 August 2014.

The Role of Echocardiography in Coronary Artery Disease and Acute Myocardial Infarction

PubMed Central

Esmaeilzadeh, Maryam; Parsaee, Mozhgan; Maleki, Majid

2013-01-01

Echocardiography is a non-invasive diagnostic technique which provides information regarding cardiac function and hemodynamics. It is the most frequently used cardiovascular diagnostic test after electrocardiography and chest X-ray. However, in a patient with acute chest pain, Transthoracic Echocardiography is essential both for diagnosing acute coronary syndrome, zeroing on the evaluation of ventricular function and the presence of regional wall motion abnormalities, and for ruling out other etiologies of acute chest pain or dyspnea, including aortic dissection and pericardial effusion. Echocardiography is a versatile imaging modality for the management of patients with chest pain and assessment of left ventricular systolic function, diastolic function, and even myocardial and coronary perfusion and is, therefore, useful in the diagnosis and triage of patients with acute chest pain or dyspnea. This review has focused on the current applications of echocardiography in patients with coronary artery disease and myocardial infarction. PMID:23646042

Caffeine reduces dipyridamole-induced myocardial ischemia

DOE Office of Scientific and Technical Information (OSTI.GOV)

Smits, P.; Aengevaeren, W.R.; Corstens, F.H.

1989-10-01

The mechanism of action of coronary vasodilation after dipyridamole may be based on inhibition of cellular uptake of circulating endogenous adenosine. Since caffeine has been reported to be a competitive antagonist of adenosine we studied the effect of caffeine on the outcome of dipiridamole-{sup 201}Tl cardiac imaging in one patient. During caffeine abstinence dipyridamole induced myocardial ischemia with down-slope ST depressions on the ECG, and reversible perfusion defects on the scintigrams. When the test was repeated 1 wk later on similar conditions, but now shortly after infusion of caffeine (4 mg/kg), the ECG showed nodepressions, and the scintigrams only slightmore » signs of ischemia. We conclude that when caffeine abstinence is not sufficient, the widespread use of coffee and related products may be responsible for false-negative findings in dipyridamole-201Tl cardiac imaging.« less

Quantitative myocardial perfusion from static cardiac and dynamic arterial CT

NASA Astrophysics Data System (ADS)

Bindschadler, Michael; Branch, Kelley R.; Alessio, Adam M.

2018-05-01

Quantitative myocardial blood flow (MBF) estimation by dynamic contrast enhanced cardiac computed tomography (CT) requires multi-frame acquisition of contrast transit through the blood pool and myocardium to inform the arterial input and tissue response functions. Both the input and the tissue response functions for the entire myocardium are sampled with each acquisition. However, the long breath holds and frequent sampling can result in significant motion artifacts and relatively high radiation dose. To address these limitations, we propose and evaluate a new static cardiac and dynamic arterial (SCDA) quantitative MBF approach where (1) the input function is well sampled using either prediction from pre-scan timing bolus data or measured from dynamic thin slice ‘bolus tracking’ acquisitions, and (2) the whole-heart tissue response data is limited to one contrast enhanced CT acquisition. A perfusion model uses the dynamic arterial input function to generate a family of possible myocardial contrast enhancement curves corresponding to a range of MBF values. Combined with the timing of the single whole-heart acquisition, these curves generate a lookup table relating myocardial contrast enhancement to quantitative MBF. We tested the SCDA approach in 28 patients that underwent a full dynamic CT protocol both at rest and vasodilator stress conditions. Using measured input function plus single (enhanced CT only) or plus double (enhanced and contrast free baseline CT’s) myocardial acquisitions yielded MBF estimates with root mean square (RMS) error of 1.2 ml/min/g and 0.35 ml/min/g, and radiation dose reductions of 90% and 83%, respectively. The prediction of the input function based on timing bolus data and the static acquisition had an RMS error compared to the measured input function of 26.0% which led to MBF estimation errors greater than threefold higher than using the measured input function. SCDA presents a new, simplified approach for quantitative perfusion imaging with an acquisition strategy offering substantial radiation dose and computational complexity savings over dynamic CT.

Nuclear medicine in the management of patients with heart failure: guidance from an expert panel of the International Atomic Energy Agency (IAEA)

PubMed Central

Peix, Amalia; Mesquita, Claudio Tinoco; Paez, Diana; Pereira, Carlos Cunha; Felix, Renata; Gutierrez, Claudia; Jaimovich, Rodrigo; Ianni, Barbara Maria; Soares, Jose; Olaya, Pastor; Rodriguez, Ma. Victoria; Flotats, Albert; Giubbini, Raffaele; Travin, Mark

2014-01-01

Heart failure is increasing worldwide at epidemic proportions, resulting in considerable disability, mortality, and increase in healthcare costs. Gated myocardial perfusion single photon emission computed tomography or PET imaging is the most prominent imaging modality capable of providing information on global and regional ventricular function, the presence of intraventricular synchronism, myocardial perfusion, and viability on the same test. In addition, 123I-mIBG scintigraphy is the only imaging technique approved by various regulatory agencies able to provide information regarding the adrenergic function of the heart. Therefore, both myocardial perfusion and adrenergic imaging are useful tools in the workup and management of heart failure patients. This guide is intended to reinforce the information on the use of nuclear cardiology techniques for the assessment of heart failure and associated myocardial disease. PMID:24781009

Cyclooxygenases, microsomal prostaglandin E synthase-1, and cardiovascular function

PubMed Central

Cheng, Yan; Wang, Miao; Yu, Ying; Lawson, John; Funk, Colin D.; FitzGerald, Garret A.

2006-01-01

We investigated the mechanisms by which inhibitors of prostaglandin G/H synthase-2 (PGHS-2; known colloquially as COX-2) increase the incidence of myocardial infarction and stroke. These inhibitors are believed to exert both their beneficial and their adverse effects by suppression of PGHS-2–derived prostacyclin (PGI2) and PGE2. Therefore, the challenge remains to identify a mechanism whereby PGI2 and PGE2 expression can be suppressed while avoiding adverse cardiovascular events. Here, selective inhibition, knockout, or mutation of PGHS-2, or deletion of the receptor for PGHS-2–derived PGI2, was shown to accelerate thrombogenesis and elevate blood pressure in mice. These responses were attenuated by COX-1 knock down, which mimics the beneficial effects of low-dose aspirin. PGE2 biosynthesis is catalyzed by the coordinate actions of COX enzymes and microsomal PGE synthase-1 (mPGES-1). We show that deletion of mPGES-1 depressed PGE2 expression, augmented PGI2 expression, and had no effect on thromboxane biosynthesis in vivo. Most importantly, mPGES-1 deletion affected neither thrombogenesis nor blood pressure. These results suggest that inhibitors of mPGES-1 may retain their antiinflammatory efficacy by depressing PGE2, while avoiding the adverse cardiovascular consequences associated with PGHS-2–mediated PGI2 suppression. PMID:16614756

Local sympathetic denervation attenuates myocardial inflammation and improves cardiac function after myocardial infarction in mice

PubMed Central

Ziegler, Karin A; Ahles, Andrea; Wille, Timo; Kerler, Julia; Ramanujam, Deepak; Engelhardt, Stefan

2018-01-01

Abstract Aims Cardiac inflammation has been suggested to be regulated by the sympathetic nervous system (SNS). However, due to the lack of methodology to surgically eliminate the myocardial SNS in mice, neuronal control of cardiac inflammation remains ill-defined. Here, we report a procedure for local cardiac sympathetic denervation in mice and tested its effect in a mouse model of heart failure post-myocardial infarction. Methods and results Upon preparation of the carotid bifurcation, the right and the left superior cervical ganglia were localized and their pre- and postganglionic branches dissected before removal of the ganglion. Ganglionectomy led to an almost entire loss of myocardial sympathetic innervation in the left ventricular anterior wall. When applied at the time of myocardial infarction (MI), cardiac sympathetic denervation did not affect acute myocardial damage and infarct size. In contrast, cardiac sympathetic denervation significantly attenuated chronic consequences of MI, including myocardial inflammation, myocyte hypertrophy, and overall cardiac dysfunction. Conclusion These data suggest a critical role for local sympathetic control of cardiac inflammation. Our model of myocardial sympathetic denervation in mice should prove useful to further dissect the molecular mechanisms underlying cardiac neural control. PMID:29186414

Two-dimensional strain echocardiography technology for evaluation of myocardial strain in swimming athletes after high-intensity exercise.

PubMed

Liang, Chen; Ma, Yun; Gao, Can; Zhang, Jianhong; Yang, Min; Chen, Gen; Fu, Shan; Zhu, Tiangang

2017-02-01

The aim of this study was to investigate the change in myocardial strain in swimming athletes before and after high-intensity exercise using two-dimensional strain echocardiography (2DSE) technology. To assess whether the local and overall myocardial function and myocardial injury are accurately measured using 2DSE technology, 15 swimming athletes were selected as research objects. We applied 2DSE technology to track the 2D ultrasound images of the apical four chambers, the apical two chambers, and the apical long axis before and after high-intensity, increasing-load exercise. We recorded indices such as the left ventricular global strain (GS) and the left ventricular segmental wall longitudinal peak systolic strain (PS) in 18 systoles and analyzed the myocardial strain change before and after exercise. After high-intensity exercise, the overall myocardial strain decreased, especially the strain of the posterior wall, posterior divider, lateral wall, lower wall, and the basal and middle segments of the anterior wall. The influence of exercise on myocardial strain was greater on the basal and middle segments than on the apical segment. One-time intensive exercise negatively affected the myocardial muscle. Myocardial muscles in the apical segment and the myocardial wall were more sensitive to intensive exercise. The 2DSE technology can precisely position the motion-sensitive areas and help locate myocardial injury. © 2017, Wiley Periodicals, Inc.

Role of cardiomyocyte circadian clock in myocardial metabolic adaptation

USDA-ARS?s Scientific Manuscript database

Marked circadian rhythmicities in cardiovascular physiology and pathophysiology exist. The cardiomyocyte circadian clock has recently been linked to circadian rhythms in myocardial gene expression, metabolism, and contractile function. For instance, the cardiomyocyte circadian clock is essential f...

Sense of coherence--a determinant of quality of life over time in older female acute myocardial infarction survivors.

PubMed

Norekvål, Tone M; Fridlund, Bengt; Moons, Philip; Nordrehaug, Jan E; Saevareid, Hans I; Wentzel-Larsen, Tore; Hanestad, Berit R

2010-03-01

To determine the relationships between different sense of coherence levels and quality of life, and in older female myocardial infarction survivors; to investigate how socio-demographic, clinical characteristics, sense of coherence self-reported symptoms and function affect quality of life; and to determine whether sense of coherence and quality of life are stable during a six-month follow-up. Myocardial infraction confers new physical and mental challenges. However, research on sense of coherence and other factors involved in maintaining physical, psychosocial and environmental aspects of quality of life in older female myocardial infraction survivors is scant. Survey. A postal survey was conducted of 145 women, aged 62-80 years, three months to five years after myocardial infarction (T1), with a follow-up after six months (T2). Self-reported socio-demographic and clinical data and hospital medical records data were collected. The sense of coherence scale (SOC-29) and the World Health Organization Quality of Life Instrument Abbreviated (WHOQOL-BREF) were used. We found a significant difference in quality of life between weak, moderate, and strong sense of coherence groups (p<0.001). Sense of coherence contributed to the level of all quality of life domains (p<0.001). Several clinical characteristics contributed to quality of life: (1) physical domain: comorbidities (p<0.001), previous myocardial infarction (p = 0.013), ejection fraction (p<0.011), length of hospital stay (p = 0.005) symptoms and function (p<0.001); (2) psychological domain: previous myocardial infarction (p = 0.031) and symptoms and function (p<0.001); and (3) environmental domain: education (p = 0.033) and symptoms and function (p = 0.003). On group level, both sense of coherence and quality of life were stable. Experiencing specific health changes (p<0.001), not major life events, influenced quality of life during the six-month follow-up. Sense of coherence was an important stable determinant of quality of life domains in female myocardial infarction survivors. Although other factors were identified, further research is needed to elucidate additional determinants of quality of life. These specific factors could guide clinicians in making treatment decisions that optimize the quality of life of their patients. Applying a salutogenic perspective through patient education may be important.

Role of cytokine hemoadsorption in cardiopulmonary bypass-induced ventricular dysfunction in a porcine model.

PubMed

Vocelka, Craig R; Jones, Krystal M; Mikhova, Krasimira M; Ebisu, Ryan M; Shar, Ashley; Kellum, John A; Verrier, Edward D; Rabkin, David G

2013-12-01

Little is known about the effect of cardiopulmonary bypass alone on cardiac function; in an attempt to illuminate this relationship and test a possible mechanism, we used Cytosorb, a device capable of removing virtually all types of circulating cytokines to test the hypothesis that hemoadsorption of cytokines during bypass attenuates bypass-induced acute organ dysfunction. Twelve Yorkshire pigs (50-65 kg) were instrumented with a left ventricular conductance catheter. Baseline mechanics and cytokine expression (tumor necrosis factor [TNF], interleukin-6 [IL-6], and interleukin-10) were measured before and hourly after 1 hour of normothermic cardiopulmonary bypass. Animals underwent bypass without (cardiopulmonary bypass [CPB], n = 6) or with (CPB+HA, n = 6) the CytosorbTM device. Data were compared with "historical" controls (n = 6) that were similarly instrumented but underwent observation instead of bypass. Five hours after separation from bypass (or observation), animals were euthanized. Myocardial water content was determined postmortem. Neither TNF nor IL-6 was significantly elevated in either experimental group versus controls at any time point. Preload recruitable stroke work and dP/dtmax were significantly depressed immediately after separation from bypass in both CPB+HA and CPB and remained depressed for the duration of the experiment. Although Tau remained unchanged, dP/dTmin was significantly diminished in both bypass groups at all time points after separation from bypass. Cytokine hemoadsorption had no effect on any measurable index of function. Differences in postmortem data were not evident between groups. One hour of normothermic CPB results in a significant and sustained decline in left ventricular function that appears unrelated to changes in cytokine expression. Because we did not appreciate a significant change in cytokine concentrations postbypass, the capacity of cytokine hemoadsorption to attenuate CPB-induced ventricular dysfunction could not be assessed.

Detailed characterization of a long-term rodent model of critical illness and recovery.

PubMed

Hill, Neil E; Saeed, Saima; Phadke, Rahul; Ellis, Matthew J; Chambers, Darren; Wilson, Duncan R; Castells, Josiane; Morel, Jerome; Freysennet, Damien G; Brett, Stephen J; Murphy, Kevin G; Singer, Mervyn

2015-03-01

To characterize a long-term model of recovery from critical illness, with particular emphasis on cardiorespiratory, metabolic, and muscle function. Randomized controlled animal study. University research laboratory. Male Wistar rats. Intraperitoneal injection of the fungal cell wall constituent, zymosan or n-saline. Following intervention, rats were followed for up to 2 weeks. Animals with zymosan peritonitis reached a clinical and biochemical nadir on day 2. Initial reductions were seen in body weight, total body protein and fat, and muscle mass. Leg muscle fiber diameter remained subnormal at 14 days with evidence of persisting myonecrosis, even though gene expression of regulators of muscle mass (e.g., MAFbx, MURF1, and myostatin) had peaked on days 2-4 but normalized by day 7. Treadmill exercise capacity, forelimb grip strength, and in vivo maximum tetanic force were also reduced. Food intake was minimal until day 4 but increased thereafter. This did not relate to appetite hormone levels with early (6 hr) rises in plasma insulin and leptin followed by persisting subnormal levels; ghrelin levels did not change. Serum interleukin-6 level peaked at 6 hours but had normalized by day 2, whereas interleukin-10 remained persistently elevated and high-density lipoprotein cholesterol persistently depressed. There was an early myocardial depression and rise in core temperature, yet reduced oxygen consumption and respiratory exchange ratio with a loss of diurnal rhythmicity that showed a gradual but incomplete recovery by day 7. This detailed physiological, metabolic, hormonal, functional, and histological muscle characterization of a model of critical illness and recovery reproduces many of the findings reported in human critical illness. It can be used to assess putative therapies that may attenuate loss, or enhance recovery, of muscle mass and function.

Acute myocardial infarction with changing axis deviation.

PubMed

Patanè, Salvatore; Marte, Filippo

2011-07-01

Changing axis deviation has been rarely reported also during atrial fibrillation or atrial flutter. Changing axis deviation has been rarely reported also during acute myocardial infarction associated with atrial fibrillation. Isolated left posterior hemiblock is a very rare finding but the evidence of transient right axis deviation with a left posterior hemiblock pattern has been reported during acute anterior myocardial infarction as related with significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery. Left anterior hemiblock development during acute inferior myocardial infarction can be an indicator of left anterior descending coronary artery lesions, multivessel coronary artery disease, and impaired left ventricular systolic function. We present a case of changing axis deviation in a 62-year-old Italian man with acute myocardial infarction. Also this case focuses attention on changing axis deviation during acute myocardial infarction. Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.

Cannabidiol Protects against Doxorubicin-Induced Cardiomyopathy by Modulating Mitochondrial Function and Biogenesis.

PubMed

Hao, Enkui; Mukhopadhyay, Partha; Cao, Zongxian; Erdélyi, Katalin; Holovac, Eileen; Liaudet, Lucas; Lee, Wen-Shin; Haskó, György; Mechoulam, Raphael; Pacher, Pál

2015-01-06

Doxorubicin (DOX) is a widely used, potent chemotherapeutic agent; however, its clinical application is limited because of its dose-dependent cardiotoxicity. DOX's cardiotoxicity involves increased oxidative/nitrative stress, impaired mitochondrial function in cardiomyocytes/endothelial cells and cell death. Cannabidiol (CBD) is a nonpsychotropic constituent of marijuana, which is well tolerated in humans, with antioxidant, antiinflammatory and recently discovered antitumor properties. We aimed to explore the effects of CBD in a well-established mouse model of DOX-induced cardiomyopathy. DOX-induced cardiomyopathy was characterized by increased myocardial injury (elevated serum creatine kinase and lactate dehydrogenase levels), myocardial oxidative and nitrative stress (decreased total glutathione content and glutathione peroxidase 1 activity, increased lipid peroxidation, 3-nitrotyrosine formation and expression of inducible nitric oxide synthase mRNA), myocardial cell death (apoptotic and poly[ADP]-ribose polymerase 1 [PARP]-dependent) and cardiac dysfunction (decline in ejection fraction and left ventricular fractional shortening). DOX also impaired myocardial mitochondrial biogenesis (decreased mitochondrial copy number, mRNA expression of peroxisome proliferator-activated receptor γ coactivator 1-alpha, peroxisome proliferator-activated receptor alpha, estrogen-related receptor alpha), reduced mitochondrial function (attenuated complex I and II activities) and decreased myocardial expression of uncoupling protein 2 and 3 and medium-chain acyl-CoA dehydrogenase mRNA. Treatment with CBD markedly improved DOX-induced cardiac dysfunction, oxidative/nitrative stress and cell death. CBD also enhanced the DOX-induced impaired cardiac mitochondrial function and biogenesis. These data suggest that CBD may represent a novel cardioprotective strategy against DOX-induced cardiotoxicity, and the above-described effects on mitochondrial function and biogenesis may contribute to its beneficial properties described in numerous other models of tissue injury.

Cannabidiol Protects against Doxorubicin-Induced Cardiomyopathy by Modulating Mitochondrial Function and Biogenesis

PubMed Central

Hao, Enkui; Mukhopadhyay, Partha; Cao, Zongxian; Erdélyi, Katalin; Holovac, Eileen; Liaudet, Lucas; Lee, Wen-Shin; Haskó, György; Mechoulam, Raphael; Pacher, Pál

2015-01-01

Doxorubicin (DOX) is a widely used, potent chemotherapeutic agent; however, its clinical application is limited because of its dose-dependent cardiotoxicity. DOX’s cardiotoxicity involves increased oxidative/nitrative stress, impaired mitochondrial function in cardiomyocytes/endothelial cells and cell death. Cannabidiol (CBD) is a nonpsychotropic constituent of marijuana, which is well tolerated in humans, with antioxidant, antiinflammatory and recently discovered antitumor properties. We aimed to explore the effects of CBD in a well-established mouse model of DOX-induced cardiomyopathy. DOX-induced cardiomyopathy was characterized by increased myocardial injury (elevated serum creatine kinase and lactate dehydrogenase levels), myocardial oxidative and nitrative stress (decreased total glutathione content and glutathione peroxidase 1 activity, increased lipid peroxidation, 3-nitrotyrosine formation and expression of inducible nitric oxide synthase mRNA), myocardial cell death (apoptotic and poly[ADP]-ribose polymerase 1 [PARP]-dependent) and cardiac dysfunction (decline in ejection fraction and left ventricular fractional shortening). DOX also impaired myocardial mitochondrial biogenesis (decreased mitochondrial copy number, mRNA expression of peroxisome proliferator-activated receptor γ coactivator 1-alpha, peroxisome proliferator-activated receptor alpha, estrogen-related receptor alpha), reduced mitochondrial function (attenuated complex I and II activities) and decreased myocardial expression of uncoupling protein 2 and 3 and medium-chain acyl-CoA dehydrogenase mRNA. Treatment with CBD markedly improved DOX-induced cardiac dysfunction, oxidative/nitrative stress and cell death. CBD also enhanced the DOX-induced impaired cardiac mitochondrial function and biogenesis. These data suggest that CBD may represent a novel cardioprotective strategy against DOX-induced cardiotoxicity, and the above-described effects on mitochondrial function and biogenesis may contribute to its beneficial properties described in numerous other models of tissue injury. PMID:25569804

Remote ischemic preconditioning and endothelial function in patients with acute myocardial infarction and primary PCI.

PubMed

Manchurov, Vladimir; Ryazankina, Nadezda; Khmara, Tatyana; Skrypnik, Dmitry; Reztsov, Roman; Vasilieva, Elena; Shpektor, Alexander

2014-07-01

Remote ischemic preconditioning by transient limb ischemia reduces myocardial ischemia-reperfusion injury in patients undergoing percutaneous coronary intervention. The aim of the study we report here was to assess the effect of remote ischemic preconditioning on endothelial function in patients with acute myocardial infarction who underwent primary percutaneous coronary intervention. Forty-eight patients with acute myocardial infarction were enrolled. All participants were randomly divided into 2 groups. In Group I (n = 23), remote ischemic preconditioning was performed before primary percutaneous coronary intervention (intermittent arm ischemia-reperfusion through 4 cycles of 5-minute inflation and 5-minute deflation of a blood-pressure cuff to 200 mm Hg). In Group II (n = 25), standard percutaneous coronary intervention without preconditioning was performed. We assessed endothelial function using the flow-mediated dilation test on baseline, then within 1-3 hours after percutaneous coronary intervention, and again on days 2 and 7 after percutaneous coronary intervention. The brachial artery flow-mediated dilation results were significantly higher on the first day after primary percutaneous coronary intervention in the preconditioning group (Group I) than in the control group (Group II) (12.1% vs 0.0%, P = .03, and 11.1% vs 6.3%, P = .016, respectively), and this difference remained on the seventh day (12.3% vs 7.4%, P = .0005, respectively). We demonstrated for the first time that remote ischemic preconditioning before primary percutaneous coronary intervention significantly improves endothelial function in patients with acute myocardial infarction, and this effect remains constant for at least a week. We suppose that the improvement of endothelial function may be one of the possible explanations of the effect of remote ischemic preconditioning. Copyright © 2014 Elsevier Inc. All rights reserved.

Nitric Oxide-Related Biological Pathways in Patients with Major Depression

PubMed Central

Baranyi, Andreas; Amouzadeh-Ghadikolai, Omid; Rothenhäusler, Hans-Bernd; Theokas, Simon; Robier, Christoph; Baranyi, Maria; Koppitz, Michael; Reicht, Gerhard; Hlade, Peter; Meinitzer, Andreas

2015-01-01

Background Major depression is a well-known risk factor for cardiovascular diseases and increased mortality following myocardial infarction. However, biomarkers of depression and increased cardiovascular risk are still missing. The aim of this prospective study was to evaluate, whether nitric-oxide (NO) related factors for endothelial dysfunction, such as global arginine bioavailability, arginase activity, L-arginine/ADMA ratio and the arginine metabolites asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) might be biomarkers for depression-induced cardiovascular risk. Methods In 71 in-patients with major depression and 48 healthy controls the Global Arginine Bioavailability Ratio (GABR), arginase activity (arginine/ornithine ratio), the L-arginine/ADMA ratio, ADMA, and SDMA were determined by high-pressure liquid chromatography. Psychiatric and laboratory assessments were obtained at baseline at the time of in-patient admittance and at the time of hospital discharge. Results The ADMA concentrations in patients with major depression were significantly elevated and the SDMA concentrations were significantly decreased in comparison with the healthy controls. Even after a first improvement of depression, ADMA and SDMA levels remained nearly unchanged. In addition, after a first improvement of depression at the time of hospital discharge, a significant decrease in arginase activity, an increased L-arginine/ADMA ratio and a trend for increased global arginine bioavailability were observed. Conclusions Our study results are evidence that in patients with major depression ADMA and SDMA might be biomarkers to indicate an increased cardiovascular threat due to depression-triggered NO reduction. GABR, the L-arginine/ADMA ratio and arginase activity might be indicators of therapy success and increased NO production after remission. PMID:26581044

Recognized Obstructive Sleep Apnea is Associated With Improved In-Hospital Outcomes After ST Elevation Myocardial Infarction.

PubMed

Mohananey, Divyanshu; Villablanca, Pedro A; Gupta, Tanush; Agrawal, Sahil; Faulx, Michael; Menon, Venugopal; Kapadia, Samir R; Griffin, Brian P; Ellis, Stephen G; Desai, Milind Y

2017-07-20

Obstructive sleep apnea (OSA) is an independent risk factor for many cardiovascular conditions such as coronary artery disease, myocardial infarction, systemic hypertension, pulmonary hypertension, and stroke. However, the association of OSA with outcomes in patients hospitalized for ST-elevation myocardial infarction remains controversial. We used the nation-wide inpatient sample between 2003 and 2011 to identify patients with a primary discharge diagnosis of ST-elevation myocardial infarction and then used the International Classification of Diseases, Clinical Modification code 327.23 to identify a group of patients with OSA. The primary outcome of interest was in-hospital mortality, and secondary outcomes were in-hospital cardiac arrest, length of stay and hospital charges. Our cohort included 1 850 625 patients with ST-elevation myocardial infarction, of which 1.3% (24 623) had documented OSA. OSA patients were younger and more likely to be male, smokers, and have chronic pulmonary disease, depression, hypertension, known history of coronary artery disease, dyslipidemia, obesity, and renal failure ( P <0.001 for all). Patients with OSA had significantly decreased in-hospital mortality (adjusted odds ratio, 0.78 [95% CI, 0.73-0.84]), longer hospital stay (5.00±4.68 versus 4.85±5.96 days), and incurred greater hospital charges ($79 460.12±70 621.91 versus $62 889.91±69 124.15). There was no difference in incidence of in-hospital cardiac arrest (adjusted odds ratio, 0.93 [95% CI, 0.84-1.03]) between these 2 groups. ST-elevation myocardial infarction patients with recognized OSA had significantly decreased mortality compared with patients without OSA. Although patients with OSA had longer hospital stays and incurred greater hospital charges, there was no difference in incidence of in-hospital cardiac arrest. © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

Early reduced myocardial diastolic function in children and adolescents with type 1 diabetes mellitus a population-based study.

PubMed

Brunvand, Leif; Fugelseth, Drude; Stensaeth, Knut Håkon; Dahl-Jørgensen, Knut; Margeirsdottir, Hanna Dis

2016-05-25

Reduced diastolic myocardial function is an early sign of diabetic cardiomyopathy. The aim of this study was to test the hypothesis that children and adolescents with type 1 diabetes mellitus (T1D), but without other known complications, have early reduced diastolic myocardial function diagnosed with echocardiographic color tissue Doppler imaging (cTDI). cTDI examination was carried out in 173 T1D patients and 62 age-matched controls. The T1D-patients were 8-18 years old with (mean (SD)) diabetes duration of 5.6 (3.4) years and HbA1c of 8.4 (1.3). All were treated with either insulin pumps or 4-6 daily insulin injections. cTDI early (E') and late (A') peak diastolic velocities and systolic peak velocity were measured from the lateral, septal, anterior and posterior mitral annulus and from the lateral tricuspidal annulus. Myocardial diastolic function was reduced in the T1D-patients with higher peak A'-velocity and lower E'/A'-ratio in all registrations. Overall mean (SD) mitral E'/A'-ratio was 2.3 (0.5) in T1D and 2.7 (0.6) in the controls (p < 0001). The overall mitral E'/A'-ratio was negative associated with blood pressure (BP) and body mass index (BMI). Stratifying all participants into three groups according to BMI (<25, 25-75, >75 centile, respectively), the T1D had lower E'/A'-values in all stratified groups, except for in the highest BMI-group where both T1D and controls had the lowest E'/A'-ratio. Systolic function did not differ in any of the measurements. There were no associations with sex, diabetes duration, carotid artery intima-media-thickness, vessel elasticity or HbA1c. Diabetic children and adolescents using modern intensive insulin treatment had echocardiographic signs of reduced diastolic myocardial function despite short duration of disease. The reduced function was associated with higher BP and higher BMI.

Comparison of usefulness of N-terminal pro-brain natriuretic peptide as an independent predictor of cardiac function among admission cardiac serum biomarkers in patients with anterior wall versus nonanterior wall ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

PubMed

Haeck, Joost D E; Verouden, Niels J W; Kuijt, Wichert J; Koch, Karel T; Van Straalen, Jan P; Fischer, Johan; Groenink, Maarten; Bilodeau, Luc; Tijssen, Jan G P; Krucoff, Mitchell W; De Winter, Robbert J

2010-04-15

The purpose of the present study was to determine the prognostic value of N-terminal pro-brain natriuretic peptide (NT-pro-BNP), among other serum biomarkers, on cardiac magnetic resonance (CMR) imaging parameters of cardiac function and infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. We measured NT-pro-BNP, cardiac troponin T, creatinine kinase-MB fraction, high-sensitivity C-reactive protein, and creatinine on the patients' arrival at the catheterization laboratory in 206 patients with ST-segment elevation myocardial infarction. The NT-pro-BNP levels were divided into quartiles and correlated with left ventricular function and infarct size measured by CMR imaging at 4 to 6 months. Compared to the lower quartiles, patients with nonanterior wall myocardial infarction in the highest quartile of NT-pro-BNP (> or = 260 pg/ml) more often had a greater left ventricular end-systolic volume (68 vs 39 ml/m(2), p <0.001), a lower left ventricular ejection fraction (42% vs 54%, p <0.001), a larger infarct size (9 vs 4 g/m(2), p = 0.002), and a larger number of transmural segments (11% of segments vs 3% of segments, p <0.001). Multivariate analysis revealed that a NT-pro-BNP level of > or = 260 pg/ml was the strongest independent predictor of left ventricular ejection fraction in patients with nonanterior wall myocardial infarction compared to the other serum biomarkers (beta = -5.8; p = 0.019). In conclusion, in patients with nonanterior wall myocardial infarction undergoing primary percutaneous coronary intervention, an admission NT-pro-BNP level of > or = 260 pg/ml was a strong, independent predictor of left ventricular function assessed by CMR imaging at follow-up. Our findings suggest that NT-pro-BNP, a widely available biomarker, might be helpful in the early risk stratification of patients with nonanterior wall myocardial infarction. Copyright 2010 Elsevier Inc. All rights reserved.

Deficiency of Rac1 Blocks NADPH Oxidase Activation, Inhibits Endoplasmic Reticulum Stress, and Reduces Myocardial Remodeling in a Mouse Model of Type 1 Diabetes

PubMed Central

Li, Jianmin; Zhu, Huaqing; Shen, E; Wan, Li; Arnold, J. Malcolm O.; Peng, Tianqing

2010-01-01

OBJECTIVE Our recent study demonstrated that Rac1 and NADPH oxidase activation contributes to cardiomyocyte apoptosis in short-term diabetes. This study was undertaken to investigate if disruption of Rac1 and inhibition of NADPH oxidase would prevent myocardial remodeling in chronic diabetes. RESEARCH DESIGN AND METHODS Diabetes was induced by injection of streptozotocin in mice with cardiomyocyte-specific Rac1 knockout and their wild-type littermates. In a separate experiment, wild-type diabetic mice were treated with vehicle or apocynin in drinking water. Myocardial hypertrophy, fibrosis, endoplasmic reticulum (ER) stress, inflammatory response, and myocardial function were investigated after 2 months of diabetes. Isolated adult rat cardiomyocytes were cultured and stimulated with high glucose. RESULTS In diabetic hearts, NADPH oxidase activation, its subunits' expression, and reactive oxygen species production were inhibited by Rac1 knockout or apocynin treatment. Myocardial collagen deposition and cardiomyocyte cross-sectional areas were significantly increased in diabetic mice, which were accompanied by elevated expression of pro-fibrotic genes and hypertrophic genes. Deficiency of Rac1 or apocynin administration reduced myocardial fibrosis and hypertrophy, resulting in improved myocardial function. These effects were associated with a normalization of ER stress markers' expression and inflammatory response in diabetic hearts. In cultured cardiomyocytes, high glucose–induced ER stress was inhibited by blocking Rac1 or NADPH oxidase. CONCLUSIONS Rac1 via NADPH oxidase activation induces myocardial remodeling and dysfunction in diabetic mice. The role of Rac1 signaling may be associated with ER stress and inflammation. Thus, targeting inhibition of Rac1 and NADPH oxidase may be a therapeutic approach for diabetic cardiomyopathy. PMID:20522592

Hypothyroidism-induced myocardial damage and heart failure: an overlooked entity.

PubMed

Shuvy, Mony; Shifman, Oshrat E Tayer; Nusair, Samir; Pappo, Orit; Lotan, Chaim

2009-01-01

Hypothyroid state may induce cardiac muscle impairment such as diastolic dysfunction and abnormal relaxation time. Advanced heart failure in hypothyroid patients has been described only in severe symptomatic cases, mostly during myxedematous coma. We describe an unusual case of asymptomatic patient with hypothyroidism who presented with severely reduced cardiac function with elevated cardiac enzymes reflecting significant myocardial injury. Comprehensive evaluation for heart failure was suggestive only for long-standing untreated hypothyroidism. Endomyocadial biopsy demonstrated unique histological findings of mucopolysaccharide accumulation attributed to hypothyroid state. Asymptomatic hypothyroidism may cause severe reduction in cardiac function accompanied with elevated cardiac enzymes. To our knowledge, this is the first description of human myocardial biopsy revealing mucopolysaccharide accumulation attributed to hypothyroid state.

New radionuclide agents for cardiac imaging: Description and application

DOE Office of Scientific and Technical Information (OSTI.GOV)

Kahn, J.K.; Pippin, J.J.; Corbett, J.R.

1989-08-01

The introduction of three new radiopharmaceuticals into clinical research and practice has broadened the potential applications and scope of nuclear cardiology examinations. Technetium-99m labeled isonitrile perfusion agents have excellent imaging characteristics allowing the accurate identification of coronary artery disease. Simultaneous assessments of ventricular function are possible with these agents. Iodine-123 phenylpentadecanoic acid myocardial scintigraphy permits assessments of myocardial perfusion and fatty acid metabolism, and permits investigations of myocardial metabolism with conventional imaging equipment. Iodine-123 meta-iodobenzyl-guanidine serves as an indicator of the functional integrity of the sympathetic nervous system and permits evaluations of the effects of various disease states on catecholaminemore » handling by the heart. 58 references.« less

Quality of life declines after first ischemic stroke

PubMed Central

Dhamoon, M.S.; Moon, Y.P.; Paik, M.C.; Boden-Albala, B.; Rundek, T.; Sacco, R.L.; Elkind, M.S.V.

2010-01-01

Objectives: Quality of life (QOL) after stroke is poorly characterized. We sought to determine long-term natural history and predictors of QOL among first ischemic stroke survivors without stroke recurrence or myocardial infarction (MI). Methods: In the population-based, multiethnic Northern Manhattan Study, QOL was prospectively assessed at 6 months and annually for 5 years using the Spitzer QOL index (QLI), a 10-point scale. Functional status was assessed using the Barthel Index (BI) at regular intervals, and cognition using the Mini-Mental State Examination at 1 year. Generalized estimating equations estimated the association between patient characteristics and repeated QOL measures over 5 years. Follow-up was censored at death, recurrent stroke, or MI. Results: There were 525 incident ischemic stroke patients ≥40 years (mean age 68.6 ± 12.4 years). QLI declined after stroke (annual change −0.10, 95% confidence interval −0.17 to −0.04), after adjusting for age, sex, race-ethnicity, education, insurance, depressed mood, stroke severity, bladder continence, and stroke laterality. This decline remained when BI ≥95 was added to the model as a time-dependent covariate, and functional status also predicted QLI. Changes in QLI over time differed by insurance status (p for interaction = 0.0017), with a decline for those with Medicaid/no insurance (p < 0.0001) but not Medicare/private insurance (p = 0.98). Conclusions: In this population-based study, QOL declined annually up to 5 years after stroke among survivors free of recurrence or MI and independently of other risk factors. QLI declined more among Medicaid patients and was associated with age, mood, stroke severity, urinary incontinence, functional status, cognition, and stroke laterality. GLOSSARY BI = Barthel Index; CAD = coronary artery disease; CHF = congestive heart failure; CI = confidence interval; CUMC = Columbia University Medical Center; DM = diabetes mellitus; GEE = generalized estimating equation; HTN = hypertension; MI = myocardial infarction; MMSE = Mini-Mental State Examination; NIHSS = NIH Stroke Scale; NOMAS = Northern Manhattan Study; QOL = quality of life; QLI = quality of life index. PMID:20574034

Open-chest 31P magnetic resonance spectroscopy of mouse heart at 4.7 Tesla.

PubMed

Lee, Joseph; Hu, Qingsong; Nakamura, Yasuhiro; Wang, Xiaohong; Zhang, Xiaoliang; Zhu, Xiaohong; Chen, Wei; Yang, Qinglin; Zhang, Jianyi

2006-12-01

To develop a rapid, robust, and accurate method for assessing myocardial energetics in mice and demonstrate its applicability to mouse models of acquired and genetic heart disease. We combined surface coil localization (10-mm diameter, tunable between (1)H and (31)P, using adiabatic half-passage radiofrequency pulses) and surgery (electrocautery removal of anterior chest wall) to create an open-chest method for acquiring in vivo (31)P nuclear magnetic resonance (NMR) cardiac spectra from mice at 4.7T within 12 minutes. Normal BALB/c mice, BALB/c with myocardial infarction (MI), cardiomyocyte-restricted peroxisome proliferator-activated receptor-delta knockout (KO) (CR-PPARd(-/-)) and control loxP-flanked Ppard (Ppard(flox/flox)) mice were examined. The mean phosphocreatine (PCr)/adenosine triphosphate (ATP) ratios in control BALB/c mice, BALB/c MI mice, Ppard(flox/flox) mice, and PPAR-delta KO mice were 2.13 +/- 0.09 (N = 11), 1.35 +/- 0.07 (N = 9, P < 0.001 vs. BALB/c control), 1.92 +/- 0.09 (N = 5), and 1.31 +/- 0.12 (N = 5, P < 0.005 vs. Ppard(flox/flox) control), respectively. The significant depression of myocardial PCr/ATP we observed in these genetic/acquired models of heart disease was in accord with previous data from analogous large animal models. No NMR signal contamination from chamber blood or adjacent skeletal muscle was identified. This new technique provides cardiac (31)P spectra suitable for accurate quantitative analysis in a relatively short acquisition time, is suitable for terminal studies of mouse myocardial energy metabolism, and could be installed in virtually any NMR laboratory to study myocardial energetics in numerous mouse models of human heart disease. (c) 2006 Wiley-Liss, Inc.

Acute myocardial infarction associated with blood transfusion: case report and literature review.

PubMed

Velibey, Yalcin; Erbay, Aliriza; Ozkurt, Enver; Usta, Emrah; Akin, Filiz

2014-04-01

A 62-year old patient with a history of chronic anemia associated with malabsorption secondary to short gut syndrome, experienced acute chest pain the second hour after the transfusion of a crossmatch-compatible erythrocyte suspension. His electrocardiogram (ECG) revealed widespread ST-segment depressions and he had an elevated troponin level. Laboratory findings and physical examination did not indicate the presence of immunological or non-immunological blood transfusion reactions. Cardiac catheterization was performed and showed angiographically non-obstructive, atherosclerotic plaques and the absence of vasospasm or thrombus formation. Following antiischemic therapy his symptoms resolved completely. The ECG obtained 24 hours after the emergence of chest pain demonstrated normal sinus rhythm with no ST-T wave changes. We present a rare case of acute myocardial infarction induced following a blood transfusion. To the best of our knowledge, a few cases of acute myocardial infarction associated with blood transfusion have been formally recorded in the medical literature and the clinical experience regarding such cases is indeed quite limited. The present case is reviewed in the context of the relevant literature as a practical resource for clinical practice. Crown Copyright © 2014. Published by Elsevier Ltd. All rights reserved.

The cGMP/PKG pathway as a common mediator of cardioprotection: translatability and mechanism

PubMed Central

Inserte, Javier; Garcia-Dorado, David

2015-01-01

Cardiomyocyte cell death occurring during myocardial reperfusion (reperfusion injury) contributes to final infarct size after transient coronary occlusion. Different interrelated mechanisms of reperfusion injury have been identified, including alterations in cytosolic Ca2+ handling, sarcoplasmic reticulum-mediated Ca2+ oscillations and hypercontracture, proteolysis secondary to calpain activation and mitochondrial permeability transition. All these mechanisms occur during the initial minutes of reperfusion and are inhibited by intracellular acidosis. The cGMP/PKG pathway modulates the rate of recovery of intracellular pH, but has also direct effect on Ca2+ oscillations and mitochondrial permeability transition. The cGMP/PKG pathway is depressed in cardiomyocytes by ischaemia/reperfusion and preserved by ischaemic postconditioning, which importantly contributes to postconditioning protection. The present article reviews the mechanisms and consequences of the effect of ischaemic postconditioning on the cGMP/PKG pathway, the different pharmacological strategies aimed to stimulate it during myocardial reperfusion and the evidence, limitations and promise of translation of these strategies to the clinical practice. Overall, the preclinical and clinical evidence suggests that modulation of the cGMP/PKG pathway may be a therapeutic target in the context of myocardial infarction. PMID:25297462

Do heart failure status and psychosocial variables moderate the relationship between leisure time physical activity and mortality risk among patients with a history of myocardial infarction?

PubMed

Oosterom-Calo, Rony; Te Velde, Saskia J; Stut, Wim; Drory, Yaacov; Brug, Johannes; Gerber, Yariv

2016-10-12

Leisure time physical activity (LTPA) is inversely related to mortality risk among patients with a history of myocardial infarction (MI). The aims were to explore if heart failure (HF) status and psychosocial variables moderate the association. Participants (n = 1169) were from a multi-center prospective cohort study. Information on LTPA (none, irregular,1-150, 151-300 and >300 weekly minutes), depression, social support and other prognostic indicators were collected 10-13 years after index MI. Cox regressions were conducted, adjusting for potential confounders. In case of significant moderation by HF-status or psychosocial variables, stratified analyses were performed. During follow-up (M = 8.4 years), 25.6 % of the sample had died. LTPA was inversely associated with mortality (p for trend < 0.01 in all models). HF did not, but psychosocial variables did, moderate the association. In the LTPA category 1-150 weekly minutes, patients with a high level of depression had a lower mortality risk in comparison to those with a low level (hazard ratios (95 % confidence intervals) were 0.43 (0.25, 0.75) versus 0.69 (0.36, 1.32)), and patients with a low level of social support had a lower mortality risk in comparison to those with a high level (0.40 (0.21, 0.77) versus 0.71 (0.39, 1.27)). In the category >300 min, patients with a high level of social support had a lower mortality risk than those with a low level (0.38 (0.19, 0.79) versus 0.51 (0.30, 0.87)). LTPA was inversely related to mortality risk of post-MI patients. HF did not moderate the relationship; depression and social support partially did.

What does age-comparative self-rated health measure? A cross-sectional study from the Northern Sweden MONICA Project.

PubMed

Waller, Göran; Janlert, Urban; Hamberg, Katarina; Forssén, Annika

2016-05-01

Self-rated health comprehensively accounts for many health domains. Using self-ratings and a knowledge of associations with health domains might help personnel in the health care sector to understand reports of ill health. The aim of this paper was to investigate associations between age-comparative self-rated health and disease, risk factors, emotions and psychosocial factors in a general population. We based our study on population-based cross-sectional surveys performed in 1999, 2004 and 2009 in northern Sweden. Participants were 25-74 years of age and 5314 of the 7500 people invited completed the survey. Comparative self-rated health was measured on a three-grade ordinal scale by the question 'How would you assess your general health condition compared to persons of your own age?' with the alternatives 'better', 'worse' or 'similar'. The independent variables were sex, age, blood pressure, cholesterol, body mass index, self-reported myocardial infarction, stroke, diabetes, physical activity, smoking, risk of unemployment, satisfaction with economic situation, anxiety and depressive emotions, education and Karasek scale of working conditions. Odds ratios using ordinal regression were calculated. Age, sex, stroke, myocardial infarction, diabetes, body mass index, physical activity, economic satisfaction, anxiety and depressive emotions were associated with comparative self-rated health. The risk of unemployment, a tense work situation and educational level were also associated with comparative self-rated health, although they were considerably weaker when adjusted for the the other variables. Anxiety, depressive emotions, low economic satisfaction and a tense work situation were common in the population. Emotions and economic satisfaction were associated with comparative self-rated health as well as some medical variables. Utilization of the knowledge of these associations in health care should be further investigated. © 2015 the Nordic Societies of Public Health.

Characteristics and Long-Term Prognosis of Holocaust Survivors Presenting with Acute Myocardial Infarction.

PubMed

Shiyovich, Arthur; Plakht, Ygal; Belinski, Katya; Gilutz, Harel

2016-05-01

Catastrophic life events are associated with the occurrence of cardiovascular incidents and worsening of the clinical course followirg-such events. To evaluate the characteristics and long-term prognosis of Holocaust survivors presenting with acute myocardial infarction (AMI) compared to non-Holocaust survivors. Israeli Jews who were born before 1941 and had been admitted to a tertiary medical center due to AMI during the period 2002-2012 were studied. Holocaust survivors were compared with non-Holocaust survivor controls using individual age matching. Overall 305 age-matched pairs were followed for up to 10 years after AMI. We found a higher prevalence of depression (5.9% vs. 3.3%, P = 0.045) yet a similar rate of cardiovascular risk factors, non-cardiovascular co-morbidity, severity of coronary artery disease, and in-hospital complications in survivors compared to controls. Throughout the follow-up period, similar mortality rates (62.95% vs. 63.9%, P = 0.801) and reduced cumulative mortality (0.9 vs. 0.96, HR = 0.780, 95% CI 0.636-0.956, P = 0.016) were found among survivors compared to age-matched controls, respectively. However, in a multivariate analysis survival was not found to be an independent predictor of mortality, although some tendency towards reduced mortality was seen (AdjHR = 0.84, 95% CI 0.68-1.03, P = 0.094). Depression disorder was associated with a 77.9% increase in the risk for mortality. Holocaust survivors presenting with AMI were older and had a higher prevalence of depression than controls. No. excessive, and possibly even mildly improved, risk of mortality.was observed in survivors compared with controls presenting with AMI. Possibly, specific traits that are associated with surviving catastrophic events counter the excess risk of such events following AMI.

Transient myocardial tissue and function changes during a marathon in less fit marathon runners.

PubMed

Gaudreault, Valerie; Tizon-Marcos, Helena; Poirier, Paul; Pibarot, Philippe; Gilbert, Philippe; Amyot, Marc; Rodés-Cabau, Josep; Després, Jean-Pierre; Bertrand, Olivier; Larose, Eric

2013-10-01

Although regular physical activity improves health, strenuous exercise might transiently increase cardiac risk. Training and fitness might provide protection. We prospectively studied 20 recreational marathon runners without known cardiovascular disease or symptoms: at peak training before, immediately after, and 3 months after a 42.2-km marathon. Changes in global/segmental myocardial function, edema, resting perfusion, and fibrosis were measured. At peak training, runners exercised 8.1 ± 2.3 hours and 62 ± 18 km per week with mean maximal oxygen consumption (VO2max) of 53.2 ± 8.3 mL/kg/min. In response to the marathon, global left ventricular and right ventricular ejection fraction decreased in half of the runners; these runners had poorer peak training distance, training time, and fitness level. Change in global left ventricular ejection fraction was associated with VO2max. Overall, 36% of segments developed edema, 53% decreased function, and 59% decreased perfusion. Significant agreement was observed between segment decreasing function, decreasing perfusion, and developing edema. Myocardial changes were reversible at 3 months. Completing a marathon leads to localized myocardial edema, diminished perfusion, and decreased function occurring more extensively in less trained and fit runners. Although reversible, these changes might contribute to the transient increase in cardiac risk reported during sustained vigorous exercise. Copyright © 2013 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction

PubMed Central

Russell, Richard O.; Rackley, Charles E.; Pombo, Jaoquin; Hunt, David; Potanin, Constantine; Dodge, Harold T.

1970-01-01

Left ventricular performance in 19 patients with acute myocardial infarction has been evaluated by measuring left ventricular response in terms of cardiac output, stroke volume, work, and power to progressive elevation of filling pressure accomplished by progressive expansion of blood volume with rapid infusion of low molecular weight dextran. Such infusion can elevate the cardiac output, stroke volume, work, and power and thus delineate the function of the left ventricle by Frank-Starling function curves. Left ventricular filling pressure in the range of 20-24 mm Hg was associated with the peak of the curves and when the filling pressure exceeded this range, the curves became flattened or decreased. An increase in cardiac output could be maintained for 4 or more hr. Patients with a flattened function curve had a high mortality in the ensuing 8 wk. The function curve showed improvement in myocardial function during the early convalescence. When left ventricular filling pressure is monitored directly or as pulmonary artery end-diastolic pressure, low molecular weight dextran provides a method for assessment of left ventricular function. Images PMID:5431663

What can we learn about treating heart failure from the heart's response to acute exercise? Focus on the coronary microcirculation.

PubMed

Heinonen, Ilkka; Sorop, Oana; de Beer, Vincent J; Duncker, Dirk J; Merkus, Daphne

2015-10-15

Coronary microvascular function and cardiac function are closely related in that proper cardiac function requires adequate oxygen delivery through the coronary microvasculature. Because of the close proximity of cardiomyocytes and coronary microvascular endothelium, cardiomyocytes not only communicate their metabolic needs to the coronary microvasculature, but endothelium-derived factors also directly modulate cardiac function. This review summarizes evidence that the myocardial oxygen balance is disturbed in the failing heart because of increased extravascular compressive forces and coronary microvascular dysfunction. The perturbations in myocardial oxygen balance are exaggerated during exercise and are due to alterations in neurohumoral influences, endothelial function, and oxidative stress. Although there is some evidence from animal studies that the myocardial oxygen balance can partly be restored by exercise training, it is largely unknown to what extent the beneficial effects of exercise training include improvements in endothelial function and/or oxidative stress in the coronary microvasculature and how these improvements are impacted by risk factors such as diabetes, obesity, and hypercholesterolemia. Copyright © 2015 the American Physiological Society.

MicroRNA-133 overexpression promotes the therapeutic efficacy of mesenchymal stem cells on acute myocardial infarction.

PubMed

Chen, Yueqiu; Zhao, Yunfeng; Chen, Weiqian; Xie, Lincen; Zhao, Zhen-Ao; Yang, Junjie; Chen, Yihuan; Lei, Wei; Shen, Zhenya

2017-11-25

Our study aim was to evaluate the therapeutic efficacy and mechanisms of miR-133-overexpressing mesenchymal stem cells (MSCs) on acute myocardial infarction. Rat MSCs were isolated and purified by whole bone marrow adherent culturing. After transfection with the agomir or antagomir of miR-133, MSCs were collected for assay of cell vitality, apoptosis, and cell cycle progression. At the same time, exosomes were isolated from the supernatant to analyze the paracrine miR-133. For in-vivo studies, constitutive activation of miR-133 in MSCs was achieved by lentivirus-mediated miR-133 overexpression. A rat myocardial infarction model was created by ligating the left anterior descending coronary artery, while control MSCs (vector-MSCs) or miR-133-overexpressed MSCs (miR-133-MSCs) were injected into the zone around the myocardial infarction. Subsequently, myocardial function was evaluated by echocardiography on days 7 and 28 post infarction. Finally the infarcted hearts were collected on days 7 and 28 for myocardial infarct size measurement and detection of snail 1 expression. Hypoxia-induced apoptosis of MSCs obviously reduced, along with enhanced expression of total poly ADP-ribose polymerase protein, after miR-133 agomir transfection, while the apoptosis rate increased in MSCs transfected with miR-133 antagomir. However, no change in cell viability and cell-cycle distribution was observed in control, miR-133-overexpressed, and miR-133-interfered MSCs. Importantly, rats transplanted with miR-133-MSCs displayed more improved cardiac function after acute myocardial infarction, compared with those that received vector-MSC injection. Further studies indicated that cardiac expression of snail 1 was significantly repressed by adjacent miR-133-overexpressing MSCs, and both the inflammatory level and the infarct size decreased in miR-133-MSC-injected rat hearts. miR-133-MSCs obviously improved cardiac function in a rat model of myocardial infarction. Transplantation of miR-133-overexpressing MSCs provides an effective strategy for cardiac repair and modulation of cardiac-related diseases.

[Psychological stress and sudden death].

PubMed

Pignalberi, Carlo; Ricci, Renato; Santini, Massimo

2002-10-01

Recent studies provide relevant evidence that psychological stress significantly influences the pathogenesis of sudden cardiac death. Psychological stress expresses a situation of imbalance, derived from a real or perceived disparity between environmental demands and the individual's ability to cope with these demands. A situation of psychological stress may include different components: personality factors and character traits, anxiety and depression, social isolation and acute or chronic adverse life events. In particular, it has been documented that a sudden extremely hard event, such as an earthquake or a war strike, can significantly increase the incidence of sudden death. Nevertheless, each one of these factors, if not present, can balance a partially unfavorable situation; this overview suggests a multifactorial situation where almost all elements are present and in which the relative influence of each one varies according to the individual examined. Sudden death occurs when a transient disruption (such as acute myocardial ischemia, platelet activation or neuroendocrine variations), occurring in a patient with a diseased myocardium (such as one with a post-necrotic scar or hypertrophy), triggers a malignant arrhythmia. Psychological stress acts at both levels: by means of a "chronic" action it contributes to create the myocardial background, while by means of an acute action it can create the transient trigger precipitating sudden death. In the chronic action two possible mechanisms can be detected: the first is a direct interaction, which contributes to cause a hypertension status or to exacerbate coronary atherosclerosis consequent to endothelial dysfunction; the second one acts through adverse health behaviors, such as a poor diet, alcohol consumption or smoking. In case of acute psychological stress, the mechanisms involved are mainly the ability to trigger myocardial ischemia, to promote arrhythmogenesis, to stimulate platelet function, and to increase blood viscosity. Finally, some individuals have a sympathetic nervous system hyper-responsitivity, manifesting as exaggerated heart rate and blood pressure responses which result in accelerated atherosclerosis.

[The cardioprotective effects of ischemic postconditioning on myocardial interstitium following ischemic/reperfusion in rats].

PubMed

Lu, Yan-Zhen; Wang, Jia; Zhang, Cui-Ying; Song, Juan; Li, Bao-Hong; Song, Xiao-Liang

2014-09-01

To investigate the effects of ischemic postconditioning (IPTC) on the changes of matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) protein and mRNA levels in rat heart subjected to ischemia/reperfusion, and explore the mechanism by which IPTC protects myocardial interstitium following ischemic/reperfusion (I/R). Twenty four healthy male SD rats were randomly divided into 3 groups (n = 8): sham control (SC) group, I/R group and IPTC group. The parameters of left ventricular function including left ventricular systolic pressure (LVSP) and its derivate (±dp/dt) were measured; the amount of myocardial collagen contents was determined by hydroxyproline quantification; the plasma activity of creatine kinase (CK) and lactate dehydrogenase (LDH) was detected; the protien levels of MMP-2 and TIMP-2 was measured by Western blot and the mRNA levels of MMP-2 and TIMP-2 was detected by real-time PCR. The myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were significantly decreased in I/R group compared with those of SC group, wherease the activities of CK and LDH in the plasma and the protein and mRNA levels of MMP-2 were significantly enhanced in I/R group when compared to SC group. Compared with I/R group, the myocardial collagen contents, left ventricular function and the protein and mRNA levels of TIMP-2 were increased in IPTC group, the activities of CK and LDH in the plasma and the protein and mRNA level of MMP-2 were decreased in IPTC group. These findings indicate that IPTC has protective effects on myocardial interstitial after the myocardial ischemia/reperfusion injury, and IPTC may exert its cardioprotectve effect via inhibiting MMP-2 and enhancing TIMP-2 expression in cardiac muscle.

Early diagnosis of interferon-induced myocardial disorder in patients with chronic hepatitis C: evaluation by myocardial imaging with 123I-BMIPP.

PubMed

Kondo, Y; Yukinaka, M; Nomura, M; Nakaya, Y; Ito, S

2000-01-01

Interferon (IFN) therapy for chronic hepatitis C is sometimes associated with cardiac complications. In the present study, we performed myocardial imaging with 123I-labeled beta-methyl-p-iodophenylpentadecanoic acid (123I-BMIPP) in order to evaluate myocardial disorders caused by IFN. We studied 40 healthy subjects (H group) and 25 patients with chronic hepatitis C who had been treated with IFN (IFN group). A Holter electrocardiogram (ECG) was performed and the autonomic nervous function was assessed by analyzing the spectral variability and 1/f fluctuation of heart rate. Myocardial planner imaging with 123I-BMIPP was performed to obtain the time activity curve for 20min immediately after administration of 123I-BMIPP (dynamic study). Early and delayed myocardial single photon emission computed tomography (SPECT) images were expressed as Bull's eyes and the myocardium was divided into four segments to calculate the washout rate for each segment on early and late SPECT images (early and late SPECT study). No significant differences in autonomic nervous function were observed between the two groups in heart rate variability. In a dynamic study, the reduction rate from the time activity curve was significantly higher in the IFN group compared with the H group (reduction rate, IFN group, 5.3 +/- 3.7% vs H group, 1.2 +/- 3.3%; P < 0.05). In the early and delayed myocardial SPECT study, the washout rate for the IFN group was significantly increased in all myocardial areas compared to that in the H group. However, the metabolic disorder of fatty acids caused by IFN was reversed on the second 123I-BMIPP myocardial scintigraphy examination several months after IFN therapy. These results indicate that metabolic disorders of fatty acids caused by IFN therapy can be detected before abnormalities are observed by Holter-ECG or echocardiography.

The effect of perioperative insulin treatment on cardiodepression in mild adiposity in mice.

PubMed

Boly, Chantal A; Eringa, Etto C; Bouwman, R Arthur; van den Akker, Rob F P; de Man, Frances S; Schalij, Ingrid; Loer, Stephan A; Boer, Christa; van den Brom, Charissa E

2016-09-20

While most studies focus on cardiovascular morbidity following anesthesia and surgery in excessive obesity, it is unknown whether these intraoperative cardiovascular alterations also occur in milder forms of adiposity without type 2 diabetes and if insulin is a possible treatment to improve intraoperative myocardial performance. In this experimental study we investigated whether mild adiposity without metabolic alterations is already associated with cardiometabolic dysfunction during anesthesia, mechanical ventilation and surgery and whether these myocardial alterations can be neutralized by intraoperative insulin treatment. Mice were fed a western (WD) or control diet (CD) for 4 weeks. After metabolic profiling, mice underwent general anesthesia, mechanical ventilation and surgery. Cardiac function was determined with echocardiography and left-ventricular pressure-volume analysis. Myocardial perfusion was determined with contrast-enhanced echocardiography. WD-fed mice were subsequently treated with insulin by hyperinsulinemic euglycemic clamping followed by the same measurements of cardiac function and perfusion. Western-type diet feeding led to a 13 % increase in bodyweight, (p < 0.0001) and increased adipose tissue mass, without metabolic alterations. Despite this mild phenotype, WD-fed mice had decreased systolic and diastolic function (end-systolic elastance was 2.0 ± 0.5 versus 4.1 ± 2.4 mmHg/μL, p = 0.01 and diastolic beta was 0.07 ± 0.03 versus 0.04 ± 0.01 mmHg/μL, p = 0.02) compared to CD-fed mice. Ventriculo-arterial coupling and myocardial perfusion were decreased by 48 % (p = 0.003) and 43 % (p = 0.03) respectively. Insulin treatment in WD-fed mice improved echo-derived systolic function (fractional shortening 42 ± 5 % to 46 ± 3, p = 0.05), likely due to decreased afterload, but there was no effect on load-independent measures of systolic function or myocardial perfusion. However, there was a trend towards improved diastolic function after insulin treatment (43 % improvement, p = 0.05) in WD-fed mice. Mild adiposity without metabolic alterations already affected cardiac function and perfusion during anesthesia, mechanical ventilation and surgery in mice. Intraoperative insulin may be beneficial to reduce afterload and enhance intraoperative ventricular relaxation, but not to improve ventricular contractility or myocardial perfusion.

Increase in mean platelet volume in patients with myocardial bridge.

PubMed

Bilen, Emine; Tanboga, Ibrahim Halil; Kurt, Mustafa; Kocak, Umran; Ayhan, Huseyin; Keles, Telat; Bozkurt, Engin

2013-01-01

Myocardial bridge is associated with atherosclerosis altered in shear stress and endothelial dysfunction. Mean platelet volume (MPV), a determinant of platelet activation, is shown to be related with atherosclerosis and endothelial dysfunction. In this study, we aimed to evaluate platelet function assessed by MPV in patients with myocardial bridge. Forty-two patients with myocardial bridge in the left anterior descending artery (LAD) and 43 age- and gender-matched healthy participants were included in the study. Myocardial bridging was defined as an intramyocardial systolic compression or milking of a segment of an epicardial coronary artery on angiography. For the entire study population, MPV was measured using an automatic blood counter. The study population consisted of 42 patients with myocardial bridge (52.7 ± 10.2, 76.2% male) and 43 age- and sex-matched healthy control participants (52.1 ± 10.4, 74.4% male). Compared to the control group, MPV value was significantly higher in patients with myocardial bridge (8.9 ± 1.24 vs 8.3 ± 0.78; P = .01). Further, there were no significant differences between groups regarding hemoglobin level, platelet count, fasting blood glucose, and creatinine levels. Our study findings indicated that myocardial bridge is associated with elevated MPV values. Our results might partly explain the increased cardiovascular events in patients with myocardial bridge.

Titanium dioxide nanoparticle-induced cytotoxicity and the underlying mechanism in mouse myocardial cells

NASA Astrophysics Data System (ADS)

Zhou, Yingjun; Hong, Fashui; Wang, Ling

2017-11-01

Exposure to fine particulate matter (PM) is known to cause cardiovascular disease. While extensive research has focused on the risk of atmospheric PM to public health, particularly heart disease, limited studies to date have attempted to clarify the molecular mechanisms underlying myocardial cell damage caused by exposure to titanium dioxide nanoparticles (TiO2 NPs). Data from the current investigation showed that TiO2 NPs are deposited in myocardial mitochondria via the blood circulation accompanied by obvious ultrastructural changes and impairment of mitochondrial structure and function in mouse myocardial cells, including reduction in mitochondrial membrane potential and ATP production, aggravation of oxidative stress along with increased levels of reactive oxygen species, malondialdehyde and protein carbonyl, and decreased glutathione content and enzymatic activities, including superoxide dismutase and glutathione peroxidase. Furthermore, TiO2 NPs induced a significant decrease in the activities of complex I, complex II, complex III, complex IV, succinate dehydrogenase, NADH oxidase, Ca2+-ATPase, Na+/K+-ATPase, and Ca2+/Mg2+-ATPase, and upregulation of cytokine expression (including cytochrome c, caspase-3, and p-JNK) in mitochondria-mediated apoptosis while downregulating Bcl-2 expression in mouse myocardial cells. Our results collectively indicate that chronic exposure to TiO2 NPs induces damage in mitochondrial structure and function as well as mitochondria-mediated apoptosis in mouse myocardial cells, which may be closely associated with heart disease in animals and humans.

Assessment of diastolic function by tissue Doppler echocardiography: comparison with standard transmitral and pulmonary venous flow

NASA Technical Reports Server (NTRS)

Farias, C. A.; Rodriguez, L.; Garcia, M. J.; Sun, J. P.; Klein, A. L.; Thomas, J. D.

1999-01-01

The objective of this study was to determine the utility of Doppler tissue echocardiography in the evaluation of diastolic filling and in discriminating between normal subjects and those with various stages of diastolic dysfunction. We measured myocardial velocities in 51 patients with various stages of diastolic dysfunction and in 27 normal volunteers. The discriminating power of each of the standard Doppler indexes of left ventricular filling, pulmonary venous flow, and myocardial velocities was determined with the use of Spearman rank correlation and analysis of variance F statistics. Early diastolic myocardial velocity (E(m)) was higher in normal subjects (16.0 +/- 3.8 cm/s) than in patients with either delayed relaxation (n = 15, 7.5 +/- 2.2 cm/s), pseudonormal filling (n = 26, 7.6 +/- 2.3 cm/s), or restrictive filling (n = 10, 7.4 +/- 2.4 cm/s, P <.0001). E(m ) was the best single discriminator between control subjects and patients with diastolic dysfunction (P =.7, F = 64.5). Myocardial velocities assessed by Doppler tissue echocardiography are useful in differentiating patients with normal from those with abnormal diastolic function. Myocardial velocity remains reduced even in those stages of diastolic dysfunction characterized by increased preload compensation.

Development of bioartificial myocardium using stem cells and nanobiotechnology templates.

PubMed

Chachques, Juan Carlos

2010-12-29

Cell-based regenerative therapy is undergoing experimental and clinical trials in cardiology, in order to limit the consequences of decreased contractile function and compliance of damaged ventricles following myocardial infarction. Over 1000 patients have been treated worldwide with cell-based procedures for myocardial regeneration. Cellular cardiomyoplasty seems to reduce the size and fibrosis of infarct scars, limit adverse postischemic remodelling, and improve diastolic function. The development of a bioartificial myocardium is a new challenge; in this approach, tissue-engineered procedures are associated with cell therapy. Organ decellularization for bioscaffolds fabrication is a new investigated concept. Nanomaterials are emerging as the main candidates to ensure the achievement of a proper instructive cellular niche with good drug release/administration properties. Investigating the electrophysiological properties of bioartificial myocardium is the challenging objective of future research, associating a multielectrode network to provide electrical stimulation could improve the coupling of grafted cells and scaffolds with host cardiomyocytes. In summary, until now stem cell transplantation has not achieved clear hemodynamic benefits for myocardial diseases. Supported by relevant scientific background, the development of myocardial tissue engineering may constitute a new avenue and hope for the treatment of myocardial diseases.

Chronic exposure to cocaine binging predisposes to an accelerated course of dilated cardiomyopathy in conscious dogs following rapid ventricular pacing.

PubMed

Parikh, Pratik; Nikolaidis, Lazaros A; Stolarski, Carol; Shen, You-Tang; Shannon, Richard P

2005-12-01

Despite extensive study, the extent to which cocaine use predisposes to cardiac injury remains unknown. We hypothesized that chronic cocaine binging would increase susceptibility to a subsequent cardiac insult, even in the absence of demonstrable effects on baseline hemodynamics. We studied progression of dilated cardiomyopathy (DCM) induced by rapid ventricular pacing (240 beats per minute) in five conscious, chronically instrumented dogs, after exposure to repetitive cocaine binging (COC) in the form of four consecutive 1 mg/kg i.v. boluses daily for 8 days, to simulate human cocaine abuse. We compared the results with nine control dogs (CON) undergoing the exact pacing protocol, without prior cocaine exposure. Baseline hemodynamics were not significantly altered by chronic cocaine exposure. Following 2 weeks of pacing, COC dogs exhibited accelerated progression to DCM, depressed plasma nitric oxide levels (CON, 17 +/- 2 microM; COC, 10 +/- 2 microM, p < 0.05), and a significantly greater increase in plasma epinephrine (CON, 33 +/- 6 pg/ml; COC, 104 +/- 24 pg/ml). After only 2 weeks of pacing, COC dogs demonstrated progressive DCM of a magnitude comparable with end-stage pacing-induced DCM. Chronic cocaine binging increases susceptibility to a subsequent myocardial insult and accelerates progression of DCM in conscious dogs following rapid pacing. These data suggest that although chronic cocaine use alone may not affect myocardial function, it predisposes to greater susceptibility to a superimposed insult.

Evaluation of prescription of exercise, for rehabilitation of coronary artery disease patients by myocardial scintigraphy.

PubMed

Meneghelo, Romeu S; Magalhães, Hélio M; Smanio, Paola E P; Fuchs, Angela R C N; Ferraz, Almir S; Buchler, Rica D D; Buglia, Susimeire; Mastrocolla, Luiz E; Thom, Anneliese F

2008-10-01

It is advisable that the intensity of the exercises for rehabilitation of patients with coronary artery disease does not cause myocardial ischemia. Compare the capacity of myocardial tomographic scintigraphy with the electrocardiogram capacity in ischemia detection during rehabilitation session. Twenty six patients with coronary artery disease, undergoing the rehabilitation program and with previous scintigraphy, with transient hypo-uptake have been administered a new injection of MIBI-Tc-99m during a training session when they were also monitored with dynamic electrocardiography. The rest scintigraphies, after ergometric treadmill test and rehabilitation session, were assessed in a semi-quantitative way using scores from 0 to 4 to classify each one of the chosen segments (0 = normal; 1 = discrete hypo-uptake; 2 = moderate; 3 = intense; 4 = lack of uptake). The means of the total scores found were: at rest = 12.9; after treadmill test = 19.3; after rehabilitation session = 15.1. There were statistically significant differences among them. An individual assessment showed that in 14 cases (53.8 %) hypo-uptake to some degree was identified during rehabilitation and in 12 cases (46.6%) it was not. Monitoring with the Holter system didn't show in any of the cases a ST segment depression equal or greater than 1mm. The exercises prescribed for patients with coronary artery disease, according to recommendations found in the literature, may trigger myocardial ischemia, assessed by scintigraphy during a rehabilitation session.

Febuxostat pretreatment attenuates myocardial ischemia/reperfusion injury via mitochondrial apoptosis.

PubMed

Wang, Shulin; Li, Yunpeng; Song, Xudong; Wang, Xianbao; Zhao, Cong; Chen, Aihua; Yang, Pingzhen

2015-07-02

Febuxostat is a selective inhibitor of xanthine oxidase (XO). XO is a critical source of reactive oxygen species (ROS) during myocardial ischemia/reperfusion (I/R) injury. Inhibition of XO is therapeutically effective in I/R injury. Evidence suggests that febuxostat exerts antioxidant effects by directly scavenging ROS. The present study was performed to investigate the effects of febuxostat on myocardial I/R injury and its underlying mechanisms. We utilized an in vivo mouse model of myocardial I/R injury and an in vitro neonatal rat cardiomyocyte (NRC) model of hypoxia/reoxygenation (H/R) injury. Mice were randomized into five groups: Sham, I/R (I/R + Vehicle), I/R + FEB (I/R + febuxostat), AL + I/R (I/R + allopurinol) and FEB (febuxostat), respectively. The I/R + FEB mice were pretreated with febuxostat (5 mg/kg; i.p.) 24 and 1 h prior to I/R. NRCs received febuxostat (1 and 10 µM) at 24 and 1 h before exposure to hypoxia for 3 h followed by reoxygenation for 3 h. Cardiac function, myocardial infarct size, serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH), and myocardial apoptotic index (AI) were measured in order to ascertain the effects of febuxostat on myocardial I/R injury. Hypoxia/reperfusion (H/R) injury in NRCs was examined using MTT, LDH leakage assay and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The underlying mechanisms were determined by measuring ROS production, mitochondrial membrane potential (ΔΨm), and expression of cytochrome c, cleaved caspases as well as Bcl-2 protein levels. Myocardial I/R led to an elevation in the myocardial infarct size, serum levels of CK and LDH, cell death and AI. Furthermore, I/R reduced cardiac function. These changes were significantly attenuated by pretreatment with febuxostat and allopurinol, especially by febuxostat. Febuxostat also protected the mitochondrial structure following myocardial I/R, inhibited H/R-induced ROS generation, stabilized the ΔΨm, alleviated cytosolic translocation of mitochondrial cytochrome C, inhibited activation of caspase-3 and -9, upregulated antiapoptotic proteins and downregulated proapoptotic proteins. This study revealed that febuxostat pretreatment mediates the cardioprotective effects against I/R and H/R injury by inhibiting mitochondrial-dependent apoptosis.

Quantitative evaluation of collateral circulation in patients with previous myocardial infarction: relation to myocardial ischemia, angiographic appearance and functional improvement of myocardium.

PubMed

Vukcevic, Vladan; Beleslin, Branko; Ostojic, Miodrag; Stojkovic, Sinisa; Stankovic, Goran; Nedeljkovic, Milan; Orlic, Dejan; Djordjevic-Dikic, Ana; Stepanovic, Jelena; Giga, Vojislav; Arandjelovic, Aleksandra; Dikic, Miodrag; Kostic, Jelena; Nedeljkovic, Ivana; Nedeljkovic-Beleslin, Biljana; Saponjski, Jovica

2009-04-01

Evaluation of coronary pressures during angioplasty may functionally quantify collateral circulation. The aim of the study was to evaluate the relation between the amount of collateral circulation and development of myocardial ischemia during balloon occlusion, anatomic degree of collaterals, and functional improvement of myocardium. Study population consisted of 31 pts (mean age 53 +/- 7 years; 25 male) with previous myocardial infarction and significant one-vessel stenosis undergoing angioplasty. Collateral circulation was calculated as the ratio between distal coronary pressure during balloon occlusion (P(w)) and aortic pressure (P(a)). Angiographic appearance of collaterals was evaluated by Rentrop classification. Patients were evaluated by echo for functional improvement of myocardium in the follow-up period. Mean P(w)/P(a) was 0.24 +/- 0.10 (range of 0.07-0.51). Rentrop grade 0 of collaterals was present in 16 patients (52%), grade 1 in11 patients (35%), and grade 2 in 4 patients (13%). A mild correlation between angio and hemodynamic evaluation of collaterals was observed (r = 0.38, P = 0.035). In patients without ECG changes during angioplasty (21 pts, 68%), P(w)/P(a) was significantly higher in comparison to patients with ECG changes (0.28 +/- 0.09 vs. 0.15 +/- 0.06, P < 0.001; area under the curve 0.93). In patients with myocardial functional improvement during follow-up (21 pts, 68%), P(w)/P(a) was significantly higher than in the patients without echo improvement (0.26 +/- 0.10 vs. 0.18 +/- 0.08, P = 0.035). The amount of recruitable collaterals is not negligible even in the patients with no angio visible collaterals. Low values of P(w)/P(a) are associated with ECG changes during balloon occlusion. Higher P(w)/P(a) was associated with better functional improvement of myocardium.

Myocardial Dysfunction and Shock after Cardiac Arrest

PubMed Central

Jentzer, Jacob C.; Chonde, Meshe D.; Dezfulian, Cameron

2015-01-01

Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies. PMID:26421284

Myocardial Dysfunction and Shock after Cardiac Arrest.

PubMed

Jentzer, Jacob C; Chonde, Meshe D; Dezfulian, Cameron

2015-01-01

Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies.

[The role of the adreno-cholinergic interaction in the pulmonary hemodynamics changes following myocardial ischemia].

PubMed

Evlakhov, V I; Poiasov, I Z

2014-06-01

In acute experiments in anesthetized rabbits the pulmonary hemodynamics changes were studied following 60 s myocardial ischemia in the region of the descendent left coronary artery in control state and after the blockade of M- or N-cholinoreceptors and acetylcholine infusion. Following myocardial ischemia in control animals the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance was not changed. Following myocardial ischemia after the blockade of M-cholinoreceptors by atropine the changes of pulmonary hemodynamics were the same as in control animals, the cardiac output decreased twice as more as in control animals. Following myocardial ischemia after the blockade of N-cholinoreceptors by hexamethonium the pulmonary hemodynamics changes were the same as in the control rabbits. Following myocardial ischemia after the acetylcholine infusion the pulmonary artery flow decreased more than the cardiac output, the pulmonary vascular resistance was diminished. The disbalance of the cardiac output and pulmonary artery flow changes has revealed the significance of the adreno-cholinergic interaction in the changes of the pulmonary vessels capacitance and resistive functions following myocardial ischemia.

Evaluation of cerebral-cardiac syndrome using echocardiography in a canine model of acute traumatic brain injury.

PubMed

Qian, Rong; Yang, Weizhong; Wang, Xiumei; Xu, Zhen; Liu, Xiaodong; Sun, Bing

2015-01-01

Previous studies have confirmed that traumatic brain injury (TBI) can induce general adaptation syndrome (GAS), which subsequently results in myocardial dysfunction and damage in some patients with acute TBI; this condition is also termed as cerebral-cardiac syndrome. However, most clinicians ignore the detection and treatment of myocardial dysfunction, and instead concentrate only on the serious neural damage that is observed in acute TBI, which is one of the most important fatal factors. Therefore, clarification is urgently needed regarding the relationship between TBI and myocardial dysfunction. In the present study, we evaluated 18 canine models of acute TBI, by using real-time myocardial contrast echocardiography and strain rate imaging to accurately evaluate myocardial function and regional microcirculation, including the strain rate of the different myocardial segments, time-amplitude curves, mean ascending slope of the curve, and local myocardial blood flow. Our results suggest that acute TBI often results in cerebral-cardiac syndrome, which rapidly progresses to the serious stage within 3 days. This study is the first to provide comprehensive ultrasonic characteristics of cerebral-cardiac syndrome in an animal model of TBI.

Current Status of 3-Dimensional Speckle Tracking Echocardiography: A Review from Our Experiences

PubMed Central

Ishizu, Tomko; Aonuma, Kazutaka

2014-01-01

Cardiac function analysis is the main focus of echocardiography. Left ventricular ejection fraction (LVEF) has been the clinical standard, however, LVEF is not enough to investigate myocardial function. For the last decade, speckle tracking echocardiography (STE) has been the novel clinical tool for regional and global myocardial function analysis. However, 2-dimensional imaging methods have limitations in assessing 3-dimensional (3D) cardiac motion. In contrast, 3D echocardiography also has been widely used, in particular, to measure LV volume measurements and assess valvular diseases. Joining the technology bandwagon, 3D-STE was introduced in 2008. Experimental studies and clinical investigations revealed the reliability and feasibility of 3D-STE-derived data. In addition, 3D-STE provides a novel deformation parameter, area change ratio, which have the potential for more accurate assessment of overall and regional myocardial function. In this review, we introduced the features of the methodology, validation, and clinical application of 3D-STE based on our experiences for 7 years. PMID:25031794

Suppression of miR-34a Expression in the Myocardium Protects Against Ischemia-Reperfusion Injury Through SIRT1 Protective Pathway.

PubMed

Fu, Bi-Cheng; Lang, Ji-Lu; Zhang, Dong-Yang; Sun, Lu; Chen, Wei; Liu, Wei; Liu, Kai-Yu; Ma, Chong-Yi; Jiang, Shu-Lin; Li, Ren-Ke; Tian, Hai

2017-09-01

MicroRNA-34a (miR-34a) is expressed in the myocardium and expression is altered after myocardial injury. We investigated the effects of miR-34a on heart function after ischemia-reperfusion (IR) injury. Cardiomyocytes were isolated from neonatal rat hearts and simulated IR injury was induced in vitro. Following IR injury in rats, infarct size was measured and left ventricular (LV) function was evaluated using echocardiography. Protein expression of silent information regulator 1 (SIRT1), acetylated p53 (ac-p53), Bcl-2 and Bax, and miR-34a and SIRT1 gene levels were analyzed. miR-34a overexpression exacerbated myocardial injury by increasing apoptosis and infarct size and decreasing LV function. Suppression of miR-34a attenuated myocardial IR injury. SIRT1 was negatively regulated by miR-34a and the expression of downstream genes, such as ac-p53, Bcl-2, and Bax were altered correspondingly. Increased expression of miR-34a aggravates injury after IR; miR-34a suppression therapy may represent a new line of treatment for myocardial IR injury.

Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses

EPA Science Inventory

Acrolein is an irritating aldehyde generated during combustion of organic compounds. Altered autonomic activity has been documented following acrolein inhalation, possibly impacting myocardial synchrony and function. Given the ubiquitous nature of acrolein in the environment, we ...

Left ventricular vascular and metabolic adaptations to high-intensity interval and moderate intensity continuous training: a randomized trial in healthy middle-aged men.

PubMed

Eskelinen, Jari-Joonas; Heinonen, Ilkka; Löyttyniemi, Eliisa; Hakala, Juuso; Heiskanen, Marja A; Motiani, Kumail K; Virtanen, Kirsi; Pärkkä, Jussi P; Knuuti, Juhani; Hannukainen, Jarna C; Kalliokoski, Kari K

2016-12-01

High-intensity interval training (HIIT) has become popular, time-sparing alternative to moderate intensity continuous training (MICT), although the cardiac vascular and metabolic effects of HIIT are incompletely known. We compared the effects of 2-week interventions with HIIT and MICT on myocardial perfusion and free fatty acid and glucose uptake. Insulin-stimulated myocardial glucose uptake was decreased by training without any significantly different response between the groups, whereas free fatty acid uptake remained unchanged. Adenosine-stimulated myocardial perfusion responded differently to the training modes (change in mean HIIT: -19%; MICT: +9%; P = 0.03 for interaction) and was correlated with myocardial glucose uptake for the entire dataset and especially after HIIT training. HIIT and MICT induce similar metabolic and functional changes in the heart, although myocardial vascular hyperaemic reactivity is impaired after HIIT, and this should be considered when prescribing very intense HIIT for previously untrained subjects. High-intensity interval training (HIIT) is a time-efficient way of obtaining the health benefits of exercise, although the cardiac effects of this training mode are incompletely known. We compared the effects of short-term HIIT and moderate intensity continuous training (MICT) interventions on myocardial perfusion and metabolism and cardiac function in healthy, sedentary, middle-aged men. Twenty-eight healthy, middle-aged men were randomized to either HIIT or MICT groups (n = 14 in both) and underwent six cycle ergometer training sessions within 2 weeks (HIIT session: 4-6 × 30 s all-out cycling/4 min recovery, MICT session 40-60 min at 60% V̇O2 peak ). Cardiac magnetic resonance imaging (CMRI) was performed to measure cardiac structure and function and positron emission tomography was used to measure myocardial perfusion at baseline and during adenosine stimulation, insulin-stimulated glucose uptake (MGU) and fasting free fatty acid uptake (MFFAU). End-diastolic and end-systolic volumes increased and ejection fraction slightly decreased with both training modes, although no other changes in CMRI were observed. MFFAU and basal myocardial perfusion remained unchanged. MGU was decreased by training (HIIT from 46.5 to 35.9; MICT from 47.4 to 44.4 mmol 100 g -1  min -1 , P = 0.007 for time, P = 0.11 for group × time). Adenosine-stimulated myocardial perfusion responded differently to the training modes (change in mean HIIT: -19%; MICT: +9%; P = 0.03 for group × time interaction). HIIT and MICT induce similar metabolic and functional changes in the heart, although myocardial vascular hyperaemic reactivity is impaired after HIIT. This should be taken into account when prescribing very intense HIIT for previously untrained subjects. © 2016 The Authors. The Journal of Physiology © 2016 The Physiological Society.

Left ventricular vascular and metabolic adaptations to high‐intensity interval and moderate intensity continuous training: a randomized trial in healthy middle‐aged men

PubMed Central

Eskelinen, Jari‐Joonas; Heinonen, Ilkka; Löyttyniemi, Eliisa; Hakala, Juuso; Heiskanen, Marja A.; Motiani, Kumail K.; Virtanen, Kirsi; Pärkkä, Jussi P.; Knuuti, Juhani; Hannukainen, Jarna C.

2016-01-01

Key points High‐intensity interval training (HIIT) has become popular, time‐sparing alternative to moderate intensity continuous training (MICT), although the cardiac vascular and metabolic effects of HIIT are incompletely known.We compared the effects of 2‐week interventions with HIIT and MICT on myocardial perfusion and free fatty acid and glucose uptake.Insulin‐stimulated myocardial glucose uptake was decreased by training without any significantly different response between the groups, whereas free fatty acid uptake remained unchanged.Adenosine‐stimulated myocardial perfusion responded differently to the training modes (change in mean HIIT: –19%; MICT: +9%; P = 0.03 for interaction) and was correlated with myocardial glucose uptake for the entire dataset and especially after HIIT training.HIIT and MICT induce similar metabolic and functional changes in the heart, although myocardial vascular hyperaemic reactivity is impaired after HIIT, and this should be considered when prescribing very intense HIIT for previously untrained subjects. Abstract High‐intensity interval training (HIIT) is a time‐efficient way of obtaining the health benefits of exercise, although the cardiac effects of this training mode are incompletely known. We compared the effects of short‐term HIIT and moderate intensity continuous training (MICT) interventions on myocardial perfusion and metabolism and cardiac function in healthy, sedentary, middle‐aged men. Twenty‐eight healthy, middle‐aged men were randomized to either HIIT or MICT groups (n = 14 in both) and underwent six cycle ergometer training sessions within 2 weeks (HIIT session: 4–6 × 30 s all‐out cycling/4 min recovery, MICT session 40–60 min at 60% V˙O2 peak ). Cardiac magnetic resonance imaging (CMRI) was performed to measure cardiac structure and function and positron emission tomography was used to measure myocardial perfusion at baseline and during adenosine stimulation, insulin‐stimulated glucose uptake (MGU) and fasting free fatty acid uptake (MFFAU). End‐diastolic and end‐systolic volumes increased and ejection fraction slightly decreased with both training modes, although no other changes in CMRI were observed. MFFAU and basal myocardial perfusion remained unchanged. MGU was decreased by training (HIIT from 46.5 to 35.9; MICT from 47.4 to 44.4 mmol 100 g–1 min–1, P = 0.007 for time, P = 0.11 for group × time). Adenosine‐stimulated myocardial perfusion responded differently to the training modes (change in mean HIIT: –19%; MICT: +9%; P = 0.03 for group × time interaction). HIIT and MICT induce similar metabolic and functional changes in the heart, although myocardial vascular hyperaemic reactivity is impaired after HIIT. This should be taken into account when prescribing very intense HIIT for previously untrained subjects. PMID:27500951

Quantification of regional nonuniformity and paradoxical intramural mechanics in hypertrophic cardiomyopathy by high frame rate ultrasound myocardial strain mapping.

PubMed

Sengupta, Partho P; Mehta, Vimal; Arora, Ramesh; Mohan, Jagdish C; Khandheria, Bijoy K

2005-07-01

This study tested the hypothesis that linear mapping of regional myocardial strain comprehensively assesses variations in regional myocardial function in hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is characterized by disorganized myocardial architecture that results in spatial and temporal nonuniformity of regional function. Left ventricular deformation was quantified in 20 patients with hypertrophic cardiomyopathy and compared with 25 age- and sex-matched control subjects. Abnormalities in subendocardial strain ranged from reduced longitudinal shortening to paradoxical systolic lengthening and delayed regional longitudinal contractions that were often located in small subsegmental areas. These variations were underestimated significantly by arbitrary measurements compared with linear mapping, in which a region of interest was moved across the longitudinal length of left ventricle (difference of peak and least strain, 10.7% +/- 5.1% vs 17% +/- 5.5%; P < .001). Echocardiographic assessment of variations in regional strain requires careful mapping and may be inappropriately assessed if left ventricular segments are sampled at arbitrary focal locations.

PET measurements of myocardial blood flow post myocardial infarction: Relationship to invasive and cardiac magnetic resonance studies and potential clinical applications.

PubMed

Gewirtz, Henry

2017-12-01

This review focuses on clinical studies concerning assessment of coronary microvascular and conduit vessel function primarily in the context of acute and sub acute myocardial infarction (MI). The ability of quantitative PET measurements of myocardial blood flow (MBF) to delineate underlying pathophysiology and assist in clinical decision making in this setting is discussed. Likewise, considered are physiological metrics fractional flow reserve, coronary flow reserve, index of microvascular resistance (FFR, CFR, IMR) obtained from invasive studies performed in the cardiac catheterization laboratory, typically at the time of PCI for MI. The role both of invasive studies and cardiac magnetic resonance (CMR) imaging in assessing microvascular function, a key determinant of prognosis, is reviewed. The interface between quantitative PET MBF measurements and underlying pathophysiology, as demonstrated both by invasive and CMR methodology, is discussed in the context of optimal interpretation of the quantitative PET MBF exam and its potential clinical applications.

Prevalence of ECG changes during adenosine stress and its association with perfusion defect on myocardial perfusion scintigraphy.

PubMed

Taywade, Sameer K; Ramaiah, Vijayaraghavan L; Basavaraja, Harish; Venkatasubramaniam, Parameswaran R; Selvakumar, Job

2017-04-01

Myocardial perfusion scintigraphy (MPS) is a valuable, noninvasive imaging modality in the evaluation of patients with coronary artery disease. Adenosine stress may occasionally be associated with ECG changes. This study evaluated the strength of association between adenosine stress-related ECG changes and perfusion defects on Tc-MPS. 117 (mean age: 61.25±9.27 years; sex: men 87, women 30) patients with known/suspected coronary artery disease underwent adenosine stress MPS. ECG was monitored continuously during adenosine stress for ST-depression. On the basis of the summed difference score, reversible perfusion defects were categorized as follows: normal: less than 4, mild: 4-8, moderate: 9-13, and severe: more than 13. ST-depression was observed in 27/117 (23.1%) and reversible perfusion defects were observed in 18/27 (66.66%) patients. 2/27, 6/27, and 10/27 patients had mild, moderate, and severe ischemia, respectively. 9/27 patients had normal perfusion. ECG changes and perfusion defects showed a moderate strength of association (correlation coefficient r=0.35, P=0.006). The sensitivity, specificity, positive predictive value, and negative predictive value of ECG findings for prediction of ischemia were 35.29, 86.36, 67.67, and 63.33%, respectively. ECG changes during adenosine stress are not uncommon. It shows a moderate strength of association with reversible perfusion defects. ECG changes during adenosine merit critical evaluation of MPS findings.

Phaeochromocytoma in a 86-year-old patient presenting with reversible myocardial dysfunction.

PubMed

Szwench, Elżbieta; P Czkowska, Mariola; Marczewski, Krzysztof; Klisiewicz, Anna; Micha Owska, Ilona; Ciuba, Iwona; Januszewicz, Magdalena; Prejbisz, Aleksander; Hoffman, Piotr; Januszewicz, Andrzej

2011-12-01

BACKGROUND. Phaeochromocytomas and paragangliomas are rare, mostly benign catecholamine-producing tumours of chromaffin cells of the adrenal medulla or of extra-adrenal paraganglia. Phaeochromocytoma may occur at any age, the greatest frequency being in the fourth and fifth decades. Only on extremely rare occasions does the tumour develop in the very old patients. METHODS. We are describing an 86-year-old patient with phaeochromocytoma, presenting with reversible myocardial dysfunction. RESULTS. This very old patient with phaeochromocytoma had hypertension characterized by labile blood pressure values and increased daytime blood pressure variability. This patient exhibited reversible myocardial dysfunction suggestive for "catecholaminergic cardiomyopathy", as the complication of phaeochromocytoma. After surgical removal of the tumour, recovery of left ventricular function was documented by echocardiography showing normalization of systolic function and improvement of diastolic function. CONCLUSION. Phaeochromocytomas are rare forms of secondary hypertension, but should be considered in the differential diagnosis, regardless of age, even in very old patients.

Depression following myocardial infarction--an overseen complication with prognostic importance.

PubMed

Larsen, Karen Kjær

2013-08-01

Myocardial infarction (MI) is a severe life event that is accompanied by an increased risk of depression. Mounting evidence suggests that post-MI depression is associated with adverse outcomes, but the underlying mechanisms of this association remain unclear, and no previous studies have examined whether the mental burden of MI is so heavy that it increases the risk of suicide. Although post-MI depression is common and burdensome, the condition remains under-recognised and under-treated. The development of new strategies to improve the quality of care for people with post-MI depression requires thorough understanding of the mechanisms that influence the prognosis as well as knowledge of the present care provided. The purpose of this PhD thesis is accordingly subdivided into four specific aims: 1. To estimate the prevalence of depression in people with MI after three months, and to estimate the provided hospital-based psychosocial rehabilitation (Paper I); 2. To examine GPs' practice of screening for depression in people with MI, and to analyse whether the screening rate varied among subgroups of people with a particularly high risk of post-MI depression (Paper II); 3. To examine the association between post-MI depression and new cardiovascular events or death, taking potential mediators into account (Paper III); 4. To examine the association between MI and suicide (Paper IV). Two different study designs were employed: a population-based cohort study using data obtained from registers and questionnaires sent to MI patients and their GPs (Paper I-III); a nationwide population-based matched case-control study using data obtained from registers (Paper IV). Three months after having suffered MI, about one fifth of the patients in our study had depression according to the Hospital Anxiety and Depression Scale (HADS). Upwards of half of the patients had participated in some rehabilitation, thirty per cent had participated in psychosocial support and three per cent reported that they had been examined for depression by questionnaire during the hospital-based rehabilitation. The rate of participation in psychosocial support and examination for depression was the same for patients with or without depression at three months following MI. A good fourth of the patients' GPs stated that they had screened the patient for depression within the first year after the patient suffered an MI. Three months after the MI, the screening rate was higher among patients with a history of mental illness and among patients with anxiety or depression than among patients without these conditions. Most of the GPs who performed screening followed guidelines by asking about specific depressive symptoms. According to the HADS, depression three months after MI was associated with an increased risk of a new cardiovascular event or death. This association was partly explained by the underlying cardiac disease severity and physical inactivity, but depression remained an independent prognostic risk factor after adjusting for these potential confounders. We found a tendency towards a weaker association with increasing physical activity and among users of antidepressants. MI was strongly associated with an increased risk of suicide. This risk was particularly high immediately after the MI, but remained high for more than five years after the MI. The association between MI and suicide remained stable throughout the study period (1981-2006), although many other factors changed (e.g. suicide rate, treatment of MI). This thesis demonstrated that post-MI depression is common, under-recognized and has a strong prognostic impact. About one in five patients have depression three months after MI. Guidelines recommend screening for depression, but the guidelines have not been systematically implemented either in the hospital-based rehabilitation or in Danish general practice. In the absence of systematic screening, we found that a significant part of those who had depression were not recognized. MI increases the risk of suicide, and depression following MI impairs the overall prognosis. The thesis indicates that physical activity and antidepressants modify the adverse prognosis in patients with post-MI depression, but larger studies are needed to clarify the impact of these potential modifiers and to evaluate how they may be catered for in the treatment of post-MI patients with depression.

The helical ventricular myocardial band: global, three-dimensional, functional architecture of the ventricular myocardium.

PubMed

Kocica, Mladen J; Corno, Antonio F; Carreras-Costa, Francesc; Ballester-Rodes, Manel; Moghbel, Mark C; Cueva, Clotario N C; Lackovic, Vesna; Kanjuh, Vladimir I; Torrent-Guasp, Francisco

2006-04-01

We are currently witnessing the advent of new diagnostic tools and therapies for heart diseases, but, without serious scientific consensus on fundamental questions about normal and diseased heart structure and function. During the last decade, three successive, international, multidisciplinary symposia were organized in order to setup fundamental research principles, which would allow us to make a significant step forward in understanding heart structure and function. Helical ventricular myocardial band of Torrent-Guasp is the revolutionary new concept in understanding global, three-dimensional, functional architecture of the ventricular myocardium. This concept defines the principal, cumulative vectors, integrating the tissue architecture (i.e. form) and net forces developed (i.e. function) within the ventricular mass. Here we expose the compendium of Torrent-Guasp's half-century long functional anatomical investigations in the light of ongoing efforts to define the integrative approach, which would lead to new understanding of the ventricular form and function by linking across multiple scales of biological organization, as defined in ongoing Physiome project. Helical ventricular myocardial band of Torrent-Guasp may also, hopefully, allow overcoming some difficulties encountered in contemporary efforts to create a comprehensive mathematical model of the heart.

Cannabinoid receptor 1 inhibition improves cardiac function and remodelling after myocardial infarction and in experimental metabolic syndrome.

PubMed

Slavic, Svetlana; Lauer, Dilyara; Sommerfeld, Manuela; Kemnitz, Ulrich Rudolf; Grzesiak, Aleksandra; Trappiel, Manuela; Thöne-Reineke, Christa; Baulmann, Johannes; Paulis, Ludovit; Kappert, Kai; Kintscher, Ulrich; Unger, Thomas; Kaschina, Elena

2013-07-01

The cannabinoid receptors, CB1 and CB2, are expressed in the heart, but their role under pathological conditions remains controversial. This study examined the effect of CB1 receptor blockade on cardiovascular functions after experimental MI and in experimental metabolic syndrome. MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with the CB1 receptor antagonist rimonabant (10 mg/kg i.p. daily) started 7 days before or 6 h after MI and continued for 6 weeks. Haemodynamic parameters were measured via echocardiography and intracardiac Samba catheter. CB1 blockade improved systolic and diastolic heart function, decreased cardiac collagen and hydroxyproline content and down-regulated TGF-β1. Additionally, rimonabant decreased arterial stiffness, normalised QRS complex duration and reduced brain natriuretic peptide levels in serum. In primary cardiac fibroblasts, rimonabant decreased MMP-9 activity and TGF-β1 expression. Furthermore, rimonabant improved depressed systolic function of spontaneously hypertensive obese rats and reduced weight gain. Blocking of CB1 receptor with rimonabant improves cardiac functions in the early and late stages after MI, decreases arterial stiffness and reduces cardiac remodelling. Rimonabant also has cardioprotective actions in rats characterised by the metabolic syndrome. Inhibition of proteolysis and TGF-β1 expression and reduced collagen content by rimonabant may attenuate destruction of the extracellular matrix and decrease fibrosis after MI.

Simultaneous assessment of myocardial perfusion and function during mental stress in patients with chronic coronary artery disease.

PubMed

Arrighi, James A; Burg, Matthew; Cohen, Ira S; Soufer, Robert

2003-01-01

Mental stress (MS) is an important provocateur of myocardial ischemia in many patients with chronic coronary artery disease. The majority of laboratory assessments of ischemia in response to MS have included measurements of either myocardial perfusion or function alone. We performed this study to determine the relationship between alterations in perfusion and ventricular function during MS. Methods and results Twenty-eight patients with reversible perfusion defects on exercise or pharmacologic stress myocardial perfusion imaging (MPI) underwent simultaneous technetium 99m sestamibi single photon emission computed tomography (SPECT) MPI and transthoracic echocardiography at rest and during MS according to a mental arithmetic protocol. In all cases the MS study was performed within 4 weeks of the initial exercise or pharmacologic MPI that demonstrated ischemia. SPECT studies were analyzed visually with the use of a 13-segment model and quantitatively by semiautomated circumferential profile analysis. Echocardiograms were graded on a segmental model for regional wall motion on a 4-point scale. Of 28 patients, 18 (64%) had perfusion defects and/or left ventricular dysfunction develop during MS: 9 (32%) had myocardial perfusion defects develop, 6 (21%) had regional or global left ventricular dysfunction develop, and 3 (11%) had both perfusion defects and left ventricular dysfunction develop. The overall concordance between perfusion and function criteria for ischemia during MS was only 46%. Among 9 patients with MS-induced left ventricular dysfunction, 5 had new regional wall motion abnormalities and 4 had a global decrement in function. In patients with MS-induced ischemia by SPECT, the number of reversible perfusion defects was similar during both MS and exercise/pharmacologic stress (2.8 +/- 2.0 vs 3.5 +/- 1.8, P =.41). Hemodynamic changes during MS were similar whether patients were divided on the basis of perfusion defects or left ventricular dysfunction during MS. These data indicate the feasibility of simultaneous assessment of perfusion and function responses during MS. Flow and function responses to MS are frequently not concordant. These data suggest that MS-induced changes in perfusion may represent a different phenomenon than MS-induced changes in left ventricular function (either globally or regionally).

The Hypertensive Heart: An Integrated Understanding Informed by Imaging

PubMed Central

Raman, Subha V.

2010-01-01

Clinical sequelae of hypertension include heart failure, arrhythmias, and ischemic events, especially myocardial infarction and stroke. Recognizing the hypertensive heart has both diagnostic as well as prognostic implications. Current imaging techniques offer noninvasive approaches to detecting myocardial fibrosis, ischemia, hypertrophy, and disordered metabolism that form the substrate for hypertensive heart disease. In addition, recognition of aortopathy and atrial myopathy as contributors to myocardial disease warrant incorporation of aortic and atrial functional measurements into a comprehensive understanding of the hypertensive heart. PMID:20117376

Advanced Echocardiography in Adult Zebrafish Reveals Delayed Recovery of Heart Function after Myocardial Cryoinjury

PubMed Central

Kossack, Mandy; Juergensen, Lonny; Fuchs, Dieter; Katus, Hugo A.; Hassel, David

2015-01-01

Translucent zebrafish larvae represent an established model to analyze genetics of cardiac development and human cardiac disease. More recently adult zebrafish are utilized to evaluate mechanisms of cardiac regeneration and by benefiting from recent genome editing technologies, including TALEN and CRISPR, adult zebrafish are emerging as a valuable in vivo model to evaluate novel disease genes and specifically validate disease causing mutations and their underlying pathomechanisms. However, methods to sensitively and non-invasively assess cardiac morphology and performance in adult zebrafish are still limited. We here present a standardized examination protocol to broadly assess cardiac performance in adult zebrafish by advancing conventional echocardiography with modern speckle-tracking analyses. This allows accurate detection of changes in cardiac performance and further enables highly sensitive assessment of regional myocardial motion and deformation in high spatio-temporal resolution. Combining conventional echocardiography measurements with radial and longitudinal velocity, displacement, strain, strain rate and myocardial wall delay rates after myocardial cryoinjury permitted to non-invasively determine injury dimensions and to longitudinally follow functional recovery during cardiac regeneration. We show that functional recovery of cryoinjured hearts occurs in three distinct phases. Importantly, the regeneration process after cryoinjury extends far beyond the proposed 45 days described for ventricular resection with reconstitution of myocardial performance up to 180 days post-injury (dpi). The imaging modalities evaluated here allow sensitive cardiac phenotyping and contribute to further establish adult zebrafish as valuable cardiac disease model beyond the larval developmental stage. PMID:25853735

ST-depression in right precordial leads with inferior STEMI and occluded right coronary artery: intertwined anatomy and ischemic areas.

PubMed

De Gennaro, Luisa; Brunetti, Natale Daniele; Ruggiero, Massimo; Rutigliano, David; Locuratolo, Nicola; Di Biase, Matteo; Caldarola, Pasquale

2017-10-01

Right coronary artery (RCA) occlusion in inferior acute myocardial infarction is usually heralded by ST-elevation both in inferior and in right precordial leads. We report the case of a 68-year-old male, who presented marked ST-elevation in inferior leads, mirrored by ST-depression in anterior-septal and lateral leads. Right precordial lead electrocardiogram unexpectedly showed ST-depression V1R-V5R leads. Coronary angiography showed mid-left anterior descending (LAD) coronary near-complete occlusion with distal wrapping LAD. Left circumflex artery was not occluded, while RCA was occluded mid tract. The patient was treated with coronary angioplasty on RCA and LAD. Absence of ST-elevation in right precordial leads may be presumably explained by the presence of a large ischemic area distal to mid-LAD near-occlusive stenosis and of a long-wrapping LAD. Complex coronary anatomy and intertwined ischemic areas may underlie apparently discording electrocardiograms.

The association between major depressive disorder in childhood and risk factors for cardiovascular disease in adolescence.

PubMed

Rottenberg, Jonathan; Yaroslavsky, Ilya; Carney, Robert M; Freedland, Kenneth E; George, Charles J; Baji, Ildikó; Dochnal, Roberta; Gádoros, Júlia; Halas, Kitti; Kapornai, Krisztina; Kiss, Eniko; Osváth, Viola; Varga, Hedvig; Vetró, Agnes; Kovacs, Maria

2014-02-01

Depression in adults is associated with risk factors for cardiovascular disease (CVD). It is unclear, however, when the association between clinical depression and cardiac risk factors develops or how early in life this association can be detected. In an ongoing study of pediatric depression, we compared CVD risk factors including smoking, obesity, physical activity level, sedentary behavior, and parental history of CVD across three samples of adolescents: probands with established histories of childhood-onset major depressive disorder (n = 210), never-depressed siblings of probands (n = 195), and controls with no history of any major psychiatric disorder (n = 161). When assessed during adolescence, 85% of the probands were not in a major depressive episode. Nevertheless, at that assessment, probands had a higher prevalence of regular smoking (odds ratio [OR] = 12.54, 95% confidence interval [CI] = 4.36-36.12) and were less physically active than controls (OR = 0.59, CI = 0.43-0.81) and siblings (OR = 0.70, CI = 0.52-0.94) and had a higher rate of obesity than did controls (OR = 3.67, CI = 1.42-9.52). Parents of probands reported high rates of CVD (significantly higher than did parents of controls), including myocardial infarction and CVD-related hospitalization (ORs = 1.62-4.36, CIs = 1.03-15.40). Differences in CVD risk factors between probands and controls were independent of parental CVD. Major depression in childhood is associated with an unfavorable CVD risk profile in adolescence, and risks for pediatric depression and CVD may coincide in families. Effective prevention and treatment of childhood depression may be a means to reduce the incidence of adult CVD.

Analysis of the relationship between community characteristics and depression using geographically weighted regression.

PubMed

Choi, Hyungyun; Kim, Ho

2017-01-01

Achieving national health equity is currently a pressing issue. Large regional variations in the health determinants are observed. Depression, one of the most common mental disorders, has large variations in incidence among different populations, and thus must be regionally analyzed. The present study aimed at analyzing regional disparities in depressive symptoms and identifying the health determinants that require regional interventions. Using health indicators of depression in the Korea Community Health Survey 2011 and 2013, the Moran's I was calculated for each variable to assess spatial autocorrelation, and a validated geographically weighted regression analysis using ArcGIS version 10.1 of different domains: health behavior, morbidity, and the social and physical environments were created, and the final model included a combination of significant variables in these models. In the health behavior domain, the weekly breakfast intake frequency of 1-2 times was the most significantly correlated with depression in all regions, followed by exposure to secondhand smoke and the level of perceived stress in some regions. In the morbidity domain, the rate of lifetime diagnosis of myocardial infarction was the most significantly correlated with depression. In the social and physical environment domain, the trust environment within the local community was highly correlated with depression, showing that lower the level of trust, higher was the level of depression. A final model was constructed and analyzed using highly influential variables from each domain. The models were divided into two groups according to the significance of correlation of each variable with the experience of depression symptoms. The indicators of the regional health status are significantly associated with the incidence of depressive symptoms within a region. The significance of this correlation varied across regions.

The Association between Major Depressive Disorder in Childhood and Risk Factors for Cardiovascular Disease in Adolescence

PubMed Central

Rottenberg, Jonathan; Yaroslavsky, Ilya; Carney, Robert M.; Freedland, Kenneth E.; George, Charles J.; Baji, Ildikó; Dochnal, Roberta; Gádoros, Júlia; Halas, Kitti; Kapornai, Krisztina; Kiss, Enikő; Osváth, Viola; Varga, Hedvig; Vetró, Ágnes; Kovacs, Maria

2014-01-01

Objective Depression in adults is associated with risk factors for cardiovascular disease (CVD). It is unclear, however, when the association between clinical depression and cardiac risk factors develops, or how early in life this association can be detected. Methods In an ongoing study of pediatric depression, we compared CVD risk factors, including smoking, obesity, physical activity level, sedentary behavior, and parental history of CVD, across three samples of adolescents: probands with established histories of childhood-onset major depressive disorder (MDD; N=210), never-depressed siblings of probands (N=195), and controls with no history of any major psychiatric disorder (N=161). Results When assessed during adolescence, 85% of the probands were not in a major depressive episode. Nevertheless, at that assessment, probands had a higher prevalence of regular smoking ([odds ratio [OR] 12.54, 95% confidence interval [CI] = 4.36–36.12) and were less physically active than controls (OR .59, CI = .43–.81) and siblings (OR .70, CI = .52–.94), and had a higher rate of obesity than did controls (OR 3.67, CI = 1.42–9.52). Parents of probands reported high rates of CVD (significantly higher than did parents of controls), including myocardial infarction and CVD-related hospitalization (ORs 1.62–4.36; CIs = 1.03–15.40). Differences in CVD risk factors between probands and controls were independent of parental CVD. Conclusions Major depression in childhood is associated with an unfavorable CVD risk profile in adolescence, and risks for pediatric depression and CVD may coincide in families. Effective prevention and treatment of childhood depression may be a means to reduce the incidence of adult CVD. PMID:24470130

Obesity-metabolic derangement exacerbates cardiomyocyte loss distal to moderate coronary artery stenosis in pigs without affecting global cardiac function.

PubMed

Li, Zi-Lun; Ebrahimi, Behzad; Zhang, Xin; Eirin, Alfonso; Woollard, John R; Tang, Hui; Lerman, Amir; Wang, Shen-Ming; Lerman, Lilach O

2014-04-01

Obesity associated with metabolic derangements (ObM) worsens the prognosis of patients with coronary artery stenosis (CAS), but the underlying cardiac pathophysiologic mechanisms remain elusive. We tested the hypothesis that ObM exacerbates cardiomyocyte loss distal to moderate CAS. Obesity-prone pigs were randomized to four groups (n = 6 each): lean-sham, ObM-sham, lean-CAS, and ObM-CAS. Lean and ObM pigs were maintained on a 12-wk standard or atherogenic diet, respectively, and left circumflex CAS was then induced by placing local-irritant coils. Cardiac structure, function, and myocardial oxygenation were assessed 4 wk later by computed-tomography and blood oxygenation level dependent (BOLD) MRI, the microcirculation with micro-computed-tomography, and injury mechanisms by immunoblotting and histology. ObM pigs showed obesity, dyslipidemia, and insulin resistance. The degree of CAS (range, 50-70%) was similar in lean and ObM pigs, and resting myocardial perfusion and global cardiac function remained unchanged. Increased angiogenesis distal to the moderate CAS observed in lean was attenuated in ObM pigs, which also showed microvascular dysfunction and increased inflammation (M1-macrophages, TNF-α expression), oxidative stress (gp91), hypoxia (BOLD-MRI), and fibrosis (Sirius-red and trichrome). Furthermore, lean-CAS showed increased myocardial autophagy, which was blunted in ObM pigs (downregulated expression of unc-51-like kinase-1 and autophagy-related gene-12; P < 0.05 vs. lean CAS) and associated with marked apoptosis. The interaction diet xstenosis synergistically inhibited angiogenic, autophagic, and fibrogenic activities. ObM exacerbates structural and functional myocardial injury distal to moderate CAS with preserved myocardial perfusion, possibly due to impaired cardiomyocyte turnover.

Conditioning the heart to prevent myocardial reperfusion injury during PPCI

PubMed Central

2012-01-01

For patients presenting with a ST-segment elevation myocardial infarction (STEMI), early myocardial reperfusion by primary percutaneous coronary intervention (PPCI) remains the most effective treatment strategy for limiting myocardial infarct size, preserving left ventricular systolic function, and preventing the onset of heart failure. Recent advances in PCI technology to improve myocardial reperfusion and the introduction of novel anti-platelet and anti-thrombotic agents to maintain the patency of the infarct-related coronary artery continue to optimize PPCI procedure. However, despite these improvements, STEMI patients still experience significant major adverse cardiovascular events. One major contributing factor has been the inability to protect the heart against the lethal myocardial reperfusion injury, which accompanies PPCI. Past attempts to translate cardioprotective strategies, discovered in experimental studies to prevent lethal myocardial reperfusion injury, into the clinical setting of PPCI have been disappointing. However, a number of recent proof-of-concept clinical studies suggest that the heart can be ‘conditioned’ to protect itself against lethal myocardial reperfusion injury, as evidenced by a reduction in myocardial infarct size. This can be achieved using either mechanical (such as ischaemic postconditioning, remote ischaemic preconditioning, therapeutic hypothermia, or hyperoxaemia) or pharmacological (such as cyclosporin-A, natriuretic peptide, exenatide) ‘conditioning’ strategies as adjuncts to PPCI. Furthermore, recent developments in cardiac magnetic resonance (CMR) imaging can provide a non-invasive imaging strategy for assessing the efficacy of these novel adjunctive therapies to PPCI in terms of key surrogate clinical endpoints such as myocardial infarct size, myocardial salvage, left ventricular ejection fraction, and the presence of microvascular obstruction or intramyocardial haemorrhage. In this article, we review the therapeutic potential of ‘conditioning’ to protect the heart against lethal myocardial reperfusion injury in STEMI patients undergoing PPCI. PMID:24062884

Real-time myocardial perfusion imaging for pharmacologic stress testing: added value to single photon emission computed tomography.

PubMed

Korosoglou, Grigorios; Dubart, Alain-Eric; DaSilva, K Gaspar C; Labadze, Nino; Hardt, Stefan; Hansen, Alexander; Bekeredjian, Raffi; Zugck, Christian; Zehelein, Joerg; Katus, Hugo A; Kuecherer, Helmut

2006-01-01

Little is known about the incremental value of real-time myocardial contrast echocardiography (MCE) as an adjunct to pharmacologic stress testing. This study was performed to evaluate the diagnostic value of MCE to detect abnormal myocardial perfusion by technetium Tc 99m sestamibi-single photon emission computed tomography (SPECT) and anatomically significant coronary artery disease (CAD) by angiography. Myocardial contrast echocardiography was performed at rest and during vasodilator stress in consecutive patients (N = 120) undergoing SPECT imaging for known or suspected CAD. Myocardial opacification, wall motion, and tracer uptake were visually analyzed in 12 myocardial segments by 2 pairs of blinded observers. Concordance between the 2 methods was assessed using the kappa statistic. Of 1356 segments, 1025 (76%) were interpretable by MCE, wall motion, and SPECT. Sensitivity of wall motion was 75%, specificity 83%, and accuracy 81% for detecting abnormal myocardial perfusion by SPECT (kappa = 0.53). Myocardial contrast echocardiography and wall motion together yielded significantly higher sensitivity (85% vs 74%, P < .05), specificity of 83%, and accuracy of 85% (kappa = 0.64) for the detection of abnormal myocardial perfusion. In 89 patients who underwent coronary angiography, MCE and wall motion together yielded higher sensitivity (83% vs 64%, P < .05) and accuracy (77% vs 68%, P < .05) but similar specificity (72%) compared with SPECT for the detection of high-grade, stenotic (> or = 75%) coronary lesions. Assessment of myocardial perfusion adds value to conventional stress echocardiography by increasing its sensitivity for the detection of functionally abnormal myocardial perfusion. Myocardial contrast echocardiography and wall motion together provide higher sensitivity and accuracy for detection of CAD compared with SPECT.

[Application of IMA and H-FABP in Forensic Diagnosis of Sudden Cardiac Death].

PubMed

Zhu, Z L; Wang, P; You, J B; Yue, Q; Wang, P F; Wang, X L; Zhang, C N; Zhang, G H

2017-08-01

Acute myocardial ischemia is the most common cause of sudden cardiac death. The diagnosis of early myocardial ischemia is a hot point in forensic medicine, which is also an early and important part for a prevention against myocardial infarction. This paper conducts a comprehensive discussion of the structure, function, clinical value and forensic medicine application prospect of ischemia modified albumin （IMA） and heart-type fatty acid binding protein （H-FABP), aiming to determine whether the two proteins can be used as biochemical detection indicators of early myocardial ischemia for the diagnosis of sudden cardiac death in forensic medicine. Copyright© by the Editorial Department of Journal of Forensic Medicine.

Cardiometabolic disease and features of depression and bipolar disorder: population-based, cross-sectional study.

PubMed

Martin, Daniel J; Ul-Haq, Zia; Nicholl, Barbara I; Cullen, Breda; Evans, Jonathan; Gill, Jason M R; Roberts, Beverly; Gallacher, John; Mackay, Daniel; McIntosh, Andrew; Hotopf, Matthew; Craddock, Nick; Deary, Ian J; Pell, Jill P; Smith, Daniel J

2016-04-01

The relative contribution of demographic, lifestyle and medication factors to the association between affective disorders and cardiometabolic diseases is poorly understood. To assess the relationship between cardiometabolic disease and features of depresion and bipolar disorder within a large population sample. Cross-sectional study of 145 991 UK Biobank participants: multivariate analyses of associations between features of depression or bipolar disorder and five cardiometabolic outcomes, adjusting for confounding factors. There were significant associations between mood disorder features and 'any cardiovascular disease' (depression odds ratio (OR) = 1.15, 95% CI 1.12-1.19; bipolar OR = 1.28, 95% CI 1.14-1.43) and with hypertension (depression OR = 1.15, 95% CI 1.13-1.18; bipolar OR = 1.26, 95% CI 1.12-1.42). Individuals with features of mood disorder taking psychotropic medication were significantly more likely than controls not on psychotropics to report myocardial infarction (depression OR = 1.47, 95% CI 1.24-1.73; bipolar OR = 2.23, 95% CI 1.53-3.57) and stroke (depression OR = 2.46, 95% CI 2.10-2.80; bipolar OR = 2.31, 95% CI 1.39-3.85). Associations between features of depression or bipolar disorder and cardiovascular disease outcomes were statistically independent of demographic, lifestyle and medication confounders. Psychotropic medication may also be a risk factor for cardiometabolic disease in individuals without a clear history of mood disorder. © The Royal College of Psychiatrists 2016.

Long-term health outcomes in patients with Prader-Willi Syndrome: a nationwide cohort study in Denmark.

PubMed

Hedgeman, E; Ulrichsen, S P; Carter, S; Kreher, N C; Malobisky, K P; Braun, M M; Fryzek, J; Olsen, M S

2017-10-01

Prader-Willi syndrome (PWS) is a rare congenital disease that affects growth, sexual development, cognitive function and behavior. Individuals exhibit food preoccupation and hyperphagia, which may lead to obesity with premature morbidity and mortality. The aim of this work was to evaluate the risk of venous thromboembolisms (VTEs), myocardial infarction, pulmonary hypertension, sleep apnea, depression, anxiety and all-cause mortality among persons with PWS as compared with an age- and sex-matched general-population cohort. All persons diagnosed with PWS (n=155) were identified in the Danish Health Registries; an age- and sex-matched comparison group was selected from the general population of Denmark (n=15 500); diseases of interest were identified through the health registry and cause of death register. Follow-up began on date of birth or first medical record availability through to first occurrence of an outcome of interest; follow-up ceased at emigration from Denmark or end of study. Incidence rates (IRs) were calculated and Cox's proportional hazards models were used to understand the relative risk (RR) of disease. The IRs for VTE among patients with PWS was 144 (60-347) per 100 000 person-years. Risks for VTE events and all-cause mortality were 9.4 times (95% confidence interval (CI): 3.7-23.5) and 11.0 times (95% CI: 5.7-21.1) higher, respectively, for patients with PWS versus the general population. Increased risks were also found individually for deep venous thromboses (DVTs) (RR: 9.1; 95% CI: 3.2-25.2), pulmonary embolisms (RR: 11.0; 95% CI: 1.4-86.9), myocardial infarction (RR: 7.2; 95% CI: 1.7-30.2) and anxiety (RR: 2.8; 95% CI: 1.0-7.5). No cases of pulmonary hypertension, sleep apnea or depressive disorders were identified within this PWS cohort. Multiple cardiovascular and behavioral illnesses are more likely to occur among patients with PWS than within the general population. These increased risks may provide an impetus for enhanced disease prevention, screening, diagnosis and treatment.

Acrolein inhalation causes myocardial strain delay and decreased cardiac performance as detected by high-frequency echocardiography in mice

EPA Science Inventory

Acrolein, an unsaturated aldehyde found in air pollution, impairs Ca2+ flux and contraction in cardiomyocytes in vitro. To better define direct and delayed functional cardiac effects, we hypothesized that a single exposure to acrolein would modify myocardial strain and performanc...

Acetyl salicylic acid protected against heat stress damage in chicken myocardial cells and may associate with induced Hsp27 expression.

PubMed

Wu, Di; Xu, Jiao; Song, Erbao; Tang, Shu; Zhang, Xiaohui; Kemper, N; Hartung, J; Bao, Endong

2015-07-01

We investigated whether acetyl salicylic acid (ASA) protects chicken myocardial cells from heat stress-mediated damage in vivo and whether the induction of Hsp27 expression is connected with this function. Pathological changes, damage-related enzyme levels, and Hsp27 expression were studied in chickens following heat stress (40 ± 1 °C for 0, 1, 2, 3, 5, 7, 10, 15, or 24 h, respectively) with or without ASA administration (1 mg/kg BW, 2 h prior). Appearance of pathological lesions such as degenerations and karyopyknosis as well as the myocardial damage-related enzyme activation indicated that heat stress causes considerable injury to the myocardial cells in vivo. Myocardial cell injury was most serious in chickens exposed to heat stress without prior ASA administration; meanwhile, ASA pretreatment acted protective function against high temperature-induced injury. Hsp27 expression was induced under all experimental conditions but was one-fold higher in the ASA-pretreated animals (0.3138 ± 0.0340 ng/mL) than in untreated animals (0.1437 ± 0.0476 ng/mL) 1 h after heat stress exposure, and such an increase was sustained over the length of the experiment. Our findings indicate that pretreatment with ASA protects chicken myocardial cells from acute heat stress in vivo with almost no obvious side effects, and this protection may involve an enhancement of Hsp27 expression. However, the detailed mechanisms underlying this effect require further investigation.

Intestinal microbiota determine severity of myocardial infarction in rats

PubMed Central

Lam, Vy; Su, Jidong; Koprowski, Stacy; Hsu, Anna; Tweddell, James S.; Rafiee, Parvaneh; Gross, Garrett J.; Salzman, Nita H.; Baker, John E.

2012-01-01

Signals from the intestinal microbiota are important for normal host physiology; alteration of the microbiota (dysbiosis) is associated with multiple disease states. We determined the effect of antibiotic-induced intestinal dysbiosis on circulating cytokine levels and severity of ischemia/reperfusion injury in the heart. Treatment of Dahl S rats with a minimally absorbed antibiotic vancomycin, in the drinking water, decreased circulating leptin levels by 38%, resulted in smaller myocardial infarcts (27% reduction), and improved recovery of postischemic mechanical function (35%) as compared with untreated controls. Vancomycin altered the abundance of intestinal bacteria and fungi, measured by 16S and 18S ribosomal DNA quantity. Pretreatment with leptin (0.12 μg/kg i.v.) 24 h before ischemia/reperfusion abolished cardioprotection produced by vancomycin treatment. Dahl S rats fed the commercially available probiotic product Goodbelly, which contains the leptin-suppressing bacteria Lactobacillus plantarum 299v, also resulted in decreased circulating leptin levels by 41%, smaller myocardial infarcts (29% reduction), and greater recovery of postischemic mechanical function (23%). Pretreatment with leptin (0.12 μg/kg i.v.) abolished cardioprotection produced by Goodbelly. This proof-of-concept study is the first to identify a mechanistic link between changes in intestinal microbiota and myocardial infarction and demonstrates that a probiotic supplement can reduce myocardial infarct size.—Lam, V., Su, J., Koprowski, S., Hsu, A., Tweddell, J. S., Rafiee, P., Gross, G. J., Salzman, N. H., Baker, J. E. Intestinal microbiota determine severity of myocardial infarction in rats. PMID:22247331

Clinical results with beta-methyl-p-(123I)iodophenylpentadecanoic acid, single-photon emission computed tomography in cardiac disease.

PubMed

Nishimura, T; Uehara, T; Shimonagata, T; Nagata, S; Haze, K

1994-01-01

This study was undertaken to evaluate the relationships, between myocardial perfusion and metabolism. Simultaneous beta-methyl-p(123I)iodophenylpentadecanoic acid (123I-BMIPP) and thallium 201 myocardial single-photon emission computed tomography (SPECT) were performed in 25 patients with myocardial infarction (group A) and 16 patients with hypertrophic cardiomyopathy (group B). The severity scores of 123I-BMIPP and 201Tl myocardial SPECT images were evaluated semiquantitatively by segmental analysis. In Group A, dissociations between thallium- and 123I-BMIPP-imaged defects were frequently observed in patients with successful reperfusion compared with those with no reperfusion and those with reinfarction. In four patients with successful reperfusion, repeated 123I-BMIPP and 201Tl myocardial SPECT showed gradual improvement of the 123I-BMIPP severity score compared with the thallium severity score. In group B, dissociations between thallium- and 123I-BMIPP-imaged defects were also demonstrated in hypertrophic myocardium. In addition, nonhypertrophic myocardium also had decreased 123I-BMIPP uptake. In groups A and B, 123I-BMIPP severity scores correlated well with left ventricular function compared with thallium severity scores. These findings indicate that 123I-BMIPP is a suitable agent for the assessment of functional integrity, because left ventricular wall motion is energy dependent and 123I-BMIPP may reflect an aspect of myocardial energy production. This agent may be useful for the early detection and patient management of various heart diseases as an alternative to positron emission tomographic study.

Relation of coronary flow pattern to myocardial blush grade in patients with first acute myocardial infarction

PubMed Central

Hoffmann, R; Haager, P; Lepper, W; Franke, A; Hanrath, P

2003-01-01

Background: Analysis of myocardial blush grade (MBG) and coronary flow velocity pattern has been used to obtain direct or indirect information about microvascular damage and reperfusion injury after percutaneous transluminal coronary angiography for acute myocardial infarction. Objective: To evaluate the relation between coronary blood flow velocity pattern and MBG immediately after angioplasty plus stenting for acute myocardial infarction. Design: The coronary blood flow velocity pattern in the infarct related artery was determined immediately after angioplasty in 35 patients with their first acute myocardial infarct using a Doppler guide wire. Measurements were related to MBG as a direct index of microvascular function in the infarct zone. Results: Coronary flow velocity patterns were different between patients with absent myocardial blush (n = 14), reduced blush (n = 7), or normal blush (n = 14). The following variables (mean (SD)) differed significantly between the three groups: systolic peak flow velocity (cm/s): absent blush 10.9 (4.2), reduced blush 14.2 (6.4), normal blush 19.2 (11.2); p = 0.036; diastolic deceleration rate (ms): absent blush 103 (58), reduced blush 80 (65), normal blush 50 (19); p = 0.025; and diastolic–systolic velocity ratio: absent blush 4.06 (2.18), reduced blush 2.02 (0.55), normal blush 1.88 (1.03); p = 0.002. In a multivariate analysis MBG was the only variable with a significant impact on the diastolic deceleration rate (p = 0.034,) while age, infarct location, time to revascularisation, infarct vessel diameter, and maximum creatine kinase had no significant impact. Conclusions: The coronary flow velocity pattern in the infarct related epicardial artery is primarily determined by the microvascular function of the dependent myocardium, as reflected by MBG. PMID:12975402

The role of PET quantification in cardiovascular imaging.

PubMed

Slomka, Piotr; Berman, Daniel S; Alexanderson, Erick; Germano, Guido

2014-08-01

Positron Emission Tomography (PET) has several clinical and research applications in cardiovascular imaging. Myocardial perfusion imaging with PET allows accurate global and regional measurements of myocardial perfusion, myocardial blood flow and function at stress and rest in one exam. Simultaneous assessment of function and perfusion by PET with quantitative software is currently the routine practice. Combination of ejection fraction reserve with perfusion information may improve the identification of severe disease. The myocardial viability can be estimated by quantitative comparison of fluorodeoxyglucose ( 18 FDG) and rest perfusion imaging. The myocardial blood flow and coronary flow reserve measurements are becoming routinely included in the clinical assessment due to enhanced dynamic imaging capabilities of the latest PET/CT scanners. Absolute flow measurements allow evaluation of the coronary microvascular dysfunction and provide additional prognostic and diagnostic information for coronary disease. Standard quantitative approaches to compute myocardial blood flow from kinetic PET data in automated and rapid fashion have been developed for 13 N-ammonia, 15 O-water and 82 Rb radiotracers. The agreement between software methods available for such analysis is excellent. Relative quantification of 82 Rb PET myocardial perfusion, based on comparisons to normal databases, demonstrates high performance for the detection of obstructive coronary disease. New tracers, such as 18 F-flurpiridaz may allow further improvements in the disease detection. Computerized analysis of perfusion at stress and rest reduces the variability of the assessment as compared to visual analysis. PET quantification can be enhanced by precise coregistration with CT angiography. In emerging clinical applications, the potential to identify vulnerable plaques by quantification of atherosclerotic plaque uptake of 18 FDG and 18 F-sodium fluoride tracers in carotids, aorta and coronary arteries has been demonstrated.

Hyperinsulinemic Normoglycemia does not meaningfully improve Myocardial Performance during Cardiac Surgery: A Randomized Trial

PubMed Central

Duncan, Andra E.; Kashy, Babak Kateby; Sarwar, Sheryar; Singh, Akhil; Stenina-Adognravi, Olga; Christoffersen, Steffen; Alfirevic, Andrej; Sale, Shiva; Yang, Dongsheng; Thomas, James D.; Gillinov, Marc; Sessler, Daniel I.

2015-01-01

Background Glucose-insulin-potassium (GIK) administration during cardiac surgery inconsistently improves myocardial function, perhaps because hyperglycemia negates the beneficial effects of GIK. The hyperinsulinemic normoglycemic clamp (HNC) technique may better enhance the myocardial benefits of GIK. We extended previous GIK investigations by: 1) targeting normoglycemia while administering a glucose-insulin-potassium infusion (HNC); 2) using improved echocardiographic measures of myocardial deformation, specifically myocardial longitudinal strain and strain rate; and, 3) assessing activation of glucose metabolic pathways. Methods 100 patients having aortic valve replacement for aortic stenosis were randomly assigned to HNC (high-dose insulin with concomitant glucose infusion titrated to normoglycemia) versus standard therapy (insulin treatment if glucose >150 mg/dL). Our primary outcomes were left ventricular longitudinal strain and strain rate, assessed using speckle-tracking echocardiography. Right atrial tissue was analyzed for activation of glycolysis/pyruvate oxidation and alternative metabolic pathways. Results Time-weighted mean glucose concentrations were lower with HNC (127±19 mg/dL) than standard care (177±41 mg/dL; P<0.001). Echocardiographic data were adequate in 72 patients for strain analysis and 67 patients for strain rate analysis. HNC did not improve myocardial strain, with an HNC minus standard therapy difference of −1.2 (97.5%CI: −2.9, 0.5)%; P=0.11. Strain rate was significantly better, but by a clinically unimportant amount: −0.16 (−0.30, −0.03) sec−1, P = 0.007. There was no evidence of increased glycolytic, pyruvate oxidation, or hexosamine biosynthetic pathway activation in right atrial samples (n = 20, HNC; 22, standard therapy). Conclusions Administration of glucose and insulin while targeting normoglycemia during aortic valve replacement did not meaningfully improve myocardial function. PMID:26200180

Enalapril protects against myocardial ischemia/reperfusion injury in a swine model of cardiac arrest and resuscitation

PubMed Central

Wang, Guoxing; Zhang, Qian; Yuan, Wei; Wu, Junyuan; Li, Chunsheng

2016-01-01

There is strong evidence to suggest that angiotensin-converting enzyme inhibitors (ACEIs) protect against local myocardial ischemia/reperfusion (I/R) injury. This study was designed to explore whether ACEIs exert cardioprotective effects in a swine model of cardiac arrest (CA) and resuscitation. Male pigs were randomly assigned to three groups: sham-operated group, saline treatment group and enalapril treatment group. Thirty minutes after drug infusion, the animals in the saline and enalapril groups were subjected to ventricular fibrillation (8 min) followed by cardiopulmonary resuscitation (up to 30 min). Cardiac function was monitored, and myocardial tissue and blood were collected for analysis. Enalapril pre-treatment did not improve cardiac function or the 6-h survival rate after CA and resuscitation; however, this intervention ameliorated myocardial ultrastructural damage, reduced the level of plasma cardiac troponin I and decreased myocardial apoptosis. Plasma angiotensin (Ang) II and Ang-(1–7) levels were enhanced in the model of CA and resuscitation. Enalapril reduced the plasma Ang II level at 4 and 6 h after the return of spontaneous circulation whereas enalapril did not affect the plasma Ang-(1–7) level. Enalapril pre-treatment decreased the myocardial mRNA and protein expression of angiotensin-converting enzyme (ACE). Enalapril treatment also reduced the myocardial ACE/ACE2 ratio, both at the mRNA and the protein level. Enalapril pre-treatment did not affect the upregulation of ACE2, Ang II type 1 receptor (AT1R) and MAS after CA and resuscitation. Taken together, these findings suggest that enalapril protects against ischemic injury through the attenuation of the ACE/Ang II/AT1R axis after CA and resuscitation in pigs. These results suggest the potential therapeutic value of ACEIs in patients with CA. PMID:27633002

Myosin Activator Omecamtiv Mecarbil Increases Myocardial Oxygen Consumption and Impairs Cardiac Efficiency Mediated by Resting Myosin ATPase Activity.

PubMed

Bakkehaug, Jens Petter; Kildal, Anders Benjamin; Engstad, Erik Torgersen; Boardman, Neoma; Næsheim, Torvind; Rønning, Leif; Aasum, Ellen; Larsen, Terje Steinar; Myrmel, Truls; How, Ole-Jakob

2015-07-01

Omecamtiv mecarbil (OM) is a novel inotropic agent that prolongs systolic ejection time and increases ejection fraction through myosin ATPase activation. We hypothesized that a potentially favorable energetic effect of unloading the left ventricle, and thus reduction of wall stress, could be counteracted by the prolonged contraction time and ATP-consumption. Postischemic left ventricular dysfunction was created by repetitive left coronary occlusions in 7 pigs (7 healthy pigs also included). In both groups, systolic ejection time and ejection fraction increased after OM (0.75 mg/kg loading for 10 minutes, followed by 0.5 mg/kg/min continuous infusion). Cardiac efficiency was assessed by relating myocardial oxygen consumption to the cardiac work indices, stroke work, and pressure-volume area. To circumvent potential neurohumoral reflexes, cardiac efficiency was additionally assessed in ex vivo mouse hearts and isolated myocardial mitochondria. OM impaired cardiac efficiency; there was a 31% and 23% increase in unloaded myocardial oxygen consumption in healthy and postischemic pigs, respectively. Also, the oxygen cost of the contractile function was increased by 63% and 46% in healthy and postischemic pigs, respectively. The increased unloaded myocardial oxygen consumption was confirmed in OM-treated mouse hearts and explained by an increased basal metabolic rate. Adding the myosin ATPase inhibitor, 2,3-butanedione monoxide abolished all surplus myocardial oxygen consumption in the OM-treated hearts. Omecamtiv mecarbil, in a clinically relevant model, led to a significant myocardial oxygen wastage related to both the contractile and noncontractile function. This was mediated by that OM induces a continuous activation in resting myosin ATPase. © 2015 American Heart Association, Inc.

Defective branched chain amino acid catabolism contributes to cardiac dysfunction and remodeling following myocardial infarction.

PubMed

Wang, Wei; Zhang, Fuyang; Xia, Yunlong; Zhao, Shihao; Yan, Wenjun; Wang, Helin; Lee, Yan; Li, Congye; Zhang, Ling; Lian, Kun; Gao, Erhe; Cheng, Hexiang; Tao, Ling

2016-11-01

Cardiac metabolic remodeling is a central event during heart failure (HF) development following myocardial infarction (MI). It is well known that myocardial glucose and fatty acid dysmetabolism contribute to post-MI cardiac dysfunction and remodeling. However, the role of amino acid metabolism in post-MI HF remains elusive. Branched chain amino acids (BCAAs) are an important group of essential amino acids and function as crucial nutrient signaling in mammalian animals. The present study aimed to determine the role of cardiac BCAA metabolism in post-MI HF progression. Utilizing coronary artery ligation-induced murine MI models, we found that myocardial BCAA catabolism was significantly impaired in response to permanent MI, therefore leading to an obvious elevation of myocardial BCAA abundance. In MI-operated mice, oral BCAA administration further increased cardiac BCAA levels, activated the mammalian target of rapamycin (mTOR) signaling, and exacerbated cardiac dysfunction and remodeling. These data demonstrate that BCAAs act as a direct contributor to post-MI cardiac pathologies. Furthermore, these BCAA-mediated deleterious effects were improved by rapamycin cotreatment, revealing an indispensable role of mTOR in BCAA-mediated adverse effects on cardiac function/structure post-MI. Of note, pharmacological inhibition of branched chain ketoacid dehydrogenase kinase (BDK), a negative regulator of myocardial BCAA catabolism, significantly improved cardiac BCAA catabolic disorders, reduced myocardial BCAA levels, and ameliorated post-MI cardiac dysfunction and remodeling. In conclusion, our data provide the evidence that impaired cardiac BCAA catabolism directly contributes to post-MI cardiac dysfunction and remodeling. Moreover, improving cardiac BCAA catabolic defects may be a promising therapeutic strategy against post-MI HF. Copyright © 2016 the American Physiological Society.

Anxiety and depression in patients three months after myocardial infarction: Association with markers of coagulation and the relevance of age.

PubMed

Geiser, Franziska; Urbach, Anne Sarah; Harbrecht, Ursula; Conrad, Rupert; Pötzsch, Bernd; Amann, Nele; Kiesewetter, Katharina; Sieke, Alexandra; Wolffs, Kyra; Skowasch, Dirk

2017-08-01

Anxiety and depression are associated with an activation of coagulation and an impairment of fibrinolysis, which may contribute to the increased cardiovascular risk associated with the two disorders. However, very few studies have examined the impact of psychological distress on coagulation factors in coronary artery disease patients. The aim of this study was to assess the correlation between anxiety/depression and factors of coagulation and fibrinolysis in patients who had suffered an acute MI three months prior. In 148 patients, anxiety and depression were assessed by the Hospital Anxiety and Depression Scale (HADS) shortly after MI and three months later. At the second time of assessment, plasma levels of fibrinogen, factor VII, factor VIII, von Willebrand factor, prothrombin-fragment 1 and 2, tissue-plasminogen-activator, plasminogen activator inhibitor-1, D-dimer, and homocysteine were measured. In 32% of the patients, elevated levels of anxiety and depression were found three months after a MI. Multiple regression analyses showed that coagulation and fibrinolysis markers were not significantly associated with HADS anxiety and depression scores. We found that age, gender, BMI, and smoking status were significant predictors for haemostasis factors. A higher age was associated with a higher coagulability but lower anxiety levels. We measured parameters of coagulation and fibrinolysis in patients three months after MI and found no predictive value of HADS anxiety and depression scores shortly after MI or at the time of blood sampling. The effects of age on the relationship between anxiety and haemostasis should be further investigated. Copyright © 2017 Elsevier Inc. All rights reserved.

Effects of short-term continuous positive airway pressure on myocardial sympathetic nerve function and energetics in patients with heart failure and obstructive sleep apnea: a randomized study.

PubMed

Hall, Allison B; Ziadi, Maria C; Leech, Judith A; Chen, Shin-Yee; Burwash, Ian G; Renaud, Jennifer; deKemp, Robert A; Haddad, Haissam; Mielniczuk, Lisa M; Yoshinaga, Keiichiro; Guo, Ann; Chen, Li; Walter, Olga; Garrard, Linda; DaSilva, Jean N; Floras, John S; Beanlands, Rob S B

2014-09-09

Heart failure with reduced ejection fraction and obstructive sleep apnea (OSA), 2 states of increased metabolic demand and sympathetic nervous system activation, often coexist. Continuous positive airway pressure (CPAP), which alleviates OSA, can improve ventricular function. It is unknown whether this is due to altered oxidative metabolism or presynaptic sympathetic nerve function. We hypothesized that short-term (6-8 weeks) CPAP in patients with OSA and heart failure with reduced ejection fraction would improve myocardial sympathetic nerve function and energetics. Forty-five patients with OSA and heart failure with reduced ejection fraction (left ventricular ejection fraction 35.8±9.7% [mean±SD]) were evaluated with the use of echocardiography and 11C-acetate and 11C-hydroxyephedrine positron emission tomography before and ≈6 to 8 weeks after randomization to receive short-term CPAP (n=22) or no CPAP (n=23). Work metabolic index, an estimate of myocardial efficiency, was calculated as follows: (stroke volume index×heart rate×systolic blood pressure÷Kmono), where Kmono is the monoexponential function fit to the myocardial 11C-acetate time-activity data, reflecting oxidative metabolism. Presynaptic sympathetic nerve function was measured with the use of the 11C-hydroxyephedrine retention index. CPAP significantly increased hydroxyephedrine retention versus no CPAP (Δretention: +0.012 [0.002, 0.021] versus -0.006 [-0.013, 0.005] min(-1); P=0.003). There was no significant change in work metabolic index between groups. However, in those with more severe OSA (apnea-hypopnea index>20 events per hour), CPAP significantly increased both work metabolic index and systolic blood pressure (P<0.05). In patients with heart failure with reduced ejection fraction and OSA, short-term CPAP increased hydroxyephedrine retention, indicating improved myocardial sympathetic nerve function, but overall did not affect energetics. In those with more severe OSA, CPAP may improve cardiac efficiency. Further outcome-based investigation of the consequences of CPAP is warranted. http://www.clinicaltrials.gov. Unique identifier: NCT00756366. © 2014 American Heart Association, Inc.

Left ventricular systolic and diastolic function improve after acute myocardial infarction treated with acute percutaneous coronary intervention, but are not influenced by intracoronary injection of autologous mononuclear bone marrow cells: a 3 year serial echocardiographic sub-study of the randomized-controlled ASTAMI study.

PubMed

Beitnes, Jan Otto; Gjesdal, Ola; Lunde, Ketil; Solheim, Svein; Edvardsen, Thor; Arnesen, Harald; Forfang, Kolbjørn; Aakhus, Svend

2011-02-01

To clarify long-term changes in global, regional, and diastolic left ventricular (LV) function after intracoronary injection of autologous mononuclear bone marrow cells (mBMCs) in acute myocardial infarction (AMI). In the Autologous Stem cell Transplantation in Acute Myocardial Infarction (ASTAMI) study, 100 patients with anterior ST-elevation myocardial infarction and percutaneous coronary intervention on the left anterior descending artery (LAD) were randomized to receive intracoronary injection of mBMCs or not. Transthoracic echocardiography was performed at baseline, 3, 6, 12 months, and 3 years. Regional LV function was assessed by two-dimensional speckle-tracking echocardiography. From baseline to 3 years, LV ejection fraction changed from 45.7 to 47.5% in the mBMC group, and from 46.9 to 46.8% in the control group (P = 0.87 for difference in change over time between groups). Longitudinal strain in the LAD territory improved from -9.7 to -12.2% in the mBMC group and from -9.9 to -12.8% in the control group (P = 0.45). E/e' decreased from 14.7 to 12.9 in the mBMC group and from 14.8 to 11.9 in the control group (P = 0.31). There were no significant differences between groups in change of LV volumes, global systolic function, regional function, or diastolic function during 3 years follow-up. No differences between groups indicating beneficial effect of intracoronary mBMC injection could be identified. Both groups in ASTAMI experienced improvement of global, regional, and diastolic LV function after 3-6 months, with effects sustained at 3 years.

Non-Compact Cardiomyopathy or Ventricular Non-Compact Syndrome?

PubMed Central

2014-01-01

Ventricular myocardial non-compaction has been recognized and defined as a genetic cardiomyopathy by American Heart Association since 2006. The argument on the nomenclature and pathogenesis of this kind of ventricular myocardial non-compaction characterized by regional ventricular wall thickening and deep trabecular recesses often complicated with chronic heart failure, arrhythmia and thromboembolism and usually overlap the genetics and phenotypes of other kind of genetic or mixed cardiomyopathy still exist. The proper classification and correct nomenclature of the non-compact ventricles will contribute to the precisely and completely understanding of etiology and its related patho-physiological mechanism for a better risk stratification and more personalized therapy of the disease individually. All of the genetic heterogeneity and phenotypical overlap and the variety in histopathological, electromechanical and clinical presentation indicates that some of the cardiomyopathies might just be the different consequence of myocardial development variations related to gene mutation and phenotype of one or group genes induced by the interacted and disturbed process of gene modulation at different links of gene function expression and some other etiologies. This review aims to establish a new concept of "ventricular non-compaction syndrome" based on the demonstration of the current findings of etiology, epidemiology, histopathology and echocardiography related to the disorder of ventricular myocardial compaction and myocardial electromechanical function development. PMID:25580189

Fibroblast growth factor 2 is an essential cardioprotective factor in a closed‐chest model of cardiac ischemia‐reperfusion injury

PubMed Central

House, Stacey L.; Wang, Joy; Castro, Angela M.; Weinheimer, Carla; Kovacs, Attila; Ornitz, David M.

2015-01-01

Abstract Fibroblast growth factor 2 (FGF2) is cardioprotective in in vivo models of myocardial infarction; however, whether FGF2 has a protective role in in vivo ischemia‐reperfusion (IR) injury, a model that more closely mimics acute myocardial infarction in humans, is not known. To assess the cardioprotective efficacy of endogenous FGF2, mice lacking a functional Fgf2 gene (Fgf2−/−) and wild‐type controls were subjected to closed‐chest regional cardiac IR injury (90 min ischemia, 7 days reperfusion). Fgf2−/− mice had significantly increased myocardial infarct size and significantly worsened cardiac function compared to wild‐type controls at both 1 and 7 days post‐IR injury. Pathophysiological analysis showed that at 1 day after IR injury Fgf2−/− mice have worsened cardiac strain patterns and increased myocardial cell death. Furthermore, at 7 days post‐IR injury, Fgf2−/− mice showed a significantly reduced cardiac hypertrophic response, decreased cardiac vessel density, and increased vessel diameter in the peri‐infarct area compared to wild‐type controls. These data reveal both acute cardioprotective and a longer term proangiogenic potential of endogenous FGF2 in a clinically relevant, in vivo, closed‐chest regional cardiac IR injury model that mimics acute myocardial infarction. PMID:25626875

Cardiaprotective effect of crocetin by attenuating apoptosis in isoproterenol induced myocardial infarction rat model.

PubMed

Zhang, Weili; Li, Yuhui; Ge, Zhiming

2017-09-01

Given study evaluates the cardioprotective effect of crocetin in myocardial infracted (MI) rats. MI was produced by administering isoproterenol (90mg/kg/day, i.p.) in rats for two consecutive days. all the animals were divided in to four groups such as control group receives only saline; MI group which receives only isoproterenol and crocetin treated group which receives crocetin (50, 100 and 200mg/kg/day, p.o.) for the duration of 15 days. At the end of dosing left ventricular functions was assessed to estimate its effect on cardiac functions. Catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), creatine kinase (CK-MB), lactate dehydrogenase (LDH) and inflammatory cytokines were determined in the cardiac tissue homogenate. Histopathology study was also carried out using hematoxylin and eosin staining. Immunohistochemistry was done for the estimation of Caspase-3, Bcl-2, Bax and Nrf-2 level in the myocardial tissues of MI rats. Result of the study suggested that GSH, CAT, CK-MB, and LDH were (p<0.01) increased in the tissue homogenate of crocetin treated group than MI group. However crocetin significantly (p<0.01) decreases the level of MDA and activity of SOD in the tissue homogenate than MI group. It was observed that treatment with crocetin attenuates the level of inflammatory cytokines in the myocardial tissues of MI rats. Moreover level of caspase-3, Bax and Nrf-2 significantly reduced and Bcl-2 enhanced in the myocardial tissues of MI rats than MI group. The altered cellular architecture of heart tissue sections in the myocardial infracted rats were reversed by administration of crocetin treatment. Taking all these data together, it may be suggested that the crocetin act as a possible protective agent in myocardial infarction by decreasing oxidative stress and inflammatory cytokines and thereby attenuates the apoptosis of myocardial cells. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Myocardial perfusion imaging with PET

PubMed Central

Nakazato, Ryo; Berman, Daniel S; Alexanderson, Erick; Slomka, Piotr

2013-01-01

PET-myocardial perfusion imaging (MPI) allows accurate measurement of myocardial perfusion, absolute myocardial blood flow and function at stress and rest in a single study session performed in approximately 30 min. Various PET tracers are available for MPI, and rubidium-82 or nitrogen-13-ammonia is most commonly used. In addition, a new fluorine-18-based PET-MPI tracer is currently being evaluated. Relative quantification of PET perfusion images shows very high diagnostic accuracy for detection of obstructive coronary artery disease. Dynamic myocardial blood flow analysis has demonstrated additional prognostic value beyond relative perfusion imaging. Patient radiation dose can be reduced and image quality can be improved with latest advances in PET/CT equipment. Simultaneous assessment of both anatomy and perfusion by hybrid PET/CT can result in improved diagnostic accuracy. Compared with SPECT-MPI, PET-MPI provides higher diagnostic accuracy, using lower radiation doses during a shorter examination time period for the detection of coronary artery disease. PMID:23671459

Role of (123)I-Iobenguane Myocardial Scintigraphy in Predicting Short-term Left Ventricular Functional Recovery: An Interesting Image.

PubMed

Feola, Mauro; Chauvie, Stephane; Biggi, Alberto; Testa, Marzia

2015-01-01

(123)I-iobenguane myocardial scintigraphy (MIBG) has been shown to be a predictor of sudden cardiac mortality in patients with heart failure. One patient with recent anterior myocardial infarction (MI) treated with coronary angioplasty and having left ventricular ejection fraction (LVEF) of 30% underwent early MIBG myocardial scintigraphy/tetrofosmin single-photon emission computed tomography (SPECT) in order to help evaluate his eligibility for implantable cardioverter defibrillator (ICD). The late heart/mediastinum (H/M) ratio was calculated to be 1.32% and the washout rate was 1%. At 40-day follow-up after angioplasty, LVEF proved to be 32%, New York Heart Association (NYHA) class was still II-III, and an ICD was placed in order to reduce mortality from ventricular arrhythmias. MIBG myocardial scintigraphy might be a promising method for evaluating left ventricular recovery in post-MI patients.

Parametric techniques for characterizing myocardial tissue by magnetic resonance imaging (part 1): T1 mapping.

PubMed

Perea Palazón, R J; Ortiz Pérez, J T; Prat González, S; de Caralt Robira, T M; Cibeira López, M T; Solé Arqués, M

2016-01-01

The development of myocardial fibrosis is a common process in the appearance of ventricular dysfunction in many heart diseases. Magnetic resonance imaging makes it possible to accurately evaluate the structure and function of the heart, and its role in the macroscopic characterization of myocardial fibrosis by late enhancement techniques has been widely validated clinically. Recent studies have demonstrated that T1-mapping techniques can quantify diffuse myocardial fibrosis and the expansion of the myocardial extracellular space in absolute terms. However, further studies are necessary to validate the usefulness of this technique in the early detection of tissue remodeling at a time when implementing early treatment would improve a patient's prognosis. This article reviews the state of the art for T1 mapping of the myocardium, its clinical applications, and its limitations. Copyright © 2016 SERAM. Published by Elsevier España, S.L.U. All rights reserved.

Zinc and Zinc Transporters: Novel Regulators of Ventricular Myocardial Development.

PubMed

Lin, Wen; Li, Deqiang

2018-06-01

Ventricular myocardial development is a well-orchestrated process involving different cardiac structures, multiple signal pathways, and myriad proteins. Dysregulation of this important developmental event can result in cardiomyopathies, such as left ventricle non-compaction, which affect the pediatric population and the adults. Human and mouse studies have shed light upon the etiology of some cardiomyopathy cases and highlighted the contribution of both genetic and environmental factors. However, the regulation of ventricular myocardial development remains incompletely understood. Zinc is an essential trace metal with structural, enzymatic, and signaling function. Perturbation of zinc homeostasis has resulted in developmental and physiological defects including cardiomyopathy. In this review, we summarize several mechanisms by which zinc and zinc transporters can impact the regulation of ventricular myocardial development. Based on our review, we propose that zinc deficiency and mutations of zinc transporters may underlie some cardiomyopathy cases especially those involving ventricular myocardial development defects.

Influence of presenting electrocardiographic findings on the treatment and outcomes of patients with non-ST-segment elevation myocardial infarction.

PubMed

Patel, Jigar H; Gupta, Raghav; Roe, Matthew T; Peng, S Andrew; Wiviott, Stephen D; Saucedo, Jorge F

2014-01-15

The influence of the presenting electrocardiographic (ECG) findings on the treatment and outcomes of patients with non-ST-segment elevation myocardial infarction (NSTEMI) has not been studied in contemporary practice. We analyzed the clinical characteristics, in-hospital management, and in-hospital outcomes of patients with NSTEMI in the Acute Coronary Treatment and Intervention Outcomes Network Registry-Get With The Guidelines (ACTION Registry-GWTG) according to the presenting ECG findings. A total of 175,556 patients from 485 sites from January 2007 to September 2011 were stratified by the ECG findings on presentation: ST depression (n = 40,146, 22.9%), T-wave inversions (n = 24,627, 14%), transient ST-segment elevation (n = 5,050, 2.9%), and no ischemic changes (n = 105,733, 60.2%). Patients presenting with ST-segment depression were the oldest and had the greatest prevalence of major cardiac risk factors. Coronary angiography was performed most frequently in the transient ST-segment elevation group, followed by the T-wave inversion, ST-segment depression, and no ischemic changes groups. The angiogram revealed that patients with ST-segment depression had more left main, proximal left anterior descending, and 3-vessel coronary artery disease and underwent coronary artery bypass grafting most often. In contrast, patients with transient ST-segment elevation had 1-vessel CAD and underwent percutaneous coronary intervention the most. The unadjusted mortality was highest in the ST-segment depression group, followed by the no ischemic changes, transient ST-segment elevation, and T-wave inversion group. Adjusted mortality using the ACTION Registry-GWTG in-hospital mortality model with the no ischemic changes group as the reference showed that in-hospital mortality was similar in the transient ST-segment elevation (odds ratio 1.15, 95% confidence interval 0.97 to 1.37; p = 0.10), higher in the ST-segment depression group (odds ratio 1.46, 95% confidence interval 1.37 to 1.54; p <0.0001), and lower in the T-wave inversion group (odds ratio 0.91, 95% confidence interval 0.83 to 0.99; p = 0.026). In conclusion, the clinical and angiographic characteristics and treatment and outcomes of patients with NSTEMI differed substantially according to the presenting ECG findings. Patients with ST-segment depression have a greater burden of co-morbidities and coronary atherosclerosis and have a greater risk of adjusted in-hospital mortality compared with the other groups. These findings highlight the importance of integrating the presenting ECG findings into the risk stratification algorithm for patients with NSTEMI. Copyright © 2014 Elsevier Inc. All rights reserved.

Role of Personality Functioning in the Quality of Life of Patients with Depression.

PubMed

Crempien, Carla; Grez, Marcela; Valdés, Camila; López, María José; de la Parra, Guillermo; Krause, Mariane

2017-09-01

Depression is associated with reduced quality of life (QoL), and personality pathology is associated with higher impairment and poorer treatment outcomes in patients with depression. This study aims to analyze the effects of personality functioning on the QoL of patients with depression. Severity of depressive symptoms (Beck Depression Inventory), level of personality functioning (Operationalized Psychodynamic Diagnosis Structure Questionnaire), and QoL (Medical Outcome Study 36-item Short-Form) were assessed in a sample of 84 depressive outpatients. Personality functioning showed main effects on both the mental and physical components of QoL. A moderating effect of personality functioning on the relationship between depressive symptoms and QoL was tested but not confirmed. Severity of depressive symptoms was found to mediate the effect of personality functioning on the mental component of QoL. These results suggest that the effect of personality functioning on the QoL of patients with depression may be related to the higher severity of depressive symptoms found in patients with lower levels of personality functioning.

No association between anxiety and depression and adverse clinical outcome among patients with cardiovascular disease: findings from the DANREHAB trial.

PubMed

Kornerup, Henriette; Zwisler, Ann-Dorthe Olsen; Prescott, Eva

2011-10-01

Anxiety and depression have been linked to adverse prognostic outcome in patients with cardiovascular disease (CVD) with mixed results. The timing of anxiety and depression measurement has received little attention so far. The study sample consisted of 536 patients admitted to hospital for CVD and followed in a rehabilitation trial. Symptoms were assessed using the Hospital Anxiety and Depression Scale at baseline and after 1 year. Cox proportional hazards model was used to describe the association between anxiety and depression and adverse outcome (myocardial infarction (MI), heart failure (HF), stroke, death and a combined endpoint) after 5 years. Prevalence of anxiety and depression at baseline was 32% and 13%, respectively. There were 303 combined events; 140 deaths, 60 patients had MI, 177 patients were admitted to hospital with HF and 60 patients had a stroke. Neither anxiety nor depression at any time was associated with mortality or the combined endpoint. Anxiety in IHD patients at baseline and at 1 year was associated with increased risk of MI (HR 2.74; 95% CI: 1.10-6.83) but was attenuated after adjusting for other risk factors (HR 1.18; 95% CI: 0.39-3.55). Both anxiety and depression at 1 year were associated with increased risk of stroke: HR 2.25 (95% CI: 1.05-4.82) and 2.34 (95% CI: 0.99-5.50), respectively, but risk associated with anxiety was attenuated after adjustment. There were no gender differences. Contrary to conclusions from recent meta-analyses, anxiety and depression measured at baseline and after 1 year were not associated with adverse outcome in CVD patients after multivariable adjustment. Copyright © 2011 Elsevier Inc. All rights reserved.

Postinfarction Functional Recovery Driven by a Three-Dimensional Engineered Fibrin Patch Composed of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells.

PubMed

Roura, Santiago; Soler-Botija, Carolina; Bagó, Juli R; Llucià-Valldeperas, Aida; Férnandez, Marco A; Gálvez-Montón, Carolina; Prat-Vidal, Cristina; Perea-Gil, Isaac; Blanco, Jerónimo; Bayes-Genis, Antoni

2015-08-01

Considerable research has been dedicated to restoring myocardial cell slippage and limiting ventricular remodeling after myocardial infarction (MI). We examined the ability of a three-dimensional (3D) engineered fibrin patch filled with human umbilical cord blood-derived mesenchymal stem cells (UCBMSCs) to induce recovery of cardiac function after MI. The UCBMSCs were modified to coexpress luciferase and fluorescent protein reporters, mixed with fibrin, and applied as an adhesive, viable construct (fibrin-cell patch) over the infarcted myocardium in mice (MI-UCBMSC group). The patch adhered well to the heart. Noninvasive bioluminescence imaging demonstrated early proliferation and differentiation of UCBMSCs within the construct in the postinfarct mice in the MI-UCBMSC group. The implanted cells also participated in the formation of new, functional microvasculature that connected the fibrin-cell patch to both the subjacent myocardial tissue and the host circulatory system. As revealed by echocardiography, the left ventricular ejection fraction and fractional shortening at sacrifice were improved in MI-UCBMSC mice and were markedly reduced in mice treated with fibrin alone and untreated postinfarction controls. In conclusion, a 3D engineered fibrin patch composed of UCBMSCs attenuated infarct-derived cardiac dysfunction when transplanted locally over a myocardial wound. ©AlphaMed Press.

Development and Evaluation of Heartbeat: A Machine Perfusion Heart Preservation System.

PubMed

Li, Yongnan; Zeng, Qingdong; Liu, Gang; Du, Junzhe; Gao, Bingren; Wang, Wei; Zheng, Zhe; Hu, Shengshou; Ji, Bingyang

2017-11-01

Static cold storage is accompanied with a partial safe ischemic interval for donor hearts. In this current study, a machine perfusion system was built to provide a better preservation for the donor heart and assessment for myocardial function. Chinese mini-swine (weight 30-35 kg, n = 16) were randomly divided into HTK, Celsior, and Heartbeat groups. All donor hearts were respectively preserved for 8 hours under static cold storage or machine perfusion. The perfusion solution is aimed to maintain its homeostasis based on monitoring the Heartbeat group. The ultrastructure of myocardium suggests better myocardial protection in the Heartbeat group compared with HTK or Celsior-preserved hearts. The myocardial and coronary artery structural and functional integrity was evaluated by immunofluorescence and Western blots in the Heartbeat. In the Heartbeat group, donor hearts maintained a high adenosine triphosphate level. Bcl-2 and Beclin-1 protein demonstrates high expression in the Celsior group. The Heartbeat system can be used to preserve donor hearts, and it could guarantee the myocardial and endothelial function of hearts during machine perfusion. Translating Heartbeat into clinical practice, it is such as to impact on donor heart preservation for cardiac transplantation. © 2017 International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc.

Complications of Cushing's syndrome: state of the art.

PubMed

Pivonello, Rosario; Isidori, Andrea M; De Martino, Maria Cristina; Newell-Price, John; Biller, Beverly M K; Colao, Annamaria

2016-07-01

Cushing's syndrome is a serious endocrine disease caused by chronic, autonomous, and excessive secretion of cortisol. The syndrome is associated with increased mortality and impaired quality of life because of the occurrence of comorbidities. These clinical complications include metabolic syndrome, consisting of systemic arterial hypertension, visceral obesity, impairment of glucose metabolism, and dyslipidaemia; musculoskeletal disorders, such as myopathy, osteoporosis, and skeletal fractures; neuropsychiatric disorders, such as impairment of cognitive function, depression, or mania; impairment of reproductive and sexual function; and dermatological manifestations, mainly represented by acne, hirsutism, and alopecia. Hypertension in patients with Cushing's syndrome has a multifactorial pathogenesis and contributes to the increased risk for myocardial infarction, cardiac failure, or stroke, which are the most common causes of death; risks of these outcomes are exacerbated by a prothrombotic diathesis and hypokalaemia. Neuropsychiatric disorders can be responsible for suicide. Immune disorders are common; immunosuppression during active disease causes susceptibility to infections, possibly complicated by sepsis, an important cause of death, whereas immune rebound after disease remission can exacerbate underlying autoimmune diseases. Prompt treatment of cortisol excess and specific treatments of comorbidities are crucial to prevent serious clinical complications and reduce the mortality associated with Cushing's syndrome. Copyright © 2016 Elsevier Ltd. All rights reserved.

Myocardial Mapping With Cardiac Magnetic Resonance: The Diagnostic Value of Novel Sequences.

PubMed

Sanz, Javier; LaRocca, Gina; Mirelis, Jesús G

2016-09-01

Cardiac magnetic resonance has evolved into a crucial modality for the evaluation of cardiomyopathy due to its ability to characterize myocardial structure and function. In the last few years, interest has increased in the potential of "mapping" techniques that provide direct and objective quantification of myocardial properties such as T1, T2, and T2* times. These approaches enable the detection of abnormalities that affect the myocardium in a diffuse fashion and/or may be too subtle for visual recognition. This article reviews the current state of myocardial T1 and T2-mapping in both health and disease. Copyright © 2016 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

Mesenchymal stem cells and their conditioned medium improve integration of purified induced pluripotent stem cell-derived cardiomyocyte clusters into myocardial tissue.

PubMed

Rubach, Martin; Adelmann, Roland; Haustein, Moritz; Drey, Florian; Pfannkuche, Kurt; Xiao, Bing; Koester, Annette; Udink ten Cate, Floris E A; Choi, Yeong-Hoon; Neef, Klaus; Fatima, Azra; Hannes, Tobias; Pillekamp, Frank; Hescheler, Juergen; Šarić, Tomo; Brockmeier, Konrad; Khalil, Markus

2014-03-15

Induced pluripotent stem cell-derived cardiomyocytes (iPS-CMs) might become therapeutically relevant to regenerate myocardial damage. Purified iPS-CMs exhibit poor functional integration into myocardial tissue. The aim of this study was to investigate whether murine mesenchymal stem cells (MSCs) or their conditioned medium (MScond) improves the integration of murine iPS-CMs into myocardial tissue. Vital or nonvital embryonic murine ventricular tissue slices were cocultured with purified clusters of iPS-CMs in combination with murine embryonic fibroblasts (MEFs), MSCs, or MScond. Morphological integration was assessed by visual scoring and functional integration by isometric force and field potential measurements. We observed a moderate morphological integration of iPS-CM clusters into vital, but a poor integration into nonvital, slices. MEFs and MSCs but not MScond improved morphological integration of CMs into nonvital slices and enabled purified iPS-CMs to confer force. Coculture of vital slices with iPS-CMs and MEFs or MSCs resulted in an improved electrical integration. A comparable improvement of electrical coupling was achieved with the cell-free MScond, indicating that soluble factors secreted by MSCs were involved in electrical coupling. We conclude that cells such as MSCs support the engraftment and adhesion of CMs, and confer force to noncontractile tissue. Furthermore, soluble factors secreted by MSCs mediate electrical coupling of purified iPS-CM clusters to myocardial tissue. These data suggest that MSCs may increase the functional engraftment and therapeutic efficacy of transplanted iPS-CMs into infarcted myocardium.

Mesenchymal Stem Cells and Their Conditioned Medium Improve Integration of Purified Induced Pluripotent Stem Cell–Derived Cardiomyocyte Clusters into Myocardial Tissue

PubMed Central

Rubach, Martin; Adelmann, Roland; Haustein, Moritz; Drey, Florian; Pfannkuche, Kurt; Xiao, Bing; Koester, Annette; Udink ten Cate, Floris E.A.; Choi, Yeong-Hoon; Neef, Klaus; Fatima, Azra; Hannes, Tobias; Pillekamp, Frank; Hescheler, Juergen; Šarić, Tomo; Brockmeier, Konrad

2014-01-01

Induced pluripotent stem cell–derived cardiomyocytes (iPS-CMs) might become therapeutically relevant to regenerate myocardial damage. Purified iPS-CMs exhibit poor functional integration into myocardial tissue. The aim of this study was to investigate whether murine mesenchymal stem cells (MSCs) or their conditioned medium (MScond) improves the integration of murine iPS-CMs into myocardial tissue. Vital or nonvital embryonic murine ventricular tissue slices were cocultured with purified clusters of iPS-CMs in combination with murine embryonic fibroblasts (MEFs), MSCs, or MScond. Morphological integration was assessed by visual scoring and functional integration by isometric force and field potential measurements. We observed a moderate morphological integration of iPS-CM clusters into vital, but a poor integration into nonvital, slices. MEFs and MSCs but not MScond improved morphological integration of CMs into nonvital slices and enabled purified iPS-CMs to confer force. Coculture of vital slices with iPS-CMs and MEFs or MSCs resulted in an improved electrical integration. A comparable improvement of electrical coupling was achieved with the cell-free MScond, indicating that soluble factors secreted by MSCs were involved in electrical coupling. We conclude that cells such as MSCs support the engraftment and adhesion of CMs, and confer force to noncontractile tissue. Furthermore, soluble factors secreted by MSCs mediate electrical coupling of purified iPS-CM clusters to myocardial tissue. These data suggest that MSCs may increase the functional engraftment and therapeutic efficacy of transplanted iPS-CMs into infarcted myocardium. PMID:24219308

Surgical myocardial revascularization in patients with reduced systolic left ventricular function.

PubMed

Bruno, Piergiorgio; Iafrancesco, Mauro; Massetti, Massimo

2018-04-20

Surgical myocardial revascularization in patients with reduced left ventricular function has been a matter of debate for decades. Recently published 10-years extension follow-up of the STICH trial have conclusively demonstrated benefit of surgical myocardial revascularization in patients with significant coronary artery disease and low left ventricular ejection fraction. However, selection of patients for surgery remains challenging as well as decision to perform percutaneous rather than surgical revascularization in this class of patients. New evidence helped to clarify the role of preoperative patients' characteristics as risk factors for surgery and to identify those patients who may benefit the most from surgery. Focus of this review is to review epidemiology, aetiology and pathophysiology of coronary artery disease in patients with reduced left ventricular function, role of viability and results of observational and investigational studies on revascularization in patients with reduced left ventricular function with a particular emphasis on relative indication of coronary artery bypass grafting and percutaneous coronary intervention and the surgical implications of development of ischemic mitral regurgitation or ischemic left ventricular aneurysm.

Cardiogenic Genes Expressed in Cardiac Fibroblasts Contribute to Heart Development and Repair

PubMed Central

Furtado, Milena B.; Costa, Mauro W.; Pranoto, Edward Adi; Salimova, Ekaterina; Pinto, Alex; Lam, Nicholas T.; Park, Anthony; Snider, Paige; Chandran, Anjana; Harvey, Richard P.; Boyd, Richard; Conway, Simon J.; Pearson, James; Kaye, David M.; Rosenthal, Nadia A.

2014-01-01

Rationale Cardiac fibroblasts are critical to proper heart function through multiple interactions with the myocardial compartment but appreciation of their contribution has suffered from incomplete characterization and lack of cell-specific markers. Objective To generate an unbiased comparative gene expression profile of the cardiac fibroblast pool, identify and characterize the role of key genes in cardiac fibroblast function, and determine their contribution to myocardial development and regeneration. Methods and Results High-throughput cell surface and intracellular profiling of cardiac and tail fibroblasts identified canonical MSC and a surprising number of cardiogenic genes, some expressed at higher levels than in whole heart. Whilst genetically marked fibroblasts contributed heterogeneously to interstitial but not cardiomyocyte compartments in infarcted hearts, fibroblast-restricted depletion of one highly expressed cardiogenic marker, Tbx20, caused marked myocardial dysmorphology and perturbations in scar formation upon myocardial infarction. Conclusions The surprising transcriptional identity of cardiac fibroblasts, the adoption of cardiogenic gene programs and direct contribution to cardiac development and repair provokes alternative interpretations for studies on more specialized cardiac progenitors, offering a novel perspective for reinterpreting cardiac regenerative therapies. PMID:24650916

GPCR-autoantibodies in chronic heart failure.

PubMed

Boivin-Jahns, Valerie; Jahns, Roland

2018-06-01

Chronic heart failure (CHF) is a syndrome characterized by shortness of breath, fluid retention, and a progressive reduction in cardiac function. More than 60% of the cases are ischemic in origin (i.e., due to myo-cardial infarction) and about 30% are caused by non-ischemic myocardial damage (i.e., due to genetic or non-genetic causes like myocardial inflammation). Because of alterations in both cellular and humoral immunity patients with non-ischemic CHF often develop abnormal or misled immune responses, including cross-reacting antibodies and/or autoantibodies to various cardiac anti-gens. Non-ischemic myo-cardial damage was found to progress to CHF particularly, when associated (a) with the generation of autoantibodies directed against distinct myocyte membrane proteins critically involved in cardiac function - like G-protein coup-led membrane receptors (GPCRs), or (b) with virus persistence in the myocardium. This article will review current knowledge on the pathophysiological relevance of GPCR-autoreactivity in CHF by giving an overview on the so far available evidence from pre-clinical, clinical and epidemiological studies on the CHF-inducing potential of GPCR-autoantibodies and thereon based novel therapeutic approaches in GPCR autoantibody-associated CHF.

[Cardiac protection is a clinical evidence].

PubMed

Guarracino, F; Doroni, L; Cariello, C; Baldassarri, R; Vullo, C

2004-05-01

Anaesthetics may have protective effect against myocardial ischemia. We aimed to investigate if sevoflurane administration could exert myocardial protection during following coronary occlusion in patients with coronary artery disease. a). prospective, randomized study. b). University Hospital, cardiac surgical operative theatre. c). 42 patients with coronary artery disease, scheduled to undergo coronary surgery. severe coronary stenosis of anterior descending coronary artery; no collateral flow on angiography; at least two normokinetic segments in the myocardial region supplied by the vessel being bypassed. PATIENTS were randomized to receive (group S) or not (group C) sevoflurane administration for 15 min just before coronary occlusion. d). Transoesophageal Tissue Doppler echocardiographic examination of myocardial systolic and early diastolic velocities in both groups basally and 60 s after coronary occlusion by the surgeon. e). systolic and early diastolic velocities were registered by Tissue Doppler from a long-axis view of the interventricular septum or the anterior wall of the left ventricle. In group C a significant reduction of systolic and diastolic intramyocardial velocities was found during myocardial ischemia due to coronary occlusion. Treatment with sevoflurane before coronary occlusion seem effective in reducing functional myocardial impairment due to ischemia.

Childhood obesity and cardiac remodeling: from cardiac structure to myocardial mechanics.

PubMed

Tadic, Marijana; Cuspidi, Cesare

2015-08-01

Epidemic of obesity, especially morbid obesity, among children and adolescents, is a key factor associated with the dramatic increase in prevalence of type 2 diabetes mellitus, arterial hypertension, and metabolic syndrome in this population. Furthermore, childhood obesity represents a very important predictor of obesity in adulthood that is related to cardiovascular and cerebrovascular diseases. Overweight and obesity in children and adolescents are associated with impairment of cardiac structure and function. The majority of studies investigated the influence of obesity on left ventricular remodeling. However, the impact of obesity on the right ventricle, both the atria, and myocardial mechanics has been insufficiently studied. The aim of this review article is to summarize all data about heart remodeling in childhood, from cardiac size, throughout systolic and diastolic function, to myocardial mechanics, using a wide range of mainly echocardiographic techniques and parameters. Additionally, we sought to present current knowledge about the influence of weight loss, achieved by various therapeutic approaches, on the improvement of cardiac geometry, structure, and function in obese children and adolescents.

Ergotamine-derived dopamine agonists and left ventricular function in Parkinson patients: systolic and diastolic function studied by conventional echocardiography, tissue Doppler imaging, and two-dimensional speckle tracking.

PubMed

Rasmussen, Vibeke Guldbrand; Poulsen, Steen Hvitfeldt; Dupont, Erik; Ostergaard, Karen; Safikhany, Gholamhossein; Egeblad, Henrik

2008-11-01

Ergot-derived dopamine agonists (EDDA) induce fibrotic heart valve disease. We aimed to investigate whether EDDA treatment also affects left ventricular (LV) function. Myocardial function was evaluated in 110 Parkinson patients [mean age (63.4 +/- 9.0 years)] treated for at least 6 months with either EDDA (n = 71) or non-EDDA (n = 39). LV ejection fraction did not differ between EDDA and non-EDDA patients [63 +/- 4% vs. 65 +/- 4% (ns)]. There was no difference in prevalence of diastolic dysfunction between EDDA and non-EDDA patients [7% vs. 8% (ns)]. Finally, averaged LV systolic myocardial strain and longitudinal displacement analysed by means of two-dimensional speckle tracking showed no difference between EDDA and non-EDDA patients [strain: 19 +/- 3% vs. 19 +/- 2% (ns) and longitudinal displacement: 12 +/- 2 mm vs. 12 +/- 2 mm (ns)]. Elevated p-NT-proBNP was found in 38% of EDDA patients and in 59% of non-EDDA patients (ns). In contrast to the well-established association between EDDA treatment and valvular fibrosis, EDDA did not have a detectable adverse impact on myocardial systolic and diastolic function.

The helical ventricular myocardial band of Torrent-Guasp.

PubMed

Kocica, Mladen J; Corno, Antonio F; Lackovic, Vesna; Kanjuh, Vladimir I

2007-01-01

We live in an era of substantial progress in understanding myocardial structure and function at genetic, molecular, and microscopic levels. Yet, ventricular myocardium has proven remarkably resistant to macroscopic analyses of functional anatomy. Pronounced and practically indefinite global and local structural anisotropy of its fibers and other ventricular wall constituents produces electrical and mechanical properties that are nonlinear, anisotropic, time varying, and spatially inhomogeneous. The helical ventricular myocardial band of Torrent-Guasp is a revolutionary new concept in understanding global, 3-dimensional, functional architecture of the ventricular myocardium. This concept defines the principal, cumulative vectors, integrating the tissue architecture (ie, form) and net forces developed (ie, function) within the ventricular mass. The primary purpose of this review is to emphasize the importance of this concept, in the light of collaborative efforts to establish an integrative approach, defining ventricular form and function by linking across multiple scales of biological organization, as explained in the ongoing Physiome project. Because one of the most important scientific missions in this century is integration of basic research with clinical medicine, we believe that this knowledge is not of merely academic importance, but is also the essential prerequisite in clinical evaluation and treatment of different heart diseases.

Adverse Effects on β-Adrenergic Receptor Coupling: Ischemic Postconditioning Failed to Preserve Long-Term Cardiac Function.

PubMed

Schreckenberg, Rolf; Bencsik, Péter; Weber, Martin; Abdallah, Yaser; Csonka, Csaba; Gömöri, Kamilla; Kiss, Krisztina; Pálóczi, János; Pipis, Judit; Sárközy, Márta; Ferdinandy, Péter; Schulz, Rainer; Schlüter, Klaus-Dieter

2017-12-22

Ischemic preconditioning (IPC) and ischemic postconditioning (IPoC) are currently among the most efficient strategies protecting the heart against ischemia/reperfusion injury. However, the effect of IPC and IPoC on functional recovery following ischemia/reperfusion is less clear, particularly with regard to the specific receptor-mediated signaling of the postischemic heart. The current article examines the effect of IPC or IPoC on the regulation and coupling of β-adrenergic receptors and their effects on postischemic left ventricular function. The β-adrenergic signal transduction was analyzed in 3-month-old Wistar rats for each of the intervention strategies (Sham, ischemia/reperfusion, IPC, IPoC) immediately and 7 days after myocardial infarction. Directly after the infarction a cardioprotective potential was demonstrated for both IPC and IPoC: the infarct size was reduced, apoptosis and production of reactive oxygen species were lowered, and the myocardial tissue was preserved. Seven days after myocardial ischemia, only IPC hearts showed significant functional improvement. Along with a deterioration in fractional shortening, IPoC hearts no longer responded adequately to β-adrenergic stimulation. The stabilization of β-adrenergic receptor kinase-2 via increased phosphorylation of Mdm2 (an E3-ubiquitin ligase) was responsible for desensitization of β-adrenergic receptors and identified as a characteristic specific to IPoC hearts. Immediately after myocardial infarction, rapid and transient activation of β-adrenergic receptor kinase-2 may be an appropriate means to protect the injured heart from excessive stress. In the long term, however, induction and stabilization of β-adrenergic receptor kinase-2, with the resultant loss of positive inotropic function, leads to the functional picture of heart failure. © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

Worse cardiac remodeling in response to pressure overload in type 2 diabetes mellitus.

PubMed

Gonçalves, N; Gomes-Ferreira, C; Moura, C; Roncon-Albuquerque, R; Leite-Moreira, A F; Falcão-Pires, I

2016-08-15

Diabetic cardiomyopathy is characterized by cardiac structural and functional abnormalities. Additionally, chronic pressure overload conditions are highly prevalent amongst diabetic population and this association leads to a more severe myocardial impairment. The differences in myocardial pathophysiology between type 1 and type 2 diabetes mellitus (DM) still remain to be clarified. Thus, we aimed to investigate biventricular structural and functional changes promoted by the two types of DM and the impact of concomitant chronic pressure overload. Wistar rats were injected with streptozotocin (Type 1 DM, T1DM) or fed with a hypercaloric diet (Type 2 DM, T2DM). Pressure overload was imposed in DM animals by aortic constriction and after 5weeks of DM the cardiac function and structure were evaluated. Both types of DM promoted hypertrophy, increased fibrosis and advanced glycation end-products deposition, in the two ventricles. Interestingly, the induced myocardial alterations were distinct. While T1DM stimulated a pronounced hypertrophy and extracellular matrix remodeling, T2DM induced functional impairment. The negative impact of the association of DM with aortic constriction was more pronounced in T2DM, promoting impaired function and increased stiffness, particularly in the right ventricle. Our study demonstrated that the two types of diabetes induce distinct cardiac alterations per se or when combined with chronic pressure overload. T1DM promoted a more extensive remodeling in cardiac structure while T2DM significantly impaired ventricular function. The impact of pressure overload was more notorious in T2DM as observed by worse myocardial remodeling, suggesting a higher susceptibility to the deleterious effects of chronic pressure overload, namely hypertension, among this diabetic population. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Timing of myocardial trpm7 deletion during cardiogenesis variably disrupts adult ventricular function, conduction, and repolarization.

PubMed

Sah, Rajan; Mesirca, Pietro; Mason, Xenos; Gibson, William; Bates-Withers, Christopher; Van den Boogert, Marjolein; Chaudhuri, Dipayan; Pu, William T; Mangoni, Matteo E; Clapham, David E

2013-07-09

Transient receptor potential (TRP) channels are a superfamily of broadly expressed ion channels with diverse physiological roles. TRPC1, TRPC3, and TRPC6 are believed to contribute to cardiac hypertrophy in mouse models. Human mutations in TRPM4 have been linked to progressive familial heart block. TRPM7 is a divalent-permeant channel and kinase of unknown function, recently implicated in the pathogenesis of atrial fibrillation; however, its function in ventricular myocardium remains unexplored. We generated multiple cardiac-targeted knockout mice to test the hypothesis that TRPM7 is required for normal ventricular function. Early cardiac Trpm7 deletion (before embryonic day 9; TnT/Isl1-Cre) results in congestive heart failure and death by embryonic day 11.5 as a result of hypoproliferation of the compact myocardium. Remarkably, Trpm7 deletion late in cardiogenesis (about embryonic day 13; αMHC-Cre) produces viable mice with normal adult ventricular size, function, and myocardial transcriptional profile. Trpm7 deletion at an intermediate time point results in 50% of mice developing cardiomyopathy associated with heart block, impaired repolarization, and ventricular arrhythmias. Microarray analysis reveals elevations in transcripts of hypertrophy/remodeling genes and reductions in genes important for suppressing hypertrophy (Hdac9) and for ventricular repolarization (Kcnd2) and conduction (Hcn4). These transcriptional changes are accompanied by action potential prolongation and reductions in transient outward current (Ito; Kcnd2). Similarly, the pacemaker current (If; Hcn4) is suppressed in atrioventricular nodal cells, accounting for the observed heart block. Trpm7 is dispensable in adult ventricular myocardium under basal conditions but is critical for myocardial proliferation during early cardiogenesis. Loss of Trpm7 at an intermediate developmental time point alters the myocardial transcriptional profile in adulthood, impairing ventricular function, conduction, and repolarization.

Adverse postresuscitation myocardial effects elicited by buffer-induced alkalemia ameliorated by NHE-1 inhibition in a rat model of ventricular fibrillation.

PubMed

Lamoureux, Lorissa; Radhakrishnan, Jeejabai; Mason, Thomas G; Kraut, Jeffrey A; Gazmuri, Raúl J

2016-11-01

Major myocardial abnormalities occur during cardiac arrest and resuscitation including intracellular acidosis-partly caused by CO 2 accumulation-and activation of the Na + -H + exchanger isoform-1 (NHE-1). We hypothesized that a favorable interaction may result from NHE-1 inhibition during cardiac resuscitation followed by administration of a CO 2 -consuming buffer upon return of spontaneous circulation (ROSC). Ventricular fibrillation was electrically induced in 24 male rats and left untreated for 8 min followed by defibrillation after 8 min of cardiopulmonary resuscitation (CPR). Rats were randomized 1:1:1 to the NHE-1 inhibitor zoniporide or vehicle during CPR and disodium carbonate/sodium bicarbonate buffer or normal saline (30 ml/kg) after ROSC. Survival at 240 min declined from 100% with Zoniporide/Saline to 50% with Zoniporide/Buffer and 25% with Vehicle/Buffer (P = 0.004), explained by worsening postresuscitation myocardial dysfunction. Marked alkalemia occurred after buffer administration along with lactatemia that was maximal after Vehicle/Buffer, attenuated by Zoniporide/Buffer, and minimal with Zoniporide/Saline [13.3 ± 4.8 (SD), 9.2 ± 4.6, and 2.7 ± 1.0 mmol/l; P ≤ 0.001]. We attributed the intense postresuscitation lactatemia to enhanced glycolysis consequent to severe buffer-induced alkalemia transmitted intracellularly by an active NHE-1. We attributed the worsened postresuscitation myocardial dysfunction also to severe alkalemia intensifying Na + entry via NHE-1 with consequent Ca 2+ overload injuring mitochondria, evidenced by increased plasma cytochrome c Both buffer-induced effects were ameliorated by zoniporide. Accordingly, buffer-induced alkalemia after ROSC worsened myocardial function and survival, likely through enhancing NHE-1 activity. Zoniporide attenuated these effects and uncovered a complex postresuscitation acid-base physiology whereby blood pH drives NHE-1 activity and compromises mitochondrial function and integrity along with myocardial function and survival.

Cardioprotective activity of placental growth factor combined with oral supplementation of l-arginine in a rat model of acute myocardial infarction.

PubMed

Luo, Liyun; Chen, Bairong; Huang, Yin; Liang, Zibin; Li, Songbiao; Yin, Yuelan; Chen, Jian; Wu, Wei

2016-01-01

Exogenous administration of placental growth factor (PlGF) stimulates angiogenesis and improves ventricular remodeling after acute myocardial infarction (AMI), and supplementation with l-arginine ameliorates endothelial function. The objective of the present study was to compare the cardioprotective effects of combination therapy of PlGF and l-arginine with those of direct administration of PlGF alone in a rat model of AMI. Fifty male Sprague Dawley rats were randomly divided into five groups: sham group, normal saline group, l-arginine group, PlGF group, and combination group (PlGF + l-arginine). An AMI rat model was established by ligation of the left anterior descending of coronary arteries. After 4 weeks of postligation treatment, cardiac function, scar area, angiogenesis and arteriogenesis, myocardial endothelial nitric oxide synthase (eNOS) and collagen I protein content, and plasma concentration of brain natriuretic peptide (BNP) were studied. Echocardiography, Masson's staining, immunohistochemical analyses, Western blot, and enzyme-linked immunosorbent assay were performed. Left ventricular ejection fraction (LVEF), left ventricular fraction shortening (LVFS), and capillary and arteriole densities were higher in the PlGF group than in the normal saline group ( P <0.01). Scar area, collagen I protein content, and plasma concentration of BNP were decreased in the PlGF group ( P <0.01). Myocardial eNOS protein level was elevated in the l-arginine group and PlGF + l-arginine group ( P <0.01). Compared with the PlGF group, LVEF, LVFS, myocardial eNOS, and capillary and arteriole densities were higher in the combination group ( P <0.01). Scar area, content of collagen I protein, and plasma concentration of BNP were reduced in the combination group ( P <0.01). Exogenous administration of PlGF stimulates angiogenesis and improves cardiac function. l-arginine increases the expression of the eNOS protein. PlGF and l-arginine have a more pronounced, synergistic protective effect on myocardial protection compared with that of exogenous PlGF therapy alone.

Protective effects of combination of quercetin and α-tocopherol on mitochondrial dysfunction and myocardial infarct size in isoproterenol-treated myocardial infarcted rats: biochemical, transmission electron microscopic, and macroscopic enzyme mapping evidences.

PubMed

Punithavathi, V R; Stanely Mainzen Prince, P

2010-01-01

Mitochondrial dysfunction plays an important role in the pathology of myocardial infarction. We evaluated the combined protective effects of quercetin and α-tocopherol on mitochondrial damage and myocardial infarct size in isoproterenol-induced myocardia- infarcted rats. Rats were pretreated with quercetin (10 mg/kg) alone, α-tocopherol (10 mg/kg) alone, and combination of quercetin (10 mg/kg) and α-tocopherol (10 mg/kg) orally using an intragastric tube daily for 14 days. After pretreatment, rats were induced myocardial infarction by isoproterenol (100 mg/kg) at an interval of 24 h for 2 days. Isoproterenol treatment caused significant increase in mitochondrial lipid peroxides with significant decrease in mitochondrial antioxidants. Significant decrease in the activities of isocitrate, succinate, malate, and α-ketoglutarate and NADH dehydrogenases and cytochrome-c-oxidase, significant increase in calcium, and significant decrease in adenosine triphosphate were observed in mitochondria of myocardial infarcted rats. Combined pretreatment with quercetin and α-tocopherol normalized all the biochemical parameters and preserved the integrity of heart tissue and restored normal mitochondrial function in myocardial-infarcted rats. Transmission electron microscopic findings on heart mitochondria and macroscopic enzyme mapping assay on the size of myocardial infarct also correlated with these biochemical parameters. The present study showed that combined pretreatment was highly effective than single pretreatment. Copyright 2010 Wiley Periodicals, Inc.

Pharmacological prevention of reperfusion injury in acute myocardial infarction. A potential role for adenosine as a therapeutic agent.

PubMed

Quintana, Miguel; Kahan, Thomas; Hjemdahl, Paul

2004-01-01

The concept of reperfusion injury, although first recognized from animal studies, is now recognized as a clinical phenomenon that may result in microvascular damage, no-reflow phenomenon, myocardial stunning, myocardial hibernation and ischemic preconditioning. The final consequence of this event is left ventricular (LV) systolic dysfunction leading to increased morbidity and mortality. The typical clinical case of reperfusion injury occurs in acute myocardial infarction (MI) with ST segment elevation in which an occlusion of a major epicardial coronary artery is followed by recanalization of the artery. This may occur either spontaneously or by means of thrombolysis and/or by primary percutaneous coronary intervention (PCI) with efficient platelet inhibition by aspirin (acetylsalicylic acid), clopidogrel and glycoprotein IIb/IIIa inhibitors. Although the pathophysiology of reperfusion injury is complex, the major role that neutrophils play in this process is well known. Neutrophils generate free radicals, degranulation products, arachidonic acid metabolites and platelet-activating factors that interact with endothelial cells, inducing endothelial injury and neutralization of nitrous oxide vasodilator capacity. Adenosine, through its multi-targeted pharmacological actions, is able to inhibit some of the above-mentioned detrimental effects. The net protective of adenosine in in vivo models of reperfusion injury is the reduction of the infarct size, the improvement of the regional myocardial blood flow and of the regional function of the ischemic area. Additionally, adenosine preserves the post-ischemic coronary flow reserve, coronary blood flow and the post-ischemic regional contractility. In small-scale studies in patients with acute MI, treatment with adenosine has been associated with smaller infarcts, less no-reflow phenomenon and improved LV function. During elective PCI adenosine reduced ST segment shifts, lactate production and ischemic symptoms. During the last years, three relatively large placebo-controlled clinical trials have been conducted: Acute Myocardial Infarction Study of Adenosine Trial (AMISTAD) I and II and Attenuation by Adenosine of Cardiac Complications (ATTACC). In the AMISTAD trials, the final infarct size was reduced and the LV systolic function was improved by adenosine treatment, mainly in patients with anterior MI localization. However, morbidity and mortality were not affected. In the ATTACC study, the LV systolic function was not affected by adenosine, however, trends towards improved survival were observed in patients with anterior MI localization. The possibility of obtaining a Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow in the infarct-related artery in up to 95% of patients with acute MI (increasing the occurrence of reperfusion injury) has turned back the interest towards the protection of myocardial cells from the impending ischemic and reperfusion injury in which adenosine alone or together with other cardio-protective agents may exert important clinical effects.

Employing Extracellular Volume Cardiovascular Magnetic Resonance Measures of Myocardial Fibrosis to Foster Novel Therapeutics.

PubMed

Schelbert, Erik B; Sabbah, Hani N; Butler, Javed; Gheorghiade, Mihai

2017-06-01

Quantifying myocardial fibrosis (MF) with myocardial extracellular volume measures acquired during cardiovascular magnetic resonance promises to transform clinical care by advancing pathophysiologic understanding and fostering novel therapeutics. Extracellular volume quantifies MF by measuring the extracellular compartment depicted by the myocardial uptake of contrast relative to plasma. MF is a key domain of dysfunctional but viable myocardium among others (eg, microvascular dysfunction and cardiomyocyte/mitochondrial dysfunction). Although anatomically distinct, these domains may functionally interact. MF represents pathological remodeling in the heart associated with cardiac dysfunction and adverse outcomes likely mediated by interactions with the microvasculature and the cardiomyocyte. Reversal of MF improves key measures of cardiac dysfunction, so reversal of MF represents a likely mechanism for improved outcomes. Instead of characterizing the myocardium as homogenous tissue and using important yet still generic descriptors, such as thickness (hypertrophy) and function (diastolic or systolic), which lack mechanistic specificity, paradigms of cardiac disease have evolved to conceptualize myocardial disease and patient vulnerability based on the extent of disease involving its various compartments. Specifying myocardial compartmental involvement may then implicate cellular/molecular disease pathways for treatment and targeted pharmaceutical development and above all highlight the role of the cardiac-specific pathology in heart failure among myriad other changes in the heart and beyond. The cardiology community now requires phase 2 and 3 clinical trials to examine strategies for the regression/prevention of MF and eventually biomarkers to identify MF without reliance on cardiovascular magnetic resonance. It seems likely that efficacious antifibrotic therapy will improve outcomes, but definitive data are needed. © 2017 American Heart Association, Inc.

Evaluation of mechanical dyssynchrony and myocardial perfusion using phase analysis of gated SPECT imaging in patients with left ventricular dysfunction

PubMed Central

Trimble, Mark A.; Borges-Neto, Salvador; Honeycutt, Emily F.; Shaw, Linda K.; Pagnanelli, Robert; Chen, Ji; Iskandrian, Ami E.; Garcia, Ernest V.; Velazquez, Eric J.

2010-01-01

Background Using phase analysis of gated single photon emission computed tomography (SPECT) imaging, we examined the relation between myocardial perfusion, degree of electrical dyssynchrony, and degree of SPECT-derived mechanical dyssynchrony in patients with left ventricular (LV) dysfunction. Methods and Results We retrospectively examined 125 patients with LV dysfunction and ejection fraction of 35% or lower. Fourier analysis converts regional myocardial counts into a continuous thickening function, allowing resolution of phase of onset of myocardial thickening. The SD of LV phase distribution (phase SD) and histogram bandwidth describe LV phase dispersion as a measure of dyssynchrony. Heart failure (HF) patients with perfusion abnormalities ities have higher degrees of dyssynchrony measured by median phase SD (45.5° vs 27.7°, P < .0001) and bandwidth (117.0° vs 73.0°, P = .0006). HF patients with prolonged QRS durations have higher degrees of dyssynchrony measured by median phase SD (54.1° vs 34.7°, P < .0001) and bandwidth (136.5° vs 99.0°, P = .0005). Mild to moderate correlations exist between QRS duration and phase analysis indices of phase SD (r = 0.50) and bandwidth (r = 0.40). Mechanical dyssynchrony (phase SD >43°) was 43.2%. Conclusions HF patients with perfusion abnormalities or prolonged QRS durations QRS durations have higher degrees of mechanical dyssynchrony. Gated SPECT myocardial perfusion imaging can quantify myocardial function, perfusion, and dyssynchrony and may help in evaluating patients for cardiac resynchronization therapy. PMID:18761269

Single-Dose Intracardiac Injection of Pro-Regenerative MicroRNAs Improves Cardiac Function After Myocardial Infarction.

PubMed

Lesizza, Pierluigi; Prosdocimo, Giulia; Martinelli, Valentina; Sinagra, Gianfranco; Zacchigna, Serena; Giacca, Mauro

2017-04-14

Recent evidence indicates that a few human microRNAs (miRNAs), in particular hsa-miR-199a-3p and hsa-miR-590-3p, stimulate proliferation of cardiomyocytes and, once expressed in the mouse heart using viral vectors, induce cardiac regeneration after myocardial infarction. Viral vectors, however, are not devoid of safety issues and, more notably, drive expression of the encoded miRNAs for indefinite periods of time, which might not be desirable in light of human therapeutic application. As an alternative to the use of viral vectors, we wanted to assess the efficacy of synthetic miRNA mimics in inducing myocardial repair after single intracardiac injection using synthetic lipid formulations. We comparatively analyzed the efficacy of different lipid formulations in delivering hsa-miR-199a-3p and hsa-miR-590-3p both in primary neonatal mouse cardiomyocytes and in vivo. We established a transfection protocol allowing persistence of these 2 mimics for at least 12 days after a single intracardiac injection, with minimal dispersion to other organs and long-term preservation of miRNA functional activity, as assessed by monitoring the expression of 2 mRNA targets. Administration of this synthetic formulation immediately after myocardial infarction in mice resulted in marked reduction of infarct size and persistent recovery of cardiac function. A single administration of synthetic miRNA-lipid formulations is sufficient to stimulate cardiac repair and restoration of cardiac function. © 2017 American Heart Association, Inc.

Cardiovascular Magnetic Resonance Imaging of Myocardial Infarction, Viability, and Cardiomyopathies

PubMed Central

West, Amy M.; Kramer, Christopher M.

2010-01-01

Cardiovascular magnetic resonance provides the opportunity for a truly comprehensive evaluation of patients with a history of MI, with regards to characterizing the extent of disease, impact on LV function and degree of viable myocardium. The use of contrast-enhanced CMR for first-pass perfusion and late gadolinium enhancement is a powerful technique for delineating areas of myocardial ischemia and infarction. Using a combination of T2-weighted and contrast-enhanced CMR images, information about the acuity of an infarct can be obtained. There is an extensive amount of literature using contrast-enhanced CMR to predict myocardial functional recovery with revascularization in patients with ischemic cardiomyopathies. In addition, CMR imaging in patients with cardiomyopathies can distinguish between ischemic and non-ischemic etiologies, with the ability to further characterize the underlying pathology for non-ischemic cardiomyopathies. PMID:20197150

Abnormal mitochondrial respiration in failed human myocardium.

PubMed

Sharov, V G; Todor, A V; Silverman, N; Goldstein, S; Sabbah, H N

2000-12-01

Chronic heart failure (HF) is associated with morphologic abnormalities of cardiac mitochondria including hyperplasia, reduced organelle size and compromised structural integrity. In this study, we examined whether functional abnormalities of mitochondrial respiration are also present in myocardium of patients with advanced HF. Mitochondrial respiration was examined using a Clark electrode in an oxygraph cell containing saponin-skinned muscle bundles obtained from myocardium of failed explanted human hearts due to ischemic (ICM, n=9) or idiopathic dilated (IDC, n=9) cardiomyopathy. Myocardial specimens from five normal donor hearts served as controls (CON). Basal respiratory rate, respiratory rate after addition of the substrates glutamate and malate (V(SUB)), state 3 respiration (after addition of ADP, V(ADP)) and respiration after the addition of atractyloside (V(AT)) were measured in scar-free muscle bundles obtained from the subendocardial (ENDO) and subepicardial (EPI) thirds of the left ventricular (LV) free wall, interventricular septum and right ventricular (RV) free wall. There were no differences in basal and substrate-supported respiration between CON and HF regardless of etiology. V(ADP)was significantly depressed both in ICM and IDC compared to CON in all the regions studied. The respiratory control ratio, V(ADP)/V(AT), was also significantly decreased in HF compared to CON. In both ICM and IDC, V(ADP)was significantly lower in ENDO compared to EPI. The results indicate that mitochondrial respiration is abnormal in the failing human heart. The findings support the concept of low myocardial energy production in HF via oxidative phosphorylation, an abnormality with a potentially impact on global cardiac performance. Copyright 2000 Academic Press.

Behavioral, psycho-physiological and salivary cortisol modifications after short-term alprazolam treatment in patients with recent myocardial infarction.

PubMed

Pruneti, Carlo; Giusti, Mariarosa; Boem, Adriano; Luisi, Michele

2002-01-01

The aim of this study was to determine the behavioral and physiological effects of the central nervous system depressant alprazolam on a group of cardiac patients. Immediately after hospital discharge, the Crown and Crisp Experiential Index (CCEI) was administered, the salivary cortisol was detected and a psycho-physiological profile was recorded in 52 subjects who had suffered from myocardial infarction. Half of the subjects represented the experimental group and the remaining 26 individuals acted as a control group not undergoing treatment. The benzodiazepine alprazolam (0.25 mg) was administered twice daily to the treated group only. With the exception of the administration of the drug, all recruited subjects underwent the same clinical evaluation. The CCEI data of the treated group showed significant decreases for the following scales: free floating anxiety (p < 0.001), phobic anxiety (p < 0.01), somatic complaints (p < 0.05), and depression (p < 0.01). In the same group, with regard to the physiological parameters, the skin conductance response significantly decreased during the baseline phase (p < 0.01), and almost all parameters showed decreased values during mental stress test administration. Cortisol levels also decreased during the recovery phase of the psycho-physiological profile assessment. Alprazolam seems to be able to reduce sympathetic discharge and some stress-related behavioral and physiological responses. This could be of benefit for selected cardiac patients for whom increases in sympathetic tone may constitute a risk factor.

Suicide in males and females with cardiovascular disease and comorbid depression.

PubMed

Hawkins, Michael; Schaffer, Ayal; Reis, Catherine; Sinyor, Mark; Herrmann, Nathan; Lanctôt, Krista L

2016-06-01

Myocardial infarction (MI) has been associated with an increased risk of suicide, further increased among individuals with a comorbid psychiatric illness. A paucity of studies have examined details of suicide among individuals with cardiovascular disease (CVD) and comorbid depression. We aimed to compare demographic, clinical and suicide-specific characteristics between suicide victims with CVD with depression (CVD+D) and without comorbid depression (CVD-D). Coroner data on suicide decedents with CVD (n=413) occurring in Toronto, Canada from 1998 to 2012 were collected. Characteristics were compared between the CVD+D and CVD-D groups. Regression analysis examined for gender differences in these groups. CVD+D subjects compared to CVD-D were more likely to have had a past suicide attempt (p=0.008), and to have experienced a bereavement (p=0.008) or financial stressor (p=0.005) in the past year. Each of these variables remained significantly associated with the presence of depression after the regression analysis. Within the CVD+D group, females were more likely to die from suicide by self-poisoning (p<0.0001) and males by shooting (p=0.001). Psychological autopsies were not available. The definition of CVD was broad and the accuracy of its diagnosis could not be confirmed. Individuals with CVD+D who died from suicide had significant differences in clinical characteristics and specific stressors compared to those without depression. These data may help to better characterize suicide risk and prevention in this vulnerable population. Copyright © 2016 Elsevier B.V. All rights reserved.

Air Pollution and ST-Segment Depression in Elderly Subjects

PubMed Central

Gold, Diane R.; Litonjua, Augusto A.; Zanobetti, Antonella; Coull, Brent A.; Schwartz, Joel; MacCallum, Gail; Verrier, Richard L.; Nearing, Bruce D.; Canner, Marina J.; Suh, Helen; Stone, Peter H.

2005-01-01

Increased levels of daily ambient particle pollution have been associated with increased risk of cardiovascular morbidity. Black carbon (BC) is a measure of the traffic-related component of particles. We investigated associations between ambient pollution and ST-segment levels in a repeated-measures study including 269 observations on 24 active Boston residents 61–88 years of age, each observed up to 12 times from June through September 1999. The protocol involved continuous Holter electrocardiogram monitoring including 5 min of rest, 5 min of standing, 5 min of exercise outdoors, 5 min of recovery, and 20 cycles of paced breathing. Pollution-associated ST-depression was estimated for a 10th- to 90th-percentile change in BC. We calculated the average ST-segment level, referenced to the P-R isoelectric values, for each portion of the protocol. The mean BC level in the previous 12 hr, and the BC level 5 hr before testing, predicted ST-segment depression in most portions of the protocol, but the effect was strongest in the postexercise periods. During post-exercise rest, an elevated BC level was associated with −0.1 mm ST-segment depression (p = 0.02 for 12-hr mean BC; p = 0.001 for 5-hr BC) in continuous models. Elevated BC also predicted increased risk of ST-segment depression ≥0.5 mm among those with at least one episode of that level of ST-segment depression. Carbon monoxide was not a confounder of this association. ST-segment depression, possibly representing myocardial ischemia or inflammation, is associated with increased exposure to particles whose predominant source is traffic. PMID:16002377

Revascularization with percutaneous coronary intervention does not affect androgen status in males with chronic stable angina pectoris.

PubMed

Gosai, J N; Charalampidis, P; Nikolaidou, T; Parviz, Y; Morris, P D; Channer, K S; Jones, T H; Grech, E D

2016-05-01

There is a clear association between low serum testosterone and coronary artery disease (CAD) in men. Hypotestosteronaemia is associated with accelerated atherosclerosis and a quarter of men with CAD are biochemically hypogonadal. Amongst those with CAD, hypotestosteronaemia is associated with increased mortality. Testosterone vasodilates coronary arteries, and exogenous testosterone reduces ischaemia. Whether hypotestosteronaemia is a cause or a consequence of CAD remains unanswered. The aim of this prospective observational study was to investigate whether coronary revascularization affected androgen status in men with stable angina pectoris. Twenty five men (mean age 62.7, SD 9.18) with angiographically significant CAD and symptomatic angina underwent full coronary revascularization by percutaneous coronary intervention. Androgen status and symptoms of angina, stress, depression and sexual function were assessed before, and at one and 6 months after the coronary revascularization. All patients underwent complete revascularization which was associated with a significant reduction in angina symptoms and ischaemia. No significant difference was seen in total testosterone (11.33 nmol/L baseline; 12.56, 1 month post; 13.04 at 6 months; p = 0.08). A significant and sustained rise in sex hormone-binding globulin was seen (33.99 nm/L baseline; 36.11 nm/L 1 month post PCI; 37.94 nm/L at 6 months; p = 0.03) Overall, there was no significant alteration in any other marker of androgen status including free testosterone or bioavailable testosterone. There was no change in symptoms of anxiety, depression or sexual function. Coronary revascularization has no sustained effect on androgen status. This supports the hypothesis that hypotestosteronaemia is not a consequence of angina pectoris or myocardial ischaemia. © 2016 American Society of Andrology and European Academy of Andrology.

Prevalence and associated factors for decreased appetite among patients with stable heart failure.

PubMed

Andreae, Christina; Strömberg, Anna; Årestedt, Kristofer

2016-06-01

To explore the prevalence of decreased appetite and factors associated with appetite among patients with stable heart failure. Decreased appetite is an important factor for the development of undernutrition among patients with heart failure, but there are knowledge gaps about prevalence and the factors related to appetite in this patient group. Observational, cross-sectional study. A total of 186 patients with mild to severe heart failure were consecutively recruited from three heart failure outpatient clinics. Data were obtained from medical records (heart failure diagnosis, comorbidity and medical treatment) and self-rated questionnaires (demographics, appetite, self-perceived health, symptoms of depression and sleep). Blood samples were taken to determine myocardial stress and nutrition status. Heart failure symptoms and cognitive function were assessed by clinical examinations. The Council on Nutrition Appetite Questionnaire was used to assess self-reported appetite. Bivariate correlations and multivariate linear regression analyses were conducted to explore factors associated with appetite. Seventy-one patients (38%) experienced a loss of appetite with a significant risk of developing weight loss. The final multiple regression model showed that age, symptoms of depression, insomnia, cognitive function and pharmacological treatment were associated with appetite, explaining 27% of the total variance. In this cross-sectional study, a large share of patients with heart failure was affected by decreased appetite, associated with demographic, psychosocial and medical factors. Loss of appetite is a prevalent problem among patients with heart failure that may lead to undernutrition. Health care professionals should routinely assess appetite and discuss patients' experiences of appetite, nutrition intake and body weight and give appropriate nutritional advice with respect to individual needs. © 2016 John Wiley & Sons Ltd.

Differential relationship between depression severity and patients' perceived family functioning in women versus in men.

PubMed

Febres, Jeniimarie; Rossi, Rita; Gaudiano, Brandon A; Miller, Ivan W

2011-07-01

Previous research suggests that depression and family functioning are related and that women and men may differ in how they respond to and cope with depression. Significantly less attention has been paid to whether sex moderates the relationship between family functioning and depression. In the current study, the relationship between depression severity and perceived family functioning, both generally and in specific areas, was examined in women and men (N = 117) hospitalized with major depression. The level of depression severity was not significantly different in men and in women. Correlations between depression severity and most domains of family functioning were significant and positive for men only. Furthermore, sex statistically moderated the associations between depression severity and family functioning in the areas of problem solving, communication, affective responsiveness, and behavior control. The implications for the assessment and treatment of family dysfunction in severely depressed patients are discussed.

Right ventricular involvement in patients with inferior myocardial infarction, correlation of electrocardiographic findings with echocardiography data.

PubMed

Javed, Sumbul; Rajani, Ali Raza; Govindaswamy, Pushparani; Radaideh, Ghazi Ahmed; Abubaraka, Harb Ahmed; Qureshi, Tariq Ilyas; Arshad, Hassaan Bin

2017-03-01

To determine the right ventricular involvement in patients with inferior myocardial infarction by echocardiography in relation to electrocardiographic findings. This observational, prospective study was conducted at Rashid Hospital, Dubai, the United Arab Emirates, from January to September 2013, and comprised patients with inferior myocardial infarction. All patients aged above 18 years were included. Right ventricular myocardial infarction was defined by the electrocardiographic criteria of > 1mV ST elevation in V4R-V5R leads. RV infarction was assessed on echocardiography by fractional area change, tricuspid annular plane systolic excursion and tricuspid annular systolic velocity by tissue Doppler imaging. SPSS 21 was used for data analysis. Of the 73 patients, there were 68(93%) men and 5(7%) women. The three modalities used to assess the right ventricular infarction showed right ventricular involvement in 36(49.3%) cases by fractional area change, 28(38.4%) cases by tricuspid annular plane systolic excursion and 31(42.5%) cases by tissue Doppler imaging in patients with inferior myocardial infarction. Tissue Doppler imaging and right ventricular function showed low degree of negative correlation (p=0.16) while the correlation between tricuspid annular plane systolic excursion and right ventricular function showed significant positive correlation (p<0.0001). Assessment of right ventricular infarction by echocardiography helped to diagnose right ventricular infarction in greater number of cases compared to surface electrocardiogram.

A Novel Positron Emission Tomography (PET) Approach to Monitor Cardiac Metabolic Pathway Remodeling in Response to Sunitinib Malate.

PubMed

O'Farrell, Alice C; Evans, Rhys; Silvola, Johanna M U; Miller, Ian S; Conroy, Emer; Hector, Suzanne; Cary, Maurice; Murray, David W; Jarzabek, Monika A; Maratha, Ashwini; Alamanou, Marina; Udupi, Girish Mallya; Shiels, Liam; Pallaud, Celine; Saraste, Antti; Liljenbäck, Heidi; Jauhiainen, Matti; Oikonen, Vesa; Ducret, Axel; Cutler, Paul; McAuliffe, Fionnuala M; Rousseau, Jacques A; Lecomte, Roger; Gascon, Suzanne; Arany, Zoltan; Ky, Bonnie; Force, Thomas; Knuuti, Juhani; Gallagher, William M; Roivainen, Anne; Byrne, Annette T

2017-01-01

Sunitinib is a tyrosine kinase inhibitor approved for the treatment of multiple solid tumors. However, cardiotoxicity is of increasing concern, with a need to develop rational mechanism driven approaches for the early detection of cardiac dysfunction. We sought to interrogate changes in cardiac energy substrate usage during sunitinib treatment, hypothesising that these changes could represent a strategy for the early detection of cardiotoxicity. Balb/CJ mice or Sprague-Dawley rats were treated orally for 4 weeks with 40 or 20 mg/kg/day sunitinib. Cardiac positron emission tomography (PET) was implemented to investigate alterations in myocardial glucose and oxidative metabolism. Following treatment, blood pressure increased, and left ventricular ejection fraction decreased. Cardiac [18F]-fluorodeoxyglucose (FDG)-PET revealed increased glucose uptake after 48 hours. [11C]Acetate-PET showed decreased myocardial perfusion following treatment. Electron microscopy revealed significant lipid accumulation in the myocardium. Proteomic analyses indicated that oxidative metabolism, fatty acid β-oxidation and mitochondrial dysfunction were among the top myocardial signalling pathways perturbed. Sunitinib treatment results in an increased reliance on glycolysis, increased myocardial lipid deposition and perturbed mitochondrial function, indicative of a fundamental energy crisis resulting in compromised myocardial energy metabolism and function. Our findings suggest that a cardiac PET strategy may represent a rational approach to non-invasively monitor metabolic pathway remodeling following sunitinib treatment.

A Novel Positron Emission Tomography (PET) Approach to Monitor Cardiac Metabolic Pathway Remodeling in Response to Sunitinib Malate

PubMed Central

Silvola, Johanna M. U.; Miller, Ian S.; Conroy, Emer; Hector, Suzanne; Cary, Maurice; Murray, David W.; Jarzabek, Monika A.; Maratha, Ashwini; Alamanou, Marina; Udupi, Girish Mallya; Shiels, Liam; Pallaud, Celine; Saraste, Antti; Liljenbäck, Heidi; Jauhiainen, Matti; Oikonen, Vesa; Ducret, Axel; Cutler, Paul; McAuliffe, Fionnuala M.; Rousseau, Jacques A.; Lecomte, Roger; Gascon, Suzanne; Arany, Zoltan; Ky, Bonnie; Force, Thomas; Knuuti, Juhani; Gallagher, William M.; Roivainen, Anne; Byrne, Annette T.

2017-01-01

Sunitinib is a tyrosine kinase inhibitor approved for the treatment of multiple solid tumors. However, cardiotoxicity is of increasing concern, with a need to develop rational mechanism driven approaches for the early detection of cardiac dysfunction. We sought to interrogate changes in cardiac energy substrate usage during sunitinib treatment, hypothesising that these changes could represent a strategy for the early detection of cardiotoxicity. Balb/CJ mice or Sprague-Dawley rats were treated orally for 4 weeks with 40 or 20 mg/kg/day sunitinib. Cardiac positron emission tomography (PET) was implemented to investigate alterations in myocardial glucose and oxidative metabolism. Following treatment, blood pressure increased, and left ventricular ejection fraction decreased. Cardiac [18F]-fluorodeoxyglucose (FDG)-PET revealed increased glucose uptake after 48 hours. [11C]Acetate-PET showed decreased myocardial perfusion following treatment. Electron microscopy revealed significant lipid accumulation in the myocardium. Proteomic analyses indicated that oxidative metabolism, fatty acid β-oxidation and mitochondrial dysfunction were among the top myocardial signalling pathways perturbed. Sunitinib treatment results in an increased reliance on glycolysis, increased myocardial lipid deposition and perturbed mitochondrial function, indicative of a fundamental energy crisis resulting in compromised myocardial energy metabolism and function. Our findings suggest that a cardiac PET strategy may represent a rational approach to non-invasively monitor metabolic pathway remodeling following sunitinib treatment. PMID:28129334

Neuromodulation therapy does not influence blood flow distribution or left-ventricular dynamics during acute myocardial ischemia.

PubMed

Kingma, J G; Linderoth, B; Ardell, J L; Armour, J A; DeJongste, M J; Foreman, R D

2001-08-13

Electrical stimulation of the dorsal aspect of the upper thoracic spinal cord is used increasingly to treat patients with angina pectoris refractory to conventional therapeutic strategies. The purpose of this study was to determine whether spinal cord stimulation (SCS) in dogs affects regional myocardial blood flow and left-ventricular (LV) function before and during transient obstruction of the left anterior descending coronary artery (LAD). In anesthetized dogs, regional myocardial blood flow distribution was determined using radiolabeled microspheres and left-ventricular function was measured by impedance-derived pressure-volume loops. SCS was accomplished by stimulating the dorsal T1-T2 segments of the spinal cord using epidural bipolar electrodes at 90% of motor threshold (MT) (50 Hz, 0.2-ms duration). Effects of 5-min SCS were assessed under basal conditions and during 4-min occlusion of the LAD. SCS alone evoked no change in regional myocardial blood flow or cardiovascular indices. Transient LAD occlusion significantly diminished blood flow within ischemic, but not in non-ischemic myocardial tissue. Left ventricular pressure-volume loops were shifted rightward during LAD occlusion. Cardiac indices were altered similarly during LAD occlusion and concurrent SCS. SCS does not influence the distribution of blood flow within the non-ischemic or ischemic myocardium. Nor does it modify LV pressure-volume dynamics in the anesthetized experimental preparation.

Determination of multidirectional myocardial deformations in cats with hypertrophic cardiomyopathy by using two-dimensional speckle-tracking echocardiography.

PubMed

Suzuki, Ryohei; Mochizuki, Yohei; Yoshimatsu, Hiroki; Teshima, Takahiro; Matsumoto, Hirotaka; Koyama, Hidekazu

2017-12-01

Objectives Hypertrophic cardiomyopathy, a primary disorder of the myocardium, is the most common cardiac disease in cats. However, determination of myocardial deformation with two-dimensional speckle-tracking echocardiography in cats with various stages of hypertrophic cardiomyopathy has not yet been reported. This study was designed to measure quantitatively multidirectional myocardial deformations of cats with hypertrophic cardiomyopathy. Methods Thirty-two client-owned cats with hypertrophic cardiomyopathy and 14 healthy cats serving as controls were enrolled and underwent assessment of myocardial deformation (peak systolic strain and strain rate) in the longitudinal, radial and circumferential directions. Results Longitudinal and radial deformations were reduced in cats with hypertrophic cardiomyopathy, despite normal systolic function determined by conventional echocardiography. Cats with severely symptomatic hypertrophic cardiomyopathy also had lower peak systolic circumferential strain, in addition to longitudinal and radial strain. Conclusions and relevance Longitudinal and radial deformation may be helpful in the diagnosis of hypertrophic cardiomyopathy. Additionally, the lower circumferential deformation in cats with severe hypertrophic cardiomyopathy may contribute to clinical findings of decompensation, and seems to be related to severe cardiac clinical signs. Indices of multidirectional myocardial deformations by two-dimensional speckle-tracking echocardiography may be useful markers and help to distinguish between cats with hypertrophic cardiomyopathy and healthy cats. Additionally, they may provide more detailed assessment of contractile function in cats with hypertrophic cardiomyopathy.

Nuclear cardiograph and scintigraphy

NASA Technical Reports Server (NTRS)

Mclaughlin, P.

1975-01-01

Extensive advances in the technology of detectors, data analysis systems, and tracers used have resulted in greatly expanded applications of radioisotopes to the assessment of cardiac function and disease. The development of nuclear cardiology has proceeded along four lines: (1) radionuclide angiography, (2) myocardial perfusion imaging, (3) intracoronary microsphere imaging, and (4) regional myocardial blood flow determination using inert gases.

Takotsubo-like Myocardial Dysfunction in a Patient with Botulism.

PubMed

Tonomura, Shuichi; Kakehi, Yoshiaki; Sato, Masatoshi; Naito, Yuki; Shimizu, Hisao; Goto, Yasunobu; Takahashi, Nobuyuki

2017-11-01

Botulinum toxin A (BTXA) can disrupt the neuromuscular and autonomic functions. We herein report a case of autonomic system dysfunction that manifested as Takotsubo-like myocardial dysfunction in a patient with botulism. Takotsubo syndrome results in acute cardiac insufficiency, another fatal complication of botulism in addition to respiratory muscle paralysis, particularly in patients with cardiovascular disease.

Takotsubo-like Myocardial Dysfunction in a Patient with Botulism

PubMed Central

Tonomura, Shuichi; Kakehi, Yoshiaki; Sato, Masatoshi; Naito, Yuki; Shimizu, Hisao; Goto, Yasunobu; Takahashi, Nobuyuki

2017-01-01

Botulinum toxin A (BTXA) can disrupt the neuromuscular and autonomic functions. We herein report a case of autonomic system dysfunction that manifested as Takotsubo-like myocardial dysfunction in a patient with botulism. Takotsubo syndrome results in acute cardiac insufficiency, another fatal complication of botulism in addition to respiratory muscle paralysis, particularly in patients with cardiovascular disease. PMID:28924131

Risk of incident cardiovascular events amongst individuals with anxiety and depression: A prospective cohort study in the east London primary care database.

PubMed

Mathur, R; Pérez-Pinar, M; Foguet-Boreu, Q; Ayis, S; Ayerbe, L

2016-12-01

It is unknown how risk of myocardial infarction and stroke differ for patients with and without anxiety or depression, and whether this risk can be explained by demographics, medication use, cardiovascular risk factors. The aim of this study is to quantify differences in risk of non-fatal MI or stroke among patients with anxiety or depression. Prospective cohort study examining risk of incident MI and stroke between March 2005 and March 2015 for 524,952 patients aged 30 and over from the east London primary care database for patients with anxiety or depression. Amongst 21,811 individuals with depression at baseline, 1.2% had MI and 0.4% had stroke. Of 22,128 individuals with anxiety at baseline, 1.1% had MI and 0.3% had stroke. Depression was independently associated with both MI and stroke, whereas anxiety was associated with MI only before adjustment for cardiovascular risk factors. Antidepressant use increased risk for MI but not stroke. Mean age at first MI was lower in those with anxiety, while mean age at first stroke was lower in those with depression. The study was limited to patients currently registered in the database and thus we did not have any patients that died during the course of follow-up. Patients with depression have increased risk of cardiovascular events. The finding of no increased cardiovascular risk in those with anxiety after adjusting for cardiovascular risk factors is of clinical importance and highlights that the adequate control of traditional risk factors is the cornerstone of cardiovascular disease prevention. Targeting management of classical cardiovascular risk factors and evaluating the risks of antidepressant prescribing should be prioritized. Copyright © 2016 Elsevier B.V. All rights reserved.

Meta-analysis of selective serotonin reuptake inhibitors in patients with depression and coronary heart disease.

PubMed

Pizzi, Carmine; Rutjes, Anne Wilhelmina Saskia; Costa, Grazia Maria; Fontana, Fiorella; Mezzetti, Andrea; Manzoli, Lamberto

2011-04-01

The occurrence of depression in patients with coronary heart disease (CHD) substantially increases the likelihood of a poorer cardiovascular prognosis. Although antidepressants are generally effective in decreasing depression, their use in patients with CHD is controversial. We carried out a meta-analysis to evaluate the health effects of selective serotonin reuptake inhibitors (SSRIs) versus placebo or no antidepressants in patients with CHD and depression. Observational studies and randomized controlled trials (RCTs) were searched in MEDLINE, EMBASE, PsycINFO, Cochrane Controlled Clinical Trial Register and other trial registries, and references of relevant articles. Primary outcomes were readmission for CHD (including myocardial infarction, unstable angina, and stroke) and all-cause mortality; the secondary outcome was severity of depression symptoms. Seven articles on 6 RCTs involving 2,461 participants were included. One study incorrectly randomized participants, and another was a reanalysis of RCT data. These were considered observational and analyzed separately. When only properly randomized trials were considered (n = 734 patients), patients on SSRIs showed no significant differences in mortality (risk ratio 0.39, 95% confidence interval 0.08 to 2.01) or CHD readmission rates (0.74, 0.44 to 1.23) compared to controls. Conversely, when all studies were included, SSRI use was associated with a significant decrease in CHD readmission (0.63, 0.46 to 0.86) and mortality rates (0.56, 0.35 to 0.88). A significantly greater improvement in depression symptoms was always apparent in patients on SSRIs with all selected indicators. In conclusion, in patients with CHD and depression, SSRI medication decreases depression symptoms and may improve CHD prognosis. Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.

Myocardial Blood Flow and Inflammatory Cardiac Sarcoidosis.

PubMed

Kruse, Matthew J; Kovell, Lara; Kasper, Edward K; Pomper, Martin G; Moller, David R; Solnes, Lilja; Chen, Edward S; Schindler, Thomas H

2017-02-01

This study sought to evaluate the effects of inflammatory sarcoid disease on coronary circulatory function and the response to immune-suppressive treatment. Although positron emission tomography assessment of myocardial inflammation is increasingly applied to identify active cardiac sarcoidosis, its effect on coronary flow and immune-suppressive treatment remains to be characterized. Thirty-two individuals, who were referred for positron emission tomography/computed tomography, were evaluated for known or suspected cardiac sarcoidosis applying 18 F-fluorodeoxyglucose to determine inflammation and 13 N-ammonia to assess for perfusion deficits following a high-fat/low-carbohydrate diet and fasting state >12 h to suppress myocardial glucose uptake. Inflammation was quantified with standardized uptake value and regional myocardial blood flow at rest and during regadenoson-stimulated hyperemia was determined in ml/g/min. Positron emission tomography studies were repeated in 18 cases with a median follow-up of 2.5 years (interquartile range [IQR]:1.3 to 3.4 years). Twenty-five exams had normal perfusion but evidence of regional inflammation (group 1), and 21 exams presented a regional perfusion deficit associated with inflammation (group 2). Median myocardial blood flow did not differ between inflamed and noninflamed myocardium in both groups (0.86 ml/g/min [IQR: 0.66 to 1.11 ml/g/min] vs. 0.83 ml/g/min [IQR: 0.64 to 1.12 ml/g/min] and 0.74 ml/g/min [IQR: 0.60 to 0.93 ml/g/min] vs. 0.77 ml/g/min [IQR: 0.59 to 0.95 ml/g/min], respectively). As regards median hyperemic myocardial blood flows, they were significantly lower in the inflamed than in the remote regions in group 1 and 2 (2.31 ml/g/min [IQR: 1.81 to 2.95 ml/g/min] vs. 2.70 ml/g/min [IQR: 2.07 to 3.30 ml/g/min] and 1.61 ml/g/min [IQR: 1.17 to 2.18 ml/g/min] vs. 1.94 ml/g/min [IQR: 1.49 to 2.39 ml/g/min]; p < 0.001, respectively). Immune-suppression-mediated decrease in inflammation was associated with preserved myocardial flow reserve (MFR) at follow-up, whereas MFR significantly worsened in regions without changes or even increases in inflammation (median ΔMFR: 0.07 [IQR: -0.29 to 0.45] vs. -0.24 [IQR: -0.84 to 0.21]; p < 0.001). There was an inverse correlation between pronounced alterations in myocardial inflammation (Δ regional myocardial volume with standardized uptake value >4.1) and ΔMFR (r = -0.47; p = 0.048). Sarcoid-mediated myocardial inflammation is associated with a regional impairment of coronary circulatory function. The association between immune-suppressive treatment-related alterations in myocardial inflammation and changes in coronary vasodilator capacity suggests direct adverse effect of inflammation on coronary circulatory function in cardiac sarcoidosis. Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Usefulness of myocardial parametric imaging to evaluate myocardial viability in experimental and in clinical studies.

PubMed

Korosoglou, G; Hansen, A; Bekeredjian, R; Filusch, A; Hardt, S; Wolf, D; Schellberg, D; Katus, H A; Kuecherer, H

2006-03-01

To evaluate whether myocardial parametric imaging (MPI) is superior to visual assessment for the evaluation of myocardial viability. Myocardial contrast echocardiography (MCE) was assessed in 11 pigs before, during, and after left anterior descending coronary artery occlusion and in 32 patients with ischaemic heart disease by using intravenous SonoVue administration. In experimental studies perfusion defect area assessment by MPI was compared with visually guided perfusion defect planimetry. Histological assessment of necrotic tissue was the standard reference. In clinical studies viability was assessed on a segmental level by (1) visual analysis of myocardial opacification; (2) quantitative estimation of myocardial blood flow in regions of interest; and (3) MPI. Functional recovery between three and six months after revascularisation was the standard reference. In experimental studies, compared with visually guided perfusion defect planimetry, planimetric assessment of infarct size by MPI correlated more significantly with histology (r2 = 0.92 versus r2 = 0.56) and had a lower intraobserver variability (4% v 15%, p < 0.05). In clinical studies, MPI had higher specificity (66% v 43%, p < 0.05) than visual MCE and good accuracy (81%) for viability detection. It was less time consuming (3.4 (1.6) v 9.2 (2.4) minutes per image, p < 0.05) than quantitative blood flow estimation by regions of interest and increased the agreement between observers interpreting myocardial perfusion (kappa = 0.87 v kappa = 0.75, p < 0.05). MPI is useful for the evaluation of myocardial viability both in animals and in patients. It is less time consuming than quantification analysis by regions of interest and less observer dependent than visual analysis. Thus, strategies incorporating this technique may be valuable for the evaluation of myocardial viability in clinical routine.

Angiotensin converting enzyme inhibition in chronic stable angina: effects on myocardial ischaemia and comparison with nifedipine.

PubMed Central

Ikram, H.; Low, C. J.; Shirlaw, T. M.; Foy, S. G.; Crozier, I. G.; Richards, A. M.; Khurmi, N. S.; Horsburgh, R. J.

1994-01-01

OBJECTIVES--To determine the anti-ischaemic effects of a new angiotensin converting enzyme inhibitor, benazepril, compared with nifedipine, alone and in combination, in chronic stable angina caused by coronary artery disease. DESIGN--Placebo controlled, double blind, latin square design. SETTING--Regional cardiology service for a mixed urban and rural population. SUBJECTS--40 patients with stable exertional angina producing at least 1 mm ST segment depression on exercise test with the Bruce protocol. 34 patients completed all four phases of the trial. INTERVENTIONS--Each patient was treated with placebo, benazepril (10 mg twice daily), nifedipine retard (20 mg twice daily), and a combination of benazepril and nifedipine in the same doses, in random order for periods of two weeks. MAIN OUTCOME MEASURES AND RESULTS--Total duration of exercise was not increased by any treatment. Exercise time to the development of 1 mm ST segment depression was not significantly changed with benazepril alone or in combination with nifedipine but was increased with nifedipine from 4.18 (1.8) min to 4.99 (1.6) min (95% confidence interval (95% CI) 0.28 to 1.34; p < 0.05). There was a significant relation between increase in duration of exercise and resting renin concentration (r = 0.498; p < 0.01). Myocardial ischaemia during daily activity, as assessed by ambulatory electrocardiographic monitoring, was reduced by benazepril and by the benazepril and nifedipine combination. This was significant for total ischaemic burden (451(628) min v 231(408) min; 95% CI -398 to -41 min; p < 0.05) and maximal depth of ST segment depression (-2.47(1.2) mm v -2.16 mm; 95% CI 0.04 to 0.57; p < 0.05) for the combination and for maximal ST segment depth for benazepril monotherapy (-2.47 (1.2) mm v -1.96(1.2) mm; 95% CI 0.18 to 0.91; p < 0.05). Benazepril significantly altered the circadian rhythm of cardiac ischaemia, abolishing the peak ischaemic periods at 0700 to 1200 and 1700 to 2300 (p < 0.05). CONCLUSIONS--Benazepril, an angiotensin converting enzyme inhibitor, had a modest anti-ischaemic effect in effort angina, but this effect was not as pronounced as with nifedipine. The anti-ischaemic action was more noticeable in asymptomatic ischaemia during daily activity, whereas nifedipine had little effect on this aspect of myocardial ischaemia. The combination of benazepril and nifedipine reduced ischaemia of daily activity. PMID:8297690

Role of leukocytes and platelets in acute myocardial infarction

DOE Office of Scientific and Technical Information (OSTI.GOV)

Bednar, M.M.

1986-01-01

Myocardial ischemia initiates an inflammatory-like response in which invading neutrophils exacerbate the degree of injury. The effects of nafazatrom, a new antithrombotic agent, on leukocyte function in vitro and in vivo were related to its ability to salvage ischemic myocardium in an occulsion-reperfusion model of myocardial injury in the anesthetized dogs. Measurements of the neutrophil-specific myeloperoxidase enzyme in ischemic myocardium indicate that the smaller infarct size in dogs treated with nafazatrom is accompanied by a diminished leukocyte infiltration. The results obtained with nafazatrom emphasize the important role of the neutrophil in ischemia-induced myocardial damage. The possibility that myocardial ischemia-induced plateletmore » deposition was secondary to a neutrophil-mediated event was assessed by the injection of PGI{sub 2}-washed autologous {sup 111}indium-labeled platelets and measuring the amount of radioactivity in different regions of the heart following a 90 min. occlusion of the left anterior descending coronary artery followed by reperfusion for periods up to 5 hrs. Neutropenia, induced with specific sheep anti-dog neutrophil antiserum, significantly reduced platelet accumulation in the ischemic myocardium following 5 hrs. reperfusion and abolished the transmural platelet distribution. These results suggest that myocardial platelet deposition is secondary to a neutrophil-mediated event in this occlusion-reperfusion model of myocardial injury.« less

Myocardial T2* Mapping at Ultrahigh Field: Physics and Frontier Applications

NASA Astrophysics Data System (ADS)

Huelnhagen, Till; Paul, Katharina; Ku, Min-Chi; Serradas Duarte, Teresa; Niendorf, Thoralf

2017-06-01

Cardiovascular magnetic resonance imaging (CMR) has become an indispensable clinical tool for the assessment of morphology, function and structure of the heart muscle. By exploiting quantification of the effective transverse relaxation time (T2*) CMR also affords myocardial tissue characterization and probing of cardiac physiology, both being in the focus of ongoing research. These developments are fueled by the move to ultrahigh magnetic field strengths, which permits enhanced sensitivity and spatial resolution that help to overcome limitations of current clinical MR systems with the goal to contribute to a better understanding of myocardial (patho)physiology in vivo. In this context, the aim of this report is to introduce myocardial T2* mapping at ultrahigh magnetic fields as a promising technique to non-invasively assess myocardial (patho)physiology. For this purpose the basic principles of T2* assessment, the biophysical mechanisms determining T2* and (pre)clinical applications of myocardial T2* mapping are presented. Technological challenges and solutions for T2* sensitized CMR at ultrahigh magnetic field strengths are discussed followed by a review of acquisition techniques and post processing approaches. Preliminary results derived from myocardial T2* mapping in healthy subjects and cardiac patients at 7.0 Tesla are presented. A concluding section discusses remaining questions and challenges and provides an outlook on future developments and potential clinical applications.

Alcohol and the risk of myocardial infarction.

PubMed

Flesch, M; Rosenkranz, S; Erdmann, E; Böhm, M

2001-04-01

Epidemiological studies have repeatedly demonstrated a beneficial effect of moderate alcohol consumption on the incidence of coronary heart disease, myocardial infarction and overall mortality. The latter increases with excessive alcohol consumption. Although most epidemiological studies demonstrate a beneficial effect of alcohol consumption independent from the specific kind of alcoholic beverage, there is increasing evidence that wine and in particular red wine might contain pharmacological substances, which prevent atherosclerosis and myocardial infarction independent from the wine ethanol. Pathophysiological mechanisms mediating these beneficial effects include effects of wine phenols and tannins on LDL-cholesterol oxidation status, thrombocyte aggregation, endothelial function and smooth muscle cell proliferation. Identification and characterization of the pharmacologically active substances might provide the stage for the development of new substances to be used in the prevention of coronary artery disease and myocardial infarction.

[Effect of formula of removing both phlegm and blood stasis in improving cardiac function of Chinese mini-swine with coronary heart disease of phlegm-stasis cementation syndrome].

PubMed

Li, Lei; Lin, Cheng-Ren; Ren, Jian-Xun; Miao, Lan; Yao, Ming-Jiang; Li, Dan; Shi, Yue; Ma, Yan-Lei; Fu, Jian-Hua; Liu, Jian-Xun

2014-02-01

To evaluate that the effect of formula of removing both phlegm and blood stasis in improving cardiac function of Chinese mini-swine with coronary heart disease of phlegm-stasis cementation syndrome. Totally 36 Chinese mini-swine were randomly divided to six groups: the normal control group, the model group, the Danlou tablet group, and Tanyu Tonzhi Fang(TYTZ) groups with doses of 2. 0, 1. 0 and 0. 5 g kg-1, with six in each group. Except for the normal control group, all of other groups were fed with high-fat diet for 2 weeks. Interventional balloons are adopted to injure their left anterior descending artery endothelium. After the operation, they were fed with high-fat diet for 8 weeks to prepare the coronary heart disease model of phlegm-stasis cementation syndrome. After the operation, they were administered with drugs for 8 weeks. The changes in the myocardial ischemia were observed. The changes in the cardiac function and structure were detected by cardiac ultrasound and noninvasive hemodynamic method. Compared with the normal control group, the model group showed significant increase in myocardial ischemia and SVR and obvious decrease in CO, SV and LCW in noninvasive hemodynamic parameters (P <0.05 or P <0.01). The ultrasonic cardiogram indicated notable decrease in IVSd, LVPWs, EF and FS, and remarkable increase in LVIDs (P<0. 05 orP<0.01). Compared with the model group, TYTZ could reduce the myocardial ischemia, strengthen cardiac function, and improve the abnormal cardiac structure and function induced by ischemia (P <0. 05 or P <0. 01). TYTZ shows a significant effect in improving cardiac function of Chinese mini-swine with coronary heart disease of phlegm-stasis cementation syndrome. The clinical cardiac function detection method could be adopted to correctly evaluate the changes in the post-myocardial ischemia cardiac function, and narrow the gap between clinical application and basic experimental studies.

123I-IPPA SPECT for the prediction of enhanced left ventricular function after coronary bypass graft surgery. Multicenter IPPA Viability Trial Investigators. 123I-iodophenylpentadecanoic acid.

PubMed

Verani, M S; Taillefer, R; Iskandrian, A E; Mahmarian, J J; He, Z X; Orlandi, C

2000-08-01

Fatty acids are the prime metabolic substrate for myocardial energy production. Hence, fatty acid imaging may be useful in the assessment of myocardial hibernation. The goal of this prospective, multicenter trial was to assess the use of a fatty acid, 123I-iodophenylpentadecanoic acid (IPPA), to identify viable, hibernating myocardium. Patients (n = 119) with abnormal left ventricular wall motion and a left ventricular ejection fraction (LVEF) < 40% who were already scheduled to undergo coronary artery bypass grafting (CABG) underwent IPPA tomography (rest and 30-min redistribution) and blood-pool radionuclide angiography within 3 d of the scheduled operation. Radionuclide angiography was repeated 6-8 wk after CABG. The study endpoint was a > or =10% increase in LVEF after CABG. The number of IPPA-viable abnormally contracting segments necessary to predict a positive LVEF outcome was determined by receiver operating characteristic (ROC) curves and was included in a logistic regression analysis, together with selected clinical variables. Before CABG, abnormal IPPA tomography findings were seen in 113 of 119 patients (95%), of whom 71 (60%) had redistribution in the 30-min images. The LVEF increased modestly after CABG (from 32% +/- 12% to 36% +/- 8%, P< 0.001).A > or =10% increase in LVEF after CABG occurred in 27 of 119 patients (23%). By ROC curves, the best predictor of a > or =10% increase in LVEF was the presence of > or =7 IPPA-viable segments (accuracy, 72%; confidence interval, 64%-80%). Among clinical and scintigraphic variables, the single most important predictor also was the number of IPPA-viable segments (P = 0.008). The number of IPPA-viable segments added significant incremental value to the best clinical predictor model. Asubstantial increase in LVEF occurs after CABG in only a minority of patients (23%) with depressed preoperative function. The number of IPPA-viable segments is useful in predicting a clinically meaningful increase in LVEF.

Sensitivity of mechanical and metabolic functions to changes in coronary perfusion: A metabolic basis of perfusion-contraction coupling.

PubMed

Askenasy, N

2000-05-01

Experimental evidence indicates a metabolic basis of contraction-perfusion coupling during an increase in cardiac work load. This study aims to characterize adjustment of myocardial energy metabolism in response to acute low flow ischemia (LFI), and to determine its involvement in perfusion-contraction coupling. Intracellular parameters were measured in isolated rat hearts by NMR spectroscopy and biochemical methods during 30 min of graded LFI and reperfusion as compared to continuous perfusion (control). Oxygen pressure was set to reach maximal oxygen extraction at 70% coronary flow rate (CFR), therefore oxygen limitation was proportional to coronary underperfusion. At 69, 38 and 10% CFR left ventricular pressures decreased to 71, 43 and 25% of pre-ischemic values respectively (P<0.005 v 97% in control) without an increase in diastolic tone, and recovered to 92+/-3% after 30 min of reperfusion. Despite hydrolysis of high energy phosphates and cellular acidification, ADP concentrations were stable in underperfused hearts. At 69, 38 and 10% CFR, cytosolic phosphorylation potentials (PP) decreased from 74+/-10 m M(-1)during pre-ischemia to 40+/-6, 25+/-4 and 14+/-4 m M(-1)respectively (P<0.05 v 63+/-9 m M(-1)in control), and lactate efflux increased to 256+/-18, 386+/-22 and 490+/-43 micromol /gdw respectively (P<0.005 v 186+/-22 micromol/gdw in control). Glycogen contents decreased (P<0.005 v control) and accounted for 27-30% of lactate efflux. These results indicate: (a) proportionate depression of contraction force and glycogen contents, and increased glucose uptake and anaerobic energy production in the underperfused myocardium. Coordinated modulation of these parameters attributes cytosolic PP a regulatory function; (b) resetting of cytosolic PP to lower levels mediates perfusion-contraction coupling during graded LFI. The data are consistent with the concept that glycolytic energy production improves myocardial tolerance to ischemia. Copyright 2000 Academic Press.

Ultrastructure of myocardial widened Z bands and endocardial cells in two teleostean species.

PubMed

Leknes, I L

1981-01-01

Widened myocardial Z bands and endocardial cells are described in two teleostean species Cichlasoma meeki and Corydoras aeneus. Widened Z bands containing mainly amorphous and electron-dense material were seen in a number of myocardial cells. Further, similar material may occur in large amounts beneath the sarcolemma and at intercellular junctions. Occasionally, we observed continuity between the latter material and that in expanded Z bands. In C. meeki the ventricular endocardial layer consists of two structurally different cell types, whereas in C. aeneus only one cell type was seen. The functional aspects of widened Z bands are discussed.

Circadian rhythms in myocardial metabolism and contractile function: influence of workload and oleate.

PubMed

Durgan, David J; Moore, Michael W S; Ha, Ngan P; Egbejimi, Oluwaseun; Fields, Anna; Mbawuike, Uchenna; Egbejimi, Anu; Shaw, Chad A; Bray, Molly S; Nannegari, Vijayalakshmi; Hickson-Bick, Diane L; Heird, William C; Dyck, Jason R B; Chandler, Margaret P; Young, Martin E

2007-10-01

Multiple extracardiac stimuli, such as workload and circulating nutrients (e.g., fatty acids), known to influence myocardial metabolism and contractile function exhibit marked circadian rhythms. The aim of the present study was to investigate whether the rat heart exhibits circadian rhythms in its responsiveness to changes in workload and/or fatty acid (oleate) availability. Thus, hearts were isolated from male Wistar rats (housed during a 12:12-h light-dark cycle: lights on at 9 AM) at 9 AM, 3 PM, 9 PM, and 3 AM and perfused in the working mode ex vivo with 5 mM glucose plus either 0.4 or 0.8 mM oleate. Following 20-min perfusion at normal workload (i.e., 100 cm H(2)O afterload), hearts were challenged with increased workload (140 cm H(2)O afterload plus 1 microM epinephrine). In the presence of 0.4 mM oleate, myocardial metabolism exhibited a marked circadian rhythm, with decreased rates of glucose oxidation, increased rates of lactate release, decreased glycogenolysis capacity, and increased channeling of oleate into nonoxidative pathways during the light phase. Rat hearts also exhibited a modest circadian rhythm in responsiveness to the workload challenge when perfused in the presence of 0.4 mM oleate, with increased myocardial oxygen consumption at the dark-to-light phase transition. However, rat hearts perfused in the presence of 0.8 mM oleate exhibited a markedly blunted contractile function response to the workload challenge during the light phase. In conclusion, these studies expose marked circadian rhythmicities in myocardial oxidative and nonoxidative metabolism as well as responsiveness of the rat heart to changes in workload and fatty acid availability.

Levosimendan improves postresuscitation outcomes in a rat model of CPR.

PubMed

Huang, Lei; Weil, Max Harry; Sun, Shijie; Cammarata, Gianluca; Cao, Lan; Tang, Wanchun

2005-11-01

In this study we sought to determine whether a calcium sensitizer, levosimendan, would have a more favorable effect on postresuscitation myocardial function and, consequently, postresuscitation survival than beta-adrenergic dobutamine. The extreme decrease in survival before hospital discharge of resuscitated victims is attributed, in part, to postresuscitation myocardial failure, and dobutamine has been recommended for the management of postresuscitation myocardial failure. We studied a total of 15 animals. Ventricular fibrillation was induced in Sprague-Dawley rats weighing 450 to 550 g. Cardiopulmonary resuscitation (CPR), including chest compressions and mechanical ventilation, was begun after 8 minutes of untreated cardiac arrest. Electrical defibrillation was attempted after 6 minutes of CPR. Each animal was resuscitated. Animals were randomized to undergo treatment with levosimendan, dobutamine, or saline-solution placebo. These agents were administered 10 minutes after the return of spontaneous circulation. Levosimendan was administered in a loading dose of 12 microg kg(-1) over a 10-minute period, followed by infusion of 0.3 microg kg(-1) min(-1) over the next 230 minutes. Dobutamine was continuously infused at a dosage of 3 microg kg(-1) min(-1). Saline-solution placebo was administered in the same volume and over the same amount of time as levosimendan. Levosimendan and dobutamine produced comparable increases in cardiac output and rate of left-ventricular pressure increase. However, administration of levosimendan resulted in lower heart rates and lesser increases in left ventricular diastolic pressure compared with both dobutamine and placebo. The duration of postresuscitation survival was significantly greater with levosimendan (16 +/- 2 hours), intermediate with dobutamine (11 +/- 2 hours) and least with saline-solution placebo (8 +/- 1 hour). Levosimendan and dobutamine both improved postresuscitation myocardial function. However, levosimendan produced more favorable postresuscitation myocardial function and increased the duration of postresuscitation survival.

Quantitation of stress echocardiography by tissue Doppler and strain rate imaging: a dream come true?

PubMed

Galderisi, Maurizio; Mele, Donato; Marino, Paolo Nicola

2005-01-01

Tissue Doppler (TD) is an ultrasound tool providing a quantitative agreement of left ventricular regional myocardial function in different modalities. Spectral pulsed wave (PW) TD, performed online during the examination, measures instantaneous myocardial velocities. By means of color TD, velocity images are digitally stored for subsequent off-line analysis and mean myocardial velocities are measured. An implementation of color TD includes strain rate imaging (SRI), based on post-processing conversion of regional velocities in local myocardial deformation rate (strain rate) and percent deformation (strain). These three modalities have been applied to stress echocardiography for quantitative evaluation of regional left ventricular function and detection of ischemia and viability. They present advantages and limitations. PWTD does not permit the simultaneous assessment of multiple walls and therefore is not compatible with clinical stress echocardiography while it could be used in a laboratory setting. Color TD provides a spatial map of velocity throughout the myocardium but its results are strongly affected by the frame rate. Both color TD and PWTD are also influenced by overall cardiac motion and tethering from adjacent segments and require reference velocity values for interpretation of regional left ventricular function. High frame rate (i.e. > 150 ms) post-processing-derived SRI can potentially overcome these limitations, since measurements of myocardial deformation have not any significant apex-to-base gradient. Preliminary studies have shown encouraging results about the ability of SRI to detect ischemia and viability, in terms of both strain rate changes and/or evidence of post-systolic thickening. SRI is, however, Doppler-dependent and time-consuming. Further technical refinements are needed to improve its application and introduce new ultrasound modalities to overcome the limitations of the Doppler-derived deformation analysis.

Improved biochemical preservation of heart slices during cold storage.

PubMed

Bull, D A; Reid, B B; Connors, R C; Albanil, A; Stringham, J C; Karwande, S V

2000-01-01

Development of myocardial preservation solutions requires the use of whole organ models which are animal and labor intensive. These models rely on physiologic rather than biochemical endpoints, making accurate comparison of the relative efficacy of individual solution components difficult. We hypothesized that myocardial slices could be used to assess preservation of biochemical function during cold storage. Whole rat hearts were precision cut into slices with a thickness of 200 microm and preserved at 4 degrees C in one of the following solutions: Columbia University (CU), University of Wisconsin (UW), D5 0.2% normal saline with 20 meq/l KCL (QNS), normal saline (NS), or a novel cardiac preservation solution (NPS) developed using this model. Myocardial biochemical function was assessed by ATP content (etamoles ATP/mg wet weight) and capacity for protein synthesis (counts per minute (cpm)/mg protein) immediately following slicing (0 hours), and at 6, 12, 18, and 24 hours of cold storage. Six slices were assayed at each time point for each solution. The data were analyzed using analysis of variance and are presented as the mean +/- standard deviation. ATP content was higher in the heart slices stored in the NPS compared to all other solutions at 6, 12, 18 and 24 hours of cold storage (p < 0.05). Capacity for protein synthesis was higher in the heart slices stored in the NPS compared to all other solutions at 6, 12, and 18 hours of cold storage (p < 0.05). CONCLUSIONS This myocardial slice model allows the rapid and efficient screening of cardiac preservation solutions and their components using quantifiable biochemical endpoints. Using this model, we have developed a novel preservation solution which improves the biochemical function of myocardial slices during cold storage.

Identification of Temporal and Region-Specific Myocardial Gene Expression Patterns in Response to Infarction in Swine

PubMed Central

Nonell, Lara; Puigdecanet, Eulàlia; Astier, Laura; Solé, Francesc; Bayes-Genis, Antoni

2013-01-01

Molecular mechanisms associated with pathophysiological changes in ventricular remodelling due to myocardial infarction (MI) remain poorly understood. We analyzed changes in gene expression by microarray technology in porcine myocardial tissue at 1, 4, and 6 weeks post-MI. MI was induced by coronary artery ligation in 9 female pigs (30–40 kg). Animals were randomly sacrificed at 1, 4, or 6 weeks post-MI (n = 3 per group) and 3 healthy animals were also included as control group. Total RNA from myocardial samples was hybridized to GeneChip® Porcine Genome Arrays. Functional analysis was obtained with the Ingenuity Pathway Analysis (IPA) online tool. Validation of microarray data was performed by quantitative real-time PCR (qRT-PCR). More than 8,000 different probe sets showed altered expression in the remodelling myocardium at 1, 4, or 6 weeks post-MI. Ninety-seven percent of altered transcripts were detected in the infarct core and 255 probe sets were differentially expressed in the remote myocardium. Functional analysis revealed 28 genes de-regulated in the remote myocardial region in at least one of the three temporal analyzed stages, including genes associated with heart failure (HF), systemic sclerosis and coronary artery disease. In the infarct core tissue, eight major time-dependent gene expression patterns were recognized among 4,221 probe sets commonly altered over time. Altered gene expression of ACVR2B, BID, BMP2, BMPR1A, LMNA, NFKBIA, SMAD1, TGFB3, TNFRSF1A, and TP53 were further validated. The clustering of similar expression patterns for gene products with related function revealed molecular footprints, some of them described for the first time, which elucidate changes in biological processes at different stages after MI. PMID:23372767

[The effectiveness of romifidine on myocardial function in horses with and without heart disease, evaluated with M-mode echocardiography and PW-tissue Doppler imaging].

PubMed

Nagel, Deborah; Gehlen, Heidrun

2013-01-01

The aim of this study was to evaluate to what extent the myocardial function in horses (measured by PW-tissue Doppler = PW-TDI) is affected during a sedation with romifidine (0.04 mg/kg, i. v.), particularly in case of an accompanying heart disease. Based on an echo- and electrocardiographic examination, a total of 45 horses was subdivided into group 1 (no heart disease), group 2 (heart disease without increased heart dimensions) and group 3 (heart disease with increased heart dimensions). Heart rate (HF), M-mode- (FS%) and TDI-measurements were performed before and after the application of romifidine. The velocities of the radial myocardial movement in the left and right ventricular wall were evaluated using PW-TDI. The TDI parameters included the isovolumic contraction (IVC), the systolic (S) as well as the early (E) and late diastolic maximal velocity (A). After the application of romifidine HF and FS were significantly decreased in all groups. IVC, S and E, determined by PW-TDI were also significantly decreased in both ventricular walls. A significant difference between groups was shown for the isovolumic contraction in the left ventricular wall. This was observed distinctly more in horses with heart disease and increased heart dimensions compared to horses with heart disease but no increased heart dimensions. The results of the study indicate that PW-TDI is a suitable imaging technique to analyse the effects of romifidine on equine myocardial function. The major percentage change after application of romifidine for TDI measurements compared to the M-mode parameters indicate that the parameter myocardial velocity measured with TDI appeared to be the most sensitive parameter to document romifidine--induced changes on the myocardium.

Glucose-6-phosphate dehydrogenase and NADPH redox regulates cardiac myocyte L-type calcium channel activity and myocardial contractile function.

PubMed

Rawat, Dhwajbahadur K; Hecker, Peter; Watanabe, Makino; Chettimada, Sukrutha; Levy, Richard J; Okada, Takao; Edwards, John G; Gupte, Sachin A

2012-01-01

We recently demonstrated that a 17-ketosteroid, epiandrosterone, attenuates L-type Ca(2+) currents (I(Ca-L)) in cardiac myocytes and inhibits myocardial contractility. Because 17-ketosteroids are known to inhibit glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway, and to reduce intracellular NADPH levels, we hypothesized that inhibition of G6PD could be a novel signaling mechanism which inhibit I(Ca-L) and, therefore, cardiac contractile function. We tested this idea by examining myocardial function in isolated hearts and Ca(2+) channel activity in isolated cardiac myocytes. Myocardial function was tested in Langendorff perfused hearts and I(Ca-L) were recorded in the whole-cell patch configuration by applying double pulses from a holding potential of -80 mV and then normalized to the peak amplitudes of control currents. 6-Aminonicotinamide, a competitive inhibitor of G6PD, increased pCO(2) and decreased pH. Additionally, 6-aminonicotinamide inhibited G6PD activity, reduced NADPH levels, attenuated peak I(Ca-L) amplitudes, and decreased left ventricular developed pressure and ±dp/dt. Finally, dialyzing NADPH into cells from the patch pipette solution attenuated the suppression of I(Ca-L) by 6-aminonicotinamide. Likewise, in G6PD-deficient mice, G6PD insufficiency in the heart decreased GSH-to-GSSG ratio, superoxide, cholesterol and acetyl CoA. In these mice, M-mode echocardiographic findings showed increased diastolic volume and end-diastolic diameter without changes in the fraction shortening. Taken together, these findings suggest that inhibiting G6PD activity and reducing NADPH levels alters metabolism and leads to inhibition of L-type Ca(2+) channel activity. Notably, this pathway may be involved in modulating myocardial contractility under physiological and pathophysiological conditions during which the pentose phosphate pathway-derived NADPH redox is modulated (e.g., ischemia-reperfusion and heart failure).

Heart deformation analysis for automated quantification of cardiac function and regional myocardial motion patterns: A proof of concept study in patients with cardiomyopathy and healthy subjects.

PubMed

Lin, Kai; Collins, Jeremy D; Chowdhary, Varun; Markl, Michael; Carr, James C

2016-10-01

To test the performance of HDA in characterizing left ventricular (LV) function and regional myocardial motion patterns in the context of cardiomyopathy based on cine cardiovascular magnetic resonance (CMR). Following the approval of the institutional review board (IRB), standard cine images of 45 subjects, including 15 healthy volunteers, 15 patients with hypertrophic cardiomyopathy (HCM) and 15 patients with dilated cardiomyopathy (DCM) were retrospectively analyzed using HDA. The variations of LV ejection fraction (LVEF), LV mass (LVM), and regional myocardial motion indices, including radial (Drr), circumferential (Dcc) displacement, radial (Vrr) and circumferential (Vcc) velocity, radial (Err), circumferential (Ecc) and shear (Ess) strain and radial (SRr) and circumferential (SRc) strain rate, were calculated and compared among subject groups. Inter-study reproducibility of HDA-derived myocardial motion indices were tested on 15 volunteers by using intra-class correlation coefficient (ICC) and coefficient of variation (CoV). HDA identified significant differences in cardiac function and motion indices between subject groups. DCM patients had significantly lower LVEF (33.5±9.65%), LVM (105.88±21.93g), peak Drr (0.29±0.11cm), Vrr-sys (2.14±0.72cm/s), Err (0.17±0.08), Ecc (-0.08±0.03), SRr-sys (0.91±0.44s(-1)) and SRc-sys (-0.64±0.27s(-1)) compared to the other two groups. HCM patients demonstrated increased LVM (171.69±34.19) and lower peak Vcc-dia (0.78±0.30cm/s) than other subjects. Good inter-study reproducibility was found for all HDA-derived myocardial indices in healthy volunteers (ICC=0.664-0.942, CoV=15.1%-37.1%). Without the need for operator interaction, HDA is a reproducible method for the automated characterization of global and regional LV function in the context of cardiomyopathy. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

[The relation between the low T3 syndrome in the clinical course of myocardial infarction and heart failure].

PubMed

Frączek, Magdalena Maria; Gackowski, Andrzej; Przybylik-Mazurek, Elwira; Nessler, Jadwiga

2016-06-01

It has been proven that either excess or deficiency of thyroid hormones has harmful influence on the cardiovascular system function. On the other hand, severe systemic conditions like myocardial infarction or severe heart failure may affect thyroid hormones secretion and their peripheral conversion, leading to low T3 syndrome. Amongst many mechanisms causing T4 to T3 conversion disturbances, important role plays decreased activity of D1 deiodinase and increased activity of D3 deiodinase. The animal research confirmed that thyroid hormones influence cardiomiocytes phenotype and morphology. They inhibit inflammation, apoptosis and cardiac remodelling after myocardial infarction. It was also proven that free triiodothyronine similarly to brain natriuretic peptide predict long-term prognosis in chronic and acute heart failure patients. Potential influence of low T3 syndrome on the course of myocardial infarction and heart failure may have significant impact on the future research on individualization of myocardial infarction and heart failure treatment depending on patient's thyroid status. © 2016 MEDPRESS.

Endocardial Hippo signaling regulates myocardial growth and cardiogenesis.

PubMed

Artap, Stanley; Manderfield, Lauren J; Smith, Cheryl L; Poleshko, Andrey; Aghajanian, Haig; See, Kelvin; Li, Li; Jain, Rajan; Epstein, Jonathan A

2018-08-01

The Hippo signaling pathway has been implicated in control of cell and organ size, proliferation, and endothelial-mesenchymal transformation. This pathway impacts upon two partially redundant transcription cofactors, Yap and Taz, that interact with other factors, including members of the Tead family, to affect expression of downstream genes. Yap and Taz have been shown to regulate, in a cell-autonomous manner, myocardial proliferation, myocardial hypertrophy, regenerative potential, and overall size of the heart. Here, we show that Yap and Taz also play an instructive, non-cell-autonomous role in the endocardium of the developing heart to regulate myocardial growth through release of the paracrine factor, neuregulin. Without endocardial Yap and Taz, myocardial growth is impaired causing early post-natal lethality. Thus, the Hippo signaling pathway regulates cell size via both cell-autonomous and non-cell-autonomous mechanisms. Furthermore, these data suggest that Hippo may regulate organ size via a sensing and paracrine function in endothelial cells. Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.

Selective neurocognitive deficits and poor life functioning are associated with significant depressive symptoms in alcoholism-HIV infection comorbidity.

PubMed

Sassoon, Stephanie A; Rosenbloom, Margaret J; Fama, Rosemary; Sullivan, Edith V; Pfefferbaum, Adolf

2012-09-30

Alcoholism, HIV, and depressive symptoms frequently co-occur and are associated with impairment in cognition and life function. We administered the Beck Depression Inventory-II (BDI-II), measures of life function, and neurocognitive tests to 67 alcoholics, 56 HIV+ patients, 63 HIV+ alcoholics, and 64 controls to examine whether current depressive symptom level (significant, BDI-II>14 vs. minimal, BDI-II<14) was associated with poorer cognitive or psychosocial function in alcoholism-HIV comorbidity. Participants with significant depressive symptoms demonstrated slower manual motor speed and poorer visuospatial memory than those with minimal depressive symptoms. HIV patients with depressive symptoms showed impaired manual motor speed. Alcoholics with depressive symptoms showed impaired visuospatial memory. HIV+ alcoholics with depressive symptoms reported the poorest quality of life; alcoholics with depressive symptoms, irrespective of HIV status, had poorest life functioning. Thus, significant depressive symptoms were associated with poorer selective cognitive and life functioning in alcoholism and in HIV infection, even though depressive symptoms had neither synergistic nor additive effects on cognition in alcoholism-HIV comorbidity. The results suggest the relevance of assessing and treating current depressive symptoms to reduce cognitive compromise and functional disability in HIV infection, alcoholism, and their comorbidity. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

Temporal and spatial resolution required for imaging myocardial function

NASA Astrophysics Data System (ADS)

Eusemann, Christian D.; Robb, Richard A.

2004-05-01

4-D functional analysis of myocardial mechanics is an area of significant interest and research in cardiology and vascular/interventional radiology. Current multidimensional analysis is limited by insufficient temporal resolution of x-ray and magnetic resonance based techniques, but recent improvements in system design holds hope for faster and higher resolution scans to improve images of moving structures allowing more accurate functional studies, such as in the heart. This paper provides a basis for the requisite temporal and spatial resolution for useful imaging during individual segments of the cardiac cycle. Multiple sample rates during systole and diastole are compared to determine an adequate sample frequency to reduce regional myocardial tracking errors. Concurrently, out-of-plane resolution has to be sufficiently high to minimize partial volume effect. Temporal resolution and out-of-plane spatial resolution are related factors that must be considered together. The data used for this study is a DSR dynamic volume image dataset with high temporal and spatial resolution using implanted fiducial markers to track myocardial motion. The results of this study suggest a reduced exposure and scan time for x-ray and magnetic resonance imaging methods, since a lower sample rate during systole is sufficient, whereas the period of rapid filling during diastole requires higher sampling. This could potentially reduce the cost of these procedures and allow higher patient throughput.

Gaseous signalling molecule SO2 via Hippo-MST pathway to improve myocardial fibrosis of diabetic rats

PubMed Central

Liu, Maojun; Liu, Shengquan; Tan, Wenting; Tang, Fen; Long, Junrong; Li, Zining; Liang, Biao; Chu, Chun; Yang, Jun

2017-01-01

Recent studies have indicated the existence of an endogenous sulfur dioxide (SO2)-generating system in the cardiovascular system. The present study aimed to discuss the function and regulatory mechanism of gaseous signal molecule SO2 in inhibiting apoptosis and endoplasmic reticulum stress (ERS) via the Hippo-MST signaling pathway to improve myocardial fibrosis of diabetic rats. A total of 40 male Sprague-Dawley rats were randomly divided into four groups (10 rats per group): Normal control group (control group), diabetic rats group [streptozotocin (STZ) group], SO2 intervention group (STZ+SO2 group) and diabetes mellitus rats treated with L-Aspartic acid β-hydroxamate (HDX) group (HDX group). Diabetic rats models were established by intra-peritoneal injection of STZ (40 mg/kg) Following model establishment, intra-peritoneal injection of Na2SO3/NaHSO3 solution (0.54 mmol/kg) was administered in the STZ+SO2 group, and HDX solution (25 mg/kg/week) was administered in the HDX group. A total of 4 weeks later, echocardiography was performed to evaluate rats' cardiac function; Masson staining, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and transmission electron microscopy examinations were performed to observe myocardial morphological changes. ELISA was employed to determine the SO2 content. Western blot analysis was performed to detect the expression of proteins associated with apoptosis, ERS and the Hippo-MST signalling pathway. Compared with the control group, the STZ group and HDX group had a disordered arrangement of myocardial cells with apparent myocardial fibrosis, and echocardiography indicated that the cardiac function was lowered, there was an obvious increase of apoptosis in myocardial tissue, the expression levels of apoptosis-associated protein B-cell lymphoma associated protein X, caspase-3 and caspase-9 were upregulated, and Bcl-2 expression was downregulated. The expression of ERS and Hippo-MST pathway-associated proteins, including CHOP, GRP94, MST1 and MST2, were significantly upregulated. By contrast, these above-mentioned changes were reversed by SO2 treatment. Compared with STZ group, the HDX group had a further increase of myocardial fibrosis and apoptosis, while there were no statistically significant differences in the expression of Bax/Bcl-2, caspase-3, caspase-9 and ERS and Hippo-MST pathway-associated proteins. The results of the present study demonstrated that the gaseous signal molecule SO2 can effectively improve the myocardial fibrosis of diabetic rats, and its mechanism may be associated with reduced apoptosis and ERS by downregulated Hippo-MST pathway. PMID:28990064

Gaseous signalling molecule SO2 via Hippo‑MST pathway to improve myocardial fibrosis of diabetic rats.

PubMed

Liu, Maojun; Liu, Shengquan; Tan, Wenting; Tang, Fen; Long, Junrong; Li, Zining; Liang, Biao; Chu, Chun; Yang, Jun

2017-12-01

Recent studies have indicated the existence of an endogenous sulfur dioxide (SO2)‑generating system in the cardiovascular system. The present study aimed to discuss the function and regulatory mechanism of gaseous signal molecule SO2 in inhibiting apoptosis and endoplasmic reticulum stress (ERS) via the Hippo‑MST signaling pathway to improve myocardial fibrosis of diabetic rats. A total of 40 male Sprague‑Dawley rats were randomly divided into four groups (10 rats per group): Normal control group (control group), diabetic rats group [streptozotocin (STZ) group], SO2 intervention group (STZ+SO2 group) and diabetes mellitus rats treated with L‑Aspartic acid β‑hydroxamate (HDX) group (HDX group). Diabetic rats models were established by intra‑peritoneal injection of STZ (40 mg/kg) Following model establishment, intra‑peritoneal injection of Na2SO3/NaHSO3 solution (0.54 mmol/kg) was administered in the STZ+SO2 group, and HDX solution (25 mg/kg/week) was administered in the HDX group. A total of 4 weeks later, echocardiography was performed to evaluate rats' cardiac function; Masson staining, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and transmission electron microscopy examinations were performed to observe myocardial morphological changes. ELISA was employed to determine the SO2 content. Western blot analysis was performed to detect the expression of proteins associated with apoptosis, ERS and the Hippo‑MST signalling pathway. Compared with the control group, the STZ group and HDX group had a disordered arrangement of myocardial cells with apparent myocardial fibrosis, and echocardiography indicated that the cardiac function was lowered, there was an obvious increase of apoptosis in myocardial tissue, the expression levels of apoptosis‑associated protein B‑cell lymphoma associated protein X, caspase‑3 and caspase‑9 were upregulated, and Bcl‑2 expression was downregulated. The expression of ERS and Hippo‑MST pathway‑associated proteins, including CHOP, GRP94, MST1 and MST2, were significantly upregulated. By contrast, these above‑mentioned changes were reversed by SO2 treatment. Compared with STZ group, the HDX group had a further increase of myocardial fibrosis and apoptosis, while there were no statistically significant differences in the expression of Bax/Bcl‑2, caspase‑3, caspase‑9 and ERS and Hippo‑MST pathway‑associated proteins. The results of the present study demonstrated that the gaseous signal molecule SO2 can effectively improve the myocardial fibrosis of diabetic rats, and its mechanism may be associated with reduced apoptosis and ERS by downregulated Hippo‑MST pathway.

Clinical, Functional, and Biological Correlates of Cognitive Dimensions in Major Depressive Disorder – Rationale, Design, and Characteristics of the Cognitive Function and Mood Study (CoFaM-Study)

PubMed Central

Baune, Bernhard T.; Air, Tracy

2016-01-01

Cross-sectional and longitudinal studies exploring clinical, functional, and biological correlates of major depressive disorder are frequent. In this type of research, depression is most commonly defined as a categorical diagnosis based on studies using diagnostic instruments. Given the phenotypic and biological heterogeneity of depression, we chose to focus the phenotypic assessments on three cognitive dimensions of depression including (a) cognitive performance, (b) emotion processing, and (c) social cognitive functioning. Hence, the overall aim of the study is to investigate the long-term clinical course of these cognitive dimensions in depression and its functional (psychosocial) correlates. We also aim to identify biological “genomic” correlates of these three cognitive dimensions of depression. To address the above overall aim, we created the Cognition and Mood Study (CoFaMS) with the key objective to investigate the clinical, functional, and biological correlates of cognitive dimensions of depression by employing a prospective study design and including a healthy control group. The study commenced in April 2015, including patients with a primary diagnosis of a major depressive episode of major depressive disorder or bipolar disorder according to DSM-IV-TR criteria. The assessments cover the three cognitive dimensions of depression (cognitive performance, emotion processing, and social cognition), cognitive function screening instrument, plus functional scales to assess general, work place, and psychosocial function, depression symptom scales, and clinical course of illness. Blood is collected for comprehensive genomic discovery analyses of biological correlates of cognitive dimensions of depression. The CoFaM-Study represents an innovative approach focusing on cognitive dimensions of depression and its functional and biological “genomic” correlates. The CoFaMS team welcomes collaborations with both national and international researchers. PMID:27616997

Clinical, Functional, and Biological Correlates of Cognitive Dimensions in Major Depressive Disorder - Rationale, Design, and Characteristics of the Cognitive Function and Mood Study (CoFaM-Study).

PubMed

Baune, Bernhard T; Air, Tracy

2016-01-01

Cross-sectional and longitudinal studies exploring clinical, functional, and biological correlates of major depressive disorder are frequent. In this type of research, depression is most commonly defined as a categorical diagnosis based on studies using diagnostic instruments. Given the phenotypic and biological heterogeneity of depression, we chose to focus the phenotypic assessments on three cognitive dimensions of depression including (a) cognitive performance, (b) emotion processing, and (c) social cognitive functioning. Hence, the overall aim of the study is to investigate the long-term clinical course of these cognitive dimensions in depression and its functional (psychosocial) correlates. We also aim to identify biological "genomic" correlates of these three cognitive dimensions of depression. To address the above overall aim, we created the Cognition and Mood Study (CoFaMS) with the key objective to investigate the clinical, functional, and biological correlates of cognitive dimensions of depression by employing a prospective study design and including a healthy control group. The study commenced in April 2015, including patients with a primary diagnosis of a major depressive episode of major depressive disorder or bipolar disorder according to DSM-IV-TR criteria. The assessments cover the three cognitive dimensions of depression (cognitive performance, emotion processing, and social cognition), cognitive function screening instrument, plus functional scales to assess general, work place, and psychosocial function, depression symptom scales, and clinical course of illness. Blood is collected for comprehensive genomic discovery analyses of biological correlates of cognitive dimensions of depression. The CoFaM-Study represents an innovative approach focusing on cognitive dimensions of depression and its functional and biological "genomic" correlates. The CoFaMS team welcomes collaborations with both national and international researchers.

The protective effect of fasudil pretreatment combined with ischemia postconditioning on myocardial ischemia/reperfusion injury in rats.

PubMed

Li, W-N; Wu, N; Shu, W-Q; Guan, Y-E; Jia, D-L

2014-01-01

Ischemic postconditioning (IPO) and pharmacological pretreatment may reduce myocardial necrosis and apoptosis during ischemia/reperfusion. This study aimed to determine the protective effect of fasudil pretreatment combined with IPO on myocardial ischemia/reperfusion injury in rats and explore the possible mechanisms. The SD rats were induced by intraperitoneal injection of fasudil hydrochloride (1 or 10 mg/kg) 60 min before the initiation of ischemia, while the control rats were given the same volume of saline. The hearts were hung on the Langendorff perfusion apparatus and underwent 30 min global ischemia and 120 min reperfusion. The IPO protocol was induced by six cycles of 10 sec ischemia and 10 sec reperfusion at the onset of reperfusion. The hemodynamic changes were measured, myocardial infarct size was determined by triphenyltetrazolium chloride (TTC) staining, cardiomyocyte apoptosis was detected by TUNEL staining, lactate dehydrogenase (LDH) was analyzed from coronary effluents, phosphorylation of Akt and eNOS, as well as expression of Bcl-2 and Bax were measured by western blotting analysis. The high-dose fasudil (10 mg/kg) pretreatment group and IPO group significantly improved post-ischemia cardiac function, reduced myocardial infarct size, attenuated cardiomyocyte apoptosis, decreased the release of LDH, increased expression of phospho-Akt, phospho-eNOS and Bcl-2, and reduced expression of Bax compared with the control group (p < 0.05). In addition, the high-dose fasudil pretreatment combined with IPO group could further improved post-ischemia cardiac function, reduced myocardial infarct size, attenuated cardiomyocyte apoptosis, decreased the release of LDH, increased expression of phospho-Akt, phospho-eNOS and Bcl-2, and reduced expression of Bax compared with the single treatment groups (p < 0.05). The combination of high-dose fasudil pretreatment and IPO had a synergistic protective effect on myocardial ischemia/reperfusion injury, which was mediated via upregulating the PI3K/Akt/eNOS pathway, increasing expression of antiapoptotic Bcl-2, and decreasing expression of proapoptotic Bax.