Science.gov

Sample records for post-acute myocardial infarction

  1. [Double post-acute myocardial infarction complication: rupture of the interventricular septum and acute mitral insufficiency].

    PubMed

    Curcio Ruigómez, A; Martín Jiménez, J; Wilhelmi Ayza, M; Soria Delgado, J L

    1997-02-01

    We present a case of double post acute myocardial infarction complication: ventricular septal defect and acute and severe mitral insufficiency. As a consequence of the delay in the diagnosis, the patient developed pulmonary hypertension with values at the systemic level. The patient underwent surgery in order to close the ventricular septal defect and aneurysmectomy, resulting in posterior regression of mitral insufficiency and pulmonary circuit values became normal. The ethology, diagnosis, evolution and treatment of this exceptional association of acute post myocardial infarction complications are discussed.

  2. Is type D personality an independent risk factor for recurrent myocardial infarction or all-cause mortality in post-acute myocardial infarction patients?

    PubMed

    Condén, Emelie; Rosenblad, Andreas; Wagner, Philippe; Leppert, Jerzy; Ekselius, Lisa; Åslund, Cecilia

    2017-03-01

    Background Type D personality refers to a combination of simultaneously high levels of negative affectivity and social inhibition. The present study aimed to examine whether type D personality was independently associated with recurrent myocardial infarction or all-cause mortality in post-acute myocardial infarction patients, using any of the previously proposed methods for measuring type D personality. Design This was a prospective cohort study. Methods Utilising data from the Västmanland Myocardial Infarction Study, 946 post-acute myocardial infarction patients having data on the DS14 instrument used to measure type D personality were followed-up for recurrent myocardial infarction and all-cause mortality until 9 December 2015. Data were analysed using Cox regression, adjusted for established risk factors. Results In total, 133 (14.1%) patients suffered from type D personality. During a mean follow-up time for recurrent myocardial infarction of 5.7 (3.2) years, 166 (17.5%) patients were affected by recurrent myocardial infarction, of which 26 (15.7%) had type D personality, while during a mean follow-up time for all-cause mortality of 6.3 (2.9) years, 321 (33.9%) patients died, of which 42 (13.1%) had type D personality. After adjusting for established risk factors, type D personality was not significantly associated with recurrent myocardial infarction or all-cause mortality using any of the previously proposed methods for measuring type D personality. A weak association was found between the social inhibition part of type D personality and a decreased risk of all-cause mortality, but this association was not significant after taking missing data into account in a multiple imputation analysis. Conclusions No support was found for type D personality being independently associated with recurrent myocardial infarction or all-cause mortality in post-acute myocardial infarction patients, using any of the previously proposed methods for measuring type D personality.

  3. Feasibility of Extracorporeal Shock Wave Myocardial Revascularization Therapy for Post-Acute Myocardial Infarction Patients and Refractory Angina Pectoris Patients.

    PubMed

    Myojo, Masahiro; Ando, Jiro; Uehara, Masae; Daimon, Masao; Watanabe, Masafumi; Komuro, Issei

    2017-04-06

    Extracorporeal shockwave myocardial revascularization (ESMR) is one of the new treatment options for refractory angina pectoris (RAP), and some studies have indicated its effectiveness. A single-arm prospective trial to assess the feasibility of ESMR using Cardiospec for patients with post-acute myocardial infarction (AMI) and RAP was designed and performed. The patients were treated with 9 sessions of ESMR to the ischemic areas for 9 weeks. The feasibility measures included echocardiography; cardiac magnetic resonance imaging; troponin T, creatine kinase-MB (CK-MB), and brain natriuretic peptide testing; and a Seattle Angina Questionnaire (SAQ) survey. Three post-AMI patients and 3 RAP patients were enrolled. The post-AMI patients had already undergone revascularization with percutaneous coronary intervention (PCI) in the acute phase. In two patients, adverse events requiring admission occurred: one a lumbar disc hernia in a post-AMI patient and the other congestive heart failure resulting in death in an RAP patient. No apparent elevations in CK-MB and troponin T levels during the trial were observed. Echocardiography revealed no remarkable changes of ejection fraction; however, septal E/E' tended to decrease after treatments (11.6 ± 4.8 versus 9.2 ± 2.8, P = 0.08). Concerning the available SAQ scores for two RAP patients, one patient reported improvements in angina frequency and treatment satisfaction and the other reported improvements in physical limitations and angina stability. In this feasibility study, ESMR seems to be a safe treatment for both post-AMI patients and RAP patients. The efficacy of ESMR for post-AMI patients remains to be evaluated with additional studies.

  4. Is telemedicine an answer to reducing 30-day readmission rates post-acute myocardial infarction?

    PubMed

    Ben-Assa, Eyal; Shacham, Yacov; Golovner, Michal; Malov, Nomi; Leshem-Rubinow, Eran; Zatelman, Avivit; Oren Shamir, Ayelet; Rogowski, Ori; Roth, Arie

    2014-09-01

    Patients hospitalized for an acute myocardial infarction (AMI) are at risk for early readmission. Readmission rates in the community reportedly reach approximately 20%, and 30-day readmission rates have become a quality-of-care marker. Telemedicine is one strategy for improving clinical outcomes by offering real-time biometrics tracking and rapid intervention. We retrospectively assessed the 30-day readmission rate of post-AMI members of a telemedicine system. All "SHL"-Telemedicine subscribers who sustained an AMI and those who became subscribers within 10 days from discharge post-AMI between 2009 and 2012 were assessed. Their files were reviewed for demographics, coronary risk factors, reasons for readmission, and discharge diagnoses. In total, 897 suitable patients (mean age, 62±14 years; 81% males) were included. They had made 3,318 calls to the monitor center for consultation. A mobile intensive care unit was dispatched for 158 patients, 64 were transported to the hospital, and 52 (5.8%) were readmitted (10 patients were readmitted twice). Thirty-five readmissions were for noncardiac reasons. Twelve patients had acute coronary syndrome (11 were revascularized). Readmission rates were higher in patients with repeat AMIs (11.9% versus 5.3% among those with no AMI history) and in females (9.6% versus 4.9% among males). Unlike published figures for the general population, there were no significant differences between readmitted and non-readmitted patients regarding diabetes, hypertension, or congestive heart failure. Telemedicine technology shows considerable promise for reducing 30-day readmission rates of post-AMI patients.

  5. Synthetic chemically modified mrna-based delivery of cytoprotective factor promotes early cardiomyocyte survival post-acute myocardial infarction.

    PubMed

    Huang, Chien-Ling; Leblond, Anne-Laure; Turner, Elizebeth C; Kumar, Arun Hs; Martin, Kenneth; Whelan, Derek; O'Sullivan, Donnchadh M; Caplice, Noel M

    2015-03-02

    To extend the temporal window for cytoprotection in cardiomyocytes undergoing apoptosis after hypoxia and myocardial infarction (MI), a synthetic chemically modified mRNA (modRNA) was used to drive delivery of insulin-like growth factor-1 (IGF1) within the area at risk in an in vivo murine model of MI. Delivery of IGF1 modRNA, with a polyethylenimine-based nanoparticle, augmented secreted and cell-associated IGF1, promoting cardiomyocyte survival and abrogating cell apoptosis under hypoxia-induced apoptosis conditions. Translation of modRNA-IGF1 was sufficient to induce downstream increases in the levels of Akt and Erk phosphorylation. Downregulation of IGF1 specific miRNA-1 and -133 but not miR-145 expression was also confirmed. As a proof of concept, intramyocardial delivery of modRNA-IGF1 but not control modRNA-GFP significantly decreased the level of TUNEL positive cells, augmented Akt phosphorylation, and decreased caspase-9 activity within the infarct border zone 24 h post-MI. These findings demonstrate the potential for an extended cytoprotective effect of transient IGF1 driven by synthetic modRNA delivery.

  6. The bizzare phenomenon of smokers' paradox in the immediate outcome post acute myocardial infarction: an insight into the Malaysian National Cardiovascular Database-Acute Coronary Syndrome (NCVD-ACS) registry year 2006-2013.

    PubMed

    Venkatason, Padmaa; Salleh, Norsabihin Mohd; Zubairi, Yong; Hafidz, Imran; Ahmad, Wan Azman Wan; Han, Sim Kui; Zuhdi, Ahmad Syadi Mahmood

    2016-01-01

    'Smoker's paradox' is a controversial phenomenon of an unexpected favourable outcome of smokers post acute myocardial infarction. There are conflicting evidences from the literature so far. We investigate for the existence of this phenomenon in our post acute myocardial infarction patients. We analysed 12,442 active smokers and 10,666 never-smokers diagnosed with STEMI and NSTEMI from the Malaysian National Cardiovascular Database-Acute Coronary Syndrome (NCVD-ACS) year 2006-2013 from 18 hospitals across Malaysia. Comparisons in the baseline characteristics, clinical presentation, in-hospital treatment and short term clinical outcome were made between the two groups. To compare the clinical outcome, an extensive multivariate adjustment was made to estimate the allcause mortality risk ratios for both groups. The active smokers were younger (smokers 53.7 years vs non-smokers 62.3 years P < 0.001) and had lower cardiovascular risk burden and other co-morbidities. STEMI is more common in smokers and intravenous thrombolysis was the main reperfusion therapy in both groups. Smokers had a higher rate of in-hsopital coronary revascularisation in NSTEMI group (21.6 % smokers vs 16.7 % non-smokers P < 0.001) but similar to non-smokers in the STEMI group. Multivariate adjusted mortality risk ratios showed significantly lower mortality risks of smokers at both in-hospital (RR 0.510 [95 % CI 0.442-0.613]) and 30-day post discharge (RR 0.534 [95 % CI 0.437-0.621]). Smoking seems to be associated with a favourable outcome post myocardial infarction. The phenomenon of 'smoker's paradox' is in fact a reality in our patients population. The definitive explanation for this unexpected protective effect of smoking remains unclear.

  7. Opposite predictive value of pulse pressure and aortic pulse wave velocity on heart failure with reduced left ventricular ejection fraction: insights from an Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) substudy.

    PubMed

    Regnault, Veronique; Lagrange, Jérémy; Pizard, Anne; Safar, Michel E; Fay, Renaud; Pitt, Bertram; Challande, Pascal; Rossignol, Patrick; Zannad, Faiez; Lacolley, Patrick

    2014-01-01

    Although hypertension contributes significantly to worsen cardiovascular risk, blood pressure increment in subjects with heart failure is paradoxically associated with lower risk. The objective was to determine whether pulse pressure and pulse wave velocity (PWV) remain prognostic markers, independent of treatment in heart failure with reduced left ventricular function. The investigation involved 6632 patients of the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study. All subjects had acute myocardial infarction with left ventricular ejection fraction <40% and signs/symptoms of heart failure. Carotid-femoral PWV was measured in a subpopulation of 306 subjects. In the overall population, baseline mean arterial pressure <90 mm Hg was associated with higher all-cause death (hazard ratio, 1.14 [95% confidence interval, 1.00-1.30]; P<0.05), whereas higher left ventricular ejection fraction or pulse pressure was associated with lower rates of all-cause death, cardiovascular death/hospitalization, and cardiovascular death. In the subpopulation, increased baseline PWV was associated with worse outcomes (all-cause death: 1.16 [1.03-1.30]; P<0.05 and cardiovascular deaths: 1.16 [1.03-1.31]; P<0.05), independent of age and left ventricular ejection fraction. Using multiple regression analysis, systolic blood pressure and age were the main independent factors positively associated with pulse pressure or PWV, both in the entire population or in the PWV substudy. In heart failure and low ejection fraction, our results suggest that pulse pressure, being negatively associated with outcome, is more dependent on left ventricular function and thereby no longer a marker of aortic elasticity. In contrast, increased aortic stiffness, assessed by PWV, contributes significantly to cardiovascular death.

  8. Combined baseline and one-month changes in big endothelin-1 and brain natriuretic peptide plasma concentrations predict clinical outcomes in patients with left ventricular dysfunction after acute myocardial infarction: Insights from the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) study.

    PubMed

    Olivier, A; Girerd, N; Michel, J B; Ketelslegers, J M; Fay, R; Vincent, J; Bramlage, P; Pitt, B; Zannad, F; Rossignol, P

    2017-08-15

    Increased levels of neuro-hormonal biomarkers predict poor prognosis in patients with acute myocardial infarction (AMI) complicated by left ventricular systolic dysfunction (LVSD). The predictive value of repeated (one-month interval) brain natriuretic peptides (BNP) and big-endothelin 1 (BigET-1) measurements were investigated in patients with LVSD after AMI. In a sub-study of the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS trial), BNP and BigET-1 were measured at baseline and at 1month in 476 patients. When included in the same Cox regression model, baseline BNP (p=0.0003) and BigET-1 (p=0.026) as well as the relative changes (after 1month) from baseline in BNP (p=0.049) and BigET-1 (p=0.045) were predictive of the composite of cardiovascular death or hospitalization for worsening heart failure. Adding baseline and changes in BigET-1 to baseline and changes in BNP led to a significant increase in prognostic reclassification as assessed by integrated discrimination improvement index (5.0%, p=0.01 for the primary endpoint). Both increased baseline and changes after one month in BigET-1 concentrations were shown to be associated with adverse clinical outcomes, independently from BNP baseline levels and one month changes, in patients after recent AMI complicated with LVSD. This novel result may be of clinical interest since such combined biomarker assessment could improve risk stratification and open new avenues for biomarker-guided targeted therapies. In the present study, we report for the first time in a population of patients with reduced LVEF after AMI and signs or symptoms of congestive HF, that increased baseline values of BNP and BigET-1 as well as a further rise of these markers over the first month after AMI, were independently predictive of future cardiovascular events. This approach may therefore be of clinical interest with the potential of improving risk stratification after AMI with reduced LVEF while

  9. Acute myocardial infarction.

    PubMed

    Boersma, Eric; Mercado, Nestor; Poldermans, Don; Gardien, Martin; Vos, Jeroen; Simoons, Maarten L

    2003-03-08

    Acute myocardial infarction is a common disease with serious consequences in mortality, morbidity, and cost to the society. Coronary atherosclerosis plays a pivotal part as the underlying substrate in many patients. In addition, a new definition of myocardial infarction has recently been introduced that has major implications from the epidemiological, societal, and patient points of view. The advent of coronary-care units and the results of randomised clinical trials on reperfusion therapy, lytic or percutaneous coronary intervention, and chronic medical treatment with various pharmacological agents have substantially changed the therapeutic approach, decreased in-hospital mortality, and improved the long-term outlook in survivors of the acute phase. New treatments will continue to emerge, but the greatest challenge will be to effectively implement preventive actions in all high-risk individuals and to expand delivery of acute treatment in a timely fashion for all eligible patients.

  10. Prevention of myocardial infarction.

    PubMed

    Adams, M R

    2002-12-01

    Despite the rapid advances that have been made in the treatment of coronary artery disease, myocardial infarction remains the major cause of death in the developed world and a growing problem for developing countries. To address this growing problem, a strategy aimed at prevention of events in high-risk individuals is required. This involves assessment of cardiovascular risk followed by risk reduction. At present there is no perfect technique available for risk prediction, although computed tomography and magnetic resonance imaging scanning, along with serum markers of inflammation, offer the greatest potential. The applicability of these techniques at present is also limited by cost and accessibility. Risk reduction is possible through lifestyle changes and drug therapy, and effective risk assessment is essential in selecting those most likely to benefit from these interventions.

  11. Paraganglioma causing a myocardial infarction

    PubMed Central

    DeMers, Gerard; Portouw, Steve

    2012-01-01

    Paragangliomas, extra-adrenal pheochromocytomas, are rare and classically associated with sustained or paroxysmal hypertension, headache, perspiration, palpitations, and anxiety. A 49-year-old male, parachute instructor, likely developed a hypertensive emergency when deploying his parachute leading to a myocardial infarction. A para-aortic tumor was incidentally discovered during the patient's emergency department work-up and was eventually surgically resected. He had no evidence of coronary disease during his evaluation. This case shows that a myocardial infarction may be the initial manifestation of these neuroendocrine tumors. Hypertensive emergency, much less elevated blood pressure may not be present at time of presentation. PMID:22787353

  12. [Ventricular "remodeling" after myocardial infarction].

    PubMed

    Cohen-Solal, A; Himbert, D; Guéret, P; Gourgon, R

    1991-06-01

    Cardiac failure is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.

  13. Spousal Adjustment to Myocardial Infarction.

    ERIC Educational Resources Information Center

    Ziglar, Elisa J.

    This paper reviews the literature on the stresses and coping strategies of spouses of patients with myocardial infarction (MI). It attempts to identify specific problem areas of adjustment for the spouse and to explore the effects of spousal adjustment on patient recovery. Chapter one provides an overview of the importance in examining the…

  14. Solar activity and myocardial infarction.

    PubMed

    Szczeklik, E; Mergentaler, J; Kotlarek-Haus, S; Kuliszkiewicz-Janus, M; Kucharczyk, J; Janus, W

    1983-01-01

    The correlation between the incidence of myocardial infarction, sudden cardiac death, the solar activity and geomagnetism in the period 1969-1976 was studied, basing on Wrocław hospitals material registered according to WHO standards; sudden death was assumed when a person died within 24 hours after the onset of the disease. The highest number of infarctions and sudden deaths was detected for 1975, which coincided with the lowest solar activity, and the lowest one for the years 1969-1970 coinciding with the highest solar activity. Such an inverse, statistically significant correlation was not found to exist between the studied biological phenomena and geomagnetism.

  15. Tachyarrhythmias in acute myocardial infarction.

    PubMed

    McLean, K H; Bett, J N; Saltups, A

    1975-02-01

    In 1505 patients with acute myocardial infarction (MI) serious ventricular arrhythmias were commoner in those with transmural ECG changes, and were associated with an increase in mortality and in the incidence of left ventricular failure (LVF) as well as higher peak serum lactic dehydrogenase (LDH) levels. Atrial fibrillation (AF) occurred more often in older patients and in those with LVF and clinical evidence of pericarditis.

  16. [Psychiatric disorders following myocardial infarction].

    PubMed

    Meincke, Ulrich; Hoff, Paul

    2006-05-15

    The number of patients who survive acute myocardial infarction has increased during recent decades. In addition, demographic development results in a rising incidence of cardiovascular diseases. Based on these facts, also the significance of psychiatric disorders is growing that may occur after myocardial infarction, such as depression, posttraumatic stress and anxiety disorders. Physicians are faced with the challenge to identify these clinical entities, that show a syndromal overlap with somatic complaints after myocardial infarction. After differentiation prompt start of adequate psychiatric-psychotherapeutic interventions is of relevance, not only regarding the patient's quality of life, but also in terms of cardiovascular prognosis. Indeed, depressive and anxiety disorders are known to be associated with a poor compliance as for rehabilitation and secondary prevention of cardiovascular disorders. Moreover, some studies suggest depression to be an independent risk factor of coronary heart disease. Consequently, early recognition and treatment, most often primarily in the hands of internists and cardiologists, are of enormous importance for the course and prognosis of the psychiatric disorder but also of cardiovascular disease.

  17. Left ventricular diastolic function following myocardial infarction.

    PubMed

    Thune, Jens Jakob; Solomon, Scott D

    2006-12-01

    An acute myocardial infarction causes a loss of contractile fibers which reduces systolic function. Parallel to the effect on systolic function, a myocardial infarction also impacts diastolic function, but this relationship is not as well understood. The two physiologic phases of diastole, active relaxation and passive filling, are both influenced by myocardial ischemia and infarction. Active relaxation is delayed following a myocardial infarction, whereas left ventricular stiffness changes depending on the extent of infarction and remodeling. Interstitial edema and fibrosis cause an increase in wall stiffness which is counteracted by dilation. The effect on diastolic function is correlated to an increased incidence of adverse outcomes. Moreover, patients with comorbid conditions that are associated with worse diastolic function tend to have more adverse outcomes after infarction. There are currently no treatments aimed specifically at treating diastolic dysfunction following a myocardial infarction, but several new drugs, including aldosterone antagonists, may offer promise.

  18. Myocardial revascularisation after acute myocardial infarction.

    PubMed

    Bana, A; Yadava, O P; Ghadiok, R; Selot, N

    1999-05-15

    One hundred and twenty-three patients had coronary artery bypass grafting (CABG) within 30 days of acute myocardial infarction (AMI) from May 1992 to November 1997. Commonest infarct was anterior transmural (61.8%) and commonest indication of surgery was post-infarct persistent or recurrent angina (69.1%). Ten patients were operated within 48 h and 36 between 48 h to 2 weeks of having MI. Out of these, nine patients were having infarct extension and cardiogenic shock at the time of surgery. Pre-operatively fourteen patients were on inotropes of which six also had intra-aortic balloon pump (IABP) support. All patients had complete revascularisation with 3.8+/-1.2 distal anastomoses per patient. By multivariate analysis, we found that independent predictors of post-operative morbidity [inotropes >48 h, use of IABP, ventilation >24 h, ICU stay >5 days] and complications [re-exploration, arrhythmias, pulmonary complications, wound infection, cerebrovascular accident (CVA)] were left ventricular ejection fraction (LVEF) <30%, Q-wave MI, surgery <48 h after AMI, presence of pre-operative cardiogenic shock and age >60 years (P < or = 0.01). Mortality at 30 days was 3.3%. LVEF <30%, Q-wave MI, surgery <48 h after AMI, presence of pre-operative cardiogenic shock and age >60 years were found to be independent predictors of 30 days mortality (P < or = 0.01). Ninety patients were followed up for a mean duration of 33 months (1 to 65 months). There were three late deaths and five patients developed recurrence of angina. To conclude, CABG can be carried out with low risk following AMI in stable patients for post-infarct angina. Patients who undergo urgent or emergent surgery and who have pre-operative cardiogenic shock, IABP, poor left ventricular functions, age >60 years and Q-wave MI are at increased risk.

  19. Arrhythmias in Post-Myocardial Infarction Patients

    ClinicalTrials.gov

    2017-07-24

    Myocardial Infarction; Coronary Artery Disease; Arrythmia; ECG Electrical Alternans; Atrioventricular Block; Atrial Fibrillation; Atrial Flutter; Ventricular Tachycardia; Ventricular Fibrillation; Ventricular Arrythmia

  20. Prophylactic lidocaine for myocardial infarction.

    PubMed

    Martí-Carvajal, Arturo J; Simancas-Racines, Daniel; Anand, Vidhu; Bangdiwala, Shrikant

    2015-08-21

    Coronary artery disease is a major public health problem affecting both developed and developing countries. Acute coronary syndromes include unstable angina and myocardial infarction with or without ST-segment elevation (electrocardiogram sector is higher than baseline). Ventricular arrhythmia after myocardial infarction is associated with high risk of mortality. The evidence is out of date, and considerable uncertainty remains about the effects of prophylactic use of lidocaine on all-cause mortality, in particular, in patients with suspected myocardial infarction. To determine the clinical effectiveness and safety of prophylactic lidocaine in preventing death among people with myocardial infarction. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (2015, Issue 3), MEDLINE Ovid (1946 to 13 April 2015), EMBASE (1947 to 13 April 2015) and Latin American Caribbean Health Sciences Literature (LILACS) (1986 to 13 April 2015). We also searched Web of Science (1970 to 13 April 2013) and handsearched the reference lists of included papers. We applied no language restriction in the search. We included randomised controlled trials assessing the effects of prophylactic lidocaine for myocardial infarction. We considered all-cause mortality, cardiac mortality and overall survival at 30 days after myocardial infarction as primary outcomes. We performed study selection, risk of bias assessment and data extraction in duplicate. We estimated risk ratios (RRs) for dichotomous outcomes and measured statistical heterogeneity using I(2). We used a random-effects model and conducted trial sequential analysis. We identified 37 randomised controlled trials involving 11,948 participants. These trials compared lidocaine versus placebo or no intervention, disopyramide, mexiletine, tocainide, propafenone, amiodarone, dimethylammonium chloride, aprindine and pirmenol. Overall, trials were underpowered and had high risk of bias. Ninety-seven per cent of trials (36

  1. Perioperative myocardial infarction in patients undergoing myocardial revascularization surgery

    PubMed Central

    Pretto, Pericles; Martins, Gerez Fernandes; Biscaro, Andressa; Kruczan, Dany David; Jessen, Barbara

    2015-01-01

    Introduction Perioperative myocardial infarction adversely affects the prognosis of patients undergoing coronary artery bypass graft and its diagnosis was hampered by numerous difficulties, because the pathophysiology is different from the traditional instability atherosclerotic and the clinical difficulty to be characterized. Objective To identify the frequency of perioperative myocardial infarction and its outcome in patients undergoing coronary artery bypass graft. Methods Retrospective cohort study performed in a tertiary hospital specialized in cardiology, from May 01, 2011 to April 30, 2012, which included all records containing coronary artery bypass graft records. To confirm the diagnosis of perioperative myocardial infarction criteria, the Third Universal Definition of Myocardial Infarction was used. Results We analyzed 116 cases. Perioperative myocardial infarction was diagnosed in 28 patients (24.1%). Number of grafts and use and cardiopulmonary bypass time were associated with this diagnosis and the mean age was significantly higher in this group. The diagnostic criteria elevated troponin I, which was positive in 99.1% of cases regardless of diagnosis of perioperative myocardial infarction. No significant difference was found between length of hospital stay and intensive care unit in patients with and without this complication, however patients with perioperative myocardial infarction progressed with worse left ventricular function and more death cases. Conclusion The frequency of perioperative myocardial infarction found in this study was considered high and as a consequence the same observed average higher troponin I, more cases of worsening left ventricular function and death. PMID:25859867

  2. [Cardiac rehabilitation after myocardial infarction].

    PubMed

    Ghannem, M; Ghannem, L; Ghannem, L

    2015-12-01

    Although the proofs of the benefits of cardiac rehabilitation accumulate, many patients are not sent to rehabilitation units, especially younger and very elderly patients. As the length of stay in acute care units decreases, rehabilitation offers more time to fully assess the patients' conditions and needs. Meta-analyses of randomised trials suggest that mortality can be improved by as much as 20-30%. In addition, rehabilitation helps managing risk factors, including hyperlipidemia, diabetes, smoking and sedentary behaviours. Physical training also helps improving exercise capacity. Because of all of these effects, cardiac rehabilitation for post-myocardial infarction patients has been given a class IA recommendation in current guidelines.

  3. [A case of rupture of the left ventricle free wall with papillary muscle dysfunction following acute myocardial infarction, operated on successfully].

    PubMed

    de Lima, R; Perdigão, C; Neves, L; Cravino, J; Dantas, M; Bordalo, A; Pais, F; Diogo, A N; Ferreira, R; Ribeiro, C

    1990-09-01

    The authors present a case of left ventricular free wall rupture post acute myocardial infarction, associated with mitral papillary posterior muscle necrosis, operated by infartectomy and mitral valvular protesis replacement. They refer the various complications occurred during the hospital staying, and discuss its medical and surgical approach. The patient was discharged alive and six months after the infarction keeps a moderate activity.

  4. Computational modeling of acute myocardial infarction.

    PubMed

    Sáez, P; Kuhl, E

    2016-01-01

    Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.

  5. Computational modeling of acute myocardial infarction

    PubMed Central

    Sáez, P.; Kuhl, E.

    2015-01-01

    Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step towards simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size. PMID:26583449

  6. Myocardial Infarction in the Elderly

    PubMed Central

    Carro, Amelia; Kaski, Juan Carlos

    2011-01-01

    Advances in pharmacological treatment and effective early myocardial revascularization have –in recent years- led to improved clinical outcomes in patients with acute myocardial infarction (AMI). However, it has been suggested that compared to younger subjects, elderly AMI patients are less likely to receive evidence-based treatment, including myocardial revascularization therapy. Several reasons have been postulated to explain this trend, including uncertainty regarding the true benefits of the interventions commonly used in this setting as well as increased risk mainly associated with comorbidities. The diagnosis, management, and post-hospitalization care of elderly patients presenting with an acute coronary syndrome pose many difficulties at present. A complex interplay of variables such as comorbidities, functional and socioeconomic status, side effects associated with multiple drug administration, and individual biologic variability, all contribute to creating a complex clinical scenario. In this complex setting, clinicians are often required to extrapolate evidence-based results obtained in cardiovascular trials from which older patients are often, implicitly or explicitly, excluded. This article reviews current recommendations regarding management of AMI in the elderly. PMID:22396870

  7. [Circadian rhythm in myocardial infarct].

    PubMed

    Enciso, R; Ramos, M A; Badui, E; Hurtado, R

    1988-01-01

    In order to determine if the beginning of the Myocardial Infarction (MI) is at random along the day or if it follows a circadian rhythm, we analyzed the clinical charts of 819 patients admitted to the Coronary Care Unite. Among them, 645 were male and 174 female. It was established that the beginning of the MI follows a circadian rhythm with maximal frequency between 8 and 9 a.m. and minimal at 0 hours (p greater than 0.01). This rhythm is sex independent. In patients younger than 45 years as well as those who received beta-block agents in less than 24 hours previous the MI no circadian rhythm was observed.

  8. Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers

    ClinicalTrials.gov

    2017-03-02

    Acute Myocardial Infarction (AMI); Acute Coronary Syndrome (ACS); ST Elevation (STEMI) Myocardial Infarction; Ischemic Reperfusion Injury; Non-ST Elevation (NSTEMI) Myocardial Infarction; Angina, Unstable

  9. [Stem cell perspectives in myocardial infarctions].

    PubMed

    Aceves, José Luis; Archundia, Abel; Díaz, Guillermo; Páez, Araceli; Masso, Felipe; Alvarado, Martha; López, Manuel; Aceves, Rocío; Ixcamparij, Carlos; Puente, Adriana; Vilchis, Rafael; Montaño, Luis Felipe

    2005-01-01

    Myocardial infarction is the leading cause of congestive heart failure and death in industrializated countries. The cellular cardiomyoplasty has emerged as an alternative treatment in the regeneration of infarted myocardial tissue. In animals' models, different cellular lines such as cardiomyocites, skeletal myoblasts, embryonic stem cells and adult mesenchymal stem cells have been used, resulting in an improvement in ventricular function and decrease in amount of infarcted tissue. The first three cells lines have disvantages as they are allogenics and are difficult to obtain. The adult mesenchymal stem cells are autologous and can be obtained throught the aspiration of bone marrow or from peripherical circulation, after stimulating with cytokines (G-CSF). The implantation in humans with recent and old myocardial infarction have shown improvements similar to those shown in animal models. These findings encourage the continued investigation in the mechanism of cellular differentiation and implantation methods in infarcted myocardial tissue.

  10. [The new universal definition of myocardial infarction].

    PubMed

    Hod, Hanoch; Halon, David; Hammerman, Haim; Hasdai, David; Zahger, Doron; Lewis, Basil; Mosseri, Morris; Atar, Shaul

    2009-01-01

    Given the considerable advances in recent years in myocardial infarction diagnosis and management, the European Society of Cardiology (ESC), the American College of Cardiology (ACC), the American Heart Association (AHA), together with the World Heart Federation [WHF] recently published an expert consensus document to establish a universal definition for myocardial infarction. The consensus document recognizes five separate myocardial infarction categories based on the differences in pathophysiology, and whether percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) surgery is involved. The new consensus document expands the criteria for defining myocardial infarction by adding new ECG criteria and imaging modalities, and also includes patients who present with sudden death. The Israel Heart Society has adopted the new universal definition and recommends its use by clinicians, researchers and epidemiologists. .

  11. 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.

  12. 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.

  13. Novel adjunctive treatments of myocardial infarction

    PubMed Central

    Schmidt, Michael Rahbek; Pryds, Kasper; Bøtker, Hans Erik

    2014-01-01

    Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve clinical outcome, but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic and pharmacological conditioning, but despite decades of research, the translation into clinical effects has been challenging. Recently published clinical studies, however, prompt optimism as novel techniques allow for improved clinical applicability. Cyclosporine A, the GLP-1 analogue exenatide and rapid cooling by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising, three follow-up studies of the effect of remote ischemic conditioning (RIC) show clinical prognostic benefit in patients undergoing coronary surgery and percutaneous coronary intervention. The discovery that RIC can be performed noninvasively using a blood pressure cuff on the upper arm to induce brief episodes of limb ischemia and reperfusion has facilitated the translation of RIC into the clinical arena. This review focus on novel advances in adjunctive therapies in relation to acute and elective coronary procedures. PMID:24976915

  14. Molecular genetics of myocardial infarction

    PubMed Central

    Ichihara, Sahoko; Nishida, Tamotsu

    2008-01-01

    Abstract Myocardial infarction (MI) is an important clinical problem because of its large contribution to mortality. The main causal and treatable risk factors for MI include hypertension, hypercholesterolemia or dyslipidemia, diabetes mellitus, and smoking. In addition to these risk factors, recent studies have shown the importance of genetic factors and interactions between multiple genes and environmental factors. Disease prevention is an important strategy for reducing the overall burden of MI, with the identification of markers for disease risk being key both for risk prediction and for potential intervention to lower the chance of future events. Although genetic linkage analyses of families and sib-pairs as well as candidate gene and genome-wide association studies have implicated several loci and candidate genes in predisposition to coronary heart disease (CHD) or MI, the genes that contribute to genetic susceptibility to these conditions remain to be identified definitively. In this review, we summarize both candidate loci for CHD or MI identified by linkage analyses and candidate genes examined by association studies. We also review in more detail studies that have revealed the association with MI or CHD of polymorphisms in MTHFR, LPL, and APOE by the candidate gene approach and those in LTA and at chromosomal region 9p21.3 by genome-wide scans. Such studies may provide insight into the function of implicated genes as well as into the role of genetic factors in the development of CHD and MI. PMID:18704761

  15. [Occupational stress and myocardial infarction].

    PubMed

    Consoli, Silla M

    2015-01-01

    Besides the best-known role of depressed mood, occupational stress deserves to be taken as a coronary risk factor. There are two basic models to define occupational stress: Karasek's model (high job psychological demands associated with low decision latitude, or even low social support at work) and Siegrist's model (imbalance between efforts and rewards received). The combination of the two models better reflects the coronary risk than each model alone. Occupational stress appears both as a risk factor and a prognostic factor after the occurrence of myocardial infarction. The relevance of the models is best in men or in younger age subjects. In women, role conflicts (occupational/domestic), the existence of excessive "intrinsic" efforts (job over investment) and association with marital stress provide more specific information. Burnout, particularly among health professionals, and bullying at work are also linked to cardiovascular risk. Occupational stress is a collective indicator of health at work, valuable to the employer. At an individual level, it can lead to therapeutic preventive approaches. Copyright © 2015 Elsevier Masson SAS. All rights reserved.

  16. Exosomes and cardiac repair after myocardial infarction.

    PubMed

    Sahoo, Susmita; Losordo, Douglas W

    2014-01-17

    Myocardial infarction is a leading cause of death among all cardiovascular diseases. The analysis of molecular mechanisms by which the ischemic myocardium initiates repair and remodeling indicates that secreted soluble factors are key players in communication to local and distant tissues, such as bone marrow. Recently, actively secreted membrane vesicles, including exosomes, are being recognized as new candidates with important roles in intercellular and tissue-level communication. In this review, we critically examine the emerging role of exosomes in local and distant microcommunication mechanisms after myocardial infarction. A comprehensive understanding of the role of exosomes in cardiac repair after myocardial infarction could bridge a major gap in knowledge of the repair mechanism after myocardial injury.

  17. Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure - demographics, etiologic and pulmonary histologic analysis

    PubMed Central

    de Matos Soeiro, Alexandre; Ruppert, Aline D; Canzian, Mauro; Capelozzi, Vera L; Serrano, Carlos V

    2012-01-01

    OBJECTIVES: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life. METHODS: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression. RESULTS: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema. CONCLUSIONS: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has

  18. Risk stratification after myocardial infarction. Clinical overview

    SciTech Connect

    O'Rourke, R.A. )

    1991-09-01

    Many patients with an acute myocardial infarction can be stratified into subgroups that are at high risk for morbidity and mortality on the basis of clinical characteristics that indicate recurrent myocardial ischemia, persistent left ventricular dysfunction, and/or recurrent cardiac arrhythmias. In patients with uncomplicated myocardial infarction the assessment of symptoms, physical findings, and ECG changes during predischarge exercise testing often identifies patients at increased risk for further cardiac events. Because of the suboptimum sensitivity and specificity of the exercise ECG for detecting myocardial ischemia, myocardial perfusion imaging with 201Tl and/or assessment of global and segmental ventricular function by two-dimensional echocardiography or radionuclide cineangiography during or immediately after exercise are often added to the predischarge risk stratification.

  19. Postmortem detection of inapparent myocardial infarction

    PubMed Central

    McVie, J. G.

    1970-01-01

    Two methods of detecting early inapparent myocardial infarcts have been studied and their value in diagnostic practice compared. The better method proved to be the determination of the potassium to sodium ratio (ionic ratio) which falls in infarcted tissue within minutes of the onset of anoxia. The second method was nitro blue tetrazolium staining of gross sections of myocardium which revealed any infarct older than three and a half hours. As staining is dependent upon enzyme activity, the latter method is disturbed by autolysis. It was shown, on the other hand, that the ionic ratio (K+/Na+) was not affected by autolysis and was therefore well suited to forensic practice. Sixteen non-infarcted control hearts, plus the nine from cases of sudden death due to causes other than myocardial infarction, all yielded high ionic ratios (K+/Na+), average 1·4, and stained normally with tetrazolium (the normal controls). Positive control was provided by 20 histologically proven infarcts of which the ionic ratios (K+/Na+) were all low (average 0·7). Histochemical staining with tetrazolium delineated infarcted areas in each case. In a series of 29 sudden deaths, a cause of death other than myocardial infarction was found at necropsy in nine, mentioned above as normal controls. The remaining 20 hearts were not infarcted histologically, but were shown to be infarcted by examination of the ionic ratios (K+/Na+). These ratios were low (average 0·8) including three borderline ratios. Confirmatory evidence of infarction included nitro blue tetrazolium staining which revealed infarcts in 10 of the 20 cases, and clinical and necropsy observations. The ionic ratio (K+/Na+) decreases as the age of the infarct increases for at least 24 hours. Thereafter as healing proceeds, the ratio gradually reverts to normal. Thus, previous infarction and replacement fibrosis do not significantly alter the ionic ratio (K+/Na+). Nor is it changed by left ventricular hypertrophy, the presence of

  20. Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

    PubMed Central

    Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V; Carruthers, Kathryn; Vesey, Alex T; Alam, Shirjel R; Sills, Andrew; Hoo, Teng Y; Melville, Adam J; Langlands, Sarah P; Jenkins, William S A; Uren, Neal G; Mills, Nicholas L; Fletcher, Alison M; van Beek, Edwin J R; Rudd, James H F; Fox, Keith A A; Dweck, Marc R; Newby, David E

    2015-01-01

    Background Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans. Methods and Results Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non–ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI. Conclusions The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization

  1. Thallium-201 myocardial scintigraphy in acute myocardial infarction and ischemia

    SciTech Connect

    Wackers, F.J.

    1982-04-01

    Thallium-201 scintigraphy provides a sensitive and reliable method of detecting acute myocardial infarction and ischemia when imaging is performed with understanding of the temporal characteristics and accuracy of the technique. The results of scintigraphy are related to the time interval between onset of symptoms and time of imaging. During the first 6 hr after chest pain almost all patients with acute myocardial infarction and approximately 50% of the patients with unstable angina will demonstrate /sup 201/TI pefusion defects. Delayed imaging at 2-4 hr will permit distinction between ischemia and infarction. In patients with acute myocardial infarction, the size of the perfusion defect accurately reflects the extent of the infarcted and/or jeopardized myocardium, which may be used for prognostic stratification. In view of the characteristics of /sup 201/TI scintigraphy, the most practical application of this technique is in patients in whom myocardial infarction has to be ruled out, and for early recognition of patients at high risk for complications.

  2. Myocardial Infarction: Symptoms and Treatments.

    PubMed

    Lu, Lei; Liu, Min; Sun, RongRong; Zheng, Yi; Zhang, Peiying

    2015-07-01

    Myocardial infarction (MI) is a term used for an event of heart attack which is due to formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include, taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and loosing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. In this article the causes, symptoms and treatments of MI are described.

  3. Nanog expression in heart tissues induced by acute myocardial infarction.

    PubMed

    Luo, Huanhuan; Li, Qiong; Pramanik, Jogen; Luo, Jiankai; Guo, Zhikun

    2014-10-01

    Nanog is a potential stem cell marker and is considered a regeneration factor during tissue repair. In the present study, we investigated expression patterns of nanog in the rat heart after acute myocardial infarction by semi-quantitative RT-PCR, immunohistochemistry and Western blot analyses. Our results show that nanog at both mRNA and protein levels is positively expressed in myocardial cells, fibroblasts and small round cells in different myocardial zones at different stages after myocardial infarction, showing a spatio-temporal and dynamic change. After myocardial infarction, the nanog expression in fibroblasts and small round cells in the infarcted zone (IZ) is much stronger than that in the margin zone (MZ) and remote infarcted zone (RIZ). From day 7 after myocardial infarction, the fibroblasts and small cells strongly expressed nanog protein in the IZ, and a few myocardial cells in the MZ and the RIZ and the numbers of nanog-positive fibroblasts and small cells reached the highest peak at 21 days after myocardial infarction, but in this period the number of nanog-positive myocardial cells decreased gradually. At 28 days after myocardial infarction, the numbers of all nanog-positive cells decreased into a low level. Therefore, our data suggest that all myocardial cells, fibroblasts and small round cells are involved in myocardial reconstruction after cardiac infarction. The nanog-positive myocardial cells may respond to early myocardial repair, and the nanog-positive fibroblasts and small round cells are the main source for myocardial reconstruction after cardiac infarction.

  4. Coincidence of cerebrovascular accident and silent myocardial infarction.

    PubMed

    Badui, E; Estañol, B; Garcia-Rubi, D

    1982-11-01

    Although it is well known that a myocardial and a cerebral infarction may be coincident, the nature of this association is not clear. The problem is further complicated because the myocardial infarction may be silent. This is a report of 3 patients with cerebral infarct in whom a silent recent myocardial infarction was found. All patients with cerebrovascular disease should be screened for a possible myocardial lesion.

  5. Myocardial infarction in Antigua. 1990 to 1995.

    PubMed

    Martin, T C; Van Longhuyzen, H W; Amaraswamy, R; Tangutoori, R; Bennett, B

    1997-09-01

    Between January 1990 and May 1995, 117 patients were admitted to the Intensive Care Unit at Holberton Hospital, Antigua, for chest pain due to suspected acute myocardial infarction. 39 (45%) of 86 patients whose records were available for retrospective review had confirmed (27 patients) or probable (12 patients) acute myocardial infarction. Risk factors identified among the patients included hypertension, diabetes, tobacco smoking, hypercholesterolaemia and obesity. On admission, 82% were Killip class I and 18% were Killip class II. Medications in the Intensive Care Unit included nitrates, aspirin, calcium channel blockers, beta-adrenergic blockers, heparin and angiotensin converting enzyme inhibitors (21%). No thrombolytic agents were available. The average hospital stay was 10 days and the in-hospital mortality rate was 13%. These data indicate that early mortality from acute myocardial infarction can be reduced in developing countries by early admission to an Intensive Care Unit and use of drugs known to be effective in its treatment.

  6. Winter weather conditions and myocardial infarctions.

    PubMed

    Ohlson, C G; Bodin, L; Bryngelsson, I L; Helsing, M; Malmberg, L

    1991-03-01

    The daily number of cases of myocardial infarctions admitted to a hospital in middle Sweden over three winter seasons 1984-87 was correlated to the weather conditions on a day-to-day basis. The study encompassed 634 days and all cases younger than 70 years, living within the catchment area, in all 382 subjects. Information on temperature, wind force, precipitation and atmospheric pressure was obtained from the Swedish Institute of Meteorology and Hydrology. A low number of myocardial infarctions was seen on Saturdays and Sundays with a mild wind chill factor and on days with moderate snowfall and high atmospheric pressure. A high number was observed for workdays, especially Mondays, as day of diagnosis. Heterogeneity of the study population and a misclassification of the time relationships between dates of diagnosis and weather changes may have caused an underestimation of the impact of weather conditions. However, weather conditions do not seem to be a major triggering factor of myocardial infarctions in Sweden.

  7. Neuroendocrine activation after acute myocardial infarction.

    PubMed Central

    McAlpine, H M; Morton, J J; Leckie, B; Rumley, A; Gillen, G; Dargie, H J

    1988-01-01

    The extent of neuroendocrine activation, its time course, and relation to left ventricular dysfunction and arrhythmias were investigated in 78 consecutive patients with suspected acute myocardial infarction. High concentrations of arginine vasopressin were found within six hours of symptoms, even in the absence of myocardial infarction (n = 18). Plasma catecholamine concentrations also were highest on admission, whereas renin and angiotensin II concentrations rose progressively over the first three days, not only in those with heart failure but also in patients with no clinical complications. Heart failure, ventricular tachycardia, and deaths were associated with extensive myocardial infarction, low left ventricular ejection fraction, and persistently high concentrations of catecholamines, renin, and angiotensin II up to 10 days after admission, whereas in uncomplicated cases concentrations had already returned to normal. PMID:3415870

  8. [Mosaic portrait method in the prognosis of myocardial infarct complications].

    PubMed

    Iakovlev, G M; Ardashev, V N; Kats, M D; Galkina, T A

    1981-06-01

    A mosaic portrait of variants of the course of myocardial infarction differing in the clinical picture of the first days of the disease was created by means of methods of Boolean algebra and electronic computers. A total of 354 patients with transmural myocardial infarction were examined., The created models allow the development of some complications of myocardial infarction to be prognosticated exact within 90%.

  9. [Frovatriptan possibly causing acute myocardial infarction].

    PubMed

    Møller-Helgestad, Ole Kristian; Kaltoft, Anne Kjer; Kasch, Helge

    2015-03-23

    Globally migraine affects more than 10% of the adult population and it is treated with simple analgesics, combined with a triptan for a stronger treatment effect. Triptans cause arterial vasoconstriction, and this is a case report of vasospasm-induced acute myocardial infarction in a 61-year-old woman with frequent episodic migraine attacks treated with triptans. She was possibly also suffering from medication overuse headache. We suggest that regular frovatriptan use may have contributed to the myocardial infarction and that long-term triptan use may have caused the medication overuse headache.

  10. Decreased selenium levels in acute myocardial infarction

    SciTech Connect

    Kok, F.J.; Hofman, A.; Witteman, J.C.M.; de Bruijn, A.M.; Kruyssen, D.H.C.M.; de Bruin, M.; Valkenburg, H.A. )

    1989-02-24

    To study the association between selenium status and the risk of myocardial infarction, the authors compared plasma, erythrocyte, and toenail selenium levels and the activity of erythrocyte glutathione peroxidase among 84 patients with acute myocardial infarction and 84 population controls. Mean concentrations of all selenium measurements were lower in cases than controls. The differences were statistically significant, except for the plasma selenium level. A positive trend in the risk of acute myocardial infarction from high to low toenail selenium levels was observed, which persisted after adjustment for other risk factors for myocardial infarction. In contrast, erythrocyte glutathione peroxidase activity was significantly higher in cases than controls. Because toenail selenium level reflects blood levels up to one year before sampling, these findings suggest that a low selenium status was present before the infarction and, thus, may be of etiologic relevance. The higher glutathione peroxidase activity in the cases may be interpreted as a defense against increased oxidant stress either preceding or following the acute event.

  11. Molecular Imaging of Healing After Myocardial Infarction

    PubMed Central

    Naresh, Nivedita K; Ben-Mordechai, Tamar; Leor, Jonathan

    2011-01-01

    The progression from acute myocardial infarction (MI) to heart failure continues to be a major cause of morbidity and mortality. Potential new therapies for improved infarct healing such as stem cells, gene therapy, and tissue engineering are being investigated. Noninvasive imaging plays a central role in the evaluation of MI and infarct healing, both clinically and in preclinical research. Traditionally, imaging has been used to assess cardiac structure, function, perfusion, and viability. However, new imaging methods can be used to assess biological processes at the cellular and molecular level. We review molecular imaging techniques for evaluating the biology of infarct healing and repair. Specifically, we cover recent advances in imaging the various phases of MI and infarct healing such as apoptosis, inflammation, angiogenesis, extracellular matrix deposition, and scar formation. Significant progress has been made in preclinical molecular imaging, and future challenges include translation of these methods to clinical practice. PMID:21869911

  12. Myocardial infarction and water hardness in the WHO myocardial infarction registry network

    PubMed Central

    Masironi, R.; Piša, Z.; Clayton, D.

    1979-01-01

    The negative association between water hardness and cardiovascular disease found by several authors in different countries has also been found in the present investigation. All cases of myocardial infarction were registered in a standardized way at 15 WHO Collaborating Centres in Europe; information on the hardness of drinking water used by the population studied was also collected. Higher rates of myocardial infarction were usually found in towns served by softer water. PMID:312161

  13. Myocardial infarction and water hardness in the WHO myocardial infarction registry network.

    PubMed

    Masironi, R; Pisa, Z; Clayton, D

    1979-01-01

    The negative association between water hardness and cardiovascular disease found by several authors in different countries has also been found in the present investigation. All cases of myocardial infarction were registered in a standardized way at 15 WHO Collaborating Centres in Europe; information on the hardness of drinking water used by the population studied was also collected. Higher rates of myocardial infarction were usually found in towns served by softer water.

  14. Lymphangiogenesis in myocardial remodelling after infarction

    PubMed Central

    Ishikawa, Y; Akishima-Fukasawa, Y; Ito, K; Akasaka, Y; Tanaka, M; Shimokawa, R; Kimura-Matsumoto, M; Morita, H; Sato, S; Kamata, I; Ishii, T

    2007-01-01

    Ishikawa Y, Akishima-Fukasawa Y, Ito K, Akasaka Y, Tanaka M, Shimokawa R, Kimura-Matsumoto M, Morita H, Sato S, Kamata I & Ishii T (2007) Histopathology51, 345–353 Lymphangiogenesis in myocardial remodelling after infarction Aims The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI). Methods and results Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages. Conclusion In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid. PMID:17727476

  15. Rehabilitation of Patients Following Myocardial Infarction.

    ERIC Educational Resources Information Center

    Blumenthal, James A.; Emery, Charles F.

    1988-01-01

    Examines three behavioral strategies in cardiac rehabilitation (CR) for formal treatment for physical and psychosocial sequelae of myocardial infarction (MI): exercise therapy, Type A modification, and nonspecific psychological therapies. Concludes CR improves the quality of life among post-MI patients, but does not prolong life or significantly…

  16. [Myocardial infarction after conduction electrical weapon shock].

    PubMed

    Ben Ahmed, H; Bouzouita, K; Selmi, K; Chelli, M; Mokaddem, A; Ben Ameur, Y; Boujnah, M R

    2013-04-01

    Controversy persists over the safety of conducted electrical weapons, which are increasingly used by law enforcement agencies around the world. We report a case of 33-year-old man who had an acute inferior myocardial infarction after he was shot in the chest with an electrical weapon. Copyright © 2012 Elsevier Masson SAS. All rights reserved.

  17. Perceived Neighborhood Social Cohesion and Myocardial Infarction

    PubMed Central

    Kim, Eric S.; Hawes, Armani M.; Smith, Jacqui

    2015-01-01

    Background The main strategy for alleviating heart disease has been to target individuals and encourage them to change their health behaviors. Though important, emphasis on individuals has diverted focus and responsibility away from neighborhood characteristics, which also strongly influence people’s behaviors. Although a growing body of research has repeatedly demonstrated strong associations between neighborhood characteristics and cardiovascular health, it has typically focused on negative neighborhood characteristics. Only a few studies have examined the potential health enhancing effects of positive neighborhood characteristics, such as perceived neighborhood social cohesion. Methods Using multiple logistic regression models, we tested whether higher perceived neighborhood social cohesion was associated with lower incidence of myocardial infarction. Prospective data from the Health and Retirement Study—a nationally representative panel study of American adults over the age of 50—were used to analyze 5,276 participants with no history of heart disease. Respondents were tracked for four years and analyses adjusted for relevant sociodemographic, behavioral, biological, and psychosocial factors. Results In a model that adjusted for age, gender, race, marital status, education, and total wealth, each standard deviation increase in perceived neighborhood social cohesion was associated with a 22% reduced odds of myocardial infarction (OR = 0.78, 95% CI, 0.63–0.94. The association between perceived neighborhood social cohesion and myocardial infarction remained even after adjusting for behavioral, biological, and psychosocial covariates. Conclusions Higher perceived neighborhood social cohesion may have a protective effect against myocardial infarction. PMID:25135074

  18. Rehabilitation of Patients Following Myocardial Infarction.

    ERIC Educational Resources Information Center

    Blumenthal, James A.; Emery, Charles F.

    1988-01-01

    Examines three behavioral strategies in cardiac rehabilitation (CR) for formal treatment for physical and psychosocial sequelae of myocardial infarction (MI): exercise therapy, Type A modification, and nonspecific psychological therapies. Concludes CR improves the quality of life among post-MI patients, but does not prolong life or significantly…

  19. Myocardial infarction. Considerations for geriatric patients.

    PubMed Central

    Sinclair, D.

    1994-01-01

    Myocardial infarction is common among the elderly. Presentation is often atypical, and symptoms include confusion, weakness, chest pain, dyspnea, and vomiting. Serial electrocardiograms and cardiac enzyme determination lead to diagnosis. Postmyocardial treatments include acetylsalicylic acid, beta-blockers, nitrates, and angiotensin-converting enzyme inhibitors. Thrombolytic agents are safe and useful. Angioplasty and cardiac surgery should be considered for certain patients. PMID:7912578

  20. Porcine (Sus scrofa) Chronic Myocardial Infarction Model Development

    DTIC Science & Technology

    2015-04-03

    Myocardial Infarction Model Development.” PRINCIPAL INVESTIGATOR (PI) / TRAINING COORDINATOR (TC): Lt Col. Daren Danielson DEPARTMENT: 60MSGS/SGCH...invasively, a myocardial infarction that was isolated to the mid-anterior, left ventricular wall. In doing so, we were able to create an infarct that...be used to investigate new methodologies for treatment of chronic myocardial infarction in individuals afflicted with chronic ischemic

  1. Targeting inflammatory pathways in myocardial infarction

    PubMed Central

    Christia, Panagiota; Frangogiannis, Nikolaos G

    2013-01-01

    Acute cardiomyocyte necrosis in the infarcted heart generates Damage-Associated Molecular Patterns (DAMPs), activating complement and Toll-Like Receptor (TLR)/Interleukin (IL)-1 signaling, and triggering an intense inflammatory reaction. Infiltrating leukocytes clear the infarct from dead cells, while activating reparative pathways that lead to formation of a scar. As the infarct heals the ventricle remodels; the geometric, functional and molecular alterations associated with post-infarction remodeling are driven by the inflammatory cascade and are involved in the development of heart failure. Because unrestrained inflammation in the infarcted heart induces matrix degradation and cardiomyocyte apoptosis, timely suppression of the post-infarction inflammatory reaction may be crucial to protect the myocardium from dilative remodeling and progressive dysfunction. Inhibition and resolution of post-infarction inflammation involves mobilization of inhibitory mononuclear cell subsets and requires activation of endogenous STOP signals. Our manuscript discusses the basic cellular and molecular events involved in initiation, activation and resolution of the post-infarction inflammatory response, focusing on identification of therapeutic targets. The failure of anti-integrin approaches in patients with myocardial infarction and a growing body of experimental evidence suggest that inflammation may not increase ischemic cardiomyocyte death, but accentuates matrix degradation causing dilative remodeling. Given the pathophysiologic complexity of post-infarction remodeling, personalized biomarker-based approaches are needed to target patient subpopulations with dysregulated inflammatory and reparative responses. Inhibition of pro-inflammatory signals (such as IL-1 and Monocyte Chemoattractant Protein-1) may be effective in patients with defective resolution of post-infarction inflammation who exhibit progressive dilative remodeling. In contrast, patients with predominant

  2. Coffee consumption and myocardial infarction in women.

    PubMed

    Palmer, J R; Rosenberg, L; Rao, R S; Shapiro, S

    1995-04-15

    Whether coffee consumption increases the risk of coronary heart disease has not yet been established. In a case-control study of nonfatal myocardial infarction among Massachusetts women aged 45-69 years in 1986-1990, 858 cases with first infarctions were compared with 858 community controls matched on age and town precinct. Detailed information on coffee drinking, cigarette smoking, and other factors was obtained by telephone interview. Relative risks (as estimated by odds ratios) and their 95% confidence intervals were computed from multiple logistic regression analyses that controlled for smoking and other risk factors. The risk of myocardial infarction increased with increasing number of cups per day among both drinkers of any type of coffee and drinkers of caffeine-containing coffee only: tests for trend, p = 0.002 and p = 0.0004, respectively. For consumption of caffeine-containing coffee alone, the relative risk estimates for 5-6 cups, 7-9 cups, and 10 or more cups per day relative to less than 1 cup per day were 1.4 (95% confidence interval (CI) 0.8-2.5), 2.1 (95% CI 0.9-4.9), and 2.5 (95% CI 1.0-6.5), respectively. No increase was observed for fewer than 5 cups per day. The positive association with heavy coffee drinking was present among nonsmokers as well as smokers. These findings and other recent studies suggest that heavy coffee consumption increases the risk of myocardial infarction.

  3. Bivalirudin versus Heparin Monotherapy in Myocardial Infarction.

    PubMed

    Erlinge, David; Omerovic, Elmir; Fröbert, Ole; Linder, Rikard; Danielewicz, Mikael; Hamid, Mehmet; Swahn, Eva; Henareh, Loghman; Wagner, Henrik; Hårdhammar, Peter; Sjögren, Iwar; Stewart, Jason; Grimfjärd, Per; Jensen, Jens; Aasa, Mikael; Robertsson, Lotta; Lindroos, Pontus; Haupt, Jan; Wikström, Helena; Ulvenstam, Anders; Bhiladvala, Pallonji; Lindvall, Bo; Lundin, Anders; Tödt, Tim; Ioanes, Dan; Råmunddal, Truls; Kellerth, Thomas; Zagozdzon, Leszek; Götberg, Matthias; Andersson, Jonas; Angerås, Oskar; Östlund, Ollie; Lagerqvist, Bo; Held, Claes; Wallentin, Lars; Scherstén, Fredrik; Eriksson, Peter; Koul, Sasha; James, Stefan

    2017-09-21

    The comparative efficacy of various anticoagulation strategies has not been clearly established in patients with acute myocardial infarction who are undergoing percutaneous coronary intervention (PCI) according to current practice, which includes the use of radial-artery access for PCI and administration of potent P2Y12 inhibitors without the planned use of glycoprotein IIb/IIIa inhibitors. In this multicenter, randomized, registry-based, open-label clinical trial, we enrolled patients with either ST-segment elevation myocardial infarction (STEMI) or non-STEMI (NSTEMI) who were undergoing PCI and receiving treatment with a potent P2Y12 inhibitor (ticagrelor, prasugrel, or cangrelor) without the planned use of glycoprotein IIb/IIIa inhibitors. The patients were randomly assigned to receive bivalirudin or heparin during PCI, which was performed predominantly with the use of radial-artery access. The primary end point was a composite of death from any cause, myocardial infarction, or major bleeding during 180 days of follow-up. A total of 6006 patients (3005 with STEMI and 3001 with NSTEMI) were enrolled in the trial. At 180 days, a primary end-point event had occurred in 12.3% of the patients (369 of 3004) in the bivalirudin group and in 12.8% (383 of 3002) in the heparin group (hazard ratio, 0.96; 95% confidence interval [CI], 0.83 to 1.10; P=0.54). The results were consistent between patients with STEMI and those with NSTEMI and across other major subgroups. Myocardial infarction occurred in 2.0% of the patients in the bivalirudin group and in 2.4% in the heparin group (hazard ratio, 0.84; 95% CI, 0.60 to 1.19; P=0.33), major bleeding in 8.6% and 8.6%, respectively (hazard ratio, 1.00; 95% CI, 0.84 to 1.19; P=0.98), definite stent thrombosis in 0.4% and 0.7%, respectively (hazard ratio, 0.54; 95% CI, 0.27 to 1.10; P=0.09), and death in 2.9% and 2.8%, respectively (hazard ratio, 1.05; 95% CI, 0.78 to 1.41; P=0.76). Among patients undergoing PCI for myocardial

  4. [Climatologic parameters and myocardial infarction].

    PubMed

    Larcan, A; Gilgenkrantz, J M; Stoltz, J F; Lambert, H; Laprevote-Heully, M C; Evrard, D; Kempf, J B; Lambert, J

    1983-01-01

    535 patients admitted to hospital with myocardium infarct which was confirmed in a determined period and within a 80 kilometers radius from a city of the East of France were compared to the meteorological parameters of the day when the infarct occurred and of the day preceding its occurrence. On one hand, climatic parameters were selected: atmospheric pressure, temperature of the air under shelter, relative humidity, wind speed and wind direction, hydrometeors and electrometeors; on the other hand, parameters of solar and planetary activity: daily flare index, AA index, Ap index or daily planetary index, phases of the moon. The analytic study concerning all acute vascular accidents (infarcts and cerebral accidents all together) enabled to us to notice a higher frequency of vascular accidents in various meteorological circumstances: atmospheric pressure lower than 990 mb, temperature lower than 12 degrees, wind of sector North to South-South West, hoar-frost with fog, rain, snow, first quarter of the moon, daily flare index lower than 530, magnetic activity lower than 6. A factorial analysis of correspondence enabled to us to understand the problem better and to determine "an infarct area" in which main meteorological factors appeared: low or decreasing atmospheric pressure, relative or increasing humidity, clear or increasing solar activity, steady magnetic activity; other factors could play an apparently less important role: low temperature, snow, decrease of wind speed, full moon, wind of sector East to North-East, South-South West. Consequently it appeared in that study that the occurrence of myocardium infarct corresponded to a climatic tendency corresponding to cold, bad or deteriorating weather.

  5. A study on quality of life in patients following myocardial infarction.

    PubMed

    Gupta, Supriya; Das, Shobha; Sahewalla, Rini; Gupta, Dhruv; Gupta, Ipshita; Prakash, Ratna; Bansal, Sandeep; Rastogi, Rajeev

    2012-01-01

    Subjective well being has been widely researched in the past few decades and in practical terms it is a term that encompasses the various ways people evaluate their lives including concepts such as life satisfaction, work and health etc. Since, it is well known, that psychological factors including stress, anxiety, poor sleeping habits etc are known to be important causes of life style disorders like myocardial infraction, we started with the hypothesis that subjective well being of post acute MI patients must be poorer compared to normal subjects in the same age group. A comparative study between normal subjects and post acute myocardial infarction patients was undertaken to compare their subjective well being and current mental health status, at Safdarjung Hospital, New Delhi using standardized questionnaires. The results showed significantly higher negative affect like inadequate mental mastery over immediate environment, perceived ill health including disturbed sleep, deficiency in social contacts, and a general ill being about life in the MI group (P<0.05). Regarding the positive emotions, the normal subjects showed a higher general well being positive affect, higher transcedence and higher perception of social support. (P<0.05). The GHQ also yielded significantly better sleeping habits, less anxiety, better perception of health and more satisfaction with life in the normal subjects compared to post acute MI patients. (P<0.05).

  6. Atypical myocardial infarction on a cruise ship.

    PubMed

    Taylor, Christopher

    2015-01-01

    A previously asymptomatic 44-year-old male crewmember on a cruise ship experienced several brief episodes of acute chest pain within a short time frame. He was ultimately diagnosed with myocardial infarction; 5 h earlier he had been discharged from the ship's medical centre after almost 8 h of monitoring to rule-out infarction. Subsequent angiography ashore revealed a 99% occlusion of the right coronary artery. This case highlights the dangers of over-reliance on shipboard cardiac enzyme testing to clear a patient with chest pain.

  7. [Methylphenidate induced ST elevation acute myocardial infarction].

    PubMed

    Ruwald, Martin Huth; Ruwald, Anne-Christine Huth; Tønder, Niels

    2012-03-05

    Adult attention deficit and hyperkinetic disorder (ADHD) is increasingly diagnosed and treated with methylphenidate. We present the case of an 20 year-old man, who was diagnosed with ADHD and suffered a ST elevation acute myocardial infarction due to coronary vasospasm related to an overdose, and subsequent episodes of myocardial injury due to the use and misuse of methylphenidate over a period of two years. We recommend an increased attention to the subscription of methylphenidate to patients, who are at risk of misuse and patients, who have a cardiovascular history.

  8. Aspergillus coronary embolization causing acute myocardial infarction.

    PubMed

    Laszewski, M; Trigg, M; de Alarcon, P; Giller, R

    1988-05-01

    An increased frequency of disseminated aspergillosis has been observed in the last decade, mostly occurring in immunocompromised patients including the bone marrow transplant population. Cardiac involvement by Aspergillus remains rare. We report the clinical and postmortem findings of an unusual case of Aspergillus pancarditis in a 7-year-old bone marrow transplant patient with Aspergillus embolization to the coronary arteries leading to a massive acute myocardial infarction. This case suggests that myocardial injury secondary to disseminated aspergillosis should be included in the differential diagnosis of chest pain in the immunocompromised pediatric patient.

  9. How reliable is myocardial imaging in the diagnosis of acute myocardial infarction

    SciTech Connect

    Willerson, J.T.

    1983-01-01

    Myocardial scintigraphic techniques available presently allow a sensitive and relatively specific diagnosis of acute myocardial infarction when they are used correctly, although every technique has definite limitations. Small myocardial infarcts (less than 3 gm.) may be missed, and there are temporal limitations in the usefulness of the scintigraphic techniques. The development of tomographic methodology that may be used with single-photon radionuclide emitters (including technetium and /sup 201/Tl will allow the detection of relatively small abnormalities in myocardial perfusion and regions of myocardial infarction and will help to provide a more objective interpretation of the myocardial scintigrams. The use of overlay techniques allowing simultaneous assessment of myocardial perfusion, infarct-avid imaging, and radionuclide ventriculograms will provide insight into the relevant aspects of the extent of myocardial damage, the relationship of damage to myocardial perfusion, and the functional impact of myocardial infarction on ventricular performance.

  10. Amphetamine Abuse Related Acute Myocardial Infarction.

    PubMed

    Sinha, Archana; Lewis, O'Dene; Kumar, Rajan; Yeruva, Sri Lakshmi Hyndavi; Curry, Bryan H

    2016-01-01

    Amphetamine abuse is a global problem. The cardiotoxic manifestations like acute myocardial infarction (AMI), heart failure, or arrhythmia related to misuse of amphetamine and its synthetic derivatives have been documented but are rather rare. Amphetamine-related AMI is even rarer. We report two cases of men who came to emergency department (ED) with chest pain, palpitation, or seizure and were subsequently found to have myocardial infarction associated with the use of amphetamines. It is crucial that, with increase in amphetamine abuse, clinicians are aware of this potentially dire complication. Patients with low to intermediate risk for coronary artery disease with atypical presentation may benefit from obtaining detailed substance abuse history and urine drug screen if deemed necessary.

  11. Painless acute myocardial infarction on Mount Kilimanjaro.

    PubMed

    Jamal, Nasiruddin; Rajhy, Mubina; Bapumia, Mustaafa

    2016-03-17

    An individual experiencing dyspnoea or syncope at high altitude is commonly diagnosed to have high-altitude pulmonary edema or cerebral edema. Acute myocardial infarction (AMI) is generally not considered in the differential diagnosis. There have been very rare cases of AMI reported only from Mount Everest. We report a case of painless ST segment elevation myocardial infarction (STEMI) that occurred while climbing Mount Kilimanjaro. A 51-year-old man suffered dyspnoea and loss of consciousness near the mountain peak, at about 5600 m. At a nearby hospital, he was treated as a case of high-altitude pulmonary edema. ECG was not obtained. Two days after the incident, he presented to our institution with continued symptoms of dyspnoea, light-headedness and weakness, but no pain. He was found to have inferior wall and right ventricular STEMI complicated by complete heart block. He was successfully managed with coronary angioplasty, with good recovery. 2016 BMJ Publishing Group Ltd.

  12. Amphetamine Abuse Related Acute Myocardial Infarction

    PubMed Central

    Lewis, O'Dene; Kumar, Rajan; Yeruva, Sri Lakshmi Hyndavi; Curry, Bryan H.

    2016-01-01

    Amphetamine abuse is a global problem. The cardiotoxic manifestations like acute myocardial infarction (AMI), heart failure, or arrhythmia related to misuse of amphetamine and its synthetic derivatives have been documented but are rather rare. Amphetamine-related AMI is even rarer. We report two cases of men who came to emergency department (ED) with chest pain, palpitation, or seizure and were subsequently found to have myocardial infarction associated with the use of amphetamines. It is crucial that, with increase in amphetamine abuse, clinicians are aware of this potentially dire complication. Patients with low to intermediate risk for coronary artery disease with atypical presentation may benefit from obtaining detailed substance abuse history and urine drug screen if deemed necessary. PMID:26998366

  13. Silent myocardial infarction during hypoglycemic coma.

    PubMed

    Mahajan, Varun Vijay; Dogra, Vikas; Pargal, Iesha; Singh, Navtej

    2012-01-01

    Hypoglycemia is a common complication of treatment of diabetes mellitus. The potential neurological complications of hypoglycemia as seizures and coma are well-recognized entities. A hypoglycemic episode is a risk factor for a patient with diabetes to have cardiovascular complications. Myocardial ischemia and infarction are known to occur in the setting of hypoglycemia. In view of the potential association of the two, the diabetic patients should undergo a routine ECG in such circumstances.

  14. Incidence of myocardial infarction and weather

    NASA Astrophysics Data System (ADS)

    Staiger, Henning

    1982-08-01

    Extreme values of temperature and/or humidity in the temperate climate of Hamburg are not able to explain the influence of weather on day-to-day fluctuations of morbidity. Short term changes in weather are described by two objective classifications as deviation from the meteorological past: 1. the temperature-humidity-environment, derived from values of temperature and water vapour pressure at 07.00 h, 2. changes in the cyclonality, derived from the difference of 500 and 850 mbar vorticity values. Their suitability for human biometeorology is illustrated with a material of 1262 subjects who suffered from acute myocardial infarction. For these investigated cases it was known whether angina pectoris was already manifest before the infarction or not. The daily weather conditions have a significant effect on the incidence of acute myocardial infarction according to angina pectoris. Compared to subjects with angina pectoris those without angina pectoris show an increased susceptibility to infarction during changes in weather conditions to warmer/more humid and also during all strong changes in the cyclonality whereby the temperature-humidity-environment seems to leave only the role of an indicator too. Persons with a preceeding angina pectoris are more sensitive agains rapid changes in weather conditions.

  15. Lymphangiogenesis in myocardial remodelling after infarction.

    PubMed

    Ishikawa, Y; Akishima-Fukasawa, Y; Ito, K; Akasaka, Y; Tanaka, M; Shimokawa, R; Kimura-Matsumoto, M; Morita, H; Sato, S; Kamata, I; Ishii, T

    2007-09-01

    The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI). Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages. In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid.

  16. Adaptation to cardiac dysfunction after myocardial infarction.

    PubMed

    Gaudron, P; Eilles, C; Ertl, G; Kochsiek, K

    1993-05-01

    Survival after myocardial infarction decreases with left ventricular dilatation, although dilatation at 4 weeks was found to be compensatory. To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 days (range, 2-6 days) and 4 weeks (range, 3-5 weeks) to 6 months (range, 5-8 months) after infarction and were repeated during supine bicycle exercise at 50 W. In patients with small infarction, end-diastolic volume (mL/m2) decreased from 4 days to 6 months; ejection fraction (%), stroke volume (mL/m2), and end-systolic volume (mL/m2) remained unchanged. Stroke index rose during exercise at 4 weeks and 6 months. In patients after large infarction (n = 37), left ventricular end-systolic volume index (4 days, 38 +/- 3; 4 weeks, 47 +/- 3*; 6 months, 52 +/- 3*; *p < 0.05 versus 4 days) and end-diastolic volume indexes (4 days, 72 +/- 3; 4 weeks, 86 +/- 5*; 6 months, 92 +/- 5*; *p < 0.05 versus 4 days, +p < 0.05 versus 4 weeks) increased at constant wedge pressure. Stroke index remained restored beyond 4 weeks after infarction (4 days, 35 +/- 2; 4 weeks, 42 +/- 2*; 6 months, 42 +/- 2*; p < 0.05 versus 4 days) and rose during exercise at 4 weeks (rest, 45 +/- 2; exercise, 55 +/- 3; p < 0.05) but not at 6 months (rest, 42 +/- 3; exercise, 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

  17. Type 2 myocardial infarction: the chimaera of cardiology?

    PubMed

    Collinson, Paul; Lindahl, Bertil

    2015-11-01

    The term type 2 myocardial infarction first appeared as part of the universal definition of myocardial infarction. It was introduced to cover a group of patients who had elevation of cardiac troponin but did not meet the traditional criteria for acute myocardial infarction although they were considered to have an underlying ischaemic aetiology for the myocardial damage observed. Since first inception, the term type 2 myocardial infarction has always been vague. Although attempts have been made to produce a systematic definition of what constitutes a type 2 myocardial infarction, it has been more often characterised by what it is not rather than what it is. Clinical studies that have used type 2 myocardial infarction as a diagnostic criterion have produced disparate incidence figures. The range of associated clinical conditions differs from study to study. Additionally, there are no agreed or evidence-based treatment strategies for type 2 myocardial infarction. The authors believe that the term type 2 myocardial infarction is confusing and not evidence-based. They consider that there is good reason to stop using this term and consider instead the concept of secondary myocardial injury that relates to the underlying pathophysiology of the primary clinical condition.

  18. Prognostic Value of the Thrombolysis in Myocardial Infarction Risk Score in ST-Elevation Myocardial Infarction Patients With Left Ventricular Dysfunction (from the EPHESUS Trial).

    PubMed

    Popovic, Batric; Girerd, Nicolas; Rossignol, Patrick; Agrinier, Nelly; Camenzind, Edoardo; Fay, Renaud; Pitt, Bertram; Zannad, Faiez

    2016-11-15

    The Thrombolysis in Myocardial Infarction (TIMI) risk score remains a robust prediction tool for short-term and midterm outcome in the patients with ST-elevation myocardial infarction (STEMI). However, the validity of this risk score in patients with STEMI with reduced left ventricular ejection fraction (LVEF) remains unclear. A total of 2,854 patients with STEMI with early coronary revascularization participating in the randomized EPHESUS (Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study) trial were analyzed. TIMI risk score was calculated at baseline, and its predictive value was evaluated using C-indexes from Cox models. The increase in reclassification of other variables in addition to TIMI score was assessed using the net reclassification index. TIMI risk score had a poor predictive accuracy for all-cause mortality (C-index values at 30 days and 1 year ≤0.67) and recurrent myocardial infarction (MI; C-index values ≤0.60). Among TIMI score items, diabetes/hypertension/angina, heart rate >100 beats/min, and systolic blood pressure <100 mm Hg were inconsistently associated with survival, whereas none of the TIMI score items, aside from age, were significantly associated with MI recurrence. Using a constructed predictive model, lower LVEF, lower estimated glomerular filtration rate (eGFR), and previous MI were significantly associated with all-cause mortality. The predictive accuracy of this model, which included LVEF and eGFR, was fair for both 30-day and 1-year all-cause mortality (C-index values ranging from 0.71 to 0.75). In conclusion, TIMI risk score demonstrates poor discrimination in predicting mortality or recurrent MI in patients with STEMI with reduced LVEF. LVEF and eGFR are major factors that should not be ignored by predictive risk scores in this population.

  19. Galectin-3 and post-myocardial infarction cardiac remodeling.

    PubMed

    Meijers, Wouter C; van der Velde, A Rogier; Pascual-Figal, Domingo A; de Boer, Rudolf A

    2015-09-15

    This review summarizes the current literature regarding the involvement and the putative role(s) of galectin-3 in post-myocardial infarction cardiac remodeling. Post-myocardial infarction remodeling is characterized by acute loss of myocardium, which leads to structural and biomechanical changes in order to preserve cardiac function. A hallmark herein is fibrosis formation, both in the early and late phase following acute myocardial infarction. Galectin-3, a β-galactoside-binding lectin, which is a shared factor in fibrosis formation in multiple organs, has an established role in cardiac fibrosis in the setting of pressure overload, neuro-endocrine activation and hypertension, but its role in post- myocardial infarction remodeling has received less attention. However, accumulative experimental studies have shown that myocardial galectin-3 expression is upregulated after myocardial infarction, both on mRNA and protein level. This already occurs shortly after myocardial infarction in the infarcted and border zone area, and also at a later stage in the spared myocardium, contributing to tissue repair and fibrosis. This is associated with typical aspects of fibrosis formation, such as apposition of matricellular proteins and increased factors of collagen turnover. Interestingly, myocardial fibrosis in experimental post-myocardial infarction cardiac remodeling could be attenuated by galectin-3 inhibition. In clinical studies, circulating galectin-3 levels have been shown to identify patients at risk for new-onset heart failure and atrial fibrillation. Circulating galectin-3 levels also predict progressive left ventricular dilatation after myocardial infarction. From literature we conclude that galectin-3 is an active player in cardiac remodeling after myocardial infarction. Future studies should focus on the dynamics of galectin-3 activation after myocardial infarction, and study the possibilities to target galectin-3.

  20. Do depressive symptoms predict the incidence of myocardial infarction independent of hopelessness?

    PubMed

    Pössel, Patrick; Mitchell, Amanda M; Ronkainen, Kimmo; Kaplan, George A; Kauhanen, Jussi; Valtonen, Maarit

    2015-01-01

    Depression and hopelessness predict myocardial infarction, but it is unclear whether depression and hopelessness are independent predictors of myocardial infarction incidents. Hopelessness, depression, and myocardial infarction incidence rate 18 years later were measured in 2005 men. Cox regressions were conducted with hopelessness and depression serving as individual predictors of myocardial infarction. Another Cox model examined whether the two predictors predict myocardial infarction when adjusting for each other. Depression and hopelessness predicted myocardial infarction in independent regressions, but when adjusting for each other, hopelessness, but not depression, predicted myocardial infarction incidents. Thus, these results suggest that depression and hopelessness are not independent predictors of myocardial infarction. © The Author(s) 2013.

  1. Clinical value of delayed thallium-201 myocardial imaging in suspected acute myocardial infarction.

    PubMed Central

    McKillop, J H; Turner, J G; Gray, H W; Bessent, R G; Greig, W R

    1978-01-01

    Fifty patients with acute chest pain had thallium-201 myocardial imaging performed three to six days after emergency admission to hospital. The image was abnormal in 20 out of 22 patients with acute transmural myocardial infarcts but in only 1 of 5 with acute subendocardial infarcts. Indistinguishable scan abnormalities caused by old infarcts were seen in 7 patients, and caused by myocardial ischaemia in 1 patient. A single thallium-201 myocardial scan some days after the onset of symptoms appears to be of little value in the clinical assessment of patients with suspected acute myocardial infarction. Images PMID:687488

  2. Creation of Chronic Myocardial Infarction in a Pig (Sus Scrofa) Model

    DTIC Science & Technology

    2015-09-01

    Objectives: The goal of this protocol was to create myocardial infarctions in mini pigs using polystyrenemicrospheres to infarct a portion of the...underwent myocardial infarctions without misadventure. Infusion of polystyrene beads into a diagonal branch of the LAD resulted In a repeatable and...controlled myocardial Infarction.Conclusion: The method reported here provided consistent and repeatable myocardial infarcts with minimal morbidity.

  3. Acute Anterior Myocardial Infarction Accompanied by Acute Inferior Myocardial Infarction: A Very Rare Coronary Artery Anomaly.

    PubMed

    Alsancak, Y; Sezenöz, B; Duran, M; Unlu, S; Turkoglu, S; Yalcın, R

    2015-01-01

    Coronary artery anomalies are rare and mostly silent in clinical practice. First manifestation of this congenital abnormality can be devastating as syncope, acute coronary syndrome, and sudden cardiac death. Herein we report a case with coronary artery anomaly complicated with ST segment myocardial infarction in both inferior and anterior walls simultaneously diagnosed during primary percutaneous coronary intervention.

  4. The allometric model in chronic myocardial infarction

    PubMed Central

    2012-01-01

    Background An allometric relationship between different electrocardiogram (ECG) parameters and infarcted ventricular mass was assessed in a myocardial infarction (MI) model in New Zealand rabbits. Methods A total of fifteen animals were used, out of which ten underwent left anterior descending coronary artery ligation to induce infarction (7–35% area). Myocardial infarction (MI) evolved and stabilized during a three month-period, after which, rabbits were sacrificed and the injured area was histologically confirmed. Right before sacrifice, ECGs were obtained to correlate several of its parameters to the infarcted mass. The latter was normalized after combining data from planimetry measurements and heart weight. The following ECG parameters were studied: RR and PR intervals, P-wave duration (PD), QRS duration (QRSD) and amplitude (QRSA), Q-wave (QA), R-wave (RA) and S-wave (SA) amplitudes, T-wave peak amplitude (TA), the interval from the peak to the end of the T-wave (TPE), ST-segment deviation (STA), QT interval (QT), corrected QT and JT intervals. Corrected QT was analyzed with different correction formulae, i.e., Bazett (QTB), Framingham (QTFRA), Fridericia (QTFRI), Hodge (QTHO) and Matsunaga (QTMA) and compared thereafter. The former variables and infarcted ventricular mass were then fitted to the allometric equation in terms of deviation from normality, in turn derived after ECGs in 5 healthy rabbits. Results Six variables (JT, QTB, QA, SA, TA and STA) presented statistical differences among leads. QT showed the best allometric fit (r = 0.78), followed by TA (r = 0.77), STA (r = 0.75), QTFRA (r = 0.72), TPE (r = 0.69), QTFRI (r = 0.68) and QTMA (r = 0.68). Corrected QT’s (QTFRA, QTFRI and QTMA) performed worse than the uncorrected counterpart (QT), the former scaling allometrically with similar goodness of fits. Conclusions QT, TA, STA and TPE could possibly be used to assess infarction extent in an old MI event through the

  5. Oxygen Therapy in Suspected Acute Myocardial Infarction.

    PubMed

    Hofmann, Robin; James, Stefan K; Jernberg, Tomas; Lindahl, Bertil; Erlinge, David; Witt, Nils; Arefalk, Gabriel; Frick, Mats; Alfredsson, Joakim; Nilsson, Lennart; Ravn-Fischer, Annica; Omerovic, Elmir; Kellerth, Thomas; Sparv, David; Ekelund, Ulf; Linder, Rickard; Ekström, Mattias; Lauermann, Jörg; Haaga, Urban; Pernow, John; Östlund, Ollie; Herlitz, Johan; Svensson, Leif

    2017-08-28

    Background The clinical effect of routine oxygen therapy in patients with suspected acute myocardial infarction who do not have hypoxemia at baseline is uncertain. Methods In this registry-based randomized clinical trial, we used nationwide Swedish registries for patient enrollment and data collection. Patients with suspected myocardial infarction and an oxygen saturation of 90% or higher were randomly assigned to receive either supplemental oxygen (6 liters per minute for 6 to 12 hours, delivered through an open face mask) or ambient air. Results A total of 6629 patients were enrolled. The median duration of oxygen therapy was 11.6 hours, and the median oxygen saturation at the end of the treatment period was 99% among patients assigned to oxygen and 97% among patients assigned to ambient air. Hypoxemia developed in 62 patients (1.9%) in the oxygen group, as compared with 254 patients (7.7%) in the ambient-air group. The median of the highest troponin level during hospitalization was 946.5 ng per liter in the oxygen group and 983.0 ng per liter in the ambient-air group. The primary end point of death from any cause within 1 year after randomization occurred in 5.0% of patients (166 of 3311) assigned to oxygen and in 5.1% of patients (168 of 3318) assigned to ambient air (hazard ratio, 0.97; 95% confidence interval [CI], 0.79 to 1.21; P=0.80). Rehospitalization with myocardial infarction within 1 year occurred in 126 patients (3.8%) assigned to oxygen and in 111 patients (3.3%) assigned to ambient air (hazard ratio, 1.13; 95% CI, 0.88 to 1.46; P=0.33). The results were consistent across all predefined subgroups. Conclusions Routine use of supplemental oxygen in patients with suspected myocardial infarction who did not have hypoxemia was not found to reduce 1-year all-cause mortality. (Funded by the Swedish Heart-Lung Foundation and others; DETO2X-AMI ClinicalTrials.gov number, NCT01787110 .).

  6. Defibrillator implantation early after myocardial infarction.

    PubMed

    Steinbeck, Gerhard; Andresen, Dietrich; Seidl, Karlheinz; Brachmann, Johannes; Hoffmann, Ellen; Wojciechowski, Dariusz; Kornacewicz-Jach, Zdzisława; Sredniawa, Beata; Lupkovics, Géza; Hofgärtner, Franz; Lubinski, Andrzej; Rosenqvist, Mårten; Habets, Alphonsus; Wegscheider, Karl; Senges, Jochen

    2009-10-08

    The rate of death, including sudden cardiac death, is highest early after a myocardial infarction. Yet current guidelines do not recommend the use of an implantable cardioverter-defibrillator (ICD) within 40 days after a myocardial infarction for the prevention of sudden cardiac death. We tested the hypothesis that patients at increased risk who are treated early with an ICD will live longer than those who receive optimal medical therapy alone. This randomized, prospective, open-label, investigator-initiated, multicenter trial registered 62,944 unselected patients with myocardial infarction. Of this total, 898 patients were enrolled 5 to 31 days after the event if they met certain clinical criteria: a reduced left ventricular ejection fraction (< or = 40%) and a heart rate of 90 or more beats per minute on the first available electrocardiogram (ECG) (criterion 1: 602 patients), nonsustained ventricular tachycardia (> or = 150 beats per minute) during Holter monitoring (criterion 2: 208 patients), or both criteria (88 patients). Of the 898 patients, 445 were randomly assigned to treatment with an ICD and 453 to medical therapy alone. During a mean follow-up of 37 months, 233 patients died: 116 patients in the ICD group and 117 patients in the control group. Overall mortality was not reduced in the ICD group (hazard ratio, 1.04; 95% confidence interval [CI], 0.81 to 1.35; P=0.78). There were fewer sudden cardiac deaths in the ICD group than in the control group (27 vs. 60; hazard ratio, 0.55; 95% CI, 0.31 to 1.00; P=0.049), but the number of nonsudden cardiac deaths was higher (68 vs. 39; hazard ratio, 1.92; 95% CI, 1.29 to 2.84; P=0.001). Hazard ratios were similar among the three groups of patients categorized according to the enrollment criteria they met (criterion 1, criterion 2, or both). Prophylactic ICD therapy did not reduce overall mortality among patients with acute myocardial infarction and clinical features that placed them at increased risk. (Clinical

  7. Acetaminophen and myocardial infarction in dogs.

    PubMed

    Merrill, Gary F; Rork, Tyler H; Spiler, Norell M; Golfetti, Roseli

    2004-11-01

    The hypothesis that acetaminophen can reduce necrosis during myocardial infarction was tested in male dogs. Two groups were studied: vehicle- (n=10) and acetaminophen-treated (n=10) dogs. All dogs were obtained from the same vendor, and there were no significant differences in their ages (18 +/- 2 mo), weights (24 +/- 1 kg), or housing conditions. Selected physiological data, e.g., coronary blood flow, nonspecific collateral flow, epicardial temperature, heart rate, systemic mean arterial pressure, left ventricular developed pressure, the maximal first derivative of left ventricular developed pressure, blood gases, and pH, were collected at baseline and during regional myocardial ischemia and reperfusion. There were no significant differences in coronary blood flow, nonspecific collateral flow, epicardial temperature, heart rate, systemic mean arterial pressure, or blood gases and pH between the two groups at any of the three time intervals, even though there was a trend toward improved function in the presence of acetaminophen. Infarct size, the main objective of the investigation, was markedly and significantly reduced by acetaminophen. For example, when expressed as a percentage of ventricular wet weight, infarct size was 8 +/- 1 versus 3 +/- 1%(P <0.05) in vehicle- and acetaminophen-treated hearts, respectively. When infarct size was expressed as percentage of the area at risk, it was 35 +/- 3 versus 13 +/- 2% (P <0.05) in vehicle- and acetaminophen-treated groups, respectively. When area at risk was expressed as percentage of total ventricular mass, there were no differences in the two groups. Results reveal that the recently reported cardioprotective properties of acetaminophen in vitro can now be extended to the in vivo arena. They suggest that it is necessary to add acetaminophen to the growing list of pharmaceuticals that possess cardioprotective efficacy in mammals.

  8. Predictors of Appraisal and Coping Dimensions in Myocardial Infarction Victims.

    ERIC Educational Resources Information Center

    Lee, Hyong Sil; Martin, Peter

    This study attempted to identify predictors of perception and coping after the occurrence of a myocardial infarction. Sixty males and 17 females who had suffered from a myocardial infarction within 3 months prior to the research were recruited from a hospital rehabilitation program. Subjects completed the Peri-Life Events Scale, the 16-PF…

  9. Low High-Density Lipoprotein and Risk of Myocardial Infarction.

    PubMed

    Ramirez, A; Hu, P P

    2015-01-01

    Low HDL is an independent risk factor for myocardial infarction. This paper reviews our current understanding of HDL, HDL structure and function, HDL subclasses, the relationship of low HDL with myocardial infarction, HDL targeted therapy, and clinical trials and studies. Furthermore potential new agents, such as alirocumab (praluent) and evolocumab (repatha) are discussed.

  10. Tissue engineering for post-myocardial infarction ventricular remodeling.

    PubMed

    Kolettis, T M; Vilaeti, A; Dimos, K; Tsitou, N; Agathopoulos, S

    2011-03-01

    Myocardial tissue engineering involves the design of biomaterial scaffolds, aiming at regenerating necrotic myocardium after myocardial infarction. Biomaterials provide mechanical support to the infarct area and they can be used as vehicles for sustained and controlled local administration of cells and growth factors. Although promising results have been reported in experimental studies, many issues need to be addressed before human use.

  11. Predictors of Appraisal and Coping Dimensions in Myocardial Infarction Victims.

    ERIC Educational Resources Information Center

    Lee, Hyong Sil; Martin, Peter

    This study attempted to identify predictors of perception and coping after the occurrence of a myocardial infarction. Sixty males and 17 females who had suffered from a myocardial infarction within 3 months prior to the research were recruited from a hospital rehabilitation program. Subjects completed the Peri-Life Events Scale, the 16-PF…

  12. Acute posteroinferior wall myocardial infarction secondary to football chest trauma.

    PubMed

    Espinosa, R; Badui, E; Castaño, R; Madrid, R

    1985-12-01

    Myocardial infarction secondary to nonpenetrating chest trauma is rare. We present the case of a sportsman who developed an acute transmural posteroinferior wall myocardial infarction due to chest trauma by a football. The angiographic study revealed total obstruction of the proximal right coronary artery.

  13. [TIMI group study of thrombolysis in myocardial infarction].

    PubMed

    Braunwald, Eugene

    2009-01-01

    The article presents the history of development of various methods of reperfusion therapy in myocardial infarction. The method of intracoronary thrombolysis was developed and used in Russia in 1976. In 1984 the TIMI Study Group initiated large-scale long-term trial of thrombolytic therapy in myocardial infarction and unstable angina pectoris. Some basic results of the study are outlined.

  14. Acute myocardial infarction in a young woman on isotretinoin treatment.

    PubMed

    Lorenzo, Natalia; Antuña, Paula; Dominguez, Lourdes; Rivero, Fernando; Bastante, Teresa; Alfonso, Fernando

    2015-02-15

    The use of isotretinoin has been associated with mild changes in the metabolic profile of adolescents. In very rare cases, a possible association with myocardial infarction, stroke and thromboembolic events has been reported. In this report we describe the potential association of isotretinoin with the occurrence of an acute myocardial infarction in a very young girl. OCT provided unique visualization of the culprit lesion.

  15. Compensatory mechanisms for cardiac dysfunction in myocardial infarction.

    PubMed

    Ertl, G; Gaudron, P; Eilles, C; Schorb, W; Kochsiek, K

    1991-01-01

    Loss of contractile myocardial tissue by myocardial infarction would result in depressed cardiac output if compensatory mechanisms would not be operative. Frank-Straub-Starling-mechanism and increased heart rate and contractility due to sympathetic stimulation are unlikely to chronically compensate for cardiac dysfunction. Structural left ventricular dilatation may be compensatory, but results in increased wall stress and, ultimately, in progressive dilatation and heart failure. In patients with myocardial infarction, we have shown left-ventricular dilatation in dependence of infarct size and time after infarction. Dilatation is compensatory first and normalizes stroke volume. However, left ventricular dilatation progresses without further hemodynamic profit and, thus, may participate in development of heart failure.

  16. [Prognosis of the outcome of recurrent myocardial infarct].

    PubMed

    Ustinskova, N M; Syrkin, A L; Markova, A I; Zhuravel', A A

    1979-05-01

    The authors developed a method for prognosticating the outcome of recurrent myocardial infarction with the use of the Bayes formula. The diagnosis of recurrent myocardial infarction was made when necroses recurred in the myocardium during in-patient treatment for acute myocardial infarction. The prognosis was determined 72 hours after the recurrence of the necrosis. The prognostic signs characterized predominantly the degree of congestive circulatory failure and the frequency of disorders of cardiac rhythm in the acute period of myocardial infarction and recurrent myocardial infarction as well as in the interval betwen them (10 signs with informativeness of 0.117 to 0.05 were used.) The prognosis was erroneous in 8 of 70 patients who recovered from the disease and in 1 of 17 who died.

  17. Inferior ST-Elevation Myocardial Infarction Associated with Takotsubo Cardiomyopathy

    PubMed Central

    Koeth, Oliver; Zeymer, Uwe; Schiele, Rudolf; Zahn, Ralf

    2010-01-01

    Takotsubo cardiomyopathy (TCM) is usually characterized by transient left ventricular apical ballooning. Due to the clinical symptoms which include chest pain, electrocardiographic changes, and elevated myocardial markers, Takotsubo cardiomyopathy is frequently mimicking ST-elevation myocardial infarction in the absence of a significant coronary artery disease. Otherwise an acute occlusion of the left anterior descending coronary artery can produce a typical Takotsubo contraction pattern. ST-elevation myocardial infarction (STEMI) is frequently associated with emotional stress, but to date no cases of STEMI triggering TCM have been reported. We describe a case of a female patient with inferior ST-elevation myocardial infarction complicated by TCM. PMID:20811565

  18. Silent ST segment elevation myocardial infarction with multi-segmental renal infarction: an unusual presentation.

    PubMed

    Chang, Hung-Yu; Yang, Yung-Nien

    2011-01-01

    A 36-year-old diabetic man came to our institution presenting with constant left flank pain. Left renal embolic infarction was found by abdominal computed tomography. Silent ST segment elevation myocardial infarction was noted on 12-lead electrocardiogram. Emergent coronary angiography revealed large thrombus burdens with complete occlusion at the left anterior descending artery ostium, which may be the embolic origin. Silent ST segment elevation myocardial infarction with acute flank pain and multiple segmental renal infarction is an unusual presentation. High vigilance may prevent delay of the "golden hour" to treat acute myocardial infarction.

  19. Ventricular Septal Dissection Complicating Inferior Wall Myocardial Infarction

    PubMed Central

    Kalvin, Lindsey; Yousefzai, Rayan; Khandheria, Bijoy K.; Paterick, Timothy E.

    2017-01-01

    Postmyocardial infarction ventricular septal defect is an increasingly rare mechanical complication of acute myocardial infarction. We present a case of acute myocardial infarction from right coronary artery occlusion that developed hypotension and systolic murmur 12 hours after successful percutaneous coronary intervention. Although preoperative imaging suggested a large ventricular septal defect and a pseudoaneurysm, intraoperative findings concluded a serpiginous dissection of the ventricular septum. The imaging technicalities are discussed.

  20. Characterization of nontransmural myocardial infarction by positron-emission tomography

    SciTech Connect

    Geltman, E.M.; Biello, D.; Welch, M.J.; Ter-Pogossian, M.M.; Roberts, R.; Sobel, B.E.

    1982-04-01

    The present study was performed to determine whether positron emission tomography (PET) performed after i.v. 11C-palmitate permits detection and characterization of nontransmural myocardial infarction. PET was performed after the i.v. injection of 11C-palmitate in 10 normal subjects, 24 patients with initial nontransmural myocardial infarction (defined electrocardiographically), and 22 patients with transmural infarction. Depressed accumulation of 11C-palmitate was detected with sagittal, coronal and transverse reconstructions, and quantified based on 14 contiguous transaxial reconstructions. Defects with homogeneously intense depression of accumulation of tracer were detected in all 22 patients with transmural infarction (100%). Abnormalities of the distribution of 11C-palmitate in the myocardium were detected in 23 patients with nontransmural infarction (96%). Thallium scintigrams were abnormal in only 11 of 18 patients with nontransmural infarction (61%). Tomographically estimated infarct size was greater among patients with transmural infarction (50.4 +/- 7.8 PET-g-Eq/m2 (+/- SEM SEM)) compared with those with nontransmural infarction (19 +/- 4 PET-g-Eq, p less than 0.01). Residual accumulation of 11C-palmitate within regions of infarction was more intensely depressed among patients with transmural compared to nontransmural infarction (33 +/- 1 vs 39 +/- 1% maximal myocardial radioactivity, p less than 0.01). Thus, PET and metabolic imaging with 11C-palmitate is a sensitive means of detecting, quantifying and characterizing nontransmural and transmural myocardial infarction.

  1. Association of urinary cadmium and myocardial infarction

    SciTech Connect

    Everett, Charles J. Frithsen, Ivar L.

    2008-02-15

    We conducted a cross-sectional analysis of individuals 45-79 years old in the National Health and Nutrition Examination Survey III (1988-1994) (NHANES III). Myocardial infarction was determined by electrocardiogram (ECG). Our sample included 4912 participants, which when weighted represented 52,234,055 Americans. We performed adjusted logistic regressions with the Framingham risk score, pack-years of smoking, race-ethnicity, and family history of heart attack, and diabetes as covariates. Urinary cadmium {>=}0.88 {mu}g/g creatinine had an odds ratio of 1.86 (95% CI 1.26-2.75) compared to urinary cadmium <0.43 {mu}g/g creatinine. This result supports the hypothesis that cadmium is associated with coronary heart disease. When logistic regressions were done by gender, women, but not men, showed a significant association of urinary cadmium with myocardial infarction. Women with urinary cadmium {>=}0.88 {mu}g/g creatinine had an odds ratio of 1.80 (95% CI 1.06-3.04) compared to urinary cadmium <0.43 {mu}g/g creatinine. When the analysis was restricted to never smokers (N=2187) urinary cadmium {>=}0.88 {mu}g/g creatinine had an odds ratio of 1.85 (95% CI 1.10-3.14) compared to urinary cadmium <0.43 {mu}g/g creatinine.

  2. Infant acute myocarditis mimicking acute myocardial infarction

    PubMed Central

    Tilouche, Samia; Masmoudi, Tasnim; Sahnoun, Maha; Chkirbène, Youssef; Mestiri, Sarra; Boughamoura, Lamia; Ben Dhiab, Mohamed; Souguir, Mohamed Kamel

    2016-01-01

    Myocarditis is an inflammatory disease of the myocardium with heterogeneous clinical manifestations and progression. In clinical practice, although there are many methods of diagnosis of acute myocarditis, the diagnosis remains an embarrassing dilemma for clinicians. The authors report the case of 9-month-old infant who was brought to the Pediatric Emergency Department with sudden onset dyspnea. Examination disclosed heart failure and resuscitation was undertaken. The electrocardiogram showed an ST segment elevation in the anterolateral leads with a mirror image. Cardiac enzyme tests revealed a significant elevation of troponin and creatine phosphokinase levels. A diagnosis of acute myocardial infarction was made, and heparin therapy was prescribed. The infant died on the third day after admission with cardiogenic shock. The autopsy showed dilatation of the ventricles and massive edema of the lungs. Histological examinations of myocardium samples revealed the presence of a marked lymphocytic infiltrate dissociating myocardiocytes. Death was attributed to acute myocarditis. The authors call attention to the difficulties of differential diagnosis between acute myocarditis and acute myocardial infarction especially in children, and to the important therapeutic implications of a correct diagnosis. PMID:28210569

  3. Sevoflurane preconditioning during myocardial ischemia-reperfusion reduces infarct size and preserves autonomic control of circulation in rats.

    PubMed

    Pasqualin, Rubens Campana; Mostarda, Cristiano Teixeira; Souza, Leandro Ezequiel de; Vane, Matheus Fachini; Sirvente, Raquel; Otsuki, Denise Aya; Torres, Marcelo Luís Abramides; Irigoyen, Maria Cláudia Costa; Auler, José Otávio Costa

    2016-05-01

    To investigate the myocardial ischemia-reperfusion with sevoflurane anesthetic preconditioning (APC) would present beneficial effects on autonomic and cardiac function indexes after the acute phase of a myocardial ischemia-reperfusion. Twenty Wistar rats were allocated in three groups: control (CON, n=10), myocardial infarction with sevoflurane (SEV, n=5) and infarcted without sevoflurane (INF, n=5). Myocardial ischemia (60 min) and reperfusion were performed by temporary coronary occlusion. Twenty-one days later, the systolic and diastolic function were evaluated by echocardiography; spectral analysis of the systolic arterial pressure (SAPV) and heart rate variability (HRV) were assessed. After the recording period, the infarct size (IS) was evaluated. The INF group presented greater cardiac dysfunction and increased sympathetic modulation of the SAPV, as well as decreased alpha index and worse vagal modulation of the HRV. The SEV group exhibited attenuation of the systolic and diastolic dysfunction and preserved vagal modulation (square root of the mean squared differences of successive R-R intervals and high frequency) of HRV, as well as a smaller IS. Sevoflurane preconditioning better preserved the cardiac function and autonomic modulation of the heart in post-acute myocardial infarction period.

  4. Oxygen therapy for acute myocardial infarction.

    PubMed

    Cabello, Juan B; Burls, Amanda; Emparanza, José I; Bayliss, Susan E; Quinn, Tom

    2016-12-19

    Oxygen (O2) is widely used in people with acute myocardial infarction (AMI). Previous systematic reviews concluded that there was insufficient evidence to know whether oxygen reduced, increased or had no effect on heart ischaemia or infarct size. Our first Cochrane review in 2010 also concluded there was insufficient evidence to know whether oxygen should be used. Since 2010, the lack of evidence to support this widely used intervention has attracted considerable attention, prompting further trials of oxygen therapy in myocardial infarction patients. It is thus important to update this Cochrane review. To assess the effects of routine use of inhaled oxygen for acute myocardial infarction (AMI). We searched the following bibliographic databases on 6 June 2015: the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, MEDLINE (OVID), Embase (OVID), CINAHL (EBSCO) and Web of Science (Thomson Reuters). LILACS (Latin American and Caribbean Health Sciences Literature) was last searched in September 2016. We also contacted experts to identify eligible studies. We applied no language restrictions. Randomised controlled trials in people with suspected or proven AMI (ST-segment elevation myocardial infarction (STEMI) or non-STEMI) within 24 hours after onset, in which the intervention was inhaled oxygen (at normal pressure) compared to air, regardless of co-therapies provided to participants in both arms of the trial. Two authors independently reviewed the titles and abstracts of identified studies to see if they met the inclusion criteria and independently undertook the data extraction. We assessed the quality of studies and the risk of bias according to guidance in the Cochrane Handbook for Systematic Reviews of Interventions. The primary outcome was death. The measure of effect used was the risk ratio (RR) with a 95% confidence interval (CI). We used the GRADE approach to evaluate the quality of the evidence and the GRADE profiler (GRADEpro) to

  5. [Recurrent myocardial infarctions: specific changes in biomarkers and in myocardial remodeling (case-control study)].

    PubMed

    Volkova, E G; Malykhina, O P; Levashov, S Iu

    2007-01-01

    Basing on a case-control study (n=81) with the use of standard methods of myocardial infarction verification, examination of hemogram, troponin T, C-reactive protein, echocardiography data it was established that markers of myocardial infarction (troponin T level) and inflammation (C reactive protein level, lymphopenia) during recurrent infarctions are less pronounced than during first infarctions. Remodeling in recurrent infarctions had the following specific characteristics: increase of left ventricular end diastolic dimension, myocardial mass index, diastolic dysfunction and stroke volume with unchanged ejection fraction.

  6. [Physiopathology of left ventricular remodeling after myocardial infarction].

    PubMed

    Bassand, J P; Anguenot, T

    1991-12-01

    The geometry of both the infarcted and non-infarcted zone of the left ventricle changes after myocardial infarction. Two mechanisms are involved: expansion of the infarcted zone and secondary dilatation of the non-infarcted zone. The necrosed area undergoes an inflammatory reaction followed by fibrosis which end up as a sca within a period of a few days to a few weeks. During this period if fibrous scarring the infarcted, thinned myocardium undergoes progressive expansion which starts in the first hours of the myocardial infarction. The loss of left ventricular systolic function related to the infarct and volumic overload created by expansion of the infarct influence the secondary development of dilatation of the non-infarcted zones. This dilatation results in restoration of left ventricular stroke volume but at the price of increased wall stress, which itself induces compensatory wall hypertrophy. These phenomena are more pronounced when the initial infarction is extensive and if they are sustained, they result in definitive myocardial failure. Several factors influence remodeling: the size of the infarct, arterial patency, wall stress and the quality of the scarring process itself. Therapeutic interventions of each of these factors can influence the remodeling. Limitation of infarct size by thrombolytic therapy, arterial revascularisation, even when performed late, seem capable of limiting expansion of the necrosed zone. Pharmacodynamic intervention of left ventricular afterload also affects ventricular remodeling. Nitrate derivatives, vasodilator therapy in general and converting enzyme inhibitors have been shown to be effective.

  7. 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.

  8. [Environmental pollution with lead and myocardial infarction morbidity].

    PubMed

    Dulskiene, Virginija

    2003-01-01

    The aim of the study was to assess the effect of exposure to ambient lead and other environmental factors on first myocardial infarction incidence. Epidemiological case-control study comprised 579 male cases (25-64 year old) of myocardial infarction, treated in Kaunas hospitals and 1777 controls of the same age group without ischemic heart disease. Myocardial infarction incidence in the area of low exposure to lead was 2.34 per 1000, while in the high exposure area it was 2.61 per 1000. We determined the distribution of potential myocardial infarction risk factors among cases and controls and calculated corresponding crude odds ratios. Variables considered for inclusion in multivariate logistic regression model were those with higher prevalence among cases and values of odds ratios greater than 1.5. The analysis revealed that smoking, arterial hypertension and stress significantly increased the risk of first myocardial infarction among 25-64 year old men. Occupational exposure to chemical substances increased myocardial infarction risk by 26%, while residential exposure to ambient lead concentrations, exceeding 0.225 microg/m (3), tended to increase myocardial infarction risk by 12% (95% PI 0.94-1.34).

  9. [Sexuality in acute myocardial infarction patients].

    PubMed

    Casado Dones, Ma J; de Andrés Gimeno, B; Moreno González, C; Fernández Balcones, C; Cruz Martín, R Ma; Colmenar García, C

    2002-01-01

    We as nurses in the Coronary Unit we do not see the sexuality of the patients sufficiently addressed neither by us nor by the patients themselves. In this article we are trying to analize the reasons and to emphasize the need to include this subject in our Nursing Problem List. In it we explaine the fears and the wrong ideas that we have identified in our patients. The sexual function is not affected by a myocardial infarction but psychological factors, age, drugs and other associated diseases might be a reason. A quiet enviroment, a fit training plan and looking for personalise proper alternatives may help the patient to start a satisfactory sexual life again.

  10. Recovery of midlife women from myocardial infarction.

    PubMed

    Stevens, Sherri; Thomas, Sandra P

    2012-01-01

    We conducted this qualitative study to elicit the experiences of midlife women who survived myocardial infarctions (MIs) and returned home to recover. We selected a phenomenological research method based on the philosophy of Merleau-Ponty. The researcher interviewed eight women ranging in age from 45 to 65. The interviews were transcribed and analyzed using the approach of Thomas and Pollio. For the women in this study, figural themes of the experience of the MI and recovery must be understood within the existential grounds of the body and others. Themes included the following: (a) interference, (b) freedom/unfreedom, (c) knowing/not knowing, and (d) living in fear. Based on the findings of this study, we suggest that women need to be better educated before leaving the hospital. Returning home post MI was a difficult time, and the women in this study felt a support group for female MI survivors was needed.

  11. Pizza and risk of acute myocardial infarction.

    PubMed

    Gallus, S; Tavani, A; La Vecchia, C

    2004-11-01

    Pizza eating has been favourably related to the risk of cardiovascular disease, but the data are limited. To evaluate the potential role of pizza consumption on the risk of acute myocardial infarction (AMI), we considered data from an Italian study. We conducted a hospital-based case-control study on 507 cases of nonfatal AMI and 478 controls in Milan, Italy, between 1995 and 1999. The multivariate odds ratios were 0.78 for occasional, 0.62 for regular and 0.44 for frequent eaters. The estimates were similar across strata of age, sex, smoking and other major covariates. Some of the ingredients of pizza have been shown to have a favourable influence on the risk of cardiovascular disease. However, there is no single explanation for the present findings. Pizza may in fact represent a general indicator of Italian diet, that has been shown to have potential cardiovascular benefits.

  12. Gender and circadian effects of myocardial infarctions.

    PubMed

    Matura, Lea Ann

    2010-02-01

    This study determines if there are differences in circadian effects of myocardial infarctions (MIs) and MI type, non-ST elevation MI (NSTEMI) and ST elevation MI (STEMI), between females and males. A two-group, nonexperimental chart review was conducted. A total of 273 randomly selected patients with an acute MI were included. Data analysis included descriptive statistics, t test and chi square to determine differences between the groups. Of the 109 females, 26% had MI symptoms begin at night, 30% in the morning, 29% in the afternoon, and 15% in the evening (p = .067). In comparison, of the 164 males, 27% had MIs at night, 30% morning, 32% afternoon, and 11% evening (p < .001). There was no circadian difference between females and males and the time of day MI-related symptoms began (p = .887) or a MItype circadian effect (p = 0.466). The majority of patients had MIs during the daytime hours.

  13. Secondary prevention of myocardial infarction with drugs.

    PubMed

    Klimt, C R; Forman, S A

    1983-05-01

    Clinical trials in the field of secondary prevention of myocardial infarctions are reviewed, with emphasis on those studies that were randomized and included at least 100 patients. Standardized total mortality data, when available, are provided. Five groups of drugs are reviewed: 1) antiarrhythmic drugs, including studies of phenytoin, tocainide, mexiletine and aprindine. Important, commonly used drugs in this group, which apparently have not been submitted to clinical trials, include procainamide and lidocaine; 2) lipid-lowering drugs, including estradiol, conjugated equine estrogen, dextrothyroxine, clofibrate and nicotinic acid; 3) anticoagulant drugs, the oldest and most controversial preventive drug measure. In this group, only the oral drug derivatives of indandione or coumarin have been tested, and no appropriate studies of parenteral heparin were found; 4) platelet-active drugs--six studies dealing with aspirin alone, one combining aspirin and dipyridamole, and one study of sulfinpyrazone are reviewed; and 5) beta-adrenergic blocking drugs, including practolol and timolol.

  14. [Myocardial infarction with normal coronary arteries].

    PubMed

    Espinosa, R; Badui, E; Narvaez, M G; Hurtado, R

    1986-01-01

    We retrospectively studied 36 cases of myocardial Infarction (MI) with normal coronary arteries, which had been obtained from a total of 538 patients with MI admitted to our Hospital in the last 3 years. All patients had coronary angiogram and left ventriculogram. The following data was reviewed: age, sex, coronary risk factors, clinical picture, short and long term follow up. The angiography findings were correlated. The average age of the patients was 42 years, 75% were male and 25% female. The 36 cases represent 7% of the total MI. Cigarette smoking was the only important risk factor. MI was the first manifestation of ischemic heart disease in 94% of the cases. The ejection fraction was normal in 94%; 27.6% presented some complication during the acute event. In the long term follow; up to 88% of the patients are asymptomatic. The physiopathologic mechanisms are analyzed.

  15. Myocardial infarction following convulsive and nonconvulsive seizures.

    PubMed

    Montepietra, Sara; Cattaneo, Luigi; Granella, Franco; Maurizio, Annarita; Sasso, Enrico; Pavesi, Giovanni; Bortone, Ermelinda

    2009-06-01

    Myocardial infarction (MI) has been rarely reported in association with seizures, and only of convulsive type. We describe a series of five patients observed over a 4-year period, who presented MI immediately following seizures, either convulsive or nonconvulsive. Patient 1 had pre-existent coronary disease (CD) and presented multiple focal nonconvulsive seizures. Patient 2 had no CD, normal coronary angiography and presented secondary generalized convulsive seizures. Patient 3 had no history of CD, normal angiography and had a first single convulsive seizure. Patient 4 had severe CD and suffered from a single convulsive event. Patient 5 had a partial and a generalized seizure and had no known CD. MI following seizures is not an exceptional event and can occur in a spectrum of conditions including single or repeated, convulsive or nonconvulsive seizures, in patients with or without pre-existing coronary disease. We suggest that the occurrence of MI should be considered in epileptic patients during and shortly after seizures.

  16. Noncontraceptive estrogens and nonfatal myocardial infarction.

    PubMed

    Jick, H; Dinan, B; Rothman, K J

    1978-04-03

    We obtained information on 107 women younger than 46 years discharged from a hospital with a diagnosis of acute myocardial infarction. In the series there were 17 women aged 39 to 45 years who were otherwise apparently healthy and had had a natural menopause, hysterectomy, or tubal ligation or whose spouse had had a vasectomy. Among them, nine (53%) were taking noncontraceptive estrogens just prior to admission. Among 34 control women, four (12%) were taking estrogens. The relative risk estimate, comparing estrogen users with nonusers, is 7.5, with 90% confidence limits of 2.4 and 24. All but one of the 17 ml subjects were cigarette smokers. While this illness is rare in most healthy young women, the risk in women older than about 38 years who both smoke and take estrogens appears to be substantial.

  17. Vitamin D and acute myocardial infarction

    PubMed Central

    Milazzo, Valentina; De Metrio, Monica; Cosentino, Nicola; Marenzi, Giancarlo; Tremoli, Elena

    2017-01-01

    Vitamin D deficiency is a prevalent condition, cutting across all ethnicities and among all age groups, and occurring in about 30%-50% of the population. Besides vitamin D established role in calcium homeostasis, its deficiency is emerging as a new risk factor for coronary artery disease. Notably, clinical investigations have suggested that there is an association between hypovitaminosis D and acute myocardial infarction (AMI). Not only has it been linked to incident AMI, but also to increased morbidity and mortality in this clinical setting. Moreover, vitamin D deficiency seems to predispose to recurrent adverse cardiovascular events, as it is associated with post-infarction complications and cardiac remodeling in patients with AMI. Several mechanisms underlying the association between vitamin D and AMI risk can be involved. Despite these observational and mechanistic data, interventional trials with supplementation of vitamin D are controversial. In this review, we will discuss the evidence on the association between vitamin D deficiency and AMI, in terms of prevalence and prognostic impact, and the possible mechanisms mediating it. Further research in this direction is warranted and it is likely to open up new avenues for reducing the risk of AMI. PMID:28163832

  18. Cardiovascular gene therapy for myocardial infarction

    PubMed Central

    Scimia, Maria C; Gumpert, Anna M; Koch, Walter J

    2014-01-01

    Introduction Cardiovascular gene therapy is the third most popular application for gene therapy, representing 8.4% of all gene therapy trials as reported in 2012 estimates. Gene therapy in cardiovascular disease is aiming to treat heart failure from ischemic and non-ischemic causes, peripheral artery disease, venous ulcer, pulmonary hypertension, atherosclerosis and monogenic diseases, such as Fabry disease. Areas covered In this review, we will focus on elucidating current molecular targets for the treatment of ventricular dysfunction following myocardial infarction (MI). In particular, we will focus on the treatment of i) the clinical consequences of it, such as heart failure and residual myocardial ischemia and ii) etiological causes of MI (coronary vessels atherosclerosis, bypass venous graft disease, in-stent restenosis). Expert opinion We summarise the scheme of the review and the molecular targets either already at the gene therapy clinical trial phase or in the pipeline. These targets will be discussed below. Following this, we will focus on what we believe are the 4 prerequisites of success of any gene target therapy: safety, expression, specificity and efficacy (SESE). PMID:24328708

  19. Biomaterial strategies for alleviation of myocardial infarction

    PubMed Central

    Venugopal, Jayarama Reddy; Prabhakaran, Molamma P.; Mukherjee, Shayanti; Ravichandran, Rajeswari; Dan, Kai; Ramakrishna, Seeram

    2012-01-01

    World Health Organization estimated that heart failure initiated by coronary artery disease and myocardial infarction (MI) leads to 29 per cent of deaths worldwide. Heart failure is one of the leading causes of death in industrialized countries and is expected to become a global epidemic within the twenty-first century. MI, the main cause of heart failure, leads to a loss of cardiac tissue impairment of left ventricular function. The damaged left ventricle undergoes progressive ‘remodelling’ and chamber dilation, with myocyte slippage and fibroblast proliferation. Repair of diseased myocardium with in vitro-engineered cardiac muscle patch/injectable biopolymers with cells may become a viable option for heart failure patients. These events reflect an apparent lack of effective intrinsic mechanism for myocardial repair and regeneration. Motivated by the desire to develop minimally invasive procedures, the last 10 years observed growing efforts to develop injectable biomaterials with and without cells to treat cardiac failure. Biomaterials evaluated include alginate, fibrin, collagen, chitosan, self-assembling peptides, biopolymers and a range of synthetic hydrogels. The ultimate goal in therapeutic cardiac tissue engineering is to generate biocompatible, non-immunogenic heart muscle with morphological and functional properties similar to natural myocardium to repair MI. This review summarizes the properties of biomaterial substrates having sufficient mechanical stability, which stimulates the native collagen fibril structure for differentiating pluripotent stem cells and mesenchymal stem cells into cardiomyocytes for cardiac tissue engineering. PMID:21900319

  20. Sorafenib Cardiotoxicity Increases Mortality after Myocardial Infarction

    PubMed Central

    Trappanese, Danielle; Gross, Polina; Husain, Sharmeen; Dunn, Jonathan; Lal, Hind; Sharp, Thomas E.; Starosta, Timothy; Vagnozzi, Ronald J.; Berretta, Remus M.; Barbe, Mary; Yu, Daohai; Gao, Erhe; Kubo, Hajime; Force, Thomas; Houser, Steven R

    2014-01-01

    Rationale Sorafenib is an effective treatment for renal cell carcinoma, but recent clinical reports have documented its cardiotoxicity through an unknown mechanism. Objective Determining the mechanism of sorafenib-mediated cardiotoxicity. Methods and Results Mice treated with sorafenib or vehicle for 3 weeks underwent induced myocardial infarction (MI) after 1 week of treatment. Sorafenib markedly decreased 2-week survival relative to vehicle-treated controls but echocardiography at 1 and 2 weeks post-MI detected no differences in cardiac function. Sorafenib-treated hearts had significantly smaller diastolic and systolic volumes and reduced heart weights. High doses of sorafenib induced necrotic death of isolated myocytes in vitro, but lower doses did not induce myocyte death or affect inotropy. Histological analysis documented increased myocyte cross-sectional area despite smaller heart sizes following sorafenib treatment, further suggesting myocyte loss. Sorafenib caused apoptotic cell death of cardiac- and bone-derived c-kit+ stem cells in vitro and decreased the number of BrdU+ myocytes detected at the infarct border zone in fixed tissues. Sorafenib had no effect on infarct size, fibrosis or post-MI neovascularization. When sorafenib-treated animals received metoprolol treatment post-MI, the sorafenib-induced increase in post MI mortality was eliminated, cardiac function was improved, and myocyte loss was ameliorated. Conclusions Sorafenib cardiotoxicity results from myocyte necrosis rather than from any direct effect on myocyte function. Surviving myocytes undergo pathological hypertrophy. Inhibition of c-kit+ stem cell proliferation by inducing apoptosis exacerbates damage by decreasing endogenous cardiac repair. In the setting of MI, which also causes large-scale cell loss, sorafenib cardiotoxicity dramatically increases mortality. PMID:24718482

  1. An Unusual Complication Following Transarterial Chemoembolization: Acute Myocardial Infarction

    SciTech Connect

    Lai Yiliang; Chang Weichou; Kuo Wuhsien; Huang Tienyu; Chu Hengcheng; Hsieh Tsaiyuan; Chang Weikuo

    2010-02-15

    Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellular carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.

  2. Acute myocardial infarction and sudden death in Sioux Indians.

    PubMed

    Hrabovsky, S L; Welty, T K; Coulehan, J L

    1989-04-01

    While some Indian tribes have low rates of acute myocardial infarction, Northern Plains Indians, including the Sioux, have rates of morbidity and mortality from acute myocardial infarction higher than those reported for the United States population in general. In a review of diagnosed cases of acute myocardial infarction over a 3-year period in 2 hospitals serving predominantly Sioux Indians, 8% of cases were found misclassified, and 22% failed to meet rigorous diagnostic criteria, although the patients did indeed have ischemic heart disease. Patients had high frequencies of complications and risk factors and a fatality rate of 16% within a month of admission. Sudden deaths likely due to ischemic heart disease but in persons not diagnosed as having acute myocardial infarction by chart review occurred 3 times more frequently than deaths occurring within a month of clinical diagnosis.

  3. Increased Sensitivity to Heparin Following Acute Myocardial Infarction

    PubMed Central

    Dufault, C.

    1965-01-01

    In vivo increased sensitivity to heparin has been demonstrated in patients following an acute myocardial infarction. An intravenous injection of 10,000 units of heparin was given to each of 18 patients with recent myocardial infarction in order to compare them with 17 patients who were not suffering from any acute illness. The changes in whole blood clotting time, recalcified plasma clotting time and prothrombin time were greater and more prolonged in the patients with recent myocardial infarction. Of the three tests, the one-stage prothrombin time provided the simplest and the most precise measurement of heparin sensitivity. The reason for this was not clear: it is possible that it is related to shock and congestive heart failure which were complications of the clinical course following myocardial infarction. PMID:14216140

  4. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction.

    PubMed

    Stub, Dion; Smith, Karen; Bernard, Stephen; Nehme, Ziad; Stephenson, Michael; Bray, Janet E; Cameron, Peter; Barger, Bill; Ellims, Andris H; Taylor, Andrew J; Meredith, Ian T; Kaye, David M

    2015-06-16

    Oxygen is commonly administered to patients with ST-elevation-myocardial infarction despite previous studies suggesting a possible increase in myocardial injury as a result of coronary vasoconstriction and heightened oxidative stress. We conducted a multicenter, prospective, randomized, controlled trial comparing oxygen (8 L/min) with no supplemental oxygen in patients with ST-elevation-myocardial infarction diagnosed on paramedic 12-lead ECG. Of 638 patients randomized, 441 patients had confirmed ST-elevation-myocardial infarction and underwent primary end-point analysis. The primary end point was myocardial infarct size as assessed by cardiac enzymes, troponin I, and creatine kinase. Secondary end points included recurrent myocardial infarction, cardiac arrhythmia, and myocardial infarct size assessed by cardiac magnetic resonance imaging at 6 months. Mean peak troponin was similar in the oxygen and no oxygen groups (57.4 versus 48.0 μg/L; ratio, 1.20; 95% confidence interval, 0.92-1.56; P=0.18). There was a significant increase in mean peak creatine kinase in the oxygen group compared with the no oxygen group (1948 versus 1543 U/L; means ratio, 1.27; 95% confidence interval, 1.04-1.52; P=0.01). There was an increase in the rate of recurrent myocardial infarction in the oxygen group compared with the no oxygen group (5.5% versus 0.9%; P=0.006) and an increase in frequency of cardiac arrhythmia (40.4% versus 31.4%; P=0.05). At 6 months, the oxygen group had an increase in myocardial infarct size on cardiac magnetic resonance (n=139; 20.3 versus 13.1 g; P=0.04). Supplemental oxygen therapy in patients with ST-elevation-myocardial infarction but without hypoxia may increase early myocardial injury and was associated with larger myocardial infarct size assessed at 6 months. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01272713. © 2015 American Heart Association, Inc.

  5. Circulatory responses to hypoxia in experimental myocardial infarction.

    NASA Technical Reports Server (NTRS)

    Schroll, M.; Robison, S. C.; Harrison, D. C.

    1971-01-01

    Three levels of decreased arterial oxygen saturation elicited a graded circulatory response in dogs, manifested by stepwise increases in cardiac output, left ventricular dp/dt, and stroke volume, and decreases in systemic vascular resistance. Responses to similar hypoxia challenges after experimental myocardial infarction were qualitatively similar but quantitatively less. Although the circulatory compensation for hypoxia was less effective after myocardial infarction, no further deterioration of the haemodynamics was noted.

  6. Circulatory responses to hypoxia in experimental myocardial infarction.

    NASA Technical Reports Server (NTRS)

    Schroll, M.; Robison, S. C.; Harrison, D. C.

    1971-01-01

    Three levels of decreased arterial oxygen saturation elicited a graded circulatory response in dogs, manifested by stepwise increases in cardiac output, left ventricular dp/dt, and stroke volume, and decreases in systemic vascular resistance. Responses to similar hypoxia challenges after experimental myocardial infarction were qualitatively similar but quantitatively less. Although the circulatory compensation for hypoxia was less effective after myocardial infarction, no further deterioration of the haemodynamics was noted.

  7. Inhalation of decomposed chlorodifluoromethane (freon-22) and myocardial infarction.

    PubMed

    Sjögren, Bengt; Gunnare, Sara; Sandler, Håkan

    2002-06-01

    After exposure to decomposed chlorodifluoromethane (freon-22), a 65-year-old man developed respiratory symptoms such as cough, blood-stained sputum, and increasing dyspnea. Three weeks later, his family doctor diagnosed infectious bronchitis. Another week later he died due to myocardial infarction. The discussion focuses on an inflammatory process caused by the inhalation of decomposed freon and its possible association with myocardial infarction.

  8. PSYCHO SOCIAL FACTORS INFLUENCING THE RECOVERY AFTER MYOCARDIAL INFARCTION

    PubMed Central

    Reddy, Karri Rama; Channabasavanna, S.M.

    1987-01-01

    SUMMARY A group of 41 consecutive patients with proven diagnosis of Myocardial Infarction were studied. The severity of the Myocardial Infarction, the personality, social back ground, stressful life events preceding the onset of illness and the psychological reaction occuring in the hospital were correlated with the Psychological, Social and Physical recoveries 4 months after the onset of illness. Social and Psychological recoveries did not depend entirely on physical recovery. All the three were independently influenced by different bio-psychosocial factors. PMID:21927231

  9. Early-phase myocardial infarction: Evaluation by MR imaging

    SciTech Connect

    Tscholakoff, D.; Higgins, C.B.; McNamara, M.T.; Derugin, N.

    1986-06-01

    In vivo gated magnetic resonance (MR) imaging was performed in 12 dogs immediately after occlusion of the left anterior descending coronary artery and serially up to 5 hours and again between 4 and 14 days. This was done to evaluate the appearance of acute myocardial infarcts and to determine how soon after coronary artery occlusion MR imaging can demonstrate the site of acute myocardial ischemia. In nine dogs with postmortem evidence of myocardial infarction, regional increase of signal intensity of the myocardium was present by 3 hours after coronary occlusion and conformed to the site of myocardial infarct found at autopsy. The signal intensity on T2-weighted images of the infarcted on T2-weighted images of the infarcted myocardium was significantly greater than that of normal myocardium at 3, 4, and 5 hours after occlusion. The T2 (spin-spin) relaxation time was significantly prolonged in the region of myocardial infarct at 3, 4, and 5 hours post-occlusion compared with normal myocardium. Myocardial wall thinning and increased intracavitary flow signal were found in six dogs with comparable pre- and postocclusion images in late systole.

  10. Hospital mortality of acute myocardial infarction in the thrombolytic era

    PubMed Central

    Mahon, N; O'Rorke, C; Codd, M; McCann, H; McGarry, K; Sugrue, D

    1999-01-01

    OBJECTIVE—To examine the management and outcome of an unselected consecutive series of patients admitted with acute myocardial infarction to a tertiary referral centre.
DESIGN—A historical cohort study over a three year period (1992-94) of consecutive unselected admissions with acute myocardial infarction identified using the HIPE (hospital inpatient enquiry) database and validated according to MONICA criteria for definite or probable acute myocardial infarction.
SETTING—University teaching hospital and cardiac tertiary referral centre.
RESULTS—1059 patients were included. Mean age was 67 years; 60% were male and 40% female. Rates of coronary care unit (CCU) admission, thrombolysis, and predischarge angiography were 70%, 28%, and 32%, respectively. Overall in-hospital mortality was 18%. Independent predictors of hospital mortality by multivariate analysis were age, left ventricular failure, ventricular arrhythmias, cardiogenic shock, management outside CCU, and reinfarction. Hospital mortality in a small cohort from a non-tertiary referral centre was 14%, a difference largely explained by the lower mean age of these patients (64 years). Five year survival in the cohort was 50%. Only age and left ventricular failure were independent predictors of mortality at follow up.
CONCLUSIONS—In unselected consecutive patients the hospital mortality of acute myocardial infarction remains high (18%). Age and the occurrence of left ventricular failure are major determinants of short and long term mortality after acute myocardial infarction.


Keywords: myocardial infarction; mortality; thrombolysis PMID:10212164

  11. Rethinking the epidemiology of acute myocardial infarction: challenges and opportunities.

    PubMed

    Yeh, Robert W; Go, Alan S

    2010-05-10

    During the previous decade, many strategies for preventing acute myocardial infarction found to be efficacious in randomized controlled trials have been adopted by physicians in the community. Although evaluations of quality improvement typically focus on process measures at the hospital, practice, or clinician level, assessment of improvements in health outcomes remains the true test for the successful translation of evidence into practice. We performed a review of the current literature examining trends in the incidence of myocardial infarction in communities. We focused specifically on the group of population-based studies that have examined trends in myocardial infarction incidence. Few population-based studies have examined recent temporal trends in the incidence of myocardial infarction, overall and by type. Existing studies have been largely limited by modest sample sizes, limited diversity within the study populations, the use of composite end points that combine disparate outcomes, and the inability to characterize the effect of long-term outpatient medication use on observed trends in incidence and severity of myocardial infarction. More contemporary assessments of community-wide changes in the epidemiology of myocardial infarction are needed to help assess the effectiveness of primary prevention and to identify areas for potential improvement.

  12. Prognostic value of radionuclide exercise testing after myocardial infarction

    SciTech Connect

    Schocken, D.D.

    1984-08-01

    Abnormal systolic ventricular function and persistent ischemia are sensitive indicators of poor prognosis following myocardial infarction. The use of exercise improves the utility of both radionuclide ventriculography and myocardial perfusion scintigraphy in the identification of postinfarction patients at high risk of subsequent cardiac events. 51 references.

  13. Coronary Slow Flow Phenomenon Leads to ST Elevation Myocardial Infarction.

    PubMed

    Sen, Taner

    2013-03-01

    The exact etiology of the coronary slow flow phenomenon (CSFP) is not certain. CSFP is not a normal variant as it is an absolutely pathological entity. Furthermore, CSFP not only leads to myocardial ischemia but it can also cause classical acute ST elevation myocardial infarction, which necessitates coronary angiography for a definite diagnosis.

  14. ECG findings after myocardial infarction in children after Kawasaki disease

    SciTech Connect

    Nakanishi, T.; Takao, A.; Kondoh, C.; Nakazawa, M.; Hiroe, M.; Matsumoto, Y.

    1988-10-01

    Standard 12-lead ECGs were evaluated in 17 children with myocardial infarction and 78 children without myocardial infarction after Kawasaki disease; sensitivity and specificity of the ECG infarction criteria were determined. The presence or absence of myocardial infarction was determined from either clinical examination results (coronary angiography, ventriculography, and thallium-201 myocardial imaging) or autopsy findings. Of seven patients with inferior infarction, abnormally deep Q waves in lead II, III, or aVF were observed in six, but the duration was greater than 0.04 second in only one (14%). The sensitivity and specificity of inferior infarction criteria based on Q wave amplitude were 86% and 97%, respectively. Of eight patients with anterior infarction, seven (88%) had abnormally deep and wide (greater than or equal to 0.04 second) Q waves in anterior chest leads. The sensitivity and specificity of the infarction criteria based on the amplitude and duration of the Q wave were 75% and 99%, respectively. Of seven patients with lateral infarction, Q waves were observed in lead I, aVL, or both in four patients, and in all of these patients Q waves were wider than 0.04 second. In two patients with both inferior and anterior infarction, Q waves were observed only in leads II, III, and aVF; in only one patient were the Q waves wider than 0.04 second. Thus deep Q waves in lead II, III, or aVF that are not wider than 0.04 second may indicate inferior infarction in children. Q waves in lead I, aVL, and chest leads associated with anterolateral infarction are in most instances deep and wide.

  15. Radionuclide imaging of myocardial infarction using Tc-99m TBI

    SciTech Connect

    Holman, B.L.; Campbell, S.; Kirshenbaum, J.M.; Lister-James, J.; Jones, A.G.; Davison, A.; Antman, E.

    1985-05-01

    The cationic complex Tc-99m t-butylisonitrile (TBI) concentrates in the myocardial tissue of several animal species. Its myocardial distribution is proportional to blood flow both in zones of ischemia and in normal myocardium at rest. Planar, tomographic, and gated myocardial images have been obtained using Tc-99m TBI in the human. The authors investigated the potential application of Tc-99m TBI imaging to detect and localize myocardial infarction. Four subjects without clinical evidence of cardiovascular disease and five patients with ECG evidence of previous myocardial infarction were studied. Tc-99m TBI (10mCi) was injected intravenously with the patient in a resting state with planar imaging in the anterior, 30 and 70 degree LAO projections beginning one hr after injection. The distribution of the tracer was homogeneous throughout the left ventricular wall in the normal subjects. Regional perfusion defects were present in 4/5 of the patients with myocardial infarction. Location of the defects corresponded to the location of the infarct using ECG criteria (2 inferoposterior and 2 anterior). The patient in whom the Tc-99m TBI image appeared normal had sustained a subendocardial myocardial infarct which could not be localized by ECG; the other 4 pts had transmural infarcts. Anterior and 30 degree LAO images were of excellent quality in all cases; there was overlap of the liver on the inferior wall of the left ventricle on the 70 degree LAO views. The authors conclude that accurate perfusion imaging may be possible using Tc-99m TBI in patients with transmural myocardial infarction.

  16. Ventricular septal rupture following acute myocardial infarction.

    PubMed

    Koh, Angela S; Loh, Yee Jim; Lim, Yeong Phang; Le Tan, Ju

    2011-04-01

    Ventricular septal rupture (VSR) is a complication of acute myocardial infarction (AMI) that is associated with significant mortality. We aim to review the clinical outcome in the current era. Patients admitted to a single tertiary centre from 1997 to 2008 with VSR post-AMI were identified from the local cardiac registry. We performed a retrospective review on 25 patients. Mean age (15 women) was 71 years. Most patients had cardiovascular risk factors (84%); the commonest was hypertension (72%). Anterior AMI (80%) and apical VSR (84%) formed the majority of the cases. Eleven patients (44%) received prior coronary reperfusion therapy either via thrombolysis or PCI. Median time to rupture was 1 day from diagnosis of infarction. More than half (60%) of the patients were in Killip class 3 or 4 at diagnosis of rupture. Mean left ventricular ejection fraction (LVEF) was 33 +/- 10%. Most patients (80%) required IABP for haemodynamic support. All patients who underwent surgery had ventricular septal repair; amongst them 47% had concomitant CABG. Those managed conservatively were older (P = 0.01). Overall mortality rate was 44%. Most died within the first four days (82%). Surgical and non-surgical survival rates were 68% and 17%, respectively (P= 0.039). Patient demographics, prior coronary reperfusion techniques, Killip class status and LVEF were not significant predictors of mortality. However, non-anterior wall AMI and non-apical VSR were significantly associated with poorer survival (P = 0.009, P = 0.026 respectively). While the occurrence ofVSR post-AMI appears to be low compared to earlier studies, it continues to be associated with significant mortality. Non-anterior wall AMI and non-apical VSR were associated with poorer survival and surgical repair conferred survival advantage over conservative management.

  17. Morphine Does Not Affect Myocardial Salvage in ST-Segment Elevation Myocardial Infarction

    PubMed Central

    Song, Young Bin; Kim, Eun Kyoung; Jang, Woo Jin; Yang, Jeong Hoon; Hahn, Joo-Yong; Choi, Seung-Hyuk; Choi, Jin-Ho; Lee, Sang Hoon; Choe, Yeon Hyeon; Ahn, Joonghyun; Carriere, Keumhee Chough; Gwon, Hyeon-Cheol

    2017-01-01

    Recent studies have proposed intravenous (IV) morphine is associated with delayed action of antiplatelet agents in acute myocardial infarction. However, it is unknown whether morphine results in increased myocardial damage in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). We investigated myocardial salvage index (MSI) to determine whether IV morphine affects myocardial injury adversely in STEMI patients undergoing primary PCI. 299 STEMI patients underwent contrast-enhanced magnetic resonance imaging a median of 3 days after PCI. Infarct size was measured on delayed-enhancement imaging, and area at risk was quantified on T2-weighted imaging. MSI was calculated as ‘[area at risk–infarct size] X 100 / area at risk’. IV morphine was administrated in 32.1% of patients. Patients treated with morphine had shorter symptom to balloon time and higher prevalence of Thrombolysis in Myocardial Infarction flow grade 0 or 1. The morphine group showed a trend toward larger MSI and infarct size and significantly greater area at risk than the non-morphine group. After propensity score matching (90 pairs), MSI was similar between the morphine and non-morphine group (46.1% versus 43.5%, P = .11), and infarct size and area at risk showed no difference. In propensity score-matched analysis, IV morphine prior to primary PCI in STEMI patients did not cause adverse impacts on myocardial salvage. PMID:28081269

  18. Coronary collateral vessels in patients with previous myocardial infarction

    SciTech Connect

    Nakatsuka, M.; Matsuda, Y.; Ozaki, M.; Ogawa, H.; Moritani, K.; Khono, M.; Miura, T.; Shimizu, T.; Furutani, Y.; Kusukawa, R.

    1987-12-01

    To assess the degree of collateral vessels after myocardial infarction, coronary angiograms, left ventriculograms, and exercise thallium-201 myocardial scintigrams of 36 patients with previous myocardial infarction were reviewed. All 36 patients had total occlusion of infarct-related coronary artery and no more than 70% stenosis in other coronary arteries. In 19 of 36 patients with transient reduction of thallium-201 uptake in the infarcted area during exercise (Group A), good collaterals were observed in 10 patients, intermediate collaterals in 7 patients, and poor collaterals in 2 patients. In 17 of 36 patients without transient reduction of thallium-201 uptake in the infarcted area during exercise (Group B), good collaterals were seen in 2 patients, intermediate collaterals in 7 patients, and poor collaterals in 8 patients (p less than 0.025). Left ventricular contractions in the infarcted area were normal or hypokinetic in 10 patients and akinetic or dyskinetic in 9 patients in Group A. In Group B, 1 patient had hypokinetic contraction and 16 patients had akinetic or dyskinetic contraction (p less than 0.005). Thus, patients with transient reduction of thallium-201 uptake in the infarcted area during exercise had well developed collaterals and preserved left ventricular contraction, compared to those in patients without transient reduction of thallium-201 uptake in the infarcted area during exercise. These results suggest that the presence of viable myocardium in the infarcted area might be related to the degree of collateral vessels.

  19. Risk stratification after acute myocardial infarction: which studies are best?

    PubMed

    Figueredo, V M

    1996-04-01

    The prognosis for a patient who has survived an acute myocardial infarction depends on three general prognostic factors: (1) residual left ventricular function, (2) remaining viable myocardium at risk (residual ischemia), and (3) presence of substrate for the development of malignant arrhythmias. Multiple clinical and historical factors predict the presence of one or more of these prognostic indicators. Electrocardiographic exercise treadmill testing needs to be done in all patients with uncomplicated infarctions. Guidelines of the American College of Cardiology/American Heart Association Task Force are recommended for risk stratification in most patients after acute myocardial infarction.

  20. [Myocardial infarct immediately after a normal exercise test].

    PubMed

    Gómez-Jaume, A; González-Hermosillo, J A; Iturralde, P; Romero, L; Colín, L; Villarreal, A

    1990-01-01

    Two cases of myocardial infarction immediately following a normal stress testing, are described. The incidence and possible pathophysiological mechanisms are discussed. In one of the patients it was difficult to establish the pathophysiological mechanism which was the cause of the ischemic event. In the other, the coronary arteriography revealed only minimal obstructive disease. Therefore, coronary vasospasm with thrombus formation as a cause of the infarction ia an interesting speculative possibility in view of the angiographic findings. Acute myocardial infarction after a normal electrocardiographic response to maximal exercise testing is extremely rare, and the precise pathophysiologic mechanism that leads to his complication is not clear.

  1. Nitroglycerin Use in Myocardial Infarction Patients: Risks and Benefits

    PubMed Central

    Ferreira, Julio C.B.; Mochly-Rosen, Daria

    2012-01-01

    Acute myocardial infarction and its sequelae are leading causes of morbidity and mortality worldwide. Nitroglycerin remains a first-line treatment for angina pectoris and acute myocardial infarction. Nitroglycerin achieves its benefit by giving rise to nitric oxide, which causes vasodilation and increases blood flow to the myocardium. However, continuous delivery of nitroglycerin results in tolerance, limiting the use of this drug. Nitroglycerin tolerance is due, at least in part, to inactivation of aldehyde dehydrogenase 2 (ALDH2), an enzyme that converts nitroglycerin to the vasodilator, nitric oxide. We have recently found that, in addition to nitroglycerin’s effect on the vasculature, sustained treatment with nitroglycerin negatively affects cardiomyocyte viability following ischemia, thus resulting in increased infarct size in a myocardial infarction model in animals. Co-administration of Alda-1, an activator of ALDH2, with nitroglycerin improves metabolism of reactive aldehyde adducts and prevents the nitroglycerin-induced increase in cardiac dysfunction following myocardial infarction. In this review, we describe the molecular mechanisms associated with the benefits and risks of nitroglycerin administration in myocardial infarction. (167 of 200). PMID:22040938

  2. Use of thallium 201 myocardial imaging to exclude myocardial infarction after dissection in congenital coarctation of the aorta

    SciTech Connect

    Halon, D.A.; Weiss, A.T.; Tzivoni, D.; Atlan, H.; Gotsman, M.S.

    1981-10-01

    The use of a mobile gamma camera with thallium 201 myocardial imaging is described to exclude myocardial infarction in a patient admitted to the coronary care unit in shock and with clinical, enzyme, and ECG changes consistent with infarction. The patient suffered from acute aortic dissection associated with congenital coarctation of the aorta. The myocardial scan excluded transmural myocardial injury.

  3. Guidelines for management of acute myocardial infarction.

    PubMed

    Banerjee, Amal Kumar; Kumar, Soumitra

    2011-12-01

    These Guidelines summarize and evaluate all currently available evidence on Acute Myocardial Infarction (AMI) with the aim of assisting physicians in selecting the best management strategies for a typical patient, suffering from AMI, taking into account the impact on outcome, as well as the risk/benefit ratio of particular diagnostic or therapeutic means. Rapid diagnosis and early risk stratification of patients presenting with AMI are important to identify patients in whom early interventions can improve outcome. AMI can be defined from a number of different perspectives related to clinical, electrocardiographic (ECG), biochemical, and pathological characteristics. Quantitative assessment of risk is useful for clinical decision making. For patients with the clinical presentation of AMI within 12 h after symptom onset, early mechanical (PCI) or pharmacological reperfusion should be performed. Platelet activation and subsequent aggregation play a dominant role in the propagation of arterial thrombosis and consequently are the key therapeutic targets in the management of AMI. Adjunctive therapy with antiplatelets and antithrombotics is essential. A recommendation for routine urgent PCI (within 24 h) following successful fibrinolysis seems to be most practical option. In India, pharmacoinvasive therapy is the best option.

  4. [Thrombolytic therapy of acute myocardial infarct].

    PubMed

    Murín, J; Kasper, J; Bulas, J; Uhliar, R

    1993-08-01

    In the period of two years the authors treated at the coronary care unit 146 patients inflicted by the acute myocardial infarction (AMI). In 15 of them (13 men, 2 women, 13 times Q and twice non-Q, 5 times anterior, 10 times inferior) they performed intravenous thrombolytic treatment by use of streptokinase. The success rate of the thrombolytic therapy was evaluated by noninvasive markers: 1.) rapid withdrawal of chest pain, 2.) rapid (in 6 hours) and essential improvement of ST segment elevation and 3.) presence of reperfusion arrhythmias (in 6 hours). The authors detected insufficient medicinal conciousness among their health district population as regard to their response after the AMI origin (absolute majority of patients delayed their arrival). Minor complications due to therapy (allergy and minor local hemorrhage) occurred in 4 patients. Nobody died. Only those cases were considered as being successful, in which all three success rate markers were present. This condition was fulfilled in 8 patients (i.e. in 53% of cases) and with minor insufficiencies in further two patients (which would increase the percentage of the success rate to 67%). This success rate of the thrombolytic therapy ranges within the limits given by literature. In five patients the authors evaluated the behaviour of the left ventricular asynergy (its range and index) prior to and following the thrombolytic therapy and this examination they consider to be appropriate for observance of the thrombolytic therapy success rate in patients with AMI. (Tab. 3, Ref. 20.).

  5. Monocyte subsets in myocardial infarction: A review.

    PubMed

    Arfvidsson, John; Ahlin, Fredrik; Vargas, Kris G; Thaler, Barbara; Wojta, Johann; Huber, Kurt

    2017-03-15

    Monocytes form an important part of the human innate immune system by taking part in inflammatory reactions. With time, monocytes have gained interest in the role they may play during the event of myocardial infarction (MI). The current paradigm suggests that monocytes consist of three subdivisions which differ in phenotypic and dynamic patterns after an MI. In the inflammation that ensues, the different subsets have been shown to have an impact on reparative processes and patient recovery. We searched Medline and Embase until April 5, 2016, for observational studies or clinical trials regarding monocyte functions and dynamics in MI. Apart from studies in humans, extensive work has been done in mice in an effort to understand the complex nature of monocyte dynamics. Animal models might add useful information on mapping these processes. The question still remains whether animal data can, to a certain degree, be extrapolated to monocyte functions during human MI. This review aims to summarize current available evidence on both mice and men with particular focus on the understanding of monocyte subsets dynamics and effects in human MI. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  6. Daylight savings time and myocardial infarction

    PubMed Central

    Sandhu, Amneet; Seth, Milan; Gurm, Hitinder S

    2014-01-01

    Background Prior research has shown a transient increase in the incidence of acute myocardial infarction (AMI) after daylight savings time (DST) in the spring as well as a decrease in AMI after returning to standard time in the fall. These findings have not been verified in a broader population and if extant, may have significant public health and policy implications. Methods We assessed changes in admissions for AMI undergoing percutaneous coronary intervention (PCI) in the Blue Cross Blue Shield of Michigan Cardiovascular Consortium (BMC2) database for the weeks following the four spring and three fall DST changes between March 2010 and September 2013. A negative binomial regression model was used to adjust for trend and seasonal variation. Results There was no difference in the total weekly number of PCIs performed for AMI for either the fall or spring time changes in the time period analysed. After adjustment for trend and seasonal effects, the Monday following spring time changes was associated with a 24% increase in daily AMI counts (p=0.011), and the Tuesday following fall changes was conversely associated with a 21% reduction (p=0.044). No other weekdays in the weeks following DST changes demonstrated significant associations. Conclusions In the week following the seasonal time change, DST impacts the timing of presentations for AMI but does not influence the overall incidence of this disease. PMID:25332784

  7. The Relative Importance of Post-Acute Care and Readmissions for Post-Discharge Spending.

    PubMed

    Huckfeldt, Peter J; Mehrotra, Ateev; Hussey, Peter S

    2016-10-01

    To understand what patterns of health care use are associated with higher post-hospitalization spending. Medicare hospital, skilled nursing, inpatient rehabilitation, and home health agency claims, and Medicare enrollment data from 2007 and 2008. For 10 common inpatient conditions, we calculated variation across hospitals in price-standardized and case mix-adjusted Medicare spending in the 30 days following hospital discharge. We estimated the fraction of spending differences between low- and high-spending hospitals attributable to readmissions versus post-acute care, and within post-acute care between inpatient rehabilitation facility (IRF) versus skilled nursing facility (SNF) use. For each service, we distinguished between differences in probability of use and spending conditional on use. We identified index hospital claims and examined hospital and post-acute care occurring within a 30-day period following hospital discharge. For each Medicare Severity Diagnosis-Related Group (MS-DRG) at each hospital, we calculated average price-standardized Medicare payments for readmissions, SNFs, IRFs, and post-acute care overall (also including home health agencies and long-term care hospitals). There was extensive variation across hospitals in Medicare spending in the 30 days following hospital discharge. For example, the interquartile range across hospitals ranged from $1,245 for chronic obstructive pulmonary disease to over $4,000 for myocardial infarction MS-DRGs. The proportion of differences attributable to readmissions versus post-acute care differed across conditions. For myocardial infarction, 74 to 93 percent of the variation was due to readmissions. For hip and femur procedures and joint replacement, 72 to 92 percent of the variation was due to differences in post-acute care spending. There was also variation in the relative importance of the type of post-acute spending. For hip and femur procedures, joint replacement, and stroke, whether patients received IRF

  8. Comparison of radionuclide and enzymatic estimate of infarct size in patients with acute myocardial infarction

    SciTech Connect

    Hirsowitz, G.S.; Lakier, J.B.; Marks, D.S.; Lee, T.G.; Goldberg, A.D.; Goldstein, S.

    1983-06-01

    A comparison was made of the estimated size of the myocardial infarction occurring in 26 patients with a first infarction using creatine kinase (CK) enzyme release between radionuclide gated blood pool measurement of total and regional ventricular function and thallium-201 scintigraphic measurement of myocardial perfusion defects. Creatine kinase estimates of infarct size (enzymatic infarct size) correlated closely with the percent of abnormal contracting regions, left ventricular ejection fraction and thallium-201 estimates of percent of abnormal perfusion area (r . 0.78, 0.69 and 0.74, respectively, p less than 0.01). A close correlation also existed between percent abnormal perfusion area and percent of abnormal contracting regions (r . 0.81, p less than 0.01) and left ventricular ejection fraction (r . 0.69, p less than 0.01). Enzymatic infarct size was larger in anterior (116 +/- 37 CK-g-Eq) than inferior (52 +/- 29 CK-g-Eq) myocardial infarction (p less than 0.01) and was associated with significantly more left ventricular functional impairment as determined by left ventricular ejection fraction (33 +/- 7 versus 60 +/- 10%) (p less than 0.01) and percent abnormal perfusion area (58 +/- 14 versus 13 +/- 12) (p less than 0.01). No significant correlation was observed between enzymatic infarct size and right ventricular ejection fraction. These different methods of estimating infarct size correlated closely with each other in these patients with a first uncomplicated myocardial infarction.

  9. Treatment and outcomes of type 2 myocardial infarction and myocardial injury compared with type 1 myocardial infarction.

    PubMed

    Smilowitz, Nathaniel R; Subramanyam, Pritha; Gianos, Eugenia; Reynolds, Harmony R; Shah, Binita; Sedlis, Steven P

    2017-07-25

    Type 2 myocardial infarction (MI) is defined by a rise and fall of cardiac biomarkers and evidence of ischemia without unstable coronary artery disease (CAD) because of a mismatch in myocardial oxygen supply and demand. Myocardial injury is similar but does not fulfill the clinical criteria for MI. There is uncertainty in terms of the clinical characteristics, management, and outcomes of type 2 MI and myocardial injury in comparison with type 1 MI. Patients admitted to a Veterans Affairs tertiary care hospital with a rise and fall in cardiac troponin were identified. MI and injury subtypes, presentation, management, and outcomes were determined. Type 1 MI, type 2 MI, and myocardial injury occurred in 137, 146, and 175 patients, respectively. Patients with type 2 MI were older (P=0.02), had lower peak cardiac troponin (P<0.001), and were less likely to receive aspirin and statin at discharge (P<0.001) than type 1 MI survivors. All-cause mortality (median follow-up: 1.8 years) was not different between patient groups (type 1 MI mortality: 29.9%, type 2 MI: 30.8%, myocardial injury: 29.7%; log rank P=0.94). A significant proportion of deaths were attributed to cardiovascular causes in all subgroups (type 1 MI: 34.1%, type 2 MI: 17.8%, myocardial injury: 30.8%). Patients with type 2 MI and myocardial injury were less likely to receive medical therapy for CAD than those with type 1 MI. No differences in all-cause mortality among MI subtypes were observed. Additional studies to determine optimal medical therapy and risk stratification strategies for these high-risk populations are warranted.

  10. Regional mechanics determine collagen fiber structure in healing myocardial infarcts.

    PubMed

    Fomovsky, Gregory M; Rouillard, Andrew D; Holmes, Jeffrey W

    2012-05-01

    Following myocardial infarction, the mechanical properties of the healing infarct are an important determinant of heart function and the risk of progression to heart failure. In particular, mechanical anisotropy (having different mechanical properties in different directions) in the healing infarct can preserve pump function of the heart. Based on reports of different collagen structures and mechanical properties in various animal models, we hypothesized that differences in infarct size, shape, and/or location produce different patterns of mechanical stretch that guide evolving collagen fiber structure. We tested the effects of infarct shape and location using a combined experimental and computational approach. We studied mechanics and collagen fiber structure in cryoinfarcts in 53 Sprague-Dawley rats and found that regardless of shape or orientation, cryoinfarcts near the equator of the left ventricle stretched primarily in the circumferential direction and developed circumferentially aligned collagen, while infarcts at the apex stretched similarly in the circumferential and longitudinal directions and developed randomly oriented collagen. In a computational model of infarct healing, an effect of mechanical stretch on fibroblast and collagen alignment was required to reproduce the experimental results. We conclude that mechanical environment determines collagen fiber structure in healing myocardial infarcts. Our results suggest that emerging post-infarction therapies that alter regional mechanics will also alter infarct collagen structure, offering both potential risks and novel therapeutic opportunities.

  11. Characterization of acute myocardial infarction by magnetic resonance imaging.

    PubMed

    Johnston, D L; Wendt, R E; Mulvagh, S L; Rubin, H

    1992-05-15

    The T2-weighted spin-echo technique is currently the most frequently used magnetic resonance imaging (MRI) method to visualize acute myocardial infarction. However, image quality is often degraded by ghost artifacts from blood flow, and respiratory and cardiac contractile motion. To enhance the usefulness of this technique for detailed characterization of infarction, a velocity-compensated spin-echo pulse sequence was tested by imaging a flow phantom, 6 normal subjects and 17 patients with acute myocardial infarction. After preliminary studies were performed in 7 patients to determine optimal imaging parameters, a standardized imaging protocol was used in the next 10. The location of myocardial infarction identified by the electrocardiogram and coronary anatomy was correctly identified in 10 of 10 patients. Distribution of the injury within the left ventricle was clearly visualized, and showed that patients often had a mixture of transmural and nontransmural injury. Heterogenous distribution of signal intensity within the infarction suggested the presence of hemorrhage. Papillary muscle involvement was readily apparent. Signal intensity of the infarction (brightest segment) was increased by 89 +/- 31% compared with the mean of the remote segments. The myocardial/skeletal muscle ratio was significantly (p less than 0.001) increased for the infarction segments compared with that for remote myocardium, allowing quantitative analysis of segmental signal intensity. The MRI wall motion study obtained as part of this protocol demonstrated wall thickening in 58% of the infarction segments and in 6 of 10 patients. This finding suggested the presence of reversibly injured myocardium. In conclusion, the results demonstrate the potential of MRI for detailed tissue characterization after acute myocardial infarction.

  12. A review of strategies for infarct size reduction during acute myocardial infarction.

    PubMed

    Parviz, Yasir; Vijayan, Sethumadhavan; Lavi, Shahar

    2017-02-08

    Advances in medical and interventional therapy over the last few decades have revolutionized the treatment of acute myocardial infarction. Despite the ability to restore epicardial coronary artery patency promptly through percutaneous coronary intervention, tissue level damage may continue. The reported 30-day mortality after all acute coronary syndromes is 2 to 3%, and around 5% following myocardial infarction. Post-infarct complications such as heart failure continue to be a major contributor to cardiovascular morbidity and mortality. Inadequate microvascular reperfusion leads to worse clinical outcomes and potentially strategies to reduce infarct size during periods of ischemia-reperfusion can improve outcomes. Many strategies have been tested, but no single strategy alone has shown a consistent result or benefit in large scale randomised clinical trials. Herein, we review the historical efforts, current strategies, and potential novel concepts that may improve myocardial protection and reduce infarct size.

  13. Multicenter double blind trial of autologous bone marrow mononuclear cell transplantation through intracoronary injection post acute myocardium infarction – MiHeart/AMI study

    PubMed Central

    Dohmann, Hans FR; Silva, Suzana A; Sousa, André LS; Braga, Alcione MS; Branco, Rodrigo VC; Haddad, Andréa F; Oliveira, Mônica A; Moreira, Rodrigo C; Tuche, Fabio AA; Peixoto, Cíntia M; Tura, Bernardo R; Borojevic, Radovan; Ribeiro, Jorge P; Nicolau, José C; Nóbrega, Antonio C; Carvalho, Antonio CC

    2008-01-01

    Background Myocardial infarction remains as a major cause of mortality worldwide and a high rate of survivors develop heart failure as a sequel, resulting in a high morbidity and elevated expenditures for health system resources. We have designed a multicenter trial to test for the efficacy of autologous bone marrow (ABM) mononuclear cell (MC) transplantation in this subgroup of patients. The main hypothesis to be tested is that treated patients will have a significantly higher ejection fraction (EF) improvement after 6 months than controls. Methods A sample of 300 patients admitted with ST elevation acute myocardial infarction (STEMI) and left ventricle (LV) systolic dysfunction, and submitted to successful mechanical or chemical recanalization of the infarct-related coronary artery will be selected for inclusion and randomized to either treated or control group in a double blind manner. The former group will receive 100 × 106 MC suspended in saline with 5% autologous serum in the culprit vessel, while the latter will receive placebo (saline with 5% autologous serum). Implications Many phase I/II clinical trials using cell therapy for STEMI have been reported, demonstrating that cell transplantation is safe and may lead to better preserved LV function. Patients with high risk to develop systolic dysfunction have the potential to benefit more. Larger randomized, double blind and controlled trials to test for the efficacy of cell therapies in patients with high risk for developing heart failure are required. Trial Register This trial is registered at the NIH registry under the number NCT00350766. PMID:18598362

  14. Reducing myocardial infarct size: challenges and future opportunities

    PubMed Central

    Bulluck, Heerajnarain; Yellon, Derek M; Hausenloy, Derek J

    2016-01-01

    Despite prompt reperfusion by primary percutaneous coronary intervention (PPCI), the mortality and morbidity of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) remain significant with 9% death and 10% heart failure at 1 year. In these patients, one important neglected therapeutic target is ‘myocardial reperfusion injury’, a term given to the cardiomyocyte death and microvascular dysfunction which occurs on reperfusing ischaemic myocardium. A number of cardioprotective therapies (both mechanical and pharmacological), which are known to target myocardial reperfusion injury, have been shown to reduce myocardial infarct (MI) size in small proof-of-concept clinical studies—however, being able to demonstrate improved clinical outcomes has been elusive. In this article, we review the challenges facing clinical cardioprotection research, and highlight future therapies for reducing MI size and preventing heart failure in patients presenting with STEMI at risk of myocardial reperfusion injury. PMID:26674987

  15. Reducing myocardial infarct size: challenges and future opportunities.

    PubMed

    Bulluck, Heerajnarain; Yellon, Derek M; Hausenloy, Derek J

    2016-03-01

    Despite prompt reperfusion by primary percutaneous coronary intervention (PPCI), the mortality and morbidity of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) remain significant with 9% death and 10% heart failure at 1 year. In these patients, one important neglected therapeutic target is 'myocardial reperfusion injury', a term given to the cardiomyocyte death and microvascular dysfunction which occurs on reperfusing ischaemic myocardium. A number of cardioprotective therapies (both mechanical and pharmacological), which are known to target myocardial reperfusion injury, have been shown to reduce myocardial infarct (MI) size in small proof-of-concept clinical studies-however, being able to demonstrate improved clinical outcomes has been elusive. In this article, we review the challenges facing clinical cardioprotection research, and highlight future therapies for reducing MI size and preventing heart failure in patients presenting with STEMI at risk of myocardial reperfusion injury.

  16. Human Umbilical Cord Blood for Transplantation Therapy in Myocardial Infarction

    PubMed Central

    Acosta, Sandra A; Franzese, Nick; Staples, Meaghan; Weinbren, Nathan L.; Babilonia, Monica; Patel, Jason; Merchant, Neil; Simancas, Alejandra Jacotte; Slakter, Adam; Caputo, Mathew; Patel, Milan; Franyuti, Giorgio; Franzblau, Max H.; Suarez, Lyanne; Gonzales-Portillo, Chiara; Diamandis, Theo; Shinozuka, Kazutaka; Tajiri, Naoki; Sanberg, Paul R.; Kaneko, Yuji; Miller, Leslie W.; Borlongan, Cesar V.

    2013-01-01

    Cell-based therapy is a promising therapy for myocardial infarction. Endogenous repair of the heart muscle after myocardial infarction is a challenge because adult cardiomyocytes have a limited capacity to proliferate and replace damaged cells. Pre-clinical and clinical evidence has shown that cell based therapy may promote revascularization and replacement of damaged myocytes after myocardial infarction. Adult stem cells can be harvested from different sources including bone marrow, skeletal myoblast, and human umbilical cord blood cells. The use of these cells for the repair of myocardial infarction presents various advantages over other sources of stem cells. Among these are easy harvesting, unlimited differentiation capability, and robust angiogenic potential. In this review, we discuss the milestone findings and the most recent evidence demonstrating the therapeutic efficacy and safety of the transplantation of human umbilical cord blood cells as a stand-alone therapy or in combination with gene therapy, highlighting the importance of optimizing the timing, dose and delivery methods, and a better understanding of the mechanisms of action that will guide the clinical entry of this innovative treatment for ischemic disorders, specifically myocardial infarction. PMID:24307973

  17. Human Umbilical Cord Blood for Transplantation Therapy in Myocardial Infarction.

    PubMed

    Acosta, Sandra A; Franzese, Nick; Staples, Meaghan; Weinbren, Nathan L; Babilonia, Monica; Patel, Jason; Merchant, Neil; Simancas, Alejandra Jacotte; Slakter, Adam; Caputo, Mathew; Patel, Milan; Franyuti, Giorgio; Franzblau, Max H; Suarez, Lyanne; Gonzales-Portillo, Chiara; Diamandis, Theo; Shinozuka, Kazutaka; Tajiri, Naoki; Sanberg, Paul R; Kaneko, Yuji; Miller, Leslie W; Borlongan, Cesar V

    2013-07-01

    Cell-based therapy is a promising therapy for myocardial infarction. Endogenous repair of the heart muscle after myocardial infarction is a challenge because adult cardiomyocytes have a limited capacity to proliferate and replace damaged cells. Pre-clinical and clinical evidence has shown that cell based therapy may promote revascularization and replacement of damaged myocytes after myocardial infarction. Adult stem cells can be harvested from different sources including bone marrow, skeletal myoblast, and human umbilical cord blood cells. The use of these cells for the repair of myocardial infarction presents various advantages over other sources of stem cells. Among these are easy harvesting, unlimited differentiation capability, and robust angiogenic potential. In this review, we discuss the milestone findings and the most recent evidence demonstrating the therapeutic efficacy and safety of the transplantation of human umbilical cord blood cells as a stand-alone therapy or in combination with gene therapy, highlighting the importance of optimizing the timing, dose and delivery methods, and a better understanding of the mechanisms of action that will guide the clinical entry of this innovative treatment for ischemic disorders, specifically myocardial infarction.

  18. Risk profile in women with acute myocardial infarction.

    PubMed

    Târlea, Mihaela; Deleanu, D; Bucşa, A; Zarma, L; Croitoru, M; Platon, P; Ginghină, Carmen

    2009-01-01

    The studies in the literature of the past years have noticed the particular characteristics of the ischemic heart disease in women, who seem to be lacking early diagnosis and invasive treatment of coronary heart disease. They especially emphasize that the evolution, complications and mortality in myocardial infarction in women are more severe. The evaluation of clinical, investigational and therapeutic aspects in a lot of women with acute myocardial infarction (AMI) versus a lot of men with the same pathology, hospitalised in the same period. 78 women hospitalised in the Emergency Institute of Cardiovascular Diseases between 1st January 1999 and 30th October 2001 with acute myocardial infarction. 109 men hospitalised in the Emergency Institute of Cardiovascular Diseases with acute myocardial infarction in the same period. acute myocardial infarction, coronary angiography +/=left ventriculography. The lot of study and the witness lot were divided into 3 subgroups based on the severity of coronary lesions: Group I: left main stenoses, Group II: stenoses >60% on the other epicardial coronary vessels, Group III: stenoses <60% on the other epicardial coronary vessels. The risk factors, clinical data, cardiac performance indices and medical and invasive treatment were compared between the two groups. The women hospitalised with AMI were older than men, had more diabetes and hypertension as main risk factors than men, with the exception of smoking, had more frequent heart failure and diastolic dysfunction of left ventricle. The favorite invasive treatment in women was the angioplasty with application of stent and in men--coronary bypass.

  19. Helicobacter pylori seropositivity in subjects with acute myocardial infarction.

    PubMed Central

    Rathbone, B.; Martin, D.; Stephens, J.; Thompson, J. R.; Samani, N. J.

    1996-01-01

    OBJECTIVE: To determine whether Helicobacter pylori infection increases the risk of myocardial infarction. DESIGN: Case-control study. SETTING: University teaching hospital. METHODS: Serological evidence of H pylori infection was determined in 342 consecutive patients with acute myocardial infarction admitted into the coronary care unit and in 236 population-based controls recruited from visitors to patients on medical and surgical wards. RESULTS: 206/342 (60.2%) of cases were H pylori positive compared with 132/236 (55.9%) of controls (P = 0.30). Age and sex stratified odds ratio for myocardial infarction associated with H pylori seropositivity was 1.05 (95% CI 0.7 to 1.53, P = 0.87) and this remained non-significant (P = 0.46) when other risk factors for ischaemic heart disease were taken into account using logistic regression analysis. H pylori seropositivity was not associated with several coronary risk factors in either cases or controls. CONCLUSION: No increase was found in H pylori seropositivity in subjects with acute myocardial infarction. This suggests that previous H pylori infection is not a major risk factor for acute myocardial infarction. Images PMID:8983674

  20. Acute Myocardial Infarction in Adult Congenital Patients with Bodily Isomerism.

    PubMed

    Loomba, Rohit S; Aggarwal, Saurabh; Buelow, Matthew; Nijhawan, Karan; Gupta, Navdeep; Alla, Venkata; Arora, Rohit R

    2016-12-01

    Children born with congenital malformations of the heart are increasingly surviving into adulthood. This population of patients possesses lesion-specific complication risks while still being at risk for common illnesses. Bodily isomerism or heterotaxy, is a unique clinical entity associated with congenital malformations of the heart which further increases the risk for future cardiovascular complications. We aimed to investigate the frequency of myocardial infarction in adults with bodily isomerism. We utilized the 2012 iteration of the Nationwide Inpatient Sample to identify adult inpatient admissions associated with acute myocardial infarction in patients with isomerism. Data regarding demographics, comorbidities and various procedures were collected and compared between those with and without isomerism. A total of 6,907,109 admissions were analyzed with a total of 172,394 admissions being associated with an initial encounter for acute myocardial infarction. The frequency of myocardial infarction did not differ between those with and without isomerism and was roughly 2% in both groups. Similarly, the number of procedures and in-hospital mortality did not differ between the two groups. The frequency and short-term prognosis of acute myocardial infarction is similar in patients with and without isomerism. © 2016 Wiley Periodicals, Inc.

  1. Infarct tissue characteristics of patients with versus without early revascularization for acute myocardial infarction: a contrast-enhancement cardiovascular magnetic resonance imaging study.

    PubMed

    Olimulder, M A G M; Kraaier, K; Galjee, M A; Scholten, M F; van Es, J; Wagenaar, L J; van der Palen, J; von Birgelen, C

    2012-05-01

    Histopathological studies have suggested that early revascularization for acute myocardial infarction (MI) limits the size, transmural extent, and homogeneity of myocardial necrosis. However, the long-term effect of early revascularization on infarct tissue characteristics is largely unknown. Cardiovascular magnetic resonance (CMR) imaging with contrast enhancement (CE) allows non-invasive examination of infarct tissue characteristics and left ventricular (LV) dimensions and function in one examination. A total of 69 patients, referred for cardiac evaluation for various clinical reasons, were examined with CE-CMR >1 month (median 6, range 1-213) post-acute MI. We compared patients with (n = 33) versus without (n = 36) successful early revascularization for acute MI. Cine-CMR measurements included the LV end-diastolic and end-systolic volumes (ESV), LV ejection fraction (LVEF, %), and wall motion score index (WMSI). CE images were analyzed for core, peri, and total infarct size (%), and for the number of transmural segments. In our population, patients with successful early revascularization had better LVEFs (46 ± 16 vs. 34 ± 14%; P < 0.01), superior WMSIs (0.53, range 0.00-2.29 vs. 1.42, range 0.00-2.59; P < 0.01), and smaller ESVs (121 ± 70 vs. 166 ± 82; P = 0.02). However, there was no difference in core (9 ± 6 vs. 11 ± 6%), peri (9 ± 4 vs. 10 ± 4%), and total infarct size (18 ± 9 vs. 21 ± 9%; P > 0.05 for all comparisons); only transmural extent (P = 0.07) and infarct age (P = 0.06) tended to be larger in patients without early revascularization. CMR wall motion abnormalities are significantly better after revascularization; these differences are particularly marked later after infarction. The difference in scar size is more subtle and does not reach significance in this study.

  2. Stem cell therapy for the treatment of myocardial infarction.

    PubMed

    Dauwe, D F; Janssens, S P

    2011-10-01

    Despite timely reperfusion and subsequent optimal postinfarct pharmacotherapy and device-based treatment, the outcome in patients with severe myocardial infarction remains unfavourable. Myocardial salvage is incomplete, resulting in adverse left ventricular remodeling with concomitant morbidity and mortality. The combined risk of recurrent myocardial infarction, death or readmission for heart failure amounts to 25 % within the first year, highlighting the need for additional treatment strategies. Recent and rapidly evolving insights in cardiac biology, recognizing endogenous repair capabilities of the adult human heart, paved the path towards progenitor or stem cell based cardiac protection and repair strategies following ischemic injury. We critically report on the major randomized controlled clinical trials published so far concerning intracoronary transfer of autologous bone marrow cells in the setting of acute myocardial infarction. Moreover, underlying mechanisms, practical aspects, remaining questions and future challenges are highlighted. Taken together, these trials confirm the safety and feasibility of intracoronary progenitor cell transfer in the setting of myocardial infarction. Efficacy data suggests its potential to improve left ventricular function recovery beyond current state of the art therapy, but results are mixed, modest at best and do not support true cardiomyogenesis. Hence, due to its complexity, costs and remaining uncertainties, it is still too early to implement progenitor cell therapy in its current form in standard treatment strategies for ischemic heart disease. Future studies on strategies for cardiomyocyte regeneration in combination with myocardial protection are needed.

  3. Radionuclide imaging of myocardial perfusion and viability in assessment of acute myocardial infarction

    SciTech Connect

    Berman, D.S.; Kiat, H.; Maddahi, J.; Shah, P.K.

    1989-07-18

    Technical advances in radionuclide imaging have important implications for the management of patients with acute myocardial infarction. Single-photon emission computerized tomography with thallium 201 (TI-201) offers greater accuracy than planar imaging in detecting, localizing and sizing myocardial perfusion defects. Use of single-photon emission computerized tomography with TI-201 should allow for a more accurate assessment of prognosis after myocardial infarction. A new radiopharmaceutical, technetium 99-m methoxyisobutyl isonitrile, provides a number of advantages over TI-201, including higher quality images, lack of redistribution, and the ability to assess first-pass ventricular function. Applications of TI-201 and technetium 99-m methoxyisobutyl isonitrile include assessment of arterial patency and myocardial salvage immediately after thrombolytic therapy, detection of resting ischemia after thrombolytic therapy, targeting of subsets of patients for further intervention, and predischarge assessment to predict the future course of patients after an acute myocardial infarction.

  4. [Early statin therapy in acute myocardial infarction].

    PubMed

    Ruiz-Bailén, M; Romero-Bermejo, F J; Expósito-Ruiz, M; Zamora-Zamora, F; Martínez-Ramírez, M J; Castillo-Rivera, A M; Ramos-Cuadra, J A; Ramírez-Sánchez, M; Vázquez-García, R

    2014-01-01

    To evaluate the effects of the early administration of statins during acute myocardial infarction (MI). A retrospective cohort study was carried out. National (Spain). Patients included in the ARIAM registry from January 1999 to December 2008 with a diagnosis of MI. None. We used logistic regression analysis and propensity scoring to determine whether the administration of statins during the first 24h of MI acts as a protective factor against: 1) mortality, 2) the incidence of lethal arrhythmias, or 3) cardiogenic shock. A total of 36 842 patients were included in the study. Statins were administered early in 50.2% of the patients. Statin administration was associated with younger patients with known previous dyslipidemia, obesity, a history of ischemic heart disease, heart failure, presence of sinus tachycardia, use of beta-blockers, angiotensin-converting enzyme inhibitors, thrombolysis and percutaneous coronary intervention. Mortality was 8.2% (13.2% without statin versus 3% with statin, P<.001). Multivariate analysis demonstrated that statin administration acted as a protective factor against mortality (adjusted OR 0.518, 95%CI 0.447 to 0.601). Continued use of statins was associated with a reduction in mortality (adjusted OR 0.597, 95%CI 0.449 to 0.798), and the start of treatment was a protective factor against mortality (adjusted OR 0.642, 95%CI 0.544 -0.757). Statin therapy also exerted a protective effect against the incidence of lethal arrhythmias and cardiogenic shock. These results suggest that early treatment with statins in patients with MI is associated with reduced mortality. Copyright © 2012 Elsevier España, S.L. and SEMICYUC. All rights reserved.

  5. Sinoatrial disease in acute myocardial infarction. Long-term prognosis.

    PubMed Central

    Hatle, L; Bathen, J; Rokseth, R

    1976-01-01

    Of 32 patients with acute myocardial infarction complicated by sinoatrial disease, 23 survived. All 23 had inferior infarction. During follow-up lasting 4 to 6 years only one patient developed severe chronic sinoatrial disease (sick sinus syndrome) necessitating permanent pacemaker treatment; twelve others died during this time. In 2 of them death was sudden 5 and 6 months after infarction. Atrial pacing studies in 7 of the 11 patients still alive showed no gross abnormalities. A review of 71 patients with chronic sinoatrial disease treated with a permanent pacemaker revealed only 5 with previous documented infarction. The present data suggest that sinus node dysfunction in patients surviving acute infarction is most often only temporary as is atrioventricular block. Occasionally, however, severe chronic sinoatrial disease requiring a permanent pacemaker may develop later, and this course of events is most likely to occur in those patients who had additional complications during the acute infarct. PMID:1267985

  6. [Lay theories regarding myocardial infarction in a transcultural comparison].

    PubMed

    Bermejo, Isaac; Bursch, Stephanie; Muthny, Fritz A

    2006-08-01

    Culturally influenced lay theories about myocardial infarction which exist in healthy individuals have an impact on treatment compliance. However, empirical data on the subject is rare. Using healthy subjects, a transcultural survey comparing three different ethnic groups was conducted. The groups were: Germans in Germany, Spaniards in Spain, and 1st generation Spaniards in Germany. Subjects were paralleled according to age, sex, and education. The groups were compared regarding cultural differences in casual attributions and locus of control with respect to myocardial infarction. While all three groups show a psycho-social understanding of myocardial infarction, it is most predominate in the German group. The results show both common factors as well as some significant differences between Germans and Spaniards, the Spaniards reporting more external attributions. Consequences for prevention concepts and medical care in a multicultural society were derived from the results.

  7. Infection and inflammation as risk factors for myocardial infarction.

    PubMed

    Nieminen, M S; Mattila, K; Valtonen, V

    1993-12-01

    Recent studies have illustrated that in addition to the well known risk factors, such as lipoproteins, smoking, hypertension, there are others that cause atherosclerosis and myocardial infarction. Our knowledge of atherosclerotic lesions has increased. We now know that atherosclerotic changes are due to inflammatory cell infiltration as well as to increases in migration of vascular smooth muscle cells. Endothelial cells play a major role in the pathology of vascular changes. In recent years a new risk factor for coronary artery disease has been discovered: chlamydia pneumonial infections. Herpes class viruses have also been associated with pathology of atherosclerotic lesions. Studies show that dental status and bacterial infections are also related to the risk of myocardial infarction. This review discusses the possible mechanisms of infection and inflammation and whether they are major or modifying risk factors for atherosclerosis and myocardial infarction.

  8. Cardiovascular collapse after myocardial infarction due to centipede bite.

    PubMed

    Üreyen, Çağin Mustafa; Arslan, Şakir; Baş, Cem Yunus

    2015-07-01

    Centipede bites have been reported to cause localized and/or systemic symptoms including local pain, erythema and edema, nausea and vomiting, palpitations, headache, lymphadenopathy, and rhabdomyolysis. However, acute myocardial infarction due to centipede envenomation is reported in only three cases in English medical literature.We present a case of 31-year-old male bitten by a golden colored centipede leading to myocardial infarction and cardiopulmonary arrest which is seen very rarely. The patient was admitted to emergency department with a swollen and painful right foot. However, typical chest pain became the major complaint and cardiopulmonary arrest developed while electrocardiography was being obtained. The patient was resuscitated successfully for 5 min and acute infero-posterolateral myocardial infarction was detected on electrocardiography.

  9. Amphetamine Containing Dietary Supplements and Acute Myocardial Infarction

    PubMed Central

    Hritani, Abdulwahab; Antoun, Patrick

    2016-01-01

    Weight loss is one of the most researched and marketed topics in American society. Dietary regimens, medications that claim to boost the metabolism, and the constant pressure to fit into society all play a role in our patient's choices regarding new dietary products. One of the products that are well known to suppress appetite and cause weight loss is amphetamines. While these medications suppress appetite, most people are not aware of the detrimental side effects of amphetamines, including hypertension, tachycardia, arrhythmias, and in certain instances acute myocardial infarction. Here we present the uncommon entity of an acute myocardial infarction due to chronic use of an amphetamine containing dietary supplement in conjunction with an exercise regimen. Our case brings to light further awareness regarding use of amphetamines. Clinicians should have a high index of suspicion of use of these substances when young patients with no risk factors for coronary artery disease present with acute arrhythmias, heart failure, and myocardial infarctions. PMID:27516911

  10. [Cardiogenic shock in acute myocardial infarct. Its coronary angioplasty treatment].

    PubMed

    Fernández Valadez, E; García y Otero, J M; Escobar, G P; Frutos Rangel, E; Zúñiga Sedano, J; García García, R; Verduzco Bazavilvazo, S; López Aranda, J; López Ruiz, J

    1993-01-01

    Ventricular dysfunction is the most common cause of in-hospital death in patients with acute myocardial infarction. When cardiogenic shock is manifested the mortality is very high. Seven patients with cardiogenic shock complicating acute myocardial infarction were treated with emergency coronary angioplasty. Four patients required cardiopulmonary resuscitation (CPR), 2 intraaortic balloon pump support and one femoro-femoral bypass pump support during the coronary angioplasty. The angiography success rate was 86%. Two patients died, one in the catheterization laboratory and the other one 24 hours later. The hospital mortality was 29%. Of the patients who survived 4 are in functional class I and one in functional class II (NYHA). Coronary angioplasty therapy in patients with cardiogenic shock complicating acute myocardial infarction plays a decisive role in the reduction of mortality.

  11. [Cardiac remodeling after myocardial infarction : Clinical practice update].

    PubMed

    Ertl, G; Brenner, S; Angermann, C E

    2017-02-01

    Heart failure remains a frequent cause of death and is the leading reason for hospitalization in Germany although therapeutic options have significantly increased over the past years particularly in heart failure with reduced ejection fraction. Clinical symptoms are usually preceded by cardiac remodeling, which was originally defined only by left ventricular dilatation and depressed function but is also associated with typical cellular and molecular processes. Healing after acute myocardial infarction is characterized by inflammation, cellular migration and scar formation. Cardiac remodeling is accompanied by adaptive changes of the peripheral cardiovascular system. Since prevention is the primary goal, rapid diagnosis and treatment of myocardial infarction are mandatory. Early reperfusion therapy limits infarct size and enables the best possible preservation of left ventricular function. Standard pharmacotherapy includes angiotensin-converting enzyme inhibitors, angiotensin-1-receptor blockers and beta blockers. In addition, mineralocorticoid receptor antagonists have proven beneficial. Compounds specifically targeting infarct healing processes are currently under development.

  12. [Thrombolysis by tissue plasminogen activator in acute myocardial infarct].

    PubMed

    Keltai, M; Dékány, P; Németh, J; Palik, I; Sitkei, E; Szente, A; Arvay, A

    1991-09-15

    The authors participated in the European multicenter investigation, ESPRIT, organized by the Wellcome Research Laboratories. Thrombolytic treatment by intravenous tissue plasminogen activator was performed in 25 patients with early (less than 6h) myocardial infarction. The efficacy of the treatment was controlled by repeat coronary arteriography at 60 minutes, at 90 minutes and at 24 hours of the tpA treatment. The infarct related artery was reperfused in 9/25 patients at 60 minutes, in 16/25 at 90 minutes and 17/18 at 24 hours. Four patients died after unsuccessful treatment or reocclusion. In two patients significant bleeding occurred at the puncture site but no transfusion was required. No other untoward effect was registered. The left ventricular function did not change significantly during the first day of infarction. It is concluded, that tpA is a safe thrombolytic agent in myocardial infarction. Its thrombolytic efficacy is similar to that of streptokinase.

  13. Sequential thallium-201 myocardial scintigraphy after acute infarction in man

    SciTech Connect

    Fletcher, J.W.; Mueller, H.S.; Rao, P.S.

    1980-07-01

    Three sequential Tl-201 myocardial perfusion studies were performed in 21 patients (18 men, 3 women) with first acute transmural myocardia infarction. The Tl-201 image defect size was determined with a semiquantitative visual scoring method and temporal changes in image defect size were compared to CK-MB infarct size and enzymatic evidence of progressive myocardial necrosis and infarct extension. Progressive decreases in Tl-201 image defect size were observed and the visual score in all 21 patients decreased significantly from 6.5 +- 3.7 (mean +- SD) on day 1 to 4.9 +- 3.5 on day 12. Eleven patients without evidence of infarct extension had significantly lower infarct size, a significant decrease in visual score by the 12th day and had significantly smaller Tl-201 defects at all three study times compared to 10 patients with infarct extension. Seven of 10 (70%) with extension had an initial visual score greater than or equal to 7 compared to only 2/11 (18%) without extension. The temporal behavior of Tl-201 image defects is related to the size of the infarction and presence or absence of extension. Sequential studies comparing early initial and subsequent defect size may assist in evaluating the behavior of ischemic and infarcted myocardium in the postinfarction period.

  14. Comparison of enzymic with cineangiocardiographic estimations of myocardial infarct size.

    PubMed Central

    Sammel, N L; Stuckey, J G; Brandt, P W; Norris, R M

    1980-01-01

    Comparisons were made between enzymic indices of myocardial infarct size (total creatine kinase appearance and peak enzyme activity) measured during the acute state of a first myocardial infarct in 32 male patients, and analysis of contraction abnormalities in biplane left ventricular cineangiocardiograms performed one month later. The cineangiocardiograms were analysed independently by two radiologists, each using two different methods for quantification of subjectively classified abnormalities of left ventricular wall motion. A very strong correlation was found between the two enzymic indices of infarct size and somewhat weaker correlations between assessment of contractility abnormalities made by the two radiologists using the same method, or by the same radiologist using the two different methods. Comparisons between enzymic and angiocardiographic indices for all infarcts showed correlation coefficients (r) within the range of 0.53 to 0.72. With all comparisons of enzymic with radiological indices r values were higher for anterior infarcts than for inferior infarcts, and there was a tendency for higher enzyme levels for a given degree of left ventricular damage in inferior than in anterior infarction. This may be the result of variable degrees of right ventricular damage in inferior infarction. PMID:7426141

  15. Asymptomatic myocardial infarction in Kawasaki disease: Long-term prognosis

    SciTech Connect

    Shiraishi, I.; Onouchi, Z.; Hayano, T.; Hamaoka, K.; Kiyosawa, N. )

    1991-04-01

    Eight patients with Kawasaki disease who had sustained asymptomatic myocardial infarction 8-15 years ago (mean, 13.1 years) were reexamined by various noninvasive cardiac function tests to assess long-term prognosis. At present, electrocardiograms (ECGs) are normal in six patients. However, all eight patients had a prolonged preejection period (PEP) to left ventricular ejection time (LVET) ratio 30 s after amylnitrate (AN) inhalation. Six patients had perfusion defects by exercise thallium-201 myocardial scintigraphy, and two patients developed ST segment depression in treadmill exercise testing. These patients are symptom-free even though their physical activity has not been restricted. Yet they proved to have serious abnormalities suggesting sequelae of myocardial infarction or existing myocardial ischemia. Judging from the results of noninvasive cardiac function tests and recently performed coronary angiography, five of the eight patients require coronary bypass surgery.

  16. Cannabis: a trigger for acute myocardial infarction? A case report.

    PubMed

    Cappelli, Francesco; Lazzeri, Chiara; Gensini, Gian Franco; Valente, Serafina

    2008-07-01

    Cannabis smoking is consistently increasing in Europe and after alcohol it is the most common recreational drug in the western world. Users and lay people believe that marijuana or hashish is safe. Over the past four decades, however, it has been well established that cannabis has pathophysiological effects on the cardiovascular system. Information concerning the link between cannabis consumption and myocardial infarction is limited and existing data are controversial on this topic. In our case report, we describe a case of a young man who after smoking marijuana experienced ST elevation myocardial infarction caused by acute thrombosis of the descending artery, submitted to efficacious primary coronary angioplasty.

  17. ST-elevation acute myocardial infarction in pregnancy: 2016 update.

    PubMed

    Ismail, Sahar; Wong, Cynthia; Rajan, Priya; Vidovich, Mladen I

    2017-02-13

    Acute myocardial infarction (AMI) during pregnancy or the early postpartum period is rare, but can be devastating for both the mother and the fetus. There have been major advances in the diagnosis and treatment of acute coronary syndromes in the general population, but there is little consensus on the approach to diagnosis and treatment of pregnant women. This article reviews the literature relating to the pathophysiology of AMI in pregnant patients and the challenges in diagnosis and treatment of ST-elevation myocardial infarction (STEMI) in this unique population. From a cardiologist, maternal-fetal medicine specialist, and anesthesiologist's perspective, we provide recommendations for the diagnosis and management of STEMI occurring during pregnancy.

  18. Acute myocardial infarction in young adults: causes and management

    PubMed Central

    Osula, S; Bell, G; Hornung, R

    2002-01-01

    The case report in this review illustrates an acute myocardial infarction in a young adult probably due to arterial thrombosis that can be attributed to a hypercoagulable state resulting from the nephrotic syndrome. Although rare, acute myocardial infarction should be considered in young adults presenting with chest pain. A detailed clinical history may help to identify the aetiology, and guide subsequent management, but diagnostic coronary angiography is essential. Careful risk factor modification and treatment of the underlying cause should reduce the incidence of recurrent cardiac events. PMID:11796868

  19. [Change of lifestyle as a relevant therapy after myocardial infarction].

    PubMed

    Janion, M; Bakowski, D

    2000-01-01

    The risk of ischemic heart disease is connected with the definite mode of life. Improper nourishment, smoking, alcohol abuse, sedentary lifestyle and excessive mental stress cause disturbances leading to development of atherosclerosis. The change of the lifestyle may prevent from coronary heart disease and may play a main role in secondary prevention, making the prognosis after myocardial infarction much better. The epidemiological and clinical studies have shown the significance of particular risk factors reduction on survival after myocardial infarction and allowed to create the optimal preventive mode of life. Therefore the change of lifestyle should become the priority in the postinfarction therapy.

  20. Echocardiography in the Assessment of Complications of Myocardial Infarction

    PubMed Central

    Wilansky, Susan

    1991-01-01

    The value of echocardiography as a tool for evaluating the prognosis of patients after myocardial infarction lies in its ability to define the region and extent of ischemic damage. Additionally, echocardiography is useful in assessing and predicting postinfarction complications. Wall motion abnormalities, pericardial effusion, left ventricular thrombi, and left ventricular aneurysms and pseudoaneurysms can be detected using echocardiography. The severity of mitral regurgitation and the location of interventricular septal repture can also be assessed using echocardiography. This diagnostic tool can provide vital information regarding the appropriate clinical management of patients after myocardial infarction. (Texas Heart Institute Journal 1991; 18:237-42) Images PMID:15227405

  1. Postoperative myocardial infarction in an orthognatic jaw surgery.

    PubMed

    Vieira Marques, F; Montenegro Sá, F; Lapa, T; Simões, I

    2017-07-29

    Cardiovascular complications, in particular perioperative myocardial infarctions, are central contributors to morbidity and mortality after non-cardiac surgery. We present a case of a 41-year-old male, smoker and dyslipidemic, who underwent bimaxillary orthognathic jaw surgery with the development of an acute coronary syndrome in the immediate postoperative period. We managed to early diagnose the myocardial infarction and promptly performed a percutaneous transluminal coronary angioplasty, resulting in a positive outcome. Copyright © 2017 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.

  2. Hair zinc and copper concentration in survivors of myocardial infarction.

    PubMed

    Białkowska, M; Hoser, A; Szostak, W B; Dybczyński, R; Sterliński, S; Nowicka, G; Majchrzak, J; Kaczorowski, J; Danko, B

    1987-01-01

    Increased Zn/Cu ratio in the diet, and consequently in the body, was suggested to be of importance in the pathogenesis of atherosclerosis. Head hair of 29 male survivors of myocardial infarction and of 23 control males was studied for the concentration of Zn and Cu. The Zn hair concentration and Zn/Cu ratio in survivors of myocardial infarction was significantly higher in comparison with controls. The inclusion of the Zn/Cu ratio into the discriminant analysis using total cholesterol and HDL cholesterol considerably improved the coefficient R2 and decreased the number of cases not properly classified.

  3. 3D cardiac wall thickening assessment for acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Khalid, A.; Chan, B. T.; Lim, E.; Liew, Y. M.

    2017-06-01

    Acute myocardial infarction (AMI) is the most severe form of coronary artery disease leading to localized myocardial injury and therefore irregularities in the cardiac wall contractility. Studies have found very limited differences in global indices (such as ejection fraction, myocardial mass and volume) between healthy subjects and AMI patients, and therefore suggested regional assessment. Regional index, specifically cardiac wall thickness (WT) and thickening is closely related to cardiac function and could reveal regional abnormality due to AMI. In this study, we developed a 3D wall thickening assessment method to identify regional wall contractility dysfunction due to localized myocardial injury from infarction. Wall thickness and thickening were assessed from 3D personalized cardiac models reconstructed from cine MRI images by fitting inscribed sphere between endocardial and epicardial wall. The thickening analysis was performed in 5 patients and 3 healthy subjects and the results were compared against the gold standard 2D late-gadolinium-enhanced (LGE) images for infarct localization. The notable finding of this study is the highly accurate estimation and visual representation of the infarct size and location in 3D. This study provides clinicians with an intuitive way to visually and qualitatively assess regional cardiac wall dysfunction due to infarction in AMI patients.

  4. Spatial analysis of myocardial infarction in Iran: National report from the Iranian myocardial infarction registry.

    PubMed

    Ahmadi, Ali; Soori, Hamid; Mehrabi, Yadollah; Etemad, Koorosh

    2015-05-01

    Myocardial infarction (MI) is a leading cause of mortality and morbidity in Iran. No spatial analysis of MI has been conducted to date. The present study was conducted to determine the pattern of MI incidence and to identify the associated factors in Iran by province. This study has two parts. One part is prospective and hospital-based, and the other part is an ecological study. In this study, the data of 20,750 new MI cases registered in Iranian Myocardial Infarction Registry in 2012 were used. For spatial analysis in global and local, spatial autocorrelation, Moran's I, Getis-Ord, and logistic regression models were used. Data were analyzed by Stata software and ArcGIS 9.3. Based on autocorrelation coefficient, a specific pattern was observed in the distribution of MI incidence in different provinces (Moran's I: 0.75, P < 0.001). Spatial pattern of incidence was approximately the same in men and women. MI incidence was clustering in six provinces (North Khorasan, Yazd, Kerman, Semnan, Golestan, and Mazandaran). Out of the associated factors with clustered MI in six provinces, temperature, humidity, hypertension, smoking, and body mass index (BMI) could be mentioned. Hypertension, smoking, and BMI contributed to clustering with, respectively, 2.36, 1.31, and 1.31 odds ratio. Addressing the place-based pattern of incidence and clarifying their epidemiologic dimension, including spatial analysis, has not yet been implemented in Iran. Report on MI incidence rate by place and formal borders is useful and is used in the planning and prioritization in different levels of health system.

  5. Spatial analysis of myocardial infarction in Iran: National report from the Iranian myocardial infarction registry

    PubMed Central

    Ahmadi, Ali; Soori, Hamid; Mehrabi, Yadollah; Etemad, Koorosh

    2015-01-01

    Background: Myocardial infarction (MI) is a leading cause of mortality and morbidity in Iran. No spatial analysis of MI has been conducted to date. The present study was conducted to determine the pattern of MI incidence and to identify the associated factors in Iran by province. Materials and Methods: This study has two parts. One part is prospective and hospital-based, and the other part is an ecological study. In this study, the data of 20,750 new MI cases registered in Iranian Myocardial Infarction Registry in 2012 were used. For spatial analysis in global and local, spatial autocorrelation, Moran's I, Getis-Ord, and logistic regression models were used. Data were analyzed by Stata software and ArcGIS 9.3. Results: Based on autocorrelation coefficient, a specific pattern was observed in the distribution of MI incidence in different provinces (Moran's I: 0.75, P < 0.001). Spatial pattern of incidence was approximately the same in men and women. MI incidence was clustering in six provinces (North Khorasan, Yazd, Kerman, Semnan, Golestan, and Mazandaran). Out of the associated factors with clustered MI in six provinces, temperature, humidity, hypertension, smoking, and body mass index (BMI) could be mentioned. Hypertension, smoking, and BMI contributed to clustering with, respectively, 2.36, 1.31, and 1.31 odds ratio. Conclusion: Addressing the place-based pattern of incidence and clarifying their epidemiologic dimension, including spatial analysis, has not yet been implemented in Iran. Report on MI incidence rate by place and formal borders is useful and is used in the planning and prioritization in different levels of health system. PMID:26487871

  6. Systemic Effects of Electromagnetic Fields in Patients with Myocardial Infarction

    NASA Astrophysics Data System (ADS)

    Cañedo-Dorantes, L.; Valle, L.; Uruchurtu, E.; Medel, A.; García-Mayen, F.; Serrano-Luna, G.

    2003-09-01

    Healing of acute myocardial infarction (AMI) is associated with inflammatory response, which promotes healing and scar formation. Activation of a local inflammatory response in patients with sequel of AMI could have an important role to enhance angiogenesis and regeneration of hibernating myocardial tissue. Chronic arterial leg ulcers have a similar etiology, and healing has been promoted by exposure to extremely low frequency electromagnetic fields (ELF). We report the evolution of three AMI patients with sequel of AMI that were exposed to ELF.

  7. Early menopause predicts angina after myocardial infarction

    PubMed Central

    Parashar, Susmita; Reid, Kimberly J.; Spertus, John A.; Shaw, Leslee J.; Vaccarino, Viola

    2011-01-01

    Objective Population studies have shown that age at menopause (AAM) predicts coronary heart disease. It is unknown, however, whether early menopause predicts post–myocardial infarction (MI) angina. We examined whether younger AAM increases risk of post-MI angina. Methods In a prospective multicenter MI registry, 493 postmenopausal women were enrolled (mean ± SD age, 65.4 ± 11.3 y, and mean ± SD AAM, 45.2 ± 7.8 y). We categorized AAM into 40 years or younger, 41 to 49 years, and 50 years or older. In the multivariable analysis, we examined whether AAM predicted 1-year post-MI angina and severity of angina after adjusting for angina before MI, demographics, comorbidities, MI severity, and quality of care (QOC). Results Women with early AAM (≤40 y; n = 132, 26.8%) were younger and more often smokers but were as likely to have comorbidities as were women with an AAM of 50 years or older. Although there were no differences in pre-MI angina, MI severity, obstructive coronary disease, and QOC based on AAM, the rate of 1-year angina was higher in women with an AAM of 40 years or younger (32.4%) than in women with an AAM of 50 years or older (12.2%). In the multivariable analysis, women with an AAM of 40 years or younger had more than twice the risk of angina (relative risk, 2.09; 95% CI, 1.38–3.17) and a higher severity of angina (odds ratio, 2.65; 95% CI, 1.34–5.22 for a higher severity level) compared with women with an AAM of 50 years or older. Conclusions Women with early menopause are at higher risk of angina after MI, independent of comorbidities, severity of MI, and QOC. The use of a simple question regarding AAM may help in the identification of women who need closer follow-up, careful evaluation, and intervention to improve their symptoms and quality of life after MI. PMID:20651619

  8. Ventricular Assist Device in Acute Myocardial Infarction

    PubMed Central

    Achary, Deepak; Loyaga-Rendon, Renzo Y.; Pamboukian, Salpy V.; Tallaj, Jose A.; Holman, William L.; Cantor, Ryan S.; Naftel, David C.; Kirklin, James K.

    2016-01-01

    Background Patients with acute myocardial infarction (AMI) complicated by acute heart failure or cardiogenic shock have high mortality with conventional management. Objectives We evaluated outcomes of patients with AMI who received durable ventricular assist devices (VADs). Methods Patients with AMI in the INTERMACS registry who underwent VAD placement were included and compared to patients who received VADs for non-AMI indications. Results VADs were implanted in 502 patients with AMI: 443 left ventricular assist devices; 33 biventricular assist devices; and 26 total artificial hearts. Median age was 58.3 years, and 77.1% were male. At implant, 66% were INTERMACS profile 1. A higher proportion of AMI than non- AMI patients had preoperative intra-aortic balloon pumps (57.6% vs. 25.3%; p < 0.01), intubation (58% vs. 8.3%; p < 0.01), extracorporeal membrane oxygenation (17.9% vs. 1.7%, p < 0.01), cardiac arrest (33.5% vs. 3.3%, p < 0.01), and higher-acuity INTERMACS profiles. At 1 month post-VAD, 91.8% of AMI patients were alive with ongoing device support, 7.2 % had died on device, and 1% had been transplanted. At 1 year post-VAD, 52% of AMI patients were alive with ongoing device support, 25.7% had been transplanted, 1.6% had LVADs explanted for recovery, and 20.7% had died on device. The AMI group had higher unadjusted early-phase hazard (HR: 1.24; p = 0.04) and reduced late-phase hazard of death (HR: 0.57; p = 0.04) than the non-AMI group. After accounting for established risk factors, the AMI group no longer had higher early mortality hazard (HR: 0.89; p = 0.3), but had lower late mortality hazard (HR: 0.55; p = 0.02). Conclusion Patients with AMI who receive VADs have outcomes similar to other VAD populations, despite being more critically ill pre-implantation. VAD therapy is an effective strategy for patients with AMI in whom medical therapy is failing. PMID:27102502

  9. Horizontal ECG in acute anterolateral myocardial infarction.

    PubMed

    Erdogan, Okan; Dalkilic, Bahar; Kepez, Alper

    2016-07-01

    The present study aims to compare the amount of ST segment changes recorded by horizontal electrocardiography (hECG) with standard ECG (sECG) in patients with acute anterior and/or lateral ST segment elevation myocardial infarction (STEMI). Consecutive eligible patients (n = 58) who were diagnosed with acute anterior and/or lateral STEMI were included in the study. After recording simultaneous sECG and hECG by placing precordial leads (V3-6) horizontally on the left 4th intercostal space, ST segment changes were compared. The mean ST segment changes (mV) on hECG were significantly higher than sECG in V4 (0.27 ± 0.2 vs. 0.21 ± 0.21, p = 0.001), V5 (0.21 ± 0.17 vs. 0.12 ± 0.16, p < 0.001) and V6 (0.09 ± 0.1 vs. 0.04 ± 0.12, p < 0.001), respectively. When hECG and sECG were compared in patients with BMI < 30 kg/m(2), mean ST segment changes (mV) on hECG were significantly higher than sECG in V4 (0.29 ± 0.21 vs. 0.21 ± 0.24, p = 0.004), V5 (0.22 ± 0.19 vs. 0.13 ± 0.17, p < 0.001) and V6 (0.11 ± 0.11 vs. 0.04 ± 0.11, p < 0.001), respectively. Mean ST segment changes in patients with anterior and/or lateral STEMI were significantly higher and easily detectable on hECG compared with sECG. We suggest that hECG be used in conjunction with sECG to diagnose anterior and lateral wall STEMI in cases of diagnostic doubt.

  10. Low molecular weight heparin for treatment of acute myocardial infarction (FAMI): Fragmin (dalteparin sodium) in acute myocardial infarction.

    PubMed

    Kakkar, V V; Iyengar, S S; De Lorenzo, F; Hargreaves, J R; Kadziola, Z A

    2000-01-01

    The benefit of using subcutaneous low molecular weight heparin for the treatment of acute myocardial infarction is not known. The aim of this study was to determine the efficacy of a low molecular weight heparin (dalteparin sodium) for the treatment of acute myocardial infarction in patients not treated with thrombolytic therapy. Twenty-nine cardiological centres from leading hospitals in India participated in this prospective, multicentre, double-blind, placebo-controlled study in two phases which included 1128 patients with acute myocardial infarction. In the acute phase (between day 1 and 3 of admission) all the patients received a weight-adjusted dose of subcutaneous dalteparin (120 IU/kg twice daily). In the second, double-blind phase of acute myocardial infarction, patients were randomised to receive a fixed dose of dalteparin (7,500 IU) or an identical placebo injection for 30 days. A composite primary endpoint of death, reinfarction, recurrence of angina and emergency revascularisation was used. All the 1128 patients with acute myocardial infarction were included in the trial. In the acute phase, the composite primary endpoint was observed in 58 (5.1%) patients. Of 1037 paients who were randomly assigned to receive a fixed dose of dalteparin (n=519) or placebo (n=518), the composite primary event rate was 6.7 percent and 7.0 percent, respectively (RR 0.97; 95% CI 0.62-1.52; p=0.90). To conclude, treatment with dalteparin administered subcutaneously in a weight-adjusted dose of 120 IU/kg twice daily resulted in a lower than expected mortality during the acute phase of myocardial infarction. A lower fixed once daily dose of 7,500 IU during the chronic phase did not confer additional protection.

  11. Current trend of acute myocardial infarction in Korea (from the Korea Acute Myocardial Infarction Registry from 2006 to 2013).

    PubMed

    Kook, Hyun Yi; Jeong, Myung Ho; Oh, Sangeun; Yoo, Sung-Hee; Kim, Eun Jung; Ahn, Youngkeun; Kim, Ju Han; Chai, Leem Soon; Kim, Young Jo; Kim, Chong Jin; Chan Cho, Myeong

    2014-12-15

    Although the incidence of acute myocardial infarction (AMI) in Korea has been rapidly changed because of westernization of diet, lifestyle, and aging of the population, the recent trend of the myocardial infarction have not been reported by classification. We investigated recent trends in the incidence and mortality associated with the 2 major types of AMI. We reviewed 39,978 patients registered in the Korea Acute Myocardial Infarction Registry for either ST-segment elevation acute myocardial infarction (STEMI) or non-ST-segment elevation acute myocardial infarction (NSTEMI) from 2006 to 2013. When the rate for AMI were investigated according to each year, the incidence rates of STEMI decreased markedly from 60.5% in 2006 to 48.1% in 2013 (p <0.001). In contrast, a gradual increase in the incidence rates of NSTEMI was observed from 39.5% in 2006 to 51.9% in 2013 (p <0.001). As risk factors, hypertension, diabetes mellitus, and dyslipidemia were much more common in patients with NSTEMI than STEMI. Among medical treatments, the use of β blockers, angiotensin receptor blocker, and statin were increased from 2006 to 2013 in patients with STEMI and NSTEMI. Patients with STEMI and NSTEMI were more inclined to be increasingly treated by invasive treatments with percutaneous coronary intervention. In conclusion, this study demonstrated that the trend of myocardial infarction has been changed rapidly in the aspect of risk factors, ratio of STEMI versus NSTEMI, and therapeutic strategies during the recent 8 years in Korea.

  12. Holmium:YAG laser coronary angioplasty in acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Topaz, On; Luxenberg, Michael; Schumacher, Audrey

    1994-07-01

    Patients who sustain complicated acute myocardial infarction in whom thrombolytic agents either fail or are contraindicated often need mechanical revascularization other than PTCA. In 24 patients with acute infarction complicated by continuous chest pain and ischemia who either received lytics or with contraindication to lytics, a holmium:YAG laser (Eclipse Surgical Technologies, Palo Alto, CA) was utilized for thrombolysis and plaque ablation. Clinical success was achieved in 23/24 patients, with 23 patients (94%) surviving the acute infarction. Holmium:YAG laser is very effective and safe in thrombolysis and revascularization in this complicated clinical setting.

  13. Pseudo-myocardial infarction in diabetic ketoacidosis with hyperkalemia.

    PubMed

    Bellazzini, Marc A; Meyer, Tom

    2010-10-01

    Hyperkalemia-induced electrocardiogram changes such as dysrhythmias and altered T wave morphology are well described in the medical literature. Pseudo-infarction hyperkalemia-induced changes are less well known, but present a unique danger for the clinician treating these critically ill patients. This article describes a case of pseudo anteroseptal myocardial infarction in a type 1 diabetic with hyperkalemia. The most common patterns of pseudo-infarct and their associated potassium concentrations are then summarized from a literature review of 24 cases.

  14. Spontaneous changes in /sup 201/Tl myocardial perfusion imaging after myocardial infarction

    SciTech Connect

    Buda, A.J.; Dubbin, J.D.; MacDonald, I.L.; Strauss, H.D.; Orr, S.A.; Meindok, H.

    1982-12-01

    To examine regional myocardial perfusion after myocardial infarction, 26 patients underwent exercise electrocardiographic testing with /sup 201/Tl myocardial perfusion imaging 3 weeks and 3 months after infarction. At 3 weeks, 9 of 26 patients (35%) had myocardial ischemia by exercise electrocardiographic testing, whereas 18 of 26 (69%) had ischemia by /sup 201/Tl imaging. The /sup 201/Tl scintigrams were scored by dividing each image, in 3 views, into 5 segments, using a 5-point scoring scheme. The exercise /sup 201/Tl score was 44.3 +/- 1.2 and increased to 47.3 +/- 1.2 in the redistribution study (p less than 0.001). Three months after infarction, although there was a significantly greater rate-pressure product which would predict a larger ischemic defect and a decrease in the stress /sup 201/Tl score, the stress score was improved (48.3 +/- 1.1, p less than 0.001). The redistribution score was similar, that is, 48.9 +/- 1.0. The improvement in /sup 201/Tl myocardial perfusion was associated with a loss of stress-induced ischemia in 8 patients (30%). These results indicate that spontaneous improvements in /sup 201/Tl myocardial perfusion imaging may occur after myocardial infarction.

  15. Myocardial sympathetic innervation, function, and oxidative metabolism in non-infarcted myocardium in patients with prior myocardial infarction.

    PubMed

    Aoki, Hirofumi; Matsunari, Ichiro; Nomura, Yusuke; Fujita, Wataru; Komatsu, Ryoko; Miyazaki, Yoshiharu; Nekolla, Stephan G; Kajinami, Kouji

    2013-07-01

    The purpose of this study was to investigate the relationship between sympathetic innervation, contractile function, and the oxidative metabolism of the non-infarcted myocardium in patients with prior myocardial infarction. In 19 patients (14 men, 5 women, 65 ± 9 years) after prior myocardial infarction, sympathetic innervation was assessed by (11)C-hydroxyephedrine (HED) positron emission tomography (PET). Oxidative metabolism was quantified using (11)C-acetate PET. Left ventricular systolic function was measured by echocardiography with speckle tracking technique. The (11)C-HED retention was positively correlated with left ventricular ejection fraction (LVEF) (r = 0.566, P < 0.05), and negatively with peak longitudinal strain in systole in the non-infarcted myocardium (r = -0.561, P < 0.05). Kmono, as an index of oxidative metabolism, was significantly correlated with rate pressure product (r = 0.649, P < 0.01), but not with (11)C-HED retention (r = 0.188, P = 0.442). Furthermore, there was no significant correlation between Kmono and LVEF (r = 0.106, P = 0.666) or peak longitudinal strain in systole (r = -0.256, P = 0.291) in the non-infarcted myocardium. When the patients were divided into two groups based on the median value of left ventricular end-systolic volume index (LVESVI) (41 mL), there were no significant differences in age, sex, and rate pressure product between the groups. However, the large LVESVI group (>41 mL) was associated with reduced (11)C-HED retention and peak longitudinal strain in systole, whereas Kmono was similar between the groups. This study indicates that remodeled LV after myocardial infarction is associated with impaired sympathetic innervation and function even in the non-infarcted myocardial tissue. Furthermore, oxidative metabolism in the non-infarcted myocardium seems to be operated by normal regulatory mechanisms rather than pre-synaptic sympathetic neuronal function.

  16. Primary coronary angioplasty in patients with acute myocardial infarction.

    PubMed Central

    Popma, J J; Chuang, Y C; Satler, L F; Kleiber, B; Leon, M B

    1994-01-01

    In some patients with acute myocardial infarction, thrombolytic therapy may be limited by its failure to reperfuse the occluded artery, by recurrent ischemia (despite initially successful reperfusion), and by major hemorrhagic complications. Primary coronary angioplasty may circumvent these limitations. This article reviews the results of primary angioplasty reported in patients with myocardial infarction and makes recommendations for its use. The review includes pertinent articles found in the English language literature from July 1987 to July 1993 on MEDLINE. Nonrandomized series of primary angioplasty in acute myocardial infarction have demonstrated high procedural success rates (86% to 99%) and infrequent recurrent ischemia (4%). Two randomized trials comparing primary angioplasty and thrombolytic therapy have shown that primary angioplasty results in lower mortality, less recurrent ischemia, shorter length of hospital stay, and improved left ventricular function. Two other randomized studies have shown little benefit from primary angioplasty on myocardial salvage, recurrent ischemia, or ventricular function. One major limitation of primary angioplasty is that it requires 24-hour availability of a catheterization laboratory and experienced surgical personnel. Primary angioplasty may be the preferred approach in patients with extensive myocardial infarction who have immediate (< 120 min) access to a cardiac catheterization laboratory with experienced personnel. Patients having 1) contraindications to thrombolytic therapy, 2) cardiogenic shock, 3) prior coronary bypass surgery, or 4) "stuttering" onset of pain may also benefit from primary angioplasty. Poor candidates for this procedure are those with a small myocardial infarction, those in whom undue delays in access to a cardiac catheterization facility would be expected, or those with complex coronary anatomy, including left main coronary artery disease. PMID:8061539

  17. Acute myocardial infarction and renal failure following naphtha ingestion.

    PubMed

    Roberge, R J; Crippen, D R; Jayadevappa, D; Kosek, T L

    2001-10-01

    We present a case of a non-Q wave myocardial infarction and acute renal failure following an ingestion of naphtha, a petroleum distillate composed primarily of hydrocarbons. The patient's renal, metabolic, and cardiac status improved over several days with aggressive volume replacement and bicarbonate therapy. Acute cardiotoxic effects of hydrocarbon exposure generally manifest as dysrhythmias, secondary to myocardial sensitization to circulating catecholamines, or, possibly, coronary vasospasm. Ischemia from associated hypotension or direct myocardial toxicity are other potential causes of naphtha-related cardiac injury.

  18. Space weather and myocardial infarction diseases at subauroral latitudes

    NASA Astrophysics Data System (ADS)

    Samsonov, Sergey; Kleimenova, Natalia; Petrova, Palmira

    The relationship of the number of calls for the emergency medical care in Yakutsk (subauroral latitudes) in connection with myocardial infarction diseases during years near the maximum (1992) and minimum (1998) of the 11-year geomagnetic disturbance cycle to space weather parameters has been studied. It is found that at subauroral latitudes, the increase of geomagnetic activity, namely, the occurrence of night magnetospheric substorms, plays the important role in the exacerbation of myocardial infarctions. Substorms are accompanied by Pi1 irregular geomagnetic pulsations with periods of (0.5-3.0) Hz, coinciding with heart rhythms of a human being, thus, these waves can be a biotropic factor negatively influencing on the occurrence of myocardial infarctions. The comparison of seasonal change of the number of calls for emergency medical care to patients at subauroral latitudes with a simultaneous seasonal change of fatal endings because of an infarction at low latitudes (Bulgaria) has shown their essential difference. Thus, in Bulgaria the maximum of infarctions have been marked in winter, and minimum - in summer, and in Yakutsk a few maxima coinciding with the sharp and considerable increases of the level of the planetary geomagnetic disturbances have been observed. In this case, in Bulgaria the infarctions could be connected with availability of the Pc1 geomagnetic pulsations. Thus, the stable quasi-sinusoidal Pc1 pulsations can be a biotropic factor influencing on the development of myocardial infarctions at middle latitudes and the Pi1 irregular geomagnetic pulsations, which do not propagate to the lower latitudes, could be a biotropic factor at subauroral latitudes.

  19. Type 2 myocardial infarction due to supply-demand mismatch.

    PubMed

    Mihatov, Nino; Januzzi, James L; Gaggin, Hanna K

    2017-08-01

    The best-accepted definition of myocardial infarction (MI) is provided by statements from the Universal Definition of MI Global Task force. This article, now in its third iteration, defines MI as myocardial cell death due to prolonged myocardial ischemia. It further delineates an increasingly incident subclassification of MI known as type 2 MI (T2MI). T2MI identifies instances of myocardial necrosis in which an imbalance between myocardial oxygen supply and/or demand occurs for reasons other than atherosclerotic plaque disruption. While associated with considerable risk (comparable to that of type 1 MI, which has well-defined management strategies), the spectrum of potential etiologies for T2MI makes development of precise diagnostic criteria and therapeutic implications of the diagnosis challenging. Copyright © 2017 Elsevier Inc. All rights reserved.

  20. Does Cardiac Rehabilitation After Myocardial Infarction Favorably Affect Prognosis?

    ERIC Educational Resources Information Center

    Shephard, Roy J.

    1988-01-01

    This article discusses the limitations of 14 randomized controlled trials of exercise rehabilitation for patients who sustained myocardial infarction. The difficulty of sampling patients and controlling the sample size is discussed and the benefits of pooled statistical evidence are considered. (JL)

  1. Controlled Trial of Psychological Intervention in Myocardial Infarction.

    ERIC Educational Resources Information Center

    Oldenburg, Brian; And Others

    1985-01-01

    Compared hospital-based psychological interventions for improving the physical, psychological, and life-style status of patients after myocardial infarction with routine medical and nursing care. Follow-ups showed intervention groups performed significantly better on measures of psychological and life-style functioning; they also reported fewer…

  2. Adaptation to a Myocardial Infarction from a Developmental Perspective.

    ERIC Educational Resources Information Center

    Meyer, Robert

    1983-01-01

    Explored the interactional effect between victims' (N=30) adult developmental stage and their coping and emotional reactions following a myocardial infarction (MI). The findings point to the usefulness of adult developmental psychology in understanding the divergent emotional and coping reactions of MI patients across the life-cycle. (Author/JAC)

  3. Group Counseling Approaches with Persons Who Have Sustained Myocardial Infarction.

    ERIC Educational Resources Information Center

    Livneh, Hanoch; Sherwood-Hawes, Ardis

    1993-01-01

    Presents group counseling strategies for working with clients who have sustained myocardial infarctions, or heart attacks. MI victims can be assisted with transition from hospital, readjustment to daily life, coping with fears and frustrations of life and the illness. Advantages of counseling, primary goals, and common topics are discussed.…

  4. Return to work after myocardial infarction: a retrospective study.

    PubMed

    Waszkowska, Małgorzata; Szymczak, Wiesław

    2009-01-01

    To evaluate the occupational functioning and identify health-related determinants of the continuation of occupational activity in workers with a recent myocardial infarction. The project was a retrospective study concerning 183 male workers, aged 39-65 years, who had suffered a primary uncomplicated myocardial infarction approximately three years prior to the study. The study group comprised both the persons who returned to work after the incident and those who did not. The subjects' mental health as well as quality of life and occupational functioning were evaluated using NHP scale, Beck Depression Inventory, STAI questionnaire by Spielberger et al., WAI, and own questionnaire "My work". Data analysis revealed that the persons who returned to work after myocardial infarction were characterized by a younger age and a higher level of education, self-rated health and quality of life than the persons who did not resume their occupational activity. The occupationally active individuals showed a varying degree of readaptation to work. In the maladapted group, such disturbances occurred as depression, anxiety and lowered work ability. The study results indicate that in workers with a recent myocardial infarction, the current procedure for assessment of work ability, which is based solely on the evaluation of physical health, is insufficient and should be supplemented with the assessment of their mental health. The employers should also undertake activities for a better adjustment of working conditions to the abilities of workers who have experienced a cardiac incident.

  5. Cardiac remodeling and physical training post myocardial infarction

    PubMed Central

    Garza, Michael A; Wason, Emily A; Zhang, John Q

    2015-01-01

    After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus that exercise training may beneficially alter the course of post-MI myocardial remodeling and improve cardiac function. This review summarizes the present state of knowledge regarding the effect of post-MI exercise training on infarcted hearts. Due to the degree of difficulty to study a viable human heart at both protein and molecular levels, most of the detailed studies have been performed by using animal models. Although there are some negative reports indicating that post-MI exercise may further cause deterioration of the wounded hearts, a growing body of research from both human and animal experiments demonstrates that post-MI exercise may beneficially alter the course of wound healing and improve cardiac function. Furthermore, the improved function is likely due to exercise training-induced mitigation of renin-angiotensin-aldosterone system, improved balance between matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1, favorable myosin heavy chain isoform switch, diminished oxidative stress, enhanced antioxidant capacity, improved mitochondrial calcium handling, and boosted myocardial angiogenesis. Additionally, meta-analyses revealed that exercise-based cardiac rehabilitation has proven to be effective, and remains one of the least expensive therapies for both the prevention and treatment of cardiovascular disease, and prevents re-infarction. PMID:25717353

  6. Acute myocardial infarction in a young man using anabolic steroids.

    PubMed

    Wysoczanski, Mariusz; Rachko, Maurice; Bergmann, Steven R

    2008-01-01

    Anabolic-androgenic steroids are used worldwide to help athletes gain muscle mass and strength. Their use and abuse is associated with numerous side effects, including acute myocardial infarction (MI). We report a case of MI in a young 31-year-old bodybuilder. Because of the serious cardiovascular complications of anabolic steroids, physicians should be aware of their abuse and consequences.

  7. Phaeochromocytoma presenting with ST segment elevation myocardial infarction.

    PubMed

    Ahmed, Mohamed A; Abdullah, Abdullah Sayied; Kiernan, Thomas John

    2016-02-08

    Phaeochromocytoma is a rare endocrine disorder with different cardiovascular presentations. In this brief report, we discuss a case of a 59-year-old woman who presented with acute ST segment elevation myocardial infarction secondary to phaeochromocytoma. Coronary angiogram showed non-obstructive coronary artery disease. 2016 BMJ Publishing Group Ltd.

  8. Thrombolytic therapy for myocardial infarction. Treatment introduced in northern Ontario.

    PubMed Central

    Hutten-Czapski, P.

    1993-01-01

    In remote regions of Canada, most patients with acute myocardial infarctions (MI) are treated by general practitioners. In hospitals served by cardiologists, intravenous thrombolytic therapy for MI is now routinely available. In a survey of northern Ontario general hospitals, 32 of 45 offered IV thrombolytic therapy. The use of streptokinase in one family physician-run hospital was also reviewed. PMID:8257484

  9. Adaptation to a Myocardial Infarction from a Developmental Perspective.

    ERIC Educational Resources Information Center

    Meyer, Robert

    1983-01-01

    Explored the interactional effect between victims' (N=30) adult developmental stage and their coping and emotional reactions following a myocardial infarction (MI). The findings point to the usefulness of adult developmental psychology in understanding the divergent emotional and coping reactions of MI patients across the life-cycle. (Author/JAC)

  10. Does Cardiac Rehabilitation After Myocardial Infarction Favorably Affect Prognosis?

    ERIC Educational Resources Information Center

    Shephard, Roy J.

    1988-01-01

    This article discusses the limitations of 14 randomized controlled trials of exercise rehabilitation for patients who sustained myocardial infarction. The difficulty of sampling patients and controlling the sample size is discussed and the benefits of pooled statistical evidence are considered. (JL)

  11. Group Counseling Approaches with Persons Who Have Sustained Myocardial Infarction.

    ERIC Educational Resources Information Center

    Livneh, Hanoch; Sherwood-Hawes, Ardis

    1993-01-01

    Presents group counseling strategies for working with clients who have sustained myocardial infarctions, or heart attacks. MI victims can be assisted with transition from hospital, readjustment to daily life, coping with fears and frustrations of life and the illness. Advantages of counseling, primary goals, and common topics are discussed.…

  12. Controlled Trial of Psychological Intervention in Myocardial Infarction.

    ERIC Educational Resources Information Center

    Oldenburg, Brian; And Others

    1985-01-01

    Compared hospital-based psychological interventions for improving the physical, psychological, and life-style status of patients after myocardial infarction with routine medical and nursing care. Follow-ups showed intervention groups performed significantly better on measures of psychological and life-style functioning; they also reported fewer…

  13. A History of Streptokinase Use in Acute Myocardial Infarction

    PubMed Central

    Sikri, Nikhil; Bardia, Amit

    2007-01-01

    A serendipitous discovery by William Smith Tillett in 1933, followed by many years of work with his student Sol Sherry, laid a sound foundation for the use of streptokinase as a thrombolytic agent in the treatment of acute myocardial infarction. The drug found initial clinical application in combating fibrinous pleural exudates, hemothorax, and tuberculous meningitis. In 1958, Sherry and others started using streptokinase in patients with acute myocardial infarction and changed the focus of treatment from palliation to “cure.” Initial trials that used streptokinase infusion produced conflicting results. An innovative approach of intracoronary streptokinase infusion was initiated by Rentrop and colleagues in 1979. Subsequently, larger trials of intracoronary infusion achieved reperfusion rates ranging from 70% to 90%. The need for a meticulously planned and systematically executed randomized multicenter trial was fulfilled by the Gruppo Italiano per la Sperimentazione della Streptochinasi nell'Infarto Miocardico (GISSI) trial in 1986, which not only validated streptokinase as an effective therapeutic method but also established a fixed protocol for its use in acute myocardial infarction. Currently, despite the wide use of tissue plasminogen activator in developed nations, streptokinase remains essential to the management of acute myocardial infarction in developing nations. PMID:17948083

  14. Modeling Myocardial Infarction in Mice: Methodology, Monitoring, Pathomorphology

    PubMed Central

    Ovsepyan, A.A.; Panchenkov, D.N.; Prokhortchouk, E.B.; Telegin, G.B.; Zhigalova, N.A.; Golubev, E.P.; Sviridova, T.E.; Matskeplishvili, S.T.; Skryabin, K.G.; Buziashvili, U.I.

    2011-01-01

    Myocardial infarction is one of the most serious and widespread diseases in the world. In this work, a minimally invasive method for simulating myocardial infarction in mice is described in the Russian Federation for the very first time; the procedure is carried out by ligation of the coronary heart artery or by controlled electrocoagulation. As a part of the methodology, a series of anesthetic, microsurgical and revival protocols are designed, owing to which a decrease in the postoperational mortality from the initial 94.6 to 13.6% is achieved. ECG confirms the development of large-focal or surface myocardial infarction. Postmortal histological examination confirms the presence of necrosis foci in the heart muscles of 87.5% of animals. Altogether, the medical data allow us to conclude that an adequate mouse model for myocardial infarction was generated. A further study is focused on the standardization of the experimental procedure and the use of genetically modified mouse strains, with the purpose of finding the most efficient therapeutic approaches for this disease. PMID:22649679

  15. Cardiomyocyte transplantation in a porcine myocardial infarction model.

    PubMed

    Watanabe, E; Smith, D M; Delcarpio, J B; Sun, J; Smart, F W; Van Meter, C H; Claycomb, W C

    1998-01-01

    Transplantation of cardiomyocytes into the heart is a potential treatment for replacing damaged cardiac muscle. To investigate the feasibility and efficiency of this technique, either a cardiac-derived cell line (HL-1 cells), or normal fetal or neonatal pig cardiomyocytes were grafted into a porcine model of myocardial infarction. The myocardial infarction was created by the placement of an embolization coil in the distal portion of the left anterior descending artery in Yorkshire pigs (n = 9). Four to 5 wk after creation of an infarct, the three preparations of cardiomyocytes were grafted, at 1 x 10(6) cells/20 microL into normal and into the middle of the infarcted myocardium. The hearts were harvested and processed for histologic examinations 4 to 5 wk after the cell grafts. Histologic evaluation of the graft sites demonstrated that HL-1 cells and fetal pig cardiomyocytes formed stable grafts within the normal myocardium without any detrimental effect including arrhythmia. In addition, a marked increase in angiogenesis was observed both within the grafts and adjacent host myocardium. Electron microscopy studies demonstrated that fetal pig cardiomyocytes and the host myocardial cells were coupled with adherens-type junctions and gap junctions. Histologic examination of graft sites from infarct tissue failed to show the presence of grafted HL-1 cells, fetal, or neonatal pig cardiomyocytes. Cardiomyocyte transplantation may provide the potential means for cell-mediated gene therapy for introduction of therapeutic molecules into the heart.

  16. Acute myocardial infarction mortality in Cuba, 1999-2008.

    PubMed

    Armas, Nurys B; Ortega, Yanela Y; de la Noval, Reinaldo; Suárez, Ramón; Llerena, Lorenzo; Dueñas, Alfredo F

    2012-10-01

    Acute myocardial infarction is one of the leading causes of death in the world. This is also true in Cuba, where no national-level epidemiologic studies of related mortality have been published in recent years. Describe acute myocardial infarction mortality in Cuba from 1999 through 2008. A descriptive study was conducted of persons aged ≥25 years with a diagnosis of acute myocardial infarction from 1999 through 2008. Data were obtained from the Ministry of Public Health's National Statistics Division database for variables: age; sex; site (out of hospital, in hospital or in hospital emergency room) and location (jurisdiction) of death. Proportions, age- and sex-specific rates and age-standardized overall rates per 100,000 population were calculated and compared over time, using the two five-year time frames within the study period. A total of 145,808 persons who had suffered acute myocardial infarction were recorded, 75,512 of whom died, for a case-fatality rate of 51.8% (55.1% in 1999-2003 and 49.7% in 2004-2008). In the first five-year period, mortality was 98.9 per 100,000 population, falling to 81.8 per 100,000 in the second; most affected were people aged ≥75 years and men. Of Cuba's 14 provinces and special municipality, Havana, Havana City and Camagüey provinces, and the Isle of Youth Special Municipality showed the highest mortality; Holguín, Ciego de Ávila and Granma provinces the lowest. Out-of-hospital deaths accounted for the greatest proportion of deaths in both five-year periods (54.8% and 59.2% in 1999-2003 and 2004-2008, respectively). Although risk of death from acute myocardial infarction decreased through the study period, it remains a major health problem in Cuba. A national acute myocardial infarction case registry is needed. Also required is further research to help elucidate possible causes of Cuba's high acute myocardial infarction mortality: cardiovascular risk studies, studies of out-of-hospital mortality and quality of care

  17. Regional left ventricular myocardial contractility and stress in a finite element model of posterobasal myocardial infarction.

    PubMed

    Wenk, Jonathan F; Sun, Kay; Zhang, Zhihong; Soleimani, Mehrdad; Ge, Liang; Saloner, David; Wallace, Arthur W; Ratcliffe, Mark B; Guccione, Julius M

    2011-04-01

    Recently, a noninvasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study a sheep with anteroapical infarction (Sun et al., 2009, "A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm," ASME J. Biomech. Eng., 131(11), p. 111001). Using the methodology developed in the previous study (Sun et al., 2009, "A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm," ASME J. Biomech. Eng., 131(11), p. 111001), which incorporates tagged magnetic resonance images, three-dimensional myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction were investigated. Active material parameters in the noninfarcted border zone (BZ) myocardium adjacent to the infarct (T(max_B)), in the myocardium remote from the infarct (T(max_R)), and in the infarct (T(max_I)) were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized T(max_B) was found to be significantly depressed relative to T(max_R), while T(max_I) was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure.

  18. [Readaptation to work after myocardial infarction: model considerations].

    PubMed

    Turczyn-Jabłońska, Katarzyna; Waszkowska, Małgorzata

    2005-01-01

    In Poland only 50-60% of persons who have experienced myocardial infarction return to work. Bearing in mind that psychophysical condition changes after such an event, this group of people has to be readapted to work. Factors that determine good work performance among post-infarction workers have been not yet investigated. The aim of our study is to identify those factors and to define their role in the readaptation process. The first stage of our project involved the development of a theoretical model of readaptation to work after myocardial infarction. This model is described in this paper. It comprises the following components: medical evaluation of the workers' health status, his or her subjective assessment of work ability, expectations (optimistic vs. pessimistic attitude), motivation to work, social support, and job characteristics.

  19. 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% O2, 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

  20. Single coronary artery presenting as acute myocardial infarction.

    PubMed

    Jurado-Román, Alfonso; Sánchez-Pérez, Ignacio; Lozano-Ruíz-Poveda, Fernando; Pinilla-Echeverri, Natalia; López-Lluva, María T; Moreno-Arciniegas, Andrea; Marina-Breysse, Manuel; Piqueras-Flores, Jesús

    2017-02-01

    A single coronary artery is one of the most rarely seen coronary artery anomalies. In addition, the specific subtype (Lipton RII-A) that our patient presented is one of the least common, and its clinical presentation as myocardial infarction and cardiac arrest has not been described in the literature. The case shows that although it is essential to exclude a malignant interarterial course of the vessel, cardiac arrest is a possible clinical presentation produced by myocardial ischemia in the context of acute myocardial infarction and should be managed according to clinical practice guidelines. Copyright © 2016 Sociedade Portuguesa de Cardiologia. Publicado por Elsevier España, S.L.U. All rights reserved.

  1. 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

  2. Dysfunctional nitric oxide signalling increases risk of myocardial infarction.

    PubMed

    Erdmann, Jeanette; Stark, Klaus; Esslinger, Ulrike B; Rumpf, Philipp Moritz; Koesling, Doris; de Wit, Cor; Kaiser, Frank J; Braunholz, Diana; Medack, Anja; Fischer, Marcus; Zimmermann, Martina E; Tennstedt, Stephanie; Graf, Elisabeth; Eck, Sebastian; Aherrahrou, Zouhair; Nahrstaedt, Janja; Willenborg, Christina; Bruse, Petra; Brænne, Ingrid; Nöthen, Markus M; Hofmann, Per; Braund, Peter S; Mergia, Evanthia; Reinhard, Wibke; Burgdorf, Christof; Schreiber, Stefan; Balmforth, Anthony J; Hall, Alistair S; Bertram, Lars; Steinhagen-Thiessen, Elisabeth; Li, Shu-Chen; März, Winfried; Reilly, Muredach; Kathiresan, Sekar; McPherson, Ruth; Walter, Ulrich; Ott, Jurg; Samani, Nilesh J; Strom, Tim M; Meitinger, Thomas; Hengstenberg, Christian; Schunkert, Heribert

    2013-12-19

    Myocardial infarction, a leading cause of death in the Western world, usually occurs when the fibrous cap overlying an atherosclerotic plaque in a coronary artery ruptures. The resulting exposure of blood to the atherosclerotic material then triggers thrombus formation, which occludes the artery. The importance of genetic predisposition to coronary artery disease and myocardial infarction is best documented by the predictive value of a positive family history. Next-generation sequencing in families with several affected individuals has revolutionized mutation identification. Here we report the segregation of two private, heterozygous mutations in two functionally related genes, GUCY1A3 (p.Leu163Phefs*24) and CCT7 (p.Ser525Leu), in an extended myocardial infarction family. GUCY1A3 encodes the α1 subunit of soluble guanylyl cyclase (α1-sGC), and CCT7 encodes CCTη, a member of the tailless complex polypeptide 1 ring complex, which, among other functions, stabilizes soluble guanylyl cyclase. After stimulation with nitric oxide, soluble guanylyl cyclase generates cGMP, which induces vasodilation and inhibits platelet activation. We demonstrate in vitro that mutations in both GUCY1A3 and CCT7 severely reduce α1-sGC as well as β1-sGC protein content, and impair soluble guanylyl cyclase activity. Moreover, platelets from digenic mutation carriers contained less soluble guanylyl cyclase protein and consequently displayed reduced nitric-oxide-induced cGMP formation. Mice deficient in α1-sGC protein displayed accelerated thrombus formation in the microcirculation after local trauma. Starting with a severely affected family, we have identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalling and myocardial infarction risk, possibly through accelerated thrombus formation. Reversing this defect may provide a new therapeutic target for reducing the risk of myocardial infarction.

  3. Role of myocardial perfusion imaging in evaluating thrombolytic therapy for acute myocardial infarction

    SciTech Connect

    Beller, G.A.

    1987-03-01

    Myocardial thallium-201 scintigraphy is being increasingly employed as a method for assessing the efficacy of coronary reperfusion in acute myocardial infarction. New thallium uptake after intracoronary tracer administration after successful recanalization indicates that nutrient blood flow has been successfully restored. One may also presume that some myocardial salvage occurred if thallium administered in this manner is transported intracellularly by myocytes with intact sarcolemmal membranes. However, if one injects thallium by way of the intracoronary route immediately after reperfusion, the initial uptake of thallium in reperfused myocardium may predominantly represent hyperemic flow and regional thallium counts measured may not be proportional to the mass of viable myocytes. When thallium is injected intravenously during the occlusion phase the degree of redistribution after thrombolysis is proportional to the degree of flow restoration and myocardial viability. When thallium is injected for the first time intravenously immediately after reperfusion, an overestimation of myocardial salvage may occur because of excess thallium uptake in the infarct zone consequent to significant hyperemia. Another approach to myocardial thallium scintigraphy in patients undergoing thrombolytic therapy is to administer two separate intravenous injections before and 24 hours or later after treatment. Finally, patients with acute myocardial infarction who receive intravenous thrombolytic therapy are candidates for predischarge exercise thallium-201 scintigraphy for risk stratification and detection of residual ischemia.

  4. Depression increases sympathetic activity and exacerbates myocardial remodeling after myocardial infarction: evidence from an animal experiment.

    PubMed

    Shi, Shaobo; Liang, Jinjun; Liu, Tao; Yuan, Xiaoran; Ruan, Bing; Sun, Lifang; Tang, Yanhong; Yang, Bo; Hu, Dan; Huang, Congxin

    2014-01-01

    Depression is an independent risk factor for cardiovascular events and mortality in patients with myocardial infarction (MI). Excessive sympathetic activation and serious myocardial remodeling may contribute to this association. The aim of this study was to discuss the effect of depression on sympathetic activity and myocardial remodeling after MI. Wild-type (WT) rats were divided into a sham group (Sham), a myocardial infarction group (MI), a depression group (D), and a myocardial infarction plus depression group (MI+D). Compared with controls, the MI+D animals displayed depression-like behaviors and attenuated body weight gain. The evaluation of sympathetic activity showed an increased level in plasma concentrations of epinephrine and norepinephrine and higher expression of myocardial tyrosine hydroxylase in the MI+D group than the control groups (p<0.05 for all). Cardiac function and morphologic analyses revealed a decreased fractional shortening accompanied by increased left ventricular dimensions, thinning myocardium wall, and reduced collagen repair in the MI+D group compared with the MI group (p<0.05 for all). Frequent premature ventricular contractions, prolonged QT duration and ventricular repolarization duration, shorted effective refractory period, and increased susceptibility to ventricular arrhythmia were displayed in MI+D rats. These results indicate that sympathetic hyperactivation and exacerbated myocardial remodeling may be a plausible mechanism linking depression to an adverse prognosis after MI.

  5. Pathological observation of acute myocardial infarction in Chinese miniswine

    PubMed Central

    Wang, Chuang; Wang, Shao-Xin; Dong, Ping-Shuan; Wang, Li-Ping; Duan, Na-Na; Wang, Yan-Yu; Wang, Ke; Li, Zhuan-Zhen; Wei, Li-Juan; Meng, Ya-Li; Cheng, Jian-Xin

    2015-01-01

    The acute myocardial infarction (AMI) model in Chinese miniswine was built by percutaneous coronary artery occlusion. Pathological observation of AMI was performed, and the expression of tumor necrosis factor alpha (TNF-α) in the infarct sites was detected at different days after modeling in Chinese miniswine. The experimental findings may be used as the basis for blood flow reconstruction and intervention after AMI. Seven experimental Chinese miniswine were subjected to general anesthesia and Seldinger right femoral artery puncture. After coronary angiography, the gelfoam was injected via the microtube to occlude the obtuse marginal branch (OM branch). At 1 d, 3 d, 5 d, 7 d, 10 d, 14 d and 17 d after modeling, hetatoxylin-eosin (HE) staining was performed to observe the pathological changes and to detect the expression of TNF-α in the myocardial tissues. Cytoplasmic acidophilia of the necrotic myocardial tissues at 1 d after modeling was enhanced, and cytoplasmic granules were formed; at 3 d, the margins of the necrotic myocardial tissues were infiltrated by a large number of inflammatory cells; at 5 d, the nuclei of the necrotic myocardial cells were fragmented; at 7 d, extensive granulation tissues were formed at the margin of the necrotic myocardial tissues; at 10 d, part of the granulation tissues were replaced by fibrous scar tissues; at 14-17 d, all granulation tissues were replaced by fibrous scar tissues. Immunohistochemical detection indicated that no TNF-α expression in normal myocardial tissues. The TNF-α expression was first detected at 3 d in the necrotic myocardial tissues and then increased at 5 d and 7 d. After reaching the peak at 10 d, the expression began to decrease at 14 d and the decrease continued at 17 d. Coronary angiography showed the disappearance of blood flow at the distal end of OM branch occluded by gelfoam, indicating that AMI model was constructed successfully. The repair of the infarcted myocardium began at 10-17 d after

  6. Ventricular function and infarct size: the Western Washington Intravenous Streptokinase in Myocardial Infarction Trial

    SciTech Connect

    Ritchie, J.L.; Cerqueira, M.; Maynard, C.; Davis, K.; Kennedy, J.W.

    1988-04-01

    The Western Washington Intravenous Streptokinase in Acute Myocardial Infarction Trial randomized 368 patients with symptoms and signs of acute myocardial infarction of less than 6 h duration to either conventional care or 1.5 million units of intravenous streptokinase. The mean time to randomization was 209 min and 52% of patients were randomized within 3 h of symptom onset. Quantitative, tomographic thallium-201 infarct size and radionuclide ejection fraction were measured at 8.2 +/- 7.5 weeks in 207 survivors who lived within a 100 mile radius of a centralized laboratory. Overall, infarct size as a percent of the left ventricle was 19 +/- 13% for control subjects and 15 +/- 13% for treatment patients (p = 0.03). For anterior infarction in patients entered within 3 h of symptom onset, infarct size was 28 +/- 13% in the control group versus 19 +/- 15% for the treatment group (p = 0.09). Left ventricular ejection fraction was 47 +/- 15% in the control versus 51 +/- 15% in the treatment group (p = 0.08). For anterior infarction of less than 3 h duration, the ejection fraction was 38 +/- 16% in the control versus 48 +/- 20% in the treatment group (p = 0.13). By statistical analysis incorporating the nonsurvivors, p values for all of these variables were less than or equal to 0.08. There was no benefit for patients with inferior infarction or for anterior infarction of greater than 3 h duration. It is concluded that intravenous streptokinase, when given within 3 h of symptom onset to patients with anterior infarction, reduces infarct size and improves ventricular function.

  7. Histological diagnosis of myocardial infarction: the role of calcium.

    PubMed

    Chatelain, P; Kapanci, Y

    1984-01-01

    The value of a histochemical method (alizarin red S) based on the detection of calcium in myocytes in early myocardial infarction was tested on 20 human and 30 rat hearts. After alizarin red S stain, a yellow-gold aspect of myocytes allowed to diagnose myocardial infarction in 18/20 human hearts, whereas with macroscopic examination and conventional histology the diagnosis was made only in 12/20 cases. In the rat, 30 min after coronary ligation, the ischaemic zone appeared yellow-gold with alizarin red S. This suggested that such a staining would also indicate an early infarct in human hearts. However, the yellow-gold aspect of myocytes with alizarin red S is unusual for calcium staining, which is generally orange. Consequently, the notion of calcium overload in 'yellow-gold' myocytes needed confirmation. This was done using a scanning electron microprobe quantometer (SEMQ), which showed a significantly high calcium level in the alizarin red S yellow-gold-stained myocytes. Our findings suggest that a single histochemical method for calcium (alizarin red S) is useful for detecting irreversible ischaemia and helps to diagnose very early myocardial infarction morphologically.

  8. Protein therapeutics for cardiac regeneration after myocardial infarction.

    PubMed

    Segers, Vincent F M; Lee, Richard T

    2010-10-01

    Although most medicines have historically been small molecules, many newly approved drugs are derived from proteins. Protein therapies have been developed for treatment of diseases in almost every organ system, including the heart. Great excitement has now arisen in the field of regenerative medicine, particularly for cardiac regeneration after myocardial infarction. Every year, millions of people suffer from acute myocardial infarction, but the adult mammalian myocardium has limited regeneration potential. Regeneration of the heart after myocardium infarction is therefore an exciting target for protein therapeutics. In this review, we discuss different classes of proteins that have therapeutic potential to regenerate the heart after myocardial infarction. Protein candidates have been described that induce angiogenesis, including fibroblast growth factors and vascular endothelial growth factors, although thus far clinical development has been disappointing. Chemotactic factors that attract stem cells, e.g., hepatocyte growth factor and stromal cell-derived factor-1, may also be useful. Finally, neuregulins and periostin are proteins that induce cell-cycle reentry of cardiomyocytes, and growth factors like IGF-1 can induce growth and differentiation of stem cells. As our knowledge of the biology of regenerative processes and the role of specific proteins in these processes increases, the use of proteins as regenerative drugs could develop as a cardiac therapy.

  9. Cardiac Telocytes in Regeneration of Myocardium After Myocardial Infarction.

    PubMed

    Zhaofu, Liao; Dongqing, Cai

    2016-01-01

    Recent research progress has revealed that a novel type of interstitial cells termed cardiac telocytes (CTs) is found in the interstitium of the heart. We demonstrated that CTs are distributed both longitudinally and within the cross network in the myocardium and that the density of CTs in the atrium-atria and base of the myocardium is higher than that in the middle of the myocardium, while the density of CTs in the epicardium is higher than that in the endocardium. In addition, we documented, for the first time, that the network of CTs in the infarct zone of the myocardium is destroyed during myocardial infarction (MI). This fact shows that, in addition to the death of cardiac myocytes, the previously unrecognized death of CTs is an important mechanism that contributes to the structural damage and poor healing and regeneration observed in the infarcted myocardium. Furthermore, we demonstrated, for the first time, that transplantation of CTs in cases of MI decreases the infarct size and improves myocardial function. The mechanisms behind the beneficial effects of CT transplantation are increased angiogenesis at the infarct site and the border zone, decreased fibrosis in the infarct and non-infarct zones, improved pathological reconstruction of the left ventricle, and increased regeneration of CTs in the infarct zone. Our findings reveal that CTs can be specifically identified by the following characteristics: very small cell bodies, extreme prolongation with some dilation, predisposition to cell death under ischemia, and expression of molecular markers such as c-Kit, CD34, vimentin, and PDGFR-β. CTs act as a structural and functional niche microenvironment in the myocardium and play an essential role in maintaining the integrity of the myocardium and in the regeneration of damaged myocardium.

  10. Cells involved in extracellular matrix remodeling after acute myocardial infarction

    PubMed Central

    Garcia, Larissa Ferraz; Mataveli, Fábio D’Aguiar; Mader, Ana Maria Amaral Antônio; Theodoro, Thérèse Rachell; Justo, Giselle Zenker; Pinhal, Maria Aparecida da Silva

    2015-01-01

    Objective Evaluate the effects of VEGF165 gene transfer in the process of remodeling of the extracellular matrix after an acute myocardial infarct. Methods Wistar rats were submitted to myocardial infarction, after the ligation of the left descending artery, and the left ventricle ejection fraction was used to classify the infarcts into large and small. The animals were divided into groups of ten, according to the size of infarcted area (large or small), and received or not VEGF165 treatment. Evaluation of different markers was performed using immunohistochemistry and digital quantification. The primary antibodies used in the analysis were anti-fibronectin, anti-vimentin, anti-CD44, anti-E-cadherin, anti-CD24, anti-alpha-1-actin, and anti-PCNA. The results were expressed as mean and standard error, and analyzed by ANOVA, considering statistically significant if p≤0.05. Results There was a significant increase in the expression of undifferentiated cell markers, such as fibronectin (protein present in the extracellular matrix) and CD44 (glycoprotein present in the endothelial cells). However, there was decreased expression of vimentin and PCNA, indicating a possible decrease in the process of cell proliferation after treatment with VEGF165. Markers of differentiated cells, E-cadherin (adhesion protein between myocardial cells), CD24 (protein present in the blood vessels), and alpha-1-actin (specific myocyte marker), showed higher expression in the groups submitted to gene therapy, compared to non-treated group. The value obtained by the relation between alpha-1-actin and vimentin was approximately three times higher in the groups treated with VEGF165, suggesting greater tissue differentiation. Conclusion The results demonstrated the important role of myocytes in the process of tissue remodeling, confirming that VEGF165 seems to provide a protective effect in the treatment of acute myocardial infarct. PMID:25993074

  11. Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents

    PubMed Central

    Rodrigues, Bruno; Figueroa, Diego Mendrot Taboas; Fang, Jiao; Rosa, Kaleizu Teodoro; Llesuy, Suzana; De Angelis, Kátia; Irigoyen, Maria Cláudia

    2011-01-01

    OBJECTIVES: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. INTRODUCTION: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. METHODS: Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. RESULTS: The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23±3%) when compared with the myocardial infarction (42±7%, p<0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32±3; diabetes + myocardial infarction: 35±0.7; control-sham: 12±2; myocardial infarction: 16±0.1 pmol min-1 mg-1 protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001). CONCLUSIONS: These data suggest that short

  12. [Dispersion of the Q-T interval after myocardial infarct].

    PubMed

    Kaliská, G; Alberty, R; Kmec, P; Kovár, F; Szentiványi, M

    1997-01-01

    Non-homogenity of ventricular myocardial repolarization is a substrate for the reentry mechanism of ventricular arrhythmias. It is manifestant by dispersion of Q-T and Q-Tc intervals on the standard ECG curve. The authors studied the possibility of using the dispersity of Q-T and Q-Tc intervals in clinical practice. They evaluated the dispersion of these intervals within the set of 21 patients after myocardial infarction with sustained ventricular tachycardia, and compared it with the dispersion within the control set of 17 patients after myocardial infarction without an arrhythmic episode. By means of comparison, they have discovered that: 1) the dispersion of Q-T and Q-Tc intervals is significantly higher in patients with ventricular tachycardia: Q-T (mean +/- SE) 82.8 +/- 7.8 msec vs 42.2 +/- 4.8 msec, Q-Tc 93.0 +/- 10.2 msec vs 47.1 +/- 4.8 msec, p > 0.001, 2) the dispersion of Q-Tc when higher than 60 msec is an optimum discrimination value for the prognosis of sudden arrhythmic death after myocardial infarction (sensitivity 81%, specificity 76%) and 3) the dispersion of Q-T and Q-Tc intervals has no relation to the function of the left ventricle. Therefore the authors consider the dispersion of Q-T and Q-Tc intervals as being a useful marker of malignant ventricular arrhythmia which could be included into the algorithm of assessment of the risk of sudden arrhythmic death after myocardial infarction.

  13. Improved detection of myocardial infarction by emission computed tomography with thallium-201. Relation to infarct size.

    PubMed Central

    Tamaki, S; Kambara, H; Kadota, K; Suzuki, Y; Nohara, R; Kawai, C; Tamaki, N; Torizuka, K

    1984-01-01

    Emission computed tomography with thallium-201 was compared with planar imaging in its ability to detect myocardial infarctions of various sizes four weeks after the onset. Tomography was performed after planar imaging at rest in 160 patients with a first myocardial infarction, in whom infarct size was prospectively estimated by the peak value of creatine kinase activity at the time of the acute episode and in 39 patients without infarction. The planar images and the transaxial, short axial, and long axial tomograms were interpreted qualitatively. Tomography was significantly more sensitive than planar imaging in detecting anterior (87% v 96%), inferior (73% v 97%), and non-transmural (47% v 87%) infarcts. The increased sensitivity was confined to detecting small infarcts as assessed by the peak creatine kinase value (44% v 89% when peak creatine kinase activity was less than or equal to 1000 IU/l). The overall sensitivity was 96% for tomography and 78% for planar imaging. The specificity was similar (92%) with the two techniques. Thus emission computed tomography can improve the detection rate of small infarcts that cannot be identified on planar images, by showing the three dimensional distribution of thallium-201, and increases the diagnostic value of thallium-201 scintigraphy. Images PMID:6334533

  14. 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

  15. Management of acute perioperative myocardial infarction: a case report of concomitant acute myocardial infarction and tumor bleeding in the transverse colon

    PubMed Central

    Li, Yu-Feng; Gao, Wen-Qian; Li, Yuan-Xin; Feng, Quan-Zhou; Zhu, Ping

    2016-01-01

    Acute myocardial infarction complicated by bleeding colon tumor is problematic with regard to management, and appropriate balance of antiplatelet or anticoagulation therapy and hemostasis or surgery is crucial for effective treatment. Here, we present a case of concomitant acute myocardial infarction and bleeding tumor in the transverse colon, and share our experience of successfully balancing anticoagulation therapy and hemostasis. PMID:26937182

  16. Prognostic Value of Troponin I for Infarct Size to Improve Preclinical Myocardial Infarction Small Animal Models

    PubMed Central

    Frobert, Aurélien; Valentin, Jérémy; Magnin, Jean-Luc; Riedo, Erwin; Cook, Stéphane; Giraud, Marie-Noëlle

    2015-01-01

    Coronary artery ligations to induce myocardial infarction (MI) in mice and rats are widely used in preclinical investigation. However, myocardial ischemic damage and subsequent infarct size are highly variable. The lack of standardization of the model impairs the probability of effective translation to the clinic. Cardiac Troponin I (cTnI) is a major clinically relevant biomarker. Aim: In the present study, we investigated the prognostic value of cTnI for early estimation of the infarct size. Methods and Results: Infarcts of different sizes were induced in mice and rats by ligation, at a random site, of the coronary artery. Kinetics of the plasma levels of cTnI were measured. Heart function was evaluated by echocardiography, the percentage of infarcted left ventricle and infarct expansion index were assessed from histological section. We observed that plasma cTnI level peaked at 24 h in the infarcted rats and between 24 and 48 h in mice. Sham operated animals had a level of cTnI below 15 ng/mL. Infarct expansion index (EI) assessed 4 weeks after ligation showed a large variation coefficient of 63 and 71% in rats and mice respectively. We showed a significative correlation between cTnI level and the EI demonstrating its predictive value for myocardial injury in small animal models. Conclusion: we demonstrated the importance of cTnI plasma level as a major early marker to assist in the optimal and efficient management of MI in laboratory animals model. The presented results stress the need for comparable biomarkers in the animal model and clinical trials for improved translation. PMID:26640441

  17. Cardiovascular magnetic resonance assessment of myocardial infarction and post-infarct complications.

    PubMed

    Assomull, Ravi; Cannell, Timothy M; Prasad, Sanjay K

    2005-09-01

    The article discusses the growing role of cardiovascular magnetic resonance in both the diagnosis of myocardial infarction and its subsequent management, including the management of any resulting complications. The current roles of magnetic resonance coronary angiography and magnetic resonance perfusion are also reviewed.

  18. Myocardial Infarction after Endoscopic Removal of Foreign Body.

    PubMed

    Maraboto, Carola; Lupercio, Florentino; Piña, Ileana L

    2017-01-01

    The development of cardiac complications during or after endoscopic procedures is rare. However, mortality from myocardial ischemia, particularly in the elderly population, is elevated. We illustrate the rare case of a 79-year-old man with multiple cardiovascular risk factors who developed a non-ST elevation myocardial infarction (NSTEMI) after endoscopic removal of a foreign body. This case report summarizes a rare complication of a low-risk procedure and highlights the importance of considering this potential adverse event, particularly in patients with significant cardiovascular risk factors, to promote early diagnosis and proper treatment.

  19. Myocardial Infarction after Endoscopic Removal of Foreign Body

    PubMed Central

    Lupercio, Florentino; Piña, Ileana L.

    2017-01-01

    The development of cardiac complications during or after endoscopic procedures is rare. However, mortality from myocardial ischemia, particularly in the elderly population, is elevated. We illustrate the rare case of a 79-year-old man with multiple cardiovascular risk factors who developed a non-ST elevation myocardial infarction (NSTEMI) after endoscopic removal of a foreign body. This case report summarizes a rare complication of a low-risk procedure and highlights the importance of considering this potential adverse event, particularly in patients with significant cardiovascular risk factors, to promote early diagnosis and proper treatment. PMID:28337347

  20. Left ventricular muscle and fluid mechanics in acute myocardial infarction.

    PubMed

    Nucifora, Gaetano; Delgado, Victoria; Bertini, Matteo; Marsan, Nina Ajmone; Van de Veire, Nico R; Ng, Arnold C T; Siebelink, Hans-Marc J; Schalij, Martin J; Holman, Eduard R; Sengupta, Partho P; Bax, Jeroen J

    2010-11-15

    Left ventricular (LV) diastolic filling is characterized by the formation of intraventricular rotational bodies of fluid (termed "vortex rings") that optimize the efficiency of LV ejection. The aim of the present study was to evaluate the morphology and dynamics of LV diastolic vortex ring formation early after acute myocardial infarction (AMI), in relation to LV diastolic function and infarct size. A total of 94 patients with a first ST-segment elevation AMI (59 ± 11 years; 78% men) were included. All patients underwent primary percutaneous coronary intervention. After 48 hours, the following examinations were performed: 2-dimensional echocardiography with speckle-tracking analysis to assess the LV systolic and diastolic function, the vortex formation time (VFT, a dimensionless index for characterizing vortex formation), and the LV untwisting rate; contrast echocardiography to assess LV vortex morphology; and myocardial contrast echocardiography to identify the infarct size. Patients with a large infarct size (≥ 3 LV segments) had a significantly lower VFT (p <0.001) and vortex sphericity index (p <0.001). On univariate analysis, several variables were significantly related to the VFT, including anterior AMI, LV end-systolic volume, LV ejection fraction, grade of diastolic dysfunction, LV untwisting rate, and infarct size. On multivariate analysis, the LV untwisting rate (β = -0.43, p <0.001) and infarct size (β = -0.33, p = 0.005) were independently associated with VFT. In conclusion, early in AMI, both the LV infarct size and the mechanical sequence of diastolic restoration play key roles in modulating the morphology and dynamics of early diastolic vortex ring formation.

  1. Regional myocardial lidocaine concentration following continuous intravenous infusion early and later after myocardial infarction

    SciTech Connect

    Zito, R.A.; Caride, V.J.; Holford, T.; Zaret, B.L.

    1982-09-01

    The regional concentration of lidocaine using a double constant infusion technique (250 micrograms/kg/min x 15 minutes followed by 35 micrograms/kg/mg/min x 120 minutes) was studied immediately (2 hours) in seven dogs and 24 hours (six dogs) after myocardial infarction. Tissue levels were determined by gas chromatography and related to regional myocardial blood flow as determined by the radioactive microsphere technique in multiple samples. At 2 hours after infarction a significantly higher lidocaine concentration (4.1 +/- 0.42 micrograms/g) was found in zones with greatly reduced blood flow (regional myocardial blood flow less than 0.2 ml/min per g) when compared with that (2.6 +/- 0.19 micrograms/g) in zones with normal blood flow (regional myocardial blood flow greater than 0.8 ml/min per g) (p less than 0.01). In contrast, in the 24 hour model the opposite situation was observed. Although the concentration of lidocaine in the infarct zone was substantial, a significant decline in lidocaine tissue concentration was found in the zones of lowest blood flow (regional myocardial blood flow less than 0.2 ml/min per g) when compared with that in normal zones (1.76 +/- 0.21 versus 3.38 +/- 0.21 micrograms/g, p less than 0.001). In addition, no significant differences in lidocaine concentrations were found between endocardium and epicardium in any of the groups other than those related to regional myocardial blood flow. Thus, with the double constant infusion technique, lidocaine reached normal and ischemic myocardium in concentrations equivalent to therapeutic plasma concentrations, even in lower infarct blood flow zones, with no significant differences between endocardium and epicardium. Of perhaps greater significance, the age of the ischemic insult is an important determinant of lidocaine tissue distribution in infarcted myocardium.

  2. Disappearance of myocardial bridging of the left anterior descending coronary artery after inferior myocardial infarction.

    PubMed

    Yıldız, Bekir Serhat; Esin, Fatma; Alihanoğlu, Yusuf Izzettin; Kılıç, Ismail Doğu; Evrengül, Harun

    2014-06-01

    Myocardial bridging (MB) is defined as the intramural course of a major epicardial coronary artery, and is mostly confined to the left ventricle and the left anterior descending coronary artery (LAD). MB is a common congenital abnormality of a coronary artery, and is usually thought to be a benign anatomical variant. Although rare, previous studies have reported that patients with MB may suffer from myocardial ischemia, myocardial infarction (MI), arrhythmias, and even sudden death. Therefore, the diagnosis and treatment of MB are both important. Since MB is congenital, its disappearance is unlikely. We here report a very rare case of disappearance of MB after inferior MI.

  3. 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

  4. Polycythemia vera presenting as acute myocardial infarction: An unusual presentation

    PubMed Central

    Bahbahani, Hussain; Aljenaee, Khaled; Bella, Abdelhaleem

    2014-01-01

    Acute myocardial infarction (AMI) is usually seen in the setting of atherosclerosis and its associated risk factors. Myocardial infarction in the young poses a particular challenge, as the disease is less likely, due to atherosclerosis. We report the case of a 37-year-old female patient who presented with ST segment elevation anterolateral AMI. The only abnormality on routine blood investigation was raised hemoglobin and hematocrit. After further testing, she was diagnosed according to the World Health Organization (WHO) criteria with polycythemia vera. This case illustrates the importance of recognizing polycythemia vera as an important cause of thrombosis, which can present initially as AMI, and to emphasize the early recognition of the disease in order to initiate appropriate management strategies. PMID:25544823

  5. Evaluating variable selection methods for diagnosis of myocardial infarction.

    PubMed Central

    Dreiseitl, S.; Ohno-Machado, L.; Vinterbo, S.

    1999-01-01

    This paper evaluates the variable selection performed by several machine-learning techniques on a myocardial infarction data set. The focus of this work is to determine which of 43 input variables are considered relevant for prediction of myocardial infarction. The algorithms investigated were logistic regression (with stepwise, forward, and backward selection), backpropagation for multilayer perceptrons (input relevance determination), Bayesian neural networks (automatic relevance determination), and rough sets. An independent method (self-organizing maps) was then used to evaluate and visualize the different subsets of predictor variables. Results show good agreement on some predictors, but also variability among different methods; only one variable was selected by all models. Images Figure 1 PMID:10566358

  6. Myocardial infarction: stem cell transplantation for cardiac regeneration.

    PubMed

    Carvalho, Edmund; Verma, Paul; Hourigan, Kerry; Banerjee, Rinti

    2015-11-01

    It is estimated that by 2030, almost 23.6 million people will perish from cardiovascular disease, according to the WHO. The review discusses advances in stem cell therapy for myocardial infarction, including cell sources, methods of differentiation, expansion selection and their route of delivery. Skeletal muscle cells, hematopoietic cells and mesenchymal stem cells (MSCs) and embryonic stem cells (ESCs)-derived cardiomyocytes have advanced to the clinical stage, while induced pluripotent cells (iPSCs) are yet to be considered clinically. Delivery of cells to the sites of injury and their subsequent retention is a major issue. The development of supportive scaffold matrices to facilitate stem cell retention and differentiation are analyzed. The review outlines clinical translation of conjugate stem cell-based cellular therapeutics post-myocardial infarction.

  7. Stressors and stress management--1 month after myocardial infarction.

    PubMed

    Miller, P; Garrett, M J; Stoltenberg, M; McMahon, M; Ringel, K

    1990-01-01

    Stressors and stress management behaviors reported by 52 myocardial infarction (MI) patients were identified from a content analysis of transcriptions of nurse/patient/spouse interactions that took place 30 days postinfarction. Subjects defined stress primarily in terms of distress related to appraisals of harm, loss, or threat. Stressors and stress management behaviors varied, although subjects were similar in age and occupation and were in the same phase of recovery. Most stressors related to recent myocardial infarction and pertained to thoughts and feelings more than to external events. Others, related to family and/or work, were ongoing before the MI. Stress management behaviors comprised a continuum of physical, cognitive, and verbal behaviors ranging from active to passive. Avoidance of situations, ignoring situations, expressing feelings, and thinking things through were the four major modes of stress management behaviors. Implications for rehabilitation nursing practice are identified.

  8. Significance of U wave polarities in previous anterior myocardial infarction

    SciTech Connect

    Kanemoto, N.; Imaoka, C.; Suzuki, Y. )

    1991-04-01

    The significance of the polarity of U waves in left precordial leads was evaluated in relation to myocardial perfusion (T1 201 myocardial scintigraphy) and left ventricular function (99m Tc radionuclide ventriculography) in 63 patients with clinical and electrocardiographic evidence of a previous anterior myocardial infarction. Patients were divided into three groups according to the polarity of the U waves: positive U waves, flat U waves, and negative U waves. Twelve matched patients served as normal controls. The following parameters were analyzed: (1) total number of abnormal Q waves; (2) total myocardial perfusion index and regional myocardial perfusion index; (3) global ejection fraction; (4) regional ejection fraction; and (5) number of diseased coronary arteries. The total myocardial perfusion index values were 43.9 {plus minus} 1.0 in controls, 40.8 {plus minus} 3.4 in the positive U wave group, 33.4 {plus minus} 3.5 in the flat U wave group, and 30.3 {plus minus} 4.4 in the patients with negative U waves. Global ejection fractions in these groups were, respectively, 63.9 {plus minus} 8.6%, 65.0 {plus minus} 11.8%, 53.6 {plus minus} 8.1%, and 36.5 {plus minus} 13.6%. The sensitivity of negative U waves suggesting a global ejection fraction of less than 45% was 91.6%, and the specificity was 82.1%. Therefore the size of myocardial infarction increased and left ventricular function decreased, in order, from patients with positive U waves, to those with flat U waves, to those with negative U waves, with statistically significant differences.

  9. Fractional Flow Reserve-Guided Multivessel Angioplasty in Myocardial Infarction.

    PubMed

    Smits, Pieter C; Abdel-Wahab, Mohamed; Neumann, Franz-Josef; Boxma-de Klerk, Bianca M; Lunde, Ketil; Schotborgh, Carl E; Piroth, Zsolt; Horak, David; Wlodarczak, Adrian; Ong, Paul J; Hambrecht, Rainer; Angerås, Oskar; Richardt, Gert; Omerovic, Elmir

    2017-03-30

    In patients with ST-segment elevation myocardial infarction (STEMI), the use of percutaneous coronary intervention (PCI) to restore blood flow in an infarct-related coronary artery improves outcomes. The use of PCI in non-infarct-related coronary arteries remains controversial. We randomly assigned 885 patients with STEMI and multivessel disease who had undergone primary PCI of an infarct-related coronary artery in a 1:2 ratio to undergo complete revascularization of non-infarct-related coronary arteries guided by fractional flow reserve (FFR) (295 patients) or to undergo no revascularization of non-infarct-related coronary arteries (590 patients). The FFR procedure was performed in both groups, but in the latter group, both the patients and their cardiologist were unaware of the findings on FFR. The primary end point was a composite of death from any cause, nonfatal myocardial infarction, revascularization, and cerebrovascular events at 12 months. Clinically indicated elective revascularizations performed within 45 days after primary PCI were not counted as events in the group receiving PCI for an infarct-related coronary artery only. The primary outcome occurred in 23 patients in the complete-revascularization group and in 121 patients in the infarct-artery-only group that did not receive complete revascularization, a finding that translates to 8 and 21 events per 100 patients, respectively (hazard ratio, 0.35; 95% confidence interval [CI], 0.22 to 0.55; P<0.001). Death occurred in 4 patients in the complete-revascularization group and in 10 patients in the infarct-artery-only group (1.4% vs. 1.7%) (hazard ratio, 0.80; 95% CI, 0.25 to 2.56), myocardial infarction in 7 and 28 patients, respectively (2.4% vs. 4.7%) (hazard ratio, 0.50; 95% CI, 0.22 to 1.13), revascularization in 18 and 103 patients (6.1% vs. 17.5%) (hazard ratio, 0.32; 95% CI, 0.20 to 0.54), and cerebrovascular events in 0 and 4 patients (0 vs. 0.7%). An FFR-related serious adverse event occurred

  10. Venlafaxine induced acute myocardial infarction with normal coronary arteries.

    PubMed

    Godkar, Darshan; Stensby, Jessica; Sinnapunayagam, Selvaratnam; Niranjan, Selva

    2009-01-01

    We describe the case of a 51-year-old female with no risk factors for coronary artery disease who had an episode of a non-ST-elevation myocardial infarction in association with an overdose of Venlafaxine. Cardiac catheterization revealed normal coronary arteries. Because no other obvious exacerbating factors for ischemia were observed, we assume that this drug may have contributed to the development of an acute ischemic event because of its pharmacologic properties.

  11. Life Expectancy after Myocardial Infarction by Hospital Performance

    PubMed Central

    Bucholz, Emily M.; Butala, Neel M.; Ma, Shuangge; Normand, Sharon-Lise T.; Krumholz, Harlan M.

    2016-01-01

    Background Thirty-day risk-standardized mortality rates after acute myocardial infarction are commonly used to evaluate and compare hospital performance. However, it is not known whether differences between hospitals in early patient survival are associated with differences in long-term survival. Methods We analyzed data from the Cooperative Cardiovascular Project, a study of Medicare beneficiaries hospitalized for acute myocardial infarction between 1994-96 with 17 years of follow-up. We grouped hospitals into five strata based on case-mix severity. Within each case-mix stratum, we compared life expectancy in patients admitted to high and low-performing hospitals, as defined by quintiles of thirty-day risk-standardized mortality rates. Cox proportional hazards models were used to calculate life expectancy. Results The study sample included 119,735 patients with acute myocardial infarction admitted to 1,824 hospitals. Within each case-mix stratum, survival curves for patients admitted to hospitals in each risk-standardized mortality rate quintile separated within the first 30 days and then remained parallel over 17 years of follow-up. Estimated life expectancy declined as hospital risk-standardized mortality rate quintile increased. On average, patients treated at high-performing hospitals lived between 1.14 and 0.84 years longer than patients treated at low-performing hospitals, depending on hospital case-mix. When 30-day survivors were examined separately, there was no difference in unadjusted or adjusted life expectancy across hospital risk-standardized mortality rate quintiles. Conclusion Patients admitted to high-performing hospitals after acute myocardial infarction had longer life expectancies than patients treated in low-performing hospitals. This survival benefit arose in the first 30 days and persisted over the long term. PMID:27705249

  12. Acute myocardial infarction and stress cardiomyopathy following the Christchurch earthquakes.

    PubMed

    Chan, Christina; Elliott, John; Troughton, Richard; Frampton, Christopher; Smyth, David; Crozier, Ian; Bridgman, Paul

    2013-01-01

    Christchurch, New Zealand, was struck by 2 major earthquakes at 4:36 am on 4 September 2010, magnitude 7.1 and at 12:51 pm on 22 February 2011, magnitude 6.3. Both events caused widespread destruction. Christchurch Hospital was the region's only acute care hospital. It remained functional following both earthquakes. We were able to examine the effects of the 2 earthquakes on acute cardiac presentations. Patients admitted under Cardiology in Christchurch Hospital 3 week prior to and 5 weeks following both earthquakes were analysed, with corresponding control periods in September 2009 and February 2010. Patients were categorised based on diagnosis: ST elevation myocardial infarction, Non ST elevation myocardial infarction, stress cardiomyopathy, unstable angina, stable angina, non cardiac chest pain, arrhythmia and others. There was a significant increase in overall admissions (p<0.003), ST elevation myocardial infarction (p<0.016), and non cardiac chest pain (p<0.022) in the first 2 weeks following the early morning September earthquake. This pattern was not seen after the early afternoon February earthquake. Instead, there was a very large number of stress cardiomyopathy admissions with 21 cases (95% CI 2.6-6.4) in 4 days. There had been 6 stress cardiomyopathy cases after the first earthquake (95% CI 0.44-2.62). Statistical analysis showed this to be a significant difference between the earthquakes (p<0.05). The early morning September earthquake triggered a large increase in ST elevation myocardial infarction and a few stress cardiomyopathy cases. The early afternoon February earthquake caused significantly more stress cardiomyopathy. Two major earthquakes occurring at different times of day differed in their effect on acute cardiac events.

  13. Acute Myocardial Infarction and Stress Cardiomyopathy following the Christchurch Earthquakes

    PubMed Central

    Chan, Christina; Elliott, John; Troughton, Richard; Frampton, Christopher; Smyth, David; Crozier, Ian; Bridgman, Paul

    2013-01-01

    Background Christchurch, New Zealand, was struck by 2 major earthquakes at 4:36am on 4 September 2010, magnitude 7.1 and at 12:51pm on 22 February 2011, magnitude 6.3. Both events caused widespread destruction. Christchurch Hospital was the region's only acute care hospital. It remained functional following both earthquakes. We were able to examine the effects of the 2 earthquakes on acute cardiac presentations. Methods Patients admitted under Cardiology in Christchurch Hospital 3 week prior to and 5 weeks following both earthquakes were analysed, with corresponding control periods in September 2009 and February 2010. Patients were categorised based on diagnosis: ST elevation myocardial infarction, Non ST elevation myocardial infarction, stress cardiomyopathy, unstable angina, stable angina, non cardiac chest pain, arrhythmia and others. Results There was a significant increase in overall admissions (p<0.003), ST elevation myocardial infarction (p<0.016), and non cardiac chest pain (p<0.022) in the first 2 weeks following the early morning September earthquake. This pattern was not seen after the early afternoon February earthquake. Instead, there was a very large number of stress cardiomyopathy admissions with 21 cases (95% CI 2.6–6.4) in 4 days. There had been 6 stress cardiomyopathy cases after the first earthquake (95% CI 0.44–2.62). Statistical analysis showed this to be a significant difference between the earthquakes (p<0.05). Conclusion The early morning September earthquake triggered a large increase in ST elevation myocardial infarction and a few stress cardiomyopathy cases. The early afternoon February earthquake caused significantly more stress cardiomyopathy. Two major earthquakes occurring at different times of day differed in their effect on acute cardiac events. PMID:23844213

  14. Structural racism and myocardial infarction in the United States

    PubMed Central

    Lukachko, Alicia; Hatzenbuehler, Mark L.; Keyes, Katherine M.

    2014-01-01

    There is a growing research literature suggesting that racism is an important risk factor undermining the health of Blacks in the United States. Racism can take many forms, ranging from interpersonal interactions to institutional/structural conditions and practices. Existing research, however, tends to focus on individual forms of racial discrimination using self-report measures. Far less attention has been paid to whether structural racism may disadvantage the health of Blacks in the United States. The current study addresses gaps in the existing research by using novel measures of structural racism and by explicitly testing the hypothesis that structural racism is a risk factor for myocardial infarction among Blacks in the United States. State-level indicators of structural racism included four domains: (1) political participation; (2) employment and job status; (3) educational attainment; and (4) judicial treatment. State-level racial disparities across these domains were proposed to represent the systematic exclusion of Blacks from resources and mobility in society. Data on past-year myocardial infarction were obtained from the National Epidemiologic Survey on Alcohol and Related Conditions (non-Hispanic Black: N = 8245; non-Hispanic White: N = 24,507), a nationally representative survey of the U.S. civilian, non-institutionalized population aged 18 and older. Models were adjusted for individual-level confounders (age, sex, education, household income, medical insurance) as well as for state-level disparities in poverty. Results indicated that Blacks living in states with high levels of structural racism were generally more likely to report past-year myocardial infarction than Blacks living in low-structural racism states. Conversely, Whites living in high structural racism states experienced null or lower odds of myocardial infarction compared to Whites living in low-structural racism states. These results raise the provocative possibility that structural

  15. More frequent diagnosis of acute myocardial infarction among Navajo Indians.

    PubMed

    Klain, M; Coulehan, J L; Arena, V C; Janett, R

    1988-10-01

    In an earlier study, we failed to confirm a clinical impression that the incidence of acute myocardial infarction (AMI) was increasing in Navajo men. Extending our data collection an additional three years, through 1986, we observed that the attack rate in men more than doubled and there was a gradual increase among women. Most Navajos who sustain AMI are hypertensive (51 per cent), diabetic (50 per cent) or both (31 per cent), but few smoke cigarettes.

  16. More frequent diagnosis of acute myocardial infarction among Navajo Indians.

    PubMed Central

    Klain, M; Coulehan, J L; Arena, V C; Janett, R

    1988-01-01

    In an earlier study, we failed to confirm a clinical impression that the incidence of acute myocardial infarction (AMI) was increasing in Navajo men. Extending our data collection an additional three years, through 1986, we observed that the attack rate in men more than doubled and there was a gradual increase among women. Most Navajos who sustain AMI are hypertensive (51 per cent), diabetic (50 per cent) or both (31 per cent), but few smoke cigarettes. PMID:3421396

  17. An unusual presentation of mad honey poisoning: acute myocardial infarction.

    PubMed

    Akinci, Sinan; Arslan, Uğur; Karakurt, Kamber; Cengel, Atiye

    2008-09-26

    An unusual type of food poisoning is commonly seen in the Black Sea coast of Turkey due to grayanotoxin containing toxic honey so called "mad honey" ingestion. In cases of toxication bradycardia and rhythm disturbances are commonly observed. Herein, we present a case of a patient who was admitted to the hospital because of acute myocardial infarction with normal coronary arteries after "mad honey" ingestion.

  18. [Use of cytoflavin for correction of complications of myocardial infarction].

    PubMed

    Bul'on, V V; Khnychenko, L K; Sapronov, N S; Kovalenko, A L; Alekseeva, L E

    2002-01-01

    The possibility of using a combined preparation cytoflavine was studied on rats with myocardial infarction induced by coronary artery occlusion. The drug produces a positive action upon the energy exchange and the lipid peroxidation process and normalizes functioning of the system of antioxidant protection of the ischemized myocardium. Cytoflavine treatment led to a more favorable course of ischemic and necrotic processes and optimum organization of the necrosis zones.

  19. Aircraft noise, air pollution, and mortality from myocardial infarction.

    PubMed

    Huss, Anke; Spoerri, Adrian; Egger, Matthias; Röösli, Martin

    2010-11-01

    Myocardial infarction has been associated with both transportation noise and air pollution. We examined residential exposure to aircraft noise and mortality from myocardial infarction, taking air pollution into account. We analyzed the Swiss National Cohort, which includes geocoded information on residence. Exposure to aircraft noise and air pollution was determined based on geospatial noise and air-pollution (PM10) models and distance to major roads. We used Cox proportional hazard models, with age as the timescale. We compared the risk of death across categories of A-weighted sound pressure levels (dB(A)) and by duration of living in exposed corridors, adjusting for PM10 levels, distance to major roads, sex, education, and socioeconomic position of the municipality. We analyzed 4.6 million persons older than 30 years who were followed from near the end of 2000 through December 2005, including 15,532 deaths from myocardial infarction (ICD-10 codes I 21, I 22). Mortality increased with increasing level and duration of aircraft noise. The adjusted hazard ratio comparing ≥60 dB(A) with <45 dB(A) was 1.3 (95% confidence interval = 0.96-1.7) overall, and 1.5 (1.0-2.2) in persons who had lived at the same place for at least 15 years. None of the other endpoints (mortality from all causes, all circulatory disease, cerebrovascular disease, stroke, and lung cancer) was associated with aircraft noise. Aircraft noise was associated with mortality from myocardial infarction, with a dose-response relationship for level and duration of exposure. The association does not appear to be explained by exposure to particulate matter air pollution, education, or socioeconomic status of the municipality.

  20. [Acute myocardial infarction during tocolytic treatment with ritodrine].

    PubMed

    Fornet, I; Calvo, M; Gimeno, M; Canser, E; Alonso, E; Gilsanz, F

    2006-05-01

    Ritodrine, a beta2-adrenergic agonist with a selective effect on the uterine muscle, is prescribed to prevent premature labor and to treat a hypertonic uterus. At therapeutic doses ritodrine has chronotropic and peripheral vasodilator effects. At high doses it has been related to sporadic cases of subendocardial necrosis, pulmonary edema, and death in pregnancy. We report the case of a pregnant woman who had a non-Q wave acute myocardial infarction after administration of ritodrine.

  1. Persistent Hypoxemia After Acute Myocardial Infarction: An Unexpected Culprit.

    PubMed

    Tralhão, António; Freitas, Pedro; Rodrigues, Gustavo; Café, Hugo; Ferreira, António Miguel; Mesquita Gabriel, Henrique; Bruges, Luís; Aguiar, Carlos; Ferreira, Jorge

    2017-07-29

    Hypoxemia after myocardial infarction (MI) is usually explained by common culprits, including congestive heart failure, pre-existing lung disease, and pulmonary infection. We report a case of a 60-year-old woman who experienced severe persistent hypoxemia caused by a patent foramen ovale in the setting of anterior MI complicated by a contained left ventricular rupture. Copyright © 2017 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

  2. Acute Myocardial Infarction following Naltrexone Consumption; a Case Report

    PubMed Central

    Dadpour, Bita; Gholoobi, Arash; Tajoddini, Shahrad; Habibi, Amir

    2017-01-01

    Cardiovascular effects of opioid withdrawal have long been studied. It was reported that patients with underlying ischemic heart disease and atherosclerotic vessels may be complicated by a sudden physical and emotional stress due to withdrawal syndrome. But some other believes sudden increase in catecholamine level as a sympathetic overflow might effect on heart with and without underlying ischemia. In the current study, a patient on methadone maintenance therapy (MMT) who experienced myocardial infarction (MI) after taking naltrexone was described. PMID:28286852

  3. Mucosal tolerance induction in autoimmune myocarditis and myocardial infarction.

    PubMed

    Li, Jin; Göser, Stefan; Leuschner, Florian; Volz, H Christian; Buss, Sebastian; Andrassy, Martin; Öttl, Renate; Pfitzer, Gabriele; Katus, Hugo A; Kaya, Ziya

    2013-01-20

    Antigen-specific therapy is a compelling approach for the treatment of autoimmune conditions. Primary goal is to induce the specific tolerization of self-reactive immune cells without altering host immunity against pathogens. We studied the effects of mucosal tolerance induction on cTnI-induced experimental autoimmune myocarditis (EAM) and post-infarct remodeling. Mucosal tolerance was induced by intranasal application of cTnI, alternatively anti-CD3 p.o. Protocols varied in frequency, dosage and time point of application before EAM. We then applied the most effective regimen to mice undergoing myocardial infarction in order to verify its effectiveness in post-infarct cardiac remodeling. The myocardium was evaluated on histological slides and for the cytokine secretion pattern, while echocardiography determined cardiac function. A single dose of 100 μg of cTnI 7 days prior to myocarditis appeared to be most effective in suppressing inflammation and fibrosis (p = 0.03), while improving fractional shortening (p = 0.02). Treatment with intranasal cTnI upregulated IL-10 expression. On the other hand, frequent intranasal application of high doses of cTnI increased myocardial inflammation. Anti-CD3 p.o. showed the propensity to reduce myocardial inflammation and improve cardiac function. The single dose regimen of i.n. cTnI applied 7 days before a myocardial infarction reduced inflammation by trend (p=0.07) and improved heart function (p=0.002). Moreover, expression of matrix metalloproteinases 9 and 14 significantly decreased when treated with intranasal cTnI (p<0.01). Depending on the optimal amount, the time period and the choice of antigen, effective mucosal tolerance can be achieved and represents an appealing therapeutic approach in the inflammatory process of cardiac remodeling. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

  4. Incidence of acute myocardial infarction in patients with exercise-induced silent myocardial ischemia

    SciTech Connect

    Assey, M.E.; Walters, G.L.; Hendrix, G.H.; Carabello, B.A.; Usher, B.W.; Spann, J.F. Jr.

    1987-03-01

    Fifty-five patients with angiographically proved coronary artery disease (CAD) underwent Bruce protocol exercise stress testing with thallium-201 imaging. Twenty-seven patients (group I) showed myocardial hypoperfusion without angina pectoris during stress, which normalized at rest, and 28 patients (group II) had a similar pattern of reversible myocardial hypoperfusion but also had angina during stress. Patients were followed for at least 30 months. Six patients in group I had an acute myocardial infarction (AMI), 3 of whom died, and only 1 patient in group II had an AMI (p = 0.05), and did not die. Silent myocardial ischemia uncovered during exercise stress thallium testing may predispose to subsequent AMI. The presence of silent myocardial ischemia identified in this manner is of prognostic value, independent of angiographic variables such as extent of CAD and left ventricular ejection fraction.

  5. Thrombospondins in the transition from myocardial infarction to heart failure.

    PubMed

    Kirk, Jonathan A; Cingolani, Oscar H

    2016-01-01

    The heart's reaction to ischemic injury from a myocardial infarction involves complex cross-talk between the extra-cellular matrix (ECM) and different cell types within the myocardium. The ECM functions not only as a scaffold where myocytes beat synchronously, but an active signaling environment that regulates the important post-MI responses. The thrombospondins are matricellular proteins that modulate cell--ECM interactions, functioning as "sensors" that mediate outside-in and inside-out signaling. Thrombospondins are highly expressed during embryonic stages, and although their levels decrease during adult life, can be re-expressed in high quantities in response to cardiac stress including myocardial infarction and heart failure. Like a Swiss-army knife, the thrombospondins possess many tools: numerous binding domains that allow them to interact with other elements of the ECM, cell surface receptors, and signaling molecules. It is through these that the thrombospondins function. In the present review, we provide basic as well as clinical evidence linking the thrombospondin proteins with the post myocardial infarction response, including inflammation, fibrotic matrix remodeling, angiogenesis, as well as myocyte hypertrophy, apoptosis, and contractile dysfunction in heart failure. We will describe what is known regarding the intracellular signaling pathways that are involved with these responses, paving the road for future studies identifying these proteins as therapeutic targets for cardiac disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

  6. Acute Myocardial Infarction Quality of Care: The Strong Heart Study

    PubMed Central

    Best, Lyle G.; Butt, Amir; Conroy, Britt; Devereux, Richard B.; Galloway, James M.; Jolly, Stacey; Lee, Elisa T.; Silverman, Angela; Yeh, Jeun-Liang; Welty, Thomas K.; Kedan, Ilan

    2014-01-01

    Objectives Evaluate the quality of care provided patients with acute myocardial infarction and compare with similar national and regional data. Design Case series. Setting The Strong Heart Study has extensive population-based data related to cardiovascular events among American Indians living in three rural regions of the United States. Participants Acute myocardial infarction cases (72) occurring between 1/1/2001 and 12/31/2006 were identified from a cohort of 4549 participants. Outcome measures The proportion of cases that were provided standard quality of care therapy, as defined by the Healthcare Financing Administration and other national organizations. Results The provision of quality services, such as administration of aspirin on admission and at discharge, reperfusion therapy within 24 hours, prescription of beta blocker medication at discharge, and smoking cessation counseling were found to be 94%, 91%, 92%, 86% and 71%, respectively. The unadjusted, 30 day mortality rate was 17%. Conclusion Despite considerable challenges posed by geographic isolation and small facilities, process measures of the quality of acute myocardial infarction care for participants in this American Indian cohort were comparable to that reported for Medicare beneficiaries nationally and within the resident states of this cohort. PMID:21942161

  7. Pseudo myocardial infarction - a condition in need to be redefined?

    PubMed

    Nunes, José Pedro L

    2010-02-01

    Since the introduction of cardiac plasma troponin measurements, a significant number of patients were seen with chest pain, elevated troponin levels but no significant coronary artery disease. Pulmonary embolism, aortic valve disease, myocarditis, sepsis, trauma, arrythmias, stress cardiomyopathy and dilated cardiomyopathy stand among possible causes for this syndrome. In some cases, myocardial strain could be the mechanism underlying this phenomenon, since it is known that the stimulation of stretch-responsive integrins may lead to the release of cardiac troponin I. In the present text, a case is made in favour of classifying this syndrome, of chest pain with increased values for plasma cardiac troponin, with or without ECG changes, in the absence of definite myocardial infarction or coronary artery disease, as pseudo myocardial infarction (PMI). This constitutes a new definition for a concept with decades, formerly centered on clinical and electrocardiographic changes mimicking infarct. The case is based on the search of scientific truth, on avoidance of unnecessary cardiac examinations, on avoidance of unnecessary drug therapy and on avoidance of unnecessary legal liability. PMI should be seen as a working diagnosis, since a more definitive diagnosis can be reached at all time. It should also be seen as a heterogeneous group of patients - several different diseases and conditions can lead to this phenomenon. But it must certainly not be seen as a benign condition, since published studies point in a totally different direction.

  8. Contrast-enhanced MRI of murine myocardial infarction - part II.

    PubMed

    Coolen, Bram F; Paulis, Leonie E M; Geelen, Tessa; Nicolay, Klaas; Strijkers, Gustav J

    2012-08-01

    Mouse models are increasingly used to study the pathophysiology of myocardial infarction in vivo. In this area, MRI has become the gold standard imaging modality, because it combines high spatial and temporal resolution functional imaging with a large variety of methods to generate soft tissue contrast. In addition, (target-specific) MRI contrast agents can be employed to visualize different processes in the cascade of events following myocardial infarction. Here, the MRI sequence has a decisive role in the detection sensitivity of a contrast agent. However, a straightforward translation of clinically available protocols for human cardiac imaging to mice is not feasible, because of the small size of the mouse heart and its extremely high heart rate. This has stimulated intense research in the development of cardiac MRI protocols specifically tuned to the mouse with regard to timing parameters, acquisition strategies, and ECG- and respiratory-triggering methods to find an optimal trade-off between sensitivity, scan time, and image quality. In this review, a detailed analysis is given of the pros and cons of different mouse cardiac MR imaging methodologies and their application in contrast-enhanced MRI of myocardial infarction. Copyright © 2012 John Wiley & Sons, Ltd.

  9. Serum irisin levels, precocious myocardial infarction, and healthy exceptional longevity.

    PubMed

    Emanuele, Enzo; Minoretti, Piercarlo; Pareja-Galeano, Helios; Sanchis-Gomar, Fabian; Garatachea, Nuria; Lucia, Alejandro

    2014-09-01

    Skeletal muscles produce irisin. Growing controversy exists on the association between this myokine and chronic disease risk. On the basis of the potential protective effects that irisin could exert on both vascular function and skeletal muscle mass, we hypothesized that an elevated level of this molecule may contribute to successful aging. Serum irisin levels were measured using enzyme-linked immunosorbent assay in disease-free centenarians, young healthy controls, and patients with precocious acute myocardial infarction. We found the highest levels of serum irisin in disease-free centenarians (35.3 ± 5.5 ng/mL) compared with young healthy controls (20.7 ± 6.3 ng/mL) and especially with young patients with acute myocardial infarction (15.1 ± 5.4 ng/mL). Our study demonstrates that healthy centenarians are characterized by increased serum irisin levels, whereas levels of this molecule were found to be significantly lower in young patients with myocardial infarction. Our findings may prompt further research into the role played by irisin not only in vascular disorders but also in life span modulation. Copyright © 2014 Elsevier Inc. All rights reserved.

  10. Multifunctional MR monitoring of the healing process after myocardial infarction.

    PubMed

    Bönner, Florian; Jacoby, Christoph; Temme, Sebastian; Borg, Nadine; Ding, Zhaoping; Schrader, Jürgen; Flögel, Ulrich

    2014-01-01

    Healing of the myocardium after infarction comprises a variety of local adaptive processes which contribute to the functional outcome after the insult. Therefore, we aimed to establish a setting for concomitant assessment of regional alterations in contractile function, morphology, and immunological state to gain prognostic information on cardiac recovery after infarction. For this, mice were subjected to myocardial ischemia/reperfusion (I/R) and monitored for 28 days by cine MRI, T2 mapping, late gadolinium enhancement (LGE), and (19)F MRI. T2 values were calculated from gated multi-echo sequences. (19)F-loaded nanoparticles were injected intravenously for labelling circulating monocytes and making them detectable by (19)F MRI. In-house developed software was used for regional analysis of cine loops, T2 maps, LGE, and (19)F images to correlate local wall movement, tissue damage as well as monocyte recruitment over up to 200 sectors covering the left ventricle. This enabled us to evaluate simultaneously zonal cardiac necrosis, oedema, and inflammation patterns together with sectional fractional shortening (FS) and global myocardial function. Oedema, indicated by a rise in T2, showed a slightly better correlation with FS than LGE. Regional T2 values increased from 19 ms to above 30 ms after I/R. In the course of the healing process oedema resolved within 28 days, while myocardial function recovered. Infiltrating monocytes could be quantitatively tracked by (19)F MRI, as validated by flow cytometry. Furthermore, (19)F MRI proved to yield valuable insight on the outcome of myocardial infarction in a transgenic mouse model. In conclusion, our approach permits a comprehensive surveillance of key processes involved in myocardial healing providing independent and complementary information for individual prognosis.

  11. Prognostic implications of cardiac scintigraphic parameters obtained in the early phase of acute myocardial infarction

    SciTech Connect

    Suzuki, A.; Matsushima, H.; Satoh, A.; Hayashi, H.; Sotobata, I.

    1988-06-01

    A cohort of 76 patients with acute myocardial infarction was studied with infarct-avid scan, radionuclide ventriculography, and thallium-201 myocardial perfusion scintigraphy. Infarct area, left ventricular ejection fraction, and defect score were calculated as radionuclide indices of the extent of myocardial infarction. The correlation was studied between these indices and cardiac events (death, congestive heart failure, postinfarction angina, and recurrence of myocardial infarction) in the first postinfarction year. High-risk patients (nonsurvivors and patients who developed heart failure) had a larger infarct area, a lower left ventricular ejection fraction, and a larger defect score than the others. Univariate linear discriminant analysis was done to determine the optimal threshold of these parameters for distinguishing high-risk patients from others. Radionuclide parameters obtained in the early phase of acute myocardial infarction were useful for detecting both patients with grave complications and those with poor late prognosis during a mean follow-up period of 2.6 years.

  12. QT dispersion and early arrhythmic risk during acute myocardial infarction.

    PubMed

    Paventi, S; Bevilacqua, U; Parafati, M A; Di Luzio, E; Rossi, F; Pelliccioni, P R

    1999-03-01

    It has been suggested that QT dispersion (maximal minus minimal QT interval calculated on a standard 12-lead electrocardiogram) could reflect regional variations of ventricular repolarization and could provide a substrate for reentry ventricular arrhythmias. The present study evaluates QT dispersion in patients with acute myocardial infarction, assessing its relation with early severe ventricular arrhythmias and some clinical features. Three hundred three patients with acute myocardial infarction and a control group of 297 healthy subjects were studied. QT and QTc dispersion were determined on the electrocardiogram taken after 12 hours and on days 3 and 10 after symptoms onset and on the electrocardiogram taken in the control group. The average values of QT and QTc dispersions (ms) were as follows: 70.5 +/- 42.5-87 +/- 45.6 (12th hour), 66.7 +/- 37.6-76.8 +/- 43.6 (day 3), 68.8 +/- 42.7-76.8 +/- 42.8 (day 10), versus 43 +/- 13.2-53.9 +/- 16.2 (control group). There were statistically significant differences between QT and QTc dispersion recorded in normal subjects and in each of the three electrocardiograms taken in patients with infarction. A greater QT dispersion was recorded in patients with anterior infarction (78.9 +/- 38.5 vs 64.9 +/- 42.8 in inferior/lateral infarction). In the first 3 days QT dispersion was not different in patients treated and untreated with thrombolysis, whereas on day 10 it was greater in untreated patients (74.9 +/- 45.3 vs 60.5 +/- 37.2). Creatine kinase peak level did not influence QT dispersion. In the first 72 hours of infarction, 37 patients developed ventricular fibrillation or sustained ventricular tachycardia. Higher early values of QT and QTc dispersion were found in patients who developed severe ventricular arrhythmias (107.8 +/- 62 and 124.8 +/- 67.5 ms) than in patients without serious arrhythmias (62.9 +/- 32.2 and 80.1 +/- 37.9 ms). These data suggest that: (1) QT dispersion increased during acute myocardial infarction. (2

  13. [Acute myocardial infarct and the kinetics of creatine kinase].

    PubMed

    Sochman, J; Fabiían, J; Englis, M; Belán, A

    1989-10-01

    The authors criticize contemporary views on creatine kinase kinetics in relation to the patency or occlusion of the coronary artery in the area of the infarction focus. In the investigation proper the time needed to achieve the peak plasma creatine kinase activity after the onset of infarction pain in patients with necroses in different areas of the left ventricle is assessed. Although the interpretation of the observed phenomenon is not clear so far, this finding makes the informative value of the hitherto used time parameter of the kinetics of this enzyme doubtful, in particular in thrombolytic treatment of myocardial infarction. In practice it is thus not possible to evaluate the restored patency of the artery to the necrotic focus on the basis of the above parameter.

  14. Relation between the kinetics of thallium-201 in myocardial scintigraphy and myocardial metabolism in patients with acute myocardial infarction

    PubMed Central

    Yamagishi, H; Akioka, K; Takagi, M; Tanaka, A; Takeuchi, K; Yoshikawa, J; Ochi, H

    1998-01-01

    Objective—To investigate the relations between myocardial metabolism and the kinetics of thallium-201 in myocardial scintigraphy.
Methods—46 patients within six weeks after the onset of acute myocardial infarction underwent resting myocardial dual isotope, single acquisition, single photon emission computed tomography (SPECT) using radioiodinated 15-iodophenyl 3-methyl pentadecaenoic acid (BMIPP) and thallium-201, exercise thallium-201 SPECT, and positron emission tomography (PET) using nitrogen-13 ammonia (NH3) and [F18]fluorodeoxyglucose (FDG) under fasting conditions. The left ventricle was divided into nine segments, and the severity of defects was assessed visually.
Results—In the resting SPECT, less BMIPP uptake than thallium-201 uptake was observed in all of 40 segments with reverse redistribution of thallium-201, and in 21 of 88 segments with a fixed defect of thallium-201 (p < 0.0001); and more FDG uptake than NH3 uptake (NH3-FDG mismatch) was observed in 35 of 40 segments with reverse redistribution and in 38 of 88 segments with fixed defect (p < 0.0001). Less BMIPP uptake in the resting SPECT was observed in 49 of 54 segments with slow stress redistribution in exercise SPECT, and in nine of 17 segments with rapid stress redistribution (p < 0.0005); NH3-FDG mismatch was observed in 42 of 54 segments with slow stress redistribution and in five of 17 segments with rapid stress redistribution (p < 0.0005).
Conclusions—Thallium-201 myocardial scintigraphy provides information about not only myocardial perfusion and viability but also about myocardial metabolism in patients with acute myocardial infarction.

 Keywords: thallium-201 SPECT;  BMIPP SPECT;  FDG PET;  myocardial infarction;  redistribution PMID:9764055

  15. Fibroblasts in myocardial infarction: a role in inflammation and repair

    PubMed Central

    Shinde, Arti V.; Frangogiannis, Nikolaos G.

    2014-01-01

    Fibroblasts do not only serve as matrix-producing reparative cells, but exhibit a wide range of functions in inflammatory and immune responses, angiogenesis and neoplasia. The adult mammalian myocardium contains abundant fibroblasts enmeshed within the interstitial and perivascular extracellular matrix. The current review manuscript discusses the dynamic phenotypic and functional alterations of cardiac fibroblasts following myocardial infarction. Extensive necrosis of cardiomyocytes in the infarcted heart triggers an intense inflammatory reaction. In the early stages of infarct healing, fibroblasts become pro-inflammatory cells, activating the inflammasome and producing cytokines, chemokines and proteases. Pro-inflammatory cytokines (such as Interleukin-1) delay myofibroblast transformation, until the wound is cleared from dead cells and matrix debris. Resolution of the inflammatory infiltrate is associated with fibroblast migration, proliferation, matrix protein synthesis and myofibroblast conversion. Growth factors and matricellular proteins play an important role in myofibroblast activation during the proliferative phase of healing. Formation of a mature cross-linked scar is associated with clearance of fibroblasts, as poorly-understood inhibitory signals restrain the fibrotic response. However, in the non-infarcted remodeling myocardium, local fibroblasts may remain activated in response to volume and pressure overload and may promote interstitial fibrosis. Considering their abundance, their crucial role in cardiac inflammation and repair, and their involvement in myocardial dysfunction and arrhythmogenesis, cardiac fibroblasts may be key therapeutic targets in cardiac remodeling. PMID:24321195

  16. The snow-shoveler's ST elevation myocardial infarction.

    PubMed

    Janardhanan, Rajesh; Henry, Zachary; Hur, David J; Lin, Christine M; Lopez, David; Reagan, Patrick M; Rudnick, Sean R; Koshko, Travis J; Keeley, Ellen C

    2010-08-15

    Heavy snowfall, cold temperatures, and low atmospheric pressure during the winter months have been associated with increased adverse cardiovascular events. However, only a few cases of the "snow shoveler's infarction" have been reported. The investigators describe their experience with 6 patients presenting with ST elevation myocardial infarctions, all within a 24-hour period during an unprecedented snowfall (4 of whom were shoveling snow), and provide a detailed review of previously reported cases of snow shoveler's infarction. Consistent with other reports, most patients reported here had the traditional cardiac risk factors of hypertension, hyperlipidemia, diabetes mellitus, tobacco use, and sedentary lifestyle. Unique to this case series, however, was that the 4 patients who had histories of coronary artery disease and previous coronary artery stenting all presented with subacute stent thromboses documented on coronary angiography performed emergently. Moreover, these patients constituted 25% of all subacute stent thromboses diagnosed in the cardiac catheterization laboratory in the preceding 12 months. In conclusion, these findings suggest that in typically sedentary individuals with cardiac risk factors or histories of coronary artery disease, snow shoveling may trigger ST elevation myocardial infarction and therefore should be avoided. This may be most critical in patients with histories of coronary stent placement, considering that these findings suggest that snow shoveling may precipitate subacute stent thrombosis.

  17. Prolonged preconditioning with natural honey against myocardial infarction injuries.

    PubMed

    Eteraf-Oskouei, Tahereh; Shaseb, Elnaz; Ghaffary, Saba; Najafi, Moslem

    2013-07-01

    Potential protective effects of prolonged preconditioning with natural honey against myocardial infarction were investigated. Male Wistar rats were pre-treated with honey (1%, 2% and 4%) for 45 days then their hearts were isolated and mounted on a Langendorff apparatus and perfused with a modified Krebs-Henseleit solution during 30 min regional ischemia fallowed by 120 min reperfusion. Two important indexes of ischemia-induced damage (infarction size and arrhythmias) were determined by computerized planimetry and ECG analysis, respectively. Honey (1% and 2%) reduced infarct size from 23±3.1% (control) to 9.7±2.4 and 9.5±2.3%, respectively (P<0.001). At the ischemia, honey (1%) significantly reduced (P<0.05) the number and duration of ventricular tachycardia (VT). Honey (1% and 2%) also significantly decreased number of ventricular ectopic beats (VEBs). In addition, incidence and duration of reversible ventricular fibrillation (Rev VF) were lowered by honey 2% (P<0.05). During reperfusion, honey produced significant reduction in the incidences of VT, total and Rev VF, duration and number of VT. The results showed cardioprotective effects of prolonged pre-treatment of rats with honey following myocardial infarction. Maybe, the existence of antioxidants and energy sources (glucose and fructose) in honey composition and improvement of hemodynamic functions may involve in those protective effects.

  18. Gemella Endocarditis Presenting as an ST-Segment-Elevation Myocardial Infarction

    PubMed Central

    Chaudhry, Sunit-Preet; Stockwell, Philip H.

    2016-01-01

    Acute myocardial infarction from septic embolization is a rare initial presentation of endocarditis. We report the case of a 67-year-old man who presented with acute chest pain, in whom emergency cardiac catheterization revealed findings that suggested coronary embolism. The patient was found to have Gemella endocarditis, with its initial presentation an embolic acute ST-segment-elevation myocardial infarction. We suggest that endocarditis be considered among the potential causes of acute myocardial infarction. PMID:27303246

  19. Regional sympathetic denervation after myocardial infarction: a follow-up study using [123I]MIBG.

    PubMed

    Podio, V; Spinnler, M T; Spandonari, T; Moretti, C; Castellano, G; Bessone, M; Brusca, A

    1995-12-01

    Previous studies in dogs have shown that experimental infarction produces myocardial sympathetic denervation not only in the infarcted area, but also in a region apical to the infarction. In these dogs MIBG myocardial scintigraphy detected denervation but returned to normal in a few months at which time reinnervation was shown to have occurred. Myocardial sympathetic denervation was studied with MIBG scintigraphy in ten patients after their first acute transmural myocardial infarction; scans were repeated at 4 months, one year and 30 months to follow the time course of possible reinnervation. Except during the first 48 hours following the infarction, no therapy except for antiaggregants was administered to the patients; during this follow-up period no cardiac events were seen. One week after infarction, comparison of MIBG images with perfusion scans revealed that the denervated area was larger than the infarcted area; no difference in MIBG uptake by the infarcted myocardium was found during the 30 months follow-up.

  20. Assessment and classification of patients with myocardial injury and infarction in clinical practice

    PubMed Central

    Chapman, Andrew R; Adamson, Philip D

    2017-01-01

    Myocardial injury is common in patients without acute coronary syndrome, and international guidelines recommend patients with myocardial infarction are classified by aetiology. The universal definition differentiates patients with myocardial infarction due to plaque rupture (type 1) from those due to myocardial oxygen supply-demand imbalance (type 2) secondary to other acute illnesses. Patients with myocardial necrosis, but no symptoms or signs of myocardial ischaemia, are classified as acute or chronic myocardial injury. This classification has not been widely adopted in practice, because the diagnostic criteria for type 2 myocardial infarction encompass a wide range of presentations, and the implications of the diagnosis are uncertain. However, both myocardial injury and type 2 myocardial infarction are common, occurring in more than one-third of all hospitalised patients. These patients have poor short-term and long-term outcomes with two-thirds dead in 5 years. The classification of patients with myocardial infarction continues to evolve, and future guidelines are likely to recognise the importance of identifying coronary artery disease in type 2 myocardial infarction. Clinicians should consider whether coronary artery disease has contributed to myocardial injury, as selected patients are likely to benefit from further investigation and in these patients targeted secondary prevention has the potential to improve outcomes. PMID:27806987

  1. Preventive effects of p-coumaric acid on lysosomal dysfunction and myocardial infarct size in experimentally induced myocardial infarction.

    PubMed

    Jyoti Roy, Abhro; Stanely Mainzen Prince, P

    2013-01-15

    The present study was designed to evaluate the preventive effects of p-coumaric acid on lysosomal dysfunction and myocardial infarct size in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated with p-coumaric acid (8 mg/kg body weight) daily for a period of 7 days after which isoproterenol (100mg/kg body weight) was injected subcutaneously into rats twice at an interval of 24h (8th and 9th day).The activity/levels of serum cardiac diagnostic markers, heart lysosomal lipid peroxidation products and the activities of lysosomal enzymes (β-glucuronidase, β-galactosidase, cathepsin-B and cathepsin-D) were significantly (P<0.05) increased in the serum and heart of isoproterenol induced myocardial infarcted rats. Isoproterenol also lowered the activities of β-glucuronidase and cathepsin-D in the lysosomal fraction. The pretreatment with p-coumaric acid significantly (P<0.05) prevented the changes in the levels of lysosomal lipid peroxidation products and the activities of lysosomal enzymes. In addition, p-coumaric acid greatly reduced myocardial infarct size. p-Coumaric acid pretreatment (8 mg/kg body weight) to normal rats did not show any significant effect. Thus, this study showed that p-coumaric acid prevents lysosomal dysfunction against cardiac damage induced by isoproterenol and brings back the levels of lipid peroxidation products and activities of lysosomal enzymes to near normal levels. The in vitro study also revealed the free radical scavenging activity of p-coumaric acid. Thus, the observed effects are due to p-coumaric acid's free radical scavenging and membrane stabilizing properties.

  2. Life Expectancy after Myocardial Infarction, According to Hospital Performance.

    PubMed

    Bucholz, Emily M; Butala, Neel M; Ma, Shuangge; Normand, Sharon-Lise T; Krumholz, Harlan M

    2016-10-06

    Thirty-day risk-standardized mortality rates after acute myocardial infarction are commonly used to evaluate and compare hospital performance. However, it is not known whether differences among hospitals in the early survival of patients with acute myocardial infarction are associated with differences in long-term survival. We analyzed data from the Cooperative Cardiovascular Project, a study of Medicare beneficiaries who were hospitalized for acute myocardial infarction between 1994 and 1996 and who had 17 years of follow-up. We grouped hospitals into five strata that were based on case-mix severity. Within each case-mix stratum, we compared life expectancy among patients admitted to high-performing hospitals with life expectancy among patients admitted to low-performing hospitals. Hospital performance was defined by quintiles of 30-day risk-standardized mortality rates. Cox proportional-hazards models were used to calculate life expectancy. The study sample included 119,735 patients with acute myocardial infarction who were admitted to 1824 hospitals. Within each case-mix stratum, survival curves of the patients admitted to hospitals in each risk-standardized mortality rate quintile separated within the first 30 days and then remained parallel over 17 years of follow-up. Estimated life expectancy declined as hospital risk-standardized mortality rate quintile increased. On average, patients treated at high-performing hospitals lived between 0.74 and 1.14 years longer, depending on hospital case mix, than patients treated at low-performing hospitals. When 30-day survivors were examined separately, there was no significant difference in unadjusted or adjusted life expectancy across hospital risk-standardized mortality rate quintiles. In this study, patients admitted to high-performing hospitals after acute myocardial infarction had longer life expectancies than patients treated in low-performing hospitals. This survival benefit occurred in the first 30 days and

  3. Atrial fibrillation, progression of coronary atherosclerosis and myocardial infarction.

    PubMed

    Bayturan, Ozgur; Puri, Rishi; Tuzcu, E Murat; Shao, Mingyuan; Wolski, Kathy; Schoenhagen, Paul; Kapadia, Samir; Nissen, Steven E; Sanders, Prashanthan; Nicholls, Stephen J

    2017-03-01

    Background Despite atrial fibrillation representing an established risk factor for stroke, the association between atrial fibrillation and both progression of coronary atherosclerosis and major adverse cardiovascular events is not well characterized. We assessed the serial measures of coronary atheroma burden and cardiovascular outcomes in patients with and without atrial fibrillation. Methods Data were analyzed from nine clinical trials involving 4966 patients with coronary artery disease undergoing serial intravascular ultrasonography at 18-24 month intervals to assess changes in percent atheroma volume (PAV). Using a propensity weighted analysis, and following adjustment for baseline variables, patients with ( n = 190) or without ( n = 4776) atrial fibrillation were compared with regard to coronary plaque volume and major adverse cardiovascular events (death, myocardial infarction, and stroke). Results Atrial fibrillation patients demonstrated lower baseline PAV (36.0 ± 8.9 vs. 38.1 ± 8.9%, p = 0.002) and less PAV progression (-0.07 ± 0.34 vs. + 0.23 ± 0.34%, p = 0.001) compared with the non-atrial fibrillation group. Multivariable analysis revealed atrial fibrillation to independently predict both myocardial infarction [HR, 2.41 (1.74,3.35), p<0.001] 2.41 (1.74, 3.35), p < 0.00) and major adverse cardiovascular events [HR, 2.2, (1.66, 2.92), p<0.001] 2.20 (1.66, 2.92), p < 0.001]. Kaplan-Meier analysis showed that atrial fibrillation compared with non-atrial fibrillation patients had a significantly higher two-year cumulative incidence of overall major adverse cardiovascular events (4.4 vs. 2.0%, log-rank p = 0.02) and myocardial infarction (3.3 vs. 1.5%, log-rank p = 0.05). Conclusions The presence of atrial fibrillation independently associates with a heightened risk of myocardial infarction despite a lower baseline burden and progression rate of coronary atheroma. Further studies are necessary to define

  4. Emergency coronary bypass grafting for evolving myocardial infarction. Effects on infarct size and left ventricular function

    SciTech Connect

    Flameng, W.; Sergeant, P.; Vanhaecke, J.; Suy, R.

    1987-07-01

    Emergency aorta-coronary bypass grafting was performed early in the course of evolving myocardial infarction in 48 patients. The time interval between the onset of symptoms and reperfusion was 169 +/- 80 minutes. Quantitative assessment of postoperative thallium 201 myocardial scans in 19 patients revealed a significant salvage of myocardium after surgical reperfusion: The size of the residual infarction was less than 50% of that in a matched, medically treated, prospective control group (n = 39) (p less than 0.05). Postoperative equilibrium-gated radionuclide blood pool studies (technetium 99m) showed an enhanced recovery of regional and global ejection fraction after operation as compared to after medical treatment (p less than 0.05). Ultrastructural evaluation of biopsy specimens obtained during the operation delineated subendocardial necrosis in the majority of cases (72%), but subepicardial necrosis was found in only 6% of instances. Q-wave abnormalities were observed on the postoperative electrocardiogram in 50% of cases. Operative mortality was 0% in low-risk patients (i.e., hemodynamically stable condition, n = 26) and 18% in high-risk patients (i.e., cardiogenic shock including total electromechanical dysfunction, n = 22). Survival rate at 18 months was 92% +/- 4%, and 95% +/- 4% of the survivors were event free. It is concluded that early surgical reperfusion of evolving myocardial infarction limits infarct size significantly, enhances functional recovery, and may be a lifesaving operation in patients having cardiogenic shock associated with unsuccessful resuscitation.

  5. [Myocardial infarction and acute coronary syndrome: definitions, classification, and diagnostic criteria].

    PubMed

    Zaĭrat'iants, O V; Mishnev, O D; Kakturskiĭ, L V

    2014-01-01

    The review gives the definitions and classification of and diagnostic criteria for myocardial infarction and acute coronary syndrome in accordance with the "The third universal definition of myocardial infarction" adopted in 2012 (Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction, 2012). It also discusses the clinical and morphological comparisons of and the problems in the differential diagnosis of myocardial infarction as a nosological entity within coronary heart disease with other coronarogenic and non-coronarogenic necroses of the myocardium.

  6. Erythrocytosis and severe asphyxia: two different causes of neonatal myocardial infarction.

    PubMed

    Caruso, Elio; Di Pino, Alfredo; Poli, Daniela; Manuri, Lucia; Guccione, Paolo

    2014-02-01

    Neonatal acute myocardial infarction is a rare event that carries a high mortality rate. We describe the cases of two newborns who survived acute myocardial infarction and discuss the management. The first neonate was born with severe asphyxia and left ventricular myocardial infarction with ventricular tachycardia. In this patient, systemic flow was maintained by right-to-left shunting through the patent ductus arteriosus. The second neonate presented with a haematocrit of 80% and an inferolateral myocardial infarction. Intensive treatment of low cardiac output syndrome led to survival of both high-risk neonates. In the follow-up, at 48 and 4 months, respectively, ventricular function recovered in both patients.

  7. Changes in red cell deformability and other haemorrheological variables after myocardial infarction.

    PubMed Central

    Dodds, A J; Boyd, M J; Allen, J; Bennett, E D; Flute, P T; Dormandy, J A

    1980-01-01

    Haemorrheological variables were studied in 43 patients after acute myocardial infarction. Red cell deformability, by a filtration method, was significantly lower within 12 hours of infarction than subsequently. This drop was greater in the presence of haemodynamic complications. Blood viscosity, particularly when adjusted to a standard haematocrit, rose in the week after infarction, as did plasma viscosity and plasma fibrinogen. Haematocrit, however, fell over this period. These changes could increase myocardial ischaemia and lead to extension of the area of infarction. PMID:7437189

  8. Role of adenosine as adjunctive therapy in acute myocardial infarction.

    PubMed

    Forman, Mervyn B; Stone, Gregg W; Jackson, Edwin K

    2006-01-01

    Although early reperfusion and maintained patency is the mainstay therapy for ST elevation myocardial infarction, experimental studies demonstrate that reperfusion per se induces deleterious effects on viable ischemic cells. Thus "myocardial reperfusion injury" may compromise the full potential of reperfusion therapy and may account for unfavorable outcomes in high-risk patients. Although the mechanisms of reperfusion injury are complex and multifactorial, neutrophil-mediated microvascular injury resulting in a progressive decrease in blood flow ("no-reflow" phenomenon) likely plays an important role. Adenosine is an endogenous nucleoside found in large quantities in myocardial and endothelial cells. It activates four well-characterized receptors producing various physiological effects that attenuate many of the proposed mechanisms of reperfusion injury. The cardio-protective effects of adenosine are supported by its role as a mediator of pre- and post-conditioning. In experimental models, administration of adenosine in the peri-reperfusion period results in a marked reduction in infarct size and improvement in ventricular function. The cardioprotective effects in the canine model have a narrow time window with the drug losing its effect following three hours of ischemia. Several small clinical studies have demonstrated that administration of adenosine with reperfusion therapy reduces infarct size and improves ventricular function. In the larger AMISTAD and AMISTAD II trials a 3-h infusion of adenosine as an adjunct to reperfusion resulted in a striking reduction in infarct size (55-65%). Post hoc analysis of AMISTAD II showed that this was associated with significantly improved early and late mortality in patients treated within 3.17 h of symptoms. An intravenous infusion of adenosine for 3 h should be considered as adjunctive therapy in high risk-patients undergoing reperfusion therapy.

  9. Surgery for Post-Myocardial Infarct Ventricular Septal Defect

    PubMed Central

    Daggett, Willard M.; Guyton, Robert A.; Mundth, Eldred D.; Buckley, Mortimer J.; McEnany, M. Terry; Gold, Herman K.; Leinbach, Robert C.; Austen, W. Gerald

    1977-01-01

    Forty-three patients (mean age 62 ± 1 years) were treated for ventricular septal defect (VSD) secondary to myocardial infarction. Whenever possible, operation was postponed until six weeks post-onset chest pain. However, hemodynamic instability, evidenced by cardiogenic shock, refractory pulmonary edema, or a rising blood urea nitrogen (BUN) forced operation in 21 patients within 21 days post-infarct (Group I). In seven patients operation was performed three to six weeks post-infarct (Group II). In only eight patients could operation be delayed beyond six weeks post-infarct (Group III). Clinical deterioration, once begun, progressed rapidly, and could be reversed only temporarily by intra-aortic balloon pumping, used in 26 patients for safe conduct of cardiac catheterization and for peri-operative hemodynamic support. Hospital survival was achieved in 24 of the 36 operated patients (66%). In Group I patients, ten of 21 survived. In Group II, six of seven survived. In Group III, eight of eight patients survived. There have been five late deaths with a mean follow-up of 41 months in survivors. Improved survival has been achieved recently by the greater use of prosthetic material to replace necrotic muscle and by a transinfarct incision regardless of infarct location. Operative mortality before 1973 was 47%; mortality after 1973 was only 18%, with a concomitant reduction of mortality (30%) even in Group I patients. ImagesFig. 7c. PMID:302110

  10. [Infarct size and left ventricular function in patients after thrombolytic therapy of acute myocardial infarct].

    PubMed

    Sochman, J; Málek, I; Ouhrabková, R; Englis, M; Fabián, J

    1989-06-01

    The authors give an account of factors which influence left ventricular function after thrombolytic treatment of an occluded coronary artery. They found that improvement of left ventricular function following a three-week interval after recanalization of the artery the occlusion of which led to myocardial infarction, depends on the size of the necrotic focus. Improvement of global left ventricular function and above all of the regional function of the infarction segment can be expected if the size of the focus is such that less than 40 gram-equivalent of total creatine kinase are liberated from it.

  11. [Return to work after myocardial infarction: evaluation and decision].

    PubMed

    Broustet, J P; Blaquière, C; Douard, H; Oysel, N; Rougier, P

    1992-11-01

    Working capacity after myocardial infarction depends on the physical and cardiovascular status, psychological repercussions and conditions of work. The latter two are much more important than the first two factors. Cardiovascular functional status is readily assessed by the large number of available investigations which leave little unknown. Exercise stress testing during the second week is the most cost-efficient investigation, providing reliable and sufficiently quantifiable data about the possible sequellae of cardiac failure on effort, ischemia and arrhythmias: an idea of the patient's functional capacity and circulatory responses (athletic, hyperkinetic) may also be obtained allowing adjustment of treatment to improve exercise capacity which goes much further than the statistical hope of prolonging survival. However, it would be naive to think that a satisfactory exercise stress test guarantees the patients' capacity to return to work. Psychological and sociological factors are more important by far. The dominant trait of the post-infarction psychological syndrome must be identified (anxiety, depression, negation): the positive and negative influences of the family, social and professional environment must be evaluated. A good knowledge of the patient's working conditions is essential to go against a number of taboos hindering the return to work (stress, stairs, restaurant meals, etc...). Finally, the medico-legal relationship between the infarct and work should not be neglected: the management of myocardial infarction when an occupational disease must respect the legislative and judicial texts which do not always correspond with everyday clinical practice. There is a lack of structures for cardiac function testing for assessing physical aptitude: we suggest that in the context of the proposed hospital reforms, departmental heads should consider setting up such units which would have a specific task respecting the spirit of these reforms. Nevertheless

  12. [Myocardial infarct morbidity among men and women in Krasnoyarsk from the viewpoint of age].

    PubMed

    Ivanov, A G

    1986-01-01

    A comparative analysis of the time course of age-related acute myocardial infarction incidence rates among men and women was based upon the results of an epidemiological study in Krasnoyarsk. Myocardial infarction incidence rates in men aged 20 to 69 (general as well as primary and secondary infarction incidence) were twice as high as in women of the same age. The time course of primary and secondary myocardial infarction incidence had common regularities. Under 60, incidence rates in men were higher than in women, over 60 just the opposite. Incidence rates in younger age groups were higher than in older age groups. No growth in the general morbidity of myocardial infarction was established in the period of the study. However its significant growth in men aged 50 to 59 ("rejuvenation" of myocardial infarction) was revealed.

  13. Myocardial Infarct Size Measurement in the Mouse Chronic Infarction Model: Comparison of Area- and Length-Based Approaches

    PubMed Central

    Takagawa, Junya; Zhang, Yan; Wong, Maelene L.; Sievers, Richard E.; Kapasi, Neel K.; Wang, Yan; Yeghiazarians, Yerem; Lee, Randall J.; Grossman, William; Springer, Matthew L.

    2009-01-01

    Efficacy of potential treatments for myocardial infarction (MI) is commonly assessed by histological measurement of infarct size in rodent models. In experiments involving an acute MI setting, measurement of the infarcted area in tissue sections of the left ventricle (LV) is a standard approach to determine infarct size. This approach has also been used in the chronic infarct setting to measure infarct area several weeks post-MI. We tested the hypothesis that due to wall thinning that is known to occur in the chronic setting, the area measurement approach would be less appropriate. We compared infarct measurements in tissue sections based on (1) infarct area, (2) epicardial and endocardial infarct arc lengths, and (3) midline infarct arc length. Infarct size from all three measurement approaches correlated significantly with LV ejection fraction (LVEF) and wall motion abnormality. However, the infarct size values derived from area measurement were significantly smaller than those from the other measurements, and the range of values obtained was compressed 0.4-fold. The midline method was able to detect the expected size differences between infarcts of variable severity resulting from proximal vs. distal ligation of the coronary artery. Segmental infarct size was correlated with segmental wall motion abnormality. We conclude that both area- and length-based measurements can determine relative infarct size over a wide range of severity but the area-based measurements are substantially more compressed due to wall thinning, and that the estimation of infarct midlines is a simple, reliable approach to infarct size assessment. PMID:17347379

  14. Work-related risk factors of myocardial infarction.

    PubMed

    Bortkiewicz, Alicja; Gadzicka, Elżbieta; Siedlecka, Jadwiga; Szyjkowska, Agata; Viebig, Piotr; Wranicz, Jerzy K; Kurpesa, Małgorzata; Dziuba, Michał; Trzos, Ewa; Makowiec-Dąbrowska, Teresa

    2010-01-01

    The aim of the study was to find out which occupational factors account for the risk of the myocardial infarction. A questionnaire survey was performed during the period of one calendar year in all patients (1053 subjects, 692 men and 361 women) hospitalized at the Medical University of Łódź because of the first myocardial infarction. The questionnaire was prepared especially for the purpose of this study and consisted of two parts. The first part comprised: demographic data, health status at admittance, traditional risk factors for the ischaemic heart disease and was filled-in by physicians. Part II was done by occupational hygiene specialists and referred to education, job title and characteristics, employment data, self assessment of work-related and general stress, fatigue, socio-economic status, physical activity, alcohol intake, tobacco smoking, dietary habits. Mean age in the study group was 59.9 ± 10.4 years (26-85 years), 58.7 ± 10.0 (26-84 years) for men and 62.3 ± 10.7 (32-85 years) for women, employment duration was 32.9±8.8 (4-65 years), for men 34.0 ± 8.6 (5-65 years), for women 30.7 ± 8.8 (4-60 years. Most of myocardial infarction cases both in the group of men and women were noted in the age interval 56-60 years, 22.3% vs. 17.4%, respectively. The majority of examined men were farmers, low and middle management and self-employed workers. Among women prevailed clerks, seamstresses and farmers. The most frequent occupational risk factors were: work-related stress, experienced by 54.2% of the examined subjects, occupational noise (45,5%), dust (41,7%) and various chemical factors (33%). A majority of the study group (76.5% women and 54.4% men) linked the cardiac infarction with stress, while 39.1% men vs. 16.5% women correlated it with physical effort. Our studies indicate that, among a wide spectrum of occupational factors, stress, noise and fine particulate dust are major contributors to the increased risk of myocardial infarction.

  15. Thallium-201 versus technetium-99m pyrophosphate myocardial imaging in detection and evaluation of patients with acute myocardial infarction

    SciTech Connect

    Pitt, B.; Thrall, J.H.

    1980-12-18

    Thallium-201 myocardial imaging is of value in the early detection and evaluation of patients with suspected acute infarction. Thallium imaging may have a special value in characterizing patients with cardiogenic shock and in detecting patients at risk for subsequent infarction or death or death or both, before hospital discharge. Approximately 95 percent of pateints with transmural or nontransmural myocardial infarction can be detected with technetium-99m pyrophosphate myocardial imaging if the imaging is performed 24 to 72 hours after the onset of symptoms. Pyrophosphate imaging may have an important role in the evaluation of patients during the early follow-up period after hospital discharge from an episode of acute infarction. The finding of a persistently positive pyrophosphate image suggests a poor prognosis and is associated with a relatively large incidence of subsequent myocardial infarction and death.

  16. Changes in IGFs in cardiac tissue following myocardial infarction.

    PubMed

    Matthews, K G; Devlin, G P; Conaglen, J V; Stuart, S P; Mervyn Aitken, W; Bass, J J

    1999-12-01

    We have studied changes in the IGF axis in an ovine model of myocardial infarction (MI), in order to determine the relationship between time-based changes in post-infarct myocardium and IGF levels. IGF localization was studied by immunocytochemistry, production by in situ hybridization, and specific binding by radioligand studies. In surviving tissue, IGF-I peptide localized to cardiomyocytes, with strongest immunostaining at 1 and 2 days post-infarct in the immediate border area adjoining the infarct, where IGF-I mRNA also increased, reaching a maximum at 2 days. Binding of radiolabelled IGF-I in surviving tissue was initially lower than that seen in cardiomyocytes in control myocardium, subsequently increasing to become significantly greater by 6 days post-infarct. In necrotic tissue, IGF-I peptide was still detectable in cardiomyocytes at 0.5 days post-infarct, but had cleared from this area by 1 day, becoming detectable again at 6 days post-infarct in macrophages and fibroblasts infiltrating the repair zone. IGF-I mRNA was not detected in necrotic tissue until 6 days, when probe hybridized to macrophages and fibroblasts. Within the necrotic zone, high levels of radiolabelled IGF-I binding to a combination of receptors and binding proteins were observed in cardiomyocytes in islands of viable tissue located close to the border. Weak immunostaining for IGF-II was observed in cardiomyocytes of the surviving tissue. IGF-II mRNA was not detected in either surviving or necrotic areas. Binding of radiolabelled IGF-II was predominantly to macrophages in both surviving and infarct areas, although as with IGF-I, high levels of binding of radiolabelled IGF-II to a combination of receptors and binding proteins were observed in islands of viable tissue close to the border within the necrotic area. We conclude that, following MI, surviving cardiomyocytes at the infarct border show marked changes in IGF-I localization, production, and specific binding, indicating that the IGF

  17. Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction

    PubMed Central

    de Couto, Geoffrey; Liu, Weixin; Tseliou, Eleni; Sun, Baiming; Makkar, Nupur; Kanazawa, Hideaki; Arditi, Moshe; Marbán, Eduardo

    2015-01-01

    Ischemic injury in the heart induces an inflammatory cascade that both repairs damage and exacerbates scar tissue formation. Cardiosphere-derived cells (CDCs) are a stem-like population that is derived ex vivo from cardiac biopsies; they confer both cardioprotection and regeneration in acute myocardial infarction (MI). While the regenerative effects of CDCs in chronic settings have been studied extensively, little is known about how CDCs confer the cardioprotective process known as cellular postconditioning. Here, we used an in vivo rat model of ischemia/reperfusion (IR) injury–induced MI and in vitro coculture assays to investigate how CDCs protect stressed cardiomyocytes. Compared with control animals, animals that received CDCs 20 minutes after IR had reduced infarct size when measured at 48 hours. CDCs modified the myocardial leukocyte population after ischemic injury. Specifically, introduction of CDCs reduced the number of CD68+ macrophages, and these CDCs secreted factors that polarized macrophages toward a distinctive cardioprotective phenotype that was not M1 or M2. Systemic depletion of macrophages with clodronate abolished CDC-mediated cardioprotection. Using both in vitro coculture assays and a rat model of adoptive transfer after IR, we determined that CDC-conditioned macrophages attenuated cardiomyocyte apoptosis and reduced infarct size, thereby recapitulating the beneficial effects of CDC therapy. Together, our data indicate that CDCs limit acute injury by polarizing an effector macrophage population within the heart. PMID:26214527

  18. L-carnitine for the treatment of acute myocardial infarction.

    PubMed

    Dinicolantonio, James J; Niazi, Asfandyar K; McCarty, Mark F; Lavie, Carl J; Liberopoulos, Evangelos; O'Keefe, James H

    2014-01-01

    Although the therapeutic strategies available for treating acute myocardial infarction (AMI) have evolved dramatically in recent decades, coronary artery disease remains the leading cause of death in our society, and the rates of recurrent myocardial infarction and mortality are still unacceptably high. Therefore, exploration of alternative therapeutic strategies for AMI is of utmost importance. One such strategy is to target metabolic pathways via L-carnitine supplementation. L-carnitine is a physiologically essential metabolic cofactor that has been shown to provide a plethora of benefits when administered after AMI. L-carnitine has been shown to lessen infarct size, to reduce ventricular arrhythmias, left ventricular dilation, and heart failure incidence, as well as improve survival. These benefits may, in part, be related to its ability to boost glucose oxidation in ischemic tissues, while moderating increases in fatty acyl-coenzyme A levels that can impair mitochondrial efficiency and promote oxidative stress and inflammation. This article summarizes the evidence pertinent to the therapeutic use of L-carnitine for AMI.

  19. Holmium:YAG laser angioplasty: treatment of acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Topaz, On

    1993-06-01

    We report our clinical experience with a group of 14 patients who presented with acute myocardial infarction. A holmium:YAG laser was applied to the infarct-related artery. This laser emits 250 - 600 mJ per pulse, with a pulse length of 250 microseconds and repetition rate of 5 Hz. Potential benefits of acute thrombolysis by lasers include the absence of systemic lytic state; a shortened thrombus clearing time relative to using thrombolytics; safe removal of the intracoronary thrombus and facilitation of adjunct balloon angioplasty. Potential clinical difficulties include targeting the obstructive clot and plaque, creation of debris and distal emboli and laser-tissue damage. It is conceivable that holmium:YAG laser can be a successful thrombolytic device as its wave length (2.1 microns) coincides with strong water absorption peaks. Since it is common to find an atherosclerotic plaque located under or distal to the thrombotic occlusion, this laser can also be applied for plaque ablation, and the patient presenting with acute myocardial infarction can clearly benefit from the combined function of this laser system.

  20. Symptom-limited maximal treadmill testing after myocardial infarction.

    PubMed

    Roberts, K C; Logan, R L

    1980-11-12

    In this paper we report our experience of routine symptom limited maximal treadmill assessment, and the methodology used with patients at the end of their convalescence after myocardial infarction. Sixty-one of 68 (90 percent) consecutive patients, mean age 55.7 years (21 to 69 years), were studied at the median time after infarction of six weeks (three to 16 weeks). No complications occurred during or after the tests. Fifty-six percent of the patients studied achieved a work capacity which was within the average range reported for healthy people of the smae age. Thirty-two percent experienced chest pain thought to be angina and 31 percent developed ST segment depression of at least 1 mm without chest pain. Although ventricular premature beats occurred in half the tests the only arrhythmia requiring any treatment was a supraventricular tachycardia. The assessment of work capacity and limiting symptoms in this way after myocardial infarction is safe and is of considerable help in patient management.

  1. Employment after myocardial infarction amongst previously healthy men.

    PubMed

    Watson, P A; Mayberry, J F; Calcraft, B; Colbourne, G

    1986-06-01

    A postal questionnaire was sent to 55 men 18 months after their first myocardial infarction; information obtained was supplemented by interview with two of the authors (PW and GC). Fifty-three men had been in full-time employment prior to their illness, 38 of them in manual work. Their return to work and changes in employment were examined and, in addition, enquiries were made about subsequent health, assistance from trade unions and the local Disabled Resettlement Officer (DRO). Details of attitude to subsequent physical exercise and sexual activity were also recorded. Eighteen months after myocardial infarction, only 35% of these men were employed and 27% asymptomatic. Patients in heavy manual work were largely unable to return to their previous job and little assistance was obtained from trade unions. Even when patients were made aware of the existence of the DRO, few approached him for advice. A counselling service is needed for patients recovering from an infarct to encourage them to return to an active and profitable life.

  2. Macrophages mediate cardioprotective cellular postconditioning in acute myocardial infarction.

    PubMed

    de Couto, Geoffrey; Liu, Weixin; Tseliou, Eleni; Sun, Baiming; Makkar, Nupur; Kanazawa, Hideaki; Arditi, Moshe; Marbán, Eduardo

    2015-08-03

    Ischemic injury in the heart induces an inflammatory cascade that both repairs damage and exacerbates scar tissue formation. Cardiosphere-derived cells (CDCs) are a stem-like population that is derived ex vivo from cardiac biopsies; they confer both cardioprotection and regeneration in acute myocardial infarction (MI). While the regenerative effects of CDCs in chronic settings have been studied extensively, little is known about how CDCs confer the cardioprotective process known as cellular postconditioning. Here, we used an in vivo rat model of ischemia/reperfusion (IR) injury-induced MI and in vitro coculture assays to investigate how CDCs protect stressed cardiomyocytes. Compared with control animals, animals that received CDCs 20 minutes after IR had reduced infarct size when measured at 48 hours. CDCs modified the myocardial leukocyte population after ischemic injury. Specifically, introduction of CDCs reduced the number of CD68+ macrophages, and these CDCs secreted factors that polarized macrophages toward a distinctive cardioprotective phenotype that was not M1 or M2. Systemic depletion of macrophages with clodronate abolished CDC-mediated cardioprotection. Using both in vitro coculture assays and a rat model of adoptive transfer after IR, we determined that CDC-conditioned macrophages attenuated cardiomyocyte apoptosis and reduced infarct size, thereby recapitulating the beneficial effects of CDC therapy. Together, our data indicate that CDCs limit acute injury by polarizing an effector macrophage population within the heart.

  3. Pesticides and myocardial infarction incidence and mortality among male pesticide applicators in the Agricultural Health Study.

    PubMed

    Mills, Katherine T; Blair, Aaron; Freeman, Laura E Beane; Sandler, Dale P; Hoppin, Jane A

    2009-10-01

    Acute organophosphate and carbamate pesticide poisonings result in adverse cardiac outcomes. The cardiac effects of chronic low-level pesticide exposure have not been studied. The authors analyzed self-reported lifetime use of pesticides reported at enrollment (1993-1997) and myocardial infarction mortality through 2006 and self-reported nonfatal myocardial infarction through 2003 among male pesticide applicators in the Agricultural Health Study. Using proportional hazard models, the authors estimated the association between lifetime use of 49 pesticides and fatal and nonfatal myocardial infarction. There were 476 deaths from myocardial infarction among 54,069 men enrolled in the study and 839 nonfatal myocardial infarctions among the 32,024 participants who completed the follow-up interview. Fatal and nonfatal myocardial infarctions were associated with commonly reported risk factors, including age and smoking. There was little evidence of an association between having used pesticides, individually or by class, and myocardial infarction mortality (e.g., insecticide hazard ratio (HR) = 0.91, 95% confidence interval (CI): 0.67, 1.24; herbicide HR = 0.74, 95% CI: 0.49, 1.10) or nonfatal myocardial infarction incidence (e.g., insecticide HR = 0.85, 95% CI: 0.66, 1.09; herbicide HR = 0.91, 95% CI: 0.61, 1.36). There was no evidence of a dose response with any pesticide measure. In a population with low risk for myocardial infarction, the authors observed little evidence of increased risk of myocardial infarction mortality or nonfatal myocardial infarction associated with the occupational use of pesticides.

  4. Altered phosphate metabolism in myocardial infarction: P-31 MR spectroscopy

    SciTech Connect

    Bottomley, P.A.; Herfkens, R.J.; Smith, L.S.; Bashore, T.M.

    1987-12-01

    The high-energy myocardial phosphate metabolism of four patients with acute anterior myocardial infarction after coronary angioplasty and drug therapy was evaluated with cardiac-gated phosphorus magnetic resonance (MR) depth-resolved surface coil spectroscopy (DRESS) 5-9 days after the onset of symptoms. Significant reductions (about threefold) in the phosphocreatine (PCr) to inorganic phosphate (Pi) ratio and elevations in the Pi to adenosine triphosphate (ATP) ratio were observed in endocardially or transmurally derived MR spectra when compared with values from epicardially displaced spectra and values from seven healthy volunteers (P less than .05). High-energy phosphate metabolites and Pi ratios did not vary significantly during the cardiac cycle in healthy volunteers. However, contamination of Pi resonances by phosphomonoester components, including blood 2,3-diphosphoglycerate, precluded accurate spectral quantification of Pi and pH. The results indicate that localized P-31 MR spectroscopy may be used to directly assess cellular energy reserve in clinical myocardial infarction and to evaluate metabolic response to interventions.

  5. Weather fronts and acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Kveton, Vit

    1991-03-01

    Some methodological aspects are discussed of the investigation of acute infarct myocarditis (AIM) in relation to weather fronts. Results of a new method of analysis are given. Data were analysed from about the hour of the onset of symptoms, and led to the diagnosis of AIM either immediately or within a few hours or days (3019 cases observed over 4.5 years during 1982 1986 in Plzen, Czechoslovakia). Weather classification was based on three factors (the type of the foregoing front, the type of the subsequent front, the time section of the time interval demarcated by the passage of the surfaces of the fronts). AIM occurrence increased in particular types of weather fronts: (i) by 30% during 7 12 h after a warm front, if the time span between fronts exceeded 24 h; (ii) by 10% in time at least 36 h distant from the foregoing cold or occlusion front and from the succeeding warm or occlusion front; (iii) by 20% during 0 2 h before the passage of the front, provided the foregoing front was not warm and the interval between fronts exceeded 5 h. AIM occurrence decreased by 15% 20% for time span between fronts > 24 h at times 6 11, 6 23 and 6 35 h before a coming warm or occlusion front (for interfrontal intervals 25 48, 49 72 and possibly > 72 h), and also at 12 23 and possibly 12 35 h before a cold front (for intervals 49 72 and possibly > 72 h), if the foregoing front was cold or an occlusion front.

  6. Assessment of Myocardial Infarction by Cardiac Magnetic Resonance Imaging and Long-Term Mortality

    PubMed Central

    Petriz, João Luiz Fernandes; Gomes, Bruno Ferraz de Oliveira; Rua, Braulio Santos; Azevedo, Clério Francisco; Hadlich, Marcelo Souza; Mussi, Henrique Thadeu Periard; Taets, Gunnar de Cunto; do Nascimento, Emília Matos; Pereira, Basílio de Bragança; e Silva, Nelson Albuquerque de Souza

    2015-01-01

    Background Cardiac magnetic resonance imaging provides detailed anatomical information on infarction. However, few studies have investigated the association of these data with mortality after acute myocardial infarction. Objective To study the association between data regarding infarct size and anatomy, as obtained from cardiac magnetic resonance imaging after acute myocardial infarction, and long-term mortality. Methods A total of 1959 reports of “infarct size” were identified in 7119 cardiac magnetic resonance imaging studies, of which 420 had clinical and laboratory confirmation of previous myocardial infarction. The variables studied were the classic risk factors – left ventricular ejection fraction, categorized ventricular function, and location of acute myocardial infarction. Infarct size and acute myocardial infarction extent and transmurality were analyzed alone and together, using the variable named “MET-AMI”. The statistical analysis was carried out using the elastic net regularization, with the Cox model and survival trees. Results The mean age was 62.3 ± 12 years, and 77.3% were males. During the mean follow-up of 6.4 ± 2.9 years, there were 76 deaths (18.1%). Serum creatinine, diabetes mellitus and previous myocardial infarction were independently associated with mortality. Age was the main explanatory factor. The cardiac magnetic resonance imaging variables independently associated with mortality were transmurality of acute myocardial infarction (p = 0.047), ventricular dysfunction (p = 0.0005) and infarcted size (p = 0.0005); the latter was the main explanatory variable for ischemic heart disease death. The MET-AMI variable was the most strongly associated with risk of ischemic heart disease death (HR: 16.04; 95%CI: 2.64-97.5; p = 0.003). Conclusion The anatomical data of infarction, obtained from cardiac magnetic resonance imaging after acute myocardial infarction, were independently associated with long-term mortality, especially for

  7. Prehospital care pathway delays: gender and myocardial infarction.

    PubMed

    O'Donnell, Sharon; Condell, Sarah; Begley, Cecily; Fitzgerald, Tony

    2006-02-01

    This paper reports the findings of a study that identified gender specific prehospital care pathway delays amongst Irish women and men with myocardial infarction. Women are more likely to experience a poorer prognosis than their male counterparts following hospitalization for myocardial infarction, yet research shows that women continue to experience prehospital care pathway delays. A 1-year prospective census was carried in six major academic teaching hospitals in Dublin, Ireland in 2001-2002. A total of 277 (31%) female and 613 (69%) male patients with confirmed myocardial infarction were included in the study. Women were more likely to experience prolonged 'initial symptom-onset to A&E delays' (14 hours vs. 2.8 hours P < 0.0001), and 'intense symptom-onset to A&E delays' (3.1 hours vs. 1.8 hours , P < 0.0001), i.e. arrival at a hospital accident and emergency department. Advancing age was associated with greater prehospital delays (P < 0.0001), whilst patients with private health insurance had shorter delays than public patients (without private health insurance) or those with medical cards (entitling them to means-tested medical benefits) (P = 0.001). Patients who drove themselves by car to hospital had shorter median prehospital times than those arriving by any other admission mode (P < 0.0001), whilst those referred by their general practitioner had longer delays than those who were self-referred (5 hours vs. 1.7 hours, P < 0.0001). Female gender, advancing age, referral source, insurance status and mode of transport to hospital are independent factors contributing to prehospital patient delays. Nurses who care for patients with coronary artery disease have a unique opportunity to educate people about the most appropriate action to be taken in the event of experiencing symptoms.

  8. Apelin modulates pathological remodeling of lymphatic endothelium after myocardial infarction

    PubMed Central

    Renaud-Gabardos, Edith; Godet, Anne-Claire; Hantelys, Fransky; Pujol, Francoise; Calise, Denis; Viars, Fanny; Valet, Philippe; Masri, Bernard; Prats, Anne-Catherine; Garmy-Susini, Barbara

    2017-01-01

    Lymphatic endothelium serves as a barrier to control fluid balance and immune cell trafficking to maintain tissue homeostasis. Long-term alteration of lymphatic vasculature promotes edema and fibrosis, which is an aggravating factor in the onset of cardiovascular diseases such as myocardial infarction. Apelin is a bioactive peptide that plays a central role in angiogenesis and cardiac contractility. Despite an established role of apelin in lymphangiogenesis, little is known about its function in the cardiac lymphatic endothelium. Here, we show that apelin and its receptor APJ were exclusively expressed on newly formed lymphatic vasculature in a pathological model of myocardial infarction. Using an apelin-knockout mouse model, we identified morphological and functional defects in lymphatic vasculature associated with a proinflammatory status. Surprisingly, apelin deficiency increased the expression of lymphangiogenic growth factors VEGF-C and VEGF-D and exacerbated lymphangiogenesis after myocardial infarction. Conversely, the overexpression of apelin in ischemic heart was sufficient to restore a functional lymphatic vasculature and to reduce matrix remodeling and inflammation. In vitro, the expression of apelin prevented the alteration of cellular junctions in lymphatic endothelial cells induced by hypoxia. In addition, we demonstrated that apelin controls the secretion of the lipid mediator sphingosine-1-phosphate in lymphatic endothelial cells by regulating the level of expression of sphingosine kinase 2 and the transporter SPNS2. Taken together, our results show that apelin plays a key role in lymphatic vessel maturation and stability in pathological settings. Thus, apelin may represent a novel candidate to prevent pathological lymphatic remodeling in diseases. PMID:28614788

  9. Apelin modulates pathological remodeling of lymphatic endothelium after myocardial infarction.

    PubMed

    Tatin, Florence; Renaud-Gabardos, Edith; Godet, Anne-Claire; Hantelys, Fransky; Pujol, Francoise; Morfoisse, Florent; Calise, Denis; Viars, Fanny; Valet, Philippe; Masri, Bernard; Prats, Anne-Catherine; Garmy-Susini, Barbara

    2017-06-15

    Lymphatic endothelium serves as a barrier to control fluid balance and immune cell trafficking to maintain tissue homeostasis. Long-term alteration of lymphatic vasculature promotes edema and fibrosis, which is an aggravating factor in the onset of cardiovascular diseases such as myocardial infarction. Apelin is a bioactive peptide that plays a central role in angiogenesis and cardiac contractility. Despite an established role of apelin in lymphangiogenesis, little is known about its function in the cardiac lymphatic endothelium. Here, we show that apelin and its receptor APJ were exclusively expressed on newly formed lymphatic vasculature in a pathological model of myocardial infarction. Using an apelin-knockout mouse model, we identified morphological and functional defects in lymphatic vasculature associated with a proinflammatory status. Surprisingly, apelin deficiency increased the expression of lymphangiogenic growth factors VEGF-C and VEGF-D and exacerbated lymphangiogenesis after myocardial infarction. Conversely, the overexpression of apelin in ischemic heart was sufficient to restore a functional lymphatic vasculature and to reduce matrix remodeling and inflammation. In vitro, the expression of apelin prevented the alteration of cellular junctions in lymphatic endothelial cells induced by hypoxia. In addition, we demonstrated that apelin controls the secretion of the lipid mediator sphingosine-1-phosphate in lymphatic endothelial cells by regulating the level of expression of sphingosine kinase 2 and the transporter SPNS2. Taken together, our results show that apelin plays a key role in lymphatic vessel maturation and stability in pathological settings. Thus, apelin may represent a novel candidate to prevent pathological lymphatic remodeling in diseases.

  10. Relation Between Myocardial Infarction Deaths and Solar Activity in Mexico

    NASA Astrophysics Data System (ADS)

    Diaz-Sandoval, R.

    2002-05-01

    We study the daily incidence of myocardial infarction deaths in Mexico for 4 years (1996-99) with a total of 129 917 cases in all the country, collected at the General Directorate of Epidemiology (National Ministry of Health). We divided the cases by sex and age and perform two kinds of analysis. First, we did an spectral analysis using the Maximum Entropy Method, considering the complete period, and minimum and maximum epochs of solar activity. The results show that the most persistent periodicity at higher frequencies in the myocardial infarction death occurrence is that of seven days. Considering the solar cycle phases, we found that during solar minimum times some frequencies are not detectable compared with solar maximum epochs, particularly that of seven days. Biological rhythms close to seven days, the circaseptans, are in general thought to be only the result of the social organization of life. However, this cannot be the only explanation, because the 7-days periodicity has been encountered in lower organisms not related with our rhythms of life. Thus, it has been proposed that biological rhythms could be evolutionary adaptations to environmental conditions, particularly, solar activity. In the second analysis we compared two solar activity-related phenomena: the Forbush decreases of cosmic rays and the geomagnetic index Ap for various levels of geomagnetic perturbations. The results show that during decreases of cosmic ray fluxes, for most cases there is a higher average myocardial infarction deaths occurrence, compared with the average incidence in days of no decreases. For geomagnetic activity we find the same situation in most cases. Furthermore, this behavior is more pronounced as the level of the perturbation increases and in times of maximum solar activity.

  11. Telemedicine for post-myocardial infarction patients: an observational study.

    PubMed

    Roth, Arie; Malov, Nomi; Steinberg, David M; Yanay, Yigal; Elizur, Mayera; Tamari, Mira; Golovner, Michal

    2009-01-01

    "SHL" Telemedicine (established 1987 in Israel) provides professional care to subscribers who use cardiobeepers and contact its medical call center via telecommunication networks. The extended 6-month Acute Coronary Syndrome Israel Survey (ACSIS) 2004 involved all 26 intensive cardiac care units in Israeli hospitals. We compared the 1-year survival rates of the "SHL" Telemedicine subscribers and ACSIS participants who survived hospitalization after sustaining an acute myocardial infarction. The myocardial infarction data for the ACSIS cohort (3,899 patients) and the SHL Telemedicine cohort (699 subscribers) were provided for this study by the ACSIS executive and SHL's files, respectively. One-year mortality was ascertained by telephone contacts with patients or their relatives. Mortality at 1 year was 4.4% for the "SHL" patients and 9.7% for the ACSIS patients (p < 0.0001). The "SHL" cohort was significantly older (p < 0.0001) than the ACSIS cohort (mean age [+/-SD] 69 +/- 11 versus 63 +/- 13 years), had significantly more past myocardial infarctions (p < 0.001), more past strokes (p < 0.0032), more heart failure (p < 0.0001), more hypertension (p = 0.002), and more hyperlipidemia (p < 0.0001). Gender distribution and diabetes status were similar for both groups. In spite of having more risk factors than the ACSIS subjects, the "SHL" Telemedicine subscribers had significantly higher survival rates at 1 year compared to the ACSIS patients, whose outcome is consistent with that of the Western world. Availability of medical call centers in the out-of-hospital setting for patients with suspected cardiac symptoms improves their motivation to seek timely and appropriate medical assistance.

  12. Body Mass Index and Mortality in Acute Myocardial Infarction Patients

    PubMed Central

    Bucholz, Emily M.; Rathore, Saif S.; Reid, Kimberly J.; Jones, Philip G.; Chan, Paul S.; Rich, Michael W.; Spertus, John A.; Krumholz, Harlan M.

    2012-01-01

    Background Previous studies have described an “obesity paradox” with heart failure, whereby higher body mass index (BMI) is associated with lower mortality. However, little is known about the impact of obesity on survival after acute myocardial infarction. Methods Data from 2 registries of patients hospitalized in the United States with acute myocardial infarction between 2003–04 (PREMIER) and 2005–08 (TRIUMPH) were used to examine the association of BMI with mortality. Patients (n=6359) were categorized into BMI groups (kg/m2) using baseline measurements. Two sets of analyses were performed using Cox proportional hazards regression with fractional polynomials to model BMI as categorical and continuous variables. To assess the independent association of BMI with mortality, analyses were repeated adjusting for 7 domains of patient and clinical characteristics. Results Median BMI was 28.6. BMI was inversely associated with crude 1-year mortality (normal, 9.2%; overweight, 6.1%; obese, 4.7%; morbidly obese; 4.6%; p<0.001), which persisted after multivariable adjustment. When BMI was examined as a continuous variable, the hazards curve declined with increasing BMI and then increased above a BMI of 40. Compared with patients with a BMI of 18.5, patients with higher BMIs had a 20% to 68% lower mortality at 1 year. No interactions between age (p=0.37), gender (p=0.87) or diabetes mellitus (p=0.55) were observed. Conclusions There appears to be an “obesity paradox” among acute myocardial infarction patients such that higher BMI is associated with lower mortality, an effect that was not modified by patient characteristics and was comparable across age, gender, and diabetes subgroups. PMID:22483510

  13. Extracellular Matrix and Fibroblast Communication Following Myocardial Infarction

    PubMed Central

    Ma, Yonggang; Halade, Ganesh V.; Lindsey, Merry L.

    2012-01-01

    The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion, and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing. PMID:22926488

  14. The immediate antecedents of myocardial infarction in active men

    PubMed Central

    Kavanagh, T.; Shephard, R. J.

    1973-01-01

    The antecedents of myocardial infarction have been reviewed in 102 patients (117 episodes) undergoing a program of rehabilitation. The year prior to the first attack was characterized by business and social problems, with some weight gain; in the week before the attach there was added tiredness, poor general health and, in some cases, increasing anginal pain. Heavy lifting and/or unusual exercise were common immediately before or during an attack; five attacks were related to the shovelling of wet snow. Both bed and the normal place of work were uncommon sites for an attack. More than 50% of patients had 30 minutes' warning of infarction. The relevance of these findings to a safe program of therapeutic exercise is discussed. PMID:4717086

  15. Myocardial infarction and intramyocardial injection models in swine.

    PubMed

    McCall, Frederic C; Telukuntla, Kartik S; Karantalis, Vasileios; Suncion, Viky Y; Heldman, Alan W; Mushtaq, Muzammil; Williams, Adam R; Hare, Joshua M

    2012-07-12

    Sustainable and reproducible large animal models that closely replicate the clinical sequelae of myocardial infarction (MI) are important for the translation of basic science research into bedside medicine. Swine are well accepted by the scientific community for cardiovascular research, and they represent an established animal model for preclinical trials for US Food and Drug Administration (FDA) approval of novel therapies. Here we present a protocol for using porcine models of MI created with a closed-chest coronary artery occlusion-reperfusion technique. This creates a model of MI encompassing the anteroapical, lateral and septal walls of the left ventricle. This model infarction can be easily adapted to suit individual study design and enables the investigation of a variety of possible interventions. This model is therefore a useful tool for translational research into the pathophysiology of ventricular remodeling and is an ideal testing platform for novel biological approaches targeting regenerative medicine. This model can be created in approximately 8-10 h.

  16. Evaluation and simplified measurement of infarct size by myocardial contrast echocardiography in a rat model of myocardial infarction.

    PubMed

    Chen, Xianghui; Cui, Kai; Xiu, Jiancheng; Lin, Huanbing; Lao, Yi; Zhou, Biying; Liang, Feixue; Zha, Daogang; Bin, Jianping; Liu, Yili

    2009-10-01

    To test the feasibility and accuracy of myocardial contrast echocardiography (MCE) for predicting infarct size (IS) in a rat model of myocardial infarction (MI) and to compare a simplified single plane-based measurement of IS with the conventional three plane-based approach. Fifty male SD rats underwent left anterior descending artery ligation and were evaluated by MCE 8 h post MI. IS was calculated by the single and three plane-based approaches, compared to that determined by triphenyltetrazolium chloride (TTC) staining method. Simplified single plane-based MCE approach and TTC method showed similar IS values (38.48 +/- 16.80% vs. 35.72 +/- 15.33%, P > 0.05) and presented a favorable positive correlation (r = 0.851, P < 0.001). IS values derived from simplified single plane-based approach was also highly significantly correlated with that by the conventional MCE method (r = 0.973, P < 0.001). Bland-Altman plots also displayed satisfactory agreement between them. MCE was validated as a novel technique to quantify infarct area in rats with MI. A single measurement at the mid-papillary muscle level may become a simple, efficient and reliable approach for in vivo IS assessment.

  17. A novel, minimally invasive, segmental myocardial infarction with a clear healed infarct borderzone in rabbits.

    PubMed

    Ziv, Ohad; Schofield, Lorraine; Lau, Emily; Chaves, Lenny; Patel, Divyang; Jeng, Paul; Peng, Xuwen; Choi, Bum-Rak; Koren, Gideon

    2012-06-01

    Ventricular arrhythmias in the setting of a healed myocardial infarction have been studied to a much lesser degree than acute and subacute infarction, due to the pericardial scarring, which results from the traditional open-chest techniques used for myocardial infarction (MI) induction. We sought to develop a segmental MI with low perioperative mortality in the rabbit that allows optimal visualization and therefore improved study of the infarction borderzone. Rabbits underwent MI using endovascular coil occlusion of the first obtuse marginal artery. Three weeks postprocedure, we evaluated our model by echocardiography and electrophysiology studies, optical mapping of isolated hearts, and histological studies. Seventeen rabbits underwent the protocol (12 MI and 5 sham) with a 92% survival to completion of the study (11 MI and 5 sham). MI rabbits demonstrated wall motion abnormalities on echocardiography while shams did not. At electrophysiological study, two MI rabbits had inducible ventricular tachycardia and one had inducible ventricular fibrillation. Isolated hearts demonstrated no pericardial scarring with a smooth, easily identifiable infarct borderzone. Optical mapping of the borderzone region showed successful mapping of peri-infarct reentry formation, with ventricular fibrillation inducible in 11 of 11 MI hearts and 1 of 5 sham hearts. We demonstrate successful high resolution mapping in the borderzone, showing delayed conduction in this region corresponding to late deflections in the QRS on ECG. We report the successful development of a minimally invasive MI via targeted coil delivery to the obtuse marginal artery with an exceptionally high rate of procedural survival and an arrhythmogenic phenotype. This model mimics human post-MI on echocardiography, gross pathology, histology, and electrophysiology.

  18. Multiscale Characterization of Impact of Infarct Size on Myocardial Remodeling in an Ovine Infarct Model.

    PubMed

    Zhang, Pei; Li, Tielou; Griffith, Bartley P; Wu, Zhongjun J

    2015-01-01

    The surviving myocardium initially compensates the loss of injured myocardium after myocardial infarction (MI) and gradually becomes progressively dysfunctional. There have been limited studies on the effect of infarct size on temporal and spatial alterations in the myocardium during progressive myocardial remodeling. MI with three infarct sizes, i.e. 15, 25 and 35% of the left ventricular (LV) wall, was created in an ovine infarction model. The progressive LV remodeling over a 12-week period was studied. Echocardiography, sonomicrometry, and histological and molecular analyses were carried out to evaluate cardiac function, regional tissue contractile function, structural remodeling and cardiomyocyte hypertrophy, and calcium handling proteins. Twelve weeks after MI, the 15, 25 and 35% MI groups had normalized LV end diastole volumes of 1.4 ± 0.2, 1.7 ± 0.3 and 2.0 ± 0.4 ml/kg, normalized end systole volumes of 1.0 ± 0.1, 1.0 ± 0.2 and 1.3 ± 0.3 ml/kg and LV ejection fractions of 43 ± 3, 42 ± 6 and 34 ± 4%, respectively. They all differed from the sham group (p < 0.05). All the three MI groups exhibited larger wall areal expansion (remodeling strain), larger cardiomyocyte size and altered expression of calcium handing proteins in the adjacent myocardium compared to the remote counterpart from the infarct. A significant correlation was found between cardiomyocyte size and remodeling strain in the adjacent zone. A comparative analysis among the three MI groups showed that a larger infarct size (35 vs. 15% MI) was associated with larger remodeling strain, more serious impairment in the cellular structure and composition, and regional contractile function at regional tissue level and LV function at organ level.

  19. Studies on the Na+-K+-ATPase in myocardial infarction.

    PubMed

    Kobayashi, Y; Sasai, Y; Nakamura, N; Katagiri, T

    1981-11-01

    Changes in the cardiac sarcolemma in myocardial infarction were studied by both determination of Na+-K+-ATPase activity and SDS gel electrophoretic analysis of sarcolemmal proteins in the canine heart. Ninety minutes after coronary ligation, Na+-K+-ATPase activity in ischemic myocardium was decreased significantly to approximately 36% of that of non-ischemic myocardium, and it remained at the lower level for 28 days. By SDS gel electrophoresis, reduction of the protein band with molecular weight of 111,000, which is suggestive of the main component of ATPase, was observed simultaneously with the reduction of Na+-K+-ATPase activity. These results indicate that ischemia for 90 minutes produces substructural changes in the sarcolemma indicating irreversible myocardial changes.

  20. Unusual mechanism of myocardial infarction in prosthetic valve endocarditis

    PubMed Central

    Atik, Fernando A; Campos, Vanessa G; da Cunha, Claudio R; de Oliveira, Felipe Bezerra Martins; Otto, Maria Estefânia Bosco; Monte, Guilherme U

    2015-01-01

    A 46-year-old man with bicuspid aortic valve and severe calcific aortic stenosis was submitted to aortic valve replacement with a stented bioprosthesis. He developed Staphylococcus epidermidis prosthetic valve endocarditis a month later, presenting in the emergency room with acute myocardial infarction. The mechanism of myocardial ischemia was a large aortic root abscess causing left main extrinsic compression. He was urgently taken to the operating room, and an aortic root replacement with cryopreserved homograft was performed, associated with autologous pericardium patch closure of aortic to right atrium fistula and coronary artery bypass grafting of the left anterior descending. After a difficult postoperative period with multiple problems, he was eventually discharged home. At 36-month follow-up, he is asymptomatic with no recurrent infection, and the left main coronary artery is widely patent on control chest computed tomography. PMID:26045678

  1. Structural racism and myocardial infarction in the United States.

    PubMed

    Lukachko, Alicia; Hatzenbuehler, Mark L; Keyes, Katherine M

    2014-02-01

    There is a growing research literature suggesting that racism is an important risk factor undermining the health of Blacks in the United States. Racism can take many forms, ranging from interpersonal interactions to institutional/structural conditions and practices. Existing research, however, tends to focus on individual forms of racial discrimination using self-report measures. Far less attention has been paid to whether structural racism may disadvantage the health of Blacks in the United States. The current study addresses gaps in the existing research by using novel measures of structural racism and by explicitly testing the hypothesis that structural racism is a risk factor for myocardial infarction among Blacks in the United States. State-level indicators of structural racism included four domains: (1) political participation; (2) employment and job status; (3) educational attainment; and (4) judicial treatment. State-level racial disparities across these domains were proposed to represent the systematic exclusion of Blacks from resources and mobility in society. Data on past-year myocardial infarction were obtained from the National Epidemiologic Survey on Alcohol and Related Conditions (non-Hispanic Black: N = 8245; non-Hispanic White: N = 24,507), a nationally representative survey of the U.S. civilian, non-institutionalized population aged 18 and older. Models were adjusted for individual-level confounders (age, sex, education, household income, medical insurance) as well as for state-level disparities in poverty. Results indicated that Blacks living in states with high levels of structural racism were generally more likely to report past-year myocardial infarction than Blacks living in low-structural racism states. Conversely, Whites living in high structural racism states experienced null or lower odds of myocardial infarction compared to Whites living in low-structural racism states. These results raise the provocative possibility that structural

  2. The Role of Unknown Risk Factors in Myocardial Infarction

    PubMed Central

    Ali, Rafighdoust Abbas; Asadollah, Mirzaee; Hossien, Rafigdoust Amir

    2010-01-01

    Background Atherosclerosis of coronary arteries is the most common cause of myocardial infarction (MI), which is initiated from childhood and progresses gradually by aging. Several risk factors influence its progress, and are categorized as classic, traditional and novel factors. The role of unknown risk factors is becoming increasingly more significant recently. The aim of this study is to underscore the novel risk factors despite the importance of classic factors and consider these factors for future studies. Methods This is a prospective study on 180 myocardial infarction cases, conducted in the cardiology ward and CCU of Imam-Reza hospital (Mashad-IRAN). A number of risk factors identified and evaluated in these patients included: hyperlipidemia, hypertension, diabetes, smoking, activity, stress, hair of external ear canal and ear lobe crease, age, and sex. Then patients without any risk factor or with one or two risk factors were distinguished. Results The majority of our patients were old men in the age range of 60 - 69 years. Amongst all patients 42.2% were smokers, 68.3% were type A personality group, 19% were active, 81% were physically inactive, 37.2% had hairy ear canal, 35% had hypertension, 21.1% were diabetic, 14.4% had hyperlipidemia and 30% had positive family history of myocardial infarction. Of great interest was the fact that of the patients whose case was studied, many did not have any risk factor or in some cases had only one. Conclusions In regard of increasing rate of cardiovascular diseases and myocardial infarction even amongst the young population, and because of considerable need to improve vascular risk detection, much research over the past decade has focused on identification of novel atherosclerotic risk factors, and some of these new risk factors are identified and some may be unknown. Amongst the new risk factors, inflammation has an important role, other risk factors that must be assessed are homocysteine, serum amyloid, and

  3. Acute myocarditis triggering coronary spasm and mimicking acute myocardial infarction

    PubMed Central

    Kumar, Andreas; Bagur, Rodrigo; Béliveau, Patrick; Potvin, Jean-Michel; Levesque, Pierre; Fillion, Nancy; Tremblay, Benoit; Larose, Éric; Gaudreault, Valérie

    2014-01-01

    A 24-year-old healthy man consulted to our center because of typical on-and-off chest-pain and an electrocardiogram showing ST-segment elevation in inferior leads. An urgent coronary angiography showed angiographically normal coronary arteries. Cardiovascular magnetic resonance imaging confirmed acute myocarditis. Although acute myocarditis triggering coronary spasm is an uncommon association, it is important to recognize it, particularly for the management for those patients presenting with ST-segment elevation and suspect myocardial infarction and angiographically normal coronary arteries. The present report highlights the role of cardiovascular magnetic resonance imaging to identify acute myocarditis as the underlying cause. PMID:25276306

  4. Acute myocarditis triggering coronary spasm and mimicking acute myocardial infarction.

    PubMed

    Kumar, Andreas; Bagur, Rodrigo; Béliveau, Patrick; Potvin, Jean-Michel; Levesque, Pierre; Fillion, Nancy; Tremblay, Benoit; Larose, Eric; Gaudreault, Valérie

    2014-09-26

    A 24-year-old healthy man consulted to our center because of typical on-and-off chest-pain and an electrocardiogram showing ST-segment elevation in inferior leads. An urgent coronary angiography showed angiographically normal coronary arteries. Cardiovascular magnetic resonance imaging confirmed acute myocarditis. Although acute myocarditis triggering coronary spasm is an uncommon association, it is important to recognize it, particularly for the management for those patients presenting with ST-segment elevation and suspect myocardial infarction and angiographically normal coronary arteries. The present report highlights the role of cardiovascular magnetic resonance imaging to identify acute myocarditis as the underlying cause.

  5. Discharge heart rate and mortality after acute myocardial infarction.

    PubMed

    Seronde, Marie France; Geha, Raghed; Puymirat, Etienne; Chaib, Aurès; Simon, Tabassome; Berard, Laurence; Drouet, Elodie; Bataille, Vincent; Danchin, Nicolas; Schiele, François

    2014-10-01

    We aimed to describe the determinants of discharge heart rate in acute coronary syndrome patients and assess the impact of discharge heart rate on 5-year mortality in hospital survivors. French Registry of Acute ST-Elevation or non-ST-elevation Myocardial Infarction (FAST-MI) 2005 is a nationwide French registry that included all consecutive patients with acute myocardial infarction over 1 month in 223 institutions in 2005. Discharge heart rate was recorded in 3079 patients discharged alive; all had 5-year follow-up. Logistic regression was used to detect predictors of high heart rate at discharge. Cox's proportional hazards model was used to assess the hazard ratio for mortality at 5 years. Heart rate was categorized into 4 groups by quartiles (<60, 61-67, 68-75, >75 beats per minute). High heart rate was defined as ≥75 beats per minute. Landmark analysis was performed at 1 year. Independent predictors of heart rate ≥75 beats per minute at discharge were female sex, ST-segment elevation myocardial infarction, diabetes, chronic obstructive pulmonary disease, bleeding/transfusion during hospitalization, left ventricular dysfunction, renal dysfunction, and prescription (type, but not dose category) of beta-blockers at discharge. Discharge heart rate was significantly related to mortality at 1 year (hazard ratio 1.13; 95% confidence interval, 1.03-1.24 per 10 beats per minute, P = .02); this was confirmed by landmark analysis, with a 39% increase (hazard ratio 1.39; 95% confidence interval 1.05-1.84) in the risk of 1-year death for discharge heart rate ≥75 beats per minute vs <75 beats per minute. This relationship was no longer significant between 2 and 5 years. After acute myocardial infarction, patients discharged with high heart rate (≥75 beats per minute) are at higher risk of death during the first year, but not later, irrespective of beta-blocker use. Copyright © 2014 Elsevier Inc. All rights reserved.

  6. [Myocardial infarction and anabolic steroid use. A case report].

    PubMed

    Godon, P; Bonnefoy, E; Guérard, S; Munet, M; Velon, S; Brion, R; Touboul, P

    2000-07-01

    The potential cardiotoxicity of anabolic steroids is not well known. The authors report the case of a young man who was a top class body builder and who developed severe ischaemic cardiomyopathy presenting with an inferior wall myocardial infarction. The clinical history revealed prolonged and intensive usage of two types of anabolic steroids to be the only risk factor. This cardiotoxicity may be related to several physiopathological mechanisms: accelerated atherogenesis by lipid changes, increased platelet aggregation, coronary spasm or a direct toxic effect on the myocytes. The apparent scarcity of the reported clinical details in the literature is probably an underestimation of the consequences of this usage.

  7. Chameleons: Electrocardiogram Imitators of ST-Segment Elevation Myocardial Infarction.

    PubMed

    Nable, Jose V; Lawner, Benjamin J

    2015-08-01

    The imperative for timely reperfusion therapy for patients presenting with ST-segment elevation myocardial infarction (STEMI) underscores the need for clinicians to have an understanding of how to distinguish patterns of STEMI from its imitators. These imitating diagnoses may confound an evaluation, potentially delaying necessary therapy. Although numerous diagnoses may mimic STEMI, several morphologic clues may allow the physician to determine if the pattern is concerning for either STEMI or a mimicking diagnosis. Furthermore, obtaining a satisfactory history, comparing previous electrocardiograms, and assessing serial tests may provide valuable clues.

  8. Subarachnoid haemorrhage mimicking transient ST-segment elevation myocardial infarction.

    PubMed

    Lai, C-H; Juan, Y-H; Chang, S-L; Lee, W-L; How, C-K; Hsu, T-F

    2015-08-01

    Patients often present to the emergency department with loss of consciousness. The differential diagnosis of such condition may be difficult because of limited clinical information. The authors present a case of subarachnoid haemorrhage (SAH) with initial electrocardiographic (ECG) finding mimicking ST-segment elevation myocardial infarction (STEMI), which was confirmed to resolve in a follow-up study. Accurate and timely diagnosis of SAH-related ST-segment elevation was important, as the therapeutic strategy for SAH is completely different from that for STEMI. If the clinicians do not have other tools for diagnosis, the follow-up ECG may help us make a most possible diagnosis.

  9. Protective effects of sinapic acid on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats.

    PubMed

    Roy, Subhro Jyoti; Stanely Mainzen Prince, Ponnian

    2012-11-01

    In the pathology of myocardial infarction, lysosomal lipid peroxidation and resulting enzyme release play an important role. We evaluated the protective effects of sinapic acid on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats. Male Wistar rats were treated with sinapic acid (12 mg/kg body weight) orally daily for 10 days and isoproterenol (100 mg/kg body weight) was injected twice at an interval of 24 h (9th and 10th day). Then, lysosomal lipid peroxidation, lysosomal enzymes in serum, heart homogenate, lysosomal fraction and myocardial infarct size were measured. Isoproterenol induced myocardial infarcted rats showed a significant increase in serum creatine kinase-MB and lysosomal lipid peroxidation. The activities of β-glucuronidase, β-galactosidase, cathepsin-B and D were significantly increased in serum, heart and the activities of β-glucuronidase and cathepsin-D were significantly decreased in lysosomal fraction of myocardial infarcted rats. Pre-and-co-treatment with sinapic acid normalized all the biochemical parameters and reduced myocardial infarct size in myocardial infarcted rats. In vitro studies confirmed the free radical scavenging effects of sinapic acid. The possible mechanisms for the observed effects are attributed to sinapic acid's free radical scavenging and membrane stabilizing properties. Thus, sinapic acid has protective effects on lysosomal dysfunction in isoproterenol induced myocardial infarcted rats.

  10. The Chinese version of the Myocardial Infarction Dimensional Assessment Scale (MIDAS): Mokken scaling

    PubMed Central

    2012-01-01

    Background Hierarchical scales are very useful in clinical practice due to their ability to discriminate precisely between individuals, and the original English version of the Myocardial Infarction Dimensional Assessment Scale has been shown to contain a hierarchy of items. The purpose of this study was to analyse a Mandarin Chinese translation of the Myocardial Infarction Dimensional Assessment Scale for a hierarchy of items according to the criteria of Mokken scaling. Data from 180 Chinese participants who completed the Chinese translation of the Myocardial Infarction Dimensional Assessment Scale were analysed using the Mokken Scaling Procedure and the 'R' statistical programme using the diagnostics available in these programmes. Correlation between Mandarin Chinese items and a Chinese translation of the Short Form (36) Health Survey was also analysed. Findings Fifteen items from the Mandarin Chinese Myocardial Infarction Dimensional Assessment Scale were retained in a strong and reliable Mokken scale; invariant item ordering was not evident and the Mokken scaled items of the Chinese Myocardial Infarction Dimensional Assessment Scale correlated with the Short Form (36) Health Survey. Conclusions Items from the Mandarin Chinese Myocardial Infarction Dimensional Assessment Scale form a Mokken scale and this offers further insight into how the items of the Myocardial Infarction Dimensional Assessment Scale relate to the measurement of health-related quality of life people with a myocardial infarction. PMID:22221696

  11. [Acute myocardial infarction complicated by acute pulmonary oedema and cardiogenic collapse during dobutamine stress echocardiography].

    PubMed

    Yameogo, Nobila Valentin; Mbaye, Alassane; Kagambega, Larissa Justine; Dioum, Momar; Diagne-Sow, Dior; Kane, Moussa; Diack, Bouna; Kane, Abdoul

    2013-06-23

    Acute myocardial infarction is a rare complication of dobutamine stress echocardiography. We describe the case of a diabetic patient who presented with an anterior myocardial infarction complicated by an acute pulmonary oedema and cardiogenic collapse during dobutamine stress echocardiography, requiring five days' hospitalisation. Coronarography could not be performed because of inadequate medical facilities.

  12. Serum creatine kinase B subunit activity in diagnosis of acute myocardial infarction.

    PubMed Central

    Ljungdahl, L; Gerhardt, W; Hofvendahl, S

    1980-01-01

    The value of serum creatine kinase B subunit activity (CK B) in the diagnosis of acute myocardial infarction was studied in 238 consecutive cases. All were admitted to a coronary care unit because of suspected acute myocardial infarction. Serum CK B activity was determined by an immunoinhibition procedure, using a CK M subunit inhibiting antibody (anti-M). For the evaluation of serum CK B, patients were classified into acute myocardial infarction and non-acute myocardial infarction groups. This classification was based on electrocardiographic findings, on quantitative determinations of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total serum creatine kinase (CK) activities, and on qualitative electrophoretic determinations of serum CK and serum lactate dehydrogenase (LD) isoenzymes. The prevalence of acute myocardial infarction in the patient material was 0.47. Serum CK B subunit activity was found to be a highly selective indicator of acute myocardial infarction with a predictive value of a positive test result of 0.97 and a predictive value of a negative test result of 0.99. The serum CK B activity increased above the acute myocardial infarction discrimination limit within 12 hours from onset of symptoms. Two non-acute myocardial infarction patients, who were resuscitated after cardiac arrest, had increased serum CK B values caused by the transient presence of CK isoenzyme BB in serum. PMID:7378210

  13. Myocardial infarction - a rare complication in Henoch-Schönlein purpura.

    PubMed Central

    Abdel-Hadi, O.; Greenstone, M. A.; Hartley, R. B.; Kidner, P. H.

    1981-01-01

    A 29-year-old man with previous Henoch-Schönlein disease presented with multiple systemic emboli and a myocardial infarction. Subsequent investigation by angiography showed normal coronary arteries. This appears to be the first reported case of Henoch-Schönlein disease and myocardial infarction probably due to coronary vasculitis. Images Fig. 1 PMID:7301688

  14. Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers.

    PubMed

    Jin, Jiyang; Chen, Min; Li, Yongjun; Wang, YaLing; Zhang, Shijun; Wang, Zhen; Wang, Lin; Ju, Shenghong

    2016-10-01

    We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (<4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction-identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.

  15. [Influences of percutaneous coronary intervention on myocardial activity in myocardial infarction patients with different viable myocardium].

    PubMed

    Li, Li-qi; Liu, Xiao-hong; Zhang, Jin; Lai, Chun-lin; He, Ye-xin

    2013-10-01

    To evaluate the effect of percutaneous coronary intervention (PCI) on left ventricular function in patients with different types of myocardial infarction and to explore the correlation factors for the left ventricular function. A total of 43 patients diagnosed as acute myocardial infarction were enrolled in this study. The perfusion and delayed enhancement magnetic resonance imaging (DE-MRI) was applied to observe the following parameters before the PCI and at month 6 after the procedure: infarct mass, left ventricular ejection fraction (LVEF) and abnormal wall motion score. The subjects were divided into the following three groups by the transmural extent of myocardial infarction manifested in the DE-MRI: the transmural enhancement group, the nontransmural group and the mixed group. Laboratory test was done to detect the level of endothelin (ET), matrix metal enzyme 9 (MMP-9) and high sensitive C reactive protein (hsCRP) before PCI and at month 6 after the procedure. The t test was used to compare the differences among the groups and the multiple regression analysis was taken to explore the correlation factors for the left ventricular function. Compared with the parameters before PCI, the infarct mass after PCI significantly decreased in the nontransmural group and the mixed group [(4.0 ± 2.9) g/cm(3) vs (9.8 ± 5.6) g/cm(3) and (6.0 ± 3.5) g/cm(3) vs (11.8 ± 6.2)g/cm(3), all P < 0.05], while LVEF was significantly improved after PCI in both groups [(52.6 ± 15.4)% vs (41.9 ± 16.3)%,(45.6 ± 15.4)% vs (38.9 ± 16.3)%, all P < 0.05]. The infarct mass was an independent correlation factor for LVEF before PCI (RR = 0.318, P < 0.05) and LVEF after PCI (RR = 0.293, P < 0.05) . LVEF before PCI was independently correlated with the level of hsCRP (RR = 0.318, P < 0.05). The effect of PCI on the improvement of left ventricular function differs in patients with different extent of myocardial infarction, which is correlated with the amount of survival myocardium and the

  16. Complement Component 3 is Necessary to Preserve Myocardium and Myocardial Function in Chronic Myocardial Infarction

    PubMed Central

    Wysoczynski, Marcin; Solanki, Mitesh; Borkowska, Sylwia; van Hoose, Patrick; Brittian, Kenneth R.; Prabhu, Sumanth D.; Ratajczak, Mariusz Z.; Rokosh, Gregg

    2014-01-01

    Activation of the complement cascade (CC) with myocardial infarction (MI) acutely initiates immune cell infiltration, membrane attack complex formation on injured myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in mobilization of stem/progenitor cells and tissue regeneration. Its role in chronic MI is unknown. Here, we consider complement component C3, in the chronic response to MI. C3 knockout (KO) mice were studied after permanent coronary artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after MI compared to WT with further impaired systolic function and LV dilation despite similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI showed C3 KO mice had more scar tissue with less viable myocardium within the infarct zone which correlated with decreased c-kitpos cardiac stem/progenitor cells (CPSC), decreased proliferating Ki67pos CSPCs and decreased formation of new BrdUpos/α-sarcomeric actinpos myocytes and increased apoptosis compared to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3 KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor cell mobilization into the peripheral blood 72 hours post-MI. These results are the first to demonstrate the CC, through C3, contributes to myocardial preservation and regeneration in response to chronic MI. Responses in the C3 KO infer that C3 activation in response to MI expands the resident CSPC population, increases new myocyte formation, increases and preserves myocardium, inflammatory response, and bone marrow stem/progenitor cell mobilization to preserve myocardial function. PMID:24806427

  17. Complement component 3 is necessary to preserve myocardium and myocardial function in chronic myocardial infarction.

    PubMed

    Wysoczynski, Marcin; Solanki, Mitesh; Borkowska, Sylwia; van Hoose, Patrick; Brittian, Kenneth R; Prabhu, Sumanth D; Ratajczak, Mariusz Z; Rokosh, Gregg

    2014-09-01

    Activation of the complement cascade (CC) with myocardial infarction (MI) acutely initiates immune cell infiltration, membrane attack complex formation on injured myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in mobilization of stem/progenitor cells and tissue regeneration. Its role in chronic MI is unknown. Here, we consider complement component C3, in the chronic response to MI. C3 knockout (KO) mice were studied after permanent coronary artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after MI compared to WT with further impaired systolic function and LV dilation despite similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI showed C3 KO mice had more scar tissue with less viable myocardium within the infarct zone which correlated with decreased c-kit(pos) cardiac stem/progenitor cells (CPSC), decreased proliferating Ki67(pos) CSPCs and decreased formation of new BrdU(pos) /α-sarcomeric actin(pos) myocytes, and increased apoptosis compared to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3 KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor cell mobilization into the peripheral blood 72 hours post-MI. These results are the first to demonstrate that CC, through C3, contributes to myocardial preservation and regeneration in response to chronic MI. Responses in the C3 KO infer that C3 activation in response to MI expands the resident CSPC population, increases new myocyte formation, increases and preserves myocardium, inflammatory response, and bone marrow stem/progenitor cell mobilization to preserve myocardial function. © 2014 AlphaMed Press.

  18. Activated platelet chemiluminescence and presence of CD45+ platelets in patients with acute myocardial infarction.

    PubMed

    Gabbasov, Zufar; Ivanova, Oxana; Kogan-Yasny, Victor; Ryzhkova, Evgeniya; Saburova, Olga; Vorobyeva, Inna; Vasilieva, Elena

    2014-01-01

    It has been found that in 15% of acute myocardial infarction patients' platelets generate reactive oxygen species that can be detected with luminol-enhanced chemiluminescence of platelet-rich plasma within 8-10 days after acute myocardial infarction. This increase in generate reactive oxygen species production coincides with the emergence of CD45(+) platelets. The ability of platelets to carry surface leukocyte antigen implies their participation in exchange of specific proteins in the course of acute myocardial infarction. Future studies of CD45(+) platelets in peripheral blood of acute myocardial infarction patients in association with generate reactive oxygen species production may provide a new insight into the complex mechanisms of cell-cell interactions associated with acute myocardial infarction.

  19. A Multidisciplinary Assessment of Remote Myocardial Fibrosis After Reperfused Myocardial Infarction in Swine and Patients.

    PubMed

    Hervas, Arantxa; Ruiz-Sauri, Amparo; Gavara, Jose; Monmeneu, Jose V; de Dios, Elena; Rios-Navarro, Cesar; Perez-Sole, Nerea; Perez, Itziar; Monleon, Daniel; Morales, Jose M; Minana, Gema; Nunez, Julio; Bonanad, Clara; Diaz, Ana; Vila, Jose M; Chorro, Francisco J; Bodi, Vicente

    2016-08-01

    In extensive nonreperfused myocardial infarction (MI), remote fibrosis has been documented. Early reperfusion by primary angioplasty represents the gold standard method to minimize the extension of the infarction. We aimed to ascertain whether fibrosis also affects remote regions in reperfused MI in swine and patients. Swine were subjected to a transient occlusion of the left anterior descending artery followed by 1-week or 1-month reperfusion. Collagen content in the remote area macroscopically, microscopically, by magnetic resonance microimaging, and at the molecular level was similar to controls. In patients with previous MI, samples from autopsies displayed a significant increase in collagen content only in the infarct region. In patients with previous MI submitted to cardiac magnetic resonance-T1 mapping, the extracellular volume fraction in remote segments was similar to that for controls. In all scenarios, the remote region did not show a significant increase of collagen content in comparison with controls.

  20. Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats

    PubMed Central

    Bozi, Luiz Henrique Marchesi; dos Santos Costa Maldonado, Izabel Regina; Baldo, Marcelo Perim; da Silva, Márcia Ferreira; Moreira, José Bianco Nascimento; Novaes, Rômulo Dias; Ramos, Regiane Maria Soares; Mill, José Geraldo; Brum, Patricia Chakur; Felix, Leonardo Bonato; Gomes, Thales Nicolau Prímola; Natali, Antônio José

    2013-01-01

    OBJECTIVES: The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. METHODS: Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05). RESULTS: Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium. CONCLUSION: Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties. PMID:23778353

  1. Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats.

    PubMed

    Bozi, Luiz Henrique Marchesi; Maldonado, Izabel Regina dos Santos Costa; Baldo, Marcelo Perim; Silva, Márcia Ferreira da; Moreira, José Bianco Nascimento; Novaes, Rômulo Dias; Ramos, Regiane Maria Soares; Mill, José Geraldo; Brum, Patricia Chakur; Felix, Leonardo Bonato; Gomes, Thales Nicolau Prímola; Natali, Antônio José

    2013-04-01

    The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05). Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium. Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties.

  2. Angiotensin-converting enzyme in acute myocardial infarction and angina pectoris.

    PubMed

    Rømer, F K; Kornerup, H J

    1981-06-01

    Serum activity of angiotensin-converting enzyme was measured by serial analysis in 19 patients with acute myocardial infarction and in eight patients with angina pectoris. As a rule no changes in enzyme activity occurred during 6 days observations. However, two patients with infarction exhibited a pronounced fall of enzyme activity which could not be related to clinical events. The analysis seems to have no place in the diagnosis and management of patients with myocardial infarction.

  3. Combined assessment of reflow and collateral blood flow by myocardial contrast echocardiography after acute reperfused myocardial infarction

    PubMed Central

    Leclercq, F; Messner-Pellenc, P; Descours, Q; Daures, J; Pasquie, J; Hager, F; Davy, J; Grolleau-Raoux, R

    1999-01-01

    OBJECTIVE—To evaluate the combined assessment of reflow and collateral blood flow by myocardial contrast echocardiography after myocardial infarction.
DESIGN—Myocardial contrast echocardiography was performed in patients with acute myocardial infarction shortly after successful coronary reperfusion (TIMI 3 patency) by direct angioplasty. Collateral flow was assessed before coronary angioplasty, and contrast reflow was evaluated 15 minutes after reperfusion. The presence of contractile reserve was assessed by low dose dobutamine echocardiography (5 to 15 µg/kg/min) at (mean (SD)) 3 (2) days after myocardial infarction. Recovery of segmental function (myocardial viability) was evaluated by resting echocardiography at a two month follow up. The study was prospective.
PATIENTS—35 consecutive patients referred for acute transmural myocardial infarction.
RESULTS—Contrast reflow was observed in 20 patients (57%) and collateral flow in 14 (40%). Contrast reflow and collateral contrast flow were both correlated with reversible dysfunction on initial dobutamine echocardiography and at follow up (p < 0.05). The presence of reflow or collateral flow on myocardial contrast echocardiography was a highly sensitive (100%) but weakly specific (60%) indicator of segmental dysfunction recovery. Simultaneous presence of contrast reflow and collateral flow was more specific of reversible dysfunction than reflow alone (90% v 60%).
CONCLUSIONS—Combined assessment of reflow and collateral blood flow enhanced the sensitivity of myocardial contrast echocardiography in predicting myocardial viability after acute, reperfused myocardial infarction. The simultaneous presence of reflow and collateral blood flow was highly specific of recovery of segmental dysfunction.


Keywords: contrast echocardiography; coronary reflow; collateral blood flow; dobutamine echocardiography; myocardial dysfunction PMID:10377311

  4. Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers

    PubMed Central

    Chen, Min; Li, Yongjun; Wang, YaLing; Zhang, Shijun; Wang, Zhen; Wang, Lin; Ju, Shenghong

    2016-01-01

    We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (<4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction—identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers. PMID:27777517

  5. Pericarditis and myocardial infarctions after Hodgkin's disease therapy

    SciTech Connect

    Cosset, J.M.; Henry-Amar, M.; Pellae-Cosset, B.; Carde, P.; Girinski, T.; Tubiana, M.; Hayat, M. )

    1991-07-01

    From 1971 to 1984, 499 patients with all stages of Hodgkin's disease received mediastinal irradiation at the Institut Gustave-Roussy by 25 MV photons from a linear accelerator. Thirty-five pericarditis (10-year cumulative incidence rate of 9.5%) and 13 myocardial infarctions (MI) (10-year cumulative incidence rate of 3.9%) were observed. In contrast, no cases were diagnosed in a parallel series of 138 Hodgkin's disease patients treated without mediastinal irradiation during the same period of time (p less than 0.005 for pericarditis, p less than 0.05 for MI). By multivariate analysis, the role of total radiation dose given to the mediastinum and that of fraction size were evaluated, adjusting for age, sex, mediastinal involvement, and type of chemotherapy. The pericarditis risk was significantly increased with total dose greater than or equal to 41 Gy (relative risk (RR) = 3.25, p = 0.006) and with dose per fraction greater than or equal to 3.0 Gy (RR = 2.0, p = 0.06). The myocardial infarction risk was not found to be related to total dose nor to fraction size in this series, possibly because of the small number of events.

  6. Adverse Remodeling and Reverse Remodeling After Myocardial Infarction.

    PubMed

    Bhatt, Ankeet S; Ambrosy, Andrew P; Velazquez, Eric J

    2017-08-01

    The purpose of this review it to summarize the current literature on remodeling after myocardial infarction, inclusive of pathophysiological considerations, imaging modalities, treatment strategies, and future directions. As patients continue to live longer after myocardial infarction (MI), the prevalence of post-MI heart failure continues to rise. Changes in the left ventricle (LV) after MI involve complex interactions between cellular and extracellular components, under neurohormonal regulation. Treatments to prevent adverse LV remodeling and promote reverse remodeling in the post-MI setting include early revascularization, pharmacotherapy aimed at neurohormonal blockade, and device-based therapies that address ventricular dyssynchrony. Despite varying definitions of adverse LV remodeling examined across multiple imaging modalities, the presence of an enlarged LV cavity and/or reduced ejection fraction is consistently associated with poor clinical outcomes. Advances in our knowledge of the neurohormonal regulation of adverse cardiac remodeling have been instrumental in generating therapies aimed at arresting adverse remodeling and promoting reserve remodeling. Further investigation into other specific mechanisms of adverse LV remodeling and pathways to disrupt these mechanisms is ongoing and may provide incremental benefit to current evidence-based therapies.

  7. Cardiac Rehabilitation After Acute Myocardial Infarction Resuscitated From Cardiac Arrest

    PubMed Central

    Kim, Chul; Choi, Hee Eun; Kang, Seong Hoon

    2014-01-01

    Objective To examine the safety and effectiveness of cardiac rehabilitation on patients resuscitated from cardiac arrest due to acute myocardial infarction. Methods The study included 23 subjects, including 8 with history of cardiac arrest and 15 without history of cardiac arrest. Both groups underwent initial graded exercise test (GXT) and subsequent cardiac rehabilitation for 6 weeks. After 6 weeks, both groups received follow-up GXT. Results Statistically significant (p<0.05) increase of VO2peak and maximal MVO2 but significant (p<0.05) decrease of submaximal MVO2 and resting heart rate were observed in both groups after 6 weeks of cardiac rehabilitation. An increasing trend of maximal heart rates was observed in both groups. However, the increase was not statistically significant (p>0.05). There was no statistically significant change of resting heart rate, maximal heart rate, maximal MVO2, or submaximal MVO2 in both groups after cardiac rehabilitation. Fatal cardiac complications, such as abnormal ECG, cardiac arrest, death or myocardial infarction, were not observed. All subjects finished the cardiac rehabilitation program. Conclusion Improvement was observed in the exercise capacity of patients after aerobic exercise throughout the cardiac rehabilitation program. Therefore, cardiac rehabilitation can be safely administered for high-risk patients with history of cardiac arrest. Similar improvement in exercise capacity can be expected in patients without cardiac arrest experience. PMID:25566479

  8. The relationship between acute myocardial infarction and periodontitis

    PubMed Central

    Khosravi Samani, Mahmoud; Jalali, Farzad; Seyyed Ahadi, Seyyed Masud; Hoseini, Seyyed Reza; Dabbagh Sattari, Farhad

    2013-01-01

    Background: Periodontitis is common in adults and cardiovascular diseases (CVD) are the most common cause of adult death in the world. This study aimed to investigate the relationship between CVD and periodontitis. Methods: Sixty patients with myocardial infarction (MI) as case and 63 subjects with periodontitis without MI as control were studied. Periodontitis was assessed according to Ramfjord periodontal diseases index and the number of missing teeth besides classic risk factors of MI were recorded. Results: The patients who lost more than 10 teeth were at more risk of myocardial infarction (OR=2.73). There was a significant relationship between mean attachment loss and MI (p=0.0001). There was also a relation between attachment loss more than 3 mm and MI with OR of 4. Significant difference between mean PDI (periodontal disease index) was seen in case and control groups (p=0.0001). Subjects with PDI>4 were at more risk of periodontal diseases (OR=7.87). Conclusion: The results show the presence of significant relation between periodontitis and MI which could serve as an alarm to treat periodontitis carefully. PMID:24009957

  9. Spontaneous splenic artery aneurysm rupture: mimicking acute myocardial infarct.

    PubMed

    Zeren, Sezgin; Bayhan, Zülfü; Sönmez, Yalcın; Mestan, Metin; Korkmaz, Mehmet; Kadıoglu, Emine; Ucar, Bercis Imge; Devir, Cigdem; Ekici, Fatih Mehmet; Sanal, Bekir

    2014-12-01

    Spontaneous splenic artery aneurysm (SAA) is a rare but a life-threatening condition. Thus, early diagnoses may increase the chance of survival. A 52-year-old female patient was admitted to the emergency department with a pain that starts from the chest and epigastric region and radiates to back and left arm. The patient prediagnosed as having acute myocardial infarct and was under observation when acute abdomen and hemorrhagic shock developed. After further investigation, the patient was diagnosed as having SAA and has undergone a successful surgery. The patient was fully cured and discharged from the hospital on the seventh postoperative day. The patient originally presented with SAA, although she was primarily observed in the emergency department with acute myocardial infarct diagnosis because of similar symptoms and clinical findings to cardiovascular diseases. When changes in the clinical picture occurred, the patient was reevaluated and had undergone an operation because of SAA rupture. Therefore, physicians should take into consideration of aneurysm rupture in the differential diagnosis of the cardiovascular conditions; otherwise, the patient may lose his/her life.

  10. Illness perception of nursing students regarding myocardial infarction.

    PubMed

    Grankvist, Gunne; Brink, Eva

    2009-01-01

    Health interventions aimed at secondary prevention of myocardial infarction (MI) are important. Patients' illness perceptions influence adherence behaviors and actions. Providing adequate infomation about the disease and lifestyle interventions is an important task for health care professionals. Therefore, a question of interest is how health care professionals perceive myocardial infarction themselves. The aim with the present study was to investigate how nursing students at a Swedish university perceived MI and to determine whether their illness perceptions changed during their six-term program of education. Illness perception was measured using the Revised Illness Perception Questionnaire (IPQ-R) in a sample of 196 students enrolled in terms 2, 4, and 6 of the nursing program. A quasi-experimental design was used. Illness perceptions among nursing students were also compared to illness perceptions in a group of patients with coronary heart disease. The belief that it is possible to control MI through medical treatment became stronger during the course of nursing education. Nursing students were found to view the consequences of MI as serious, but also as medically treatable and responsive to lifestyle changes.

  11. Exosomes Mediate the Intercellular Communication after Myocardial Infarction

    PubMed Central

    Yuan, Ming-Jie; Maghsoudi, Taneen; Wang, Tao

    2016-01-01

    The mechanisms of cardiac repair after myocardial infarction (MI) are complicated and not well-understood currently. It is known that exosomes are released from most cells, recognized as new candidates with important roles in intercellular and tissue-level communication. Cells can package proteins and RNA messages into exosome and secret to recipient cells, which regulate gene expression in recipient cells. The research on exosomes in cardiovascular disease is just emerging. It is well-known that exosomes from cardiomyocyte can transfect endothelial cells, stem cells, fibroblasts and smooth muscle cells to induce cellular changes. After myocardial infarction (MI), the exosomes play important roles in local and distant microcommunication. Nowadays, exosomal microRNAs transportation has been found to deliver signals to mediate cardiac repair after MI. However, the exosomes quality and quantities are variable under different pathological conditions. Therefore, we speculate that the monitoring of the quality and quantity of exosomes may serve as diagnosis and prognosis biomarkers of MI, and the study of exosomes will provide insights for the new therapeutics to cardiac remodeling after MI. PMID:26941569

  12. Exosomes Mediate the Intercellular Communication after Myocardial Infarction.

    PubMed

    Yuan, Ming-Jie; Maghsoudi, Taneen; Wang, Tao

    2016-01-01

    The mechanisms of cardiac repair after myocardial infarction (MI) are complicated and not well-understood currently. It is known that exosomes are released from most cells, recognized as new candidates with important roles in intercellular and tissue-level communication. Cells can package proteins and RNA messages into exosome and secret to recipient cells, which regulate gene expression in recipient cells. The research on exosomes in cardiovascular disease is just emerging. It is well-known that exosomes from cardiomyocyte can transfect endothelial cells, stem cells, fibroblasts and smooth muscle cells to induce cellular changes. After myocardial infarction (MI), the exosomes play important roles in local and distant microcommunication. Nowadays, exosomal microRNAs transportation has been found to deliver signals to mediate cardiac repair after MI. However, the exosomes quality and quantities are variable under different pathological conditions. Therefore, we speculate that the monitoring of the quality and quantity of exosomes may serve as diagnosis and prognosis biomarkers of MI, and the study of exosomes will provide insights for the new therapeutics to cardiac remodeling after MI.

  13. Differential MR Delayed Enhancement Patterns of Chronic Myocardial Infarction between Extracellular and Intravascular Contrast Media

    PubMed Central

    Wang, Jian; Xiang, Bo; Lin, Hung Yu; Liu, Hongyu; Freed, Darren; Arora, Rakesh C.; Tian, Ganghong

    2015-01-01

    Objectives Because the distribution volume and mechanism of extracellular and intravascular MR contrast media differ considerably, the enhancement pattern of chronic myocardial infarction with extracellular or intravascular media might also be different. This study aims to investigate the differences in MR enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media. Materials and Methods Twenty pigs with myocardial infarction underwent cine MRI, first pass perfusion MRI and delayed enhancement MRI with extracellular or intravascular media at four weeks after coronary occlusion. Myocardial blood flow (MBF) was determined with microsphere measurement. The infarction histopathological changes were evaluated by hematoxylin and eosin staining and Masson's trichrome method. Results Cine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium. Moreover, significant wall thinning in chronic infarction was observed in cine MRI. Peak first-pass signal intensity didn’t significantly differ between chronic infarction and normal myocardium no matter what kinds of contrast media. At the following delayed enhancement phase, extracellular media-enhanced signal intensity was significantly higher in chronic infarction than in normal myocardium. Conversely, intravascular media-enhanced signal intensity was almost equivalent among chronic infarction and normal myocardium. At four weeks after infarction, MBF in chronic infarction approached to that in normal myocardium. Large thick-walled vessels were detected at peri-infarction zones. The cardiomyocytes were replaced by scar tissue consisting of dilated blood vessels and discrete fibers of collagen. Conclusions Chronic infarction was characterized by the significantly reduced wall thickening and the definite wall thinning. First-pass myocardial perfusion defect was not detected in chronic infarction with two media due to the significantly

  14. Differential MR delayed enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media.

    PubMed

    Wang, Jian; Xiang, Bo; Lin, Hung Yu; Liu, Hongyu; Freed, Darren; Arora, Rakesh C; Tian, Ganghong

    2015-01-01

    Because the distribution volume and mechanism of extracellular and intravascular MR contrast media differ considerably, the enhancement pattern of chronic myocardial infarction with extracellular or intravascular media might also be different. This study aims to investigate the differences in MR enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media. Twenty pigs with myocardial infarction underwent cine MRI, first pass perfusion MRI and delayed enhancement MRI with extracellular or intravascular media at four weeks after coronary occlusion. Myocardial blood flow (MBF) was determined with microsphere measurement. The infarction histopathological changes were evaluated by hematoxylin and eosin staining and Masson's trichrome method. Cine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium. Moreover, significant wall thinning in chronic infarction was observed in cine MRI. Peak first-pass signal intensity didn't significantly differ between chronic infarction and normal myocardium no matter what kinds of contrast media. At the following delayed enhancement phase, extracellular media-enhanced signal intensity was significantly higher in chronic infarction than in normal myocardium. Conversely, intravascular media-enhanced signal intensity was almost equivalent among chronic infarction and normal myocardium. At four weeks after infarction, MBF in chronic infarction approached to that in normal myocardium. Large thick-walled vessels were detected at peri-infarction zones. The cardiomyocytes were replaced by scar tissue consisting of dilated blood vessels and discrete fibers of collagen. Chronic infarction was characterized by the significantly reduced wall thickening and the definite wall thinning. First-pass myocardial perfusion defect was not detected in chronic infarction with two media due to the significantly recovered MBF and well-developed collateral vessels

  15. Electrocardiographic infarct size assessment after thrombolysis: insights from the Acute Myocardial Infarction STudy ADenosine (AMISTAD) trial.

    PubMed

    Barbagelata, Alejandro; Di Carli, Marcelo F; Califf, Robert M; Garg, Jyotsna; Birnbaum, Yochai; Grinfeld, Liliana; Gibbons, Raymond J; Granger, Christopher B; Goodman, Shaun G; Wagner, Galen S; Mahaffey, Kenneth W

    2005-10-01

    Noninvasive methods are needed to evaluate reperfusion success in patients with acute myocardial infarction (MI). The AMISTAD trial was analyzed to compare MI size and myocardial salvage determined by electrocardiogram (ECG) with technetium Tc 99m sestamibi single-photon emission computerized tomography (SPECT) imaging. Of 236 patients enrolled in AMISTAD, 166 (70 %) with no ECG confounding factors and no prior MI were included in this analysis. Of these, group 1 (126 patients, 53%) had final infarct size (FIS) available by both ECG and SPECT. Group 2 (56 patients, 24%) had myocardium at risk, FIS, and salvage index (SI) assessed by both SPECT and ECG techniques. Aldrich/Clemmensen scores for myocardium at risk and the Selvester QRS score for final MI size were used. Salvage index was calculated as follows: SI = (myocardium at risk-FIS)/(myocardium at risk). In group 1, FIS was 15% (6, 24) as measured by ECG and 11% (2, 27) as measured by SPECT. In the adenosine group, FIS was 12% (6, 21) and 11% (2, 22). In the placebo group, FIS was 16.5% (7.5, 24) and 11.5% (3.0, 38.5) by ECG and SPECT, respectively. The overall correlation between SPECT and ECG for FIS was 0.58 (P = .0001): 0.60 in the placebo group (P = .0001) and 0.54 (P = .0001) in the adenosine group. In group 2, myocardium at risk was 23% (17, 30) and 26% (10, 50) with ECG and SPECT, respectively (P = .0066). Final infarct size was 17% (6, 21) and 12% (1, 24) (P < .0001). The SI was 29% (-7, 57) and 46% (15, 79) with ECG and SPECT, respectively (P = .0510). The ECG measurement of infarct size has a moderate relationship with SPECT infarct size measurements in the population with available assessments. This ECG algorithm must further be validated on clinical outcomes.

  16. Metformin and Myocardial Injury in Patients With Diabetes and ST-Segment Elevation Myocardial Infarction: A Propensity Score Matched Analysis.

    PubMed

    Basnet, Suresh; Kozikowski, Andrzej; Makaryus, Amgad N; Pekmezaris, Renee; Zeltser, Roman; Akerman, Meredith; Lesser, Martin; Wolf-Klein, Gisele

    2015-10-22

    Although animal studies have documented metformin's cardioprotective effects, the impact in humans remains elusive. The study objective was to explore the association between metformin and myocardial infarct size in patients with diabetes presenting with ST-segment elevation myocardial infarction. Data extraction used the National Cardiovascular Data CathPCI Registry in all patients with diabetes aged >18 years presenting with ST-segment elevation myocardial infarction at 2 academic medical centers from January 2010 to December 2013. The exposure of interest was ongoing metformin use before the event. Propensity score matching was used for the metformin and nonmetformin groups on key prognostic variables. All matched pairs had acceptable D scores of <10%, confirming an efficient matching procedure. The primary outcome was myocardial infarct size, reflected by peak serum creatine kinase-myocardial band, troponin T, and hospital discharge left ventricular ejection fraction. Of all 1726 ST-segment elevation myocardial infarction cases reviewed, 493 patients had diabetes (28.5%), with 208 metformin users (42.1%) and 285 nonusers. Matched pairs analysis yielded 137 cases per group. The difference between metformin and nonmetformin groups was -18.1 ng/mL (95% CI -55.0 to 18.8; P=0.56) for total peak serum creatine kinase-myocardial band and -1.1 ng/mL (95% CI -2.8 to 0.5; P=0.41) for troponin T. Median discharge left ventricular ejection fraction in both groups was 45, and the difference between metformin and nonmetformin users was 0.7% (95% CI -2.2 to 3.6; P=0.99). No statistically significant association of cardioprotection was found between metformin and myocardial infarct size in patients with diabetes and acute ST-segment elevation myocardial infarction. © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

  17. Clinical efforts to reduce myocardial infarct size--the next step.

    PubMed

    Braunwald, Eugene

    2011-01-01

    Prompt myocardial reperfusion reduces infarct size in patients experiencing coronary occlusion. However, its clinical value is limited because reperfusion also causes ischemic myocardial reperfusion injury (IMRI). Considerable research to reduce IMRI has been conducted. Three interventions appear to be promising: 1) myocardial conditioning, which consists of repetitive occlusions of coronary or other arteries prior to or at the time of myocardial reperfusion; 2) the administration of cyclosporine A; and 3) the administration of adenosine. A plan for the testing of these interventions in patients with acute myocardial infarction is described.

  18. Diagnostic and therapeutic implications of type 2 myocardial infarction: review and commentary.

    PubMed

    Alpert, Joseph S; Thygesen, Kristian A; White, Harvey D; Jaffe, Allan S

    2014-02-01

    The Task Force for the Universal Definition of Myocardial Infarction recently published updated guidelines for the clinical and research diagnosis of myocardial infarction under a variety of circumstances and in a variety of categories. A type 1 myocardial infarction (MI) is usually the result of atherosclerotic coronary artery disease with thrombotic coronary arterial obstruction secondary to atherosclerotic plaque rupture, ulceration, fissuring, or dissection, causing coronary arterial obstruction with resultant myocardial ischemia and necrosis. Patients with a type 2 MI do not have atherosclerotic plaque rupture. In this latter group of patients, myocardial necrosis occurs because of an increase in myocardial oxygen demand or a decrease in myocardial blood flow. Type 2 MI has been the subject of considerable clinical discussion and confusion. This review by knowledgeable members of the Task Force seeks to help clinicians resolve the confusion surrounding type 2 MI.

  19. Quantitative proteomic changes during post myocardial infarction remodeling reveals altered cardiac metabolism and Desmin aggregation in the infarct region.

    PubMed

    Datta, Kaberi; Basak, Trayambak; Varshney, Swati; Sengupta, Shantanu; Sarkar, Sagartirtha

    2017-01-30

    Myocardial infarction is one of the leading causes of cardiac dysfunction, failure and sudden death. Post infarction cardiac remodeling presents a poor prognosis, with 30%-45% of patients developing heart failure, in a period of 5-25years. Oxidative stress has been labelled as the primary causative factor for cardiac damage during infarction, however, the impact it may have during the process of post infarction remodeling has not been well probed. In this study, we have implemented iTRAQ proteomics to catalogue proteins and functional processes, participating both temporally (early and late phases) and spatially (infarct and remote zones), during post myocardial infarction remodeling of the heart as functions of the differential oxidative stress manifest during the remodeling process. Cardiac metabolism was the dominant network to be affected during infarction and the remodeling time points considered in this study. A distinctive expression pattern of cytoskeletal proteins was also observed with increased remodeling time points. Further, it was found that the cytoskeletal protein Desmin, aggregated in the infarct zone during the remodeling process, mediated by the protease Calpain1. Taken together, all of these data in conjunction may lay the foundation to understand the effects of oxidative stress on the remodeling process and elaborate the mechanism behind the compromised cardiac function observed during post myocardial infarction remodeling.

  20. Characterization of Circulating Endothelial Cells in Acute Myocardial Infarction

    PubMed Central

    Damani, Samir; Bacconi, Andrea; Libiger, Ondrej; Chourasia, Aparajita H.; Serry, Rod; Gollapudi, Raghava; Goldberg, Ron; Rapeport, Kevin; Haaser, Sharon; Topol, Sarah; Knowlton, Sharen; Bethel, Kelly; Kuhn, Peter; Wood, Malcolm; Carragher, Bridget; Schork, Nicholas J.; Jiang, John; Rao, Chandra; Connelly, Mark; Fowler, Velia M.; Topol, Eric J.

    2013-01-01

    Acute myocardial infarction (MI), which involves the rupture of existing atheromatous plaque, remains highly unpredictable despite recent advances in the diagnosis and treatment of coronary artery disease. Accordingly, a biomarker that can predict an impending MI is desperately needed. Here, we characterize circulating endothelial cells (CECs) using the first automated and clinically feasible CEC 3-channel fluorescence microscopy assay in 50 consecutive patients with ST-elevation myocardial infarction (STEMI) and 44 consecutive healthy controls. CEC counts were significantly elevated in MI cases versus controls with median numbers of 19 and 4 cells/ml respectively (p = 1.1 × 10−10). A receiver-operating characteristic (ROC) curve analysis demonstrated an area under the ROC curve of 0.95, suggesting near dichotomization of MI cases versus controls. We observed no correlation between CECs and typical markers of myocardial necrosis (ρ=0.02, CK-MB; ρ=−0.03, troponin). Morphologic analysis of the microscopy images of CECs revealed a 2.5-fold increase (P<0.0001) in cellular area and 2-fold increase (P<0.0001) in nuclear area of MI CECs versus healthy control, age-matched CECs, as well as CECs obtained from patients with preexisting peripheral vascular disease. The distribution of CEC images containing from 2 up to 10 nuclei demonstrates that MI patients are the only group to contain more than 3 nuclei/image, indicating that multi-cellular and multi-nuclear clusters are specific for acute MI. These data indicate that CECs may serve as promising biomarkers for the prediction of atherosclerotic plaque rupture events. PMID:22440735

  1. [Phonomecanography in recent myocardial infarction. Ventricular mechanic curve].

    PubMed

    Delage, B; Le Pailleur, C; Heulin, A; Di Matteo, J

    1976-04-01

    Repeated recordings were made of the apexcardiogram throughout the first month after myocardial infarction in 30 patients. The classical timed intervals of the systolic wave are open to some criticism. The systolic waveforms are important. In the majority of transmural anterior infarctions there is a rounded appearance to the beginning of the wave which seems to prolong the electromechanical latency, followed by a late systolic bulge, or a domed waveform. This signifies a non-contractile area, and not neccessarily an ectasia. The early diastolic "peaktrough" appearance, found very frequently wherever the necrosis is situated, is indicative of asynergic contraction of the left ventricle. All of the diastolic phases are altered, probably by increased parietal stiffness: the TRI is lengthened; the "F" wave is flattened (and often absent later on in the condition), its duration is shortened over the anterior positions, and it may contain a shallow dip if there is LVF; the stasis wave is very feeble; the "a" wave is large when the infarct is extensive, or when there is LVF, or when there is longstanding hypertension. Enlargement of the "a" wave is especially indicative of a lowering of the performance of the left ventricle.

  2. Measurement of myocardial perfusion and infarction size using computer-aided diagnosis system for myocardial contrast echocardiography.

    PubMed

    Du, Guo-Qing; Xue, Jing-Yi; Guo, Yanhui; Chen, Shuang; Du, Pei; Wu, Yan; Wang, Yu-Hang; Zong, Li-Qiu; Tian, Jia-Wei

    2015-09-01

    Proper evaluation of myocardial microvascular perfusion and assessment of infarct size is critical for clinicians. We have developed a novel computer-aided diagnosis (CAD) approach for myocardial contrast echocardiography (MCE) to measure myocardial perfusion and infarct size. Rabbits underwent 15 min of coronary occlusion followed by reperfusion (group I, n = 15) or 60 min of coronary occlusion followed by reperfusion (group II, n = 15). Myocardial contrast echocardiography was performed before and 7 d after ischemia/reperfusion, and images were analyzed with the CAD system on the basis of eliminating particle swarm optimization clustering analysis. The myocardium was quickly and accurately detected using contrast-enhanced images, myocardial perfusion was quantitatively calibrated and a color-coded map calibrated by contrast intensity and automatically produced by the CAD system was used to outline the infarction region. Calibrated contrast intensity was significantly lower in infarct regions than in non-infarct regions, allowing differentiation of abnormal and normal myocardial perfusion. Receiver operating characteristic curve analysis documented that -54-pixel contrast intensity was an optimal cutoff point for the identification of infarcted myocardium with a sensitivity of 95.45% and specificity of 87.50%. Infarct sizes obtained using myocardial perfusion defect analysis of original contrast images and the contrast intensity-based color-coded map in computerized images were compared with infarct sizes measured using triphenyltetrazolium chloride staining. Use of the proposed CAD approach provided observers with more information. The infarct sizes obtained with myocardial perfusion defect analysis, the contrast intensity-based color-coded map and triphenyltetrazolium chloride staining were 23.72 ± 8.41%, 21.77 ± 7.8% and 18.21 ± 4.40% (% left ventricle) respectively (p > 0.05), indicating that computerized myocardial contrast echocardiography can

  3. Safety of air travel following acute myocardial infarction.

    PubMed

    Roby, Howard; Lee, Anna; Hopkins, Andrew

    2002-02-01

    A randomized, single-blind, controlled trial was carried out to: 1) examine the safety of patients flying on commercial airlines 2 wk after a myocardial infarction; 2) determine whether or not the use of supplemental oxygen was associated with a reduced risk of in-flight adverse events; and 3) determine the need for a medical escort. There were 38 patients who were prospectively and randomly assigned supplemental continuous oxygen therapy (2 L x min(-1) via nasal prongs; n = 19) or no oxygen (n = 19) during the flight. Prior to flying, an escorting doctor completed a medical questionnaire for each patient. Both groups underwent Holter monitoring throughout the flight. The major end-point was the development of inflight myocardial ischemia, as detected by Holter monitoring. Minor end-points included patients complaining of chest pain or dyspnea; the detection of bigeminy or trigeminy by Holter monitoring; or oxygen desaturation to less than 90%, as measured by pulse oximetry. Of the 38 patients enrolled, there was only 1 major end-point. This patient had a brief, self-limiting, asymptomatic episode of myocardial ischemia diagnosed by Holter monitoring. Minor end-points occurred in 13 (34%) patients. One patient had asymptomatic evidence of S-T depression on a transport monitor, but not on the Holter. Five patients had transient low (<90%) oxygen saturations, two complained of chest pain, and five had complex ventricular ectopic beats or periods of transient ventricular tachycardia. None of the minor end-points were associated with Holter evidence of myocardial ischemia. Of the 30 patients with completed questionnaires and Holter results, there was no difference in the incidence of minor end-points between the oxygen (5/13) and no oxygen groups (6/15) (p = 0.93). Intervention by the medical escort consisted of commencing oxygen therapy on those patients with low oxygen saturations and those with chest pain. Use of an already dispensed glyceryl trinitrate spray was

  4. Influence of coronary architecture on the variability in myocardial infarction induced by coronary ligation in rats.

    PubMed

    Kainuma, Satoshi; Miyagawa, Shigeru; Fukushima, Satsuki; Tsuchimochi, Hirotsugu; Sonobe, Takashi; Fujii, Yutaka; Pearson, James T; Saito, Atsuhiro; Harada, Akima; Toda, Koichi; Shirai, Mikiyasu; Sawa, Yoshiki

    2017-01-01

    It has been shown that the size of myocardial infarction in rats created by coronary ligation technique is not uniform, varying from 4% to 65%. We hypothesized that infarct size variability induced by coronary artery ligation might be caused by coronary artery branching pattern. Coronary artery angiography was performed in 50 normal Lewis rats and in chronic myocardial infarction models in which coronary artery was ligated immediately below the left atrial appendage or 2mm distal to the left atrial appendage (n = 25 for each), followed by histological analysis. Unlike the human, the rats had a single major septal artery arising from the proximal part of the left coronary artery (n = 30) or right coronary artery (n = 20). There were three branching patterns of left circumflex artery (LCX): 33 (66%) had LCX branching peripherally from a long left main coronary artery (LMCA), while the remainder 17 (34%) had the LCX branching from the proximal part of the septal artery or a short LMCA. The rats with distal coronary ligation presented myocardial infarction localized to an anterior territory irrespective of LCX branching pattern. In the rats with proximal coronary ligation, 64% (n = 16) had broad myocardial infarction involving the anterior and lateral territories, while the remainder (36%, n = 9) had myocardial infarction localized to an anterior territory with the intact LCX arising proximally from a short LMCA. The interventricular septum was spared from infarction in all rats because of its anatomical location. Infarct size variations were caused not only by ligation site but also by varying LCX branching patterns. There are potential risks to create different sizes of myocardial infarction, particularly when targeting a broad range of myocardial infarction. The territory of the septal artery always appears to be spared from myocardial infarction induced by the coronary ligation technique.

  5. Physicians' perceptions of the Thrombolysis in Myocardial Infarction (TIMI) risk score in older adults with acute myocardial infarction.

    PubMed

    Feder, Shelli L; Schulman-Green, Dena; Geda, Mary; Williams, Kathleen; Dodson, John A; Nanna, Michael G; Allore, Heather G; Murphy, Terrence E; Tinetti, Mary E; Gill, Thomas M; Chaudhry, Sarwat I

    2015-01-01

    To evaluate physician-perceived strengths and limitations of the Thrombolysis in Myocardial Infarction (TIMI) risk scores for use in older adults with acute myocardial infarction (AMI). The TIMI risk scores are risk stratification models developed to estimate mortality risk for patients hospitalized for AMI. However, these models were developed and validated in cohorts underrepresenting older adults (≥75 years). Qualitative study using semi-structured telephone interviews and the constant comparative method for analysis. Twenty-two physicians completed interviews ranging 10-30 min (mean = 18 min). Median sample age was 37 years, with a median of 11.5 years of clinical experience. TIMI strengths included familiarity, ease of use, and validation. Limitations included a lack of risk factors relevant to older adults and model scope and influence. Physicians report that the TIMI models, while widely used in clinical practice, have limitations when applied to older adults. New risk models are needed to guide AMI treatment in this population. Copyright © 2015 Elsevier Inc. All rights reserved.

  6. Physicians’ Perceptions of the Thrombolysis in Myocardial Infarction (TIMI) Risk Score in Older Adults with Acute Myocardial Infarction

    PubMed Central

    Feder, Shelli L.; Schulman-Green, Dena; Geda, Mary; Williams, Kathleen; Dodson, John A.; Nanna, Michael G.; Allore, Heather G.; Murphy, Terrence E.; Tinetti, Mary E.; Gill, Thomas M.; Chaudhry, Sarwat I.

    2015-01-01

    Objectives To evaluate physician-perceived strengths and limitations of the Thrombolysis In Myocardial Infarction (TIMI) risk scores for use in older adults with acute myocardial infarction (AMI). Background The TIMI risk scores are risk stratification models developed to estimate mortality risk for patients hospitalized for AMI. However, these models were developed and validated in cohorts underrepresenting older adults (≥75 years). Methods Qualitative study using semi-structured telephone interviews and the constant comparative method for analysis. Results Twenty-two physicians completed interviews ranging 10–30 minutes (mean = 18 minutes). Median sample age was 37 years, with a median of 11.5 years of clinical experience. TIMI strengths included familiarity, ease of use, and validation. Limitations included a lack of risk factors relevant to older adults and model scope and influence. Conclusions Physicians report that the TIMI models, while widely used in clinical practice, have limitations when applied to older adults. New risk models are needed to guide AMI treatment in this population. PMID:26164651

  7. Effect of Wenxin Granule on Ventricular Remodeling and Myocardial Apoptosis in Rats with Myocardial Infarction

    PubMed Central

    Wu, Aiming; Zhai, Jianying; Zhang, Dongmei; Lou, Lixia; Zhu, Haiyan; Gao, Yonghong; Chai, Limin; Xing, Yanwei; Lv, Xiying; Zhu, Lingqun; Zhao, Mingjing; Wang, Shuoren

    2013-01-01

    Aim. To determine the effect of a Chinese herbal compound named Wenxin Granule on ventricular remodeling and myocardial apoptosis in rats with myocardial infarction (MI). Methods. Male Sprague-Dawley (SD) rats were randomly divided into four groups: the control group, the model group, the metoprolol group, and the Wenxin Granule group (WXKL group) with sample size (n) of 7 rats in each group. An MI model was established in all rats by occlusion of the left anterior descending coronary artery (the control group was without occlusion). Wenxin Granule (1.35 g/kg/day), metoprolol (12 mg/kg/day), and distilled water (5 mL/kg/day for the control and model groups) were administered orally for 4 weeks. Ultrasonic echocardiography was used to examine cardiac structural and functional parameters. Myocardial histopathological changes were observed using haematoxylin and eosin (H&E) dyeing. Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) staining. Serum angiotensin II (Ang II) concentration was measured using the enzyme-linked immunosorbent assay (ELISA). Results. It was found that Wenxin Granule could partially reverse ventricular remodeling, improve heart function, alleviate the histopathological damage, inhibit myocardial apoptosis, and reduce Ang II concentration in rats with MI. Conclusions. The results of the current study suggest that Wenxin Granule may be a potential alternative and complementary medicine for the treatment of MI. PMID:23997803

  8. [Dynamic detection of surface blood flow in rat heart and its application in real time identification of myocardial infarction model].

    PubMed

    Lei, Q; Chen, C; Wu, X L; Chen, W J; Yi, T; Ma, M D; He, Y; Shui, X R; Huang, S A; Chen, C; Lei, W

    2017-04-04

    Objective: To establish a method for monitoring the surface blood flow in the heart of rats, and to clarify the relationship between the degree of myocardial infarction and the blood perfusion on the surface of the heart, so as to provide a new indicator for the identification of rat myocardial infarction model. Methods: The rats were divided into control group (n=23) and model group (n=107), the rat hearts were scanned by the laser doppler perfusion imager before and after operation respectively, and the data was analyzed to acquire the rate of surface blood flow change of the heart. Myocardial infarction size of model group was detected by NBT. Model group were divided into three subgroups of mild myocardial infarction, moderate myocardial infarction and severe myocardial infarction according to the myocardial infarction size, and an analysis was made on the correlativity between rate of surface blood flow change of the heart and myocardial infarction size. Results: Myocardial infarction size was highly correlated to the rate of surface blood flow change of the heart in model group (r=0.849 6, P<0.000 1). There was no significant correlation between infarction size and heart blood flow in the mild myocardial infarction subgroup (r=-0.133 6, P>0.05), while the correlation in moderate myocardial infarction was significant (r=0.721 7, P<0.000 1), and the highest correlation was shown in severe myocardial infarction subgroup (r=0.910 2, P<0.000 1). Conclusion: The heart surface blood flow has a close relationship with the myocardial infarction size in rat, so the change of heart blood perfusion can beused as an effective reference to establish and identify rat myocardial infarction model.

  9. Persistent T-wave inversion predicts myocardial damage after ST-elevation myocardial infarction.

    PubMed

    Reindl, Martin; Reinstadler, Sebastian Johannes; Feistritzer, Hans-Josef; Niess, Lea; Koch, Constantin; Mayr, Agnes; Klug, Gert; Metzler, Bernhard

    2017-08-15

    Persistent T-wave inversion (PTI) after ST-elevation myocardial infarction (STEMI) is associated with worse clinical outcome; however, the underlying mechanism between PTI and poor prognosis is incompletely understood. We sought to investigate the relationship between PTI and myocardial damage assessed by cardiac magnetic resonance (CMR) following STEMI. In this prospective observational study, we included 142 consecutive revascularized STEMI patients. Electrocardiography to determine the presence and amplitude of PTI and pathological Q-waves was conducted 4months after infarction. CMR was performed within 1week after infarction and at 4months follow-up to evaluate infarct characteristics and myocardial function. Patients with PTI (n=103, 73%) showed a larger acute (21[11-29] vs. 6[1-13]%; p<0.001) and chronic infarct size (IS) (14[8-19] vs. 3[1-8]%; p<0.001) and more frequently microvascular obstruction (59 vs. 33%; p=0.02). The association between PTI and chronic IS remained significant (odds ratio: 9.02, 95%CI 3.49-23.35; p<0.001) after adjustment for pathological Q-wave and other IS estimators (high-sensitivity cardiac troponin T and C-reactive protein, N-terminal pro B-type natriuretic peptide, culprit vessel, pre-interventional TIMI flow). The value of PTI amplitude for the prediction of large chronic IS>11% (AUC: 0.84, 95%CI 0.77-0.90) was significantly higher compared to Q-wave amplitude (AUC: 0.72, 95%CI 0.63-0.80; p=0.009); the combination of PTI with pathological Q-wave (Q-wave/T-wave score) led to a net reclassification improvement of 0.43 (95% CI 0.29-0.57; p<0.001) as compared to PTI alone. PTI following STEMI is independently and incrementally associated with more extensive myocardial damage as visualized by CMR. An electrocardiographic score combining PTI with pathological Q-wave allows for a highly accurate IS estimation post-STEMI. Copyright © 2017 Elsevier B.V. All rights reserved.

  10. Effect of hydroxy safflower yellow A on myocardial apoptosis after acute myocardial infarction in rats.

    PubMed

    Zhou, M X; Fu, J H; Zhang, Q; Wang, J Q

    2015-04-10

    This study aimed to investigate the effect of hydroxy safflower yellow A (HSYA) on myocardial apoptosis after acute myocardial infarction (AMI) in rats. We randomly divided 170 male Wistar rats into 6 groups (N = 23): normal control, sham, control, SY (90 mg/kg), HSYA high-dose (HSYA-H, 40 mg/kg), and HSYA low-dose groups (HSYA-L, 20 mg/kg). Myocardial ischemic injury was induced by ligating the anterior descending coronary artery, and the degree of myocardial ischemia was evaluated using electrocardiography and nitroblue tetrazolium staining. Bax and Bcl-2 expressions in the ischemic myocardium were determined using immunohistochemical analysis. Peroxisome proliferator-activated receptor-γ (PPAR-γ) expression in the myocardium of rats with AMI was determined using reverse transcription-polymerase chain reaction. Compared to rats in the control group, those in the HYSA-H, HSYA-L, and SY groups showed a decrease in the elevated ST segments and an increase in the infarct size. The rats in the drug-treated groups showed a significantly lower percentage of Bax-positive cells and a significantly higher percentage of Bcl-2-positive cells than those in the control group (P < 0.05). Moreover, mRNA expression of PPAR-γ in the ischemic myocardium of rats in the SY, HSYA-L, and HSYA-H groups was significantly lower than that in the control group (P < 0.05). Thus, HSYA and SY can attenuate myocardial ischemia in rats, possibly by increasing the level of Bcl-2/Bax, and PPAR-γ may be not a necessary link in this process.

  11. Cost-effectiveness of eplerenone compared with placebo in patients with myocardial infarction complicated by left ventricular dysfunction and heart failure.

    PubMed

    Weintraub, William S; Zhang, Zefeng; Mahoney, Elizabeth M; Kolm, Paul; Spertus, John A; Caro, Jaime; Ishak, Jack; Goldberg, Robert; Tooley, Joseph; Willke, Richard; Pitt, Bertram

    2005-03-08

    In the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), aldosterone blockade with eplerenone decreased mortality in patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction. The present study was performed to evaluate the cost-effectiveness of eplerenone compared with placebo in these patients. A total of 6632 patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction were randomized to eplerenone or placebo and followed up for a mean of 16 months. The coprimary end points were all-cause mortality and the composite of cardiovascular mortality/cardiovascular hospitalization. The evaluation of resource use included hospitalizations, outpatient services, and medications. Eplerenone was priced at the average wholesale price, 3.60 dollars per day. Survival beyond the trial period was estimated from data from the Framingham Heart Study, the Saskatchewan Health database, and the Worcester Heart Attack Registry. The incremental cost-effectiveness of eplerenone in cost per life-year and quality-adjusted life-year gained compared with placebo was estimated. The number of life-years gained with eplerenone was 0.1014 based on Framingham (95% CI, 0.0306 to 0.1740), 0.0636 with Saskatchewan (95% CI, 0.0229 to 0.1038), and 0.1337 with Worcester (95% CI, 0.0438 to 0.2252) data. Cost was 1391 dollars higher over the trial period in the eplerenone arm (95% CI, 656 to 2165) because of drug cost. The incremental cost-effectiveness ratio was 13,718 dollars per life-year gained with Framingham (96.7% under 50,000 dollars per life-year gained), 21,876 dollars with Saskatchewan, and 10,402 dollars with Worcester. Eplerenone compared with placebo in the treatment of heart failure after acute myocardial infarction is effective in reducing mortality and is cost-effective in increasing years of life by commonly used criteria.

  12. Acute myocardial infarction after heart irradiation in young patients with Hodgkin's disease

    SciTech Connect

    Joensuu, H.

    1989-02-01

    Forty-seven patients younger than 40 years at the time of the diagnosis, and irradiated to the mediastinum for Hodgkin's disease at Turku University Central Hospital from 1977 to 1982, were regularly followed for 56 to 127 months after therapy. Two patients developed an acute myocardial infarction ten and 50 months after cardiac irradiation at the age of only 28 and 24 years, respectively. None of the patients died from lymphoma within five years from the diagnosis, but one of the infarctions was eventually fatal. Since acute myocardial infarction is rare in this age group, the result suggests strongly that prior cardiac irradiation is a risk factor for acute myocardial infarction. The possibility of radiation-induced myocardial infarction should be taken into account both in treatment planning and follow-up of patients with Hodgkin's disease.

  13. [Clinical significance of myocardial 123I-BMIPP imaging in patients with myocardial infarction].

    PubMed

    Narita, M; Kurihara, T; Shindoh, T; Honda, M

    1997-03-01

    In order to clarify the characteristics of fatty acid metabolism in patients with myocardial infarction (MI), we performed myocardial imaging with 123I-beta-methyl-p-iodophenylpentadecanoic acid (BMIPP) and we compared these findings with exercise stress (Ex) and resting myocardial perfusion imaging with 99mTc-methoxyisobutylisonitrile (MIBI) and left ventricular wall motion index (WMI) which were obtained by left ventriculography. We studied 55 patients with MI, 14 patients with recent MI (RMI) and 41 patients with old MI (OMI), and myocardial images were divided into 17 segments and myocardial uptake of the radionuclide was graded from 0 (normal) to 3 (maximal abnormality). In 28 patients we compared segmental defect score (SDS) with WMI which were obtained by centerline method at the corresponded segments. As a whole, the mean total defect scores (TDSs) of BMIPP and Ex were similar and they were greater than the mean TDS of resting perfusion. In 30 patient (55%) TDS of BMIPP was greater than that of TDS of resting perfusion. In 24 patients perfusion abnormality developed by Ex and the location of BMIPP abnormality coincided with the abnormality of Ex. But in the other 6 patients Ex did not induce any abnormality and they were all RMI and infarcted coronary artery was patent. However in the group with TDS of BMIPP identical to TDS of resting perfusion (25 patients), 92% did not show myocardial perfusion abnormality after Ex. In the comparison of SDS and WMI, myocardial segments were divided into 3 groups; both SDSs of BMIPP and resting perfusion were normal or borderline abnormality (Group 1, 82 segments), SDS of resting perfusion was normal or borderline and SDS of BMIPP was definitely abnormal (Group 2, 10 segments) and both SDSs of BMIPP and resting perfusion were definitely abnormal (Group 3, 48 segments). In Group 1, WMS (-0.41 +/- 0.77) was significantly (p < 0.001) greater than those of Group 2 (-2.14 +/- 0.50) and Group 3 (-2.32 +/- 0.67). But there was

  14. Magnetic resonance imaging dynamic contrast enhancement (DCE) characteristics of healed myocardial infarction differ from viable myocardium.

    PubMed

    Goldfarb, James W; Zhao, Wenguo

    2014-12-01

    To determine whether healed myocardial infarction alters dynamic contrast-enhancement (DCE) curve shapes as well as late gadolinium-enhancement (LGE). Twenty patients with chronic myocardial infarction underwent MR imaging at 1.5 T with blood and myocardial T1 measurements before and after contrast administration for forty minutes. Viable and infarcted myocardial partition coefficients were calculated using multipoint slope methods for ten different DCE sampling intervals and windows. Partition coefficients and coefficients of determination were compared with paired statistical tests to assess the linearity of DCE curve shapes over the 40 min time period. Calculated partition coefficients did not vary significantly between methods (p=0.325) for viable myocardium but did differ for infarcted myocardium (p<0.001), indicating a difference in infarcted DCE. There was a significant difference between viable and infarcted myocardial partition coefficients estimates for all methods with the exception of methods that included measurements during the first 10 min after contrast agent administration. Myocardial partition coefficients calculated from a slope calculation vary in healed myocardial infarction based on the selection of samples due to non-linear DCE curve shapes. Partition coefficient calculations are insensitive to data sampling effects in viable myocardium due to linear DCE curve shapes. Copyright © 2014 Elsevier Inc. All rights reserved.

  15. Acute myocardial infarction: the first manifestation of ischemic heart disease and relation to risk factors.

    PubMed

    Manfroi, Waldomiro Carlos; Peukert, Carolina; Berti, Clarissa Bacha; Noer, Clarissa; Gutierres, Danielle de Avila; Silva, Felipe Theodoro Bezerra Gaspar Carvalho da

    2002-04-01

    To assess the association between cardiovascular risk factors and acute myocardial infarction as the first manifestation of ischemic heart disease, correlating them with coronary angiographic findings. We carried out a cross-sectional study of 104 patients with previous acute myocardial infarction, who were divided into 2 groups according to the presence or absence of angina prior to acute myocardial infarction. We assessed the presence of angina preceding acute myocardial infarction and risk factors, such as age >55 years, male sex, smoking, systemic arterial hypertension, lipid profile, diabetes mellitus, obesity, sedentary lifestyle, and familial history of ischemic heart disease. On coronary angiography, the severity of coronary heart disease and presence of left ventricular hypertrophy were assessed. Of the 104 patients studied, 72.1% were males, 90.4% were white, 73.1% were older than 55 years, and 53.8% were hypertensive. Acute myocardial infarction was the first manifestation of ischemic heart disease in 49% of the patients. The associated risk factors were systemic arterial hypertension (RR=0.19; 95% CI=0.06-0.59; P=0.04) and left ventricular hypertrophy (RR=0.27; 95% CI=0,.8-0.88; P=0.03). The remaining risk factors were not statistically significant. Prevalence of acute myocardial infarction as the first manifestation of ischemic heart disease is high, approximately 50%. Hypertensive individuals more frequently have symptoms preceding acute myocardial infarction, probably due to ventricular hypertrophy associated with high blood pressure levels.

  16. Impact of type 2 diabetes mellitus on recurrent myocardial infarction in China.

    PubMed

    Li, Wentao; Li, Muwei; Gao, Chuanyu; Wang, Xianpei; Qi, Datun; Liu, Jun; Jin, Qiangsong

    2016-11-01

    To evaluate the influence of type 2 diabetes mellitus on the long-term outcomes of Chinese patients with previous myocardial infarction, we studied 864 patients with previous myocardial infarction, including 251 with type 2 diabetes mellitus and 613 without type 2 diabetes mellitus, over a median follow-up time of 2.9 years. The type 2 diabetes mellitus patients were subdivided into 95 insulin-treated diabetes mellitus and 156 non-insulin-treated diabetes mellitus subjects. The crude incidences (per 1000 patient-years) in the type 2 diabetes mellitus subjects versus the non-type 2 diabetes mellitus subjects were 43.7 versus 25.1 for recurrent myocardial infarction, 68.7 versus 28.3 for all-cause death and 99.8 versus 49.9 for the composite end point (i.e. recurrent myocardial infarction or all-cause death). Cox regression analysis showed that the adjusted hazard ratios for recurrent myocardial infarction, all-cause death and their combination were 1.67 (95% confidence interval: 1.06-2.74), 1.90 (1.25-2.90) and 1.72 (1.23-2.40), respectively. Significant associations were also observed between insulin treatment and all-cause death. Our findings suggested that type 2 diabetes mellitus is an independent risk factor for recurrent myocardial infarction, all-cause death and the composite end point among previous myocardial infarction patients.

  17. Safety Evaluation of Sevoflurane as Anesthetic Agent in Mouse Model of Myocardial Ischemic Infarction.

    PubMed

    Cheng, Xiang; Hou, Jianglong; Liu, Jiaming; Sun, Xiaorong; Sheng, Qin; Han, Pengfei; Kang, Y James

    2017-04-01

    The selection of anesthetics for patients with myocardial infarction is critically challenging. Sevoflurane is a volatile anesthetic gradually used in recent years. The intraoperative hemodynamic stability of sevoflurane was supported by several studies with some suggestions for its use for patients with cardiac events. The present study was undertaken to investigate the effect of sevoflurane on mice with myocardial infarction to evaluate the safety issue of this agent for possible application in patients with myocardial infarction. Mice of 7-12 weeks old were subjected to left anterior descending artery ligation to introduce acute myocardial infarction. The effect of sevoflurane on the hemodynamics was examined in comparison with that of currently available agent etomidate at low and moderate doses. The results showed that sevoflurane caused unstable hemodynamic changes in mice with myocardial infarction at both low and moderate inhaled concentrations relative to low and moderate doses of etomidate. In addition, the relative safety margin estimated from therapeutic index was decreased by 50 % when sevoflurane was used for mice with myocardial infarction relative to control mice, but only decreased by 20 % for etomidate. These analyses indicate that in comparison with currently available agent etomidate, sevoflurane should not be applied to patients with myocardial infarction or other cardiac events.

  18. Myocardium and microvessel endothelium apoptosis at day 7 following reperfused acute myocardial infarction.

    PubMed

    Kang, Sheng; Yang, Yue-jin; Wu, Yi-ling; Chen, Yu-tong; Li, Li; Tian, Yi

    2010-01-01

    This study was to investigate the salvaged myocardial and microvascular endothelial cells apoptosis at the first week of reperfused acute myocardial infarction (AMI). Sixteen mini swines (20-30 kg) were randomly assigned to the sham-operated group and the AMI group. The acute myocardial infarction and reperfusion model was created, and pathologic myocardial tissue was collected at day 7 following left anterior descending coronary artery reperfusion, and detected by transmission electron microscope, in situ cell apoptosis detection (TUNEL method), Real-time Quantitative Polymerase Chain Reaction and Western blot. In the AMI group, the infarcted area showed the myolysis, fibroblast and injuried endothelial cells under transmission electron microscope. The infarcted area had higher apoptotic index of microvascular endothelial cells than the marginal area, the normal area, and the sham-operated area (all P<0.05). Fas and Bax mRNA expressions in the infarcted area were higher than those in the marginal area, the normal area, and the sham-operated area (all P<0.05), and both protein overexpressions and Bcl-2 low expression in the infarcted and marginal areas compared with the normal area and the sham-operated area. The overexpressions of Fas and Bax or the low expression of Bcl-2 in the infarcted and marginal heart tissue may play an important role in the acceleration of myocardial and endothelial apoptosis at 7th day following reperfused acute myocardial infarction. Copyright 2009 Elsevier Inc. All rights reserved.

  19. Magnetic resonance imaging in patients with unstable angina: comparison with acute myocardial infarction and normals

    SciTech Connect

    Ahmad, M.; Johnson, R.F. Jr.; Fawcett, H.D.; Schreiber, M.H.

    1988-09-01

    The role of magnetic resonance imaging in characterizing normal, ischemic and infarcted segments of myocardium was examined in 8 patients with unstable angina, 11 patients with acute myocardial infarction, and 7 patients with stable angina. Eleven normal volunteers were imaged for comparison. Myocardial segments in short axis magnetic resonance images were classified as normal or abnormal on the basis of perfusion changes observed in thallium-201 images in 22 patients and according to the electrocariographic localization of infarction in 4 patients. T2 relaxation time was measured in 57 myocardial segments with abnormal perfusion (24 with reversible and 33 with irreversible perfusion changes) and in 25 normally perfused segments. T2 measurements in normally perfused segments of patients with acute myocardial infarction, unstable angina and stable angina were within normal range derived from T2 measurements in 48 myocardial segments of 11 normal volunteers (42 +/- 10 ms). T2 in abnormal myocardial segments of patients with stable angina also was not significantly different from normal. T2 of abnormal segments in patients with unstable angina (64 +/- 14 in reversibly ischemic and 67 +/- 21 in the irreversibly ischemic segments) was prolonged when compared to normal (p less than 0.0001) and was not significantly different from T2 in abnormal segments of patients with acute myocardial infarction (62 +/- 18 for reversibly and 66 +/- 11 for irreversibly ischemic segments). The data indicate that T2 prolongation is not specific for acute myocardial infarction and may be observed in abnormally perfused segments of patients with unstable angina.

  20. [The content of selen in blood plasma in patients with acute Q-wave myocardial infarction].

    PubMed

    Radchenko, E N; Nizov, A A; Ivanova, A Yu; Sidorova, Yu S

    2015-01-01

    The level of blood plasma selenium was analyzed by microfluorimetric method in in-patients and out-patients with acute coronary syndrome with ST-elevation resulting in acute Q-wave myocardial infarction. 72 patients, 40-75 years old, with acute Q-wave myocardial infarction were followed during a month. The initial decreased concentration of blood plasma selenium was recorded in most patients in the acute period of the myocardial infarction: deficiency of the microelement (< 90 mcg/l) was found in 30 subjects, the critical ranges (< 70 mcg/l) were stated in 33 patients. Just 2 patients had optimal concentration and 7 patients had a suboptimal one (90-114 mcg/l). Blood plasma level of the microelement increased in 2 weeks after myocardial infarction (in subacute stage) but it was still within deficient or critical levels. No difference was detected in selen concentration depending on gender, age, location on myocardial infarction, accompanying diseases, presence of some risk factors (smoking, alcohol abuse, hereditary predisposition to coronary artery disease). At the same time we revealed a significant Spearman rank correlation in patients with Q-wave myocardial infarction between basal level of blood serum selenium on the one hand, and electrocardiography indices (reflecting the rate of myocardial lesion and necrosis), echocardiography. data (which characterize myocardium reparation processes and remodeling), CPK (a prognostic marker of the myocardial necrosis), HDL-cholesterol (lipid profile index), blood potassium level and BMI on the other.

  1. Noninvasive electrocardiographic imaging of chronic myocardial infarct scar.

    PubMed

    Horáček, B Milan; Wang, Linwei; Dawoud, Fady; Xu, Jingjia; Sapp, John L

    2015-01-01

    Myocardial infarction (MI) scar constitutes a substrate for ventricular tachycardia (VT), and an accurate delineation of infarct scar may help to identify reentrant circuits and thus facilitate catheter ablation. One of the recent advancements in characterization of a VT substrate is its volumetric delineation within the ventricular wall by noninvasive electrocardiographic imaging. This paper compares, in four specific cases, epicardial and volumetric inverse solutions, using magnetic resonance imaging (MRI) with late gadolinium enhancement as a gold standard. For patients with chronic MI, who presented at Glasgow Western Infirmary, delayed-enhancement MRI and 120-lead body surface potential mapping (BSPM) data were acquired and 4 selected cases were later made available to a wider community as part of the 2007 PhysioNet/Computers in Cardiology Challenge. These data were used to perform patient-specific inverse solutions for epicardial electrograms and morphology-based criteria were applied to delineate infarct scar on the epicardial surface. Later, the Rochester group analyzed the same data by means of a novel inverse solution for reconstructing intramural transmembrane potentials, to delineate infarct scar in three dimensions. Comparison of the performance of three specific inverse-solution algorithms is presented here, using scores based on the 17-segment ventricular division scheme recommended by the American Heart Association. The noninvasive methods delineating infarct scar as three-dimensional (3D) intramural distribution of transmembrane action potentials outperform estimates providing scar delineation on the epicardial surface in all scores used for comparison. In particular, the extent of infarct scar (its percentage mass relative to the total ventricular mass) is rendered more accurately by the 3D estimate. Moreover, the volumetric rendition of scar border provides better clues to potential targets for catheter ablation. Electrocardiographic inverse

  2. Noninvasive electrocardiographic imaging of chronic myocardial infarct scar§

    PubMed Central

    Horáček, B. Milan; Wang, Linwei; Dawoud, Fady; Xu, Jingjia; Sapp, John L.

    2015-01-01

    Background Myocardial infarction (MI) scar constitutes a substrate for ventricular tachycardia (VT), and an accurate delineation of infarct scar may help to identify reentrant circuits and thus facilitate catheter ablation. One of the recent advancements in characterization of a VT substrate is its volumetric delineation within the ventricular wall by noninvasive electrocardiographic imaging. This paper compares, in four specific cases, epicardial and volumetric inverse solutions, using magnetic resonance imaging (MRI) with late gadolinium enhancement as a gold standard. Methods For patients with chronic MI, who presented at Glasgow Western Infirmary, delayed-enhancement MRI and 120-lead body surface potential mapping (BSPM) data were acquired and 4 selected cases were later made available to a wider community as part of the 2007 PhysioNet/Computers in Cardiology Challenge. These data were used to perform patient-specific inverse solutions for epicardial electrograms and morphology-based criteria were applied to delineate infarct scar on the epicardial surface. Later, the Rochester group analyzed the same data by means of a novel inverse solution for reconstructing intramural transmembrane potentials, to delineate infarct scar in three dimensions. Comparison of the performance of three specific inverse-solution algorithms is presented here, using scores based on the 17-segment ventricular division scheme recommended by the American Heart Association. Results The noninvasive methods delineating infarct scar as three-dimensional (3D) intramural distribution of transmembrane action potentials outperform estimates providing scar delineation on the epicardial surface in all scores used for comparison. In particular, the extent of infarct scar (its percentage mass relative to the total ventricular mass) is rendered more accurately by the 3D estimate. Moreover, the volumetric rendition of scar border provides better clues to potential targets for catheter ablation

  3. Protective mechanism of quercetin on acute myocardial infarction in rats.

    PubMed

    Li, B; Yang, M; Liu, J W; Yin, G T

    2016-03-11

    To investigate the protective mechanism of quercetin on acute myocardial infarction (AMI) rats, an AMI rat model was established by ligating the left coronary anterior descending branch. The rats were randomly divided into the model group and low- and high-dose quercetin groups. The control group comprised sham-operated rats. The rats in the low- and high-dose quercetin groups were administered 100 and 400 mg/kg quercetin, respectively, by gavage. The rats in the control and model groups were administered isometric normal saline once daily for one week. The mRNA and protein levels of TNF-α and IL-1β in the myocardial tissue of rats were detected in each group by real time polymerase chain reaction and enzyme-linked immunosorbent assay. Malondialdehyde (MDA) content in the myocardial tissue and superoxide dismutase (SOD) and catalase (CAT) activities were detected using a colorimetric method. The level of apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. Compared with those in the control group, the mRNA and protein levels of TNF-α, IL-1β and MDA content in the model, low-, and high-dose groups significantly increased. SOD and CAT activities decreased significantly. The cell apoptosis index increased significantly  (P < 0.05). Compared with those in the model group, the mRNA and protein levels of TNF-α and IL-1β and MDA content in myocardial tissue of rats in the low-dose and high-dose groups decreased significantly. SOD and CAT activities increased significantly. The cell apoptosis index significantly reduced (P < 0.05). In conclusion, quercetin has significant anti-inflammatory, antioxidant, and anti-apoptotic effects on AMI rats and can effectively protect against myocardium damage.

  4. Myocardial uptake of indium-111-labeled antimyosin in acute subendocardial infarction: Clinical, histochemical, and autoradiographic correlation of myocardial necrosis

    SciTech Connect

    Hendel, R.C.; McSherry, B.A.; Leppo, J.A. )

    1990-11-01

    Indium-111-labeled antimyosin has been utilized in the diagnosis and localization of acute transmural myocardial infarction. The present report describes a patient who presented with a massive subendocardial infarction. Two days after the injection of antimyosin, the patient's clinical status markedly deteriorated and he expired. Postmortem examination demonstrated severe three-vessel coronary artery disease with extensive myocyte death in the endocardium. Autoradiography and histochemical staining of the prosected heart demonstrated high correlation for myocardial necrosis and corresponded to clinical evidence for diffuse subendocardial infarction.

  5. n-3 fatty acids and cardiovascular events after myocardial infarction.

    PubMed

    Kromhout, Daan; Giltay, Erik J; Geleijnse, Johanna M

    2010-11-18

    Results from prospective cohort studies and randomized, controlled trials have provided evidence of a protective effect of n-3 fatty acids against cardiovascular diseases. We examined the effect of the marine n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and of the plant-derived alpha-linolenic acid (ALA) on the rate of cardiovascular events among patients who have had a myocardial infarction. In a multicenter, double-blind, placebo-controlled trial, we randomly assigned 4837 patients, 60 through 80 years of age (78% men), who had had a myocardial infarction and were receiving state-of-the-art antihypertensive, antithrombotic, and lipid-modifying therapy to receive for 40 months one of four trial margarines: a margarine supplemented with a combination of EPA and DHA (with a targeted additional daily intake of 400 mg of EPA-DHA), a margarine supplemented with ALA (with a targeted additional daily intake of 2 g of ALA), a margarine supplemented with EPA-DHA and ALA, or a placebo margarine. The primary end point was the rate of major cardiovascular events, which comprised fatal and nonfatal cardiovascular events and cardiac interventions. Data were analyzed according to the intention-to-treat principle, with the use of Cox proportional-hazards models. The patients consumed, on average, 18.8 g of margarine per day, which resulted in additional intakes of 226 mg of EPA combined with 150 mg of DHA, 1.9 g of ALA, or both, in the active-treatment groups. During the follow-up period, a major cardiovascular event occurred in 671 patients (13.9%). Neither EPA-DHA nor ALA reduced this primary end point (hazard ratio with EPA-DHA, 1.01; 95% confidence interval [CI], 0.87 to 1.17; P=0.93; hazard ratio with ALA, 0.91; 95% CI, 0.78 to 1.05; P=0.20). In the prespecified subgroup of women, ALA, as compared with placebo and EPA-DHA alone, was associated with a reduction in the rate of major cardiovascular events that approached significance (hazard ratio

  6. Estimation of infarct size by myocardial emission computed tomography with thallium-201 and its relation to creatine kinase-MB release after myocardial infarction in man

    SciTech Connect

    Tamaki, S.; Nakajima, H.; Murakami, T.

    1982-11-01

    Emission computed tomography (ECT) for thallium-201 (/sup 201/Tl) myocardial imaging was evaluated in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar /sup 201/Tl perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of /sup 201/Tl perfusion defects, the infarct area in planar images and the infarct volume in reconsturcted ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r=0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r=0.69; for the largest infarct area, r=0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS.

  7. Estimation of infarct size by myocardial emission computed tomography with /sup 201/Tl and its relation to creatine kinase-MB release after myocardial infarction in man

    SciTech Connect

    Tamaki, S.; Nakajima, H.; Murakami, T.

    1982-11-01

    We evaluated emission computed tomography (ECT) /sup 201/Tl myocardial imaging in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar /sup 201/Tl perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of /sup 201/Tl perfusion defects, the infarct area in planar images and the infarct volume in reconstructed ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r . 0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r . 0.69; for the largest infarct area, r . 0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS.

  8. Treatment of patients with myocardial infarction depends on history of cancer.

    PubMed

    Rohrmann, Sabine; Witassek, Fabienne; Erne, Paul; Rickli, Hans; Radovanovic, Dragana

    2017-09-01

    Although cancer treatment considerably affects cardiovascular health, little is known about how cancer patients are treated for an acute myocardial infarction. We aimed to investigate whether acute myocardial infarction patients with a history of cancer received the same guideline recommended treatment as those acute myocardial infarction patients without and whether they differ with respect to inhospital outcome. All patients with ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction, enrolled between 2002 and mid-2015 in the acute myocardial infarction in Switzerland (AMIS Plus) registry with comorbidity data based on the Charlson comorbidity index were analysed. Patients were classified as having cancer if one of the cancer diseases of the Charlson comorbidity index was indicated. Immediate treatment strategies and inhospital outcomes were compared between groups using propensity score matching. Of 35,249 patients, 1981 (5.6%) had a history of cancer. After propensity score matching for age, gender, Killip class >2, ST-segment elevation myocardial infarction and renal disease (1981 patients per group), significant differences were no longer found for a history of acute myocardial infarction, hypertension, diabetes, heart failure and cerebrovascular disease between cancer and non-cancer patients. However, cancer patients underwent percutaneous coronary intervention less frequently (odds ratio (OR) 0.76; 95% confidence interval (CI) 0.67-0.88) and received P2Y12 blockers (OR 0.82; 95% CI 0.71-0.94) and statins (OR 0.87; 95% CI 0.76-0.99) less frequently. Inhospital mortality was significantly higher in cancer patients (10.7% vs. 7.6%, OR 1.45; 95% CI 1.17-1.81). However, the main cause of death was cardiac in both groups ( P=0.06). Acute myocardial infarction patients with a history of cancer were less likely to receive guideline recommended treatment and had worse inhospital outcomes than non-cancer patients.

  9. Elevated risk of myocardial infarction in very young immigrants from former Yugoslavia.

    PubMed

    Wiesbauer, Franz; Blessberger, Hermann; Goliasch, Georg; Holy, Erik Walter; Pfaffenberger, Stephan; Tentzeris, Ioannis; Maurer, Gerald; Huber, Kurt; Abdolvahab, Farshid; Sodeck, Gottfried; Exner, Markus; Wojta, Johann; Schillinger, Martin

    2009-01-01

    We performed a hospital based case-control study to assess if the risk of myocardial infarction at a very young age (< or =40 years) was elevated in immigrants from the region of former Yugoslavia. Patients were classified as "exposed" if they or both their parents were born in former Yugoslavia. Consecutive myocardial infarction patients were recruited in the immediate post-infarction period from two Viennese hospitals over a 3.5-year period. Control patients free of myocardial infarction were frequency matched on age, gender, centre, and time in an approximate 1:2 ratio. Logistic regression was used for the assessment of an association between Yugoslavian descent and myocardial infarction. Overall, we recruited 102 myocardial infarction patients and 200 controls. The median age of infarction patients was 37.3 years. Yugoslavian descent was strongly associated with myocardial infarction (crude OR 7.3, 95% CI 3-18). This association was attenuated after multivariate adjustment (OR 3.9, 95% CI 1.2-13) but remained statistically significant. Using Miettinen's formula for population attributable risk, we calculated that between 15.3% (adjusted) and 17.8% (unadjusted) of myocardial infarction cases in very young patients could be attributable to immigrants from the studied region. In conclusion, we found that the risk of developing myocardial infarction at a young age is elevated in immigrants from the region of former Yugoslavia and their offspring. Even though residual confounding cannot be ruled out definitively, this risk seems to be independent of established cardiovascular risk factors.

  10. Treatment of Chronic Myocardial Infarction in a Pig (Sus scrofa) Model with Extracellular Matrix and Stem Cells

    DTIC Science & Technology

    2015-08-13

    Use additional pages If necessary.) PROTOCOL #: FDG20140039A DATE: 13 August 2015 PROTOCOL TITLE: Treatment of Chronic Myocardial Infarction in a...model developed in protocols FDG20120019A and FDG20130043A, we were able to successfully create myocardial infarctions in pigs with a high survival rate...applications.) ObJectives: The goal of this protocol was to create myocardial infarctions in miniplgs using polystyrene microspheres to Infarct a

  11. Myocardial infarction during pregnancy: report of two cases with a review of the literature

    PubMed Central

    Husaini, M. H.

    1971-01-01

    Two further cases of myocardial infarction during pregnancy are reported. From the review of the literature of forty-three cases of myocardial infarction during pregnancy and labour, it appears that myocardial infarction in the last trimester and labour is frequently fatal. Short-term anticoagulant therapy to suppress any thrombo-embolic tendency is desirable. Termination of pregnancy is indicated for patients in cardiac failure or persistent angina. For patients who are well, either assisted vaginal delivery or Caesarean section are equally good. ImagesFig. 1Fig. 2 PMID:4945869

  12. A rare case of concomitant stress (takotsubo) cardiomyopathy and acute myocardial infarction.

    PubMed

    Menezes, Miguel Nobre; Silva, Doroteia; Almeida, Ana G; Pinto, Fausto J; Brito, Dulce

    2015-01-01

    Stress cardiomyopathy and myocardial infarction are generally regarded as mutually exclusive diagnoses. We report the case of a 54-year-old woman who presented with acute chest pain. Her echocardiogram and ventriculography were typical of stress cardiomyopathy, but she had one subocclusive coronary lesion, a highly significant rise in troponin and a subendocardial myocardial infarction scar documented on cardiac magnetic resonance. This is a rare case of concomitant myocardial infarction and stress cardiomyopathy, in which the acute coronary syndrome itself may have been the stressor, given the absence of other identifiable causes. Copyright © 2014 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.

  13. Risk factors for myocardial infarction associated with the Chicago snowstorm of jan 13- 15, 1979.

    PubMed

    Glass, R I; Wiesenthal, A M; Zack, M M; Preston, M

    1981-01-09

    Sixty male survivors of acute myocardial infarction in the week after the Chicago blizzard of Jan 15, 1979, were matched by hospital and sex with 60 myocardial infarction survivors from a week without snowfall to determine whether a history of previous heart disease or of cardiac risk factors increased the risk of a postblizzard myocardial infarction. Cases did not differ significantly from control subjects with respect to age, percentage working full time, or percentage with a history of heart disease, hypertension, smoking, diabetes mellitus, obesity, or gout. Hypercholesterolemia was four times as common among cases as among controls.

  14. Tissue imaging of myocardial infarct regions by a slit-scanning Raman microscope

    NASA Astrophysics Data System (ADS)

    Ogawa, Mitsugu; Harada, Yoshinori; Yamaoka, Yoshihisa; Fujita, Katsumasa; Takamatsu, Tetsuro

    2009-02-01

    Estimating the distribution of myocardial fibrosis after myocardial infarct is important for appropriate therapeutic planning. Here, we applied a Raman confocal microscope equipped with slit scanner for molecular tissue imaging of rat infarcted hearts. Raman spectra of the cytoplasm of cardiomyocytes included the resonance Raman bands at 751, 1130 and 1582 cm-1 arising mainly from reduced b- and c- type cytochromes. Raman spectra of fibrotic tissues at the borderzone of old myocardial infarct were highly consistent with that of collagen type I. Based on these findings, we successfully obtained Raman tissue images of a cardiomyocyte and surrounding collagen at the cellular level.

  15. [Extracorporeal cardiac shock wave therapy improved myocardial micro-vascular circulation after acute myocardial infarction at early stage in pigs].

    PubMed

    Tao, Si-ming; Guo, Tao; Wang, Yue; Cai, Hong-yan; Yang, Chao

    2011-03-01

    To explore the effect of low-energy extracorporeal shock wave therapy to improve myocardial micro-vascular circulation after acute myocardial infarction at the early stage in pig model. A total of 25 domestic pigs were used in this study. Model of acute myocardial infarction (AMI) was created successfully by the implantation of angioplasty balloon in mid-distal segment of left anterior descending coronary artery (n=20). These AMI animals were divided two groups. Extracorporeal shock wave therapy to the ischemic myocardial region was performed for the group of shock wave therapy (n=15) at 3 days after acute myocardial infarction; The remaining AMI animals were treated in the same manner, but without the shock wave therapy (n=5), The other health animals (n=5) were used as blank control group. The number of endothelium cell, capillary density, VEGF mRNA level and collateral vessel Rentrop score in each group were evaluated and compared. Shock wave treatment up-regulated the mRNA expression of VEGF in the model of acute myocardial infarction (P < 0.05). Furthermore, the number of capillaries was significantly higher in the shock wave group than that of positive and blank control group (P < 0.05). The Rentrop score of collateral vessel indicated the reconstruction of collateral circulation in shock wave group. Extracorporeal cardiac shock wave therapy could effectively induce angiogenesis, up-regulate the expression of angiogenic factor, resulting in an improvement in micro-vascular circulation reconstruction of ischemic myocardial region.

  16. Raman spectroscopy of human saliva for acute myocardial infarction detection

    NASA Astrophysics Data System (ADS)

    Chen, Maowen; Chen, Yuanxiang; Wu, Shanshan; Huang, Wei; Lin, Jinyong; Weng, Guo-Xing; Chen, Rong

    2014-09-01

    Raman spectroscopy is a rapidly non-invasive technique with great potential for biomedical research. The aim of this study was to evaluate the feasibility of using Raman spectroscopy of human saliva for acute myocardial infarction (AMI) detection. Raman spectroscopy measurements were performed on two groups of saliva samples: one group from patients (n=30) with confirmed AMI and the other group from healthy controls (n=31). The diagnostic performance for differentiating AMI saliva from normal saliva was evaluated by multivariate statistical analysis. The combination of principal component analysis (PCA) and linear discriminate analysis (LDA) of the measured Raman spectra separated the spectral features of the two groups into two distinct clusters with little overlaps, rendering the sensitivity of 80.0% and specificity of 80.6%. The results from this exploratory study demonstrated that Raman spectroscopy of human saliva can serve as a potentially clinical tool for rapid AMI detection and screening.

  17. Treatment of post-myocardial infarction depressive disorder.

    PubMed

    Kuyper, Astrid M G; Honig, Adriaan

    2008-07-01

    Both major and minor depressive disorder post-myocardial infarction (MI) are associated with an increased risk of all-cause mortality, cardiac mortality and new cardiovascular events. Post-MI depressive disorder predicts slow recovery and poor quality of life. This review attends to post-MI depressive disorder, its underlying mechanisms and options for and effects of treatment. Evidence has been found for several mechanisms to be involved in the pathophysiology, including hypothalamus-pituitary-adrenal axis activity, immune activity, polyunsaturated fatty acids, serotonin, platelet activation, type D personality and negative health behavior. Five leading randomized controlled trials are discussed, showing safety and efficacy of antidepressive treatment in post-MI patients. Effects on cardiac outcome remain unclear.

  18. ST elevation myocardial infarction: recent advances and updates.

    PubMed

    Ganjehei, Leila; Rashid, Urmiya Mamoon; Payami, Sara; Saal, Andrew Kim

    2014-09-01

    ST elevation myocardial infarction (STEMI) remains a leading cause of morbidity, mortality and disability worldwide. Statistically, a trend towards improvements in morbidity and mortality has been consistent over the years, which is attributed primarily to the modification of risk factors, healthier lifestyles, treatment advances and better management of door-to-balloon times via STEMI systems. However, a major challenge in the coming years will be the baby boomers (born between the years 1946 and 1964) coming into old age. The first baby boomers turned 65 in year 2011. As the baby boomers age in the coming years, the incidence of coronary heart disease is likely to increase, and so there will be a greater need to have major advances in the management of coronary heart disease in order to deal with this additional incidence. The scope of this article is to review recent advances in the management of STEMI and to provide an updated overview.

  19. [Effect of mexicor on oxidative stress in acute myocardial infarction].

    PubMed

    Golikov, A P; Davydov, B V; Rudnev, D V; Klychnikova, E V; Bykova, N S; Riabinin, V A; Polumiskov, V Iu; Nikolaeva, N Iu; Golikov, P P

    2005-01-01

    Mexicor (5% solution and capsules) was used in 40 of 80 conventionally treated patients with acute myocardial infarction. The drug was given intravenously for 5 days, than intramuscularly (6-9 mg/kg) for 9 days and orally (0.1 mg t.i.d.) thereafter until discharge. Severity of oxidative stress was evaluated by K coefficient. Calculation of this coefficient required data on degree of oxidation of lipids in blood serum, serum levels of diene conjugates, malonic dialdehyde, alpha-tocopherol and ceruloplasmin. These parameters as well as activity of superoxide dismutase, glutathione peroxidase and catalase in erythrocytes were measured at admission, on days 2, 3, 7, 14 and at discharge. Mexicor treated compared with untreated (n=40) patients were characterized by diminished severity of oxidative stress at the account of lower levels of lipid peroxidation products and augmented compensatory potential of the endogenous antioxidant system.

  20. Climate and environmental triggers of acute myocardial infarction.

    PubMed

    Claeys, Marc J; Rajagopalan, Sanjay; Nawrot, Tim S; Brook, Robert D

    2017-04-01

    Over the past few decades, a growing body of epidemiological and clinical evidence has led to heightened concerns about the potential short- and long-term deleterious effects of the environment on cardiovascular health, including the risk for acute myocardial infarction (AMI). This review highlights the increased risk of AMI caused by exposure to air pollution and cold temperatures. These factors should be considered modifiable risk factors in the prevention of cardiovascular disease. The current body of knowledge about the biological mechanisms linking environmental changes to atherothrombotic events and the impact of climate change on cardiovascular health are discussed. Finally, recommendations for prevention and public policy are presented. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.

  1. Percutaneous coronary intervention for acute myocardial infarction with mitral regurgitation

    PubMed Central

    Tu, Yan; Zeng, Qing-Chun; Huang, Ying; Li, Jian-Yong

    2016-01-01

    Ischemic mitral regurgitation (IMR) is a common complication of acute myocardial infarction (AMI). Current evidences suggest that revascularization of the culprit vessels with percutaneous coronary artery intervention (PCI) or coronary artery bypass grafting can be beneficial for relieving IMR. A 2.5-year follow-up data of a 61-year-old male patient with ST-segment elevation AMI complicated with IMR showed that mitral regurgitation area increased five days after PCI, and decreased to lower steady level three months after PCI. This finding suggest that three months after PCI might be a suitable time point for evaluating the possibility of IMR recovery and the necessity of surgical intervention of the mitral valve for AMI patient. PMID:27582769

  2. Maximizing the benefits of thrombolytic therapy for acute myocardial infarction.

    PubMed Central

    Cairns, J; Armstrong, P W; Belenkie, I; Hirsh, J; Johnstone, D E; Knudtson, M; Lemieux, M; Massel, D; Naylor, C D; Roy, L

    1995-01-01

    Thrombolytic therapy is a huge advance in the management of acute myocardial infarction (AMI). The results of large clinical trials over the past 9 years have unequivocally demonstrated its benefit: of every 1000 patients treated 30 will be saved, at a cost of two cases of nonfatal cerebral hemorrhage and seven of noncerebral major hemorrhage. The concurrent use of acetylsalicylic acid increases the benefit of thrombolytic therapy. Sales figures for thrombolytic agents indicate that their use in Canada is less than optimal and lags behind that in several European countries. Major educational efforts are needed to promote awareness of the efficacy of thrombolytic therapy and of optimal approaches for maximizing its potential benefit for patients with AMI. PMID:7697574

  3. Patient education by videotape after myocardial infarction: an empirical evaluation.

    PubMed

    Bracken, M B; Bracken, M; Landry, A B

    1977-05-01

    Patients recovering from myocardial infarction (MI) or other heart diseases at St. Francis Hospital, Hartford, Ct, were educated by videotape or by staff lectures on alternating weeks. Both programs included the following: risk factors for MI, medications, diet, MI symptoms and life style changes. Patients were interviewed before and after the educational program. The MI patients under the age of 60 scored equally well on an informational test irrespective of the type of education program experienced. Older MI patients were significantly more likely to complete the educational program when it was given by videotape; those discontinuing attendance at lectures were less psychologically motivated to participate but were not necessarily more ill. Overall, higher education was the single most significant predictor of superior scores following patient education. Implications for the coronary care ward of the success of videotape in educating MI patients are discussed.

  4. Deciding to Seek Emergency Care for Acute Myocardial Infarction.

    PubMed

    Noureddine, Samar; Dumit, Nuhad Y; Saab, Mohammad

    2015-10-01

    The purpose of this qualitative descriptive study was to explore how patients who experience acute myocardial infarction (AMI) decide to seek emergency care. Fifty patients with AMI were interviewed at two hospitals in Lebanon. The perspective of 22 witnesses of the attack was also sought about the cardiac event. The themes that transpired from the data were as follows: making sense of the symptoms, waiting to see what happens, deciding to come to the hospital, and the family influenced the decision to seek care. The witnesses of the cardiac event, mostly family members, supported the decision to seek emergency care. Deciding to seek emergency care for AMI is complex. Nurses must solicit their patients' perception of the cardiac event to provide them with tailored education and counseling about heart attack symptoms and how to respond to them in case they recur. Family members must be included in the education process.

  5. Effectiveness of a videotape for sexual counseling after myocardial infarction.

    PubMed

    Steinke, Elaine E; Swan, James H

    2004-08-01

    A two-group randomized clinical trial was used to test the hypothesis that patients with myocardial infarction (MI) who receive both written instructions and a videotape to view at home will have greater knowledge, better quality of life, less anxiety, greater sexual satisfaction, and will resume sexual activity more quickly than will those who receive written instructions alone. The participants, 115 patients diagnosed with an MI, were pretested in the hospital and followed at home at 1, 3, and 5 months. The intervention was an educational videotape on return to sexual activity. Significant improvements in knowledge were found for the experimental group at 1 month. The videotape intervention provides an alternative method for education to facilitate recovery post-MI.

  6. [Myocardial Infarction and Stroke Among Railway Employees in Azerbaijan].

    PubMed

    Azizov, V; Rzayeva, A; Agayeva, K; Mammedbeyli, A; Khatamzade, E

    2017-02-01

    We studied the incidence of myocardial infarction (MI) and stroke in two groups of railway employees aged over 39 years including pensioners. The first (main) group included employees (n=15 671) responsible for movement of trains and exposed to `action of harmful occupational factors. The second (control) group included persons (n=19 132) who were not exposed to harmful occupational factors. Both main and control groups were divided into subgroups according to age. Prospective follow-up of persons with postinfarction atherosclerosis and consequences of stroke was also conducted during 5 years. There was no significant difference in incidence of MI between main and control groups except age subgroups 65-69 years where it was significantly higher among subjects from the main group. Incidence of stroke, mortality in acute periods of MI and stroke in main and control groups were similar.

  7. Clinical trials in thrombosis: secondary prevention of myocardial infarction.

    PubMed

    Klimt, C R; Doub, P H; Doub, N H

    1976-02-29

    Numerous in vivo and in vitro experiments, investigating the inhibition of platelet aggregation and the prevention of experimentally-induced thrombosis, suggest that anti-platelet drugs, such as aspirin or the combination of aspirin, and dipyridamole or sulfinpyrazone, may be effective anti-thrombotic agents in man. Since 1971, seven randomized prospective trials and two case-control studies have been referenced in the literature or are currently being conducted, which evaluate the effects of aspirin, sulfinpyrazone, or dipyridamole in combination with aspirin in the secondary prevention of myocardial infarction. A critical review of these trials indicates a range of evidence from no difference to a favorable trend that anti-platelet drugs may serve as anti-thrombotic agents in man. To date, a definitive answer concerning the therapeutic effects of these drugs in the secondary prevention of coronary heart disease is not available.

  8. Recurrent Myocardial Infarction in a Case of Congenital Afibrinogenemia

    PubMed Central

    Patra, Soumya; Reddy, Babu; Nagesh, C. M.; Srinivas, B. C.; Manjunath, C. N.

    2014-01-01

    Afibrinogenemia is a rare autosomal recessive bleeding disorder with an estimated prevalence of 1:1,000,000. Usual presentation of this disorder is spontaneous bleeding, bleeding after minor trauma and excessive bleeding during interventional procedures. Paradoxically, few patients with afibrinogenemia may also suffer from severe thromboembolic complications. The management of these patients is particularly challenging because they are not only at risk of thrombosis but also of bleeding. We are presenting a case of 33-year-old male patient of congenital afibrinogenemia who had two episodes myocardial infarction in a span of two years. The patient was managed conservatively with antiplatelet therapy and thrombolytic therapy was not given due to high risk for bleeding. PMID:24949183

  9. Recurrent myocardial infarction in a case of congenital afibrinogenemia.

    PubMed

    Patra, Soumya; Reddy, Babu; Nagesh, C M; Srinivas, B C; Manjunath, C N

    2014-01-01

    Afibrinogenemia is a rare autosomal recessive bleeding disorder with an estimated prevalence of 1:1,000,000. Usual presentation of this disorder is spontaneous bleeding, bleeding after minor trauma and excessive bleeding during interventional procedures. Paradoxically, few patients with afibrinogenemia may also suffer from severe thromboembolic complications. The management of these patients is particularly challenging because they are not only at risk of thrombosis but also of bleeding. We are presenting a case of 33-year-old male patient of congenital afibrinogenemia who had two episodes myocardial infarction in a span of two years. The patient was managed conservatively with antiplatelet therapy and thrombolytic therapy was not given due to high risk for bleeding.

  10. A case of acute myocardial infarction during 5-fluorouracil infusion.

    PubMed

    Canale, Maria Laura; Camerini, Andrea; Stroppa, Stefano; Porta, Romana Prosperi; Caravelli, Paolo; Mariani, Mario; Balbarini, Alberto; Ricci, Sergio

    2006-11-01

    Cardiac toxicity is an uncommon side-effect of 5-fluorouracil (5-FU) treatment, consisting mainly of chest pain episodes with or without electrocardiographic changes and dysrhythmias. Here, we describe the case of a 56-year-old male patient with a diagnosis of advanced colorectal cancer who developed an acute myocardial infarction during 5-FU infusion. The patient was not affected by prior heart disease and did not show any classic risk factors for coronary heart disease. Coronary angiography examination revealed no evidence of coronary stenosis, supporting the hypothesis of a coronary artery spasm related to 5-FU infusion. Given the great number of cancer patients receiving 5-FU containing chemotherapeutic regimens, this rare but severe cardiac side-effect may be observed in both cardiologic and oncologic clinical practice. We suggest a tight clinical monitoring of all patients receiving 5-FU infusions, even in those without a prior history of heart disease.

  11. Critical role of angiopoietins/Tie-2 in hyperglycemic exacerbation of myocardial infarction and impaired angiogenesis.

    PubMed

    Tuo, Qin-Hui; Zeng, Heng; Stinnett, Amanda; Yu, Heidi; Aschner, Judy L; Liao, Daun-Fang; Chen, Jian-Xiong

    2008-06-01

    Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) are the two ligands of the Tie-2 receptor, a receptor tyrosine kinase that is expressed on the endothelium. A balanced angiopoietin/Tie-2 system is critical for the maintenance of vascular integrity. We investigated the potential role of a disrupted angiopoietin/Tie-2 system on hyperglycemic exacerbation of myocardial infarction and impaired angiogenesis. Using streptozotocin (STZ) mice subjected to myocardial ischemia, we examined the effects of shifting the Ang-2-to-Ang-1 ratio on myocardial infarction size, apoptosis, bone marrow (BM) cell-endothelial progenitor cell (EPC) differentiation, and angiogenesis. In control mice, myocardial ischemia increased expression of both Ang-2 and Tie-2. In STZ mice, Ang-2 expression was elevated, whereas Tie-2 expression was reduced, and neither was significantly altered by ischemia. Myocardial infarct size and apoptosis were increased in STZ compared with control mice. Using in vivo administration of an adenovirus containing Ang-1 or Ang-2, we found that shifting the Ang-2-to-Ang-1 ratio to favor Ang-1 reduced myocardial apoptosis and infarct size in STZ mice, while shifting the Ang-2-to-Ang-1 ratio to favor Ang-2 resulted in a significant increase in myocardial infarct size and apoptosis in control mice. Myocardial ischemia-stimulated BM cell-EPC differentiation was inhibited and myocardial angiogenesis was reduced in STZ mice. Systemic administration of Ad-Ang-1 restored BM cell-EPC differentiation and increased myocardial VEGF expression and angiogenesis in STZ mice. Our data demonstrate that disturbed angiopoietin/Tie-2 signaling contributes to the hyperglycemic exacerbation of myocardial infarction and impaired angiogenesis. Restoration of the Ang-2-to-Ang-1 ratio may be a novel therapeutic strategy for the treatment of diabetic myocardial ischemic diseases.

  12. Race, Socioeconomic Status, and Life Expectancy After Acute Myocardial Infarction

    PubMed Central

    Bucholz, Emily M.; Ma, Shuangge; Normand, Sharon-Lise T.; Krumholz, Harlan M.

    2016-01-01

    Background Prior studies have been unable to disentangle the negative associations of black race and low socioeconomic status (SES) with long-term outcomes of patients after acute myocardial infarction (AMI). Such information could assist in efforts to address both racial and socioeconomic disparities. Methods and Results We used data from the Cooperative Cardiovascular Project, a prospective cohort study of Medicare beneficiaries hospitalized with AMI with 17-years of follow-up, to evaluate the relationship between race, area-level SES (measured by ZIP code level median household income), and life expectancy after AMI. Life expectancy was estimated using Cox proportional hazards regression with extrapolation using exponential models. Of the 141,095 patients with AMI, 6.3% were black and 6.8% resided in low SES areas; 26% of black patients lived in low SES areas compared with 5.7% of white patients. Post-myocardial infarction life expectancy estimates were shorter for black than white patients across all socioeconomic levels in patients ≤75 years of age. After adjustment for patient and treatment characteristics, the association between race and life expectancy persisted but was attenuated. Younger black patients (<68 years) had shorter life expectancies than white patients whereas older black patients had longer life expectancies. The largest white-black gap in life expectancy occurred in patients residing in high and medium SES areas (p=0.02 interaction). Conclusions Black and white patients residing in low SES areas have similar life expectancies after AMI, which are lower than those living in higher SES areas. Racial disparities were most prominent among patients living in high SES areas. PMID:26369354

  13. Thrombus aspiration during ST-segment elevation myocardial infarction.

    PubMed

    Fröbert, Ole; Lagerqvist, Bo; Olivecrona, Göran K; Omerovic, Elmir; Gudnason, Thorarinn; Maeng, Michael; Aasa, Mikael; Angerås, Oskar; Calais, Fredrik; Danielewicz, Mikael; Erlinge, David; Hellsten, Lars; Jensen, Ulf; Johansson, Agneta C; Kåregren, Amra; Nilsson, Johan; Robertson, Lotta; Sandhall, Lennart; Sjögren, Iwar; Ostlund, Ollie; Harnek, Jan; James, Stefan K

    2013-10-24

    The clinical effect of routine intracoronary thrombus aspiration before primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) is uncertain. We aimed to evaluate whether thrombus aspiration reduces mortality. We conducted a multicenter, prospective, randomized, controlled, open-label clinical trial, with enrollment of patients from the national comprehensive Swedish Coronary Angiography and Angioplasty Registry (SCAAR) and end points evaluated through national registries. A total of 7244 patients with STEMI undergoing PCI were randomly assigned to manual thrombus aspiration followed by PCI or to PCI only. The primary end point was all-cause mortality at 30 days. No patients were lost to follow-up. Death from any cause occurred in 2.8% of the patients in the thrombus-aspiration group (103 of 3621), as compared with 3.0% in the PCI-only group (110 of 3623) (hazard ratio, 0.94; 95% confidence interval [CI], 0.72 to 1.22; P=0.63). The rates of hospitalization for recurrent myocardial infarction at 30 days were 0.5% and 0.9% in the two groups, respectively (hazard ratio, 0.61; 95% CI, 0.34 to 1.07; P=0.09), and the rates of stent thrombosis were 0.2% and 0.5%, respectively (hazard ratio, 0.47; 95% CI, 0.20 to 1.02; P=0.06). There were no significant differences between the groups with respect to the rate of stroke or neurologic complications at the time of discharge (P=0.87). The results were consistent across all major prespecified subgroups, including subgroups defined according to thrombus burden and coronary flow before PCI. Routine thrombus aspiration before PCI as compared with PCI alone did not reduce 30-day mortality among patients with STEMI. (Funded by the Swedish Research Council and others; ClinicalTrials.gov number, NCT01093404.).

  14. Race, Socioeconomic Status, and Life Expectancy After Acute Myocardial Infarction.

    PubMed

    Bucholz, Emily M; Ma, Shuangge; Normand, Sharon-Lise T; Krumholz, Harlan M

    2015-10-06

    Previous studies have been unable to disentangle the negative associations of black race and low socioeconomic status (SES) with long-term outcomes of patients after acute myocardial infarction (AMI). Such information could assist in efforts to address both racial and socioeconomic disparities. We used data from the Cooperative Cardiovascular Project, a prospective cohort study of Medicare beneficiaries hospitalized with AMI with 17 years of follow-up, to evaluate the relationship between race, area-level SES (measured by zip code-level median household income), and life expectancy after AMI. Life expectancy was estimated by using Cox proportional hazards regression with extrapolation using exponential models. Of the 141 095 patients with AMI, 6.3% were black and 6.8% resided in low-SES areas; 26% of black patients lived in low-SES areas in comparison with 5.7% of white patients. Post-myocardial infarction life expectancy estimates were shorter for black patients than for white patients across all socioeconomic levels in patients ≤ 75 years of age. After adjustment for patient and treatment characteristics, the association between race and life expectancy persisted but was attenuated. Younger black patients (<68 years) had shorter life expectancies than white patients, whereas older black patients had longer life expectancies. The largest white-black gap in life expectancy occurred in patients residing in high- and medium-SES areas (P=0.02 interaction). Black and white patients residing in low-SES areas have similar life expectancies after AMI, which are lower than those living in higher-SES areas. Racial disparities were most prominent among patients living in high-SES areas. © 2015 American Heart Association, Inc.

  15. Nitrendipine binding in congestive heart failure due to myocardial infarction

    SciTech Connect

    Dixon, I.M.; Lee, S.L.; Dhalla, N.S. )

    1990-03-01

    Depressed cardiac pump function is the hallmark of congestive heart failure, and it is suspected that decreased influx of Ca2+ into the cardiac cell is responsible for depressed contractile function. Since Ca2+ channels in the sarcolemmal membrane are considered to be an important route for the entry of Ca2+, we examined the status of Ca2+ receptors/channels in failing rat hearts after myocardial infarction of the left ventricular free wall. For this purpose, the left coronary artery was ligated and hearts were examined 4, 8, and 16 weeks later; sham-operated animals served as controls. Hemodynamic assessment revealed decreased total mechanical energy (left ventricular systolic pressure x heart rate), increased left ventricular diastolic pressure, and decreased positive and negative dP/dt in experimental animals at 4, 8, and 16 weeks. Although accumulation of ascites in the abdominal cavity was evident at 4 weeks, other clinical signs of congestive heart failure in experimental rats were evident from the presence of lung congestion and cardiac dilatation at 8 and 16 weeks after induction of myocardial infarction. The density of Ca2+ receptors/channels in crude membranes, as assessed by (3H)nitrendipine binding assay, was found to be decreased in the uninfarcted experimental left ventricle at 8 and 16 weeks; however, no change in the affinity of nitrendipine was evident. A similar depression in the specific binding of another dihydropyridine compound, (3H)PN200-110, was also evident in failing hearts. Brain and skeletal muscle crude membrane preparations, unlike those of the right ventricle and liver, revealed a decrease in Ca2+ receptors/channels density in experimental animals at 16 weeks.

  16. Depressive symptoms are associated with mental stress-induced myocardial ischemia after acute myocardial infarction.

    PubMed

    Wei, Jingkai; Pimple, Pratik; Shah, Amit J; Rooks, Cherie; Bremner, J Douglas; Nye, Jonathon A; Ibeanu, Ijeoma; Murrah, Nancy; Shallenberger, Lucy; Raggi, Paolo; Vaccarino, Viola

    2014-01-01

    Depression is an adverse prognostic factor after an acute myocardial infarction (MI), and an increased propensity toward emotionally-driven myocardial ischemia may play a role. We aimed to examine the association between depressive symptoms and mental stress-induced myocardial ischemia in young survivors of an MI. We studied 98 patients (49 women and 49 men) age 38-60 years who were hospitalized for acute MI in the previous 6 months. Patients underwent myocardial perfusion imaging at rest, after mental stress (speech task), and after exercise or pharmacological stress. A summed difference score (SDS), obtained with observer-independent software, was used to quantify myocardial ischemia under both stress conditions. The Beck Depression Inventory-II (BDI-II) was used to measure depressive symptoms, which were analyzed as overall score, and as separate somatic and cognitive depressive symptom scores. There was a significant positive association between depressive symptoms and SDS with mental stress, denoting more ischemia. After adjustment for demographic and lifestyle factors, disease severity and medications, each incremental depressive symptom was associated with 0.14 points higher SDS. When somatic and cognitive depressive symptoms were examined separately, both somatic [β = 0.17, 95% CI: (0.04, 0.30), p = 0.01] and cognitive symptoms [β = 0.31, 95% CI: (0.07, 0.56), p = 0.01] were significantly associated with mental stress-induced ischemia. Depressive symptoms were not associated with ischemia induced by exercise or pharmacological stress. Among young post-MI patients, higher levels of both cognitive and somatic depressive symptoms are associated with a higher propensity to develop myocardial ischemia with mental stress, but not with physical (exercise or pharmacological) stress.

  17. Depressive Symptoms Are Associated with Mental Stress-Induced Myocardial Ischemia after Acute Myocardial Infarction

    PubMed Central

    Wei, Jingkai; Pimple, Pratik; Shah, Amit J.; Rooks, Cherie; Bremner, J. Douglas; Nye, Jonathon A.; Ibeanu, Ijeoma; Murrah, Nancy; Shallenberger, Lucy; Raggi, Paolo; Vaccarino, Viola

    2014-01-01

    Objectives Depression is an adverse prognostic factor after an acute myocardial infarction (MI), and an increased propensity toward emotionally-driven myocardial ischemia may play a role. We aimed to examine the association between depressive symptoms and mental stress-induced myocardial ischemia in young survivors of an MI. Methods We studied 98 patients (49 women and 49 men) age 38–60 years who were hospitalized for acute MI in the previous 6 months. Patients underwent myocardial perfusion imaging at rest, after mental stress (speech task), and after exercise or pharmacological stress. A summed difference score (SDS), obtained with observer-independent software, was used to quantify myocardial ischemia under both stress conditions. The Beck Depression Inventory-II (BDI-II) was used to measure depressive symptoms, which were analyzed as overall score, and as separate somatic and cognitive depressive symptom scores. Results There was a significant positive association between depressive symptoms and SDS with mental stress, denoting more ischemia. After adjustment for demographic and lifestyle factors, disease severity and medications, each incremental depressive symptom was associated with 0.14 points higher SDS. When somatic and cognitive depressive symptoms were examined separately, both somatic [β = 0.17, 95% CI: (0.04, 0.30), p = 0.01] and cognitive symptoms [β = 0.31, 95% CI: (0.07, 0.56), p = 0.01] were significantly associated with mental stress-induced ischemia. Depressive symptoms were not associated with ischemia induced by exercise or pharmacological stress. Conclusion Among young post-MI patients, higher levels of both cognitive and somatic depressive symptoms are associated with a higher propensity to develop myocardial ischemia with mental stress, but not with physical (exercise or pharmacological) stress. PMID:25061993

  18. Haemodynamic implications of exercise-induced myocardial ischaemia in patients with recent inferior myocardial infarction.

    PubMed

    De Vito, F; Giordano, A; Giannuzzi, P; Tavazzi, L

    1988-04-01

    Two hundred and forty patients with recent inferior myocardial infarction were studied by a symptom-limited ergometric test with haemodynamic monitoring (triple lumen tip-thermistor Swan-Ganz catheter) in order to investigate and quantify the haemodynamic effects of exercise-induced myocardial ischaemia in post-infarct patients and to assess whether the ST-segment changes give any indication of the degree of ventricular impairment. One hundred and thirteen patients showed no ST-segment changes during excercise; ST-segment elevation in leads with abnormal Q wave occurred in 14 patients, ST-segment depression was recorded in 88 subjects, and both ST-segment elevation and depression were found in 27 patients. In subjects with no ST-segment shift, as well as in those with exercise-induced ST-segment elevation, the resting and exertional haemodynamic patterns were normal or nearly normal. In subjects showing ST-segment depression or both ST-segment elevation and depression during exercise the mean pulmonary wedge pressure was abnormally elevated (at peak exercise 25 +/- 8 and 24 +/- 7 mm Hg, respectively). However, 31% of these showed a normal haemodynamic pattern either at rest or during exercise. The number of leads with ST-segment depression and the sum of ST-segment depressions in standard ECG does not reliably indicate the degree of ischaemia-dependent left ventricular impairment. In contrast, in patients grouped on the basis of time of ST depression appearance, the lower the ischaemic threshold the more severe was the left ventricular impairment. Finally, to assess the relative role of both scar and ischaemia in producing left ventricular dysfunction, the haemodynamic patterns of patients with and without exercise-induced ST-segment depression were compared in subsets with similar echocardiographic wall asynergy extent (inferior, infero-apical, infero-septo-apical). Among patients with small or medium-sized scar, the exertional left ventricular filling pressure

  19. The influence of lunar phases on the occurrence of myocardial infarction: fact or myth? The MONICA/KORA Myocardial Infarction Registry.

    PubMed

    Wende, R; von Klot, S; Kirchberger, I; Kuch, B; von Scheidt, W; Peters, A; Meisinger, C

    2013-04-01

    The potential influence of lunar phases on the occurrence of myocardial infarction is still controversial. The purpose of the present study was to investigate the association of the lunar cycle on the occurrence of fatal and non-fatal myocardial infarction based on a myocardial infarction registry. We studied 15,985 patients consecutively hospitalised with an acute myocardial infarction (AMI) between 1 January 1985 and 31 December 2007 with a known date of symptom onset who were recruited from a population-based myocardial infarction registry. The exact hour of AMI onset was known for 9813 events. Poisson regression analysis was performed to examine the relation between the lunar cycle and the occurrence of AMI. There was no association between new moon, full moon, waning moon and waxing moon and the occurrence of AMI. However, we observed that the three days after a new moon may be significantly protective for the occurrence of AMI, rate ratio (RR) 0.94 (95% CI 0.91-0.98), and the day before a new moon had a slightly negative effect (RR 1.06, 95% CI 1.00-1.12). Stratified analysis did not reveal any susceptible subgroups. The moon phases did not show any apparent association with AMI occurrence. However, there might be a 'cardioprotective' time three days after a new moon.

  20. Comparison between primary angioplasty and thrombolytic therapy on erectile dysfunction after acute ST elevation myocardial infarction

    PubMed Central

    Akdemir, Ramazan; Karakurt, Özlem; Orcan, Salih; Karakoyunlu, Nihat; Mucahit Balci, Mustafa; Sağnak, Levent; Ersoy, Hamit; Bulent Vatan, Mehmet; Kilic, Harun; Yeter, Ekrem

    2012-01-01

    Acute ST elevation myocardial infarction has high mortality and morbidity rates. The majority of patients with this condition face erectile dysfunction in addition to other health problems. In this study, we aimed to investigate the effects of two different reperfusion strategies, primary angioplasty and thrombolytic therapy, on the prevalence of erectile dysfunction after acute myocardial infarction. Of the 71 patients matching the selection criteria, 45 were treated with primary coronary angioplasty with stenting, and 26 were treated with thrombolytic agents. Erectile function was evaluated using the International Index of Erectile Function in the hospital to characterize each patient's sexual function before the acute myocardial infarction and 6 months after the event. The time required to restore blood flow to the artery affected by the infarct was found to be associated with the occurrence of erectile dysfunction after acute myocardial infarction. The increase in the prevalence of erectile dysfunction after acute myocardial infarction was 44.4% in the angioplasty group and 76.9% in the thrombolytic therapy group (P=0.008). In conclusion, this study has shown that reducing the time of reperfusion decreases the erectile dysfunction prevalence, and primary angioplasty is superior to thrombolytic therapy for decreasing the prevalence of erectile dysfunction after acute myocardial infarction. PMID:22796737

  1. History of Hypertension and the Effects of Eplerenone in Patients with Acute Myocardial Infarction Complicated by Systolic Heart Failure

    PubMed Central

    Pitt, Bertram; Ahmed, Ali; Love, Thomas E.; Krum, Henry; Nicolau, Jose; Silva Cardoso, José; Parkhomenko, Alexander; Aschermann, Michael; Corbalán, Ramon; Solomon, Henry; Shi, Harry; Zannad, Faiez

    2013-01-01

    In the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (n=6632), eplerenone-associated reduction in all-cause mortality was significantly greater in those with a history of hypertension (Hx-HTN). There were 4007 patients with Hx-HTN (eplerenone: n=1983) and 2625 patients without Hx-HTN (eplerenone: n=1336). Propensity scores for eplerenone use, separately calculated for patients with and without Hx-HTN, were used to assemble matched cohorts of 1838 and 1176 pairs of patients. In patients with Hx-HTN, all-cause mortality occurred in 18% of patients treated with placebo (rate, 1430/10 000 person-years) and 14% of patients treated with eplerenone (rate, 1058/10 000 person-years) during 2350 and 2457 years of follow-up, respectively (hazard ratio [HR]: 0.71; 95% CI: 0.59 to 0.85; P<0.0001). Composite end point of cardiovascular hospitalization or cardiovascular mortality occurred in 33% of placebo-treated patients (3029/10 000 person-years) and 28% of eplerenone-treated patients (2438/10 000 person-years) with Hx-HTN (HR: 0.82; 95% CI: 0.72 to 0.94; P=0.003). In patients without Hx-HTN, eplerenone reduced heart failure hospitalization (HR: 0.73; 95% CI: 0.55 to 0.97; P=0.028) but had no effect on mortality (HR: 0.91; 95% CI: 0.72 to 1.15; P=0.435) or on the composite end point (HR: 0.91; 95% CI: 0.76 to 1.10; P=0.331). Eplerenone should, therefore, be prescribed to all of the post–acute myocardial infarction patients with reduced left ventricular ejection fraction and heart failure regardless of Hx-HTN. PMID:18559720

  2. Effects of biglycan deficiency on myocardial infarct structure and mechanics

    PubMed Central

    Campbell, Patrick H.; Hunt, Darlene L.; Jones, Ying; Harwood, Fred; Amiel, David; Omens, Jeffrey H.; McCulloch, Andrew D.

    2009-01-01

    Biglycan, a small leucine-rich proteoglycan, has been shown to interact with extracellular matrix (ECM) collagen and may influence fibrillogenesis. We hypothesized that biglycan contributes to post-myocardial infarction (MI) scar development and that the absence of biglycan would result in altered scar structure and mechanics. Anterior MI was induced in biglycan hemizygous null and wild-type mice by permanent ligation of the left coronary artery. The initial extent of ischemic injury was similar in the two groups, as was the infarct size after 30 days, although there was some tendency toward reduced expansion in the biglycan-null. Electron microscopy revealed that collagen fibrils had a smaller average diameter and a narrower range in the biglycan-null scar, as well as appearing more densely packed. In vivo strain analysis showed that biglycan-null scars were stiffer than the wild-type. Remote LV collagen concentration tended to be reduced in biglycan-null hearts, but the difference was not statistically significant. Null-expression of biglycan may alter collagen fibril ultrastructure, and thereby influence scar mechanics and remodeling. PMID:18524244

  3. Desvenlafaxine reduces apoptosis in amygdala after myocardial infarction.

    PubMed

    Malick, Mandy; Gilbert, Kim; Barry, Mathieu; Godbout, Roger; Rousseau, Guy

    2014-10-01

    This study was designed to determine if desvenlafaxine (DV), a serotonin-norepinephrine reuptake inhibitor, can attenuate apoptosis observed in the limbic system after myocardial infarction (MI). MI was induced in rats by occlusion of the left descending artery for 40 min followed by reperfusion. Another group of sham (control) rats was similarly manipulated, but without occlusion. Half of the full cohort received DV (3 mg/kg/day intraperitoneal), starting 5 min after the onset of reperfusion; the other half received the vehicle (0.5 ml of 0.9% saline). Rats were sacrificed after 3 days for biochemical analyses and MI size measurements. Infarct size was significantly smaller in DV- compared to vehicle-treated rats. At 3 days post-MI, caspase-3 and -8 activities and terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling-positive cells were decreased in the amygdala of DV-treated rats compared to MI-vehicle controls. No difference was observed between the sham groups. The data indicates that DV given immediately after an acute MI event can reduce MI size and apoptosis in amygdala when measured three days post-MI. Copyright © 2014 Elsevier Inc. All rights reserved.

  4. Photoacoustic tomography of ex vivo mouse hearts with myocardial infarction

    NASA Astrophysics Data System (ADS)

    Holotta, Markus; Grossauer, Harald; Kremser, Christian; Torbica, Pavle; Völkl, Jakob; Degenhart, Gerald; Esterhammer, Regina; Nuster, Robert; Paltauf, Günther; Jaschke, Werner

    2011-03-01

    In the present study, we evaluated the applicability of ex vivo photoacoustic imaging (PAI) on small animal organs. We used photoacoustic tomography (PAT) to visualize infarcted areas within murine hearts and compared these data to other imaging techniques [magnetic resonance imaging (MRI), micro-computed tomography] and histological slices. In order to induce ischemia, an in vivo ligation of the left anterior descending artery was performed on nine wild-type mice. After varying survival periods, the hearts were excised and fixed in formaldehyde. Samples were illuminated with nanosecond laser pulses delivered by a Nd:YAG pumped optical parametric oscillator. Ultrasound detection was achieved using a Mach-Zehnder interferometer (MZI) working as an integrating line detector. The voxel data were computed using a Fourier-domain based reconstruction algorithm, followed by inverse Radon transforms. The results clearly showed the capability of PAI to visualize myocardial infarction and to produce three-dimensional images with a spatial resolution of approximately 120 μm. Regions of affected muscle tissue in PAI corresponded well with the results of MRI and histology. Photoacoustic tomography utilizing a MZI for ultrasound detection allows for imaging of small tissue samples. Due to its high spatial resolution, good soft tissue contrast and comparatively low cost, PAT offers great potentials for imaging.

  5. Injectable Hydrogels for Cardiac Tissue Repair after Myocardial Infarction.

    PubMed

    Hasan, Anwarul; Khattab, Ahmad; Islam, Mohammad Ariful; Hweij, Khaled Abou; Zeitouny, Joya; Waters, Renae; Sayegh, Malek; Hossain, Md Monowar; Paul, Arghya

    2015-11-01

    Cardiac tissue damage due to myocardial infarction (MI) is one of the leading causes of mortality worldwide. The available treatments of MI include pharmaceutical therapy, medical device implants, and organ transplants, all of which have severe limitations including high invasiveness, scarcity of donor organs, thrombosis or stenosis of devices, immune rejection, and prolonged hospitalization time. Injectable hydrogels have emerged as a promising solution for in situ cardiac tissue repair in infarcted hearts after MI. In this review, an overview of various natural and synthetic hydrogels for potential application as injectable hydrogels in cardiac tissue repair and regeneration is presented. The review starts with brief discussions about the pathology of MI, its current clinical treatments and their limitations, and the emergence of injectable hydrogels as a potential solution for post MI cardiac regeneration. It then summarizes various hydrogels, their compositions, structures and properties for potential application in post MI cardiac repair, and recent advancements in the application of injectable hydrogels in treatment of MI. Finally, the current challenges associated with the clinical application of injectable hydrogels to MI and their potential solutions are discussed to help guide the future research on injectable hydrogels for translational therapeutic applications in regeneration of cardiac tissue after MI.

  6. Temporal Effects of Catalase Overexpression on Healing Following Myocardial Infarction

    PubMed Central

    Pendergrass, Karl D.; Varghese, Susan T.; Maiellaro-Rafferty, Kathryn; Brown, Milton E.; Taylor, W. Robert; Davis, Michael E.

    2011-01-01

    Background Reactive oxygen species, such as hydrogen peroxide (H2O2), contribute to progression of dysfunction following myocardial infarction (MI). However, chronic overexpression studies do not agree with acute protein delivery studies. The purpose of the present study was to assess the temporal role of cardiomyocyte-derived H2O2 scavenging on cardiac function after infarction using an inducible system. Methods and Results We developed a tamoxifen-inducible, cardiomyocyte-specific catalase overexpressing mouse. Catalase overexpression was induced either 5 days pre or post-MI. Mice exhibited a 3-fold increase in cardiac catalase activity that was associated with a significant decrease in H2O2 levels at both 7 and 21 days. However, cardiac function improved only at the later time point. Pro-inflammatory and fibrotic genes were acutely upregulated after MI, but catalase overexpression abolished the increase, despite no acute change in function. This led to reduced overall scar formation, with lower levels of Collagen 1A and increased contractile Collagen 3A expression at 21 days. Conclusions In contrast to prior studies, there were no acute functional improvements with physiological catalase overexpression prior to MI. Scavenging of H2O2 however, reduced pro-inflammatory cytokines and altered cardiac collagen isoforms, associated with an improvement in cardiac function after 21 days. Our results suggest that sustained H2O2 levels, rather than acute levels immediately following MI, may be critical in directing remodeling and cardiac function at later time points. PMID:20971939

  7. Myocardial infarction and intramyocardial injection models in swine

    PubMed Central

    McCall, Frederic C; Telukuntla, Kartik S; Karantalis, Vasileios; Suncion, Viky Y; Heldman, Alan W; Mushtaq, Muzammil; Williams, Adam R; Hare, Joshua M

    2014-01-01

    Sustainable and reproducible large animal models that closely replicate the clinical sequelae of myocardial infarction (MI) are important for the translation of basic science research into bedside medicine. Swine are well accepted by the scientific community for cardiovascular research, and they represent an established animal model for preclinical trials for US Food and Drug Administration (FDA) approval of novel therapies. Here we present a protocol for using porcine models of MI created with a closed-chest coronary artery occlusion-reperfusion technique. This creates a model of MI encompassing the anteroapical, lateral and septal walls of the left ventricle. This model infarction can be easily adapted to suit individual study design and enables the investigation of a variety of possible interventions. This model is therefore a useful tool for translational research into the pathophysiology of ventricular remodeling and is an ideal testing platform for novel biological approaches targeting regenerative medicine. This model can be created in approximately 8–10 h. PMID:22790084

  8. Injectable Hydrogels for Cardiac Tissue Repair after Myocardial Infarction

    PubMed Central

    Khattab, Ahmad; Islam, Mohammad Ariful; Hweij, Khaled Abou; Zeitouny, Joya; Waters, Renae; Sayegh, Malek; Hossain, Md Monowar; Paul, Arghya

    2015-01-01

    Cardiac tissue damage due to myocardial infarction (MI) is one of the leading causes of mortality worldwide. The available treatments of MI include pharmaceutical therapy, medical device implants, and organ transplants, all of which have severe limitations including high invasiveness, scarcity of donor organs, thrombosis or stenosis of devices, immune rejection, and prolonged hospitalization time. Injectable hydrogels have emerged as a promising solution for in situ cardiac tissue repair in infarcted hearts after MI. In this review, an overview of various natural and synthetic hydrogels for potential application as injectable hydrogels in cardiac tissue repair and regeneration is presented. The review starts with brief discussions about the pathology of MI, its current clinical treatments and their limitations, and the emergence of injectable hydrogels as a potential solution for post MI cardiac regeneration. It then summarizes various hydrogels, their compositions, structures and properties for potential application in post MI cardiac repair, and recent advancements in the application of injectable hydrogels in treatment of MI. Finally, the current challenges associated with the clinical application of injectable hydrogels to MI and their potential solutions are discussed to help guide the future research on injectable hydrogels for translational therapeutic applications in regeneration of cardiac tissue after MI. PMID:27668147

  9. MOEMS-based cardiac enzymes detector for acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Amritsar, Jeetender; Stiharu, Ion G.; Packirisamy, Muthukumaran; Balagopal, Ganesharam; Li, Xing

    2004-10-01

    Biomedical applications of MOEMS are limited only by the mankind imagination. Precision measurements on minute amounts of biological material could be performed by optical means with a remarkable accuracy. Although available in medical laboratories for general purposes, such analyzers are making their way directly to the users in the form of dedicated equipment. Such an example is a test kit to detect the existence of cardiac enzymes in the blood stream. Apart from the direct users, the medical personnel will make use of such tools given the practicality of the kit. In a large proportion of patients admitted to the hospital suspected of Acute Myocardial Infarction (AMI), the symptoms and electrocardiographic changes are inconclusive. This necessitates the use of biochemical markers of myocardial damage for correct exclusion or conformation of AMI. In this study the concept of MOEMS is applied for the detection of enzyme reaction, in which glass spectrums are scanned optically when enzyme molecules adsorb on their surface. This paper presents the optical behavior of glass spectrums under Horseradish Peroxide (HRP) enzyme reaction. The reported experimental results provide valuable information that will be useful in the development of biosensors for enzymatic detection. This paper also reports the dynamic behavior of different glass spectrums.

  10. [Serum mitochondrial aspartate aminotransferase (ASTm) in acute myocardial infarction].

    PubMed

    Zhang, G

    1991-06-01

    The increase of serum ASTm activity might reflect the severity of damage at the subcellular level of the myocardium. 50 patients with acute myocardial infarction (AMI) were observed. The mean peak ASTm activity was 34.34 +/- 34.60 IU/L and 48 patients (96%) greater than or equal to 9 IU/L (two times median value of normal subject). The peak time (36 h) came later and the duration (120 h) was longer than that of CK-MB. ASTm/ASTt ratio in groups of AMI, non-AMI heart failure and acute ictero-hepatitis was 0.25 +/- 0.10, 0.02 +/- 0.05 and 0.05 +/- 0.02 respectively. The former was significantly greater than other two groups (P less than 0.01). The activity of ASTm in AMI cases with heart function at I, II and III + IV (Killip classification) was 21.8, 40.2 and 76.2 IU/L respectively (F = 8.407 P less than 0.01) and it was 84.9 and 24.7 IU/L in the death and surviving groups (P less than 0.01). The result showed that the estimation of serum ASTm level was helpful to the establishment of diagnosis in the patients with AMI who were sent delayed to the hospital. It held special significance in evaluating the severity of myocardial damage, heart function and in predicting the prognosis of AMI.

  11. Myocardial Infarction Triggers Chronic Cardiac Autoimmunity in Type 1 Diabetes

    PubMed Central

    Gottumukkala, Raju V.; Lv, HuiJuan; Cornivelli, Lizbeth; Wagers, Amy J.; Kwong, Raymond Y.; Bronson, Roderick; Stewart, Garrick C.; Schulze, P. Christian; Chutkow, William; Wolpert, Howard A.; Lee, Richard T.; Lipes, Myra A.

    2015-01-01

    Patients with type 1 diabetes (T1D) suffer excessive morbidity and mortality following myocardial infarction (MI) that is not fully explained by the metabolic effects of diabetes. Acute MI is known to trigger a profound innate inflammatory response with influx of mononuclear cells and production of proinflammatory cytokines that are crucial for cardiac repair. We hypothesized that these same pathways might exert ‘adjuvant effects’ and induce pathological responses in autoimmune-prone T1D hosts. Here we show that experimental MI in nonobese diabetic (NOD) mice - but not in control C57BL/6 mice - results in a severe post-infarction autoimmune (PIA) syndrome characterized by destructive lymphocytic infiltrates in the myocardium, infarct expansion, sustained cardiac IgG autoantibody production and Th1 effector cell responses against cardiac (α-)myosin. PIA was prevented by inducing tolerance to α-myosin, demonstrating that immune responses to cardiac myosin are required for this disease process. Extending these findings to humans, we developed a panel of immunoassays for cardiac autoantibody detection and found autoantibody positivity in 83% post-MI T1D patients. We further identified shared cardiac myosin autoantibody signatures between post-MI T1D patients and non-diabetic patients with myocarditis – that were absent in post-MI type 2 diabetic patients - and confirmed the presence of myocarditis in T1D by cardiac magnetic resonance imaging techniques. These data provide experimental and clinical evidence for a distinct post-MI autoimmune syndrome in T1D. Our findings suggest that PIA may contribute to worsened post-MI outcomes in T1D, and highlight a role for antigen-specific immunointervention to selectively block this pathway. PMID:22700956

  12. Early Biventricular Molecular Responses to an Acute Myocardial Infarction

    PubMed Central

    Erdal, Cenk; Karakülah, Gökhan; Fermancı, Emel; Kunter, İmge; Silistreli, Erdem; Canda, Tülay; Erdal, Esra; Hepaguslar, Hasan

    2012-01-01

    Background: Acute myocardial infarction (AMI) remains as one of the most common lethal diseases in the world and therefore it is necessary to understand its effect on molecular basis. Genome-wide microarray analysis provides us to predict potential biomarkers and signaling pathways for this purpose. Objectives: The aim of this study is to understand the molecular basis of the immediate right ventricular cellular response to left ventricular AMI. Material and Methods: A rat model of left anterior descending coronary artery ligation was used to assess the effect of left ventricular AMI on both the right ventricle as a remote zone and the left ventricle as an ischemic/infarct zone. Microarray technology was applied to detect the gene expression. Gene Ontology and KEGG pathways analysis were done to identify effected pathways and related genes. Results: We found that immune response, cell chemotaxis, inflammation, cytoskeleton organization are significantly deregulated in ischemic zone as early response within 30 min. Unexpectedly, there were several affected signaling pathways such as cell chemotaxis, regulation of endothelial cell proliferation, and regulation of caveolea regulation of anti-apoptosis, regulation of cytoskeleton organization and cell adhesion on the remote zone in the right ventricle. Conclusion: This data demonstrates that there is an immediate molecular response in both ventricles after an AMI. Although the ischemia did not histologically involve the right ventricle; there is a clear molecular response to the infarct in the left ventricle. This provides us new insights to understand molecular mechanisms behind AMI and to find more effective drug targets. PMID:22211093

  13. Intracoronary Cardiosphere-Derived Cells After Myocardial Infarction

    PubMed Central

    Malliaras, Konstantinos; Makkar, Raj R.; Smith, Rachel R.; Cheng, Ke; Wu, Edwin; Bonow, Robert O.; Marbán, Linda; Mendizabal, Adam; Cingolani, Eugenio; Johnston, Peter V.; Gerstenblith, Gary; Schuleri, Karl H.; Lardo, Albert C.; Marbán, Eduardo

    2013-01-01

    Objectives This study sought to report full 1-year results, detailed magnetic resonance imaging analysis, and determinants of efficacy in the prospective, randomized, controlled CADUCEUS (CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlar dySfunction) trial. Background Cardiosphere-derived cells (CDCs) exerted regenerative effects at 6 months in the CADUCEUS trial. Complete results at the final 1-year endpoint are unknown. Methods Autologous CDCs (12.5 to 25 × 106) grown from endomyocardial biopsy specimens were infused via the intracoronary route in 17 patients with left ventricular dysfunction 1.5 to 3 months after myocardial infarction (MI) (plus 1 infused off-protocol 14 months post-MI). Eight patients were followed as routine-care control patients. Results In 13.4 months of follow-up, safety endpoints were equivalent between groups. At 1 year, magnetic resonance imaging revealed that CDC-treated patients had smaller scar size compared with control patients. Scar mass decreased and viable mass increased in CDC-treated patients but not in control patients. The single patient infused 14 months post-MI responded similarly. CDC therapy led to improved regional function of infarcted segments compared with control patients. Scar shrinkage correlated with an increase in viability and with improvement in regional function. Scar reduction correlated with baseline scar size but not with a history of temporally remote MI or time from MI to infusion. The changes in left ventricular ejection fraction in CDC-treated subjects were consistent with the natural relationship between scar size and ejection fraction post-MI. Conclusions Intracoronary administration of autologous CDCs did not raise significant safety concerns. Preliminary indications of bioactivity include decreased scar size, increased viable myocardium, and improved regional function of infarcted myocardium at 1 year post-treatment. These results, which are consistent with therapeutic regeneration

  14. Repolarization duration in patients with conduction disturbances after myocardial infarction.

    PubMed

    Piotrowicz, Katarzyna; Zareba, Wojciech; McNitt, Scott; Moss, Arthur J

    2007-01-15

    This study compared different measurements of repolarization duration in patients after infarction with and without conduction disturbances and evaluated the prognostic significance of repolarization parameters for predicting mortality in patients with conduction abnormalities. The study population consisted of 3,282 patients after recent myocardial infarction. Repolarization duration was measured using Bazett QTc and JTc (QTc minus QRS) and Rautaharju QT and JT(RR) formulas. All-cause mortality was the end point of the predictive models. In 259 patients with conduction disturbances, 76 (2.3%) had indeterminate ventricular conduction disturbances, 126 (3.8%) had right bundle branch block, and 47 (1.4%) had left bundle branch block. Patients with left bundle branch block demonstrated excessive prolongation of the QTc interval, which was not observed when using the JT(RR) interval. There were no significant differences in repolarization duration by gender in patients with conduction abnormalities. Repolarization parameters were uniformly dichotomized at the 75th percentile (QTc interval >490 ms, JTc interval >360 ms, QT(RR,QRS) interval >433 ms, JT(RR) interval >359 ms) to determine their prognostic significance for predicting mortality. After adjustment for significant clinical predictors of mortality, the hazard ratios were 1.65 for QTc interval (p = 0.062), 1.46 for JTc interval (p = 0.168), 1.71 for QT(RR,QRS) interval (p = 0.043), and 1.70 for JT(RR) interval (p = 0.044)(.) In conclusion, patients with left bundle branch block, right bundle branch block, or indeterminate ventricular conduction disturbances show longer repolarization duration than patients without these conduction disturbances, and QT(RR,QRS) and JT(RR) intervals reflect better than QTc repolarization duration in patients with conduction disturbances. QT(RR) and JT(RR) intervals significantly and independently predict mortality in patients after infarction with conduction disturbances.

  15. Scintigraphic assessment of sympathetic innervation after transmural versus nontransmural myocardial infarction

    SciTech Connect

    Dae, M.W.; Herre, J.M.; O'Connell, J.W.; Botvinick, E.H.; Newman, D.; Munoz, L. )

    1991-05-01

    To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs. Twelve dogs underwent myocardial infarction by injection of vinyl latex into the left anterior descending coronary artery (transmural myocardial infarction, n = 6), or ligation of the left anterior descending coronary artery (nontransmural myocardial infarction, n = 6). Four dogs served as sham-operated controls. Image patterns were compared with tissue norepinephrine content and with histofluorescence microscopic findings in biopsy specimens. Hearts with transmural infarction showed zones of absent MIBG and thallium, indicating scar. Adjacent and distal regions showed reduced MIBG but normal thallium uptake, indicating viable but denervated myocardium. Denervation distal to infarction was confirmed by reduced norepinephrine content and absence of nerve fluorescence. Nontransmural myocardial infarction showed zones of wall thinning with decreased thallium uptake and a greater reduction or absence of MIBG localized to the region of the infarct, with minimal extension of denervation beyond the infarct. Norepinephrine content was significantly reduced in the infarct zone, and nerve fluorescence was absent. These findings suggest that (1) MIBG imaging can detect viable and perfused but denervated myocardium after infarction; and (2) as opposed to the distal denervation produced by transmural infarction, nontransmural infarction may lead to regional ischemic damage of sympathetic nerves, but may spare subepicardial nerve trunks that course through the region of infarction to provide a source of innervation to distal areas of myocardium.

  16. Litsea Deccanensis Ameliorates Myocardial Infarction in Wistar Rats: Evidence from Biochemical and Histological Studies

    PubMed Central

    Kumar, Bharath P; Kannan, Mari M; Quine, Darlin S

    2011-01-01

    The present study was designed to evaluate the cardioprotective effects of methanolic extract of Litsea deccanensis (MELD) against isoproterenol-induced myocardial infarction in rats by studying cardiac markers, lipid peroxidation, lipid profile, and histological changes. Male Wistar rats were treated orally with MELD (100 and 200 mg/kg) daily for a period of 21 days. After 21 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed significant (P < 0.05) increase in the levels of serum creatine kinase, lactate dehydrogenase, thiobarbituric acid reactive substances, and lipid hydro peroxides. The serum lipid levels were altered in the isoproterenol-induced myocardial infarcted rats. The histopathological findings of the myocardial tissue evidenced myocardial damage in isoproterenol-induced rats. The oral pretreatment with MELD restored the pathological alterations in the isoproterenol-induced myocardial infarcted rats. The MELD pretreatment significantly reduced the levels of biochemical markers, lipid peroxidation and regulated the lipid profile of the antioxidant system in the isoproterenol-induced rats. An inhibited myocardial necrosis was evidenced by the histopathological findings in MELD pretreated isoproterenol-induced rats. Our study shows that oral pretreatment with MELD prevents isoproterenol-induced oxidative stress in myocardial infarction. The presence of phenolic acid and flavonoid contents were confirmed by preliminary phytochemical tests. The reducing power and free radical scavenging activities of the MELD may be the possible reason for it pharmacological actions. PMID:22224035

  17. Litsea deccanensis ameliorates myocardial infarction in wistar rats: evidence from biochemical and histological studies.

    PubMed

    Kumar, Bharath P; Kannan, Mari M; Quine, Darlin S

    2011-10-01

    The present study was designed to evaluate the cardioprotective effects of methanolic extract of Litsea deccanensis (MELD) against isoproterenol-induced myocardial infarction in rats by studying cardiac markers, lipid peroxidation, lipid profile, and histological changes. Male Wistar rats were treated orally with MELD (100 and 200 mg/kg) daily for a period of 21 days. After 21 days of pretreatment, isoproterenol (100 mg/kg) was injected subcutaneously to rats at an interval of 24 h for 2 days to induce myocardial infarction. Isoproterenol-induced rats showed significant (P < 0.05) increase in the levels of serum creatine kinase, lactate dehydrogenase, thiobarbituric acid reactive substances, and lipid hydro peroxides. The serum lipid levels were altered in the isoproterenol-induced myocardial infarcted rats. The histopathological findings of the myocardial tissue evidenced myocardial damage in isoproterenol-induced rats. The oral pretreatment with MELD restored the pathological alterations in the isoproterenol-induced myocardial infarcted rats. The MELD pretreatment significantly reduced the levels of biochemical markers, lipid peroxidation and regulated the lipid profile of the antioxidant system in the isoproterenol-induced rats. An inhibited myocardial necrosis was evidenced by the histopathological findings in MELD pretreated isoproterenol-induced rats. Our study shows that oral pretreatment with MELD prevents isoproterenol-induced oxidative stress in myocardial infarction. The presence of phenolic acid and flavonoid contents were confirmed by preliminary phytochemical tests. The reducing power and free radical scavenging activities of the MELD may be the possible reason for it pharmacological actions.

  18. Estrogen receptors do not influence angiogenesis after myocardial infarction.

    PubMed

    Broberg, Agneta Månsson; Siddiqui, Anwar J; Fischer, Helene; Grinnemo, Karl-Henrik; Wardell, Eva; Andersson, Agneta B; Inzunza, José; Sylvén, Christer; Gustafsson, Jan Åke

    2011-08-01

    There is controversy on whether estrogen receptors are present and functioning in the myocardium. Aims. To explore if after myocardial infarction (MI) estrogen receptors α (ERα) and β (ERβ) are upregulated in myocardial tissue and to explore if the presence/ absence of ERα or ERβ influences angiogenesis after MI. MI was induced by ligation of the left anterior descending artery in knockout (KO) mice, ERαKO and ERβKO, respectively, and non-KO littermate-controls, C57Bl/6 mice. The hearts were harvested after 12 days. A part of the periinfarct tissue was collected for ERα and ERβ mRNA expression determination by real-time polymerase chain reaction. Using immunohistochemistry, ERα and ERβ protein expression and capillary and arteriolar densities were blindly determined in the periinfarct area. In myocardium disrupted mRNA was upregulated in both ERαKO and ERβKO, (p < 0.005) and did not change after MI. There was no change in mRNA expression of ERα or ERβ in wild type mice after MI. Expression of ERβ in ERαKO and of ERα in ERβKO did not change. Following MI ERα or ERβ could not be demonstrated by immunohistochemistry in either wild type or ERαKO or ERβKO. The capillary and arteriolar densities after MI did not differ between the groups in the periinfarct area. Although disrupted ER mRNA is upregulated in myocardium of ER knockout mice, no change in these or native receptors occurs following MI. At least in this model ER therefore seems not to have a role in myocardial arteriogenesis and angiogenesis after MI.

  19. The relationship between helicobacter pylori infection and myocardial infarction

    PubMed Central

    Azarkar, Zohreh; Jafarnejad, Majid; Sharifzadeh, Gholamreza

    2011-01-01

    Background: Coronary Artery Disease is known as the main cause of death in industrialized countries. Relation between this disease and some infections such as Helicobacter pylori (H.pylori) has been shown in several studies. The purpose of this study was to dermine the relationship between Hypylori and mycardical infarctions. Methods: Seventy-three myocardial infarction patients and 78 individuals with no history of this disease were compared. Patients and control matched for age and sex person to person by the match method. Levels of serum IgA and IgG antibodies against H. pylori were measured by Elisa method. Also, cholesterol, triglyceride, LDL, HDL measured in both groups and data were compared between two groups in terms of relation with cardiac risk factors. Results: From 151 participants, 73 were patients and 78 were control subjects. The percentage of IgG positive cases against H. pylori was 57.5% in the case group and 32.1% in the control group (p=0.002, OR: 2.87 CI: 95%; 1.5-5.6). Meanwhile, there was no significant difference in IgA positive cases between the two groups (42.5% and 48.7% in the case and control groups, respectively) (p=0.44; OR: 0.78 95% CI; 0.41-1.48). The study showed 74.2% of cases in the case group and 45.2% in the control group were positive for both IgG and IgA (p=0.01; OR: 3.5 95% CI; 1.3-9.5). No significant differences were found between two groups in terms of relation between H. pylori related antibodies level and heart disease classic risk factors (smoking, hypertension,…), sex, and age, but between dyslipidemia and H. pylori related antibodies was significant differences in case group (p=0.05). Conclusion: According to the results, it seems there is a relation between H. pylori infection and myocardial infarction. Also, between dislipidemia and H. Pylori antibodies in case group were significant difference. Therefore, H. pylori can be a new risk factor for atherosclerosis or can be exacerbate effect of other risk factors

  20. Acute myocardial infarct imaging with indium-111-labeled monoclonal antimyosin Fab

    SciTech Connect

    Khaw, B.A.; Yasuda, T.; Gold, H.K.; Leinbach, R.C.; Johns, J.A.; Kanke, M.; Barlai-Kovach, M.; Strauss, H.W.; Haber, E.

    1987-11-01

    Indium-111 monoclonal antimyosin Fab scintigraphy was used to detect myocardial necrosis in 52 of 54 patients (96.3%) with acute myocardial infarction. Infarcts were visualized when coronary arteries were persistently occluded (n = 10), became patent after thrombolysis (n = 33), or became patent after spontaneous reperfusion (n = 7). Posteroinferolateral visualizations were obtained in two patients with clinical and enzymatic evidence of infarction but normal electrocardiograms. Of the two patients in whom no infarcts were visualized, one had an anterior myocardial infarct. This patient underwent successful thrombolytic therapy, with attendant minimization of creatine kinase release. The other patient had a small, nonreperfused inferior myocardial infarct. Five patients with a history of remote infarction and acute necrosis showed antimyosin uptake only in regions concordant with the acute episodes of infarction, and radiolabeled antimyosin Fab localized in neither old infarcts nor normal, noninfarcted myocardium. Antimyosin Fab scintigraphy, thus, appears to be a highly specific means of delineating necrotic myocardium, at least in this limited and selected group of patients.

  1. Influence of acute glycaemic level on measures of myocardial infarction in non-diabetic pigs.

    PubMed

    Diemar, Sarah S; Sejling, Anne-Sophie; Iversen, Kasper K; Engstrøm, Thomas; Honge, Jesper L; Tønder, Niels; Vejlstrup, Niels; Idorn, Manja; Ekström, Kathrine; Pedersen-Bjergaard, Ulrik; Thorsteinsson, Birger; Dalsgaard, Morten

    2015-01-01

    Patients with diabetes are at increased risk of experiencing myocardial infarction. The influence of the prevailing plasma glucose level on infarction and mortality after acute ischaemia is however unknown. The aim was to study the effect of the acute plasma glucose level on the myocardial infarction size in a closed-chest pig model. 38 non-diabetic pigs were randomised to hypoglycaemic (1.8-2.2 mmol/l; n = 15), normoglycaemic (5-7 mmol/l; n = 12) or hyperglycaemic glucose clamping (22-23 mmol/l; n = 11). After 30 min within glucose target myocardial infarction was induced for 30 min followed by reperfusion for 120 min. Hereafter the heart was double-stained to delineate infarction from viable tissue within the area at risk. Mean infarction size was 201 ± 35 mm(2) (mean ± SEM) in the hypoglycaemic group, 154 ± 40 mm(2) in the normoglycaemic group and 134 ± 40 mm(2) in the hyperglycaemic group, with no differences in infarction size, infarct/area at risk ratio or troponin T levels between the groups. There was no difference in incidence of ventricular fibrillation or mortality between the groups. No statistically significant associations were observed between the acute glycaemic level and measures of myocardial infarction, rates of ventricular fibrillation and subsequent premature death in the setting of acute ischaemia and reperfusion.

  2. Persistent uptake of indium-111-antimyosin monoclonal antibody in patients with myocardial infarction

    SciTech Connect

    Matsumori, A.; Yamada, T.; Tamaki, N.; Kawai, C.; Watanabe, Y.; Yonekura, Y.; Endo, K.; Konishi, J.; Yoshida, A.; Tamaki, S. )

    1990-11-01

    Indium-111(111In)-antimyosin scintigraphy was investigated in 27 patients with myocardial infarction. {sup 111}In-antimyosin Fab was administered intravenously, and planar and single photon emission computed tomographic images were obtained 48 hours later. Uptake of {sup 111}In-antimyosin was present in 9 of 10 patients (90%) studied within 6 days of infarction. During the second week positive scans were seen in 16 of 16 patients (100%) including 13 (81%) who had normal creatine kinase levels. The mechanism of persistent positive antimyosin images in the subacute stage of myocardial infarction remains to be clarified. {sup 111}In-antimyosin scintigraphy may be useful as a noninvasive method for the detection of myocardial injury late and early after a suspected acute myocardial infarction.

  3. Imaging of acute myocardial infarction in pigs with Indium-111 monoclonal antimyosin scintigraphy and MRI

    SciTech Connect

    ten Kate, C.I.; van Kroonenburgh, M.J.; Schipperheyn, J.J.; Doornbos, J.; Hoedemaeker, P.J.; Maes, A.; v.d. Nat, K.H.; Camps, J.A.; Huysmans, H.A.; Pauwels, E.K. )

    1990-07-01

    Indium-111 antimyosin F(ab')2 was used in a series of scintigraphic studies on experimentally induced myocardial infarctions in pigs. Antimyosin distribution recorded by planar images of in vivo pigs and by single photon emission computed tomography (SPECT) of excised hearts delineated areas of myocardial necrosis if infarct volume exceeded 3.3 cm3. Scintigraphic images were compared with magnetic resonance images (MRI) obtained from excised hearts and with photographs of slices of the hearts. Infarct size and localization determined with antimyosin were compared. The MR images, with or without gadolinium-DTPA (Gd-DTPA), of the in vivo pigs were all false-negative; some myocardial wall thinning and high bloodpool signals were visible. Results show that both the antimyosin and the MR technique are specific methods for the visualization of induced myocardial necrosis in this animal model. However, the use of antimyosin is limited to a period ranging from 24 to 72 hours after infarction.

  4. Large myocardial infarction with myocardium calcium deposits associated with reperfusion injury.

    PubMed

    Rios, Elisabete; Mancio, Jennifer; Rodrigues-Pereira, Pedro; Magalhães, Domingos; Bartosch, Carla

    2014-01-01

    The clinical and autopsy findings of a 66-year-old man with myocardial infarction complicated by reperfusion injury are described, highlighting the presence of large myocardium calcium deposits. Copyright © 2014 Elsevier Inc. All rights reserved.

  5. An unusual case of silent acute ST-elevation myocardial infarction following amphetamine use.

    PubMed

    Chia-Yu Chang, Julia; Peng, Chian-Ze; How, Chorng-Kuang; Huang, Mu-Shun

    2013-07-01

    We report a case of silent acute ST-elevation myocardial infarction associated with amphetamine use in a 62 years old diabetic man. The patient was devoid of chest pain and had a normal cardiac enzyme analysis at the initial presentation. A routine electrocardiogram demonstrated acute inferior wall ST-elevation myocardial infarction. Coronary angiography confirmed a total occlusion of the posterior lateral branch of right coronary artery. The patient underwent successful percutaneous transluminal coronary angioplasty with stent placement. Amphetamine abuse may play a role in acute myocardial infarction. Adverse cardiovascular manifestations of amphetamine can occur with sudden overt chest pain or present insidiously. In view of the potential association of amphetamine and myocardial infarction, physicians should not rely only upon clinical symptoms. This report highlights the diabetic patients with amphetamine abuse should undergo a routine electrocardiogram in such circumstances.

  6. Lipoprotein(a) and risk of myocardial infarction--genetic epidemiologic evidence of causality.

    PubMed

    Kamstrup, Pia R; Tybjærg-Hansen, Anne; Nordestgaard, Børge G

    2011-04-01

    Elevated levels of lipoprotein(a) are associated with an increased risk of myocardial infarction. Our study aimed to test whether genetic data are consistent with this association being causal. Accordingly, we developed a high-throughput realtime PCR assay to genotype for the lipoprotein(a) kringle IV type 2 (KIV-2) repeat polymorphism in the LPA gene in > 40,000 individuals. The LPA KIV-2 genotype associated with plasma levels of lipoprotein(a) (trend p < 0.001), and the LPA KIV-2 genotype associated with risk of myocardial infarction (trend p < 0.001 to 0.03) in a manner consistent with its effect on plasma levels of lipoprotein(a). The association of LPA KIV-2 genotypes raising plasma levels of lipoprotein(a) with increased risk of myocardial infarction strongly supports a causal association of lipoprotein(a) with risk of myocardial infarction.

  7. Effect of decellularized tissue powders on a rat model of acute myocardial infarction.

    PubMed

    Tabuchi, Masaki; Negishi, Jun; Yamashita, Akitatsu; Higami, Tetsuya; Kishida, Akio; Funamoto, Seiichi

    2015-11-01

    Many research groups are currently investigating new treatment modalities for myocardial infarction. Numerous aspects need to be considered for the clinical application of these therapies, such as low cell integration and engraftment rates of cell injection techniques. Decellularized tissues are considered good materials for promoting regeneration of traumatic tissues. The properties of the decellularized tissues are sustained after processing to powder form. In this study, we examined the use of decellularized tissue powder in a rat model of acute myocardial infarction. The decellularized tissue powders, especially liver powder, promoted cell integration and neovascularization both in vitro and in vivo. Decellularized liver powder induced neovascularization in the infarct area, resulting in the suppression of myocardial necrosis. The results of this study suggest that decellularized liver powder has good potential for application as a blood supply material for the treatment of myocardial infarction. Copyright © 2015 Elsevier B.V. All rights reserved.

  8. No reflow phenomenon in percutaneous coronary interventions in ST-segment elevation myocardial infarction.

    PubMed

    Gupta, Sanjiv; Gupta, Madan Mohan

    2016-01-01

    Percutaneous coronary intervention (PCI) is effective in opening the infarct related artery and restoring thrombolysis in myocardial infarction flow 3 (TIMI-flow 3) in large majority of ST-elevation myocardial infarction (STEMI). However there remain a small but significant proportion of patients, who continue to manifest diminished myocardial reperfusion despite successful opening of the obstructed epicardial artery. This phenomenon is called no-reflow. Clinically it manifests with recurrence of chest pain and dyspnea and may progress to cardiogenic shock, cardiac arrest, serious arrhythmias and acute heart failure. No reflow is regarded as independent predictor of death or recurrent myocardial infarction. No reflow is a multi-factorial phenomenon. However micro embolization of atherothrombotic debris during PCI remains the principal mechanism responsible for microvascular obstruction. This review summarizes the pathogenesis, diagnostic methods and the results of various recent randomized trials and studies on the prevention and management of no-reflow.

  9. Use of copeptin for rapid rule-out of acute myocardial infarction.

    PubMed

    Mueller, Christian; Möckel, Martin; Giannitsis, Evangelos; Huber, Kurt; Mair, Johannes; Plebani, Mario; Thygesen, Kristian; Jaffe, Allan S; Lindahl, Bertil

    2017-06-01

    Copeptin is currently understood as a quantitative marker of endogenous stress. It rises rapidly in multiple acute disorders including acute myocardial infarction. As a single variable, it has only modest diagnostic accuracy for acute myocardial infarction. However, the use of copeptin within a dual-marker strategy together with conventional cardiac troponin increases the diagnostic accuracy and particularly the negative predictive value of cardiac troponin alone for acute myocardial infarction. The rapid rule-out of acute myocardial infarction is the only application in acute cardiac care mature enough to merit consideration for routine clinical care. However, the dual-marker approach seems to provide only very small incremental value when used in combination with sensitive or high-sensitivity cardiac troponin assays. This review aims to update and educate regarding the potential and the procedural details, as well as the caveats and challenges of using copeptin in clinical practice.

  10. Myocardial infarction after blunt chest trauma incurred during rugby football that later required cardiac transplantation.

    PubMed Central

    Watt, A H; Stephens, M R

    1986-01-01

    A 28 year old man sustained an extensive anterolateral myocardial infarction five minutes after a blow on the chest while playing rugby football. The resulting persistent cardiac failure necessitated orthotopic cardiac transplantation. Images Fig. 1 Fig. 2 PMID:3516188

  11. Myocardial protection of early extracorporeal membrane oxygenation (ECMO) support for acute myocardial infarction with cardiogenic shock in pigs.

    PubMed

    Zhu, Gang-jie; Sun, Li-na; Li, Xing-hai; Wang, Ning-fu; Wu, Hong-hai; Yuan, Chen-xing; Li, Qiao-qiao; Xu, Peng; Ren, Ya-qi; Mao, Bao-gen

    2015-09-01

    The aim of this study was to explore myocardial protection of early extracorporeal membrane oxygenation (ECMO) support for acute myocardial infarction with cardiogenic shock in pigs. 24 male pigs (34.6 ± 1.3 kg) were randomly divided into three groups-control group, drug therapy group, and ECMO group. Myocardial infarction model was created in drug therapy group and ECMO group by ligating coronary artery. When cardiogenic shock occurred, drugs were given in drug therapy group and ECMO began to work in ECMO group. The pigs were killed 24 h after cardiogenic shock. Compared with in drug therapy group, left ventricular end-diastolic pressure in ECMO group decreased significantly 6 h after ligation (P < 0.05). At the end of the experiments, LV - dp/dt among three groups was significantly different, drug therapy group < ECMO group < control group. There was no difference in LV + dp/dt between drug therapy group and ECMO group. Compared with drug group, myocardial infarct size of ECMO group did not reduce significantly, but myocardial enzyme and troponin-I decreased significantly. Compared with drug therapy, ECMO improves left ventricular diastolic function, and may improve systolic function. ECMO cannot reduce myocardial infarct size without revascularization, but may have positive effects on ischemic areas by avoiding further injuring.

  12. Clenbuterol and anabolic steroids: a previously unreported cause of myocardial infarction with normal coronary arteriograms.

    PubMed

    Goldstein, D R; Dobbs, T; Krull, B; Plumb, V J

    1998-08-01

    During the last 10 years, several cases of myocardial infarction associated with anabolic steroid use have been reported. Postulated mechanisms to explain this association have included changes in lipid levels, the fibrinolytic system, and platelet aggregation. Clenbuterol is a beta 2-agonist with anabolic properties that has not been seen previously with myocardial infarction. We report a case of myocardial infarction in an otherwise healthy 26-year-old body-builder who recently used clenbuterol and anabolic steroids. In this case, synergistic effects of the two agents seem likely to have played a role in the infarct. The normal coronary arteriograms before any anticoagulant or thrombolytic therapy strongly suggest coronary spasm as the mechanism of the infarct.

  13. Blood PGC-1α Concentration Predicts Myocardial Salvage and Ventricular Remodeling After ST-segment Elevation Acute Myocardial Infarction.

    PubMed

    Fabregat-Andrés, Óscar; Ridocci-Soriano, Francisco; Estornell-Erill, Jordi; Corbí-Pascual, Miguel; Valle-Muñoz, Alfonso; Berenguer-Jofresa, Alberto; Barrabés, José A; Mata, Manuel; Monsalve, María

    2015-05-01

    Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) is a metabolic regulator induced during ischemia that prevents cardiac remodeling in animal models. The activity of PGC-1α can be estimated in patients with ST-segment elevation acute myocardial infarction. The aim of the present study was to evaluate the value of blood PGC-1α levels in predicting the extent of necrosis and ventricular remodeling after infarction. In this prospective study of 31 patients with a first myocardial infarction in an anterior location and successful reperfusion, PGC-1α expression in peripheral blood on admission and at 72 hours was correlated with myocardial injury, ventricular volume, and systolic function at 6 months. Edema and myocardial necrosis were estimated using cardiac magnetic resonance imaging during the first week. At 6 months, infarct size and ventricular remodeling, defined as an increase > 10% of the left ventricular end-diastolic volume, was evaluated by follow-up magnetic resonance imaging. Myocardial salvage was defined as the difference between the edema and necrosis areas. Greater myocardial salvage was seen in patients with detectable PGC-1α levels at admission (mean [standard deviation (SD)], 18.3% [5.3%] vs 4.5% [3.9%]; P = .04). Induction of PGC-1α at 72 hours correlated with greater ventricular remodeling (change in left ventricular end-diastolic volume at 6 months, 29.7% [11.2%] vs 1.2% [5.8%]; P = .04). Baseline PGC-1α expression and an attenuated systemic response after acute myocardial infarction are associated with greater myocardial salvage and predict less ventricular remodeling. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

  14. Acute Myocardial Infarction Due to Spontaneous Dissection of the Right Coronary Artery in a Young Male

    SciTech Connect

    Papadopoulos, Dimitris P. Moyssakis, Ioannis; Perakis, Alexandros; Athanasiou, Andreas; Anagnostopoulou, Sophia; Benos, Ioannis; Votteas, Vassilios E.

    2004-09-15

    Spontaneous coronary artery dissection is a rare cause of acute myocardial infarction. We report a case of a 33-year-old male who presented with an acute inferior myocardial infarction. Coronary arteriography performed 3 hours after the episode revealed a dissection involving the middle segment of right coronary artery. Because of a spiral form of dissection and the TIMI 3 flow grade, our patient was treated medically and repeat coronary angiography 6 months later was decided.

  15. Influence of climate variability on acute myocardial infarction mortality in Havana, 2001-2012.

    PubMed

    Rivero, Alina; Bolufé, Javier; Ortiz, Paulo L; Rodríguez, Yunisleydi; Reyes, María C

    2015-04-01

    Death from acute myocardial infarction is due to many factors; influences on risk to the individual include habits, lifestyle and behavior, as well as weather, climate and other environmental components. Changing climate patterns make it especially important to understand how climatic variability may influence acute myocardial infarction mortality. Describe the relationship between climate variability and acute myocardial infarction mortality during the period 2001-2012 in Havana. An ecological time-series study was conducted. The universe comprised 23,744 deaths from acute myocardial infarction (ICD-10: I21-I22) in Havana residents from 2001 to 2012. Climate variability and seasonal anomalies were described using the Bultó-1 bioclimatic index (comprising variables of temperature, humidity, precipitation, and atmospheric pressure), along with series analysis to determine different seasonal-to-interannual climate variation signals. The role played by climate variables in acute myocardial infarction mortality was determined using factor analysis. The Mann-Kendall and Pettitt statistical tests were used for trend analysis with a significance level of 5%. The strong association between climate variability conditions described using the Bultó-1 bioclimatic index and acute myocardial infarctions accounts for the marked seasonal pattern in AMI mortality. The highest mortality rate occurred during the dry season, i.e., the winter months in Cuba (November-April), with peak numbers in January, December and March. The lowest mortality coincided with the rainy season, i.e., the summer months (May-October). A downward trend in total number of deaths can be seen starting with the change point in April 2009. Climate variability is inversely associated with an increase in acute myocardial infarction mortality as is shown by the Bultó-1 index. This inverse relationship accounts for acute myocardial infarction mortality's seasonal pattern.

  16. Takotsubo cardiomyopathy after acute myocardial infarction: An unusual case of possible association.

    PubMed

    Ferrara, Francesco; Baldi, Cesare; Malinconico, Marisa; Acri, Edvige; Cirillo, Annapaola; Citro, Rodolfo; Bossone, Eduardo

    2016-04-01

    Takotsubo cardiomyopathy is an acute reversible clinical condition mimicking an acute myocardial infarction. Although a normal coronary artery tree is frequently detected, the concurrence of coronary artery disease is a common finding in a substantial proportion of patients. We report an unusual case of takotsubo cardiomyopathy in post-menopausal women after emotional stress, occurring after inferior ST-segment elevation myocardial infarction. The possible association between takotsubo cardiomyopathy and coronary artery disease is discussed.

  17. ST-Elevation Myocardial Infarction After Sumitriptan Ingestion in Patient with Normal Coronary Arteries

    PubMed Central

    Jensen, Christian; Riddle, Mark

    2015-01-01

    Sumitriptan has been used by millions as a migraine abortant; however, there have been studies showing angina pectoris, coronary vasospasm, and even myocardial infarction in patients with predisposing cardiac risk factors. The majority are patients using the injectable form subcutaneously. We present the case of a patient who presents with ST-elevation myocardial infarction, with no cardiovascular risk factors, after ingesting oral sumitriptan for her typical migraine. PMID:26587110

  18. Prevalence and Prognosis of High-risk Myocardial Infarction Patient Candidates to Extended Antiplatelet Therapy.

    PubMed

    Marrugat, Jaume; Elosua, Roberto; Grau, María; Sayols-Baixeras, Sergi; Dégano, Irene R

    2016-05-01

    Secondary prevention in myocardial infarction patients is paramount to prevent recurrences. Dual antiplatelet therapy has been shown to reduce the risk of subsequent events up to 1 year and beyond in the PEGASUS-TIMI 54 trial. This study aimed to estimate the annual number of myocardial infarction patients with PEGASUS characteristics in Spain and to analyze short- and long-term outcomes in these patients. The number of myocardial infarction patients was estimated assuming a Poisson distribution. Myocardial infarction incidence and mortality rates obtained from population registries (IBERICA and REGICOR) were properly adjusted. The proportion of myocardial infarction patients with PEGASUS characteristics was estimated with a REGICOR cohort of consecutive patients from 2003-2009 (n=1391). This cohort follow-up was used to compare the occurrence of reinfarction and death at 1 year and at the end of the follow-up (4.7 years) in patients with and without PEGASUS characteristics by Cox regression. The estimated annual number of stable myocardial infarction patients aged ≥ 50 years and without bleeding events was 41 311. Of these, 22 493 had at least 1 PEGASUS characteristic (diabetes, previous myocardial infarction, or chronic kidney disease). At 4.7 years of follow-up, having any PEGASUS characteristic or age ≥ 65 years was associated with a higher risk of cardiovascular and all-cause death in adjusted analyses (hazard ratio=3.44 and 2.21, 95% confidence interval, 1.22-9.74 and 1.11-4.42, respectively). In Spain, more than 50% of the stable myocardial infarction patients aged ≥ 50 years are estimated to have at least 1 PEGASUS characteristic, which substantially increases the long-term risk of cardiovascular and all-cause death. Copyright © 2016 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

  19. Acute ST Elevation Myocardial Infarction in Patients With Immune Thrombocytopenia Purpura: A Case Report

    PubMed Central

    Dhillon, Sandeep K; Lee, Edwin; Fox, John; Rachko, Maurice

    2011-01-01

    Acute myocardial infarction (AMI) in patients with immune thrombocytopenic purpura (ITP) is rare. We describe a case of AMI in patient with ITP. An 81-year-old woman presented with acute inferoposterior MI with low platelet count on admission (34,000/µl). Coronary angiography revealed significant mid right coronary artery (RCA) stenosis with thrombus, subsequently underwent successful percutaneous coronary intervention (PCI). In some patients with immune thrombocytopenia purpura and acute myocardial infarction, percutaneous coronary intervention is a therapeutic option.

  20. Acute myocardial infarction following blunt chest trauma due to sea traffic accident.

    PubMed

    Vincelj, Josip; Sokol, Ivan; Samodol, Ante; Grubisić-Cabo, Robert

    2007-09-14

    Myocardial infarction as a complication of blunt chest trauma has been reported most commonly in victims of car accidents. Other cases have been very rarely reported. To our knowledge, sea traffic accident as the cause of coronary artery injury has not been described. The authors report on a rare case of acute anterior wall myocardial infarction in a 60-year-old woman following blunt chest trauma caused by sea traffic accident.

  1. A Case of an Acute Myocardial Infarction Post Thrombolytic Treatment of Ischemic Stroke - A Management Dilemma.

    PubMed

    Wagle, Kalyan; Yee, Jimmy; Kumar, Vishesh; Anuwatworn, Amornpol; Stys, Tomasz; Stys, Adam; Stanton, Christopher

    2017-08-01

    Acute ischemic stroke and myocardial infarction are emergency clinical events that require prompt intervention. Concurrent occurrence of both events magnifies the complexity of the clinical management. We present a case of a patient who presented with acute ischemic stroke, complicated by acute myocardial infarction shortly after thrombolytic was administered. This case highlights the importance of individualization of management especially in complex cases where there are no clear specific guidelines to follow. Copyright© South Dakota State Medical Association.

  2. [Myocardial infarction after butane inhalation in a 14-year-old boy].

    PubMed

    Godlewski, Krzysztof; Werner, Bozena; Sterliński, Maciej; Pytkowski, Mariusz; Szwed, Hanna; Domagała, Marek; Koc, Lucyna

    2006-03-01

    Myocardial infarction is a rare disease in children. Among many reasons the toxic damage of myocardium should be taken into consideration. The authors present the case of a 14-year-old boy with sudden cardiac arrest due to ventricular fibrillation and myocardial infarction as a result of butane gas inhalation. Coronary angiography revealed normal coronary arteries. Cardioverter-defibrillator was implanted as a secondary prophylaxis of sudden cardiac death.

  3. Liposomal amphotericin B-induced hypotension leading to ST segment elevated myocardial infarction.

    PubMed

    Golwala, Harsh; Patel, Nishit; Zacharias, Soni; Lozano, Pedro

    2011-09-01

    We hereby report a short case of 71-year-old gentleman who developed ST segment elevation myocardial infarction shortly after starting the infusion of liposomal amphotericin B for disseminated histoplasmosis. We also discuss the novel pathogenesis of specific liposomal component of amphotericin B that contributed to the acute cardiopulmonary compromise in our patient leading to subsequent myocardial infarction. (C) 2011 Lippincott Williams & Wilkins, Inc.

  4. Regional differences of myocardial infarct development and ischemic preconditioning.

    PubMed

    Schulz, Rainer; Gres, Petra; Konietzka, Ina; Heusch, Gerd

    2005-01-01

    The spatial and temporal development of myocardial infarction depends on the area at risk (AAR), the severity and duration of blood flow reduction (energy supply) as well as on heart rate and regional wall function (energy demand). Both supply and demand can vary within the AAR of a given heart, potentially resulting in differences in infarct development. We therefore retrospectively analyzed infarct size (IS, %AAR, TTC) in 24 anesthetized pigs in vivo following 90 min hypoperfusion and 120 min reperfusion of the LAD coronary artery, which supplies parts of the LV septum (LVS) and anterior free wall (LVAFW). The total LAD perfusion territory averaged 49.8 +/- 14.2 (SD) g (49.2 +/- 8.4% of LV); 61.4 +/- 8.1% of the AAR was LVAFW. IS within the LVS was 25.3 +/- 15.1%, while IS within the LVAFW was 16.6 +/-10.1% (p<0.05). While ischemic blood flow (radiolabeled microspheres) did not differ between LVS (0.05 +/- 0.02 ml/min/g) and LVAFW (0.05 +/- 0.03 ml/min/g), perivascular connective tissue (56 +/- 9 vs. 38+/-7 microm(2), p < 0.05) and the capillary-to-myocyte distance (1.65 +/- 0.23 vs. 1.18 +/- 0.23 mm, p < 0.05) were larger in LVS than in LVAFW. Interestingly, IS in LVS (9.3 +/- 9.6%, n = 24) and LVAFW (9.2 +/- 9.1%) were reduced to the same absolute extent by ischemic preconditioning with one cycle of 10 min ischemia and 15 min reperfusion, suggesting that a similar regional difference exists also in the protection afforded by ischemic preconditioning. The mechanism(s) for that remain(s) to be established. In pigs, regional differences in infarct development and protection from it exist in the LAD perfusion territory, which are independent of ischemic blood flow but apparently related to pre-existing structural differences.

  5. Noninvasive Imaging of Angiotensin Receptors After Myocardial Infarction

    PubMed Central

    Verjans, Johan W. H.; Lovhaug, Dagfinn; Narula, Navneet; Petrov, Artiom D.; Indrevoll, Bård; Bjurgert, Emma; Krasieva, Tatiana B.; Petersen, Lizette B.; Kindberg, Grete M.; Solbakken, Magne; Cuthbertson, Alan; Vannan, Mani A.; Reutelingsperger, Chris P. M.; Tromberg, Bruce J.; Hofstra, Leonard; Narula, Jagat

    2010-01-01

    OBJECTIVES The purpose of this study was to evaluate the feasibility of noninvasive imaging of angiotensin II (AT) receptor upregulation in a mouse model of post-myocardial infarction (MI) heart failure (HF). BACKGROUND Circulating AT levels do not reflect the status of upregulation of renin-angiotensin axis in the myocardium, which plays a central role in ventricular remodeling and evolution of HF after MI. Appropriately labeled AT or AT receptor blocking agents should be able to specifically target AT receptors by molecular imaging techniques. METHODS AT receptor imaging was performed in 29 mice at various time points after permanent coronary artery ligation or in controls using a fluoresceinated angiotensin peptide analog (APA) and radiolabeled losartan. The APA was used in 19 animals for intravital fluorescence microscopy on a beating mouse heart. Tc-99m losartan was used for in vivo radionuclide imaging and quantitative assessment of AT receptor expression in 10 mice. After imaging, hearts were harvested for pathological characterization using confocal and 2-photon microscopy. RESULTS No or little APA uptake was observed in control animals or within infarct regions on days 0 and 1. Distinct uptake occurred in the infarct area at 1 to 12 weeks after MI; the uptake was at maximum at 3 weeks and reduced markedly at 12 weeks after MI. Ultrasonographic examination demonstrated left ventricular remodeling, and pathologic characterization revealed localization of the APA tracer with collagen-producing myofibroblasts. Tc-99m losartan uptake in the infarct region (0.524 ± 0.212% injected dose/g) increased 2.4-fold as compared to uptake in the control animals (0.215 ± 0.129%; p < 0.05). CONCLUSIONS The present study demonstrates the feasibility of in vivo molecular imaging of AT receptors in the remodeling myocardium. Noninvasive imaging studies aimed at AT receptor expression could play a role in identification of subjects likely to develop heart failure. In addition

  6. Acute myocardial infarction: estimation of at-risk and salvaged myocardium at myocardial perfusion SPECT 1 month after infarction.

    PubMed

    Romero-Farina, Guillermo; Aguadé-Bruix, Santiago; Candell-Riera, Jaume; Pizzi, M Nazarena; Pineda, Victor; Figueras, Jaume; Cuberas, Gemma; de León, Gustavo; Castell-Conesa, Joan; García-Dorado, David

    2013-11-01

    To estimate at-risk and salvaged myocardium by using gated single photon emission computed tomography (SPECT) myocardial perfusion imaging after acute myocardial infarction (AMI). The study was approved by the hospital's Ethical Committee on Clinical Trials (trial register number, PR(HG)36/2000), and all patients gave informed consent. Forty patients (mean age, 61.78 years; eight women) with a first AMI underwent two gated SPECT examinations--one before percutaneous coronary intervention (PCI) and one 4-5 weeks after PCI. Myocardium at risk was estimated by assessing the perfusion defect at the first gated SPECT examination, and salvaged myocardium was estimated by assessing the risk area minus necrosis at the second examination. Myocardium at risk was estimated by determining the discordance between the areas of left ventricular (LV) wall motion and perfusion at the second examination. Concordance between tests was analyzed by means of linear regression analysis, the Pearson correlation, the intraclass correlation coefficient, and Bland-Altman analysis. An improvement in perfusion, wall motion, wall thickening, and LV ejection fraction (P < .001) was observed at 1 month. At 1 month, the area with abnormal wall motion was greater than the area of altered perfusion (35.47 vs 23.1 cm(2); P = .007). The extent of myocardium at risk estimated from this discordance correlated well with myocardium at risk measured at the first gated SPECT examination and with salvaged myocardium between both studies (Pearson correlation: 0.78 and 0.6, respectively). Concordance for correct classification of patients with salvaged myocardium of 50% or greater was 83% (κ = 0.65). Myocardial perfusion gated SPECT performed 1 month after early PCI in a first AMI provides potentially useful information on at-risk and salvaged myocardium. http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.13122324/-/DC1. RSNA, 2013

  7. [Impact of comorbidities on in-hospital mortality from acute myocardial infarction, 2003-2009].

    PubMed

    Gili, Miguel; Sala, José; López, Julio; Carrión, Ana; Béjar, Luís; Moreno, Julio; Rosales, Angela; Sánchez, Gabriel

    2011-12-01

    Treatment of acute myocardial infarction has changed notably in recent years. The objective of this study was to analyze trends in in-hospital mortality during the period 2003-2009 and to examine how changes in comorbidity indices affected mortality prediction models for acute myocardial infarction using the minimum basic data set. During the study period, 5275 cases of acute myocardial infarction were admitted. Mortality rates were calculated by age and sex and Charlson and Elixhauser comorbidity index scores were obtained on admission for every patient. Trends were analyzed and their validity studied. Multivariate models predictive of mortality were derived and compared. Mean age and comorbidities increased in all patients over the period 2003-2009. In spite of these trends, acute myocardial infarction mortality decreased. Comorbidity indices remained valid when the criterion "present on admission" was applied. Multivariate predictive models included age, sex, medical treatment, coronary revascularization and a comorbidity index or specific comorbidities. The model with specific comorbidities showed the best predictive ability. All models found that age and comorbidities increased the risk of death, and that coronary revascularization and treatment with anticoagulants, fibrinolytics, and platelet antiaggregants were protective factors. Despite the fact that the mean age and number of comorbidities in acute myocardial infarction patients has increased year over year, acute myocardial infarction mortality has decreased, probably because of more frequent reperfusion and revascularization therapy and better medical treatment. Copyright © 2011 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.

  8. Total antioxidant capacity from diet and risk of myocardial infarction: a prospective cohort of women.

    PubMed

    Rautiainen, Susanne; Levitan, Emily B; Orsini, Nicola; Åkesson, Agneta; Morgenstern, Ralf; Mittleman, Murray A; Wolk, Alicja

    2012-10-01

    There are no previous studies investigating the effect of all dietary antioxidants in relation to myocardial infarction. The total antioxidant capacity of diet takes into account all antioxidants and synergistic effects between them. The aim of this study was to examine how total antioxidant capacity of diet and antioxidant-containing foods were associated with incident myocardial infarction among middle-aged and elderly women. In the population-based prospective Swedish Mammography Cohort of 49-83-year-old women, 32,561 were cardiovascular disease-free at baseline. Women completed a food-frequency questionnaire, and dietary total antioxidant capacity was calculated using oxygen radical absorbance capacity values. Information on myocardial infarction was identified from the Swedish Hospital Discharge and the Cause of Death registries. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox proportional hazard models. During the follow-up (September 1997-December 2007), we identified 1114 incident cases of myocardial infarction (321,434 person-years). In multivariable-adjusted analysis, the HR for women comparing the highest quintile of dietary total antioxidant capacity to the lowest was 0.80 (95% CI, 0.67-0.97; P for trend=0.02). Servings of fruit and vegetables and whole grains were nonsignificantly inversely associated with myocardial infarction. These data suggest that dietary total antioxidant capacity, based on fruits, vegetables, coffee, and whole grains, is of importance in the prevention of myocardial infarction. Copyright © 2012 Elsevier Inc. All rights reserved.

  9. Myocardial infarction and stroke in young women: what is the impact of oral contraceptives?

    PubMed

    Lewis, M A

    1998-09-01

    Recent discussions have centered on the small apparent risk increase for venous thromboembolism found with newer oral contraceptives (third-generation oral contraceptives containing the progestins desogestrel and gestodene) compared with older oral contraceptives (second-generation). This article reviews the studies addressing the association between oral contraceptive use and thromboembolic conditions affecting the arterial system, ischemic stroke, and myocardial infarction. Differences are found between a US database study, which showed no risk of ischemic stroke or myocardial