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Sample records for myocardial infarction effects

  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. 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.

  3. 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.

  4. 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

  5. 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.

  6. Effect of coronary artery recanalization on right ventricular function in patients with acute myocardial infarction

    SciTech Connect

    Verani, M.S.; Tortoledo, F.E.; Batty, J.W.; Raizner, A.E.

    1985-05-01

    The effects of coronary artery recanalization by intracoronary administration of streptokinase on left ventricular function during acute myocardial infarction have received increasing attention in recent years. Although myocardial dysfunction is often more pronounced in the right ventricle than in the left ventricle in patients with acute inferior wall myocardial infarction, the effect of coronary artery recanalization on right ventricular dysfunction has not been previously addressed. Accordingly, in this investigation, 54 patients who participated in a prospective, controlled, randomized trial of recanalization during acute myocardial infarction were studied. Among 30 patients with inferior wall infarction, 19 had right ventricular dysfunction on admission; 11 of these 19 had positive uptake of technetium-99m pyrophosphate in the right ventricle, indicative of right ventricular infarction. Patients with successful recanalization exhibited improved right ventricular ejection fraction from admission to day 10. However, control patients and patients who did not undergo recanalization also exhibited improvement. These data indicate that the right ventricular dysfunction commonly associated with inferior wall infarction is often transient, and improvement is the rule, irrespective of early recanalization of the infarct vessel.

  7. Chronic effects of myocardial infarction on right ventricular function: a noninvasive assessment

    SciTech Connect

    Kaul, S.; Hopkins, J.M.; Shah, P.M.

    1983-10-01

    To assess the chronic effects of myocardial infarction on right ventricular function, 48 subjects were studied utilizing radionuclide angiography and two-dimensional echocardiography. Ten were normal subjects (group I), 11 had previous inferior wall myocardial infarction (group II), 10 had previous anteroseptal infarction (group III), 11 had combined anteroseptal and inferior infarction (group IV) and 6 had extensive anterolateral infarction (group V). The mean (+/- standard deviation) left ventricular ejection fraction was 0.66 +/- 0.03 in group I, 0.58 +/- 0.02 in group II, 0.52 +/- 0.02 in group III, 0.33 +/- 0.03 in group IV and 0.33 +/- 0.01 in group V. No systematic correlation between left and right ventricular ejection fraction was observed among the groups. The mean right ventricular ejection fraction was significantly reduced in the presence of inferior myocardial infarction (0.30 +/- 0.03 in group II and 0.29 +/- 0.03 in group IV compared with 0.43 +/- 0.02 in group I (p less than 0.001)). The group II and IV patients also had increased (p less than 0.001) right ventricular end-diastolic area and decreased (p less than 0.001) right ventricular free wall motion by two-dimensional echocardiography. In the presence of anteroseptal infarction (group III), right ventricular free wall motion was increased (p less than 0.05) compared with normal subjects (group I). Thus, the effects of prior myocardial infarction on right ventricular function depend more on the location of infarction than on the extent of left ventricular dysfunction. Inferior infarction was commonly associated with reduced right ventricular ejection fraction and increased right ventricular end-diastolic area. The right ventricular free wall excursion was increased in the presence of anteroseptal infarction, suggested loss of contribution of interventricular septal contraction to right ventricular ejection.

  8. 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…

  9. Myocardial Salvaging Effects of Berberine in Experimental Diabetes Co-Existing with Myocardial Infarction

    PubMed Central

    Borde, Manjusha K.; Mohanty, Ipseeta Ray; Maheshwari, Ujwala; Deshmukh, Y.A.

    2016-01-01

    Introduction Berberine, an isoquinoline alkaloid isolated from the Berberis aristata, has been shown to display a wide array of pharmacological activities (hypoglycaemic and hypolipidemic). Aim The present study was designed to investigate whether these pharmacological properties translate into the cardioprotective effects of Berberine in the setting of diabetes mellitus. Materials and Methods Necessary approval from the Institutional Animal Ethics Committee was taken for the study. Experimental diabetes was produced with single dose of Streptozotocin (STZ): 45mg/kg ip and myocardial infarction was induced by administering Isoproterenol (ISP): 85mg/kg, sc to rats on 35th & 36th day. After the confirmation of diabetes on 7th day (>200mg/dl), Berberine (100 mg/kg) was administered orally to experimental rats from day 8 and continued for 30 days thereafter. Various anti-diabetic (Glucose, HbA1c), cardioprotective (CPK-MB), metabolic (lipid profile), safety {liver function (SGPT, kidney function (Creatinine)} and histopathological indices of injury were evaluated in Healthy Control, Diabetic Control and Berberine treated groups. Results Administration of STZ-ISP resulted in a significant decrease in body weight (p<0.001), diabetic changes (increase in blood glucose, HbA1c), cardiac injury (leakage of myocardial CPK-MB), altered lipid profile, SGPT, creatinine levels (p<0.001) in the diabetic control group rats as compared to healthy control. Berberine treatment demonstrated significant antidiabetic as well as myocardial salvaging effects as indicated by restoration of blood glucose, HbA1c and CPK-MB levels (p<0.001) compared to diabetic control group. In addition, Berberine favourably modulated the lipid parameters (total cholesterol, triglycerides, HDL, LDL). Subsequent to ISP challenge, histopathological assessment of heart, pancreas and biochemical indices of injury confirmed the cardioprotective effects of Berberine in setting of diabetes. In addition, Berberine

  10. 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.

  11. Anti-inflammatory and anti-thrombotic effects of zingerone in a rat model of myocardial infarction.

    PubMed

    Hemalatha, K L; Stanely Mainzen Prince, P

    2016-11-15

    Myocardial infarction continues to be a major public health problem. Reduction in mortality rate and prevention of myocardial infarction are of utmost importance. Inflammation and thrombosis play an important role in the pathogenesis of myocardial infarction. The anti-inflammatory and anti-thrombotic effects of zingerone were evaluated in isoproterenol induced myocardial infarcted rats. Rats were pretreated with zingerone (6mg/kg body weight) daily for 14 days and were then induced myocardial infarction with isoproterenol (100mg/kg body weight) on 15th and 16th day. Isoproterenol induced myocardial infarcted rats showed significant (P<0.05) increase in the levels/ activities of cardiac troponin-I (cTnI), high sensitive C-reactive protein (Hs CRP), lysosomal hydrolases in the serum and concentration of heart lysosomal lipid peroxidation (LPO) products. RT-PCR study revealed over expression of myocardial tumour necrosis factor - alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) genes in the myocardial infarcted rats. Histopathology of heart and coronary artery revealed marked inflammation and coronary thrombosis. Zingerone pretreatment significantly (P<0.05) decreased serum cTnI, Hs CRP, lysosomal hydrolases and heart lysosomal LPO and down regulated myocardial TNF-α, IL-1β and IL-6 genes and prevented coronary thrombosis in isoproterenol induced myocardial infarcted rats. The observed effects of zingerone could be attributed to its anti-inflammatory and anti-thrombotic properties.

  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. 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.

  14. [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.

  15. Hemodynamic effects of acute digitalization several months after acute myocardial infarction.

    PubMed

    Ressl, J; Jandová, R; Jebavý, P; Kasalický, J; Widimský, J

    1975-01-01

    Left ventricular function was investigated at rest and during exercise by heart catheterization in 15 patients 3-5 months after acute myocardial infarction. The effect of 1 mg digoxin i.v. in ten patients was correlated to placebo (saline solution) in five patients. A significant decrease of the left ventricular enddiastolic pressure, increase of left ventricular systolic ejection fraction and a shift of the left ventricular function curve to left upwards was found after digoxin with no changes in the placebo group. This beneficial effect of acute digitalization in patients convalescing from uncomplicated myocardial infarction without clinical signs of manifest heart failure could have therapeutic implication.

  16. Changes in Sympathetic Innervation of Rat Caudal Artery in Experimental Myocardial Infarction. Effect of Semax Peptide.

    PubMed

    Gorbacheva, A M; Berdalin, A B; Stulova, A N; Nikogosova, A D; Lin, M D; Buravkov, S V; Gavrilova, S A; Koshelev, V B

    2016-08-01

    Activation of the sympathetic nervous system aggravates the course of myocardial infarction. Semax peptide moderated the degree of this activation and prevented the increase in the density of sympathetic endings in rat caudal artery in 28 days after ischemia or ischemia/reperfusion. The peptide reduced the density of α-adrenoreceptors in the caudal artery of rats with myocardial infarction. Semax produced no effect on β-adrenoreceptors in both experimental models. The experiments on isolated segments of the caudal artery revealed reduced vascular responsiveness to electrical stimulation and norepinephrine infusion in rats treated with Semax after ischemia/reperfusion injury.

  17. Effect of initial temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction.

    PubMed

    Qian, Yuanyu; Liu, Jie; Ma, Jinling; Meng, Qingyi; Peng, Chaoying

    2014-07-01

    In the present study, the effect of initial body temperature changes on myocardial enzyme levels and cardiac function in acute myocardial infarction (AMI) patients was investigated. A total of 315 AMI patients were enrolled and the mean temperature was calculated based on their body temperature within 24 h of admission to hospital. The patients were divided into four groups according to their normal body temperature: Group A, <36.5°C; group B, ≥36.5°C and <37.0°C; group C, ≥37.0°C and <37.5°C and group D, ≥37.5°C. The levels of percutaneous coronary intervention, myocardial enzymes and troponin T (TNT), as well as cardiac ultrasound images, were analyzed. Statistically significant differences in the quantity of creatine kinase at 12 and 24 h following admission were identified between group A and groups C and D (P<0.01). A significant difference in TNT at 12 h following admission was observed between groups A and D (P<0.05), however, this difference was not observed with groups B and C. The difference in TNT between the groups at 24 h following admission was not statistically significant (P>0.05). Significant differences in lactate dehydrogenase at 12 and 24 h following admission were observed between groups A and D (P<0.05), however, differences were not observed with groups B and C (P>0.05). Significant differences in glutamic-oxaloacetic transaminase at 12 and 24 h following admission were observed between groups A and D (P<0.05), however, differences were not observed in groups B and C (P>0.05). However, no significant differences were identified in cardiac function index between all the groups. Therefore, the results of the present study indicated that AMI patients with low initial body temperatures exhibited decreased levels of myocardial enzymes and TNT. Thus, the observation of an initially low body temperature may be used as a protective factor for AMI and may improve the existing clinical program.

  18. Human cord blood cells and myocardial infarction: effect of dose and route of administration on infarct size.

    PubMed

    Henning, Robert J; Burgos, Jose D; Vasko, Mark; Alvarado, Felipe; Sanberg, Cyndy D; Sanberg, Paul R; Morgan, Michael B

    2007-01-01

    There is no consensus regarding the optimal dose of stem cells or the optimal route of administration for the treatment of acute myocardial infarction. Bone marrow cells, containing hematopoietic and mesenchymal stem cells, in doses of 0.5 x 10(6) to >30 x 10(6) have been directly injected into the myocardium or into coronary arteries or infused intravenously in subjects with myocardial infarctions to reduce infarct size and improve heart function. Therefore, we determined the specific effects of different doses of human umbilical cord blood mononuclear cells (HUCBC), which contain hematopoietic and mesenchymal stem cells, on infarct size. In order to determine the optimal technique for stem cell administration, HUCBC were injected directly into the myocardium (IM), or into the LV cavity with the ascending aorta transiently clamped to facilitate coronary artery perfusion (IA), or injected intravenously (IV) in rats 1-2 h after the left anterior coronary artery was permanently ligated. Immune suppressive therapy was not given to any rat. One month later, the infarct size in control rat hearts treated with only Isolyte averaged 23.7 +/- 1.7% of the LV muscle area. Intramyocardial injection of HUCBC reduced the infarct size by 71% with 0.5 x 10(6) HUCBC and by 93% with 4 x 10(6) HUCBC in comparison with the controls (p < 0.001). Intracoronary injection reduced the infarction size by 47% with 0.5 x 10(6) HUCBC and by 80% with 4 x 10(6) HUCBC (p < 0.001), and IV HUCBC reduced infarct size by 51% with 0.5 x 10(6) and by 75-77% with 16-32 million HUCBC (p < 0.001) in comparison with control hearts. With 4 x 10(6) HUCBC, infarction size was 65% smaller with IM HUCBC than with IA HUCBC and 78% smaller than with IV HUCBC (p < 0.05). Nevertheless, IM, IA, and IV HUCBC all produced significant reductions in infarct size in comparison with Isolyte-treated infarcted hearts without requirements for host immune suppression. The present experiments demonstrate that the optimal dose

  19. Synergistic effects of nitric oxide and exercise on revascularisation in the infarcted ventricle in a murine model of myocardial infarction

    PubMed Central

    Ranjbar, Kamal; Nazem, Farzad; Nazari, Afshin; Gholami, Mohammadreza; Nezami, Ali Reza; Ardakanizade, Malihe; Sohrabi, Maryam; Ahmadvand, Hasan; Mottaghi, Mohammad; Azizi, Yaser

    2015-01-01

    It has been shown that density of microvessels decreases in the left ventricular after myocardial infarction (MI). The change of angiogenic and angiostatic factors as the main factors in revascularisation after exercise training in area at risk is not determined yet in MI. Therefore, the aim of the present study was the effect of exercise training and L-arginine supplementation on area at risk angiogenesis in myocardial infarction rat. Four weeks after surgery (Left Anterior Descending Coronary artery Ligation), myocardial infarction rats were divided into 4 groups: Sedentary rats (Sed-MI); L-arginine supplementation (La-MI); Exercise training (Ex-MI) and Exercise + L-arginine (Ex+La). Exercise training (ET) lasted for 10 weeks at 17 m/min for 10-50 min day−1. Rats in the L-arginine-treated groups drank water containing 4 % L-arginine. After ET and L-arginine supplementation, ventricular function was evaluated and angiogenic and angiostatic indices were measured at ~1 mm from the edge of scar tissue (area at risk). Statistical analysis revealed that gene expression of VEGF as an angiogenic factor, angiostatin as an angiostatic factor and caspase-3 at area at risk decrease significantly in response to exercise training compared to the sedentary group. The capillary and arteriolar density in the Ex groups were significantly higher than those of the Sed groups. Compared to the Ex-MI group, the Ex+La group showed a markedly increase in capillary to fiber ratio. No significant differences were found in infarct size among the four groups, but cardiac function increased in response to exercise. Exercise training increases revascularization at area at risk by reduction of angiostatin. L-arginine supplementation causes additional effects on exercise-induced angiogenesis by preventing more reduction of VEGF gene expression in response to exercise. These improvements, in turn, increase left ventricular systolic function and decrease mortality in myocardial infarction rats

  20. 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

  1. 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.

  2. Short-term effects of atmospheric particulate matter on myocardial infarction: a cumulative meta-analysis.

    PubMed

    Cai, Xianlei; Li, Zhenhong; Scott, E Marian; Li, Xiuyang; Tang, Mengyao

    2016-04-01

    Atmospheric particulate matter (PM) is hypothesized to increase the risk of myocardial infarction (MI). However, the epidemiological evidence is inconsistent. We identified 33 studies with more than 4 million MI patients and applied meta-analysis and meta-regression to assess the available evidence. Twenty-five studies presented the effects of the PM level on hospitalization for MI patients, while eight studies showed the effects on mortality. An increase in PM10 was associated with hospitalization and mortality in myocardial infarction patients (RR per 10 μg/m(3) = 1.011, 95% CI 1.006-1.016; RR per 10 μg/m(3) = 1.008, 95 % CI 1.004-1.012, respectively); PM2.5 also increased the risk of hospitalization and mortality in MI patients (RR per 10 μg/m(3) = 1.024, 95% CI 1.007-1.041 for hospitalization and RR per 10 μg/m(3) = 1.012, 95% CI 1.010-1.015 for mortality). The results of the cumulative meta-analysis indicated that PM10 and PM2.5 were associated with myocardial infarction with the addition of new studies each year. In conclusion, short-term exposure to high PM10 and PM2.5 levels revealed to increase risk of hospitalization and mortality for myocardial infarction. Policy support of pollution control and individual protection was strongly recommended.

  3. Clinical Effects of Hypertension on the Mortality of Patients with Acute Myocardial Infarction

    PubMed Central

    Kang, Dong Goo; Ahn, Yongkeun; Chae, Shung Chull; Hur, Seung Ho; Hong, Taek Jong; Kim, Young Jo; Seong, In Whan; Chae, Jei Keon; Rhew, Jay Young; Chae, In Ho; Cho, Myeong Chan; Bae, Jang Ho; Rha, Seung Woon; Kim, Chong Jin; Jang, Yang Soo; Yoon, Junghan; Seung, Ki Bae; Park, Seung Jung

    2009-01-01

    The incidence of ischemic heart disease has been increased rapidly in Korea. However, the clinical effects of antecedent hypertension on acute myocardial infarction have not been identified. We assessed the relationship between antecedent hypertension and clinical outcomes in 7,784 patients with acute myocardial infarction in the Korea Acute Myocardial Infarction Registry during one-year follow-up. Diabetes mellitus, hyperlipidemia, cerebrovascular disease, heart failure, and peripheral artery disease were more prevalent in hypertensives (n=3,775) than nonhypertensives (n=4,009). During hospitalization, hypertensive patients suffered from acute renal failure, shock, and cerebrovascular event more frequently than in nonhypertensives. During follow-up of one-year, the incidence of major adverse cardiac events was higher in hypertensives. In multi-variate adjustment, old age, Killip class ≥III, left ventricular ejection fraction <45%, systolic blood pressure <90 mmHg on admission, post procedural TIMI flow grade ≤2, female sex, and history of hypertension were independent predictors for in-hospital mortality. However antecedent hypertension was not significantly associated with one-year mortality. Hypertension at the time of acute myocardial infarction is associated with an increased rate of in-hospital mortality. PMID:19794974

  4. Molecular Basis of Cardioprotective Effect of Antioxidant Vitamins in Myocardial Infarction

    PubMed Central

    Rodrigo, Ramón; Feliú, Felipe; Hasson, Daniel

    2013-01-01

    Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage. PMID:23936799

  5. Allogeneic Mesenchymal Precursor Cell Therapy to Limit Remodeling After Myocardial Infarction: The Effect of Cell Dosage

    PubMed Central

    Hamamoto, Hirotsugu; Gorman, Joseph H.; Ryan, Liam P.; Hinmon, Robin; Martens, Timothy P.; Schuster, Michael D.; Plappert, Theodore; Kiupel, Matti; St. John-Sutton, Martin G.; Itescu, Silviu; Gorman, Robert C.

    2011-01-01

    Background This experiment assessed the dose-dependent effect of a unique allogeneic STRO-3–positive mesenchymal precursor cell (MPC) on postinfarction left ventricular (LV) remodeling. The MPCs were administered in a manner that would simulate an off-the-self, early postinfarction, preventative approach to cardiac cell therapy in a sheep transmural myocardial infarct (MI) model. Methods Allogeneic MPCs were isolated from male crossbred sheep. Forty-six female sheep underwent coronary ligation to produce a transmural LV anteroapical infarction. One hour after infarction, the borderzone myocardium received an injection of 25, 75, 225, or 450 × 106 MPCs, or cell medium. Echocardiography was performed at 4 and 8 weeks after MI to quantify LV end-diastolic (LVEDV) and end-systolic volumes (LVESV), ejection fraction (EF), and infarct expansion. CD31 and smooth muscle actin (SMA) immunohistochemical staining was performed on infarct and borderzone specimens to quantify vascular density. Results Compared with controls, low-dose (25 and 75 × 106 cells) MPC treatment significantly attenuated infarct expansion and increases in LVEDV and LVESV. EF was improved at all cell doses. CD31 and SMA immunohistochemical staining demonstrated increased vascular density in the borderzone only at the lower cell doses. There was no evidence of myocardial regeneration within the infarct. Conclusion Allogeneic STRO-3 positive MPCs attenuate the remodeling response to transmural MI in a clinically relevant large-animal model. This effect is associated with vasculogenesis and arteriogenesis within the borderzone and infarct and is most pronounced at lower cell doses. PMID:19231391

  6. The Effects of Inhalation Aromatherapy on Anxiety in Patients With Myocardial Infarction: A Randomized Clinical Trial

    PubMed Central

    Najafi, Zahra; Taghadosi, Mohsen; Sharifi, Khadijeh; Farrokhian, Alireza; Tagharrobi, Zahra

    2014-01-01

    Background: Anxiety is an important mental health problem in patients with cardiac disease. Anxiety reduces patients’ quality of life and increases the risk of different cardiac complications. Objectives: The aim of this study was to investigate the effects of inhalation aromatherapy on anxiety in patients with myocardial infarction. Patients and Methods: This was a randomized clinical trial conduced on 68 patients with myocardial infarction hospitalized in coronary care units of a large-scale teaching hospital affiliated to Kashan University of Medical Sciences, Kashan, Iran in 2013. By using the block randomization technique, patients were randomly assigned to experimental (33 patients receiving inhalation aromatherapy with lavender aroma twice a day for two subsequent days) and control (35 patients receiving routine care of study setting including no aromatherapy) groups. At the beginning of study and twenty minutes after each aromatherapy session, anxiety state of patients was assessed using the Spielberger’s State Anxiety Inventory. Data was analyzed using SPSS v. 16.0. We used Chi-square, Fisher’s exact, independent-samples T-test and repeated measures analysis of variance to analyze the study data. Results: The study groups did not differ significantly regarding baseline anxiety mean and demographic characteristics. However, after the administration of aromatherapy, anxiety mean in the experimental group was significantly lower than the control group. Conclusions: Inhalation aromatherapy with lavender aroma can reduce anxiety in patients with myocardial infarction. Consequently, healthcare providers, particularly nurses, can use this strategy to improve postmyocardial infarction anxiety management. PMID:25389481

  7. 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.

  8. Mechanisms Involved in the Beneficial Effects of Spironolactone after Myocardial Infarction

    PubMed Central

    Minicucci, Marcos F.; dos Santos, Priscila P.; Rafacho, Bruna P. M.; Gonçalves, Andrea F.; Silva, Renata A. C.; Chiuso-Minicucci, Fernanda; Azevedo, Paula S.; Polegato, Bertha F.; Okoshi, Katashi; Pereira, Elenize J.; Paiva, Sergio A. R.; Zornoff, Leonardo A. M.

    2013-01-01

    Introduction Our objective was to analyze the effect of spironolactone on cardiac remodeling after experimental myocardial infarction (MI), assessed by matricellular proteins levels, cardiac collagen amount and distribution, myocardial tissue metalloproteinase inhibitor-1(TIMP-1) concentration, myocyte hypertrophy, left ventricular architecture, and in vitro and in vivo cardiac function. Methods Wistar rats were assigned to 4 groups: control group, in which animals were submitted to simulated surgery (SHAM group; n=9); group that received spironolactone and in which animals were submitted to simulated surgery (SHAM-S group, n=9); myocardial infarction group, in which animals were submitted to coronary artery ligation (MI group, n=15); and myocardial infarction group with spironolactone supplementation (MI-S group, n=15). The rats were observed for 3 months. Results The MI group had higher values of left cardiac chambers and mass index and lower relative wall thicknesses compared with the SHAM group. In addition, diastolic and systolic functions were worse in the MI groups. However, spironolactone did not influence any of these variables. The MI-S group had a lower myocardial hydroxyproline concentration and myocyte cross-sectional area compared with the MI group. Myocardial periostin and collagen type III were lower in the MI-S group compared with the MI-group. In addition, TIMP-1 concentration in myocardium was higher in the MI-S group compared with the MI group. Conclusions The predominant consequence of spironolactone supplementation after MI is related to reductions in collagens, with discrete attenuation of other remodeling variables. Importantly, this effect may be modulated by periostin and TIMP-1 levels. PMID:24098808

  9. Effects of interleukin-37 on cardiac function after myocardial infarction in mice

    PubMed Central

    Xu, Daoying; Wang, Aiqin; Jiang, Fengqin; Hu, Junhong; Zhang, Xiuzhou

    2015-01-01

    Background: Interleukin-37 (IL-37) is a new discovered member of the interleukin family and plays anti-inflammatory effect in some inflammatory disease. A recent study found that IL-37 elevated significantly in peripheral blood of patients with acute myocardial infarction. We aimed to explore the effect IL-37 on cardiac function after mice myocardial infarction (MI) and its mechanism. Methods: Acute MI mouse model was established and divided into three groups: sham group, MI group and IL-37 treatment group. MPO expression was detected by immunohistochemistry; NF-κB signaling pathway was tested by Western blot; and cardiac function was measured by echocardiography. Results: Compared with MI mice, IL-37 treatment showed an obvious decrease of MPO expression, suppression of p-p65 expression, and improved cardiac function by decreasing left ventricular shortening fraction (LVFS). Conclusion: IL-37 may improve MI mice cardiac function via inhibition of inflammatory NF-κB signaling pathway. PMID:26191225

  10. 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

  11. [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.

  12. Beneficial Effects of Schisandrin B on the Cardiac Function in Mice Model of Myocardial Infarction

    PubMed Central

    Chen, Pengsheng; Pang, Sisi; Yang, Naiquan; Meng, Haoyu; Liu, Jia; Zhou, Ningtian; Zhang, Min; Xu, Zhihui; Gao, Wei; Chen, Bo; Tao, Zhengxian; Wang, Liansheng; Yang, Zhijian

    2013-01-01

    The fruit of Schisandra chinensis has been used in the traditional Chinese medicine for thousands of years. Accumulating evidence suggests that Schisandrin B (Sch B) has cardioprotection effect on myocardial ischemia in vitro. However, it is unclear whether Sch B has beneficial effects on continuous myocardial ischemia in vivo. The aim of the present study was to investigate whether Sch B could improve cardiac function and attenuate myocardial remodeling after myocardial infarction (MI) in mice. Mice model of MI was established by permanent ligation of the left anterior descending (LAD) coronary artery. Then the MI mice were randomly treated with Sch B or vehicle alone. After treatment for 3 weeks, Sch B could increase survival rate, improve heart function and decrease infarct size compared with vehicle. Moreover, Sch B could down-regulate some inflammatory cytokines, activate eNOS pathway, inhibit cell apoptosis, and enhance cell proliferation. Further in vitro study on H9c2 cells showed similar effects of Sch B on prevention of hypoxia-induced inflammation and cell apoptosis. Taken together, our results demonstrate that Sch B can reduce inflammation, inhibit apoptosis, and improve cardiac function after ischemic injury. It represents a potential novel therapeutic approach for treatment of ischemic heart disease. PMID:24260217

  13. The effect of ibuprofen on accumulation of /sup 111/In-labeled platelets and leukocytes in experimental myocardial infarction

    SciTech Connect

    Romson, J.L.; Hook, B.G.; Rigot, V.H.; Schork, M.A.; Swanson, D.P.; Lucchesi, B.R.

    1982-11-01

    To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 (/sup 111/In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occlusion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p . 0.005). Quantification of the platelet-associated /sup 111/In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes accumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction.

  14. The effect of ibuprofen on accumulation of indium-111-labeled platelets and leukocytes in experimental myocardial infarction

    SciTech Connect

    Romson, J.L.; Hook, B.G.; Rigot, V.H.; Schark, M.A.; Swanson, D.P.; Lucchesi, B.R.

    1982-11-01

    To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 (/sup 111/In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occulsion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p=0.005). Quantification of the platelet-associated /sup 111/In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes acumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction.

  15. Effects of histidine and vitamin C on isoproterenol-induced acute myocardial infarction in rats

    PubMed Central

    Moradi-Arzeloo, Masoumeh; Farshid, Amir Abbas; Tamaddonfard, Esmaeal; Asri-Rezaei, Siamak

    2016-01-01

    In the present study, we investigated the effects of histidine and vitamin C (alone or in combination) treatments against isoproterenol (a β-adrenergic receptor agonist)-induced acute myocardial infarction in rats. We used propranolol (a β-adrenergic receptor blocker) to compare the results. Rats were given intraperitoneal injections of histidine (40 mg kg-1) and vitamin C (40 mg kg-1) alone and combined daily for 21 days. Propranolol (10 mg kg-1) was orally administered daily for 10 days (from day 11 to day 21). Myocardial infarction was induced by subcutaneous injections of 150 mg kg-1 of isoproterenol at an interval of 24 hr on days 20 and 21. Blood and tissue samples were taken for histopathological and biochemical evaluations following electrocardiography recording on day 21. Isoproterenol elevated ST segment, increased heart weight, heart rate, serum activities of aspartate transaminase, lactate dehydrogenase, creatine kinase-MB and heart tissue content of malondialdehyde, and decreased R wave amplitude and superoxide dismutase and catalase activities of heart tissue. Necrosis, edema and inflammatory cells infiltration were observed in myocardial tissue sections. Our results indicated that histidine and vitamin C alone, and especially in combination prevent isoproterenol-induced cardiotoxicity and have similar protective effects with propranolol. Cardioprotective effects of histidine and vitamin C may be associated with their ability to reduce free radical-induced toxic effects. PMID:27226887

  16. Effects of xenon and isoflurane on apoptosis and inflammation in a porcine myocardial infarction model.

    PubMed

    Sopka, Sasa; Mertens, Christine; Roehl, Anna Bettina; Schiffl, Katharina; Rossaint, Rolf; Classen-Linke, Irmgard

    2013-03-01

    Volatile anaesthetics can reduce the infarction size in myocardial tissue when administered before and during experimentally induced ischaemia. The aim of this study was to investigate whether xenon is beneficial compared to isoflurane in limiting myocardial tissue apoptosis and inflammation induced by experimental ischaemia-reperfusion injury in a porcine right ventricular infarction model. Twenty-one animals used for this study randomly received isoflurane, xenon or thiopental, (n=6-8 per group). Myocardial infarction was induced for 90min, followed by reperfusion for 120min. Tissues from the left and right ventricles were removed from the sites of infarction, reperfusion and remote areas, and processed for immunohistochemistry. Apoptosis (caspase-3 staining) and neutrophilic infiltration (naphthol AS-D chloroacetate-specific esterase) were assessed and evaluated. Statistical analysis was performed using an ANOVA of repeated measures. Density of apoptotic cells were higher in tissues from animals that were anesthetized with xenon. This effect was significant in comparison to isoflurane (p=0.0177). Neutrophilic infiltration was significantly higher in the right compared to the left ventricle (p<0.001), whereas no significant differences in the number of granulocytes based on the anaesthetic regime or the different tissue areas were found. We conclude that xenon, in the early phase of ischaemia and reperfusion, induces a significant increase in apoptosis compared to isoflurane. Therefore, clinical use of this anaesthetic in cardiocompromised patients should be taken with care until more long-term studies have been carried out. The increased neutrophilic infiltration in the right vs. the left ventricle indicates the right ventricle being more susceptible to ischaemia-reperfusion injury.

  17. Effects of intracoronary melatonin on ischemia-reperfusion injury in ST-elevation myocardial infarction.

    PubMed

    Ekeløf, Sarah V; Halladin, Natalie L; Jensen, Svend E; Zaremba, Tomas; Aarøe, Jens; Kjærgaard, Benedict; Simonsen, Carsten W; Rosenberg, Jacob; Gögenur, Ismail

    2016-01-01

    Acute coronary occlusion is effectively treated by primary percutaneous coronary intervention. However, myocardial ischemia-reperfusion injury is at the moment an unavoidable consequence of the procedure. Oxidative stress is central in the development of ischemia-reperfusion injury. Melatonin, an endogenous hormone, acts through antioxidant mechanisms and could potentially minimize the myocardial injury. The aim of the experimental study was to examine the cardioprotective effects of melatonin in a porcine closed-chest reperfused infarction model. A total of 20 landrace pigs were randomized to a dosage of 200 mg (0.4 mg/mL) melatonin or placebo (saline). The intervention was administered intracoronary and intravenous. Infarct size, area at risk and microvascular obstruction were determined ex vivo by cardiovascular magnetic resonance imaging. Myocardial salvage index was calculated. The plasma levels of high-sensitive troponin T were assessed repeatedly. The experimenters were blinded with regard to treatment regimen. Melatonin did not significantly increase myocardial salvage index compared with placebo [melatonin 21.8% (16.1; 24.8) vs. placebo 20.2% (16.9; 27.0), p = 1.00]. The extent of microvascular obstruction was similar between the groups [melatonin 3.8% (2.7; 7.1) vs. placebo 3.7% (1.3; 7.7), p = 0.96]. The area under the curve for high-sensitive troponin T release was insignificantly reduced by 32% in the melatonin group [AUC melatonin 12,343.9 (6,889.2; 20,147.4) ng h/L vs. AUC placebo 18,285.3 (5,180.4; 23,716.8) ng h/L, p = 0.82]. Combined intracoronary and intravenous treatment with melatonin did not reduce myocardial reperfusion injury. The lack of a positive effect could be due to an ineffective dose of melatonin, a type II error or the timing of administration.

  18. Cardioprotective effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats.

    PubMed

    Gao, Yan; Gao, Jianping; Chen, Changxun; Wang, Huilin; Guo, Juan; Wu, Rong

    2015-05-01

    The purpose of this study was to explore the effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats and to elucidate the underlying mechanisms. A rat model of ventricular remodeling after myocardial infarction was established by left coronary artery ligation. Rats with coronary artery ligation were randomly divided into five groups: control, plus 40 mg/kg captopril, plus 25 mg/kg polydatin, plus 50 mg/kg polydatin, and plus 100 mg/kg polydatin. The sham-operated group was used as a negative control. Rats were administered intragastrically with the corresponding drugs or drinking water for seven weeks. At the end of the treatment, the left ventricular weight index and heart weight index were assessed. The cross-sectional size of cardiomyocytes was measured by staining myocardium tissue with hematoxylin and eosin. Collagen content was counted by Sirius red in aqueous saturated picric acid. The concentrations of angiotensin I, angiotensin II, aldosterone, and endothelin 1 in myocardium or serum were determined by radioimmunoassay. Hydroxyproline and nitric oxide concentrations and glutathione peroxidase and catalase activities in serum were measured by ultraviolet spectrophotometry. Our results showed that seven weeks of polydatin treatment resulted in a significantly reduced left ventricular weight index, heart weight index, serum concentrations of hydroxyproline and aldosterone, an increased concentration of nitric oxide as well as enhanced activities of glutathione peroxidase and catalase. Myocardial angiotensin I, angiotensin II, and endothelin 1 levels were also reduced. The cardiomyocyte cross-sectional area and collagen deposition diminished. This study suggests that polydatin may attenuate ventricular remodeling after myocardial infarction in coronary artery ligation rats through restricting the excessive activation of the renin-angiotensin-aldosterone system and inhibiting peroxidation.

  19. 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

  20. Computational Modeling of the Effects of Myocardial Infarction on Left Ventricular Hemodynamics

    NASA Astrophysics Data System (ADS)

    Vedula, Vijay; Seo, Jung Hee; Mittal, Rajat; Fortini, Stefania; Querzoli, Giorgio

    2012-11-01

    Most in-vivo and modeling studies on myocardial infarction and ischemia have been directed towards understanding the left ventricular wall mechanics including stress-strain behavior, end systolic pressure-volume correlations, ejection fraction and stroke work. Fewer studies have focused on the alterations in the intraventricular blood flow behavior due to local infarctions. Changes in the motion of the endocardium can cause local circulation and stagnation regions; these increase the blood cell residence time in the left ventricle and may eventually be implicated in thrombus formation. In the present study, we investigate the effects of myocardial infarction on the ventricular hemodynamics in simple models of the left ventricle using an immersed-boundary flow solver. Apart from the Eulerian flow features such as vorticity and velocity flow fields, pressure distribution, shear stress, viscous dissipation and pump work, we also examine the Lagrangian dynamics of the flow to gain insights into the effect of flow dynamics on thrombus formation. The study is preceded by a comprehensive validation study which is based on an in-vitro experimental model of the left ventricle and this study is also described. This research is supported by the U.S. National Science Foundation through (NSF) CDI-Type II grant IOS-1124804. Computational resources for some of the simulations were also provided in part through the NSF grant NSF-OCI-108849.

  1. 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.

  2. 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

  3. Depression following myocardial infarction: the effects of distance running.

    PubMed

    Kavanagh, T; Shephard, R J; Tuck, J A; Qureshi, S

    1977-01-01

    A proportion of postcoronary patients seen 16 to 18 months after infarction are seriously depressed (high D score on Minnesota Multiphasic Personality Inventory). A follow-up of 44 such depressed patients showed a significant (p less than 0.001) decrease of standardized D scores, from 80 to 72 units over 4 years of exercise-based rehabilitation. There were associated decreases in scores for hysteria, hypochondriasis, and psychasthenia. A decrease of D score was associated with exercise compliance. An increase of D score was associated with a significant (p less than 0.05) worsening of ST segmental sagging, suggesting that progression of the disease process had contributed to the increase of depression. All of the patients had high (feminine) scores on the masculinity/femininity scale of the MMPI test. This finding was unrelated to the daily running distance or medication; it could represent a "feminine" personality, or be a typical response in a well-educated white collar group. Evidence of successful group interaction may be indicated by reduction in scores for social introversion and schizophrenic traits.

  4. PROTECTIVE EFFECT OF HESPERIDIN ON CARDIOVASCULAR COMPLICATION IN EXPERIMENTALLY INDUCED MYOCARDIAL INFARCTION IN DIABETES IN RATS

    PubMed Central

    Kakadiya, Jagdish; Mulani, Haresh; Shah, Nehal

    2010-01-01

    Present study was designed to evaluate effect Hesperidin on Cardiovascular Complication in isoproterenol induced myocardial infarction in normal and Streptozotocin-Nicotinamide induced in diabetic rats. Hesperidin (100 mg/kg, p.o) was administered for 28 days in rats injected with single dose of Streptozotocin (65 mg/kg, i.p, STZ) and Nicotinamide (110 mg/kg, i.p, NIC) and after isoproterenol (200 mg/kg, s.c.) induced myocardial infarction in rats on 29th and 30th day. At the end of experimental period (i.e. on the day 31) serum and heart tissues sample were collected, and glucose, HbA1c and Total Cholesterol (TC), Triglycerides (TG) and High density lipoprotein (HDL) and cholesterol ester synthetase (CES), lecithin Cholesterol acyl transferase (LCAT), lipoprotein lipase (LPL), systolic and diastolic blood pressure were find out. Administration of STZ–NIC in rats showed a significant (p<0.001) increased in the levels of serum glucose, glycosylated heamoglobin (HbA1c), Total Cholesterol (TC), Triglycerides (TG) and Low density lipoprotein (LDL) whereas the levels of High density lipoprotein (HDL) were found to be non significant but significant (p<0.001) increased in the level of heart tissues CES and significant (p<0.001, p<0.01) decreased LCAT and LPL, significantly (p<0.01) increased systolic and diastolic blood pressure as compared to respective control groups. Treatment with Hesperidin significantly (P<0.05) decreased HbA1c, glucose, CES level and significantly (P<0.01) decreased LDL, TC, TG, systolic and diastolic blood pressure and significant (P<0.01) increased LCAT and LPL level but no significantly change HDL in compared to diabetic control group. We concluded that HES (100 mg/kg) is effective in controlling blood glucose levels and reduced cardiac complication in experimentally induced myocardial infarction diabetic rats. PMID:24825971

  5. Effect of myocardial infarction on the function and metabolism of the non-infarcted muscle

    SciTech Connect

    Hansen, C.A.

    1985-01-01

    Rat hearts were infarcted in vivo by ligation of the left ventricular coronary artery. After one or three weeks, the hearts were isolated and perfused in vitro. Despite the onset of hypertrophy, ventricular function was more depressed in the one- and three-week infarcted hearts than in acutely ligated hearts. These data suggested that the depressed mechanical function was due not only to the loss of viable tissue, but also to alterations occurring in the non-infarcted tissue. The inotropic response to extracellular calcium was depressed in infarcted hearts, such that the mechanical performance of the infarcted heart was likely to be limited by the availability of extracellular calcium under physiological conditions. No limitation in energy production was found as indicated by the maintenance of ATP levels, the creatine phosphate/creatine ratio and normal lactate concentrations in the infarcted hearts. Comparison of the rates of substrate oxidation with MVO/sub 2/ revealed that, in both the sham and infarcted hearts, substrate oxidation, as estimated by /sup 14/CO/sub 2/ production, could not account for the observed MVO/sub 2/. It was found that the rate of /sup 14/CO/sub 2/ production from exogenous labeled palmitate underestimated the actual rate of fatty acid oxidation. This resulted from incomplete equilibration of added (/sup 14/C)-palmitate with the fatty acyl moieties present in acyl carnitine. However, the rate of /sup 14/CO/sub 2/ production from exogenous palmitate was lower in the infarcted than sham hearts.

  6. Neutrophil accumulation in experimental myocardial infarcts: relation with extent of injury and effect of reperfusion

    SciTech Connect

    Chatelain, P.; Latour, J.G.; Tran, D.; de Lorgeril, M.; Dupras, G.; Bourassa, M.

    1987-05-01

    The effects of reperfusion on the myocardial accumulation of neutrophils and their role in the extent of injury were investigated in a canine preparation with a 3 hr coronary occlusion followed by 21 hr of reperfusion. The left anterior descending coronary artery (LAD) was permanently occluded in group 1 and reperfused after 3 hr in four others (groups 2 to 5). All but group 5 received lidocaine (1 mg/min over 8 hr). A critical stenosis was produced and left in place at reperfusion only in group 2. In groups 1 and 2, /sup 111/In-labeled autologous neutrophils were injected at the time of coronary occlusion. Group 4 animals were rendered leukopenic 2 hr before the coronary ligature and throughout the experiment by injection of an antineutrophil rabbit serum. Quantification of the radioactivity by digitized scintigraphy of the heart slices revealed an 80% increase in neutrophil accumulation in the infarct region after reperfusion (group 2) as compared with permanent occlusion (group 1). Gamma counting of myocardial tissue samples showed that the neutrophil accumulation ratio in the subendocardial central zone of the infarct was increased five times by reperfusion, whereas no difference was evident in the subepicardium. Infarct size and myocardial area at risk were not statistically different among the five groups. However LAD flow in the leukopenic group (group 4) was significantly higher 30 min after reperfusion (40.0 +/- 5 ml/min) when compared with the preocclusion value (21.7 +/- 4 ml/min). In contrast, in a parallel experiment without leukopenia (group 3), LAD flow after reperfusion did not differ from the preocclusion value.

  7. Effects of Air Pollutant Exposure on Acute Myocardial Infarction, According to Gender

    PubMed Central

    Tuan, Tássia Soldi; Venâncio, Taís Siqueira; Nascimento, Luiz Fernando Costa

    2016-01-01

    Background: There is evidence of the effects of air pollution on hospital admissions due to cardiovascular diseases, including myocardial infarction. Objective: To estimate the association between exposure to air pollutants and hospital admissions due to myocardial infarction according to gender, between January 1st 2012 and December 31st 2013, in São Jose dos Campos-SP. Methods: An ecological time series study was carried out with daily data of admissions due to AMI, pollutants CO, O3, PM10, SO2, and NO2, according to gender. We used the Poisson regression generalized linear model to estimate the relative risks of hospital admissions with lags of 0-5 days, adjusted for temperature, humidity, seasonality and days of the week. Results: There were 1837 admissions for ischemic heart diseases, with 636 women and 1201 men. For females, the risks were significant for CO in lag 0 (RR = 1,09), lag1 (RR = 1,08) and lag 5 (RR = 1,10) and SO2 in lag 0 (RR = 1,10) and 3 (RR = 1,09). For men there was significance of the CO in, lag 3 and lag 5 (RR = 1,05). There was significance, regardless of gender, for CO at lag 1 (RR = 1,05) and lag 5 (RR = 1,07) and lag 0 for SO2 (RR = 1,06). Conclusion: The data presented show the important role of CO and SO2 in the genesis of myocardial infarction admissions, and responses to pollutant exposure are different if analyzed by gender and together - hence the importance of a stratified analyses. PMID:27533257

  8. Clinical effects of anticoagulant therapy in suspected acute myocardial infarction: systematic overview of randomised trials.

    PubMed Central

    Collins, R.; MacMahon, S.; Flather, M.; Baigent, C.; Remvig, L.; Mortensen, S.; Appleby, P.; Godwin, J.; Yusuf, S.; Peto, R.

    1996-01-01

    OBJECTIVES: Most randomised trials of anticoagulant therapy for suspected acute myocardial infarction have been small and, in some, aspirin and fibrinolytic therapy were not used routinely. A systematic overview (meta-analysis) of their results is needed, in particular to assess the clinical effects of adding heparin to aspirin. DESIGN: Computer aided searches, scrutiny of reference lists, and inquiry of investigators and companies were used to identify potentially eligible studies. On central review, 26 studies were found to involve unconfounded randomised comparisons of anticoagulant therapy versus control in suspected acute myocardial infarction. Additional information on study design and outcome was sought by correspondence with study investigators. SUBJECTS: Patients with suspected acute myocardial infarction. INTERVENTIONS: No routine aspirin was used among about 5000 patients in 21 trials (including half of one small trial) that assessed heparin alone or heparin plus oral anticoagulants, and aspirin was used routinely among 68,000 patients in six trials (including the other half of one small trial) that assessed the addition of intravenous or high dose subcutaneous heparin. MAIN OUTCOME MEASUREMENTS: Death, reinfarction, stroke, pulmonary embolism, and major bleeds (average follow up of about 10 days). RESULTS: In the absence of aspirin, anticoagulant therapy reduced mortality by 25% (SD 8%; 95% confidence interval 10% to 38%; 2P = 0.002), representing 35 (11) fewer deaths per 1000. There were also 10 (4) fewer strokes per 1000 (2P = 0.01), 19 (5) fewer pulmonary emboli per 1000 (2P < 0.001), and non-significantly fewer reinfarctions, with about 13 (5) extra major bleeds per 1000 (2P = 0.01). Similar sized effects were seen with the different anticoagulant regimens studied. In the presence of aspirin, however, heparin reduced mortality by only 6% (SD 3%; 0% to 10%; 2P = 0.03), representing just 5 (2) fewer deaths per 1000. There were 3 (1.3) fewer

  9. Effects of myocardial infarction on the distribution and transport of nutrients and oxygen in porcine myocardium.

    PubMed

    Davis, Bryce H; Morimoto, Yoshihisa; Sample, Chris; Olbrich, Kevin; Leddy, Holly A; Guilak, Farshid; Taylor, Doris A

    2012-10-01

    One of the primary limitations of cell therapy for myocardial infarction is the low survival of transplanted cells, with a loss of up to 80% of cells within 3 days of delivery. The aims of this study were to investigate the distribution of nutrients and oxygen in infarcted myocardium and to quantify how macromolecular transport properties might affect cell survival. Transmural myocardial infarction was created by controlled cryoablation in pigs. At 30 days post-infarction, oxygen and metabolite levels were measured in the peripheral skeletal muscle, normal myocardium, the infarct border zone, and the infarct interior. The diffusion coefficients of fluorescein or FITC-labeled dextran (0.3-70 kD) were measured in these tissues using fluorescence recovery after photobleaching. The vascular density was measured via endogenous alkaline phosphatase staining. To examine the influence of these infarct conditions on cells therapeutically used in vivo, skeletal myoblast survival and differentiation were studied in vitro under the oxygen and glucose concentrations measured in the infarct tissue. Glucose and oxygen concentrations, along with vascular density were significantly reduced in infarct when compared to the uninjured myocardium and infarct border zone, although the degree of decrease differed. The diffusivity of molecules smaller than 40 kD was significantly higher in infarct center and border zone as compared to uninjured heart. Skeletal myoblast differentiation and survival were decreased stepwise from control to hypoxia, starvation, and ischemia conditions. Although oxygen, glucose, and vascular density were significantly reduced in infarcted myocardium, the rate of macromolecular diffusion was significantly increased, suggesting that diffusive transport may not be inhibited in infarct tissue, and thus the supply of nutrients to transplanted cells may be possible. in vitro studies mimicking infarct conditions suggest that increasing nutrients available to

  10. Effect of green tea and vitamin E combination in isoproterenol induced myocardial infarction in rats.

    PubMed

    Upaganlawar, Aman; Gandhi, Chintan; Balaraman, Ramchandran

    2009-03-01

    The present study was aimed to investigate the combined effects of green tea and vitamin E on heart weight, body weight, serum marker enzymes, lipid peroxidation, endogenous antioxidants and membrane bound ATPases in isoproterenol (ISO)-induced myocardial infarction in rats. Adult male albino rats, treated with ISO (200 mg/kg, s.c.) for 2 days at an interval of 24 h caused a significant (P<0.05) elevation of heart weight, serum marker enzymes, lipid peroxidation and Ca+2 ATPase level whereas there was a significant (P<0.05) decrease in body weight, endogenous antioxidants, Na+/ K+ ATPase and Mg+2 ATPase levels. Administration of green tea (100 mg/kg/day, p.o.) and vitamin E (100 mg/kg/day, p.o.) together for 30 consecutive days and challenged with ISO on the day 29th and 30th, showed a significant (P<0.05) decrease in heart weight, serum marker enzymes, lipid peroxidation, Ca+2 ATPase and a significant increase in the body weight, endogenous antioxidants, Na+/K+ ATPase and Mg+2 ATPase when compared with ISO treated group and green tea or vitamin E alone treated groups. These findings indicate the synergistic protective effect of green tea and vitamin E during ISO induced myocardial infarction in rats.

  11. Effect of Early Statin Treatment in Patients with Cardiogenic Shock Complicating Acute Myocardial Infarction

    PubMed Central

    Sim, Doo Sun; Cho, Kyung Hoon; Ahn, Youngkeun; Kim, Young Jo; Chae, Shung Chull; Hong, Taek Jong; Seong, In Whan; Chae, Jei Keon; Kim, Chong Jin; Cho, Myeong Chan; Rha, Seung-Woon; Bae, Jang Ho; Seung, Ki Bae; Park, Seung Jung

    2013-01-01

    Background and Objectives The benefit of early statin treatment following acute myocardial infarction (MI) complicated with cardiogenic shock (CS) has not been well studied. We sought to assess the effect of early statin therapy in patients with CS complicating acute MI. Subjects and Methods We studied 553 statin-naive patients with acute MI and CS (Killip class IV) who underwent revascularization therapy between November 2005 and January 2008 at 51 hospitals in the Korea Acute Myocardial Infarction Registry. Patients were divided into 2 groups: those who received statins during hospitalization (n=280) and those who did not (n=273). The influence of statin treatment on a 12-month clinical outcome was examined using a matched-pairs analysis (n=200 in each group) based on the propensity for receiving statin therapy during hospitalization. Results Before adjustment, patients receiving statin, compared to those not receiving statin, had a more favorable clinical profile, were less likely to suffer procedural complications, and more likely to receive adequate medical therapy. Patients receiving statin had lower unadjusted in-hospital mortality and composite rate of mortality, MI, and repeat revascularization at 12 months, which remained significantly lower after adjustment for patient risk, procedural characteristics, and treatment propensity. Conclusion In CS patients with acute MI undergoing revascularization therapy, early statin treatment initiated during hospitalization was associated with lower rates of in-hospital death and 12-month adverse cardiac events. PMID:23508129

  12. Comparative effects of cortisone, dianabol and enovid on isoprenaline-induced myocardial infarction in arteriosclerotic vs nonarteriosclerotic rats.

    PubMed Central

    Wexler, B. C.

    1976-01-01

    Male and female nonarteriosclerotic (virgin) and arteriosclerotic (breeder) Sprague-Dawley rats were subjected to acute myocardial infarction with isoprenaline. When myocardial necrosis was most intense, animals were given cortisone (high and low doses), Dianabol, or Enovid. Animals receiving large doses of cortisone manifested the best survival rate during the early stages of myocardial infarction. Although their serum enzyme levels were least elevated and their hearts showed tha least amount of damage, these animals had undergone the most intense body weight loss and began to die suddenly during the later stages of the experiment. These animals also manifested hyperlipidaemia, hyperglycaemia, septicaemia, severe disuse atrophy of their adrenal glands, and reduced Cmpd. B production. Animals treated with low doses of cortisone or with the anabolic and androgenic steroid, Dianabol, manifested none of the myocardial pretective effects of the larger dose of cortisone. These animals displayed a high incidence of left ventricular aneurysm formation concomitant with extensive cartilaginous metaplasia within the aneurysmal sites. Treatment with the contraceptive drug, Enovid, caused body weight loss, hyperlipidaemia, hyperglycaemia, gonadal atrophy and reduction of Cmpd. B production. Although the high dose of cortisone exercised definite salutary effects during early myocardial infarction, chronic treatment led to adrenal disuse atrophy and hypoadrenocorticism associated with sudden death during the later stages of myocardial repair. These findings indicate that proper adjustment of the dose and chronicity of corticosteroids used for treating the crisis of acute myocardial infarction must be made in order to provide effective protection against untoward pathophysiological conditions, acceleration of myocardial repair, but without suppression of adrenal function. Images Fig. 12 Fig. 13 Fig. 14 Fig. 15 Fig. 16 Fig. 17 PMID:1008997

  13. Comparative effects of cortisone, dianabol and enovid on isoprenaline-induced myocardial infarction in arteriosclerotic vs nonarteriosclerotic rats.

    PubMed

    Wexler, B C

    1976-12-01

    Male and female nonarteriosclerotic (virgin) and arteriosclerotic (breeder) Sprague-Dawley rats were subjected to acute myocardial infarction with isoprenaline. When myocardial necrosis was most intense, animals were given cortisone (high and low doses), Dianabol, or Enovid. Animals receiving large doses of cortisone manifested the best survival rate during the early stages of myocardial infarction. Although their serum enzyme levels were least elevated and their hearts showed tha least amount of damage, these animals had undergone the most intense body weight loss and began to die suddenly during the later stages of the experiment. These animals also manifested hyperlipidaemia, hyperglycaemia, septicaemia, severe disuse atrophy of their adrenal glands, and reduced Cmpd. B production. Animals treated with low doses of cortisone or with the anabolic and androgenic steroid, Dianabol, manifested none of the myocardial pretective effects of the larger dose of cortisone. These animals displayed a high incidence of left ventricular aneurysm formation concomitant with extensive cartilaginous metaplasia within the aneurysmal sites. Treatment with the contraceptive drug, Enovid, caused body weight loss, hyperlipidaemia, hyperglycaemia, gonadal atrophy and reduction of Cmpd. B production. Although the high dose of cortisone exercised definite salutary effects during early myocardial infarction, chronic treatment led to adrenal disuse atrophy and hypoadrenocorticism associated with sudden death during the later stages of myocardial repair. These findings indicate that proper adjustment of the dose and chronicity of corticosteroids used for treating the crisis of acute myocardial infarction must be made in order to provide effective protection against untoward pathophysiological conditions, acceleration of myocardial repair, but without suppression of adrenal function.

  14. 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

  15. 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.

  16. Dexrazoxane Shows No Protective Effect in the Acute Phase of Reperfusion during Myocardial Infarction in Pigs

    PubMed Central

    Kamat, Pranitha; Vandenberghe, Stijn; Christen, Stephan; Bongoni, Anjan K.; Meier, Bernhard; Rieben, Robert; Khattab, Ahmed A.

    2016-01-01

    Calcium and iron overload participate in the mechanisms of ischemia/reperfusion (I/R) injury during myocardial infarction (MI). Calcium overload induces cardiomyocyte death by hypercontraction, while iron catalyses generation of reactive oxygen species (ROS). We therefore hypothesized that dexrazoxane, an intracellular metal chelator, would attenuate I/R injury. MI was induced in pigs by occlusion of the left anterior descending artery for 1 hour followed by 2 hours reperfusion. Thirty minutes before reperfusion either 5 mg/ml dexrazoxane (n = 5) or saline (n = 5) was infused intravenously. Myocardial necrosis as percentage of the area at ischemic risk was found to be similar in both groups (77.2 ± 18% for dexrazoxane and 76.4 ± 14% for saline group) as determined by triphenyl tetrazolium chloride staining of the ischemic myocardium. Also, serum levels of troponin-I were similar in both groups. A conductance catheter was used to measure left ventricular pressure and volume at all times. Markers for tissue damage due to ROS (HNE), endothelial cell activation (CD31) and inflammation (IgG, C3b/c, C5b9, MCP-1) were assessed on tissue and/or in serum. No significant differences were observed between the groups for the parameters analyzed. To conclude, in this clinically relevant model of early reperfusion after acute myocardial ischemia, dexrazoxane lacked attenuating effects on I/R injury as shown by the measured parameters. PMID:28002439

  17. Acute effects of delayed reperfusion following myocardial infarction: a 3D x-ray imaging analysis

    NASA Astrophysics Data System (ADS)

    Simari, Robert D.; Bell, M. R.; Pao, Y. C.; Gersh, B. J.; Ritman, Erik L.

    1996-04-01

    Clinical and experimental data suggest that delayed reperfusion of the infarct related artery may limit infarct expansion without increasing myocardial salvage. In order to assess the potential mechanisms involved, an acute closed chest canine model of myocardial infarction and delayed reperfusion was studied. Nineteen dogs underwent 3D computed tomography in the Dynamic Spatial Reconstructor (a fast, volume imaging, CT scanner) at baseline and three and four hours later to estimate left ventricular chamber volumes, global distensibility and regional myocardial stiffness. A control group was scanned without intervention. An occlusion group underwent four hours of coronary artery occlusion. A reperfusion group underwent three hours of coronary artery occlusion followed by one hour of reperfusion. Similar infarct sizes were seen in the occlusion and reperfusion groups. Globally reperfusion was associated with increased left ventricular end diastolic pressure and prolongation of global relaxation. Regionally reperfusion was associated with increased myocardial stiffness, intramyocardial blood volume and wall thickness within the infarct zone relative to the not reperfused myocardium.

  18. TARGETED DELETION OF INDUCIBLE HEAT SHOCK PROTEIN 70 ABROGATES THE LATE INFARCT-SPARING EFFECT OF MYOCARDIAL ISCHEMIC PRECONDITIONING

    EPA Science Inventory

    Abstract submitted for 82nd annual meeting of the American Association for Thoracic Surgery, May 4-8, 2002 in Washington D.C.

    Targeted Deletion of Inducible Heat Shock Protein 70 Abrogates the Late Infarct-Sparing Effect of Myocardial Ischemic Preconditioning

    Craig...

  19. Effect of Pericardial Effusion Complicating ST-Elevation Myocardial Infarction as Predictor of Extensive Myocardial Damage and Prognosis.

    PubMed

    Jobs, Alexander; Eitel, Charlotte; Pöss, Janine; Desch, Steffen; Thiele, Holger; Eitel, Ingo

    2015-10-01

    Pericardial effusion (PE) is a common complication following ST-elevation myocardial infarction (STEMI). However, the frequency and prognostic relevance of PE complicating STEMI are unknown. Aim of this study was to investigate the exact incidence, infarct characteristics, and the prognostic impact of moderate-to-large PEs detected by cardiac magnetic resonance (CMR) in patients with acute reperfused STEMI. In total, 780 patients with STEMI reperfused by angioplasty (<12 hours after symptom onset) were enrolled in this CMR study at 8 centers. CMR was completed in median 3 days after infarction using a standardized protocol. Central core laboratory-masked analysis for the presence of moderate-to-large PE was performed. The primary clinical end point was the occurrence of major adverse cardiac events (MACE) defined as composite of all-cause death, reinfarction, and new congestive heart failure within 12 months after the index event. A moderate-to-large PE was detected in 183 patients (24%). Patients with moderate-to-large PEs had significantly larger infarcts, less myocardial salvage, a larger extent of microvascular obstruction, higher incidence of intramyocardial hemorrhage, and more pronounced left ventricular dysfunction (p <0.001 for all). Significant predictors of a moderate-to-large PE were age, Thrombolysis in Myocardial Infarction flow before percutaneous coronary intervention, and infarct size. MACE rates were significantly higher in the PE group (p = 0.003) and a moderate-to-large PE was identified as a significant independent predictor for MACE (hazard ratio 3.12, 95% confidence interval 1.49 to 6.81; p = 0.003) together with Thrombolysis in Myocardial Infarction risk score and left ventricular ejection fraction. In conclusion, a moderate-to-large PE complicating STEMI is a common finding (almost 25%) and related to more severe infarcts with subsequent significantly increased MACE rates during 1-year follow-up. Consequently, a moderate-to-large PE

  20. 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.

  1. 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.

  2. The Effect of Metformin on Diastolic Function in Patients Presenting with ST-Elevation Myocardial Infarction

    PubMed Central

    Al Ali, Lawien; Hartman, Minke T.; Lexis, Chris P. H.; Hummel, Yoran M.; Lipsic, Erik; van Melle, Joost P.; van Veldhuisen, Dirk J.; Voors, Adriaan A.; van der Horst, Iwan C. C.; van der Harst, Pim

    2016-01-01

    Introduction Diastolic dysfunction is an important predictor of poor outcome after myocardial infarction. Metformin treatment improved diastolic function in animal models and patients with diabetes. Whether metformin improves diastolic function in patients presenting with ST-segment elevation myocardial infarction (STEMI) is unknown. Methods The GIPS-III trial randomized STEMI patients, without known diabetes, to metformin or placebo initiated directly after PCI. The previously reported primary endpoint was left ventricular ejection fraction at 4 months, which was unaffected by metformin treatment. This is a predefined substudy to determine an effect of metformin on diastolic function. For this substudy trans-thoracic echocardiography was performed during hospitalization and after 4 months. Diastolic dysfunction was defined as having the combination of a functional alteration (i.e. decreased tissue velocity: mean of septal e’ and lateral e’) and a structural alteration (i.e. increased left atrial volume index (LAVI)). In addition, left ventricular mass index and transmitral flow velocity (E) to mean e' ratio (E/e’) were measured to determine an effect of metformin on individual echocardiographic markers of diastolic function. Results In 237 (63%) patients included in the GIPS-III trial diastolic function was measured during hospitalization as well as at 4 months. Diastolic dysfunction was present in 11 (9%) of patients on metformin and 11 (9%) patients on placebo treatment (P = 0.98) during hospitalization. After 4 months 22 (19%) of patients with metformin and 18 (15%) patients with placebo (P = 0.47) had diastolic dysfunction. In addition, metformin did not improve any of the individual echocardiographic markers of diastolic function. Conclusions In contrast to experimental and observational data, our randomized placebo controlled trial did not suggest a beneficial effect of short-term metformin treatment on diastolic function in STEMI patients. PMID

  3. Analysis of weekend effect on 30-day mortality among patients with acute myocardial infarction

    PubMed Central

    Noad, Rebecca; Stevenson, Michael; Herity, Niall A

    2017-01-01

    Objectives Several publications have demonstrated increased 30-day mortality in patients admitted on Saturdays or Sundays compared with weekdays. We sought to determine whether this was true for two different cohorts of patients admitted with acute myocardial infarction (MI). Methods and results Thirty-day mortality data were obtained for 3757 patients who had been admitted to the Belfast Health and Social Care Trust with acute MI between 2009 and 2015. They were subdivided into those presenting with ST elevation MI (n=2240) and non-ST elevation MI (n= 1517). We observed no excess 30-day mortality in those admitted over weekends. Conclusion Excess mortality in patients admitted at weekends is not a universal finding. This may mean that that there are patient subgroups with proportionately greater weekend hazard and points to the need for more detailed understanding of the weekend effect.

  4. Side effects of using nitrates to treat heart failure and the acute coronary syndromes, unstable angina and acute myocardial infarction.

    PubMed

    Thadani, Udho; Ripley, Toni L

    2007-07-01

    Nitrates are potent venous dilators and anti-ischemic agents. They are widely used for the relief of chest pain and pulmonary congestion in patients with acute coronary syndromes and heart failure. Nitrates, however, do not reduce mortality in patients with acute coronary syndromes. Combination of nitrates and hydralazine when given in addition to beta-blockers and angiotensin-converting enzyme (ACE) inhibitors reduce mortality and heart failure hospitalizations in patients with heart failure due to left ventricular systolic dysfunction who are of African-American origin. Side effects during nitrate therapy are common but are less well described in the literature compared with the reported side effects in patients with stable angina pectoris. The reported incidence of side effects varies highly among different studies and among various disease states. Headache is the most commonly reported side effect with an incidence of 12% in acute heart failure, 41-73% in chronic heart failure, 3-19% in unstable angina and 2-26% in acute myocardial infarction. The reported incidence of hypotension also differs: 5-10% in acute heart failure, 20% in chronic heart failure, 9% in unstable angina and < 1-48% in acute myocardial infarction, with the incidence being much higher with concomitant nitrate therapy plus angiotensin-converting enzyme inhibitors. Reported incidence of dizziness is as low as 1% in patients with acute myocardial infarction to as high as 29% in patients with heart failure. Severe headaches and/or symptomatic hypotension may necessitate discontinuation of nitrate therapy. Severe life threatening hypotension or even death may occur when nitrates are used in patients with acute inferior myocardial infarction associated with right ventricular dysfunction or infarction, or with concomitant use of phosphodiesterase-5 inhibitors or N-acetylcysteine. Despite the disturbing observational reports in the literature that continuous and prolonged use of nitrates may lead to

  5. Percutaneous carbon dioxide mist treatment has protective effects in experimental myocardial infarction.

    PubMed

    Yamaguchi, Takehiro; Yamazaki, Takanori; Nakamura, Yasuhiro; Shiota, Masayuki; Shimada, Kenei; Miura, Katsuyuki; Iwao, Hiroshi; Yoshiyama, Minoru; Izumi, Yasukatsu

    2015-04-01

    Percutaneous treatment with carbon dioxide (CO2) mist, CO2 gas dissolved in water, contributes to improved cardiac function after myocardial infarction (MI). In this study, we investigated the effects of repeated pretreatment with CO2 mist on cardiac dysfunction after MI. The CO2 mist was generated by a dry mist production unit. The whole body of rats below the axilla was wrapped in a polyethylene bag, which was sealed and filled with the CO2 mist in the draft cabinet for 30 min daily for 7 days. MI was induced by ligation of the coronary artery in untreated (UT), CO2 gas-pretreated (CG), and CO2 mist-pretreated (CM) rats. The infarct size and the increase in oxidative stress due to MI were significantly smaller in the CM rats than in the UT rats. Furthermore, the expression of inflammation-related genes, such as monocyte chemoattractant protein-1, and fibrosis-related genes, such as transforming growth factor-β1, was significantly suppressed in the CM rats. The CM rats had a better left ventricular ejection fraction than the UT rats 7 days after MI. These parameters in the CG rats were the same as in the UT group. Thus, CO2 mist preparative treatment may be potentially useful for the reduction of MI.

  6. 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

  7. Effects of phentolamine on coronary blood flow in patients with recent myocardial infarction.

    PubMed

    Gould, L; Reddy, C V; Blatt, C J; Gomprecht, R F; Hayt, D B

    1975-06-01

    The myocardial clearance of rubidium may be obtained by praecordial counting after intravenous injection of Rb-minus 86 Cl. Eight patients with recent myocardial infarction had this determination performed before and after the infusion of 10 mg phentolamine at a rate of 0.3 mg/minute. The average predrug myocardial clearance of Rb was 89.3 plus or minus 29.9 ml/min per 100 g myocardium. After phentolamine, the average myocardial clearance rose to 117.3 plus or minus 33.3 ml/min per 100 g myocardium (P LESS THAN 0.01). An explanation for this findings is presented as well as its possible clinical applications.

  8. Effects of phentolamine on coronary blood flow in patients with recent myocardial infarction.

    PubMed Central

    Gould, L; Reddy, C V; Blatt, C J; Gomprecht, R F; Hayt, D B

    1975-01-01

    The myocardial clearance of rubidium may be obtained by praecordial counting after intravenous injection of Rb-minus 86 Cl. Eight patients with recent myocardial infarction had this determination performed before and after the infusion of 10 mg phentolamine at a rate of 0.3 mg/minute. The average predrug myocardial clearance of Rb was 89.3 plus or minus 29.9 ml/min per 100 g myocardium. After phentolamine, the average myocardial clearance rose to 117.3 plus or minus 33.3 ml/min per 100 g myocardium (P LESS THAN 0.01). An explanation for this findings is presented as well as its possible clinical applications. PMID:1148064

  9. [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.

  10. Effect of additional treatment with EXenatide in patients with an Acute Myocardial Infarction (EXAMI): study protocol for a randomized controlled trial

    PubMed Central

    2011-01-01

    Background Myocardial infarction causes irreversible loss of cardiomyocytes and may lead to loss of ventricular function, morbidity and mortality. Infarct size is a major prognostic factor and reduction of infarct size has therefore been an important objective of strategies to improve outcomes. In experimental studies, glucagon-like peptide 1 and exenatide, a long acting glucagon-like peptide 1 receptor agonist, a novel drug introduced for the treatment of type 2 diabetes, reduced infarct size after myocardial infarction by activating pro-survival pathways and by increasing metabolic efficiency. Methods The EXAMI trial is a multi-center, prospective, randomized, placebo controlled trial, designed to evaluate clinical outcome of exenatide infusion on top of standard treatment, in patients with an acute myocardial infarction, successfully treated with primary percutaneous coronary intervention. A total of 108 patients will be randomized to exenatide (5 μg bolus in 30 minutes followed by continuous infusion of 20 μg/24 h for 72 h) or placebo treatment. The primary end point of the study is myocardial infarct size (measured using magnetic resonance imaging with delayed enhancement at 4 months) as a percentage of the area at risk (measured using T2 weighted images at 3-7 days). Discussion If the current study demonstrates cardioprotective effects, exenatide may constitute a novel therapeutic option to reduce infarct size and preserve cardiac function in adjunction to reperfusion therapy in patients with acute myocardial infarction. Trial registration ClinicalTrials.gov: NCT01254123 PMID:22067476

  11. Changes in rest and exercise myocardial perfusion and left ventricular function 3 to 26 weeks after clinically uncomplicated acute myocardial infarction: effects of exercise training

    SciTech Connect

    Hung, J.; Gordon, E.P.; Houston, N.; Haskell, W.L.; Goris, M.L.; DeBusk, R.F.

    1984-11-01

    The effects of exercise training on exercise myocardial perfusion and left ventricular (LV) function in the first 6 months after clinically uncomplicated acute myocardial infarction (AMI) were assessed in 53 consecutive men aged 55 +/- 9 years. Symptom-limited treadmill exercise with thallium myocardial perfusion scintigraphy and symptom-limited upright bicycle ergometry with equilibrium gated radionuclide ventriculography were performed 3, 11 and 26 weeks after AMI by 23 men randomized to training and 30 randomized to no training. Peak cycle capacity increased in both groups between 3 and 26 weeks (p less than 0.01), but reached higher levels in trained than in untrained patients (803 +/- 149 vs 648 +/- 182 kg-m/min, p less than 0.01). Reversible thallium perfusion defects were significantly more frequent at 3 than at 26 weeks: 59% and 36% of patients, respectively (p less than 0.05), without significant inter-group differences. Values of LV ejection fraction at rest, submaximal and peak exercise did not change significantly in either group. The increase in functional capacity, i.e., peak treadmill or bicycle workload, that occurred 3 to 26 weeks after infarction was significantly correlated with the increase in peak exercise heart rate (p less than 0.001), but not with changes in myocardial perfusion or LV function determined by radionuclide techniques. Changes in myocardial perfusion or LV function do not appear to account for the improvement in peak functional capacity that occurs within the first 6 months after clinically uncomplicated AMI.

  12. [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).

  13. Erythropoietin has an antiapoptotic effect after myocardial infarction and stimulates in vitro aortic ring sprouting

    SciTech Connect

    Mansson Broberg, Agneta; Grinnemo, Karl-Henrik; Genead, Rami; Danielsson, Christian; Andersson, Agneta B.; Waerdell, Eva; Sylven, Christer

    2008-06-20

    Aims were to explore if darbepoietin-{alpha} in mouse can induce angiogenesis and if moderate doses after myocardial infarction stimulates periinfarct capillary and arteriolar densities, cell proliferation, and apoptosis. Myocardial infarction was induced by ligation of LAD. Mouse aortic rings (0.8 mm) were cultured in matrigel and the angiogenic sprouting was studied after addition of darbepoietin-{alpha} with and without VEGF-165. After 12 days the hemoglobin concentration was 25% higher in the darbepoietin-{alpha} treated mice than in the control group. No difference in capillary densities in the periinfarct or noninfarcted areas was seen with darbepoietin-{alpha}. Cell proliferation was about 10 times higher in the periinfarct area than in the noninfarcted wall. Darbepoietin-{alpha} treatment led to a decrease of cell proliferation (BrdU, (p < 0.02)) and apoptosis (TUNEL, p < 0.005) with about 30% in the periinfarct area. Darbepoietin-{alpha} and VEGF-165 both independently induced sprouting from aortic rings. The results suggest that darbepoietin-{alpha} can induce angiogenesis but that moderate doses after myocardial infarction are not angiogenic but antiapoptotic.

  14. Cardioprotective effects of traditional Chinese medicine Guanmaitong on acute myocardial infarction

    PubMed Central

    Wang, Xing-Hua; Li, Guang-Ping; Yang, Wan-Song; Jiao, Zhan-Quan; Liu, Hong-Mei; Ni, Yan-Ping

    2016-01-01

    Guanmaitong (GMT) is a traditional Chinese herbal compound that has been used for the treatment of coronary heart disease (CHD) and other cardiovascular diseases. However, the efficacy of GMT in treating cardiovascular diseases remains unclear. The aim of the present study was to investigate the protective mechanisms and identify the targeted proteins and signaling networks associated with the physiological activity of GMT in a rat model of acute myocardial infarction (AMI). Sprague-Dawley rats were randomly allocated into five groups: Control group (sham-operated), the model group, and small, medium, and large dosage GMT groups. The rat model of AMI was established via ligation of the coronary artery. The results indicate that GMT was able to reduce myocardial infarction size and improve the activities of tumor necrosis factor-α (TNF-α), intercellular adhesion molecule 1 (ICAM-1) and interleukin-1. Furthermore, the reduced apoptotic index of the GMT-treated cardiocytes (P<0.05 vs. model group) was in accordance with the downregulated expression of Bax and the upregulated expression of Bcl-2. In conclusion, GMT may exert a protective potential against myocardial infarction injury by inhibiting apoptosis and inflammation of cardiomyocytes, and may offer a promising adjunct treatment for CHD. PMID:28105124

  15. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats

    PubMed Central

    Goyal, Sameer N.; Sharma, Charu; Mahajan, Umesh B.; Patil, Chandragouda R.; Agrawal, Yogeeta O.; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-01-01

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities. PMID:26593900

  16. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats.

    PubMed

    Goyal, Sameer N; Sharma, Charu; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-11-17

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities.

  17. Effect of endothelin receptor antagonist bosentan on plasma leptin concentration in acute myocardial infarction in rats.

    PubMed

    Ostrowski, Robert P.; Januszewski, Sławomir; Kowalska, Zdzisława; Kapuściński, Andrzej

    2003-09-01

    The aim of the study was to evaluate the effect of endothelin receptor antagonism on plasma leptin level after myocardial infarction (MI). In Wistar rats under chloral hydrate anesthesia, MI was performed by ligation of the left coronary artery. The animals were divided into the following groups: control-sham (thoracotomy only), and two MI groups with or without bosentan treatment. Bosentan was given daily by gavage at the dose of 100 mg/kg. Treatment of animals started 2 days before MI and continued up to the fifth day. Concentration of leptin was measured by radioimmunoassay by means of 125I labeled antigen in the following time intervals: before MI or sham operation, 4, 24 and 48 h after surgery. Electrocardiogram (ECG), blood pressure, heart rate, arterial pO(2), pCO(2) and pH were periodically monitored. Two days after the MI animals were perfused retrograde into descending aorta with 2% triphenyltetrazolium chloride (TTC) and hearts were fixed by immersion in formalin for microscopic examination. Hearts were sectioned transaxially and size of MI was quantitated with morphometric methods. ECG, TTC staining and microscopic results confirmed development of MI. Morphometric methods did not show significant differences in infarct size between bosentan treated and untreated groups. Concentration of leptin in plasma in untreated group significantly increased already 4 h after MI. In bosentan treated animals this increase appeared only after 24 h. In animals treated with bosentan also a significant diminution of MI mortality was observed. Our results indicate that bosentan has an important effect on leptin concentration in ischemic cardiovascular pathology.

  18. 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.

  19. Comparative effects of a novel angiotensin-converting enzyme inhibitor versus captopril on plasma angiotensins after myocardial infarction.

    PubMed

    Flores-Monroy, Jazmín; Ferrario, Carlos M; Valencia-Hernández, Ignacio; Hernández-Campos, Maria Elena; Martínez-Aguilar, Luisa

    2014-01-01

    The compound 4-tert-butyl-2,6-bis(thiomorpholin-4-ylmethyl)phenol (TBTIF) has molecular characteristics similar to angiotensin-converting enzyme (ACE) inhibitors of the sulfhydryl subclass. To assess its value as a new therapeutic agent, we performed a comparative analysis of the effect of TBTIF versus captopril on the circulating levels of angiotensin (Ang) peptides and bradykinin as well as ACE and ACE2 expression after myocardial infarction. Male Wistar rats were divided into four groups: (1) sham-operated rats; (2) rats subjected to 48 h of coronary artery ligation; (3) rats administered captopril (1 mg/kg, i.m.), and (4) a similar group of rats given TBTIF (1 mg/kg, i.m.). Both drugs were administered 30 min before coronary artery ligation and again 24 h later. Acute myocardial infarction lowered both systolic and left ventricular systolic blood pressures compared to the sham group and increased plasma levels of Ang I, Ang II, Ang(1-7) and Ang(1-12). Administration of either captopril or TBTIF reversed the increases in plasma angiotensins. Interestingly, the levels of plasma Ang(1-7) achieved by administration of TBTIF reached values higher than those recorded with captopril. Both agents reversed the decreases in plasma concentrations of bradykinin; in addition, TBTIF upregulated ACE expression, while both agents suppressed the ACE2 upregulation induced by myocardial infarction. These results demonstrate a beneficial effect of the novel compound TBTIF in suppressing the acute surge in the circulating renin-angiotensin system activity induced by myocardial infarction. The greater effects of this compound in augmenting plasma Ang(1-7) concentrations may be highly significant as drugs which augment the concentration of this heptapeptide will exert cardioprotective actions in part by suppressing the hypertrophic and profibrotic actions of Ang II.

  20. No large-effect low-frequency coding variation found for myocardial infarction.

    PubMed

    Holmen, Oddgeir L; Zhang, He; Zhou, Wei; Schmidt, Ellen; Hovelson, Daniel H; Langhammer, Arnulf; Løchen, Maja-Lisa; Ganesh, Santhi K; Mathiesen, Ellisiv B; Vatten, Lars; Platou, Carl; Wilsgaard, Tom; Chen, Jin; Skorpen, Frank; Dalen, Håvard; Boehnke, Michael; Abecasis, Goncalo R; Njølstad, Inger; Hveem, Kristian; Willer, Cristen J

    2014-09-01

    Genome-wide association studies have identified variants, primarily common, that are associated with coronary artery disease or myocardial infarction (MI), but have not tested the majority of the low frequency and rare variation in the genome. We explored the hypothesis that previously untested low frequency (1-5% minor allele frequency) and rare (<1% minor allele frequency) coding variants are associated with MI. We genotyped 2906 MI cases and 6738 non-MI controls from Norway using the Illumina HumanExome Beadchip, allowing for direct genotyping of 85 972 polymorphic coding variants as well as 48 known GWAS SNPs. We followed-up 34 coding variants in an additional 2350 MI cases and 2318 controls from Norway. We evaluated exome array coverage in a subset of these samples using whole exome sequencing (N = 151). The exome array provided successful genotyping for an estimated 72.5% of Norwegian loss-of-function or missense variants with frequency >1% and 66.2% of variants <1% frequency observed more than once. Despite 80% power in the two-stage study (N = 14 312) to detect association with low-frequency variants with high effect sizes [odds ratio (OR) >1.86 and >1.36 for 1 and 5% frequency, respectively], we did not identify any novel genes or single variants that reached significance. This suggests that low-frequency coding variants with large effect sizes (OR >2) may not exist for MI. Larger sample sizes may identify coding variants with more moderate effects.

  1. Antilipoperoxidative and antioxidant effects of S-allyl cysteine sulfoxide on isoproterenol-induced myocardial infarction in Wistar rats.

    PubMed

    Sangeetha, T; Quine, S Darlin

    2006-01-01

    Our study evaluates the preventive effect of S-allyl cysteine sulfoxide (SACS) on lipid peroxidative products and enzymic and nonenzymic antioxidants in isoproterenol (ISO) induced myocardial infarction in rats. The male Wistar rats were rendered myocardial infarction by ISO (150 mg kg(-1), once a day for two days). The concentrations of thiobarbituric acid reactive substances and lipid hydroperoxides were increased in hearts from ISO-treated rats, whereas the content of enzymic and nonenzymic antioxidants were declined in rats administered ISO. Oral pretreatment with SACS (40 mg kg(-1) and 80 mg kg(-1) daily for a period of 35 days) significantly (p < 0.05) decreased the lipid peroxidative products and significantly (p < 0.05) increased antioxidants in ISO-induced rats. Oral administration of SACS (40 mg kg(-1) and 80 mg kg(-1)) did not show any significant effect in normal rats. Thus, the present study shows that SACS exhibits antilipoperoxidative and antioxidant effects in experimental myocardial infarction.

  2. Triggering of Myocardial Infarction by Increased Ambient Fine Particle Concentration: Effect Modification by Source Direction

    PubMed Central

    Hopke, Philip K.; Kane, Cathleen; Utell, Mark J.; Chalupa, David C.; Kumar, Pramod; Ling, Frederick; Gardner, Blake; Rich, David Q.

    2015-01-01

    Background Previously, we reported a 18% increased odds of ST-elevation myocardial infarction (STEMI) associated with each 7.1 µg/m3 increase in PM2.5 concentration in the hour prior to MI onset. We found no association with non-ST elevation myocardial infarction (NSTEMI). We examined if this association was modified by PM2.5 source direction. Methods We used the NOAA HYbrid Single-Particle Lagrangian Trajectory (HYSPLIT) model to calculate each hourly air mass location for the 24 hours before each case or control time period in our previous PM2.5/STEMI case-crossover analysis. Using these data on patients with STEMI (n=338), hourly PM2.5 concentrations, and case-crossover methods, we evaluated whether our PM2.5/STEMI association was modified by whether the air mass passed through each of the 8 cardinal wind direction sectors in the previous 24 hours. Results When the air mass passed through the West-Southwest direction (WSW) any time in the past 24 hours, the odds of STEMI associated with each 7.1 µg/m3 increase in PM2.5 concentration in the previous hour (OR=1.27; 95% CI=1.08, 1.22) was statistically significantly (p=0.01) greater than the relative odds of STEMI associated with increased PM2.5 concentration when the wind arrived from any other direction (OR=0.99; 95% CI=0.80, 1.22). We found no other effect modification by any other source direction. Further, relative odds estimates were largest when the time spent in the WSW was 8-16 hours, compared to ≤7 hours or 17-24 hours, suggesting that particles arising from sources in this direction were more potent in triggering STEMIs. Conclusions Since relative odds estimates were higher when the air mass passed through the WSW octant in the past 24 hours, there may be specific components of the ambient aerosol that are more potent in triggering STEMIs. This direction is associated with substantial emissions from coal-fired power plants and other industrial sources of the Ohio River Valley, many of which are

  3. Preventive effects of p-coumaric acid on cardiac hypertrophy and alterations in electrocardiogram, lipids, and lipoproteins in experimentally induced myocardial infarcted rats.

    PubMed

    Roy, Abhro Jyoti; Stanely Mainzen Prince, P

    2013-10-01

    The present study evaluated the preventive effects of p-coumaric acid on cardiac hypertrophy and alterations in electrocardiogram, lipids, and lipoproteins in experimentally induced myocardial infarcted rats. Rats were pretreated with p-coumaric acid (8 mg/kg body weight) daily for a period of 7 days and then injected with isoproterenol (100mg/kg body weight) on 8th and 9th day to induce myocardial infarction. Myocardial infarction induced by isoproterenol was indicated by increased level of cardiac sensitive marker and elevated ST-segments in the electrocardiogram. Also, the levels/concentrations of serum and heart cholesterol, triglycerides and free fatty acids were increased in myocardial infarcted rats. Isoproterenol also increased the levels of serum low density and very low density lipoprotein cholesterol and decreased the levels of high density lipoprotein cholesterol. It also enhanced the activity of liver 3-hydroxy-3 methyl glutaryl-Coenzyme-A reductase. p-Coumaric acid pretreatment revealed preventive effects on all the biochemical parameters and electrocardiogram studied in myocardial infarcted rats. The in vitro study confirmed the free radical scavenging property of p-coumaric acid. Thus, p-coumaric acid prevented cardiac hypertrophy and alterations in lipids, lipoproteins, and electrocardiogram, by virtue of its antihypertrophic, antilipidemic, and free radical scavenging effects in isoproterenol induced myocardial infarcted rats.

  4. Cardioprotective effect of ethanolic extract of Urtica parviflora Roxb. against isoproterenol induced myocardial infarction in rats

    PubMed Central

    Barman, Nishith Ranjan; Nandy, Subhangkar; Datta, Rana; Kar, Prasanna Kumar

    2013-01-01

    Objective: The objective of this study is to evaluate the effect of ethanolic extract of Urtica parviflora Roxb. in isoproterenol (ISO) induced myocardial infarction (MI) in rats. Materials and Methods: U. parviflora Roxb. (350 mg/kg and 500 mg/kg, p.o) was administered for 15 days in rats. MI was induced with a single dose of ISO (200 mg/kg, s.c.) on the 14th and 15th day. At the end of the experimental period (i.e., on the day 16), serum and heart tissues were collected and total cholesterol (TC), high density lipoprotein, triglyceride and malondialdehyde, superoxide dismutase, catalase (CAT), reduced glutathione (GSH) and body weight were determined. Results: Administration of ISO in control rats showed a significant (P < 0.001) increase serum cholesterol alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and low density lipoprotein (LDL). There was a significant increase (P < 0.01) in the levels of heart tissues as compared with respective control groups. Rats treated with U. parviflora significantly (P < 0.01) decreased ALT, AST, ALP, LDL and TC. Moreover, there was an increased CAT and GSH levels in rat treated with U. parviflora Roxb. as compared with the control group. Conclusion: U. parviflora (350 and 500 mg/kg p.o.) is effective in controlling serum LDL levels and reduced cardiac complication in experimentally induced MI in rats. PMID:24130389

  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. 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

  7. Effect of β-Blockers on the Risk of Atrial Fibrillation in Patients with Acute Myocardial Infarction

    PubMed Central

    Pesaro, Antonio Eduardo; de Matos Soeiro, Alexandre; Serrano, Carlos Vicente; Giraldez, Roberto Rocha; Ladeira, Renata Teixeira; Nicolau, José Carlos

    2010-01-01

    INTRODUCTION: Oral β-blockers improve the prognosis of patients with acute myocardial infarction, while atrial fibrillation worsens the prognosis of this population. The reduction of atrial fibrillation incidence in patients treated with β-blockers could at least in part explain the benefits of this drug. OBJECTIVE: To investigate the effect of β-blockers on the incidence of atrial fibrillation in patients with acute myocardial infarction. METHODS: We analyzed 1401 patients with acute myocardial infarction and evaluated the occurrence or absence of atrial fibrillation, the use of oral β-blockers and mortality during the first 24 hours. RESULTS: a) The use of β-blockers was inversely correlated with the presence of atrial fibrillation (ρ = 0.004; OR = 0.54). b) Correlations with mortality were as follows: 31.5% in patients with atrial fibrillation, 9.2% in those without atrial fibrillation (ρ < 0.001; Odds Ratio = 4.52), and 17.5% in patients not treated with β-blockers and 6.7% in those who received the drug (ρ < 0.001; OR = 0.34). c) Adjusted Models: The presence of atrial fibrillation was independently correlated with mortality (OR = 2.48, ρ = 0.002). The use of β-blockers was inversely and independently correlated with mortality (OR = 0.53; ρ = 0.002). The patients who used β-blockers showed a lower risk of atrial fibrillation (OR = 0.59; ρ = 0.029) in the adjusted model. CONCLUSION: The presence of atrial fibrillation and the absence of oral β-blockers increased in-hospital mortality in patients with acute myocardial infarction. Oral β-blockers reduced the incidence of atrial fibrillation, which might be at least partially responsible for the drug’s benefit. PMID:20360916

  8. Effect of paroxetine on left ventricular remodeling in an in vivo rat model of myocardial infarction.

    PubMed

    Lassen, Thomas Ravn; Nielsen, Jan Møller; Johnsen, Jacob; Ringgaard, Steffen; Bøtker, Hans Erik; Kristiansen, Steen Buus

    2017-05-01

    Left ventricular (LV) remodeling following a myocardial infarction (MI) involves formation of reactive oxygen species (ROS). Paroxetine, a selective serotonin reuptake inhibitor, has an antioxidant effect in the vascular wall. We investigated whether paroxetine reduces myocardial ROS formation and LV remodeling following a MI. In a total of 32 Wistar rats, MI was induced by a 30-min ligation of the left anterior descending artery followed by 7- or 28-day reperfusion. During the 28 days of reperfusion, LV remodeling was evaluated by magnetic resonance imaging (MRI) and echocardiography (n = 20). After 28 days of reperfusion, the susceptibility to ventricular tachycardia was evaluated prior to sacrifice and histological assessment of myocyte cross-sectional area, fibrosis, and presence of myofibroblasts. Myocardial ROS formation was measured with dihydroethidium after 7 days of reperfusion in separate groups (n = 12). Diastolic LV volume, evaluated by MRI (417 ± 60 vs. 511 ± 64 µL, p < 0.05), and echocardiography (515 ± 80 vs. 596 ± 83 µL, p < 0.05) as well as diastolic LV internal diameter evaluated with echocardiography (7.2 ± 0.6 vs. 8.1 ± 0.7 mm, p < 0.05) were lower in the paroxetine group than in controls. Furthermore, myocyte cross-sectional area was reduced in the paroxetine group compared with controls (277 ± 26 vs. 354 ± 23 mm(3), p < 0.05) and ROS formation was reduced in the remote myocardium (0.415 ± 0.19 normalized to controls, p < 0.05). However, no differences in the presence of fibrosis or myofibroblasts were observed. Finally, paroxetine reduced the susceptibility to ventricular tachycardia (induced in 2/11 vs. 6/8 rats, p < 0.05). Paroxetine treatment following MI decreases LV remodeling and susceptibility to arrhythmias, probably by reducing ROS formation.

  9. Effects of Tribuli saponins on ventricular remodeling after myocardial infarction in hyperlipidemic rats.

    PubMed

    Guo, Yan; Shi, Da-Zhuo; Yin, Hui-Jun; Chen, Ke-Ji

    2007-01-01

    This experiment was designed to determine whether Tribuli saponins (TS) relieve left ventricular remodeling (VR) after myocardial infarction (MI) in a murine hyperlipemia (HL) model. MI and HL models were induced and high and low doses of TS and simvastatin were administrated to the rats. Four weeks later, echocardiographic observation was performed and the left and right ventricular weight index (LVWI, RVWI) was calculated. Echocardiographic results showed that both high dose of TS and simvastatin had a beneficial effect on increasing fractional shortening (FS) and ejection fraction (EF), reducing left ventricular end diastolic volume (LVEDV), systolic volume (LVESV), left ventricular dimension end diastole (LVDd) and systole (LVDs), and decreasing LVWI, as compared to those in the HL-MI model group (p < 0.05, 0.01). Both medicines had little impact on thickness of the anterior and posterior wall. No significant difference was observed between each treatment group (p > 0.05). In conclusion, TS not only lowered serum lipidemia, but also relieved left ventricular remodeling, and improved cardiac function in the early stage after MI.

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

    PubMed Central

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

    2015-01-01

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

  11. A quantitative analysis of the effect of glucose-insulin-potassium in acute myocardial infarction

    PubMed Central

    Rasoul, S.; Svilaas, T.; Ottervanger, J-P.; Timmer, J.R.; van 't Hof, A.W.J.; Zijlstra, F.

    2006-01-01

    Objective To review the currently available data to investigate the clinical benefit of high- and low-dose glucose-insulin-potassium (GIK) in patients with ST-segment elevation acute myocardial infarction (STEMI). Design Quantitative analysis of all randomised trials on GIK in patients with STEMI. Electronic and manual searches for randomised controlled trials of GIK in STEMI were performed with regard to inclusion criteria, dose of GIK and additional use of reperfusion therapy, and a meta-analysis with the primary endpoint 30-day mortality was performed. Patients Data from 16 randomised trials, involving 26,273 patients, were included. Results Studies were conducted between 1962 and 2005. Overall, hospital mortality was 9.6% after GIK compared with 10.2% in controls (p=0.088). GIK infusion was not associated with an increase in major adverse events. Conclusion This quantitative analysis of GIK in patients with STEMI did not show a beneficial or detrimental effect of GIK infusion on 30-day mortality. GIK infusion should not be part of the standard therapy for patients with STEMI. PMID:25696550

  12. Effects of purified herbal extract of Salvia miltiorrhiza on ischemic rat myocardium after acute myocardial infarction.

    PubMed

    Sun, Jian; Huang, Shan Hong; Tan, Benny K-H; Whiteman, Matt; Zhu, Yi Chun; Wu, Ya Jun; Ng, Yeekong; Duan, Wei; Zhu, Yi Zhun

    2005-04-29

    In the current study, we compared purified Salvia miltiorrhiza extract (PSME) with Angiotensin-converting enzyme inhibitor, Ramipril, in in vitro experiments and also in vivo using animal model of myocardial infarction. PSME was found to have a significantly higher trolox equivalent antioxidant capacity which indicated a great capacity for scavenging free radicals. PSME could also prevent pyrogallo red bleaching and DNA damage. After 2 weeks treatment with PSME or Ramipril, survival rates of rats with experimental myocardial infarction were marginally increased (68.2% and 71.4%) compared with saline (61.5%). The ratios of infarct size to left ventricular size in both PSME-and Ramipril-treated rats were significantly less than that in the saline-treated group. Activity of cardiac antioxidant enzyme superoxide dismutase (SOD) was significant higher while level of Thiobarbituric acid-reactive substances (TBARs) was lower in the PSME treated group. Purified and standardized Chinese herb could provide an alternative regimen for the prevention of ischemic heart disease.

  13. microRNA-208a in an early stage myocardial infarction rat model and the effect on cAMP-PKA signaling pathway.

    PubMed

    Feng, Gao; Yan, Zhang; Li, Chuanchuan; Hou, Yuemei

    2016-08-01

    The expression level of microRNA-208a (miR-208a) in a rat model with myocardial infarction and the effect of cAMP-PKA signaling pathway in early stage of myocardial infarction in rats were investigated. The early myocardial infarction model was established in 12 male Sprague-Dawley rats by ligation of the anterior descending coronary artery, and 12 rats were selected as the control group (sham operation group). Reverse-transcription quantitative PCR was conducted to detect the expression levels of miR-208a in the myocardium of and the expression levels of miR‑208a in the serum of rats in the two groups. Western blot analysis was used to evaluate the expression levels of cAMP-PKA protein in the rat tissues in the two groups. After stimulating high levels of miR‑208a expression in human myocardial cells (HCM), western blot analysis was used to detect the cAMP-PKA protein levels. The expression levels of miR‑208a in myocardial tissues in rats with myocardial infarction were significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The expression levels of miR‑208a in the early stage of myocardial infarction rats were also significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The level of cAMP-PKA protein in myocardial tissue in rats with chronic myocardial infarction was also significantly higher. Transfection of human myocardial cells with miR‑208a analogue significantly increased the cAMP-PKA protein levels in human myocardial cells. In conclusion, the over-expression of miR-208a in myocardial infarction tissue and the high levels of this miRNA in the serum, may be involved in the process of myocardial infarction by influencing the cAMP-PKA signaling pathway in myocardial cells.

  14. [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. .

  15. [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.

  16. Mesenchymal Stem Cells and Mononuclear Cells From Cord Blood: Cotransplantation Provides a Better Effect in Treating Myocardial Infarction

    PubMed Central

    Chen, Gecai; Yue, Aihuan; Yu, Hong; Ruan, Zhongbao; Yin, Yigang; Wang, Ruzhu; Ren, Yin

    2016-01-01

    The aim of this study was to evaluate the effect of cotransplanting mononuclear cells from cord blood (CB-MNCs) and mesenchymal stem cells (MSCs) as treatment for myocardial infarction (MI). Transplanting CD34+ cells or MSCs separately has been shown effective in treating MI, but the effect of cotransplanting CB-MNCs and MSCs is not clear. In this study, MSCs were separated by their adherence to the tissue culture. The morphology, immunophenotype, and multilineage potential of MSCs were analyzed. CB-MNCs were separated in lymphocyte separation medium 1.077. CD34+ cell count and viability were analyzed by flow cytometry. Infarcted male Sprague-Dawley rats in a specific-pathogen-free grade were divided into four treatment groups randomly: group I, saline; group II, CB-MNCs; group III, MSCs; and group IV, CB-MNCs plus MSCs. The saline, and CB-MNCs and/or MSCs were injected intramyocardially in infarcted rats. Their cardiac function was evaluated by echocardiography. The myocardial capillary density was analyzed by immunohistochemistry. Both cell types induced an improvement in the left ventricular cardiac function and increased tissue cell proliferation in myocardial tissue and neoangiogenesis. However, CB-MNCs plus MSCs were more effective in reducing the infarct size and preventing ventricular remodeling. Scar tissue was reduced significantly in the CB-MNCs plus MSCs group. MSCs facilitate engraftment of CD34+ cells and immunomodulation after allogeneic CD34+ cell transplantation. Cotransplanting MSCs and CB-MNCs might be more effective than transplanting MSCs or CB-MNCs separately for treating MI. This study contributes knowledge toward effective treatment strategies for MI. Significance This study assessed cotransplantation of hematopoietic stem cells (CD34+ cells) and mesenchymal stem cells (MSCs) for treatment of myocardial infarction (MI) in a rat model. The results demonstrate that MSCs and mononuclear cells from cord blood may have synergistic effects and

  17. Multipronged Therapeutic Effects of Chinese Herbal Medicine Qishenyiqi in the Treatment of Acute Myocardial Infarction

    PubMed Central

    Wang, Yong; Lin, Weili; Li, Chun; Singhal, Sarita; Jain, Gaurav; Zhu, Lixin; Lu, Linghui; Zhu, Ruixin; Wang, Wei

    2017-01-01

    Background: Based on global gene expression profile, therapeutic effects of Qishenyiqi (QSYQ) on acute myocardial infarction (AMI) were investigated by integrated analysis at multiple levels including gene expression, pathways involved and functional group. Methods: Sprague-Dawley (SD) rats were randomly divided into 3 groups: Sham-operated, AMI model (left anterior descending coronary artery ligation) and QSYQ-treated group. Cardiac tissues were obtained for analysing digital gene expression. Sequencing and transcriptome analyses were performed collaboratively, including analyses of differential gene expression, gene co-expression network, targeted attack on network and functional grouping. In this study, a new strategy known as keystone gene-based group significance analysis was also developed. Results: Analysis of top keystone QSYQ-regulated genes indicated that QSYQ ameliorated ventricular remodeling (VR), which is an irreversible process in the pathophysiology of AMI. At pathway level, both well-known cardiovascular diseases and cardiac signaling pathways were enriched. The most remarkable finding was the novel therapeutic effects identified from functional group analysis. This included anti-inflammatory effects mediated via suppression of arachidonic acid lipoxygenase (LOX) pathway and elevation of nitric oxide (NO); and amelioration of dyslipidaemia mediated via fatty acid oxidation. The regulatory patterns of QSYQ on key genes were confirmed by western blot, immunohistochemistry analysis and measurement of plasma lipids, which further validated the therapeutic effects of QSYQ proposed in this study. Conclusions: QSYQ exerts multipronged therapeutic effects on AMI, by concurrently alleviating VR progression, attenuating inflammation induced by arachidonic acid LOX pathway and NO production; and ameliorating dyslipidaemia. PMID:28303103

  18. Effect of Coronary Thrombectomy in Cardiogenic Shock Complicating ST-Segment Elevation Myocardial Infarction.

    PubMed

    Suzuki, Makoto; Sumiyoshi, Tetsuya; Miyachi, Hideki; Yamashita, Jun; Yamasaki, Masao; Miyauchi, Katsumi; Yamamoto, Takeshi; Nagao, Ken; Tomoike, Hitonobu; Takayama, Morimasa

    2015-06-15

    Optimal coronary reflow is the critical key issue to ameliorate clinical outcomes in patients with cardiogenic shock complicating ST-segment elevation myocardial infarction (Shock-STEMI). We investigated our hypothesis that pre-percutaneous coronary intervention (PCI) procedural coronary thrombectomy may provide clinical advantages to attempt optimal coronary reflow in patients with Shock-STEMI. Of 7,650 patients with acute myocardial infarction registered in the Tokyo CCU Network Scientific Council from January 2009 to December 2011, a total of 180 consecutive patients (144 men, 68 ± 13 years) with Shock-STEMI who showed pre-PCI procedural Thrombolysis in Myocardial Infarction flow grade 0 (absent initial coronary flow) were recruited. Achievements of post-PCI procedural Thrombolysis in Myocardial Infarction flow grade 3 (optimal coronary reflow) and also in-hospital mortality were evaluated in those in accordance with and without coronary thrombectomy. Coronary thrombectomy was performed in 128 patients with Shock-STEMI (71% of all). Overall in-hospital mortality was 41% and that in anterior Shock-STEMI with a necessity of mechanical circulatory support increased by 59% (i.e., profound shock). Coronary thrombectomy did not affect any improvements in the achievement of optimal coronary reflow (65% vs 58%, p = 0.368) and in-hospital mortality (42% vs 37%, p = 0.484) in these patients. Even when focused on 76 patients with profound shock, neither an achievement of optimal coronary reflow (56% vs 47%, p = 0.518) nor in-hospital mortality (58% vs 65%, p = 0.601) were different between with and without coronary thrombectomy. Multivariate logistic analysis did not demonstrate any association of coronary thrombectomy (p = 0.798), left main Shock-STEMI (p = 0.258), and use of mechanical circulatory support (p = 0.119) except a concentration of hemoglobin (for each 1 g/dl increase, odds ratio 1.247, 95% confidence interval 1.035 to 1.531, p = 0.019) with optimal

  19. Effect of diltiazem on myocardial infarct size estimated by enzyme release, serial thallium-201 single-photon emission computed tomography and radionuclide angiography

    SciTech Connect

    Zannad, F.; Amor, M.; Karcher, G.; Maurin, P.; Ethevenot, G.; Sebag, C.; Bertrand, A.; Pernot, C.; Gilgenkrantz, J.M.

    1988-06-01

    Diltiazem is a calcium antagonist with demonstrated experimental cardioprotective effects. Its effects on myocardial infarct size were studied in 34 patients admitted within 6 hours after the first symptoms of acute myocardial infarction. These patients were randomized, double-blind to placebo or diltiazem (10-mg intravenous bolus followed by 15 mg/hr intravenous infusion during 72 hours, followed by 4 X 60 mg during 21 days). Myocardial infarct size was assessed by plasma creatine kinase and creatine kinase-MB indexes, perfusion defect scores using single-photon emission computed tomography with thallium-201 and left ventricular ejection fraction measured by radionuclide angiography. Tomographic and angiographic scanning was performed serially before randomization, after 48 hours and 21 days later. Groups were comparable in terms of age, sex, inclusion time and baseline infarct location and size. Results showed no difference in creatine kinase and creatine kinase-MB data between controls and treated patients, a significant decrease in the perfusion defect scores in the diltiazem group (+0.1 +/- 3.0 placebo vs -2.2 +/- 1.9 diltiazem, p less than 0.02) and a better ejection fraction recovery in the diltiazem group (-4.2 +/- 7.4 placebo vs +7.7 +/- 11.2 diltiazem, p less than 0.05). Myocardial infarct size estimates from perfusion defect scores and enzyme data were closely correlated. These preliminary results suggest that diltiazem may reduce ischemic injury in acute myocardial infarction.

  20. The effect of atmospheric temperature and pressure on the occurrence of acute myocardial infarction in Kaunas.

    PubMed

    Radišauskas, Ričardas; Vaičiulis, Vidmantas; Ustinavičienė, Rūta; Bernotienė, Gailutė

    2013-01-01

    OBJECTIVE. The aim of the study was to evaluate the impact of meteorological variables (atmospheric temperature and pressure) on the daily occurrence of acute myocardial infarction (AMI). MATERIAL AND METHODS. The study used the daily values of atmospheric temperature and pressure in 2000-2007. The meteorological data were obtained from the Lithuanian Hydrometeorological Service for Kaunas. The relative risks of event occurrence were computed for 5°C atmospheric temperature and for 10-hPa atmospheric pressure variations by means of the Poisson regression model. RESULTS. The occurrence of AMI and atmospheric temperature showed an inverse linear relationship, while the occurrence of AMI and atmospheric pressure, a positive linear relationship. Among the youngest subjects (25-44 years old), no relationships were detected. Contrary, among the subjects aged 45-64 years and those aged 65 years and older, the occurrence of AMI significantly decreased with higher temperature (P=0.001 and P=0.002, respectively). A decrease in atmospheric temperature by 10ºC reduced the risk of AMI by 8.7% in the age groups of 45-64 and 65 years and older and by 19% in the age group of 25 years and older. Among the first AMI cases, the risk increased by 7.5% in the age group of 45-64-year olds and by 6.4% in the age group of 25-64-year olds. The relationship between atmospheric temperature and pressure, and AMI occurrence was found to be linear but inverse. An increase in atmospheric pressure by 10 hPa resulted in an increase in risk by 4% among the subjects aged 65 years and more and by 3% among the subjects aged 25 years and more. CONCLUSIONS. Atmospheric temperature and pressure variations had the greatest effect on middle-aged and aging subjects (starting from 45 years). At younger age, the effect of such factors on the AMI risk was considerably lower.

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

    PubMed Central

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

    2015-01-01

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

  2. Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction.

    PubMed Central

    Silke, B; Frais, M A; Verma, S P; Reynolds, G W; Hafizullah, M; Kalra, P A; Jackson, N C; Taylor, S H

    1986-01-01

    A prospective study evaluated the comparative haemodynamic effects of three Class I antiarrhythmics (lignocaine Class 1B, disopyramide Class 1A and flecainide Class 1C) in 30 patients with uncomplicated acute myocardial infarction. Three groups, each of 10 patients, were allocated to lignocaine (Group I) 1.5 mg kg-1 i.v. loading dose over 10 min followed by infusion at 3 mg kg-1 h-1, disopyramide (Group II) or flecainide (Group III), both administered as a 1.0 mg kg-1 i.v. loading bolus over 10 min followed by a 1.6 mg kg-1 h-1 infusion for 120 min. The plasma levels of each drug were in the described therapeutic range. Lignocaine decreased cardiac index (-0.3 l min-1 m-2 (9%); P less than 0.05) and stroke volume index (-5 ml m-2 (11%); P less than 0.01). Systemic blood pressure, heart rate and systemic vascular resistance index were unchanged. There was a small increase (+3 mm Hg (30%); P less than 0.01) in pulmonary artery occluded pressure (PAOP). Both disopyramide and flecainide increased systemic blood pressure; the maximum increases for mean blood pressure were +10 mm Hg (11%) and +4 mm Hg (4%) respectively. Both drugs reduced cardiac index (-0.5 l min-1 m-2 (16%): -0.4 l min-1 m-2 (11%)) and stroke volume index (-11 ml m-2 (25%): -5 ml m-2 (11%)). There were increases in heart rate (+13: +5 beats min-1) pulmonary artery occluded pressure (+2: +3 mm Hg) and systemic vascular resistance index (+696: +275 dyn s cm-5 m2).(ABSTRACT TRUNCATED AT 250 WORDS) PMID:3105568

  3. [Effect of rehabilitation after myocardial infarction on muscular metabolism. Contribution of phosphorus 31 NMR spectroscopy].

    PubMed

    Cottin, Y; Marcer, I; Walker, P; Verges, B; Caillaux, B X; Louis, P; Didier, J P; Casillas, J M; Brunotte, F; Wolf, J E

    1994-06-01

    P 31 NMR spectroscopy is a recent technique which allows a non-invasive and direct analysis of oxidative metabolism and pH changes, an indicator of acidosis due to lactic acid accumulation in the skeletal muscles. The authors investigated oxidative muscular metabolism of the sural triceps in 10 patients after myocardial infarction by performing a study after the acute phase and repeating the study after a programme of physical training. At rest, there were no significant differences. On the other hand, for the same level of maximal effort, the depletion in phosphocreatinine (PCr) and the accumulation of inorganic phosphate (Pi) were significantly lower after physical training: the PCr/PCr + Pi increased from 0.467 +/- 0.179 to 0.538 +/- 0.20 (p < 0.02) and the Pi/PCr ratio decreased from 1.570 +/- 1.440 to 1.181 +/- 1.069 (p < 0.05). The pH at the same level of maximal exercise did not change significantly between the two periods: 6.85 +/- 0.16 vs 6.88 +/- 0.15 (NS). The peak oxygen consumption (VO2) measured during bicycle ergometry increased significantly from 23.4 +/- 10.5 to 28.3 +/- 12.14 ml/min/kg after exercise training (p < 0.01). In addition, a correlation was observed between the improvement of the peripheral parameters (PCr/PCr + Pi) and the increase in VO2 max (r = 0.757, p < 0.01). The authors results confirm the effects of physical training on oxidative metabolisms of the peripheral muscles and its influence on improvement of global performance of coronary patients.

  4. Effects of acute myocardial infarction on the circulation of the conscious rat.

    PubMed

    Ratz, P H; Peres, A K; Flaim, S F

    1986-08-01

    This study was conducted to determine if experimental left coronary artery ligation resulting in a small myocardial infarction (MI, 15% of the left ventricle) affects the peripheral circulation in conscious rat during the first 48 h of recovery. At 24 or 48 h post-MI or sham surgery, animals were instrumented and evaluated using the radioactive microsphere technique. There were no overt central hemodynamic changes 24 h post-MI but at 48 h, left ventricular end diastolic pressure was significantly increased compared to the parallel control (MI: 5.9 +/- 0.6, sham 2.0 +/- 0.5 mm Hg, P less than 0.005). At 24 h post-MI, renal vascular resistance was increased and similar but non-significant changes occurred in the gut. At 48 h post-MI, vascular resistance in the skeletal muscle, spleen, gut and cutaneous circulations were significantly reduced compared to sham-operated rats. Similar changes at 24 h were seen in a separate group of conscious rats with MI which had previously undergone cardiac denervation suggesting that cardiac afferent activity was not directly responsible for the peripheral response to MI at 24 h. Denervation did eliminate the 48 h peripheral vasodilator response. In denervated animals, circulating renin levels were similar in MI and sham-operated rats and were unchanged between 24 and 48 h. Thus, small MI in conscious rat induces a sequela of effects on the peripheral circulation over 48 h. These changes are associated with cardiac afferent nerve activity but appear to be unrelated to plasma renin levels.

  5. Effects of transient increased afterload during experimentally induced acute myocardial infarction in dogs.

    PubMed

    Hammerman, H; Kloner, R A; Alker, K J; Schoen, F J; Braunwald, E

    1985-02-15

    Alterations in afterload may occur during acute myocardial infarction (AMI), but it is unknown whether such alterations cause long-term changes in the left ventricular topography or alter healing of the AMI. AMI was produced by ligation of the left anterior descending coronary artery in open-chest dogs. Eight dogs were randomized to a methoxamine group with an infusion dose of 30 micrograms/kg/min starting 1 hour after ligation for 4 hours to increase systemic systolic pressure by 40 to 50 mm Hg, and 8 were randomized to a saline control group (n = 8). Seven days later the dogs were killed and the hearts examined. The ratio of infarct wall thickness to noninfarct wall thickness was 1.13 +/- 0.03 (mean +/- standard error of the mean) in control dogs and was 0.98 +/- 0.03 in the dogs treated with methoxamine (p less than 0.005). An expansion index was determined as previously reported and expansion was considered to have occurred if this index exceeded 1.09. The expansion index was 0.98 +/- 0.06 in the control group and 1.18 +/- 0.07 in the methoxamine group (p less than 0.05). Histologic analysis suggested a lag in the healing rate in the methoxamine-treated dogs. Thus, early, brief increases in afterload cause infarct expansion and thinning and appears to slow the early healing phase of AMI in dogs.

  6. 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.

  7. Omega-3 Fatty Acids Do Not Protect Against Arrhythmias in Acute Nonreperfused Myocardial Infarction Despite Some Antiarrhythmic Effects.

    PubMed

    Mączewski, Michał; Duda, Monika; Marciszek, Mariusz; Kołodziejczyk, Joanna; Dobrzyń, Paweł; Dobrzyń, Agnieszka; Mackiewicz, Urszula

    2016-11-01

    Ventricular arrhythmias are an important cause of mortality in the acute myocardial infarction (MI). To elucidate the effect of the omega-3 polyunsaturated fatty acids (PUFAs) on ventricular arrhythmias in acute nonreperfused MI, rats were fed with normal or eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA)-enriched diet for 3 weeks. Subsequently the rats were subjected to either MI induction or sham operation. ECG was recorded for 6 h after the operation and episodes of ventricular tachycardia/fibrillation (VT/VF) were identified. Six hours after MI epicardial monophasic action potentials (MAPs) were recorded, cardiomyocyte Ca(2+) handling was assessed and expression of proteins involved in Ca(2+) turnover was studied separately in non-infarcted left ventricle wall and infarct borderzone. EPA and DHA had no effect on occurrence of post-MI ventricular arrhythmias or mortality. Nevertheless, DHA but not EPA prevented Ca(2+) overload in LV cardiomiocytes and improved rate of Ca(2+) transient decay, protecting PMCA and SERCA function. Moreover, both EPA and DHA prevented MI-induced hyperphosphorylation of ryanodine receptors (RyRs) as well as dispersion of action potential duration (APD) in the left ventricular wall. In conclusion, EPA and DHA have no antiarrhythmic effect in the non-reperfused myocardial infarction in the rat, although these omega-3 PUFAs and DHA in particular exhibit several potential antiarrhythmic effects at the subcellular and tissue level, that is, prevent MI-induced abnormalities in Ca(2+) handling and APD dispersion. In this context further studies are needed to see if these potential antiarrhythmic effects could be utilized in the clinical setting. J. Cell. Biochem. 117: 2570-2582, 2016. © 2016 Wiley Periodicals, Inc.

  8. 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

  9. 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

  10. Protective effect of S-allyl cysteine sulphoxide (alliin) on glycoproteins and hematology in isoproterenol induced myocardial infarction in male Wistar rats.

    PubMed

    Sangeetha, T; Quine, S Darlin

    2008-07-01

    The antihyperlipidemic, antilipoperoxidative and antioxidant effects of S-allyl cysteine sulphoxide (SACS) in myocardial infarcted rats were reported previously. The present study was undertaken to evaluate the preventive role of SACS on some biochemical parameters, glycoproteins and hematology in experimentally induced myocardial infarction in rats. Myocardial infarction was induced in rats by subcutaneous injection of isoproterenol (ISO) (150 mg kg(-1)) at an interval of 24 h for 2 days. ISO-treated rats showed a significant increase in the levels of serum iron, uric acid and blood glucose, Na(+) and Ca(2+) in the heart and a significant decrease in the levels of plasma iron binding capacity, serum total protein, albumin/globulin ratio, heart K(+) and heart glycogen. The levels/concentrations of glycoproteins in serum and the heart were increased in myocardial infarcted rats. Myocardial infarcted rats also showed a significant increase in red blood cells, hemoglobin, packed cell volume, white blood cells, neutrophils, platelet count and fibrinogen level and a significant decrease in erythrocyte sedimentation rate, eosinophils, lymphocytes, bleeding, clotting and prothrombin time. Oral pretreatment with SACS (40 and 80 mg kg(-1)) daily for a period of 35 days showed a positive effect on all the biochemical parameters studied in ISO-induced rats. Thus, the study showed the protective effect of SACS on ISO-induced cardiotoxicity in male Wistar rats.

  11. 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.

  12. 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.

  13. Effect of Streptokinase on Reperfusion After Acute Myocardial Infarction and Its Complications: An Ex-Post Facto Study

    PubMed Central

    Taheri, Leila; Zargham-Boroujeni, Ali; Jahromi, Marzieh Kargar; Charkhandaz, Maryam; Hojat, Mohsen

    2015-01-01

    Introduction: Emergency treatment of patients with acute myocardial infarction is very important. Streptokinase in Iran is often as the only clot-busting medication is used. The purpose of using streptokinase medication is to revive the ischemic heart tissue, although has dangerous complications too. Therefore, the present study aimed to determine the effect of streptokinase on reperfusion after acute myocardial infarction and its complications, has been designed and conducted. Materials and Methods: This is an Ex-post facto study. The study population included patients who suffer from acute myocardial infarction. The sample size was 300 patients, and 2 groups were matched, in variables of age, sex, underlying disease, frequencies and area of MI. Data collection did by researcher making questionnaire, that accept face and content validity by 10 expert researcher, the reliability was conducted with Spearman’s test (r=0.85) by Test-retest method. Data analysis did by SPSS software: V 12. Findings: Mean of EF in SK group was (46.15±8.11) and in control group was (43.11±12.57). Significant relationship was seen between SK, arrhythmia occurring and improve EF reperfusion by chi-square test (p=0.028), (p=0.020). The most arrhythmia in SK group was Ventricular Tachycardia (20.7%). Significant statistical relation between SK and mortality were found by Chi-square test (p=0.001). But a meaningful statistical relation was not found between SK and pulmonary edema incidence (p=0.071). Conclusions: Nurses of CCU should be aware about SK complications such as hypotension, bleeding and arrhythmias. Proposed compare SK and tissue plasminogen drug in reperfusion and complications effect. PMID:25946921

  14. Effect of exercise training and myocardial infarction on force development and contractile kinetics in isolated canine myocardium.

    PubMed

    Canan, Benjamin D; Haizlip, Kaylan M; Xu, Ying; Monasky, Michelle M; Hiranandani, Nitisha; Milani-Nejad, Nima; Varian, Kenneth D; Slabaugh, Jessica L; Schultz, Eric J; Fedorov, Vadim V; Billman, George E; Janssen, Paul M L

    2016-04-15

    It is well known that moderate exercise training elicits a small increase in ventricular mass (i.e., a physiological hypertrophy) that has many beneficial effects on overall cardiac health. It is also well known that, when a myocardial infarction damages part of the heart, the remaining myocardium remodels to compensate for the loss of viable functioning myocardium. The effects of exercise training, myocardial infarction (MI), and their interaction on the contractile performance of the myocardium itself remain largely to be determined. The present study investigated the contractile properties and kinetics of right ventricular myocardium isolated from sedentary and exercise trained (10-12 wk progressively increasing treadmill running, begun 4 wk after MI induction) dogs with and without a left ventricular myocardial infarction. Exercise training increased force development, whereas MI decreased force development that was not improved by exercise training. Contractile kinetics were significantly slower in the trained dogs, whereas this impact of training was less or no longer present after MI. Length-dependent activation, both evaluated on contractile force and kinetics, was similar in all four groups. The control exercise-trained group exhibited a more positive force-frequency relationship compared with the sedentary control group while both sedentary and trained post-MI dogs had a more negative relationship. Last, the impact of the β-adrenergic receptor agonist isoproterenol resulted in a similar increase in force and acceleration of contractile kinetics in all groups. Thus, exercise training increased developed force but slowed contractile kinetics in control (noninfarcted animals), actions that were attenuated or completely absent in post-MI dogs.

  15. 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

  16. Effect of siRNA silencing of inducible co-stimulatory molecule on myocardial cell hypertrophy after cardiac infarction in rats.

    PubMed

    Wang, W M; Liu, Z; Chen, G

    2016-05-20

    As the most common cardiac disease, myocardial infarction is followed by hypertrophy of cardiac myocytes and reconstruction of ventricular structure. The up-regulation of a series of factors including metalloproteinases, inflammatory factors, and growth factors after primary infarction lead to the hypertrophy, apoptosis, necrosis, and fibroblast proliferation in cardiac muscle tissues. Recent studies have reported on the potency of small interfering RNA (siRNA) in treating cardiac diseases. We thus investigated the efficacy of inducible co-stimulatory molecule (ICOS)-specific siRNA silencing in myocardial hypertrophy in a cardiac infarction rat model. This cardiac infarction model was prepared by ligating the left anterior descending coronary artery. ICOS-siRNA treatment was administered in parallel with non-sense siRNA. After 18 days, the cross-sectional area of cardiac muscle tissues and the left ventricle weight index were measured, along with ICOS mRNA and protein expression levels, and pathological staining. Compared to those in the control groups, in myocardial infarcted rats, the application of ICOS-siRNA effectively decreased the left ventricle weight index, as well as the surface area of cardiac myocytes. Both mRNA and protein levels of ICOS were also significantly decreased. HE staining was consistent with these results. In conclusion, ICOS-targeted siRNA can effectively silence gene expression of ICOS, and provided satisfactory treatment efficacy for myocardial cell hypertrophy after infarction.

  17. 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

  18. 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

  19. 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.

  20. Effect of Smoking on Infarct Size and Major Adverse Cardiac Events in Patients With Large Anterior ST-Elevation Myocardial Infarction (from the INFUSE-AMI Trial).

    PubMed

    Gennaro, Giustino; Brener, Sorin J; Redfors, Björn; Kirtane, Ajay J; Généreux, Philippe; Maehara, Akiko; Neunteufl, Thomas; Metzger, D Christopher; Mehran, Roxana; Gibson, C Michael; Stone, Gregg W

    2016-10-15

    We sought to investigate the effect of smoking on infarct size (IS) and major adverse cardiac events (MACE) in patients with large anterior ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Participants from the Intracoronary Abciximab and Aspiration Thrombectomy in Patients with Large Anterior Myocardial Infarction study were categorized according to smoking status (current or previous smoking vs no history of smoking). The primary imaging outcome was cardiac magnetic resonance imaging-assessed IS of left ventricular mass (%) at 30 days. The primary clinical outcome was the rate of MACE at 30 days and 1 year, defined as the composite of death, reinfarction, new-onset heart failure, or rehospitalization. Of 447 patients enrolled in Intracoronary Abciximab and Aspiration Thrombectomy in Patients with Large Anterior Myocardial Infarction, 271 (60.6%) were current or past smokers. Compared with nonsmokers, smokers were almost 10 years younger and had a lower prevalence of clinical co-morbidities. Smokers had better procedural success and angiographic reperfusion compared with nonsmokers. At 30 days, there were no differences between smokers and nonsmokers in median IS (16.8% vs 17.4%, p = 0.67) or metrics of left ventricular function. By multivariable linear regression analysis, smoking was not significantly associated with IS at 30 days (beta coefficient: 0.83, p = 0.42). At 1 year, smokers had lower crude rates of MACE (7.6% vs 15%, p = 0.01). After multivariable adjustment, there were no significant differences in 1-year MACE between smokers and nonsmokers (adjusted hazard ratio 0.73, 95% CI 0.40 to 1.33, p = 0.30). In conclusion, smoking history had no significant effect on IS at 30 days. Although current or previous smokers had lower rates of 1-year MACE than those with no history of smoking, adjustment for baseline characteristics rendered this association nonsignificant. These findings support the hypothesis

  1. Effects of Ginseng Fruit Saponins on Serotonin System in Sprague-Dawley Rats with Myocardial Infarction, Depression, and Myocardial Infarction Complicated with Depression

    PubMed Central

    He, Dong-Fang; Ren, Yan-Ping; Liu, Mei-Yan

    2016-01-01

    Background: Our previous studies have demonstrated that the levels of 5-hydroxytryptamine (5-HT) and 5-HT 2A receptor (5-HT2AR) in serum and platelet were associated with depression and myocardial infarction (MI), and pretreatment with ginseng fruit saponins (GFS) before MI and depression had an effect on the 5-HT system. In this study, the effects of GFS on the 5-HT system in the Sprague-Dawley (SD) rats with MI, depression, and MI + depression were evaluated. Methods: A total of eighty SD rats were allocated to four groups: MI, depression, MI + depression, and control groups (n = 20 in each group). Each group included two subgroups (n = 10 in each subgroup): Saline treatment subgroup and GFS treatment subgroup. The levels of 5-HT, 5-HT2AR, and serotonin transporter (SERT) were quantified in serum, platelet lysate, and brain tissue through the enzyme-linked immunosorbent assay method, respectively. Results: Compared with those in the saline treatment subgroups, the levels of 5-HT in serum and platelet lysate statistically significantly increased in the GFS treatment subgroups of MI, depression, and MI + depression groups (serum: all P = 0.000; platelet lysate: P = 0.002, 0.000, 0.000, respectively). However, the 5-HT levels in brain homogenate significantly decreased in the GFS treatment subgroups compared with those in the saline treatment subgroups in MI and depression groups (P = 0.025 and 0.044 respectively), and no significant difference was observed between saline and GFS treatment subgroups in MI + depression group (P = 0.663). Compared with that in GFS treatment subgroup of control group, the 5-HT2AR levels in the platelet lysate significantly decreased in GFS treatment subgroups of MI, depression, and MI + depression groups (all P = 0.000). Compared to those in the saline treatment subgroups, the serum SERT levels significantly decreased in the GFS treatment subgroups in MI, depression, and MI + depression groups (P = 0.009, 0.038, and P = 0

  2. The positive therapeutic effect in a patient of Evans syndrome combined with acute myocardial infarction

    PubMed Central

    Zhang, Yuwei; Zheng, Kai; Zheng, Miao; Liu, Qigong; Meng, Li

    2015-01-01

    Evans syndrome (ES) is a rare combination of autoimmune hemolytic anemia and thrombocytopenia. This case report details an old male ES patient with acute myocardial infarction. He was successfully treated by primary percutaneous coronary intervention in the case of low hemoglobin level (60 g/L). Considering ES recurrence after surgery, he was given human immunoglobulin, methyl prednisolone and TPO treatment. On the basis of his platelet count, the patient was required to take only one anti-platelet drug or stop all anti-platelet drugs. To the best of our knowledge, this is the first report of ES with AMI. This case suggests that primary PCI can be a useful therapeutic strategy even if patient has low hemoglobin level, but careful balance between anti-platelet therapy and efforts to raise platelet count are needed after surgery. PMID:26309630

  3. An unusual adverse effect of sildenafil citrate: acute myocardial infarction in a nitrate-free patient.

    PubMed

    Cakmak, Huseyin Altug; Ikitimur, Baris; Karadag, Bilgehan; Ongen, Zeki

    2012-10-19

    Myocardial infarction (MI) associated with sildenafil citrate is seen rarely in patients without any history of coronary artery disease. We report a nitrate-free patient with a history of cardiovascular risk factors who developed acute MI after taking sildenafil. A 44-year-old man diagnosed with acute anterior ST segment elevation MI 120 min after self-administration of 150 mg sildenafil was admitted before attempting any sexual intercourse. The coronary angiography revealed 99% occlusion of the left anterior descending artery (LAD) and a bare-metal stent was implanted. He was discharged after 5 days without any complication. Sildenafil may cause coronary steal or may lead to vasodilation causing hypotension in patient with pre-existing cardiovascular disease, especially in patients on nitrate therapy. Our patient was nitrate free, with normal blood pressure values. Emotional stimulation associated with anticipated sexual activity may have been a triggering factor for vulnerable coronary plaque rupture.

  4. 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.

  5. The Effect of Exercise Training on Diastolic and Systolic Function After Acute Myocardial Infarction

    PubMed Central

    Fontes-Carvalho, Ricardo; Azevedo, Ana Isabel; Sampaio, Francisco; Teixeira, Madalena; Bettencourt, Nuno; Campos, Lilibeth; Gonçalves, Francisco Rocha; Ribeiro, Vasco Gama; Azevedo, Ana; Leite-Moreira, Adelino

    2015-01-01

    Abstract After acute myocardial infarction (AMI), diastolic dysfunction is frequent and an important determinant of adverse outcome. However, few interventions have proven to be effective in improving diastolic function. We aimed to determine the effect of exercise training on diastolic and systolic function after AMI. One month after AMI, 188 patients were prospectively randomized (1:1) to an 8-week supervised program of endurance and resistance exercise training (n = 86; 55.9 ± 10.8 years) versus standard of care (n = 89; 55.4 ± 10.3 years). All patients were submitted to detailed echocardiography and cardiopulmonary exercise test, at baseline and immediately after the study. Diastolic function was evaluated by the determination of tissue-Doppler derived early diastolic velocities (E′ velocity at the septal and lateral sides of mitral annulus) and by the E/E′ (ratio between the E wave velocity from mitral inflow and the E’ velocity) as recommended in the consensus document for diastolic function assessment. At the end of the study, there was no significant change in E′ septal velocity or E/E′ septal ratio in the exercise group. We observed a small, although nonsignificant, improvement in E′ lateral (mean change 0.1 ± 2.0 cm/s; P = 0.40) and E/E′ lateral ratio (mean change of −0.3 ± 2.5; P = 0.24), while patients in the control group had a nonsignificant reduction in E′ lateral (mean change −0.4 ± 1.9 cm/s; P = 0.09) and an increase in E/E′ lateral ratio (mean change + 0.3 ± 3.3; P = 0.34). No relevant changes occurred in other diastolic parameters. The exercise-training program also did not improve systolic function (either tissue Doppler systolic velocities or ejection fraction). Exercise capacity improved only in the exercise-training group, with an increase of 1.6 mL/kg/min in pVO2 (P = 0.001) and of 1.9 mL/kg/min in VO2 at anaerobic threshold (P < 0.001). After AMI

  6. Experiences with ACE inhibitors early after acute myocardial infarction. Rationale and design of the German Multicenter Study on the Effects of Captopril on Cardiopulmonary Exercise parameters post myocardial infarction (ECCE).

    PubMed

    Kleber, F X; Reindl, I; Wenzel, M; Rodewyk, P; Beil, S; Kosloswki, B; Doering, W; Sabin, G V; Hinzmann, S; Winter, U J

    1993-12-01

    Left ventricular damage by necrosis of myocardial tissue can lead to compromise of left ventricular function, to left ventricular volume increase and ultimately to development of heart failure. This sequence in the pathophysiology has been shown to be blunted by ACE inhibitors. Volume increase, however, can also be helpful in restoring stroke volume and ameliorate elevation of filling pressures. Furthermore, very early institution of ACE inhibition has failed to improve short-term mortality after myocardial infarction in one large trial. The aim of the ECCE trial therefore is, to investigate the early effects of the ACE inhibitor captopril on compromise of exercise capacity, thought to be a first measurable sign of developing heart failure. The ECCE trial is a randomized, seven-center investigation, studying the effects of ACE inhibition on oxygen uptake in a double blind, placebo controlled design in a group of 204 patients. Sample size was calculated on the basis of a pilot trial. The study design and first not unblinded data of 104 patients are presented. The population consists of predominantly male patients with mostly first myocardial infarction. They were admitted to hospital within five hours of onset of chest pain. End-diastolic volumes were normal, but ejection fraction was moderately compromised. ACE inhibition was started after the first day, but within 72 hours of onset of chest pain. After four and after twelve weeks, oxygen uptake was considerably below expected values and one third of the patients had severe compromise of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

  7. 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.

  8. Timing effect of intramyocardial hydrogel injection for positively impacting left ventricular remodeling after myocardial infarction

    PubMed Central

    Yoshizumi, Tomo; Zhu, Yang; Jiang, Hongbin; D’Amore, Antonio; Sakaguchi, Hirokazu; Tchao, Jason; Tobita, Kimimasa; Wagner, William R.

    2016-01-01

    Intramyocardial injection of various injectable hydrogel materials has shown benefit in positively impacting the course of left ventricular (LV) remodeling after myocardial infarction (MI). However, since LV remodeling is a complex, time dependent process, the most efficacious time of hydrogel injection is not clear. In this study, we injected a relatively stiff, thermoresponsive and bioabsorbable hydrogel in rat hearts at 3 different time points - immediately after MI (IM), 3 d post-MI (3D), and 2 w post-MI (2W), corresponding to the beginnings of the necrotic, fibrotic and chronic remodeling phases. The employed left anterior descending coronary artery ligation model showed expected infarction responses including functional loss, inflammation and fibrosis with distinct time dependent patterns. Changes in LV geometry and contractile function were followed by longitudinal echocardiography for 10 w post-MI. While all injection times positively affected LV function and wall thickness, the 3D group gave better functional outcomes than the other injection times and also exhibited more local vascularization and less inflammatory markers than the earlier injection time. The results indicate an important role for injection timing in the increasingly explored concept of post-MI biomaterial injection therapy and suggest that for hydrogels with mechanical support as primary function, injection at the beginning of the fibrotic phase may provide improved outcomes. PMID:26774561

  9. Timing effect of intramyocardial hydrogel injection for positively impacting left ventricular remodeling after myocardial infarction.

    PubMed

    Yoshizumi, Tomo; Zhu, Yang; Jiang, Hongbin; D'Amore, Antonio; Sakaguchi, Hirokazu; Tchao, Jason; Tobita, Kimimasa; Wagner, William R

    2016-03-01

    Intramyocardial injection of various injectable hydrogel materials has shown benefit in positively impacting the course of left ventricular (LV) remodeling after myocardial infarction (MI). However, since LV remodeling is a complex, time dependent process, the most efficacious time of hydrogel injection is not clear. In this study, we injected a relatively stiff, thermoresponsive and bioabsorbable hydrogel in rat hearts at 3 different time points - immediately after MI (IM), 3 d post-MI (3D), and 2 w post-MI (2W), corresponding to the beginnings of the necrotic, fibrotic and chronic remodeling phases. The employed left anterior descending coronary artery ligation model showed expected infarction responses including functional loss, inflammation and fibrosis with distinct time dependent patterns. Changes in LV geometry and contractile function were followed by longitudinal echocardiography for 10 w post-MI. While all injection times positively affected LV function and wall thickness, the 3D group gave better functional outcomes than the other injection times and also exhibited more local vascularization and less inflammatory markers than the earlier injection time. The results indicate an important role for injection timing in the increasingly explored concept of post-MI biomaterial injection therapy and suggest that for hydrogels with mechanical support as primary function, injection at the beginning of the fibrotic phase may provide improved outcomes.

  10. Effects of increasing left ventricular filling pressure in patients with acute myocardial infarction

    PubMed Central

    Russell, Richard O.; Rackley, Charles E.; Pombo, Jaoquin; Hunt, David; Potanin, Constantine; Dodge, Harold T.

    1970-01-01

    Left ventricular performance in 19 patients with acute myocardial infarction has been evaluated by measuring left ventricular response in terms of cardiac output, stroke volume, work, and power to progressive elevation of filling pressure accomplished by progressive expansion of blood volume with rapid infusion of low molecular weight dextran. Such infusion can elevate the cardiac output, stroke volume, work, and power and thus delineate the function of the left ventricle by Frank-Starling function curves. Left ventricular filling pressure in the range of 20-24 mm Hg was associated with the peak of the curves and when the filling pressure exceeded this range, the curves became flattened or decreased. An increase in cardiac output could be maintained for 4 or more hr. Patients with a flattened function curve had a high mortality in the ensuing 8 wk. The function curve showed improvement in myocardial function during the early convalescence. When left ventricular filling pressure is monitored directly or as pulmonary artery end-diastolic pressure, low molecular weight dextran provides a method for assessment of left ventricular function. Images PMID:5431663

  11. 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

  12. Changes in ECG and enzyme activity in rat heart after myocardial infarction: effect of TPP and MnCl2.

    PubMed

    Tylicki, A; Czerniecki, J; Godlewska, A; Kieliszek, M; Zebrowski, T; Bielawski, T; Wojcik, B

    2008-06-01

    Heart infarction is one of the main causes of death in the human population. Assurance of a sufficient level of bioenergetic processes is very important for the heart after infarction. Mn2+ as well as thiamine pyrophosphate (TPP) are positive effectors of the pyruvate dehydrogenase complex (PDH) and the 2-oxoglutarate dehydrogenase complex (OGDH), both of which play a very important role in the Krebs cycle. Thus, we have established the effect of MnCl2 (10mg/kg) and TPP (20mg/kg)--4 injections every 12 h--on the activity of PDH, OGDH, lactate dehydrogenase (LDH) and malate dehydrogenase (MDH). Additionally, we perform an analysis of ECG to affirm the changes in the heart electrophysiology of healthy rats after MnCl2 and TPP treatment. We then analyzed changes in the activity of these enzymes after experimental myocardial infarction in rats. We observed a decrease of OGDH and MDH activity in rat hearts after infarction in comparison with sham-operated rats. Treatment of healthy rats with MnCl2 caused an increase of OGDH activity. Moreover both MnCl2 and TPP caused an increase of PDH activity and a decrease of MDH activity (TPP revealed a stronger effect). We found no changes in LDH activity. Electrocardiography data showed a slight shortening of the QT interval and an enhanced heartbeat rate after treatment with MnCl2. TPP caused only elongation of the QT interval. In conclusion, application of MnCl2 enhanced the activity of some very important enzymes in the respiration process (PDH and OGDH). This effect, connected with enhanced heartbeat and a slightly shortened ventricle relaxation, may have potential application during the key period of convalescence following heart infarction.

  13. 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

  14. 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.

  15. The Effect of Wenxin Keli on the mRNA Expression Profile of Rabbits with Myocardial Infarction

    PubMed Central

    Zheng, Min; Liu, Zhouying; Liu, Nana; Hou, Cuihong; Zhang, Shu

    2016-01-01

    Aims. The molecular mechanisms of Chinese traditional medicine Wenxin Keli (WXKL) were unknown. This study was aimed at exploring the effects of WXKL on the gene expression profile and pathological alteration of rabbits with myocardial infarction. Methods. Twenty male adult rabbits were randomly divided into 4 groups: sham, model, WXKL, and captopril groups. Model, WXKL, and captopril groups underwent the ligation of the left anterior descending coronary artery while sham group went through an identical procedure without ligation. WXKL (817 mg/kg/d), captopril (8 mg/kg/d), and distilled water (to model and sham groups) were administered orally to each group. After 4 weeks, the rabbits were examined with echocardiography and the hearts were taken for expression chip and pathological staining (H&E, Masson, and Tunel) studies. Results. The data revealed that WXKL downregulated genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (CTSC and TTC5), and neurohumoral system (ACE and EDN1) and upregulated angiogenesis promoting genes such as RSPO3. Moreover, the results also showed that WXKL improved cardiac function and prevented histopathological injury and apoptosis. Conclusion. The present study demonstrated that WXKL might play an important role in inhibiting inflammation, renin-angiotensin system, and apoptosis. It might be a promising Chinese medicine in the treatment of patients with myocardial infarction. PMID:27843475

  16. The Effect of Wenxin Keli on the mRNA Expression Profile of Rabbits with Myocardial Infarction.

    PubMed

    Zheng, Min; Liu, Zhouying; Liu, Nana; Hou, Cuihong; Pu, Jielin; Zhang, Shu

    2016-01-01

    Aims. The molecular mechanisms of Chinese traditional medicine Wenxin Keli (WXKL) were unknown. This study was aimed at exploring the effects of WXKL on the gene expression profile and pathological alteration of rabbits with myocardial infarction. Methods. Twenty male adult rabbits were randomly divided into 4 groups: sham, model, WXKL, and captopril groups. Model, WXKL, and captopril groups underwent the ligation of the left anterior descending coronary artery while sham group went through an identical procedure without ligation. WXKL (817 mg/kg/d), captopril (8 mg/kg/d), and distilled water (to model and sham groups) were administered orally to each group. After 4 weeks, the rabbits were examined with echocardiography and the hearts were taken for expression chip and pathological staining (H&E, Masson, and Tunel) studies. Results. The data revealed that WXKL downregulated genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (CTSC and TTC5), and neurohumoral system (ACE and EDN1) and upregulated angiogenesis promoting genes such as RSPO3. Moreover, the results also showed that WXKL improved cardiac function and prevented histopathological injury and apoptosis. Conclusion. The present study demonstrated that WXKL might play an important role in inhibiting inflammation, renin-angiotensin system, and apoptosis. It might be a promising Chinese medicine in the treatment of patients with myocardial infarction.

  17. Different angiogenesis effect of mini-TyrRS/mini-TrpRS by systemic administration of modified siRNAs in rats with acute myocardial infarction.

    PubMed

    Zeng, Rui; Chen, Yu-Cheng; Zeng, Zhi; Liu, Wei-Qiang; Liu, Xiao-Xia; Liu, Rui; Qiang, Ou; Li, Xian

    2010-07-01

    We aimed to clarify the different angiogenesis effects of mini-tyrosyl-tRNA synthetase (TyrRS)/minitryptophanyl-tRNA synthetase (TrpRS) in rodent primates with acute myocardial infarction, by delivering small interfering RNAs (siRNAs) systemically in a liposomal formulation. Left coronary artery ligation was used to establish the model of acute myocardial infarction in rats; mini-TyrRS/mini-TrpRS-specific siRNAs were encapsulated in stable nucleic acid lipid particles (SNALP), and administered by intravenous injection to rats. Rats were divided into four experiment groups: sham operated group (no left anterior descending artery [LAD] occlusion); negative control group (LAD occlusion + saline injection); mock transfection group (LAD occlusion + mock transfected injection); experiment group (LAD occlusion + mini-TyrRS/mini-TrpRS-specific siRNAs injection). Silencing efficiency was assayed by Western blotting. To determine whether mini-TyrRS/mini-TrpRS affected the angiogenesis activity of rats with myocardial infarction, we measured the myocardial infarction size by TTC staining, and the capillary density using immunohistochemistry staining, to investigate the expression of factor VIII. The myocardial infarction size and the capillary density of mini-TyrRS-siRNA group were respectively 18.89% and 8.64/0.1 mm(2) 1 month after ligation, while in the mini-TrpRS-siRNA group these values were 7.33% and 17.32/0.1 mm(2), significantly different compared with the mock transfection group (14.19%; 13.56/0.1 mm(2)) and negative control group (14.28%; 13.89/0.1 mm(2)), P < 0.05. There were no significant changes between the mock transfection group and the negative control group, P > 0.05. These results indicated that angiogenesis is either stimulated by mini-TyrRS or inhibited by mini-TrpRS in rat models with acute myocardial infarction.

  18. 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

  19. Effect of goal attainment theory based education program on cardiovascular risks, behavioral modification, and quality of life among patients with first episode of acute myocardial infarction: Randomized study.

    PubMed

    Park, Moonkyoung; Song, Rhayun; Jeong, Jin-Ok

    2017-02-24

    Effect of goal-attainment-theory-based education program on cardiovascular risks, behavioral modification, and quality of life among patients with first episode of acute myocardial infarction: randomized study BACKGROUND: The behavioral modification strategies should be explored at the time of admission to lead the maximum effect of cardiovascular risk management.

  20. Effects of Intracoronary Administration of Autologous Adipose Tissue-Derived Stem Cells on Acute Myocardial Infarction in a Porcine Model

    PubMed Central

    Lee, Hye Won; Park, Jong Ha; Kim, Bo Won; Ahn, Jinhee; Kim, Jin Hee; Park, Jin Sup; Oh, Jun-Hyok; Choi, Jung Hyun; Cha, Kwang Soo; Hong, Taek Jong; Park, Tae Sik; Kim, Sang-Pil; Song, Seunghwan; Kim, Ji Yeon; Park, Mi Hwa; Jung, Jin Sup

    2015-01-01

    Purpose Adipose-derived stem cells (ADSCs) are known to be potentially effective in regeneration of damaged tissue. We aimed to assess the effectiveness of intracoronary administration of ADSCs in reducing the infarction area and improving function after acute transmural myocardial infarction (MI) in a porcine model. Materials and Methods ADSCs were obtained from each pig's abdominal subcutaneous fat tissue by simple liposuction. After 3 passages of 14-days culture, 2 million ADSCs were injected into the coronary artery 30 min after acute transmural MI. At baseline and 4 weeks after the ADSC injection, 99mTc methoxyisobutylisonitrile-single photon emission computed tomography (MIBI-SPECT) was performed to evaluate the left ventricular volume, left ventricular ejection fraction (LVEF; %), and perfusion defects as well as the myocardial salvage (%) and salvage index. At 4 weeks, each pig was sacrificed, and the heart was extracted and dissected. Gross and microscopic analyses with specific immunohistochemistry staining were then performed. Results Analysis showed improvement in the perfusion defect, but not in the LVEF in the ADSC group (n=14), compared with the control group (n=14) (perfusion defect, -13.0±10.0 vs. -2.6±12.0, p=0.019; LVEF, -8.0±15.4 vs. -15.9±14.8, p=0.181). There was a tendency of reducing left ventricular volume in ADSC group. The ADSCs identified by stromal cell-derived factor-1 (SDF-1) staining were well co-localized by von Willebrand factor and Troponin T staining. Conclusion Intracoronary injection of cultured ADSCs improved myocardial perfusion in this porcine acute transmural MI model. PMID:26446632

  1. Protective effect of geranylgeranylacetone via enhanced induction of HSPB1 and HSPB8 in mitochondria of the failing heart following myocardial infarction in rats.

    PubMed

    Marunouchi, Tetsuro; Inomata, Satomi; Sanbe, Atsushi; Takagi, Norio; Tanonaka, Kouichi

    2014-05-05

    The mechanisms underlying mitochondrial impairment in the failing heart are not yet clear. In a previous study, we found that the levels of small heat shock proteins (HSP) such as mitochondrial HSPB1 and HSPB8 in the failing heart following myocardial infarction were decreased. In the present study, to verify the hypothesis that mitochondrial dysfunction in the failing heart is associated with alterations in mitochondrial small heat shock proteins, we examined the effects of geranylgeranylacetone, a heat shock protein inducer, on the cardiac mitochondrial function after myocardial infarction. When hemodynamic parameters of rats with myocardial infarction were measured at the 8th (8W) week after coronary artery ligation (CAL), the 8W-CAL showed signs of chronic heart failure concomitant with a reduced mitochondrial oxygen consumption rate. HSPB1 and HSPB8 contents in the mitochondrial fraction prepared from the failing heart were decreased, suggesting that an attenuation of mitochondrial translocation of HSPB1 and HSPB8 had led to an impairment of mitochondrial energy-producing ability. Geranylgeranylacetone treatment from the 2nd to 8th week after myocardial infarction attenuated the reduction in mitochondrial HSPB1 and HSPB8 contents. Furthermore, the mitochondrial energy-producing ability and cardiac pump function were preserved by orally administered geranylgeranylacetone during the development of heart failure. These results suggest that the induction of small heat shock proteins in the infarcted heart by geranylgeranylacetone treatment contributed to the preservation of mitochondrial function, leading to an improvement of cardiac contractile function.

  2. 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

  3. [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.

  4. Anti-inflammatory, Antithrombotic and Cardiac Remodeling Preventive Effects of Eugenol in Isoproterenol-Induced Myocardial Infarction in Wistar Rat.

    PubMed

    Mnafgui, Kais; Hajji, Raouf; Derbali, Fatma; Gammoudi, Anis; Khabbabi, Gaddour; Ellefi, Hedi; Allouche, Noureddine; Kadri, Adel; Gharsallah, Neji

    2016-10-01

    This study aimed to evaluate the antithrombotic, anti-inflammatory and anti-cardiac remodeling properties of eugenol in isoproterenol-induced myocardial infarction in rats. Male Wistar rats were randomly divided into four groups, control, iso [100 mg/kg body weight was injected subcutaneously into rats at an interval of 24 h for 2 days (6th and 7th day) to induce MI] and pretreated animals with clopidogrel (0.2 mg/kg) and eugenol (50 mg/kg) orally for 7 days and intoxicated with isoproterenol (Iso + Clop) and (Iso + EG) groups. Isoproterenol-induced myocardial infarcted rats showed notable changes in the ECG pattern, increase in heart weight index, deterioration in the hemodynamic function and rise in plasma level of troponin-T, CK-MB and LDH and ALT by 316, 74, 172 and 45 %, respectively, with histological myocardium necrosis and cells inflammatory infiltration. In addition, significant increases in plasma levels of inflammatory biomarkers such as fibrinogen, α1, α2, β1, β2 and γ globulins with decrease level of albumin were observed in infarcted rats as compared to normal ones. Else, the angiotensin-converting enzyme (ACE) activity in plasma, kidney and heart of the isoproterenol-induced rats was significantly increased by 34, 47 and 93 %, respectively, as compared to normal group. However, the administration of eugenol induced a clear improvement in cardiac biomarkers injury, reduced inflammatory mediators proteins, increased heart activities of superoxide dismutase and glutathione peroxidase with reduce in thiobarbituric acid-reactive substances content and inhibition of ventricular remodeling process through inhibition of ACE activity. Overall, eugenol evidences high preventive effects from cardiac remodeling process.

  5. Effect of intravenous and intracoronary melatonin as an adjunct to primary percutaneous coronary intervention for acute ST-elevation myocardial infarction: Results of the Melatonin Adjunct in the acute myocaRdial Infarction treated with Angioplasty trial.

    PubMed

    Dominguez-Rodriguez, Alberto; Abreu-Gonzalez, Pedro; de la Torre-Hernandez, Jose M; Gonzalez-Gonzalez, Julia; Garcia-Camarero, Tamara; Consuegra-Sanchez, Luciano; Garcia-Saiz, Maria Del Mar; Aldea-Perona, Ana; Virgos-Aller, Tirso; Azpeitia, Agueda; Reiter, Russel J

    2017-01-01

    The MARIA randomized trial evaluated the efficacy and safety of melatonin for the reduction of reperfusion injury in patients undergoing revascularization for ST-elevation myocardial infarction (STEMI). This was a prespecified interim analysis. A total of 146 patients presenting with STEMI within 6 hours of chest pain onset were randomized to receive intravenous and intracoronary melatonin (n=73) or placebo (n=73) during primary percutaneous coronary intervention (PPCI). Primary endpoint was myocardial infarct size as assessed by magnetic resonance imaging (MRI) at 6 ± 2 days. Secondary endpoints were changes in left ventricular volumes and ejection fraction (LVEF) at 130 ± 10 days post-PPCI and adverse events during the first year. No significant differences in baseline characteristics were observed between groups. MRI was performed in 108 patients (86.4%). Myocardial infarct size by MRI evaluated 6 ± 2 days post-PPCI, did not differ between melatonin and placebo groups (P=.63). Infarct size assessed by MRI at 130 ± 10 days post-PPCI, performed in 91 patients (72.8%), did not show statistically significant differences between groups (P=.27). The recovery of LVEF from 6 ± 2 to 130 ± 10 days post-PPCI was greater in the placebo group (60.0 ± 10.4% vs 53.1 ± 12.5%, P=.008). Both left ventricular end-diastolic and end-systolic volumes were lower in the placebo group (P=.01). The incidence of adverse events at 1 year was comparable in both groups (P=.150). Thus, in a nonrestricted STEMI population, intravenous and intracoronary melatonin was not associated with a reduction in infarct size and has an unfavourable effect on the ventricular volumes and LVEF evolution. Likewise, there is lack of toxicity of melatonin with the doses used.

  6. 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

  7. 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…

  8. [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.

  9. Berberine elicits anti-arrhythmic effects via IK1/Kir2.1 in the rat type 2 diabetic myocardial infarction model.

    PubMed

    Wang, Li-hong; Yu, Chang-hua; Fu, Ying; Li, Qiang; Sun, Yu-qian

    2011-01-01

    The purpose of this study was to explore the anti-arrhythmic mechanisms of berberine in diabetic rats with myocardial infarction. Sixty rats were divided into four groups: (1) normal control; (2) myocardial infarction group (MI); (3) Type 2 diabetes with myocardial infarction group (T2DM+MI); and (4) Type 2 diabetic with myocardial infarction berberine-treated group (BBR). Berberine (60 mg/kg/day) was administered after coronary artery ligation in the T2DM+MI group for 14 days. Currents were measured using whole-cell patch-clamp techniques. Western blot was performed for quantification of target proteins. The study showed that arrhythmias induced by myocardial infarction were aggravated in diabetic rats. Arrhythmia scores in the MI group were significantly higher than in the control group. Interestingly, the administration of berberine at a dose of 60 mg/kg/d recovered arrhythmia scores (P > 0.05). RMP (Resting membrane potential) which could be recovered by berberine (P < 0.05), was significantly reduced in both the infarction groups. I(K1) current and current density markedly decreased in the MI and T2DM+MI groups (P < 0.05) and could be reversed by berberine (P < 0.05). The relative expression of Kir2.1 in rats in the MI and T2DM+MI group were both significantly decreased (P < 0.05); berberine recovered depressed Kir2.1 to nearly normal levels. The results suggest that the effects of berberine on I(K1)/Kir2.1 may be an important mechanism for producing anti-arrhythmic effects.

  10. 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.

  11. [Protective effect of peptide semax the rat heart in acute myocardial infarction].

    PubMed

    Golubeva, A V; Gavrilova, S A; Lipina, T V; Shornikova, M V; Postnikov, A B; Andreeva, L A; Chentsov, Iu S; Koshelev, V B

    2006-06-01

    Semax, a member of ACTH-derived peptides family, has been employed in the treatment of acute ischemic stroke in patients. It decreased neurological deficit and reduced NO hyperproduction in the rat brain, caused by acute cerebral hypoperfusion. We suggested that semax is also able to protect rat heart from ischemic damage in acute myocardial infaction (AMI). AMI was induced by left coronary artery occlusion, myocardial ischemic area averaged 30 % of left ventricle. In 2 hours after coronary occlusion, the AMI group developed 11 % reduced mean arterial blood pressure and 48 % increased diastolic blood pressure in left ventricle in comparison with sham-operated control group. However, infusion of either dobutamine, which directly stimulates myocardial contractility, or sodium nitroprusside and phenylephrine, that change vascular resistance and thus cardiac afterload, did not reveal distinctions in hemodynamic parameters between groups. These data indicate absense or only moderate cardiac dysfunction in rats with AMI and are consistent wih morphometrical and histochemical studies that did not detect any necrotic or apoptotic (TUNEL-test) changes in left ventricular cardiomyocytes in spite of development of distinct ischemic disturbances of mitochondria and nuclear in about 50 % of cardiomyocytes in 2 hours after AMI. Semax (150 microg/kg), given i. p. 15 min and 2 hours after coronary occlusion, caused no effect on cardiac function, but completely prevented ischemia-induced ultrastructural changes of cardiomyocytes. This protective effect was accompanied by the ability of peptide to blunt the increase in plasma concentrations of nitrates, observed in AMI group.

  12. 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

  13. 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)

  14. 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.

  15. Short-term effects of air pollution on hospitalization for acute myocardial infarction: age effect on lag pattern.

    PubMed

    Collart, Philippe; Dramaix, Michele; Levêque, Alain; Coppieters, Yves

    2017-02-01

    The aim of the present study is to analyse the age effect on the lag patterns of relative risk of hospitalization for acute myocardial infarction and NO2, PM10 and O3. Daily hospitalizations for AMI during the period 2008-2011 were extracted from administrative data. Analyses were performed using the quasi-Poisson regression model adjusted for seasonality, long-term trend, day of the week and temperature. We observed very different patterns depending on age. For NO2 and PM10, the younger group (25-54 years) shows a more delayed effect in comparison with the two older age groups (55-64 and ≥ 65 years). Overall, the associations between NO2 and AMI are higher compared to PM10. There are no associations between O3 and AMI. This study indicates that age plays a major role in the lag pattern. Younger people have delayed effects, but they are nevertheless sensitive to air pollution.

  16. The impact of ischemia-reperfusion injury on the effectiveness of primary angioplasty in ST-segment elevation myocardial infarction

    PubMed Central

    Grygier, Marek; Lesiak, Maciej; Grajek, Stefan

    2013-01-01

    The most effective method of reperfusion in patients with ST-segment elevation myocardial infarction (STEMI) is primary percutaneous coronary intervention (PCI), assisted by aspiration thrombectomy and administration of antiplatelet agents and anticoagulants. However, effective restoration of blood flow in the infarct-related artery may paradoxically result in further damage to the heart muscle. This phenomenon, called ischemia-reperfusion injury (IRI), can significantly reduce the beneficial effects of reperfusion therapy. The rapid restoration of blood flow to the previously ischemic area causes a number of pathophysiological mechanisms leading to increased necrosis of myocytes still viable at the end of the ischemic period. It has been postulated that there are several strategies that can reduce damage to the heart muscle. Attempts to translate the results of experimental trials has been disappointing. More recently, however, some of the clinical benefits of ischemic postconditioning in which reperfusion in patients with STEMI who are undergoing PCI is interrupted with short episodes of ischemia were demonstrated. This renewed the interest in the reperfusion phase as a target for cardioprotective therapy. Research in this field has also been reinforced by the discovery of new potential targets for treatment that protects against IRI, such as the kinase pathway to protect against damage (reperfusion injury salvage kinases – RISK) and mitochondrial permeability transition pore. It seems that these findings will help to develop strategies that will improve the efficiency of mechanical reperfusion and may translate into long-term clinical effects. PMID:24570732

  17. Preventive effect of phytic acid on lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats.

    PubMed

    Brindha, E; Rajasekapandiyan, M

    2015-02-01

    This study was aimed to evaluate the preventive role of phytic acid on lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85 mg/kg) at an interval of 24 h for two days showed a significant increase in the activities of lysosomal enzymes (glucuronidase, N-acetyl glucosaminidase, galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with phytic acid (25 and 50 mg/kg) daily for a period of 56 d positively altered activities of lysosomal hydrolases in ISO-induced rats. Thus, phytic acid possesses a cardioprotective effect in ISO-induced MI in rats.

  18. 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.

  19. [The effect on myocardial perfusion and clinical outcome of intracoronary nicorandil injection prior to percutaneous coronary intervention in ST-segment elevation myocardial infarction].

    PubMed

    Wang, Z Q; Chen, M X; Liu, D L; Zheng, W X; Cao, X Z; Chen, H; Huang, M F; Luo, Z R

    2017-01-25

    Objective: To investigate the effect of intracoronary administration of nicorandil prior to primary percutaneous coronary intervention (PPCI) on myocardial perfusion and short-term clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). Methods: A total of 158 patients with STEMI undergoing PPCI from January 2014 to December 2015 in Fuzhou General Hospital were enrolled consecutively in this prospective controlled randomized trial. Patients were assigned into three groups with random number table: the nicorandil group (patients received intracoronary administration of 6 mg nicorandil after guide wire or balloon successfully crossed the target lesion, n=53), the nitroglycerin group (patients received intracoronary administration of 300 μg nitroglycerin after after guide wire or balloon successfully crossed the target lesion, n=52) and the control group(patients received routine treatment, n=53). The primary outcomes were myocardial perfusion, including the levels of corrected TIMI frame count (cTFC), and the incidence of no reflow or slow flow after PPCI. The secondary outcomes included the incidence of major adverse cardiovascular events (MACE) during hospitalization (all-cause death, reperfusion arrhythmia within 2 hours after PPCI, angina within 24 hours after PPCI, new heart failure or worsening cardiac function, and repeat revascularization) and within 3 months of follow-up (all-cause death, nonfatal myocardial infarction, repeat revascularization, post-infarction angina, and re-hospitalization for congestive heart failure). Results: The age of enrolled patients was (62.9±11.3) years old, and 130 cases (82.3%) of them were male. The median time of symptom-onset to balloon was 4.50 (3.20, 6.43) hours. There were significantly difference in cTFC immediately after PPCI((21.68±7.43)frames, (24.74±8.66)frames, and(27.06±10.40)frames), incidence of no reflow or slow flow after PPCI(5.7%(3/53), 13.5%(7/52), and 22.6%(12/53)), ST

  20. Tumour necrosis factor-α and its receptors in the beneficial effects of vagal stimulation after myocardial infarction in rats.

    PubMed

    Kong, Shan-Shan; Liu, Jin-Jun; Hwang, Tyzh-Chang; Yu, Xiao-Jiang; Lu, Yi; Zang, Wei-Jin

    2011-05-01

    1. Acute myocardial infarction (AMI) often activates the sympathetic system and inhibits the vagal system. Long-term vagal nerve stimulation (VNS) exerts several beneficial effects on the ischaemic heart, including an anti-inflammatory effect. The aim of the present study was to investigate whether short-term VNS during AMI could inhibit tumour necrosis factor (TNF)-α expression and the effect of TNF receptor (TNFR), key components in inflammatory responses to AMI, in a rodent model. 2. Adult male Sprague-Dawley rats were divided into four groups, namely a control (C), VNS (S), AMI (M) and an AMI group subjected to prior VNS (MS). In the S and MS groups, the right vagus nerve was stimulated electrically for 4 h; in the M and MS groups, AMI was induced by occlusion of the left anterior descending coronary artery. Haemodynamic data were monitored continuously using a multichannel physiological recorder. Lactate dehydrogenase (LDH) leakage, creatine kinase (CK) leakage and infarct size were determined. The expression of TNF-α and its receptors were analysed by reverse transcription-polymerase chain reaction, western blotting and ELISA. 3. Compared with the control group, rats in the M group had low blood pressure, high left ventricular (LV) end-diastolic pressure, a depressed maximum dP/dt of LV pressure, higher LDH and CK leakage, a larger infarct size, increased TNF-α levels and an increased TNFR1/TNFR2 ratio. However, these presumably harmful effects of AMI were all significantly ameliorated by VNS during AMI (MS group). 4. In conclusion, VNS can rectify ischaemia-induced cardiac dysfunction partly via inhibition of a TNF-α-mediated signalling pathway.

  1. 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.

  2. 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.

  3. 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

  4. 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.

  5. [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.

  6. [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.

  7. 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.

  8. 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

  9. The beneficial effects of ranolazine on cardiac function after myocardial infarction are greater in diabetic than in nondiabetic rats.

    PubMed

    Mourouzis, Iordanis; Mantzouratou, Polixeni; Galanopoulos, Georgios; Kostakou, Erietta; Dhalla, Arvinder K; Belardinelli, Luiz; Pantos, Constantinos

    2014-09-01

    Ranolazine (RAN) is known to exert both anti-ischemic and antidiabetic actions. Thus, this study has explored the hypothesis that RAN would have greater effect on the recovery of cardiac function in diabetic mellitus (DM) rat hearts following myocardial infarction (MI). Myocardial infarction was induced in nondiabetic (MI, n = 14) and diabetic (streptozotocin induced; DM-MI, n = 13) Wistar rats by permanent ligation of the left coronary artery. Cardiac function was evaluated using echocardiography (left ventricular ejection fraction %) and in isolated heart preparations by measuring left ventricular developed pressure (LVDP), and the positive and negative first derivative of LVDP (± dp/dt). Ranolazine (20 mg/kg, ip once a day) was administered 24 hours after surgical procedure for 4 weeks to nondiabetic (MI + RAN, n = 17) and diabetic rats (DM-MI + RAN, n = 15). The RAN improved the recovery of function in both the nondiabetic and the diabetic postinfarcted hearts but this effect was greater and achieved statistical significance only in the diabetic group. The RAN resulted in increased levels of phosphorylated protein kinase B (Akt) and mammalian target of rapamycin (mTOR, a component of Akt signaling) in both nondiabetic and diabetic infarcted hearts without changes in the activation of mitogen-activated protein kinases (MAPKs; p38 MAPK, c-Jun N-terminal kinase, and extracellular signal-regulated kinase). In addition, in diabetic hearts, RAN resulted in a significant increase in the ratio of sarcoplasmic Ca(2+)-ATPase/phospholamban (a target of Akt signaling, 2.0-fold increase) and increased levels of phosphorylated calcium-regulated adenosine monophosphate-activated protein kinase (AMPK; 2.0-fold increase). In diabetic animals, RAN increased insulin and lowered glucose levels in serum. In conclusion, the beneficial effect of RAN on the recovery of cardiac function after MI was greater in DM rats. This response was associated with activation of Akt/mTOR and AMPK

  10. 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

  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.

  12. 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.

  13. 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)

  14. 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.

  15. 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.

  16. Cardioprotective Effects of Lagenaria siceraria Fruit Juice on Isoproterenol-induced Myocardial Infarction in Wistar Rats: A Biochemical and Histoarchitecture Study.

    PubMed

    Upaganlawar, A; Balaraman, R

    2011-10-01

    The present study was designed to evaluate the cardioprotective effects of Lagenaria siceraria fruit juice in isoproterenol-induced myocardial infarction. Rats injected with isoproterenol (200 mg/kg, s.c.) showed a significant increase in the levels of serum uric acid, tissue Na(++) and Ca(++) ions and membrane-bound Ca(+2)-ATPase activity. A significant decrease in the levels of serum protein, tissue K(+) ion, vitamin E level, and the activities of Na(+)/K(+)-ATPase and mg(+2)-ATPase was observed. Isoproterenol injected rats also showed a significant increase in the intensity of lactate dehydrogenase isoenzyme and histopathologic alterations in the heart. Treatment with L. siceraria fruit juice (400 mg/kg/day, p.o.) for 30 days and administration of isoproterenol on 29(th) and 30(th) days showed a protective effect on altered biochemical and histopathologic changes. These findings indicate the cardioprotective effect of L. siceraria fruit juice in isoproterenol-induced myocardial infarction in rats.

  17. Comparative Cost-Effectiveness of Interventions to Improve Medication Adherence after Myocardial Infarction

    PubMed Central

    Ito, Kouta; Shrank, William H; Avorn, Jerry; Patrick, Amanda R; Brennan, Troyen A; Antman, Elliot M; Choudhry, Niteesh K

    2012-01-01

    Objective To evaluate the comparative cost-effectiveness of interventions to improve adherence to evidence-based medications among postmyocardial infarction (MI) patients. Data Sources/Study Setting Cost-effectiveness analysis. Study Design We developed a Markov model simulating a hypothetical cohort of 65-year-old post-MI patients who were prescribed secondary prevention medications. We evaluated mailed education, disease management, polypill use, and combinations of these interventions. The analysis was performed from a societal perspective over a lifetime horizon. The main outcome was an incremental cost-effectiveness ratio (ICER) as measured by cost per quality-adjusted life year (QALY) gained. Data Collection/Extraction Methods Model inputs were extracted from published literature. Principal Findings Compared with usual care, only mailed education had both improved health outcomes and reduced spending. Mailed education plus disease management, disease management, polypill use, polypill use plus mailed education, and polypill use plus disease management cost were $74,600, $69,200, $133,000, $113,000, and $142,900 per QALY gained, respectively. In an incremental analysis, only mailed education had an ICER of less than $100,000 per QALY and was therefore the optimal strategy. Polypill use, particularly when combined with mailed education, could be cost effective, and potentially cost saving if its price decreased to less than $100 per month. Conclusions Mailed education and a polypill, once available, may be the cost-saving strategies for improving post-MI medication adherence. PMID:22998129

  18. 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

  19. 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.

  20. Vulnerabilities to Temperature Effects on Acute Myocardial Infarction Hospital Admissions in South Korea.

    PubMed

    Kwon, Bo Yeon; Lee, Eunil; Lee, Suji; Heo, Seulkee; Jo, Kyunghee; Kim, Jinsun; Park, Man Sik

    2015-11-13

    Most previous studies have focused on the association between acute myocardial function (AMI) and temperature by gender and age. Recently, however, concern has also arisen about those most susceptible to the effects of temperature according to socioeconomic status (SES). The objective of this study was to determine the effect of heat and cold on hospital admissions for AMI by subpopulations (gender, age, living area, and individual SES) in South Korea. The Korea National Health Insurance (KNHI) database was used to examine the effect of heat and cold on hospital admissions for AMI during 2004-2012. We analyzed the increase in AMI hospital admissions both above and below a threshold temperature using Poisson generalized additive models (GAMs) for hot, cold, and warm weather. The Medicaid group, the lowest SES group, had a significantly higher RR of 1.37 (95% CI: 1.07-1.76) for heat and 1.11 (95% CI: 1.04-1.20) for cold among subgroups, while also showing distinctly higher risk curves than NHI for both hot and cold weather. In additions, females, older age group, and those living in urban areas had higher risks from hot and cold temperatures than males, younger age group, and those living in rural areas.

  1. [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.

  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. Effects of Statin Therapy on Clinical Outcomes of Survivors of Acute Myocardial Infarction with Severe Systolic Heart Failure

    PubMed Central

    Kim, Hyun Soo; Kim, Jin Bae; Kim, Woo-Shik; Kim, Kwon Sam; Jeong, Myung Ho; Kim, Weon

    2015-01-01

    Objective Large randomized trials have failed to show a beneficial effect of statin treatment in chronic HF. The investigators tried to evaluate the long-term effects of statin therapy in patients with new onset heart failure (HF) following acute myocardial infarction (AMI). Methods Between January 2008 and December 2011, a total of 13,616 AMI patients were enrolled in the Korea Acute Myocardial Infarction Registry (KAMIR) which was a prospective, multi-center, nationwide, web-based database of AMI in Korea. From this database, we studied 1,055 patients with AMI who had newly developed severe acute HF [left ventricular ejection fraction ≤ 40%] and were discharged alive. The patients were divided into two groups, a statin group (n = 756) and a no-statin group (n = 299). We investigated the one-year major adverse cardiovascular events (MACEs), including all-cause mortality, MI, and any revascularization of each group. We then performed a propensity-score matched analysis. Results In the original cohort, one-year MACEs were similar between the two groups (16.5% vs. 14.7% in the statin or no-statin groups; p = 0.47). Propensity-score matching yielded 256 pairs, and in that population we observed comparable results in terms of MACEs (18.0% vs. 12.5% in the statin or no-statin groups, p = 0.11) and mortality (5.1% vs. 3.5% in the statin or no-statin groups, p = 0.51). Cox-regression analysis revealed that statin therapy was not an independent predictor for occurrence of a MACE [Hazard ratio (HR) 1.11, 95% CI 0.79–1.57, p = 0.54] or all-cause mortality (HR 1.42, 95% CI 0.75–2.70, p = 0.28). Conclusion Statin therapy was not associated with a reduction in the long-term occurrence of MACEs or mortality in survivors of AMI with severe acute HF in this retrospective cohort study. PMID:26658751

  4. 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.

  5. Acute Effects of Intracoronary Tirofiban on No-Reflow Phenomena in Patients With ST-Segment Elevated Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

    PubMed

    Akpek, Mahmut; Sahin, Omer; Sarli, Bahadir; Baktir, Ahmet Oguz; Saglam, Hayrettin; Urkmez, Serkan; Ergin, Ali; Oguzhan, Abdurrahman; Arinc, Huseyin; Kaya, Mehmet G

    2015-07-01

    We evaluated the acute effect of intracoronary administration of tirofiban on no-reflow phenomenon in patients with ST-segment elevated myocardial infarction undergoing primary percutaneous coronary intervention. Consecutive patients (n = 162) were randomized into 2 groups based on whether intracoronary tirofiban was administered. After the administration of intracoronary tirofiban, thrombolysis in myocardial infarction (TIMI) flow grade significantly increased (P < .001) and successful reperfusion was achieved in 26 (32%) patients. In the placebo group, however, after the administration of intracoronary placebo the TIMI flow grade did not change (P = .070), and successful reperfusion was achieved only in 8 (10%) patients. In-hospital major adverse cardiac events (MACE) were significantly lower in the tirofiban group (36% vs 19%, P = .013). Intracoronary administration of tirofiban significantly improves TIMI flow grade and is associated with a lower in-hospital rate of MACE.

  6. 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

  7. 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.

  8. [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.

  9. 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…

  10. 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.

  11. Effectiveness of a Myocardial Infarction Protocol in Reducing Door-to-Ballon Time

    PubMed Central

    Correia, Luis Cláudio Lemos; Brito, Mariana; Kalil, Felipe; Sabino, Michael; Garcia, Guilherme; Ferreira, Felipe; Matos, Iracy; Jacobs, Peter; Ronzoni, Liliana; Noya-Rabelo, Márcia

    2013-01-01

    Background An adequate door-to-balloon time (<120 minutes) is the necessary condition for the efficacy of primary angioplasty in infarction to translate into effectiveness. Objective To describe the effectiveness of a quality of care protocol in reducing the door-to-balloon time. Methods Between May 2010 and August 2012, all individuals undergoing primary angioplasty in our hospital were analyzed. The door time was electronically recorded at the moment the patient took a number to be evaluated in the emergency room, which occurred prior to filling the check-in forms and to the triage. The balloon time was defined as the beginning of artery opening (introduction of the first device). The first 5 months of monitoring corresponded to the period of pre-implementation of the protocol. The protocol comprised the definition of a flowchart of actions from patient arrival at the hospital, the team's awareness raising in relation to the prioritization of time, and provision of a periodic feedback on the results and possible inadequacies. Results A total of 50 individuals were assessed. They were divided into five groups of 10 sequential patients (one group pre-and four groups post-protocol). The door-to-balloon time regarding the 10 cases recorded before protocol implementation was 200 ± 77 minutes. After protocol implementation, there was a progressive reduction of the door-to-balloon time to 142 ± 78 minutes in the first 10 patients, then to 150 ± 50 minutes, 131 ± 37 minutes and, finally, 116 ± 29 minutes in the three sequential groups of 10 patients, respectively. Linear regression between sequential patients and the door-to-balloon time (r = - 0.41) showed a regression coefficient of - 1.74 minutes. Conclusion The protocol implementation proved effective in the reduction of the door-to-balloon time. PMID:23702814

  12. 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.

  13. 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.

  14. 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

  15. 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.

  16. Clinical effectiveness of pneumococcal vaccination against acute myocardial infarction and stroke in people over 60 years: the CAPAMIS study, one-year follow-up

    PubMed Central

    2012-01-01

    Background Conflicting results have been recently reported evaluating the relationship between pneumococcal vaccination and the risk of thrombotic vascular events. This study assessed the clinical effectiveness of the 23-valent polysaccharide pneumococcal vaccine (PPV23) against acute myocardial infarction and ischaemic stroke in older adults. Methods Population-based prospective cohort study conducted from December 1, 2008 until November 30, 2009, including all individuals ≥ 60 years-old assigned to nine Primary Care Centres in Tarragona, Spain (N = 27,204 individuals). Primary outcomes were hospitalisation for acute myocardial infarction and/or ischaemic stroke. All cases were validated by checking clinical records. The association between pneumococcal vaccination and the risk of each outcome was evaluated by Multivariable Cox proportional-hazard models (adjusted by age, sex, influenza vaccine status, presence of comorbidities and cardiovascular risk factors). Results Cohort members were followed for a total of 26,444 person-years, of which 34% were for vaccinated subjects. Overall incidence rates (per 1000 person-years) were 4.9 for myocardial infarction and 4.6 for ischaemic stroke. In the multivariable analysis, vaccination was associated with a marginally significant 35% lower risk of stroke (hazard ratio [HR]: 0.65; 95% confidence interval [CI]: 0.42-0.99; p = 0.046). We found no evidence for an association between pneumococcal vaccination and reduced risk of myocardial infarction (HR: 0.83; 95% CI: 0.56-1.22; p = 0.347). Conclusions Our data supports a benefit of PPV23 against ischaemic stroke among the general population over 60 years, suggesting a possible protective role of pneumococcal vaccination against some acute thrombotic events. PMID:22436146

  17. Recovery of Monkeys After Myocardial Infarction with Ventricular Fibrillation. Effects of PGB

    DTIC Science & Technology

    1980-01-01

    Pubiishing, New cellular Comnpoinenits. G. D). Birnic, Ed. Uini- York, 1974, pp. 247-260. versity Park Press, Baltimore, 1972, pp. 42. W. Kubler and P. G...Watanabe, J. W. Covell, J. Ross , and E. 31. H. Yamazaki, M. M. Bodenheimer, V. S. Braunwald. Factors influencing infarct size Banka, J. iLewandowski

  18. Effect of Hurricane Katrina on chronobiology at onset of acute myocardial infarction during the subsequent three years.

    PubMed

    Peters, Matthew N; Katz, Morgan J; Moscona, John C; Alkadri, Mohi E; Khazi Syed, Rashad H; Turnage, Thomas A; Nijjar, Vikram S; Bisharat, Mohannad B; Delafontaine, Patrice; Irimpen, Anand M

    2013-03-15

    The onset of acute myocardial infarction (AMI) has been shown to occur in a nonrandom pattern, with peaks in midmorning and on weekdays (especially Monday). The incidence of AMI has been shown to increase locally after natural disasters, but the effect of catastrophic events on AMI biorhythms is largely unknown. To assess the differences in the chronobiology of AMI in residents of New Orleans before and after Hurricane Katrina, the onset of AMI in patients at Tulane University Health Sciences Center in the 6 years before and the 3 years after Hurricane Katrina was retrospectively examined. Compared to the pre-Katrina group, the post-Katrina cohort demonstrated significant decreases in the onset of AMI during mornings (p = 0.002), Mondays (p <0.0001), and weekdays (p <0.0001) and significant increases in onset during weekends (p <0.0001) and nights (p <0.0001). These changes persisted during all 3 years after the storm. In conclusion, the normal pattern of AMI onset was altered after Hurricane Katrina, and expected morning, weekday, and Monday peaks were eliminated.

  19. Quantitative assessment of oscillatory components in blood circulation: classification of the effect of aging, diabetes, and acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Bernjak, Alan; Stefanovska, Aneta; Urbancic-Rovan, Vilma; Azman-Juvan, Katja

    2005-04-01

    The human cardiovascular system is a complex system with the pumping activity of the heart as the main generator of oscillations. Besides the heartbeat there are several other oscillatory components which determine its dynamics. Their nonlinear nature and a weak coupling between them both require special treatment while studying this system. A particular characteristic of the oscillatory components is their frequency fluctuations in time. Consequently, their interactions also fluctuate in time. Therefore the wavelet transform is applied to trace the oscillatory components in time, and specific quantitative measures are introduced to quantify the contribution of each of the oscillatory components involved on the time scale of up to three minutes. Oscillatory components are then analysed from signals obtained by simultaneous measurements of blood flow in the microcirculation, ECG, respiration and blood pressure. Based on quantitative evaluation of the oscillatory components related to (I) the heart beat (0.6-2Hz), (II) respiration (0.145-0.6Hz), (III) intrinsic myogenic activity (0.052-0.145Hz), (IV) sympathetic activity (0.021-0.052Hz), (V, VI) endothelial related activity (0.0095-0.021Hz, 0.005 - 0.0095 Hz), 30-minutes recording taken on 109 healthy subjects, 75 patients with diabetes, and 82 patients after acute myocardial infarction (AMI) were analysed. Classification of the effect of ageing, diabetes and AMI from blood flow signals simultaneously recorded in the skin of four extremities, the heart rate and heart rate variability from R-R intervals will be presented and discussed.

  20. 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.

  1. 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.

  2. 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.

  3. Design and rationale of a multicentre, randomised, double-blind, placebo-controlled clinical trial to evaluate the effect of vitamin D on ventricular remodelling in patients with anterior myocardial infarction: the VITamin D in Acute Myocardial Infarction (VITDAMI) trial

    PubMed Central

    Tuñón, José; González-Hernández, Ignacio; Llanos-Jiménez, Lucía; Alonso-Martín, Joaquín; Escudier-Villa, Juan M; Tarín, Nieves; Cristóbal, Carmen; Sanz, Petra; Pello, Ana M; Aceña, Álvaro; Carda, Rocío; Orejas, Miguel; Tomás, Marta; Beltrán, Paula; Calero Rueda, Marta; Marcos, Esther; Serrano-Antolín, José María; Gutiérrez-Landaluce, Carlos; Jiménez, Rosa; Cabezudo, Jorge; Curcio, Alejandro; Peces-Barba, Germán; González-Parra, Emilio; Muñoz-Siscart, Raquel; González-Casaus, María Luisa; Lorenzo, Antonio; Huelmos, Ana; Goicolea, Javier; Ibáñez, Borja; Hernández, Gonzalo; Alonso-Pulpón, Luis M; Farré, Jerónimo; Lorenzo, Óscar; Mahíllo-Fernández, Ignacio; Egido, Jesús

    2016-01-01

    Introduction Decreased plasma vitamin D (VD) levels are linked to cardiovascular damage. However, clinical trials have not demonstrated a benefit of VD supplements on left ventricular (LV) remodelling. Anterior ST-elevation acute myocardial infarction (STEMI) is the best human model to study the effect of treatments on LV remodelling. We present a proof-of-concept study that aims to investigate whether VD improves LV remodelling in patients with anterior STEMI. Methods and analysis The VITamin D in Acute Myocardial Infarction (VITDAMI) trial is a multicentre, randomised, double-blind, placebo-controlled trial. 144 patients with anterior STEMI will be assigned to receive calcifediol 0.266 mg capsules (Hidroferol SGC)/15 days or placebo on a 2:1 basis during 12 months. Primary objective: to evaluate the effect of calcifediol on LV remodelling defined as an increase in LV end-diastolic volume ≥10% (MRI). Secondary objectives: change in LV end-diastolic and end-systolic volumes, ejection fraction, LV mass, diastolic function, sphericity index and size of fibrotic area; endothelial function; plasma levels of aminoterminal fragment of B-type natriuretic peptide, galectin-3 and monocyte chemoattractant protein-1; levels of calcidiol (VD metabolite) and other components of mineral metabolism (fibroblast growth factor-23 (FGF-23), the soluble form of its receptor klotho, parathormone and phosphate). Differences in the effect of VD will be investigated according to the plasma levels of FGF-23 and klotho. Treatment safety and tolerability will be assessed. This is the first study to evaluate the effect of VD on cardiac remodelling in patients with STEMI. Ethics and dissemination This trial has been approved by the corresponding Institutional Review Board (IRB) and National Competent Authority (Agencia Española de Medicamentos y Productos Sanitarios (AEMPS)). It will be conducted in accordance with good clinical practice (International Council for Harmonisation of

  4. Loss of quality adjusted days as a trial endpoint: effect of early thrombolytic treatment in suspected myocardial infarction. Grampion Region Early Anistreplase Trial (GREAT).

    PubMed Central

    Rawles, J; Light, J

    1993-01-01

    STUDY OBJECTIVES--(1) To measure the quality of life and the loss of quality adjusted days (QADS) after suspected acute myocardial infarction in patients who received thrombolytic treatment either at home or in hospital. (2) To compare the loss of QADS as a trial endpoint with the conventional endpoints of mortality and Q-wave infarction. DESIGN--Randomised double blind parallel group trial of anistreplase (30 U given intravenously) and placebo given either at home or in hospital. SETTING--Rural practices in Grampian admitting patients to teaching hospitals in Aberdeen. PATIENTS--A total of 311 patients with suspected acute myocardial infarction and no contraindications to thrombolytic treatment seen at home within four hours of the onset of symptoms. MEASUREMENTS AND MAIN RESULTS--Loss of quality adjusted days (QADS) in the first 100 days after suspected myocardial infarction (365 QADS = 1 QALY) was the main outcome measure. Compared with later administration in hospital, anistreplase at home resulted in a relative reduction of mortality of 49% (95% confidence interval 3.95%, 2p = 0.04), and a relative reduction of 26% in the proportion of survivors with infarction who had Q-waves (95% CI 7.44%, 2p = 0.007). During the 100 day follow up, the median loss of QADS was 25 for all patients. This loss was significantly greater in those who died than in survivors (65 v 18, 2p < 0.001), and in survivors with infarction than in survivors without infarction (26 v 13, 2p < 0.01). However, there was no significant difference in loss of QADS in those with infarction with or without Q-waves (29 v 21, NS), and the median loss of QADS was not significantly different in those who had thrombolytic treatment at home or in hospital (median difference 0, 95% CI -5, +4 QADS). CONCLUSIONS--Loss of QADS had two serious limitations as an outcome measure: it was less sensitive than mortality and it failed to reflect physiological benefit. Palliative treatment with no physiological effect

  5. 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

  6. 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.

  7. Cost-effectiveness of a European ST-segment elevation myocardial infarction network: results from the Catalan Codi Infart network

    PubMed Central

    Bosch, Julia; Martín-Yuste, Victoria; Rosas, Alba; Faixedas, Maria Teresa; Gómez-Hospital, Joan Antoni; Figueras, Jaume; Curós, Antoni; Cequier, Angel; Goicolea, Javier; Fernández-Ortiz, Antonio; Macaya, Carlos; Tresserras, Ricard; Pellisé, Laura; Sabaté, Manel

    2015-01-01

    Objectives To evaluate the cost-effectiveness of the ST-segment elevation myocardial infarction (STEMI) network of Catalonia (Codi Infart). Design Cost-utility analysis. Setting The analysis was from the Catalonian Autonomous Community in Spain, with a population of about 7.5 million people. Participants Patients with STEMI treated within the autonomous community of Catalonia (Spain) included in the IAM CAT II-IV and Codi Infart registries. Outcome measures Costs included hospitalisation, procedures and additional personnel and were obtained according to the reperfusion strategy. Clinical outcomes were defined as 30-day avoided mortality and quality-adjusted life-years (QALYs), before (N=356) and after network implementation (N=2140). Results A substitution effect and a technology effect were observed; aggregate costs increased by 2.6%. The substitution effect resulted from increased use of primary coronary angioplasty, a relatively expensive procedure and a decrease in fibrinolysis. Primary coronary angioplasty increased from 31% to 89% with the network, and fibrinolysis decreased from 37% to 3%. Rescue coronary angioplasty declined from 11% to 4%, and no reperfusion from 21% to 4%. The technological effect was related to improvements in the percutaneous coronary intervention procedure that increased efficiency, reducing the average length of the hospital stay. Mean costs per patient decreased from €8306 to €7874 for patients with primary coronary angioplasty. Clinical outcomes in patients treated with primary coronary angioplasty did not change significantly, although 30-day mortality decreased from 7.5% to 5.6%. The incremental cost-effectiveness ratio resulted in an extra cost of €4355 per life saved (30-day mortality) and €495 per QALY. Below a cost threshold of €30 000, results were sensitive to variations in costs and outcomes. Conclusions The Catalan STEMI network (Codi Infart) is cost-efficient. Further studies are needed in geopolitical

  8. 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.

  9. Cardioprotective effect of resveratrol analogue isorhapontigenin versus omega-3 fatty acids in isoproterenol-induced myocardial infarction in rats.

    PubMed

    Abbas, Amr M

    2016-09-01

    Myocardial infarction (MI) is a common cause of mortality worldwide. Isorhapontigenin is a derivative of stilbene with chemical structure similar to resveratrol. The omega-3 fatty acids (FA) have beneficial effects on neurodegenerative, inflammatory, and cardiovascular diseases. The aim of this study was to investigate the effects of pretreatment with isorhapontigenin and omega-3 FA on rat model of isoproterenol-induced MI. Fifty-six rats were divided into seven groups: normal, normal + isorhapontigenin, normal + omega-3 FA, MI, MI + isorhapontigenin, MI + omega-3 FA, and MI + isorhapontigenin + omega-3 FA. Serum levels of cardiac marker enzymes [lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB)], cardiac troponin I (cTnI), inflammatory markers [tumor necrosis factor-alpha (TNF-α) and interleukin-6], and lipid profile [triglycerides, total cholesterol (T.Ch), high and low density lipoproteins (HDL, LDL), and phospholipids] as well as cardiac levels of malondialdehyde and anti-oxidants [reduced glutathione (GSH), superoxide dismutase (SOD), and catalase)] were measured in all rats. ECG and histopathological examination were performed. Isoproterenol caused a significant elevation of ST segment, decreased R wave amplitude, HDL, and anti-oxidants, and increased LDH, CK-MB, cTnI, TNF-α, interleukin-6, malondialdehyde, triglycerides, T.Ch, LDL, and phospholipids. Omega-3 FA or isorhapontigenin significantly decreased the ST segment elevation, LDH, CK-MB, cTnI, TNF-α, interleukin-6, malondialdehyde, and phospholipids and increased R wave amplitude and anti-oxidants. The effects of combined omega-3 FA and isorhapontigenin were more significant than either of them alone. Therefore, we conclude that omega-3 FA and isorhapontigenin have a cardioprotective effect on rats with isoproterenol-induced MI through their anti-oxidant and anti-inflammatory actions.

  10. Cardiac rehabilitation after myocardial infarction.

    PubMed

    Contractor, Aashish S

    2011-12-01

    Cardiac rehabilitation/secondary prevention programs are recognized as integral to the comprehensive care of patients with coronary heart disease (CHD), and as such are recommended as useful and effective (Class I) by the American Heart Association and the American College of Cardiology in the treatment of patients with CHD. The term cardiac rehabilitation refers to coordinated, multifaceted interventions designed to optimize a cardiac patient's physical, psychological, and social functioning, in addition to stabilizing, slowing, or even reversing the progression of the underlying atherosclerotic processes, thereby reducing morbidity and mortality. Cardiac rehabilitation, aims at returning the patient back to normal functioning in a safe and effective manner and to enhance the psychosocial and vocational state of the patient. The program involves education, exercise, risk factor modification and counselling. A meta-analysis based on a review of 48 randomized trials that compared outcomes of exercise-based rehabilitation with usual medical care, showed a reduction of 20% in total mortality and 26% in cardiac mortality rates, with exercise-based rehabilitation compared with usual medical care. Risk stratification helps identify patients who are at increased risk for exercise-related cardiovascular events and who may require more intensive cardiac monitoring in addition to the medical supervision provided for all cardiac rehabilitation program participants. During exercise, the patients' ECG is continuously monitored through telemetry, which serves to optimize the exercise prescription and enhance safety. The safety of cardiac rehabilitation exercise programs is well established, and the occurrence of major cardiovascular events during supervised exercise is extremely low. As hospital stays decrease, cardiac rehabilitation is assuming an increasingly important role in secondary prevention. In contrast with its growing importance internationally, there are very few

  11. Hemodynamic effects of intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock: the prospective, randomized IABP shock trial.

    PubMed

    Prondzinsky, Roland; Unverzagt, Susanne; Russ, Martin; Lemm, Henning; Swyter, Michael; Wegener, Nikolas; Buerke, Ute; Raaz, Uwe; Ebelt, Henning; Schlitt, Axel; Heinroth, Konstantin; Haerting, Johannes; Werdan, Karl; Buerke, Michael

    2012-04-01

    We conducted the IABP Cardiogenic Shock Trial (ClinicalTrials.gov ID NCT00469248) as a prospective, randomized, monocentric clinical trial to determine the hemodynamic effects of additional intra-aortic balloon pump (IABP) treatment and its effects on severity of disease in patients with acute myocardial infarction complicated by cardiogenic shock (CS). Intra-aortic balloon pump counterpulsation is recommended in patients with CS complicating myocardial infarction. However, there are only limited randomized controlled trial data available supporting the efficacy of IABP following percutaneous coronary intervention (PCI) and its impact on hemodynamic parameters in patients with CS. Percutaneous coronary intervention of infarct-related artery was performed in 40 patients with acute myocardial infarction complicated by CS, within 12 h of onset of hemodynamic instability. Serial hemodynamic parameters were determined over the next 4 days and compared in patients receiving medical treatment alone with those treated with additional intra-aortic balloon counterpulsation. There were no significant differences among severity of disease (i.e., Acute Physiology and Chronic Health Evaluation II score) initially and no differences among both groups for disease improvement. We observed significant temporal improvements of cardiac output (4.8 ± 0.5 to 6.0 ± 0.5 L/min), systemic vascular resistance (926 ± 73 to 769 ± 101 dyn · s(-1) · cm(-5)), and the prognosis-validated cardiac power output (0.78 ± 0.06 to 1.01 ± 0.2 W) within the IABP group. However, there were no significant differences between the IABP group and the medical-alone group. Additional IABP treatment did not result in a significant hemodynamic improvement compared with medical therapy alone in a randomized prospective trial in patients with CS following PCI. Therefore, the use and recommendation for IABP treatment in CS remain unclear.

  12. 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

  13. Cardioprotective Effects of Essential Oil of Lavandula angustifolia on Isoproterenol-induced Acute Myocardial Infarction in Rat

    PubMed Central

    Ziaee, Mojtaba; Khorrami, Arash; Ebrahimi, Maryam; Nourafcan, Hassan; Amiraslanzadeh, Masoumeh; Rameshrad, Maryam; Garjani, Mehraveh; Garjani, Alireza

    2015-01-01

    Myocardial infarction (MI) is a common presentation of the ischemic heart disease. Lavandula angustifolia is an herbaceous plant with antioxidative effects. This study was designed to investigate the cardioprotective effects of lavandula angustifolia essential oil against isoproterenol-induced MI in rats. The dried sample was subjected to hydrodistillation by using a Clevenger and the oils were dried over anhydrous Na2SO4. Male Wistar rats were assigned to 6 groups of control, sham, isoproterenol and treatment with 5, 10, 20 mg/Kg of the essential oil. MI was induced by subcutaneous injection of Isoproterenol (100 mg/Kg) for 3 consecutive days at an interval of 24 h. The essential oil was given intraperitoneally every 24 h started at MI induction. Following anesthesia, hemodynamic parameters were measured. After sacrificing the animals, the hearts were removed to measure the heart to body weight ratio and histopathological examination. Myeloperoxidase (MPO) and Malondialdehyde (MDA) were measured in heart tissues for evaluating the activity of neutrophils and lipid peroxidation, respectively. The essential oil amended ECG pattern by suppressing ST-segment elevation and increasing R-amplitude. 10 mg/Kg of the essential oil significantly decreased heart to body weight ratio (P<0.001) and the elevation of MDA and MPO in myocardium, it also increased dp/dtmax from 2793 ± 210 to 4488 ± 253 mmHg/sec (P<0.001), and 20 mg/Kg of it significantly lowered LVEDP from 14 ± 3.43 to 4.3 ± 0.83 mmHg (P<0.001).The results demonstrated that L. angustifolia protects myocardium against isoproterenol-induced MI that it could be related to its antioxidant properties. PMID:25561934

  14. Effects of paroxetine-mediated inhibition of GRK2 expression on depression and cardiovascular function in patients with myocardial infarction

    PubMed Central

    Tian, Xiuqing; Wang, Qing; Guo, Rui; Xu, Lingling; Chen, Qin M; Hou, Yinglong

    2016-01-01

    Background Paroxetine is a selective serotonin reuptake inhibitor utilized in the treatment of depression and anxiety disorders. Recent studies have identified paroxetine as a G protein-coupled receptor kinase-2 (GRK2) inhibitor capable of reversing cardiac dysfunction and remodeling in experimental models of acute myocardial infarction (AMI). We determine the clinical importance of paroxetine on cardiac functions in patients having AMI with depression (AMID) in comparison with fluoxetine, an unrelated selective serotonin reuptake inhibitor that does not inhibit GRK2. Methods Diagnosis of depression was based on the 17-item Hamilton Depression Scale and Self-rating Depression Scale in AMI patients after hospital admission. AMID patients were randomly assigned to paroxetine or fluoxetine for treatment of depression. Heart rate variability and cardiac function were evaluated. GRK2 protein levels were measured using peripheral lymphocytes and Western blot. Results GRK2 expression in AMID patients was significantly higher than that in AMI patients without depression. In AMID patients, GRK2 levels were positively correlated with the 17-item Hamilton Depression Scale and the Self-rating Depression Scale scores, and negatively correlated with heart rate variability. Treatment of AMID patients with paroxetine significantly reduced the expression of GRK2, normalized the autonomic nervous system function, and improved cardiac performance. In contrast, fluoxetine normalized the autonomic nervous system but did not reduce the expression of GRK2 nor improved cardiac performance. Conclusion This study suggests that paroxetine is effective for improving cardiac function in patients with AMID and such effect correlates with GRK2 reduction. PMID:27695334

  15. Effect of chronic blockade of angiotensin II-receptor subtypes on aortic compliance in rats with myocardial infarction.

    PubMed

    Ceiler, D L; Nelissen-Vrancken, H J; De Mey, J G; Smits, J F

    1998-04-01

    This study was undertaken to investigate changes in aortic geometry and compliance after long-term blockade of angiotensin receptors type 1 (AT1) and AT2 receptors under basal conditions and after myocardial infarction (MI). Sham-operated (sham) or MI rats received either no treatment, AT1 antagonist GR138950C (GR; 2 mg/kg/day i.v.), or AT2 antagonist PD123319 (PD; 3 mg/kg/day s.c.). After 3 weeks, mean arterial blood pressure (MAP) was measured. Thoracic aorta diastolic diameter (D[dia]), compliance coefficient (CC), and distensibility coefficient (DC) were determined noninvasively in anesthetized rats by using ultrasound and wall tracking. After the rats were killed, histologic measurements were made on aortic cross sections. In sham rats, MAP was reduced by GR treatment (76 +/- 6 vs. 106 +/- 5 mm Hg), but not by PD. D(dia) was reduced in both GR-treated (1.74 +/- 0.08 vs. 2.09 +/- 0.05 mm) and PD-treated (1.83 +/- 0.05 vs. 2.09 +/- 0.05 mm) sham rats. CC and DC were not modified by either treatment. Although media cross-sectional area was not affected by either GR or PD treatment in sham rats, media thickness and media/lumen ratio were increased in both cases. Induction of MI had no effect on aortic structure, geometry, or mechanics; however, treatment with either GR or PD improved DC versus untreated MI rats. We conclude that AT1 and AT2 receptors are involved in angiotensin II-mediated effects on aortic geometry and mechanics under both basal conditions and after MI. Whereas blockade of AT1 receptors most likely influences vascular properties through a depressor mechanism, AT2 receptors induce pressure-independent remodeling.

  16. 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.

  17. 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

  18. Effect of Hurricane Katrina on incidence of acute myocardial infarction in New Orleans three years after the storm.

    PubMed

    Jiao, Zhen; Kakoulides, Socrates V; Moscona, John; Whittier, Jabar; Srivastav, Sudesh; Delafontaine, Patrice; Irimpen, Anand

    2012-02-15

    To detect a long-term increase in the incidence of acute myocardial infarction (AMI) after Hurricane Katrina and to investigate the pertinent contributing factors, we conducted a single-center retrospective cohort observational study. The patients admitted with AMI to Tulane University Hospital in the 2 years before Katrina and the 3 years after the hospital reopened were identified from the hospital medical records. The pre- and post-Katrina groups were compared for prespecified demographic and clinical data. In the 3-year post-Katrina group, 418 admissions (2.0%) for AMI occurred of a total census of 21,092 patients compared to 150 (0.7%) of a census of 21,079 in the 2-year pre-Katrina group (p <0.0001). The post-Katrina group had a greater prevalence of unemployment (p <0.0001), lack of medical insurance (p <0.001), smokers (p <0.01), medical noncompliance (p <0.0001), first-time hospitalizations (p <0.001), history of coronary artery disease (p <0.01), multiple vessel disease (p <0.05), and percutaneous coronary interventions (p <0.0001). The mean age of onset of AMI decreased from 62 years before Katrina to 59 years after Katrina (p <0.05), and a significantly greater percentage of patients were men (p <0.05). No significant differences were found between the two groups in terms of race, substance abuse, and a history of hypertension or diabetes mellitus. Our data suggest that chronic stress after natural disasters may significantly affect cardiovascular risk factors such as tobacco abuse and increase medical noncompliance. In conclusion, our data is consistent with a significant change in the overall health of the population and support the need for additional study into the health effects of chronic stress after natural disasters.

  19. Comparison of the Effects of Cardiac Rehabilitation Between Obese and Non-obese Patients After Acute Myocardial Infarction

    PubMed Central

    2016-01-01

    Objective To evaluate the effects of cardiac rehabilitation (CR) on functional capacity in obese and non-obese patients who have suffered acute myocardial infarction (AMI). Methods Overall, 359 patients who have suffered AMI, and were referred for CR after percutaneous coronary intervention from 2010 to 2015 and underwent an exercise tolerance test before and after phase II CR were included in this study. The patients were divided into two groups: obese group with body mass index (BMI) ≥25 kg/m2 (n=170; age, 54.32±9.98 years; BMI, 27.52±2.92 kg/m2) and non-obese group with BMI <25 kg/m2 (n=189; age, 59.12±11.50 years; BMI 22.86±2.01 kg/m2). The demographic characteristics and cardiopulmonary exercise capacity of all patients were analyzed before and after CR. Results There were significant changes in resting heart rate (HRrest) before and after CR between the obese and non-obese groups (before CR, p=0.028; after CR, p=0.046), but other cardiopulmonary exercise capacity before and after CR was not different between the groups. HRrest (p<0.001), maximal metabolic equivalents (METs, p<0.001), total exercise duration (TED, p<0.001), and maximal oxygen consumption (VO2max, p<0.001) improved significantly in the obese and non-obese groups after CR. No difference in the change in the cardiopulmonary exercise capacity rate was detected between the groups. Conclusion CR may improve functional capacity in patients who suffered AMI regardless of their obesity. PMID:27847723

  20. The effect of multiple analysers on the biochemical diagnosis of myocardial infarction using a contemporary troponin-I assay.

    PubMed

    Pethick, James; Patel, Prashanth; Davies, Timothy; Thompson, John; Nallagonda, Madhavi; Beech, Alison; Collinson, Paul; Lee, Virginia; Gupta, Pankaj

    2016-11-01

    Background The measurement of cardiac troponin is central for the diagnosis of myocardial infarction (MI). It is recommended that a coefficient of variation of ≤10% is achieved at the diagnostic threshold and significant change between serial measurements reported. Many modern laboratories use multiple analysers linked by automation where samples are randomly assigned to an analyser. It is therefore important to consider the combined effect of all analysers on the analytical performance of troponin measurement. Method The performance of a contemporary troponin-I (cTn-I) assay run on three analysers, linked by an automated track, was undertaken across a range of cTn-I concentrations. The data for the three analysers were aggregated to obtain the combined analytical coefficient of variation (CVA) and reference change values (RCVs). Results The CVA improved with increasing concentration and calculated RCVs ranged from 67.2% (±13 ng/L) to 32% (±160 ng/L) between cTn-I values 20 ng/L and 500 ng/L. Although there were significant differences in cTn-I measurement between analysers around the diagnostic threshold ( P < 0.05), the CVA was 13.6%. Conclusions We demonstrate that there are significant differences between the performances of analysers which can impact the biochemical criteria for the diagnosis of MI. We also show that the RCV varies according to baseline cTn-I values and that reporting a single RCV across the analytical range of cTn-I may not be appropriate.

  1. Effects of Treatment with Zofenopril in Men and Women with Acute Myocardial Infarction: Gender Analysis of the SMILE Program

    PubMed Central

    Franconi, Flavia; Omboni, Stefano; Ambrosioni, Ettore; Reggiardo, Giorgio; Campesi, Ilaria; Borghi, Claudio

    2014-01-01

    Background the SMILE studies proved the prognostic benefit of zofenopril vs. placebo or other ACE-inhibitors (ACEIs) in post-acute myocardial infarction (AMI). In this retrospective pooled analysis of these studies we assessed whether the zofenopril effect is influenced by gender. Methods the four double-blind, randomized, parallel-group SMILE studies, compared the efficacy and safety of 6–48 week treatment with zofenopril 60 mg/day with that of placebo, lisinopril 10 mg/day or ramipril 10 mg/day in 3630 AMI patients. This pooled analysis compared treatment efficacy (1-year combined occurrence of death or hospitalization for CV causes) in 2733 men and 897 women. Results women were older than men, had a higher prevalence of diabetes and of other major CV risk factors. The risk of a major CV event was significantly larger for women (23% vs. 17% men, p<0.001). Between-gender risk difference was more marked for people living in Southern (+54%) than in Northern Europe (+12%). In both genders zofenopril similarly reduced the 1-year risk of CV morbidity and mortality vs. placebo (−39% men, p = 0.0001; −40% women, p = 0.005). The risk reduction was more marked with zofenopril than with the other ACEIs, particularly in men (−27%, p = 0.012; women: −14%, p = 0.479). The drug safety profile was similar between genders in zofenopril-treated patients, while it was worse in women treated with other ACEIs. Conclusions post-AMI women are at higher risk of CV complications than men, particularly when living in Mediterranean countries. Their response to ACE-inhibition varies according to the type of drug and is usually better in men. PMID:25364906

  2. A Mendelian randomization study of the effect of calcium on coronary artery disease, myocardial infarction and their risk factors

    PubMed Central

    Xu, Lin; Lin, Shi Lin; Schooling, C. Mary

    2017-01-01

    Meta-analyses of randomized controlled trials (RCTs) suggest calcium could have adverse effects on cardiovascular disease, although these findings are controversial. To clarify, we assessed whether people with genetically higher calcium had a higher risk of coronary artery disease (CAD), myocardial infarction (MI) and their risk factors. We used a two-sample Mendelian randomization study. We identified genetic variants (single nucleotide polymorphisms (SNPs)) that independently contributed to serum calcium at genome-wide significance which we applied to large extensively genotyped studies of CAD, MI, diabetes, lipids, glycaemic traits and adiposity to obtain unconfounded estimates, with body mass index (BMI) as a control outcome. Based on 4 SNPs each 1 mg/dl increase in calcium was positively associated with CAD (odds ratio (OR) 1.49, 95% confidence interval (CI) 1.02–2.17), MI (OR 1.58, 95% CI 1.06–2.35), LDL-cholesterol (0.21 standard deviations, 95% CI 0.01–0.4), total cholesterol (0.21 standard deviations, 95% CI 0.03-0.38) and possibly triglycerides (0.19 standard deviations, 95% CI −0.1–0.48), but was unlikely related to BMI although the estimate lacked precision. Sensitivity analysis using 13 SNPs showed a higher risk for CAD (OR 1.87, 95% CI 1.14–3.08). Our findings, largely consistent with the experimental evidence, suggest higher serum calcium may increase the risk of CAD. PMID:28195141

  3. 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.

  4. 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.

  5. [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.

  6. 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.

  7. [Protective effect of peptide semax (ACTH(4-7)Pro-Gly-Pro) on the rat heart rate after myocardial infarction].

    PubMed

    Gavrilova, S A; Golubeva, A V; Lipina, T V; Fominykh, E S; Shornikova, M V; Postnikov, A B; Andrejeva, L A; Chentsov, Iu S; Koshelev, V B

    2006-11-01

    Semax, a member of ACTH-derived peptides family, was used in treatment of ischemic stroke in patients. It decreased neurological deficiency and reduced NO hyperproduction in the rat brain caused by acute cerebral hypoperfusion. We suggest that semax is also capable of protecting the rat heart from ischemic damage 28 days after myocardial infarction (MI) induced by left descendent coronary artery occlusion. Semax (150 microg/kg) was given i. p. in the operating day twice: 15 min and 2 hours after coronary occlusion, and once a day for the following 6 days. In 28 days after infarction, the MI group developed cardiac hypertrophy, cell growth was caused mainly by the increase of contractile filaments not supported by the appropriate mitochondrial growth that indicated an impaired energy supply of the cells. Moreover, cardiac hypertrophy was accompanied by decreased mean arterial blood pressure and cardiac contractile function and increased left ventricular end-diastolic pressure. Pharmacological change of cardiac afterload revealed that, in 28 days after MI, the rat heart was not able to change its contractile performance in response to either increase or decrease of systemic blood pressure, and as a result could not maintain its diastolic pressure. All these changes obviously reflect development of heart failure. Semax did not affect cardiac work but partially prevented end-diastolic pressure growth in left ventricle as well as ameliorated cardiomyocyte hypertrophy and disproportionate growth of contractile and mitochondrial apparatus, thus exerting beneficial effect on the left ventricular remodeling and heart failure development late after myocardial infarction.

  8. 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

  9. 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

  10. 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.

  11. 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

  12. 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

  13. 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.

  14. Safety and Effectiveness of Statins for Prevention of Recurrent Myocardial Infarction in 12 156 Typical Older Patients: A Quasi-Experimental Study

    PubMed Central

    Hughes, Peter M.; Delgado, Joao; Masoli, Jane A.; Bowman, Kirsty; Zirk-Sadowski, Jan; Mujica Mota, Ruben E.; Henley, William E.; Melzer, David

    2017-01-01

    Background: There is limited evidence on statin risk and effectiveness for patients aged 80+. We estimated risk of recurrent myocardial infarction, muscle-related and other adverse events, and statin-related incremental costs in “real-world” older patients treated with statins versus no statins. Methods: We used primary care electronic medical records from the UK Clinical Practice Research Datalink. Subhazard ratios (competing risk of death) for myocardial infarction recurrence (primary end point), falls, fractures, ischemic stroke, and dementia, and hazard ratios (Cox) for all-cause mortality were used to compare older (60+) statin users and 1:1 propensity-score-matched controls (n = 12,156). Participants were followed-up for 10 years. Results: Mean age was 76.5±9.2 years; 45.5% were women. Statins were associated with near significant reduction in myocardial infarction recurrence (subhazard ratio = 0.84, 0.69–1.02, p = .073), with protective effect in the 60–79 age group (0.73, 0.57–0.94) but a nonsignificant result in the 80+ group (1.06, 0.78–1.44; age interaction p = .094). No significant associations were found for stroke or dementia. Data suggest an increased risk of falls (1.36, 1.17–1.60) and fractures (1.33, 1.04–1.69) in the first 2 years of treatment, particularly in the 80+ group. Treatment was associated with lower all-cause mortality. Statin use was associated with health care cost savings in the 60–79 group but higher costs in the 80+ group. Conclusions: Estimates of statin effectiveness for the prevention of recurrent myocardial infarction in patients aged 60–79 years were similar to trial results, but more evidence is needed in the older group. There may be an excess of falls and fractures in very old patients, which deserves further investigation. PMID:27146371

  15. 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

  16. 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.

  17. 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.

  18. Correlation between oxidative stress and alteration of intracellular calcium handling in isoproterenol-induced myocardial infarction.

    PubMed

    Díaz-Muñoz, Mauricio; Alvarez-Pérez, Marco Antonio; Yáñez, Lucía; Vidrio, Susana; Martínez, Lidia; Rosas, Gisele; Yáñez, Mario; Ramírez, Sotero; de Sánchez, Victoria Chagoya

    2006-09-01

    Myocardial Ca(2+) overload and oxidative stress are well documented effects associated to isoproterenol (ISO)-induced myocardial necrosis, but information correlating these two issues is scarce. Using an ISO-induced myocardial infarction model, 3 stages of myocardial damage were defined: pre-infarction (0-12 h), infarction (12-24 h) and post-infarction (24-96 h). Alterations in Ca(2+) homeostasis and oxidative stress were studied in mitochondria, sarcoplasmic reticulum and plasmalemma by measuring the Ca(2+) content, the activity of Ca(2+) handling proteins, and by quantifying TBARs, nitric oxide (NO) and oxidative protein damage (changes in carbonyl and thiol groups). Free radicals generated system, antioxidant enzymes and oxidative stress (GSH/GSSG ratio) were also monitored at different times of ISO-induced cardiotoxicity. The Ca(2+) overload induced by ISO was counterbalanced by a diminution in the ryanodine receptor activity and the Na(+)-Ca(+2) exchanger as well as by the increase in both calcium ATPases activities (vanadate- and thapsigargine-sensitive) and mitochondrial Ca(2+) uptake during pre-infarction and infarction stages. Pro-oxidative reactions and antioxidant defences during the 3 stages of cardiotoxicity were observed, with maximal oxidative stress during the infarction. Significant correlations were found among pro-oxidative reactions with plasmalemma and sarcoplasmic reticulum Ca(2+) ATPases, and ryanodine receptor activities at the onset and development of ISO-induced infarction. These findings could be helpful in the design of antioxidant therapies in this pathology.

  19. [Acute myocardial infarction in a 5-year-old boy].

    PubMed

    Romero Ibarra, C; Bueno Campaña, M; Barriuso Lapresa, L M; de Miguel Medina, C; Maraví Poma, E

    1996-11-01

    We present the case of a child five and half years-old that died suddenly due to an acute myocardial infarction. The anatomopathological study showed a total obstruction of the left coronary ostium by mixoide dysplasia of the aortic valve. We revise the literature and briefly expose the more frequent causes of infarction in infancy.

  20. 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.

  1. [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.

  2. 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.

  3. 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.

  4. 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.

  5. 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

  6. Beneficial effects of intracoronary thrombolysis up to eighteen hours after onset of pain in evolving myocardial infarction

    SciTech Connect

    Smalling, R.W.; Fuentes, F.; Freund, G.C.; Reduto, L.A.; Wanta-Matthews, M.; Gaeta, J.M.; Walker, W.; Sterling, R.; Gould, K.L.

    1982-10-01

    Coronary arteriography and intracoronary streptokinase (STK) infusion were performed on 89 patients with evolving acute myocardial infarction (AMI). Ventricular function was followed in these patients during their hospitalization by gated radionuclide ventriculography. In 35 of these patients thallium imaging was performed on admission and 4 hours after reperfusion. An additional 30 patients with AMI who either met exclusion criteria for the STK protocol or refused study served as a control group. In patients admitted 0 to 6, 6 to 12, or 12 to 18 hours after onset of pain, there was no difference in change in left ventricular ejection fraction (LVEF) from admission to discharge, in percent of patients with total occlusion demonstrating reperfusion, or in percent of patients demonstrating a significant increase in LVEF. The average increase in LVEF from admission to discharge in patients reperfused ws 8% (40% +/- 14% to 48% +/- 13%, p less than 0.001). No change in LVEF was demonstrated in the control population or in patients in whom coronary reperfusion was unsuccessful. Reperfusion produced an increase in thallium uptake in the infarct-related myocardium that was accompanied by an improvement in regional function. Failure of reperfusion produced no change in either thallium uptake or regional function.

  7. 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.

  8. 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.

  9. 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

  10. Alcohol intake modulates the effect of a polymorphism of the cholesteryl ester transfer protein gene on plasma high density lipoprotein and the risk of myocardial infarction.

    PubMed Central

    Fumeron, F; Betoulle, D; Luc, G; Behague, I; Ricard, S; Poirier, O; Jemaa, R; Evans, A; Arveiler, D; Marques-Vidal, P

    1995-01-01

    A polymorphism of the CETP gene (CETP/TaqIB) with two alleles B1 (60%) and B2 (40%) has been investigated in relation to lipid variables and the risk of myocardial infarction in a large case-control study (ECTIM) of men aged 25-64. No association was observed between the polymorphism and LDL or VLDL related lipid variables. Conversely, B2 carriers had reduced levels of plasma CETP (P < 0.0001) and increased levels of HDL cholesterol (P < 0.0001) and of other HDL related lipid variables. The effects of the polymorphism on plasma CETP and HDL cholesterol were independent, suggesting the presence of at least two functional variants linked to B2. A search for these variants on the coding sequence of the CETP gene failed to identify them. The effect of B2 on plasma HDL cholesterol was absent in subjects drinking < 25 grams/d of alcohol but increased commensurably, with higher values of alcohol consumption (interaction: P < 0.0001). A similar interaction was not observed for plasma CETP. The odds-ratio for myocardial infarction of B2 homozygotes decreased from 1.0 in nondrinkers to 0.34 in those drinking 75 grams/d or more. These results provide the first demonstration of a gene-environment interaction affecting HDL cholesterol levels and coronary heart disease risk. PMID:7657837

  11. Effect of vitamin D on isoprenaline induced myocardial infarction in rats; possible role of Peroxisome Proliferator Activated Receptor- ɣ (PPAR-ɣ).

    PubMed

    El-Gohary, Ola Ahmed; Allam, Mona Maher

    2017-01-22

    Infarct-like lesion induced by isoprenaline is a well-known model to study myocardial infarction (MI). Vitamin D has been shown to have anti-inflammatory and antioxidant effects. Recent studies highlighted cross talk between vitamin D and peroxisome proliferator-activated receptor gamma (PPAR- ɣ). The present study was designed to investigate the effect of pretreatment with vitamin D on the isoprenaline-induced infarct-like lesion in rats and the role of PPAR- ɣ as a novel mechanism in vitamin D-mediated cardio protective effect. Markers chosen to assess cardiac damage included serum level of creatine kinase (CPK), lactate dehydrogenase (LDH), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Cardiac contents of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH) have been also assessed. Furthermore, ECG monitoring and measurement of injury extension were carried out. Isoprenaline increased the level of cardiac enzymes as well as inflammatory and oxidative stress biomarkers. In addition, it produced ST-segment elevation. Pretreatment with vitamin D significantly improved previous parameters. The prior treatment with PPAR- ɣ antagonist; bisphenol A diglycidyl ether; (BADGE) significantly attenuated the protective effect of vitamin D. In conclusion, vitamin D can be demonstrated as a promising cardio-protective agent in MI and PPAR- ɣ significantly contributes toward vitamin D-mediated protection.

  12. Mitochondrially targeted Endonuclease III has a powerful anti-infarct effect in an in vivo rat model of myocardial ischemia/reperfusion

    PubMed Central

    Yang, Xi-Ming; Cui, Lin; White, James; Kuck, Jamie; Ruchko, Mykhaylo V.; Wilson, Glenn L.; Alexeyev, Mikhail; Gillespie, Mark N.; Downey, James M.

    2016-01-01

    Recent reports indicate that elevating DNA glycosylase/AP lyase repair enzyme activity offers marked cytoprotection in cultured cells and a variety of injury models. In this study, we measured the effect of EndoIII, a fusion protein construct that traffics Endonuclease III, a DNA glycosylase/AP lyase, to the mitochondria, on infarct size in a rat model of myocardial ischemia/reperfusion. Open-chest, anesthetized rats were subjected to 30 min of occlusion of a coronary artery followed by 2 h of reperfusion. An intravenous bolus of EndoIII, 8 mg/kg, just prior to reperfusion reduced infarct size from 43.8 ± 1.4 % of the risk zone in control animals to 24.0 ± 1.3 % with no detectable hemodynamic effect. Neither EndoIII’s vehicle nor an enzymatically inactive EndoIII mutant (K120Q) offered any protection. The magnitude of EndoIII’s protection was comparable to that seen with the platelet aggregation inhibitor cangrelor (25.0 ± 1.8 % infarction of risk zone). Because loading with a P2Y12 receptor blocker to inhibit platelets is currently the standard of care for treatment of acute myocardial infarction, we tested whether EndoIII could further reduce infarct size in rats treated with a maximally protective dose of cangrelor. The combination reduced infarct size to 15.1 ± 0.9 % which was significantly smaller than that seen with either cangrelor or EndoIII alone. Protection from cangrelor but not EndoIII was abrogated by pharmacologic blockade of phosphatidylinositol-3 kinase or adenosine receptors indicating differing cellular mechanisms. We hypothesized that EndoIII protected the heart from spreading necrosis by preventing the release of proinflammatory fragments of mitochondrial DNA (mtDNA) into the heart tissue. In support of this hypothesis, an intravenous bolus at reperfusion of deoxyribonuclease I (DNase I) which should degrade any DNA fragments escaping into the extracellular space was as protective as EndoIII. Furthermore, the combination of EndoIII and

  13. A Meta-analysis of the effects of Exercise Training on Left Ventricular Remodeling Following Myocardial Infarction: Start early and go longer for greatest exercise benefits on remodeling

    PubMed Central

    2011-01-01

    Background The effects of variations in exercise training on Left ventricular (LV) remodeling in patients shortly after Myocardial Infarction (MI) are important but poorly understood. Methods Systematic review incorporating meta-analysis using meta-regression. Studies were identified via systematic searches of: OVID MEDLINE (1950 to 2009), Cochrane Central Register of Controlled Trials (1991 to 2009), AMED (1985 to 2009), EMBASE (1988 to 2009), PUBMED (1966 to 2009), SPORT DISCUS (1975 to 2009), SCOPUS (1950 to 2009) and WEB OF SCIENCE (1950 to 2009) using the medical subject headings: myocardial infarction, post myocardial infarction, post infarction, heart attack, ventricular remodeling, ventricular volumes, ejection fraction, left ventricular function, exercise, exercise therapy, kinesiotherapy, exercise training. Reference lists of all identified studies were also manually searched for further relevant studies. Studies selected were randomized controlled trials of exercise training interventions reporting ejection fraction (EF) and/or ventricular volumes in patients following recent MI (≤ 3 months) post-MI patients involving control groups. Studies were excluded if they were not randomized, did not have a 'usual-care' control (involving no exercise), evaluated a non-exercise intervention, or did not involve human subjects. Non-English studies were also excluded. Results After screening of 1029 trials, trials were identified that reported EF (12 trials, n = 647), End Systolic Volumes (ESV) (9 trials, n = 475) and End Diastolic Volumes (EDV) (10 trials, n = 512). Meta-regression identified that changes in EF effect size difference decreased as the time between MI and initiation of the exercise program lengthened, and increased as the duration of the program increased (Q = 25.48, df = 2, p < 0.01, R2 = 0.76). Greater reductions in ESV and EDV (as indicated by effect size decreases) occurred with earlier initiation of exercise training and with longer training

  14. 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.

  15. 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.

  16. [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.).

  17. Effect of a real-time tele-transmission system of 12-lead electrocardiogram on the first-aid for athletes with ST-elevation myocardial infarction.

    PubMed

    Zhang, Huan; Song, Donghan; An, Lina

    2016-05-01

    To study the effect of a real-time tele-transmission system of 12-lead electrocardiogram on door-to-balloon time in athletes with ST-elevation myocardial infarction. A total of 60 athletes with chest pain diagnosed as ST-elevation myocardial infarction (STEMI) from our hospital were randomly divided into group A (n=35) and group B (n=25), the patients in group A transmitted the real-time tele-transmission system of 12-lead electrocardiogram to the chest pain center before arriving in hospital, however, the patients in group B not. The median door-to-balloon time was significant shorter in-group A than group B (38min vs 94 min, p<0.01) and the ratio of door-to-balloon time below 90 min was remarkable higher in-group A (94.2% vs 60%, p<0.01). The rate of catheter laboratory occupied was 5.7% in-group A and 40% in group B respectively (p=0.001). There was no statistically difference in mortality between the two groups (5.7% vs 4%, p>0.05). The median length of stay was significant reduced in-group A (5 days vs 7 days, p<0.01). Real-time tele-transmission system of 12 lead electrocardiogram is beneficial to the pre-hospital diagnosis of STEMI.

  18. 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.

  19. 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.

  20. 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

  1. Pharmacologic Effects of Cannabidiol on Acute Reperfused Myocardial Infarction in Rabbits: Evaluated With 3.0T Cardiac Magnetic Resonance Imaging and Histopathology.

    PubMed

    Feng, Yuanbo; Chen, Feng; Yin, Ting; Xia, Qian; Liu, Yewei; Huang, Gang; Zhang, Jian; Oyen, Raymond; Ni, Yicheng

    2015-10-01

    Cannabidiol (CBD) has anti-inflammatory effects. We explored its therapeutic effects on cardiac ischemia-reperfusion injury with an experimental imaging platform. Reperfused acute myocardial infarction (AMI) was induced in rabbits with a 90-minute coronary artery occlusion followed by 24-hour reperfusion. Before reperfusion, rabbits received 2 intravenous doses of 100 μg/kg CBD (n = 10) or vehicle (control, n = 10). Evans blue was intravenously injected for later detection of the AMI core. Cardiac magnetic resonance imaging was performed to evaluate cardiac morphology and function. After euthanasia, blood troponin I (cTnI) was assessed, and the heart was excised and infused with multifunctional red iodized oil dye. The heart was sliced for digital radiography to quantify the perfusion density rate, area at risk (AAR), and myocardial salvage index, followed by histomorphologic staining. Compared with controls, CBD treatment improved systolic wall thickening (P < 0.05), significantly increased blood flow in the AAR (P < 0.05), significantly decreased microvascular obstruction (P < 0.05), increased the perfusion density rate by 1.7-fold, lowered the AMI core/AAR ratio (P < 0.05), and increased the myocardial salvage index (P < 0.05). These improvements were associated with reductions in serum cTnI, cardiac leukocyte infiltration, and myocellular apoptosis (P < 0.05). Thus, CBD therapy reduced AMI size and facilitated restoration of left ventricular function. We demonstrated that this experimental platform has potential theragnostic utility.

  2. 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

  3. 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

  4. 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.

  5. 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.

  6. 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.

  7. Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice

    PubMed Central

    Fiechter, Danielle; Kats, Suzanne; Brands, Ruud; van Middelaar, Ben; Pasterkamp, Gerard; de Kleijn, Dominique; Seinen, Willem

    2011-01-01

    Background There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphorylation of the lipid A moiety of lipopolysaccharide. The aim of this study was to investigate the effect of bovine intestinal alkaline phosphatase on reducing inflammation after acute myocardial infarction. Methods Just before permanent ligation of the left anterior descending coronary (LAD) artery to induce acute myocardial infarction in Balb/c mice, bovine intestinal alkaline phosphatase (bIAP) was administrated intravenously. After 4 hours, mice were sacrificed and the inflammatory response was assessed. Acute myocardial infarction induced the production of different cytokines, which were measured in blood. Results Treatment with bovine intestinal alkaline phosphatase resulted in a significant reduction of the pro-inflammatory cytokines IL-6, IL-1β and the chymase mouse mast cell protease-1. No difference in the production of the anti-inflammatory cytokine IL-10 was observed between the control group and the bovine intestinal alkaline phosphatase treated group. Conclusion In a mouse model of permanent LAD coronary artery ligation, bIAP diminishes the pro-inflammatory responses but does not have an effect on the anti-inflammatory response in the acute phase after acute myocardial infarction.

  8. Enhanced cardioprotective effects mediated by plasmid containing the short-hairpin RNA of angiotensin converting enzyme with a biodegradable hydrogel after myocardial infarction.

    PubMed

    Wan, Wei-Guo; Jiang, Xue-Jun; Li, Xiao-Yan; Zhang, Cui; Yi, Xin; Ren, Shan; Zhang, Xian-Zheng

    2014-10-01

    The expression of foreign gene was enhanced and prolonged by sustained releasing a target gene to cells from biodegradable dextran-poly(e-caprolactone)-2-hydroxylethylmethacrylate-poly(N-isopropylacrylamide) (Dex-PCL-HEMA/PNIPAAm) hydrogel in vitro. Moreover, we have demonstrated that injection of the same hydrogel improved post-infarct ventricular remodeling. Therefore, we hypothesized that intramyocardial injection of plasmid containing the short-hairpin RNA (shRNA) of angiotensin converting enzyme (ACE) with the same hydrogel enhances the cardioprotective effects superior to either alone or after rat myocardial infarction (MI). In this study, equal volume of phosphate-buffered solution (PBS), 10 μg ACE-shRNA plasmids, hydrogel containing 10 μg negative control ACE-shRNA plasmids and hydrogel containing 10 μg ACE-shRNA plasmids were shortly injected into the infarct area of rats after MI, respectively. We found that ACE-shRNA plasmid-loaded hydrogel extended the duration of gene expression in vivo. Moreover, it was shown that direct intramyocardial injection of ACE-shRNA plasmid-loaded hydrogel significantly decreased the expression of local ACE expression, inhibited cell apoptosis, reduced infarct size, and improved cardiac function compared with the injection of either alone 30 days after MI in rats. These results suggest that injection of ACE-shRNA plasmid-loaded hydrogel into impaired myocardium obtains more cardioprotective effects than either alone in rat with MI by prolonging the gene silencing of ACE. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 3452-3458, 2014.

  9. [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.

  10. 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.

  11. [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.

  12. Dipyridamole 201Tl scintigraphy in the evaluation of prognosis after myocardial infarction

    SciTech Connect

    Okada, R.D.; Glover, D.K.; Leppo, J.A. )

    1991-09-01

    Dipyridamole 201Tl imaging has been proposed as an alternative to exercise ECG testing for the prehospital discharge evaluation of patients recovering from myocardial infarction. The rationale is that many postinfarction patients with exercise-induced ischemia experience later cardiac events, and the sensitivity of predischarge exercise ECG testing in patients with multivessel disease ranges from only 45% to 62%. In addition, several groups of investigators have shown the sensitivity of submaximum exercise 201Tl imaging to be less than ideal. This report summarizes the current status of dipyridamole 201Tl imaging in the period of 1-13 days after myocardial infarction. Although the number of studies performed to date is limited, the following conclusions can be drawn: dipyridamole 201Tl imaging after myocardial infarction was associated with no serious side effects, and those present could be quickly reversed with aminophylline; redistribution with dipyridamole 201Tl images definitely correlates with prognosis after uncomplicated myocardial infarction; dipyridamole 201Tl imaging is definitely useful in patients unable to exercise for a variety of reasons; and future studies are definitely indicated to further define the role of dipyridamole 201Tl imaging for assessing prognosis, especially in those patients undergoing interventional therapy after acute myocardial infarction.

  13. Rationale and design of the CAPAMIS study: Effectiveness of pneumococcal vaccination against community-acquired pneumonia, acute myocardial infarction and stroke

    PubMed Central

    2010-01-01

    Background The 23-valent polysaccharide pneumococcal vaccine (PPV-23) is recommended for elderly and high-risk people, although its effectiveness is controversial. Some studies have reported an increasing risk of acute vascular events among patients with pneumonia, and a recent case-control study has reported a reduction in the risk of myocardial infarction among patients vaccinated with PPV-23. Given that animal experiments have shown that pneumococcal vaccination reduces the extent of atherosclerotic lesions, it has been hypothesized that PPV-23 could protect against acute vascular events by an indirect effect preventing pneumonia or by a direct effect on oxidized low-density lipoproteins. The main objective of this study is to evaluate the clinical effectiveness of PPV-23 in reducing the risk of pneumonia and acute vascular events (related or nonrelated with prior pneumonia) in the general population over 60 years. Methods/Design Cohort study including 27,000 individuals 60 years or older assigned to nine Primary Care Centers in the region of Tarragona, Spain. According to the reception of PPV-23 before the start of the study, the study population will be divided into vaccinated and nonvaccinated groups, which will be followed during a consecutive 30-month period. Primary Care and Hospitals discharge databases will initially be used to identify study events (community-acquired pneumonia, hospitalisation for acute myocardial infarction and stroke), but all cases will be further validated by checking clinical records. Multivariable Cox regression analyses estimating hazard ratios (adjusted for age, sex and comorbidities) will be used to estimate vaccine effectiveness. Discussion The results of the study will contribute to clarify the controversial effect of the PPV-23 in preventing community-acquired pneumonia and they will be critical in determining the posible role of pneumococcal vaccination in cardiovascular prevention. PMID:20085658

  14. 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.

  15. 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

  16. Intestinal Microbial Metabolites Are Linked to Severity of Myocardial Infarction in Rats.

    PubMed

    Lam, Vy; Su, Jidong; Hsu, Anna; Gross, Garrett J; Salzman, Nita H; Baker, John E

    2016-01-01

    Intestinal microbiota determine severity of myocardial infarction in rats. We determined whether low molecular weight metabolites derived from intestinal microbiota and transported to the systemic circulation are linked to severity of myocardial infarction. Plasma from rats treated for seven days with the non-absorbed antibiotic vancomycin or a mixture of streptomycin, neomycin, polymyxin B and bacitracin was analyzed using mass spectrometry-based metabolite profiling platforms. Antibiotic-induced changes in the abundance of individual groups of intestinal microbiota dramatically altered the host's metabolism. Hierarchical clustering of dissimilarities separated the levels of 284 identified metabolites from treated vs. untreated rats; 193 were altered by the antibiotic treatments with a tendency towards decreased metabolite levels. Catabolism of the aromatic amino acids phenylalanine, tryptophan and tyrosine was the most affected pathway comprising 33 affected metabolites. Both antibiotic treatments decreased the severity of an induced myocardial infarction in vivo by 27% and 29%, respectively. We then determined whether microbial metabolites of the amino acids phenylalanine, tryptophan and tyrosine were linked to decreased severity of myocardial infarction. Vancomycin-treated rats were administered amino acid metabolites prior to ischemia/reperfusion studies. Oral or intravenous pretreatment of rats with these amino acid metabolites abolished the decrease in infarct size conferred by vancomycin. Inhibition of JAK-2 (AG-490, 10 μM), Src kinase (PP1, 20 μM), Akt/PI3 kinase (Wortmannin, 100 nM), p44/42 MAPK (PD98059, 10 μM), p38 MAPK (SB203580, 10 μM), or KATP channels (glibenclamide, 3 μM) abolished cardioprotection by vancomycin, indicating microbial metabolites are interacting with cell surface receptors to transduce their signals through Src kinase, cell survival pathways and KATP channels. These inhibitors have no effect on myocardial infarct size in

  17. 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.

  18. Intracoronary hypothermia for acute myocardial infarction in the isolated beating pig heart

    PubMed Central

    Otterspoor, Luuk C; van Nunen, Lokien X; Rosalina, Tilaï T; Veer, Marcel van’t; Tuijl, Sjoerd Van; Stijnen, Marco; Rutten, Marcel CM; van de Vosse, Frans N; Pijls, Nico HJ

    2017-01-01

    Hypothermia may attenuate reperfusion injury and thereby improve acute myocardial infarction therapy. Systemic cooling trials failed to reduce infarct size, perhaps because the target temperature was not reached fast enough. The use of selective intracoronary hypothermia combined with intracoronary temperature monitoring allows for titrating to target temperature and optimizing the cooling rate. We aimed to the test the feasibility of intracoronary cooling for controlled, selective myocardial hypothermia in an isolated beating pig heart. In five porcine hearts the left anterior descending artery (LAD) was occluded by an over-the-wire balloon (OTWB). After occlusion, saline at 22°C was infused through the OTWB lumen for 5 minutes into the infarct area at a rate of 30 ml/min. Thereafter the balloon was deflated but infusion continued with saline at 4°C for 5 minutes. Distal coronary temperature was continuously monitored by a pressure/temperature guidewire. Myocardial temperature at several locations in the infarct and control areas was recorded using needle thermistors. In the occlusion phase, coronary temperature decreased by 11.4°C (range 9.4-12.5°C). Myocardial temperature throughout the infarct area decreased by 5.1°C (range 1.8-8.1°C) within three minutes. During the reperfusion phase, coronary temperature decreased by 6.2°C (range 4.1-10.3°C) and myocardial temperature decreased by 4.5°C (range 1.5-7.4°C). Myocardial temperature outside the infarct area was not affected. In the isolated beating pig heart with acute occlusion of the LAD, we were able to rapidly “induce, maintain, and control” a stable intracoronary and myocardial target temperature of at least 4°C below body temperature without side effects and using standard PCI equipment, justifying further studies of this technique in humans. PMID:28337283

  19. 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.

  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. Imaging Macrophage Development and Fate in Atherosclerosis and Myocardial Infarction

    PubMed Central

    Swirski, Filip K.; Nahrendorf, Matthias

    2013-01-01

    Macrophages are central regulators of disease progression in both atherosclerosis and myocardial infarction. In atherosclerosis, macrophages are the dominant leukocyte population that influences lesional development. In myocardial infarction, which is caused by atherosclerosis, macrophages accumulate readily and play important roles in inflammation and healing. Molecular imaging has grown considerably as a field and can reveal biological process at the molecular, cellular, and tissue levels. Here we explore how various imaging modalities, from intravital microscopy in mice to organ-level imaging in patients, are contributing to our understanding of macrophages and their progenitors in cardiovascular disease. PMID:23207281

  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. Randomised phase 2 trial of intra-coronary nitrite during acute myocardial infarction

    PubMed Central

    Jones, Daniel A; Pellaton, Cyril; Velmurugan, Shanti; Rathod, Krishnaraj Sinha; Andiapen, Mervyn; Antoniou, Sotiris; van Eijl, Sven; Webb, Andrew J; Westwood, Mark A; Parmar, Mahesh K; Mathur, Anthony; Ahluwalia, Amrita

    2015-01-01

    Rationale Pre-clinical evidence demonstrates that inorganic nitrite, following its in situ conversion to nitric oxide, attenuates consequent myocardial reperfusion injury. Objective We investigated whether intra-coronary injection of nitrite during primary percutaneous coronary intervention (PCI) might improve infarct size in ST-elevated myocardial infarction (STEMI). Methods and Results Patients undergoing primary PCI (n=80) were randomised to receive intracoronary (10mL) sodium nitrite (1.8μmol) or NaCl (placebo) before balloon inflation. The primary endpoint was infarct size assessed by measuring creatine kinase (CK) release. Secondary outcomes included infarct size assessed by troponin T release and by cardiac magnetic resonance imaging (CMR) on day 2. Baseline characteristics were similar between the groups. No evidence of differences in CK release (p=0.92), troponin T (p=0.85) or CMR-assessed infarct size (p=0.254) were evident. In contrast there was an improvement in myocardial salvage index (p=0.05) and reduction in MACE at 1 year (2.6% vs 15.8%, p=0.04) in the nitrite group. In a 66-patient sub-group with TIMI≤1 flow there was reduced serum CK (p=0.030) and a 19% reduction in CMR-determined infarct size (p=0.034) with nitrite. No adverse effects of nitrite were detected. Conclusions In this phase II study intra-coronary nitrite infusion did not alter infarct size although a trend to improved myocardial salvage index and a significant reduction in MACE was evident. In a sub-group of patients with TIMI flow≤1 nitrite reduced infarct size and MACE and improved myocardial salvage index indicating that a phase III clinical trial assessing intra-coronary nitrite administration as an adjunct to PCI in STEMI patients is warranted. Clinical Trial Registration URL: http://clinicaltrials.gov NCT01584453. PMID:25512434

  4. Total and high molecular weight adiponectin levels in the rat model of post-myocardial infarction heart failure.

    PubMed

    Kalisz, M; Baranowska, B; Wolinska-Witort, E; Maczewski, M; Mackiewicz, U; Tulacz, D; Gora, M; Martynska, L; Bik, W

    2015-10-01

    Adiponectin is a protein secreted primarily by adipose tissue. It has been suggested that adiponectin plays a protective role in the early phase following myocardial infarction. Our primary aim was to investigate the effects of post-myocardial infarction heart failure well-characterized by left ventricular hemodynamic parameters on the total and high molecular weight adiponectin concentrations in plasma, fat and cardiac tissue. Eight weeks after myocardial infarction or sham operation, total and high molecular weight adiponectin concentrations in plasma, fat, and cardiac tissues were assayed in rats. In addition, hemodynamic parameters and expression of the genes encoding atrial natriuretic peptide and brain natriuretic peptide in left ventricle were evaluated. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in left ventricle tissue were higher in rats with myocardial infarction-induced heart failure compared with the controls. Similarly, total adiponectin concentration was increased in left ventricle (but not in right ventricle) in rats with post-myocardial infarction heart failure. In contrast, adiponectin levels in plasma and cardiac adipose tissue in rats with post-myocardial infarction heart failure were lower than in sham-operated animals. Furthermore, there were no significant differences in levels of high molecular weight adiponectin in plasma, cardiac tissue or adipose tissue between these two groups. We conclude that in the rat model of post-myocardial infarction heart failure, adiponectin level is increased in left ventricle tissue. This is accompanied by decreased adiponectin levels in plasma and cardiac adipose tissue.

  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. Combined effects of current-smoking and the aldehyde dehydrogenase 2*2 allele on the risk of myocardial infarction in Japanese patients.

    PubMed

    Morita, Kazunori; Miyazaki, Hiroko; Saruwatari, Junji; Oniki, Kentaro; Kumagae, Naoki; Tanaka, Takahiro; Kajiwara, Ayami; Otake, Koji; Ogata, Yasuhiro; Arima, Yuichiro; Hokimoto, Seiji; Ogawa, Hisao; Nakagawa, Kazuko

    2015-01-05

    Aldehyde dehydrogenase 2 (ALDH2) detoxifies toxic aldehydes, e.g. acetaldehyde in cigarette smoke; however, the interactive effects between smoking status and the ALDH2 genotype on coronary artery disease (CAD) have not been reported. We investigated the effects of smoking status and the ALDH2 genotype, and assessed their interactive and combined effects on the risk of myocardial infarction (MI) or stable angina (SA), including 221 MI and 175 SA subjects and 473 age- and sex-matched controls without CAD. Current-smoking and the ALDH2*2 allele additively increased the risk of MI (adjusted odds ratio 4.54, 95% confidence interval 2.25-9.15), although this combination was not associated with the risk of SA. This combination also increased the peak creatine kinase (CK) level synergistically in the acute MI (AMI) subjects. Moreover, current-smoking was found to be a significant risk factor for an increased peak CK level in the ALDH2*2 allele carriers (B 2220.2IU/L, p=0.008), but not the non-carriers. Additionally, a synergistic effect of this combination on the triglycerides levels was also found in the AMI subjects. These preliminary findings suggest that the combination of current-smoking and the inactive ALDH2*2 allele may increase the risk of MI additively and the infarct size synergistically.

  7. 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.

  8. 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.

  9. 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.

  10. Effects of first myocardial infarction on left ventricular systolic and diastolic function with the use of mitral annular velocity determined by pulsed wave doppler tissue imaging.

    PubMed

    Alam, M; Wardell, J; Andersson, E; Samad, B A; Nordlander, R

    2000-05-01

    This study was undertaken to assess the effect of a first myocardial infarction (MI) on the systolic and diastolic velocity profiles of the mitral annulus determined by pulsed wave Doppler tissue imaging and thereby evaluate left ventricular (LV) function after MI. Seventy-eight patients with a first MI were examined before discharge. Peak systolic, peak early diastolic, and peak late diastolic velocities were recorded at 4 different sites on the mitral annulus corresponding to the septum, anterior, lateral, and inferior sites of the left ventricle. In addition, the amplitude of mitral annular motion at the 4 above LV sites, the ejection fraction, and conventional Doppler diastolic parameters were recorded. Nineteen age-matched healthy subjects served as controls. Compared with healthy subjects, the MI patients had a significantly reduced peak systolic velocity at the mitral annulus, especially at the infarction sites. A relatively good linear correlation was found between the ejection fraction and the mean systolic velocity from the 4 LV sites (r = 0.74, P <.001). The correlation was also good when the mean peak systolic mitral annular velocity was tested against the magnitude of the mean mitral annular motion (r = 0.77, P <.001). When the patients were divided into 2 different groups with respect to an ejection fraction > or =0.50 or <0.50, a cutoff point of mean systolic mitral annular velocity of > or =7.5 cm/s had a sensitivity of 79% and a specificity of 88% in predicting a preserved global LV systolic function. Similar to systolic velocities, the early diastolic velocity was also reduced, especially at the infarction sites. The peak mitral annular early diastolic velocity correlated well with both LV ejection fraction (r =.66, P <.001) and mean systolic mitral annular motion (r = 0.68, P <.001). However, no correlation existed between the early diastolic velocity and conventional diastolic Doppler parameters. The reduced peak systolic mitral annular velocity

  11. Is the effect of job strain on myocardial infarction risk due to interaction between high psychological demands and low decision latitude? Results from Stockholm Heart Epidemiology Program (SHEEP).

    PubMed

    Hallqvist, J; Diderichsen, F; Theorell, T; Reuterwall, C; Ahlbom, A

    1998-06-01

    The objectives are to examine if the excess risk of myocardial infarction from exposure to job strain is due to interaction between high demands and low control and to analyse what role such an interaction has regarding socioeconomic differences in risk of myocardial infarction. The material is a population-based case-referent study having incident first events of myocardial infarction as outcome (SHEEP: Stockholm Heart Epidemiology Program). The analysis is restricted to males 45-64 yr of age with a more detailed analysis confined to those still working at inclusion. In total, 1047 cases and 1450 referents were included in the analysis. Exposure categories of job strain were formed from self reported questionnaire information. The results show that high demands and low decision latitude interact with a synergy index of 7.5 (95% C.I.: 1.8-30.6) providing empirical support for the core mechanism of the job strain model. Manual workers are more susceptible when exposed to job strain and its components and this increased susceptibility explains about 25-50% of the relative excess risk among manual workers. Low decision latitude may also, as a causal link, explain about 30% of the socioeconomic difference in risk of myocardial infarction. The distinction between the interaction and the causal link mechanisms identifies new etiologic questions and intervention alternatives. The specific causes of the increased susceptibility among manual workers to job strain and its components seem to be an interesting and important research question.

  12. 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.

  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. 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.

  15. 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.

  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. Effects of ranolazine on the exercise capacity of rats with chronic heart failure induced by myocardial infarction.

    PubMed

    Aaker, A; McCormack, J G; Hirai, T; Musch, T I

    1996-09-01

    Ranolazine was previously shown to stimulate cardiac glucose oxidation. Dichloroacetate (DCA) also does and was shown to improve exercise capacity in animals, but it has long-term toxicity problems. To test the hypothesis that ranolazine would increase exercise performance in the chronic heart failure (CHF) condition, we compared the exercise endurance capacities of rats with a surgically induced myocardial infarction (MI) with those of noninfarcted sham-operated (Sham) controls both before and after 14 and 28 days of drug administration. Chronic administration of ranolazine, 50 mg/kg twice daily (b.i.d.) oral, significantly reduced the endurance capacities of both Sham and MI rats (measured after a 12-h fast to reduce liver glycogen stores), as indicated by the reductions in run times to fatigue during a progressive treadmill test. Ranolazine produced reductions in resting plasma lactate and glucose concentrations of animals fasted for 12 h (consistent with stimulating glucose oxidation); however, tissue glycogen concentrations measured in various locomotor muscles located in the animal's hindlimb were unaffected when measured 48 h after the last treadmill test and after 12 h of fasting. Chronic administration of ranolazine did not increase the endurance capacity of rats with CHF induced by MI at the dosage and with the protocol used. To the contrary, the chronic administration of ranolazine appears to reduce the work capacity of all rats, suggesting that this drug may not be useful therapeutically in the treatment of CHF. Whether the decrements in endurance capacity produced by ranolazine are related to the high plasma concentrations of the drug produced in this study as compared with previous studies in humans remains subject to further experimentation.

  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. Temperature, air pollution, and mortality from myocardial infarction in São Paulo, Brazil.

    PubMed

    Sharovsky, R; César, L A M; Ramires, J A F

    2004-11-01

    An increase in daily mortality from myocardial infarction has been observed in association with meteorological factors and air pollution in several cities in the world, mainly in the northern hemisphere. The objective of the present study was to analyze the independent effects of environmental variables on daily counts of death from myocardial infarction in a subtropical region in South America. We used the robust Poisson regression to investigate associations between weather (temperature, humidity and barometric pressure), air pollution (sulfur dioxide, carbon monoxide, and inhalable particulate), and the daily death counts attributed to myocardial infarction in the city of São Paulo in Brazil, where 12,007 fatal events were observed from 1996 to 1998. The model was adjusted in a linear fashion for relative humidity and day-of-week, while nonparametric smoothing factors were used for seasonal trend and temperature. We found a significant association of daily temperature with deaths due to myocardial infarction (P < 0.001), with the lowest mortality being observed at temperatures between 21.6 and 22.6 degrees C. Relative humidity appeared to exert a protective effect. Sulfur dioxide concentrations correlated linearly with myocardial infarction deaths, increasing the number of fatal events by 3.4% (relative risk of 1.03; 95% confidence interval = 1.02-1.05) for each 10 microg/m(3) increase. In conclusion, this study provides evidence of important associations between daily temperature and air pollution and mortality from myocardial infarction in a subtropical region, even after a comprehensive control for confounding factors.

  20. Cardioprotective effect of pioglitazone in diabetic and non-diabetic rats subjected to acute myocardial infarction involves suppression of AGE-RAGE axis and inhibition of apoptosis.

    PubMed

    Khodeer, Dina M; Zaitone, Sawsan A; Farag, Noha E; Moustafa, Yasser M

    2016-05-01

    Insulin resistance increases risk of cardiovascular diseases. This work investigated the protective effect of pioglitazone on myocardial infarction (MI) in non-diabetic and diabetic rats, focusing on its role on advanced glycated endproducts (AGEs) and cardiac apoptotic machinery. Male rats were divided into 2 experiments: experiment I and II (non-diabetic and diabetic rats) were assigned as saline, MI (isoproterenol, 85 mg/kg, daily), and MI+pioglitazone (5, 10, and 20 mg/kg). Injection of isoproterenol in diabetic rats produced greater ECG disturbances compared to non-diabetic rats. Treatment with pioglitazone (5 mg/kg) reduced the infarct size and improved some ECG findings. Pioglitazone (10 mg/kg) enhanced ECG findings, improved the histopathological picture and downregulated apoptosis in cardiac tissues. Whereas the higher dose of pioglitazone (20 mg/kg) did not improve most of the measured parameters but rather worsened some of them, such as proapoptotic markers. Importantly, a positive correlation was found between serum AGEs and cardiac AGE receptors (RAGEs) versus caspase 3 expression in the two experiments. Therefore, the current effect of pioglitazone was, at least in part, mediated through downregulation of AGE-RAGE axis and inhibition of apoptosis. Consequently, these data suggest that pioglitazone, at optimized doses, may have utility in protection from acute MI.

  1. Osteoprotegerin levels in ST-elevation myocardial infarction: Temporal profile and association with myocardial injury and left ventricular function

    PubMed Central

    Shetelig, Christian; Limalanathan, Shanmuganathan; Eritsland, Jan; Hoffmann, Pavel; Seljeflot, Ingebjørg; Gran, Jon Michael; Aukrust, Pål; Ueland, Thor; Andersen, Geir Øystein

    2017-01-01

    Background Elevated levels of osteoprotegerin (OPG) have been associated with adverse outcomes in ST-elevation myocardial infarction (STEMI). However, the role of OPG in myocardial injury and adverse remodeling in STEMI patients remains unclear. The aims of this observational cohort study were to evaluate: 1) the temporal profile of OPG during STEMI, 2) possible associations between OPG measured acutely and after 4 months, with infarct size, adverse left ventricular (LV) remodeling, microvascular obstruction (MVO) and myocardial salvage and 3) the effect of heparin administration on OPG levels. Methods Blood samples were drawn repeatedly from 272 STEMI patients treated with primary percutaneous coronary intervention (PCI). Cardiac magnetic resonance imaging (CMR) was performed in the acute phase and after 4 months. The effect of heparin administration on OPG levels was studied in 20 patients referred to elective coronary angiography. Results OPG levels measured acutely were significantly higher than Day 1 and during follow-up. OPG levels were correlated with age. No association was found between early OPG levels and CMR measurements at 4 months. Patients with >median OPG levels measured at Day 1 had larger final infarct size, lower LV ejection fraction (LVEF) at 4 months and higher frequency of MVO. There were no associations between OPG and change in end-diastolic volume or myocardial salvage. OPG remained associated with infarct size and LVEF after adjustment for relevant covariates, except peak troponin T and CRP. A 77% increase in OPG levels following heparin administration was found in patients undergoing elective coronary angiography. Conclusions OPG was found to be associated with myocardial injury, but not with LV remodeling or myocardial salvage. The use of OPG as a biomarker in STEMI patients seems to be limited by a strong association with age, confounding effect of heparin administration, and little additive value to established biomarkers. PMID

  2. Paclitaxel Induced Acute ST Elevation Myocardial Infarction: A Rare Case Report

    PubMed Central

    Yadav, Sankalp; Kumar, Raj

    2016-01-01

    Paclitaxel, is a frequently used anti-neoplastic agent and is included in various chemotherapy regimens. The life threatening cardio toxicity associated with its use and the still unclear pathophysiology, has limited the use of this drug. Acute myocardial infarction is a rare adverse event associated with this drug. We report a case of acute ST-elevation myocardial infarction induced by paclitaxel infusion in a patient of oesophageal carcinoma who was saved by percutaneous primary intervention. The authors emphasize the awareness of this side effect of Paclitaxel among the clinicians. PMID:27891444

  3. Beneficial effects of selective HDL-raising gene transfer on survival, cardiac remodelling and cardiac function after myocardial infarction in mice

    PubMed Central

    Gordts, S C; Muthuramu, I; Nefyodova, E; Jacobs, F; Van Craeyveld, E; De Geest, B

    2013-01-01

    Post-myocardial infarction (MI) ejection fraction is decreased in patients with low high-density lipoprotein (HDL) cholesterol levels, independent of the degree of coronary atherosclerosis. The objective of this study is to evaluate whether selective HDL-raising gene transfer exerts cardioprotective effects post MI. Gene transfer in C57BL/6 low-density lipoprotein receptor (LDLr)−/− mice was performed with the E1E3E4-deleted adenoviral vector AdA-I, inducing hepatocyte-specific expression of human apo A-I, or with the control vector Adnull. A ligation of the left anterior descending coronary artery was performed 2 weeks after transfer or saline injection. HDL cholesterol levels were persistently 1.5-times (P<0.0001) higher in AdA-I mice compared with controls. Survival was increased (P<0.01) in AdA-I MI mice compared with control MI mice during the 28-day follow-up period (hazard ratio for mortality 0.42; 95% confidence interval 0.24–0.76). Longitudinal morphometric analysis demonstrated attenuated infarct expansion and inhibition of left ventricular (LV) dilatation in AdA-I MI mice compared with controls. AdA-I transfer exerted immunomodulatory effects and increased neovascularisation in the infarct zone. Increased HDL after AdA-I transfer significantly improved systolic and diastolic cardiac function post MI, and led to a preservation of peripheral blood pressure. In conclusion, selective HDL-raising gene transfer may impede the development of heart failure. PMID:23759702

  4. Beneficial effects of selective HDL-raising gene transfer on survival, cardiac remodelling and cardiac function after myocardial infarction in mice.

    PubMed

    Gordts, S C; Muthuramu, I; Nefyodova, E; Jacobs, F; Van Craeyveld, E; De Geest, B

    2013-11-01

    Post-myocardial infarction (MI) ejection fraction is decreased in patients with low high-density lipoprotein (HDL) cholesterol levels, independent of the degree of coronary atherosclerosis. The objective of this study is to evaluate whether selective HDL-raising gene transfer exerts cardioprotective effects post MI. Gene transfer in C57BL/6 low-density lipoprotein receptor (LDLr)(-/-) mice was performed with the E1E3E4-deleted adenoviral vector AdA-I, inducing hepatocyte-specific expression of human apo A-I, or with the control vector Adnull. A ligation of the left anterior descending coronary artery was performed 2 weeks after transfer or saline injection. HDL cholesterol levels were persistently 1.5-times (P<0.0001) higher in AdA-I mice compared with controls. Survival was increased (P<0.01) in AdA-I MI mice compared with control MI mice during the 28-day follow-up period (hazard ratio for mortality 0.42; 95% confidence interval 0.24-0.76). Longitudinal morphometric analysis demonstrated attenuated infarct expansion and inhibition of left ventricular (LV) dilatation in AdA-I MI mice compared with controls. AdA-I transfer exerted immunomodulatory effects and increased neovascularisation in the infarct zone. Increased HDL after AdA-I transfer significantly improved systolic and diastolic cardiac function post MI, and led to a preservation of peripheral blood pressure. In conclusion, selective HDL-raising gene transfer may impede the development of heart failure.

  5. 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

  6. 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)

  7. 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…

  8. 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.…

  9. Rapid Identification of Myocardial Infarction Risk Associated With Diabetes Medications Using Electronic Medical Records

    PubMed Central

    Brownstein, John S.; Murphy, Shawn N.; Goldfine, Allison B.; Grant, Richard W.; Sordo, Margarita; Gainer, Vivian; Colecchi, Judith A.; Dubey, Anil; Nathan, David M.; Glaser, John P.; Kohane, Isaac S.

    2010-01-01

    OBJECTIVE To assess the ability to identify potential association(s) of diabetes medications with myocardial infarction using usual care clinical data obtained from the electronic medical record. RESEARCH DESIGN AND METHODS We defined a retrospective cohort of patients (n = 34,253) treated with a sulfonylurea, metformin, rosiglitazone, or pioglitazone in a single academic health care network. All patients were aged >18 years with at least one prescription for one of the medications between 1 January 2000 and 31 December 2006. The study outcome was acute myocardial infarction requiring hospitalization. We used a cumulative temporal approach to ascertain the calendar date for earliest identifiable risk associated with rosiglitazone compared with that for other therapies. RESULTS Sulfonylurea, metformin, rosiglitazone, or pioglitazone therapy was prescribed for 11,200, 12,490, 1,879, and 806 patients, respectively. A total of 1,343 myocardial infarctions were identified. After adjustment for potential myocardial infarction risk factors, the relative risk for myocardial infarction with rosiglitazone was 1.3 (95% CI 1.1–1.6) compared with sulfonylurea, 2.2 (1.6–3.1) compared with metformin, and 2.2 (1.5–3.4) compared with pioglitazone. Prospective surveillance using these data would have identified increased risk for myocardial infarction with rosiglitazone compared with metformin within 18 months of its introduction with a risk ratio of 2.1 (95% CI 1.2–3.8). CONCLUSIONS Our results are consistent with a relative adverse cardiovascular risk profile for rosiglitazone. Our use of usual care electronic data sources from a large hospital network represents an innovative approach to rapid safety signal detection that may enable more effective postmarketing drug surveillance. PMID:20009093

  10. 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.

  11. 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

  12. Effects of tirofiban on platelet activation and endothelial function in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention.

    PubMed

    Wang, Kuan; Zuo, Guoxing; Zheng, Liuying; Zhang, Cheng; Wang, Dong; Cao, Zhongnan; Hu, Sheng; Du, Xinping

    2015-01-01

    This pilot study examined, for the first time, the effect of intracoronary administration of tirofiban, an inhibitor of platelet aggregation, on platelet activation and endothelial dysfunction in patients with ST-segment-elevated myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). A total of 119 STEMI patients were randomized into either tirofiban group (n = 72, intracoronary injection of 10 μg/kg tirofiban prior to PCI, followed by intravenous infusion at 0.15 μg/kg min) or a control group (n = 47), which did not receive tirofiban. Periprocedural administration of tirofiban was associated with significantly reduced levels of platelet activation (lower levels of CD62P and PAC-1) and endothelial dysfunction (reduced levels of endothelial microparticles, VCAM-1, and ICAM-1) 48 h after PCI. At 10 days after PCI, patients in the tirofiban group had a higher incidence of complete STR (78.7 vs. 65.0%) and higher left ventricular ejection fractions (47.8 vs. 44.2) compared to those in the control group. The clinical outcomes between two groups did not differ significantly two weeks after treatment. The results demonstrated that periprocedural administration of tirofiban is associated with significantly attenuated platelet activation and endothelial dysfunction in STEMI patients undergoing PCI. This may have contributed to the improved myocardial reperfusion and preservation of left ventricular systolic function in these patients.

  13. Protective effect of fish oil on changes in the activities of membrane-bound ATPases and mineral status in experimentally induced myocardial infarction in Wistar rats.

    PubMed

    Padma, Viswanadha Vijaya; Devi, Chennam Srinivasulu Shyamala; Kalaiselvi, Palaniswamy

    2010-12-01

    The present study evaluated the protective effect of fish oil in isoproterenol-induced myocardial infarction in rats. The results of the present study indicate that the IPH administration decreases the activities of membrane-bound ATPases compared to control animals. Fish oil pretreatment brought about significant increase in the activity of these membrane-bound ATPases in IPH (isoproterenol hydrochloride)-treated animals. Significant increase in serum potassium level with concomitant decrease in the values of sodium, magnesium, and calcium were observed in IPH-treated rats compared to control rats, fish oil pretreatment reversed these changes to near normal. Significant elevation of sodium and calcium levels with concomitant decrease in the levels of potassium and magnesium were observed in the myocardial tissue of IPH-administered rats compared to control rats, fish oil pretreatment followed by IPH administration brought these levels to near normal. The levels of lipid peroxidation (LPO) in both serum and tissue were increased in IPH-treated rats compared with control rats, whereas pretreatment with fish oil in IPH-treated rats maintained near-normal LPO levels. The results of the present study reveals that the pretreatment of fish maintains the activities of membrane-bound ATPases and the mineral levels at near normal by the inhibition of lipid peroxidation.

  14. [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.

  15. Effect of Late Revascularization of a Totally Occluded Coronary Artery After Myocardial Infarction on Mortality Rates in Patients with Renal Impairment

    PubMed Central

    Hastings, Ramin; Hochman, Judith S.; Dzavik, Vladimir; Lamas, Gervasio A.; Forman, Sandra A.; Schiele, Francois; Michalis, Lampros K.; Nikas, Dimitris; Jaroch, Joanna; Reynolds, Harmony R.

    2012-01-01

    Renal dysfunction is an independent predictor of cardiovascular events and a negative prognostic indicator after myocardial infarction (MI). Randomized data comparing percutaneous coronary intervention (PCI) to medical therapy in MI patients with renal insufficiency are needed. The Occluded Artery Trial (OAT) compared optimal medical therapy alone to PCI with optimal medical therapy in 2201 high risk patients with an occluded infarct artery >24 hours post-MI with serum creatinine ≤2.5 mg/dl. The primary endpoint was a composite of death, MI, and class IV heart failure (HF). Analyses were carried out utilizing estimated glomerular filtration rates (eGFR) as a continuous variable and by eGFR categories. Long term follow up data (maximum 9 years) were used for this analysis. Lower eGFR (ml/min/1.73m2) was associated with development of the primary outcome (6-year life-table rate 16.9% in eGFR>90; 19.2% in eGFR 60–89; 34.9% in eGFR<60; p-value <0.0001), death, and class IV HF, with no difference in rates of reinfarction. On multivariable analysis, eGFR was an independent predictor of death and HF. There was no effect of treatment assignment on the primary endpoint regardless of eGFR, and there was no significant interaction between eGFR and treatment assignment on any outcome. In conclusion, lower eGFR at enrollment was independently associated with death and HF in OAT participants. Despite this increased risk, the lack of benefit from PCI in the overall trial was also seen in patients with renal dysfunction and persistent occlusion of the infarct artery in the subacute phase post MI. PMID:22728005

  16. 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.

  17. Primary percutaneous coronary intervention for acute myocardial infarction in a pediatric patient with giant coronary aneurysm due to Kawasaki disease.

    PubMed

    Mongiovì, Maurizio; Alaimo, Annalisa; Vernuccio, Federica; Pieri, Daniele

    2014-01-01

    We report a case of acute myocardial infarction in an 8-year-old boy with a history of Kawasaki disease and giant coronary aneurysms in the right and left coronary arteries. We performed coronary angiography and percutaneous coronary intervention 4 hours after the onset of symptoms. This case suggests that primary percutaneous coronary intervention might be safe and effective in the long-term treatment of acute myocardial infarction due to coronary sequelae of Kawasaki.

  18. 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.

  19. Targeting the inflammatory response in healing myocardial infarcts.

    PubMed

    Frangogiannis, Nikolaos G

    2006-01-01

    Healing of myocardial infarcts depends on an inflammatory cascade that ultimately results in clearance of dead cells and matrix debris and formation of a scar. Myocardial necrosis activates complement, Nuclear Factor (NF)-kappaB and Toll-like Receptor (TLR)-dependent pathways, and generates free radicals, triggering an inflammatory response. Chemokines and cytokines are markedly induced in the infarct and mediate recruitment and activation of neutrophils and mononuclear cells. Extravasation of platelets and plasma proteins, such as fibrinogen and fibronectin, results in formation of a clot, consisting of platelets embedded in a mesh of crosslinked fibrin. This provisional matrix provides a scaffold for migration of cells into the infarct. Monocytes differentiate into macrophages and secrete fibrogenic and angiogenic growth factors inducing formation of granulation tissue, containing myofibroblasts and neovessels. Repression of proinflammatory cytokine and chemokine synthesis, mediated in part through Transforming Growth Factor (TGF)-beta and Interleukin (IL)-10, is critical for resolution of the inflammatory infiltrate and transition to fibrous tissue deposition. Infarct myofibroblasts deposit extracellular matrix proteins and a collagen-based scar is formed. As the wound matures, fibroblasts undergo apoptosis and neovessels regress, resulting in formation of a scar with a low cellular content containing dense, cross-linked collagen. The pathologic and structural changes associated with infarct healing directly influence ventricular remodeling and affect prognosis in patients with myocardial infarction. Understanding the mechanisms involved in the regulation of the post-infarction inflammatory response, and the spatial and temporal parameters of wound healing is necessary in order to identify specific molecular targets for therapeutic intervention.

  20. 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

  1. 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.

  2. 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

  3. Human recombinant relaxin reduces heart injury and improves ventricular performance in a swine model of acute myocardial infarction.

    PubMed

    Perna, Avio-Maria; Masini, Emanuela; Nistri, Silvia; Bani Sacchi, Tatiana; Bigazzi, Mario; Bani, Daniele

    2005-05-01

    This study shows that relaxin can be effective in the treatment of acute myocardial infarction. In a swine model of heart ischemia-reperfusion currently used to test cardiotropic drugs because of its similarities with human myocardial infarction, human recombinant relaxin (2.5 and 5 microg/kg body weight), given at reperfusion after a 30-min ischemia, markedly reduced the main serum markers of myocardial damage (myoglobin, CK-MB, and troponin T) and the metabolic and histopathologic parameters of myocardial inflammation and cardiomyocyte injury, resulting in overall improvement of ventricular performance (increased cardiac index) compared to the controls. These results provide a background for future clinical trials with human relaxin as adjunctive therapy to catheter-based coronary angioplasty in patients with acute myocardial infarction.

  4. 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.

  5. Recovery of regional myocardial dysfunction after successful coronary angioplasty early after a non-Q wave myocardial infarction

    SciTech Connect

    Suryapranata, H.; Serruys, P.W.; Beatt, K.; De Feyter, P.J.; van den Brand, M.; Roelandt, J. )

    1990-08-01

    More aggressive therapy has been suggested for patients who have a non-Q wave myocardial infarction (MI) because of the frequency of subsequent unstable angina, recurrent MI, and high mortality rate compared to patients with Q wave MI. The present study was undertaken to investigate the effect of coronary angioplasty on regional myocardial function of the infarct zone in patients with angina early after a non-Q wave MI. The study population consisted of 36 patients undergoing successful coronary angioplasty within 30 days of a non-Q wave MI, in whom sequential left ventricular angiograms of adequate quality were obtained before the initial procedure and at follow-up angiography. The global ejection fraction increased significantly from 60 +/- 9% to 67 +/- 6% (p = 0.0003). This significant increase in the global ejection fraction was primarily due to a significant improvement in the regional myocardial function of the infarct zone. The results of the present study show not only that ischemic attacks early after a non-Q wave MI may lead to prolonged regional myocardial dysfunction but more important that this depressed myocardium has the potential to achieve normal contraction after successful coronary angioplasty.

  6. Does primary stenting preserve cardiac function in myocardial infarction? A case-control study

    PubMed Central

    Sasao, H; Tsuchihashi, K; Hase, M; Nakata, T; Shimamoto, K; investigators, t. N.

    2000-01-01

    OBJECTIVE—To investigate whether coronary stenting limits myocardial injury and preserves left ventricular function.
DESIGN AND SETTING—Prospective multicentre case-control study of primary percutaneous transluminal coronary angioplasty (PTCA) with and without stenting, performed in seven cardiovascular centres.
SUBJECTS AND METHODS—45 consecutive patients with acute myocardial infarction who were treated with successful primary stenting (Stent group) and did not have restenosis were paired with 45 matched control subjects with acute myocardial infarction treated by successful primary PTCA without stenting, also with no restenosis (POBA group).
RESULTS—In comparison with the POBA group, the Stent group—especially those patients with a left anterior descending coronary artery lesion—had a smaller hypokinesis area (mean (SD): 15.1 (20.0) v 34.4 (24.3) chords), reduced hypokinesis area/risk area (25.2 (31.9)% v 58.8 (40.1)%), and a larger ejection fraction (63.3 (10.2)% v 51.7 (11.7)%) evaluated by quantitative left ventriculography using the centreline method. In the Stent group, the correlation between risk area and hypokinesis area was significantly shifted downward. Multiple logistic regression analysis on infarct size limitation (hypokinesis area/risk area < 50%) identified preinfarction angina in all subjects and preinfarction angina and stenting in patients with left anterior descending coronary artery leasions as explanatory factors.
CONCLUSIONS—Primary PTCA using a coronary stent is effective in preventing myocardial injury and restoring left ventricular function in patients with anterior acute myocardial infarction.


Keywords: acute myocardial infarction; primary stenting; left ventricular function; preinfarction angina PMID:11040013

  7. ARD-353 [4-((2R,5S)-4-(R)-(4-diethylcarbamoylphenyl)(3-hydroxyphenyl)methyl)-2,5-dimethylpiperazin-1-ylmethyl)benzoic acid], a novel nonpeptide delta receptor agonist, reduces myocardial infarct size without central effects.

    PubMed

    Watson, Michael J; Holt, Jonathon D S; O'Neill, Scott J; Wei, Ke; Pendergast, William; Gross, Garrett J; Gengo, Peter J; Chang, Kwen-Jen

    2006-01-01

    A novel delta-receptor selective compound, ARD-353 [4-((2R,5S)-4-(R)-(4-diethylcarbamoylphenyl)(3-hydroxyphenyl)methyl)-2, 5-dimethylpiperazin-1-ylmethyl)benzoic acid], was evaluated for activity on infarct size in a rat model of acute myocardial infarction. ARD-353 was characterized as having delta receptor selectivity using radioligand binding and had no apparent selectivity between delta receptor subtypes as determined by [(3)H] cyclic [D-Pen(2),D-Pen(5)]enkephalin (delta(1)) and [(3)H]Deltorphin II (delta(2)) competition binding. ARD-353 also showed selective delta receptor agonist activity in mouse-isolated vas deferens. There was no evidence of any seizure-like convulsions when ARD-353 was administered to mice either i.v. or p.o., implying minimal penetration of the blood-brain barrier. ARD-353 decreased infarct size in a left anterior descending coronary artery (LAD) occlusion model of myocardial infarction. In animals pretreated with ARD-353 (i.v.) and then subjected to 30 min of LAD occlusion followed by 90 min of reperfusion, infarct size was reduced in a dose-dependent manner compared with vehicle-treated controls. The effects of ARD-353 on infarct size were blocked by the delta(1)-opioid selective antagonist 7-benzylidenenaltrexone, indicating a significant role for the delta(1)-opioid receptor in the cardioprotective mechanism of ARD-353. ARD-353 (0.3 mg/kg i.v.) produced significant protection when administered 5 min and 12 and 48 h before ischemic insult or when given immediately after the ischemic insult (at the start of reperfusion). Given the lack of central nervous system effects and beneficial efficacy in the rat model of myocardial ischemia, it is felt that ARD-353 is the first nonpeptide delta-receptor agonist with true potential for clinical use before surgically induced ischemia or in an emergency setting.

  8. [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.

  9. Acute myocardial infarction in young adults with antiphospholipid syndrome: report of two cases and literature review.

    PubMed

    Abid, Leila; Frikha, Faten; Bahloul, Zouhir; Kammoun, Samir

    2011-01-01

    Acute myocardial infarction (AMI) is rarely associated with antiphospholipid syndrome. The treatment of these patients is a clinical challenge. We report the observations of 2 young adults (1 woman and 1 man), admitted in our acute care unit for acute myocardial infarction (AMI). A coagulopathy work-up concludes the existence of antiphospholipid syndrome (APS) in the 2 cases. APS syndrome was considered primary in 2 cases. All patients presented an intense inflammatory syndrome (high level of CRP). Anticardiolipine was present in the 2 cases. However, anti B2 glycoprotein I antibodies were detected in only one case. Emergency percutaneous transluminal coronary angioplasty (PTCA) with direct stenting had been performed successfully only in the first case, and the follow-up was uncomplicated. Thereafter, long-term oral anticoagulant appeared to be effective. The last patient was admitted because of peripheral acute ischemia of legs. Standard electrocardiogram showed signs of previous silent anteroseptal wall myocardial infarction confirmed by echocardiography. The latter revealed an apical thrombus and a very low left ventricular ejection fraction. Amputation of the right leg was necessary because of consultation occurred too late. However, he died four weeks later. Primary antiphospholipid syndrome should be considered as a cause of acute myocardial infarction in young adults, and PTCA with anticoagulant treatment is effective for initial treatment of this complication.

  10. MRI evaluation of injectable hyaluronic acid-based hydrogel therapy to limit ventricular remodeling after myocardial infarction.

    PubMed

    Dorsey, Shauna M; McGarvey, Jeremy R; Wang, Hua; Nikou, Amir; Arama, Leron; Koomalsingh, Kevin J; Kondo, Norihiro; Gorman, Joseph H; Pilla, James J; Gorman, Robert C; Wenk, Jonathan F; Burdick, Jason A

    2015-11-01

    Injectable biomaterials are an attractive therapy to attenuate left ventricular (LV) remodeling after myocardial infarction (MI). Although studies have shown that injectable hydrogels improve cardiac structure and function in vivo, temporal changes in infarct material properties after treatment have not been assessed. Emerging imaging and modeling techniques now allow for serial, non-invasive estimation of infarct material properties. Specifically, cine magnetic resonance imaging (MRI) assesses global LV structure and function, late-gadolinium enhancement (LGE) MRI enables visualization of infarcted tissue to quantify infarct expansion, and spatial modulation of magnetization (SPAMM) tagging provides passive wall motion assessment as a measure of tissue strain, which can all be used to evaluate infarct properties when combined with finite element (FE) models. In this work, we investigated the temporal effects of degradable hyaluronic acid (HA) hydrogels on global LV remodeling, infarct thinning and expansion, and infarct stiffness in a porcine infarct model for 12 weeks post-MI using MRI and FE modeling. Hydrogel treatment led to decreased LV volumes, improved ejection fraction, and increased wall thickness when compared to controls. FE model simulations demonstrated that hydrogel therapy increased infarct stiffness for 12 weeks post-MI. Thus, evaluation of myocardial tissue properties through MRI and FE modeling provides insight into the influence of injectable hydrogel therapies on myocardial structure and function post-MI.

  11. MRI Evaluation of Injectable Hyaluronic Acid-Based Hydrogel Therapy to Limit Ventricular Remodeling after Myocardial Infarction

    PubMed Central

    Dorsey, Shauna M.; McGarvey, Jeremy R.; Wang, Hua; Nikou, Amir; Arama, Leron; Koomalsingh, Kevin J.; Kondo, Norihiro; Gorman, Joseph H.; Pilla, James J.; Gorman, Robert C.; Wenk, Jonathan F.; Burdick, Jason A.

    2015-01-01

    Injectable biomaterials are an attractive therapy to attenuate left ventricular (LV) remodeling after myocardial infarction (MI). Although studies have shown that injectable hydrogels improve cardiac structure and function in vivo, temporal changes in infarct material properties after treatment have not been assessed. Emerging imaging and modeling techniques now allow for serial, non-invasive estimation of infarct material properties. Specifically, cine MRI assesses global LV structure and function, late-gadolinium enhancement (LGE) MRI enables visualization of infarcted tissue to quantify infarct expansion, and spatial modulation of magnetization (SPAMM) tagging provides passive wall motion assessment as a measure of tissue strain, which can all be used to evaluate infarct properties when combined with finite element (FE) models. In this work, we investigated the temporal effects of degradable hyaluronic acid (HA) hydrogels on global LV remodeling, infarct thinning and expansion, and infarct stiffness in a porcine infarct model for 12 weeks post-MI using MRI and FE modeling. Hydrogel treatment led to decreased LV volumes, improved ejection fraction, and increased wall thickness when compared to controls. FE model simulations demonstrated that hydrogel therapy increased infarct stiffness for 12 weeks post-MI. Thus, evaluation of myocardial tissue properties through MRI and FE modeling provides insight into the influence of injectable hydrogel therapies on myocardial structure and function post-MI. PMID:26280951

  12. Role of lymphocytes in myocardial injury, healing, and remodeling after myocardial infarction.

    PubMed

    Hofmann, Ulrich; Frantz, Stefan

    2015-01-16

    A large body of evidence produced during decades of research indicates that myocardial injury activates innate immunity. On the one hand, innate immunity both aggravates ischemic injury and impedes remodeling after myocardial infarction (MI). On the other hand, innate immunity activation contributes to myocardial healing, as exemplified by monocytes' central role in the formation of a stable scar and protection against intraventricular thrombi after acute infarction. Although innate leukocytes can recognize a wide array of self-antigens via pattern recognition receptors, adaptive immunity activation requires highly specific cooperation between antigen-presenting cells and distinct antigen-specific receptors on lymphocytes. We have only recently begun to examine lymphocyte activation's relationship to adaptive immunity and significance in the context of ischemic myocardial injury. There is some experimental evidence that CD4(+) T-cells contribute to ischemia-reperfusion injury. Several studies have shown that CD4(+) T-cells, especially CD4(+) T-regulatory cells, improve wound healing after MI, whereas depleting B-cells is beneficial post MI. That T-cell activation after MI is induced by T-cell receptor signaling implicates autoantigens that have not yet been identified in this context. Also, the significance of lymphocytes in humans post MI remains unclear, primarily as a result of methodology. This review summarizes current experimental evidence of lymphocytes' activation, functional role, and crosstalk with innate leukocytes in myocardial ischemia-reperfusion injury, wound healing, and remodeling after myocardial infarction.

  13. Experimental Myocardial Infarction Induces Altered Regulatory T Cell Hemostasis, and Adoptive Transfer Attenuates Subsequent Remodeling

    PubMed Central

    Sharir, Rinat; Semo, Jonathan; Shimoni, Sara; Ben-Mordechai, Tamar; Landa-Rouben, Natalie; Maysel-Auslender, Sofia; Shaish, Aviv; Entin–Meer, Michal; Keren, Gad; George, Jacob

    2014-01-01

    Background Ischemic cardiac damage is associated with upregulation of cardiac pro-inflammatory cytokines, as well as invasion of lymphocytes into the heart. Regulatory T cells (Tregs) are known to exert a suppressive effect on several immune cell types. We sought to determine whether the Treg pool is influenced by myocardial damage and whether Tregs transfer and deletion affect cardiac remodeling. Methods and Results The number and functional suppressive activity of Tregs were assayed in mice subjected to experimental myocardial infarction. The numbers of splenocyte-derived Tregs in the ischemic mice were significantly higher after the injury than in the controls, and their suppressive properties were significantly compromised. Compared with PBS, adoptive Treg transfer to mice with experimental infarction reduced infarct size and improved LV remodeling and functional performance by echocardiography. Treg deletion with blocking anti-CD25 antibodies did not influence infarct size or echocardiographic features of cardiac remodeling. Conclusion Treg numbers are increased whereas their function is compromised in mice with that underwent experimental infarction. Transfer of exogeneous Tregs results in attenuation of myocardial remodeling whereas their ablation has no effect. Thus, Tregs may serve as interesting potential interventional targets for attenuating left ventricular remodeling. PMID:25436994

  14. 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.

  15. 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

  16. 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.

  17. 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.

  18. 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.

  19. 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.

  20. 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.

  1. Effects of Cardiac Overexpression of the Angiotensin II Type 2 Receptor on Remodeling and Dysfunction in Mice Post-Myocardial Infarction RR

    PubMed Central

    Xu, Jiang; Sun, Ying; Carretero, Oscar A; Zhu, Liping; Harding, Pamela; Shesely, Edward G.; Dai, Xiangguo; Rhaleb, Nour-Eddine; Peterson, Edward; Yang, Xiao-Ping

    2014-01-01

    Activation of the angiotensin II type 2 receptors (AT2R) has been considered cardioprotective. However, there are controversial findings regarding the role of overexpressing AT2R in the heart. Using transgenic mice with different levels of AT2R gene overexpression in the heart (1, 4 or 9 copies of the AT2R transgene, Tg1, Tg4 or Tg9), we studied the effect of AT2R overexpression on left ventricular remodeling and dysfunction post-myocardial infarction (MI). Tg1, Tg4, Tg9 and their wild-type (WT) littermates were divided into 1) sham MI, 2) MI + vehicle, and 3) MI + AT2R antagonist. Treatments were started 4 weeks after MI and continued for 8 weeks. AT2R protein and mRNA expression in the heart was significantly increased in transgenic mice and the increase positively correlated with copies of the transgene. AT1R mRNA and protein expression remained unchanged in Tg1 and Tg4 but slightly higher in Tg9 mice. Systolic blood pressure and cardiac phenotypes did not differ among strains under basal conditions. MI caused myocardial hypertrophy, interstitial fibrosis, ventricular dilatation and dysfunction associated with increased protein expression of Nox2 and transforming growth factor (TGF)-β1 expression. These pathological responses were diminished in Tg1 and Tg4 mice. Moreover, the protective effects of AT2R were abolished by AT2R antagonist and also absent in Tg9 mice. We thus conclude that whether overexpression of AT2R is beneficial or detrimental to the heart is largely dependent on expression levels and possibly via regulations of Nox2 and TGF-β1 signaling pathways. PMID:24732892

  2. 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

  3. 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.

  4. 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

  5. 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

  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. 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.

  8. 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

    Background 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. Methods 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. Results 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

  9. 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.

  10. Reduction of early ventricular arrhythmia by acebutolol in patients with acute myocardial infarction.

    PubMed Central

    Ahumada, G G; Karlsberg, R P; Jaffe, A S; Ambos, H D; Sobel, B E; Roberts, R

    1979-01-01

    To assess the effects of intravenously administered acebutolol (1-20 mg every 4 hours for 24 hours) on cardiac rhythm and performance, we studied 72 patients with evolving myocardial infarction. Twenty-five patients were treated with acebutolol beginning 6 hours after the first increase in the level of plasma creatine kinase. Enzymatically estimated infarct size was compared with that of 25 controls matched for predicted infarct size. Observed infarct sizes were not significantly different in the 2 groups (37 +/- 5 and 30 +/- 5 CK-gram equivalents, respectively). Mean heart rate, diastolic blood pressure, and cardiac output declined from control values during treatment with acebutolol, but remained within the normal range. Mean pulmonary artery pressure and pulmonary artery occlusive pressure were unchanged. In a group of 22 treated patients matched with 22 control subjects for frequency of ventricular extrasystoles, acebutolol effected a prompt reduction in frequencies of ventricular extrasystoles and repetitive arrhythmias, whereas values were not significantly changed in controls during the corresponding intervals. Accordingly, acebutolol may be a useful antiarrhythmic agent in selected patients with acute myocardial infarction with adversely altering haemodynamic stability or enzymatically estimated infarct size. PMID:465240

  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. 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.

  13. 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

  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. 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.

  16. 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

  17. Long-term effect of β-blocker in ST-segment elevation myocardial infarction in patients with preserved left ventricular systolic function: a propensity analysis.

    PubMed

    Konishi, Hirokazu; Miyauchi, Katsumi; Kasai, Takatoshi; Tsuboi, Shuta; Ogita, Manabu; Naito, Ryo; Nishizaki, Yuji; Okai, Iwao; Tamura, Hiroshi; Okazaki, Shinya; Isoda, Kikuo; Daida, Hiroyuki

    2016-04-01

    The current guidelines for acute myocardial infarction (AMI) recommended that β-blocker should be used in patients with decreased left ventricular (LV) systolic function for long-term period. However, the effect of β-blocker in AMI patients with preserved LV systolic function is uncertain. We sought to assess the long-term effect of β-blocker in AMI patients with preserved LV systolic function. During the follow-up period (1997-2011), total 3508 patients were performed percutaneous coronary intervention (PCI). Of these patients, 424 AMI patients with preserved LV systolic function [ejection fraction (EF) > 40 %] were analyzed. Median follow-up period was 4.7 years. Then, patients were divided into two groups (β-blocker group 197 patients and no-β-blocker group 227 patients). However, there are substantial differences in baseline characteristics between two groups. Therefore, we calculated propensity score to match the patients in β-blocker and no-β-blocker groups. After post-match patients (N = 206, 103 matched pair), β-blocker therapy significantly reduced cardiac death compared with no-β-blocker [hazard ratio (HR) 0.40, p = 0.04], whereas β-blocker therapy was not associated with major adverse cardiac events (MACE) and all-cause death. β-Blocker is an effective treatment for AMI patients who underwent PCI with preserved LV systolic function.

  18. Invasive surgery reduces infarct size and preserves cardiac function in a porcine model of myocardial infarction

    PubMed Central

    van Hout, Gerardus PJ; Teuben, Michel PJ; Heeres, Marjolein; de Maat, Steven; de Jong, Renate; Maas, Coen; Kouwenberg, Lisanne HJA; Koenderman, Leo; van Solinge, Wouter W; de Jager, Saskia CA; Pasterkamp, Gerard; Hoefer, Imo E

    2015-01-01

    Reperfusion injury following myocardial infarction (MI) increases infarct size (IS) and deteriorates cardiac function. Cardioprotective strategies in large animal MI models often failed in clinical trials, suggesting translational failure. Experimentally, MI is induced artificially and the effect of the experimental procedures may influence outcome and thus clinical applicability. The aim of this study was to investigate if invasive surgery, as in the common open chest MI model affects IS and cardiac function. Twenty female landrace pigs were subjected to MI by transluminal balloon occlusion. In 10 of 20 pigs, balloon occlusion was preceded by invasive surgery (medial sternotomy). After 72 hrs, pigs were subjected to echocardiography and Evans blue/triphenyl tetrazoliumchloride double staining to determine IS and area at risk. Quantification of IS showed a significant IS reduction in the open chest group compared to the closed chest group (IS versus area at risk: 50.9 ± 5.4% versus 69.9 ± 3.4%, P = 0.007). End systolic LV volume and LV ejection fraction measured by echocardiography at follow-up differed significantly between both groups (51 ± 5 ml versus 65 ± 3 ml, P = 0.033; 47.5 ± 2.6% versus 38.8 ± 1.2%, P = 0.005). The inflammatory response in the damaged myocardium did not differ between groups. This study indicates that invasive surgery reduces IS and preserves cardiac function in a porcine MI model. Future studies need to elucidate the effect of infarct induction technique on the efficacy of pharmacological therapies in large animal cardioprotection studies. PMID:26282710

  19. 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.

  20. 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

  1. 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

  2. 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

  3. Late onset oral treatment with tranilast following large myocardial infarction has no beneficial effects on cardiac remodeling and mortality in rats

    PubMed Central

    BETGE, STEFAN; KUNZ, CHRISTIAN; FIGULLA, HANS; JUNG, CHRISTIAN

    2014-01-01

    Tranilast (Tra) reduces intracardiac interstitial fibrosis in the animal models of hypertensive heart failure and diabetic cardiomyopathy by inhibiting cardiac fibroblasts. The present study examined whether Tra has long-term effects on the cardiac remodeling in the remote area of the left ventricle (LV) following myocardial infarction (MI) in the rat. Treatment with Tra (n=40; 150 mg/kg twice daily) or placebo (Plac, n=36) was started at day 28 after induction of a large MI or sham-operation (ShO, n=18) in female Lewis rats. Collagen content was determined using high-performance liquid chromatography. Large MI led to a significant hypertrophy of the two ventricles, a severe dilatation of the LV and a shift of the chamber stiffness variables in the pressure volume curves. The six-month survival rates were Tra, 62.5%; Plac, 75%; and ShO, 100%. No significant difference was identified between Tra and Plac regarding survival rate and collagen content. Treatment with the anti-inflammatory and antifibrotic drug, Tra, started four weeks after the induction of a large MI in the rat, did not attenuate or positively influence remodeling in chronic ischemic heart failure and survival. Further studies are required to explore the effects of Tra on cardiac myocytes post-MI in more detail. PMID:25371734

  4. Effect of low dose acetylsalicylic acid on the frequency and hematologic activity of left ventricular thrombus in anterior wall acute myocardial infarction

    SciTech Connect

    Kuepper, A.J.V.; Verheugt, F.W.; Peels, C.H.; Galema, T.W.; den Hollander, W.; Roos, J.P.

    1989-04-15

    In this prospective, randomized, placebo-controlled trial the effect of 100 mg acetylsalicylic acid (ASA) once daily on the incidence, hematologic activity and embolic potential of left ventricular (LV) thrombosis was studied in 100 consecutive patients with a first anterior wall acute myocardial infarction (AMI). Patients were randomized to ASA or placebo less than 12 hours after onset of symptoms. Heparin, 5,000 IU subcutaneously twice daily, was given to all patients during immobilization. Echocardiography was performed less than 24 hours, 48 to 72 hours and 1, 2, and 12 weeks after AMI. LV thrombosis was detected by echocardiography in 30 (33%) of the 92 evaluable patients (15 patients given ASA and 15 given placebo). Indium-111 platelet scintigraphy was done in 17 of the 22 patients with an LV thrombus at the second week echocardiogram. Among 7 ASA-treated patients, 4 had positive images; among 10 placebo patients, 5 had positive images. LV thrombus resolution was noted in 3 of 9 patients with a positive scan and in 5 of 8 patients with a negative platelet scan. In 7 of 10 ASA-treated patients and 5 of 12 placebo-treated patients thrombus resolution was observed (difference not significant). Systemic embolism occurred in 2 patients, both given ASA, during the first week after AMI. Thus, low dose ASA has no effect on the incidence, hematologic activity and embolic potential of LV thrombosis in anterior wall AMI.

  5. [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.

  6. 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

  7. Neural Mechanisms and Delayed Gastric Emptying of Liquid Induced Through Acute Myocardial Infarction in Rats

    PubMed Central

    Nunez, Wilson Ranu Ramirez; Ozaki, Michiko Regina; Vinagre, Adriana Mendes; Collares, Edgard Ferro; de Almeida, Eros Antonio

    2015-01-01

    Background In pathological situations, such as acute myocardial infarction, disorders of motility of the proximal gut can trigger symptoms like nausea and vomiting. Acute myocardial infarction delays gastric emptying (GE) of liquid in rats. Objective Investigate the involvement of the vagus nerve, α 1-adrenoceptors, central nervous system GABAB receptors and also participation of paraventricular nucleus (PVN) of the hypothalamus in GE and gastric compliance (GC) in infarcted rats. Methods Wistar rats, N = 8-15 in each group, were divided as INF group and sham (SH) group and subdivided. The infarction was performed through ligation of the left anterior descending coronary artery. GC was estimated with pressure-volume curves. Vagotomy was performed by sectioning the dorsal and ventral branches. To verify the action of GABAB receptors, baclofen was injected via icv (intracerebroventricular). Intravenous prazosin was used to produce chemical sympathectomy. The lesion in the PVN of the hypothalamus was performed using a 1mA/10s electrical current and GE was determined by measuring the percentage of gastric retention (% GR) of a saline meal. Results No significant differences were observed regarding GC between groups; vagotomy significantly reduced % GR in INF group; icv treatment with baclofen significantly reduced %GR. GABAB receptors were not conclusively involved in delaying GE; intravenous treatment with prazosin significantly reduced GR% in INF group. PVN lesion abolished the effect of myocardial infarction on GE. Conclusion Gastric emptying of liquids induced through acute myocardial infarction in rats showed the involvement of the vagus nerve, alpha1- adrenergic receptors and PVN. PMID:25494017

  8. Smad3 inactivation and MiR-29b upregulation mediate the effect of carvedilol on attenuating the acute myocardium infarction-induced myocardial fibrosis in rat.

    PubMed

    Zhu, Jie-Ning; Chen, Ren; Fu, Yong-Heng; Lin, Qiu-Xiong; Huang, Shuai; Guo, Lin-Lin; Zhang, Meng-Zhen; Deng, Chun-Yu; Zou, Xiao; Zhong, Shi-Long; Yang, Min; Zhuang, Jian; Yu, Xi-Yong; Shan, Zhi-Xin

    2013-01-01

    Carvedilol, a nonselective β-adrenoreceptor antagonist, protects against myocardial injury induced by acute myocardium infarction (AMI). The mechanisms underlying the anti-fibrotic effects of carvedilol are unknown. Recent studies have revealed the critical role of microRNAs (miRNAs) in a variety of cardiovascular diseases. This study investigated whether miR-29b is involved in the cardioprotective effect of carvedilol against AMI-induced myocardial fibrosis. Male SD rats were randomized into several groups: the sham surgery control, left anterior descending (LAD) surgery-AMI model, AMI plus low-dose carvedilol treatment (1 mg/kg per day, CAR-L), AMI plus medium-dose carvedilol treatment (5 mg/kg per day, CAR-M) and AMI plus high-dose carvedilol treatment (10 mg/kg per day, CAR-H). Cardiac remodeling and impaired heart function were observed 4 weeks after LAD surgery treatment; the observed cardiac remodeling, decreased ejection fraction, and fractional shortening were rescued in the CAR-M and CAR-H groups. The upregulated expression of Col1a1, Col3a1, and α-SMA mRNA was significantly reduced in the CAR-M and CAR-H groups. Moreover, the downregulated miR-29b was elevated in the CAR-M and CAR-H groups. The in vitro study showed that Col1a1, Col3a1, and α-SMA were downregulated and miR-29b was upregulated by carvedilol in a dose-dependent manner in rat cardiac fibroblasts. Inhibition of ROS-induced Smad3 activation by carvedilol resulted in downregulation of Col1a1, Col3a1, and α-SMA and upregulation of miR-29b derived from the miR-29b-2 precursor. Enforced expression of miR-29b significantly suppressed Col1a1, Col3a1, and α-SMA expression. Taken together, we found that smad3 inactivation and miR-29b upregulation contributed to the cardioprotective activity of carvedilol against AMI-induced myocardial fibrosis.

  9. Effects of beta receptor antagonists in patients with clinical evidence of heart failure after myocardial infarction: double blind comparison of metoprolol and xamoterol.

    PubMed Central

    Persson, H.; Rythe'n-Alder, E.; Melcher, A.; Erhardt, L.

    1995-01-01

    OBJECTIVE--To evaluate whether xamoterol, a partial agonist, would improve exercise time more than metoprolol in patients with mild to moderate heart failure after a myocardial infarction. DESIGN--Single-centre double blind randomised parallel group comparison of metoprolol 50-100 mg and xamoterol 100-200 mg twice daily. PATIENTS--210 patients aged 40-80 years (173 men) with clinical evidence of heart failure early after a myocardial infarction. 106 were given metoprolol and 104 xamoterol. MAIN OUTCOME MEASURES--Exercise test results and performance at three months; the exercise test, quality of life, and clinical assessments at baseline (5-7 days after the infarction) and after 3, 6, and 12 months. RESULTS--Exercise time increased at three months by 22% in the metoprolol group and 29% in the xamoterol group, but with no significant difference between the groups. Patients taking xamoterol showed overall non-significantly higher mean values of exercise time achieved with higher heart rates at rest and exercise. Improvements in quality of life, clinical signs of heart failure, and New York Heart Association functional class were seen in both treatment groups over one year, with minor benefits of xamoterol on breathlessness, peripheral oedema, and functional class. Eighteen patients taking metoprolol and 22 taking xamoterol withdrew from the study during one year, with a low mortality, reinfarction rate, and progress of heart failure in both treatment groups. Mean dose from baseline to 3 months was 135 mg metoprolol and 347 mg xamoterol. CONCLUSION--beta 1 Receptor antagonists with or without partial agonist activity are safe to use in mild to moderate heart failure after a myocardial infarction. Exercise tolerance, quality of life, and clinical signs and functional class of heart failure improve, and few patients show deterioration in their condition. Exercise tolerance is no better with xamoterol than metoprolol. PMID:7546992

  10. Chitosan hydrogel improves mesenchymal stem cell transplant survival and cardiac function following myocardial infarction in rats

    PubMed Central

    Xu, Bin; Li, Yang; Deng, Bo; Liu, Xiaojing; Wang, Lin; Zhu, Qing-Lei

    2017-01-01

    Myocardial infarction (MI) remains the leading cause of cardiovascular-associated mortality and morbidity. Improving the retention rate, survival and cardiomyocyte differentiation of mesenchymal stem cells (MSCs) is important in improving the treatment of patients with MI. In the present study, temperature-responsive chitosan hydrogel, an injectable scaffold, was used to deliver MSCs directly into the infarcted myocardium of rats following MI. Histopathology and immunohistochemical staining were used to evaluate cardiac cell survival and regeneration, and cardiac function was assessed using an echocardiograph. It was demonstrated that chitosan hydrogel increased graft size and cell retention in the ischemic heart, promoted MSCs to differentiate into cardiomyocytes and increased the effects of MSCs on neovasculature formation. Furthermore, chitosan hydrogel enhanced the effect of MSCs on the improvement of cardiac function and hemodynamics in the infarcted area of rats following MI. These findings suggest that chitosan hydrogel is an appropriate material to deliver MSCs into infarcted myocardium. PMID:28352335

  11. The economics of cardiac biomarker testing in suspected myocardial infarction.

    PubMed

    Goodacre, Steve; Thokala, Praveen

    2015-03-01

    Suspected myocardial infarction (MI) is a common reason for emergency hospital attendance and admission. Cardiac biomarker measurement is an essential element of diagnostic assessment of suspected MI. Although the cost of a routinely available biomarker may be small, the large patient population and consequences in terms of hospital admission and investigation mean that the economic impact of cardiac biomarker testing is substantial. Economic evaluation involves comparing the estimated costs and effectiveness (outcomes) of two or more interventions or care alternatives. This process creates some difficulties with respect to cardiac biomarkers. Estimating the effectiveness of cardiac biomarkers involves identifying how they help to improve health and how we can measure this improvement. Comparison to an appropriate alternative is also problematic. New biomarkers may be promoted on the basis of reducing hospital admission or length of stay, but hospital admission for low risk patients may incur significant costs while providing very little benefit, making it an inappropriate comparator. Finally, economic evaluation may conclude that a more sensitive biomarker strategy is more effective but, by detecting and treating more cases, is also more expensive. In these circumstances it is unclear whether we should use the more effective or the cheaper option. This article provides an introduction to health economics and addresses the specific issues relevant to cardiac biomarkers. It describes the key concepts relevant to economic evaluation of cardiac biomarkers in suspected MI and highlights key areas of uncertainty and controversy.

  12. [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.

  13. [The causes of death after acute myocardial infarction (author's transl)].

    PubMed

    Puletti, M; Zingales, L D; Borgia, C; La Rosa, A; Curione, M; Pozzar, F; Righetti, G; Jacobellis, G F

    1979-01-01

    Following a brief outline on problems concerning methodology, the cause of death is analysed in 110 patients dying from acute myocardial infarction during hospitalization. Autopsy studied were carried out in 78 cases. Of the various causes, the most frequent were forms of contractile insufficiency (EPA, shock, shock + EPA, biventricular congestive heart failure) which were responsible for 50.90% of cases; followed by cardiac rupture (considered in a single group with electromechanic dissociations of the patients not submitted to autopsy studies since in the experience of the Authors cardiac rupture almost always presents with this pattern) with a frequency of 29%. The frequency of arrhythmias, on the other hand, is very low, particularly in the coronary care unit where it is practically a negligible causa mortis 2.72%): even if sudden death, in patients who were not monitored, is included amongst the arrhythmias, the percentage is still only about 10%. Embolism (usually pulmonary, but systemic in one case) was the cause of death in 5 patients (4.54%). Three patients over 80 years of age died from ischemic cerebral episodes. Age, sex, and site of infarction, do not appear, in the present series, to have a determinant effect in the cause of death; a higher frequency of rupture in the female sex was not, for example, confirmed. On the basis of the observations in the present series, any relationship between cardiac rupture and anticoagulating therapy, steroid treatment, application of endocavitary stimulators, or early ambulation is excluded. It is also excluded that reanimation, as hypothesized by some Authors, may be responsible for rupture.

  14. 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

  15. Evaluation of the role of opium addiction in acute myocardial infarction as a risk factor

    PubMed Central

    Khosoosi Niaki, Mohammad Reza; Hamid, Mahdizadeh; Farshidi, Fatemeh; Mohammadpour, Mehdi; Salehi Omran, Mohammad Taghi

    2013-01-01

    Background: More than half of myocardial infracted (MI) patients have no conventional risk factors. Regarding the belief that opium addiction has a protective effect on heart diseases, addiction prevalence has unfortunately increased in recent years. This study was conducted to investigate the effect of opium addiction on patients with acute myocardial infarction. Methods: This case-control study was performed on 118 patients with acute myocardial infarction admitted to CCU ward (case group), and 118 patients with no history of MI to other wards (control group) of Shahid Beheshti Hospital in Babol, Iran. Opium addiction conventional risk factors were evaluated for both groups, and the data were analyzed using chi-square test and logistic regression model was used to adjust the conventional risk factor effects. Moreover, demographic variables as well as the extent of MI (extensive or non-extensive), and infarction type (ST-elevated or non-ST elevated) also were evaluated. Results: Sixty-seven patients in MI and 6 subjects in control group had a history of opium consumption (p<0.0001, OR=24.5). Blood pressure, hyperlipidemia, and smoking showed a significant difference between the two groups (p<0.05), whereas, no significant difference was observed for diabetes and family history. The results of adjusted model report a significant effect of opium consumption with the development of MI (OR=26.3). No significant difference was found in terms of infarction type and the extent between the addicts and non addicts in MI group. Conclusion: The results show that opium addiction is a strong risk factor for myocardial infarction. PMID:24009941

  16. Novel, selective EPO receptor ligands lacking erythropoietic activity reduce infarct size in acute myocardial infarction in rats.

    PubMed

    Kiss, Krisztina; Csonka, Csaba; Pálóczi, János; Pipis, Judit; Görbe, Anikó; Kocsis, Gabriella F; Murlasits, Zsolt; Sárközy, Márta; Szűcs, Gergő; Holmes, Christopher P; Pan, Yijun; Bhandari, Ashok; Csont, Tamás; Shamloo, Mehrdad; Woodburn, Kathryn W; Ferdinandy, Péter; Bencsik, Péter

    2016-11-01

    Erythropoietin (EPO) has been shown to protect the heart against acute myocardial infarction in pre-clinical studies, however, EPO failed to reduce infarct size in clinical trials and showed significant safety problems. Here, we investigated cardioprotective effects of two selective non-erythropoietic EPO receptor ligand dimeric peptides (AF41676 and AF43136) lacking erythropoietic activity, EPO, and the prolonged half-life EPO analogue, darbepoetin in acute myocardial infarction (AMI) in rats. In a pilot study, EPO at 100U/mL significantly decreased cell death compared to vehicle (33.8±2.3% vs. 40.3±1.5%, p<0.05) in rat neonatal cardiomyocytes subjected to simulated ischemia/reperfusion. In further studies (studies 1-4), in vivo AMI was induced by 30min coronary occlusion and 120min reperfusion in male Wistar rats. Test compounds and positive controls for model validation (B-type natriuretic peptide, BNP or cyclosporine A, CsA) were administered iv. before the onset of reperfusion. Infarct size (IS) was measured by standard TTC staining. In study 1, 5000U/kg EPO reduced infarct size significantly compared to vehicle (45.3±4.8% vs. 59.8±4.5%, p<0.05). In study 2, darbepoetin showed a U-shaped dose-response curve with maximal infarct size-reducing effect at 5μg/kg compared to the vehicle (44.4±5.7% vs. 65.9±2.7%, p<0.01). In study 3, AF41676 showed a U-shaped dose-response curve, where 3mg/kg was the most effective dose compared to the vehicle (24.1±3.9% vs. 44.3±2.5%, p<0.001). The positive control BNP significantly decreased infarct size in studies 1-3 by approximately 35%. In study 4, AF43136 at 10mg/kg decreased infarct size, similarly to the positive control CsA compared to the appropriate vehicle (39.4±5.9% vs. 58.1±5.4% and 45.9±2.4% vs. 63.8±4.1%, p<0.05, respectively). This is the first demonstration that selective, non-erythropoietic EPO receptor ligand dimeric peptides AF41676 and AF43136 administered before reperfusion are able to reduce

  17. Solar Activity, Different Geomagnetic Activity Levels and Acute Myocardial Infarction

    NASA Astrophysics Data System (ADS)

    Dimitrova, Svetla; Jordanova, Malina; Stoilova, Irina; Taseva, Tatiana; Maslarov, Dimitar

    Results on revealing a possible relationship between solar activity (SA) and geomagnetic activity (GMA) and acute myocardial infarction (AMI) morbidity are presented. Studies were based on medical data covering the period from 1.12.1995 to 31.12.2004 and concerned daily distribution of patients with AMI diagnose (in total 1192 cases) from Sofia region on the day of admission at the hospital. Analysis of variance (ANOVA) was applied to check the significance of GMA intensity effect and the type of geomagnetic storms, those caused by Magnetic Clouds (MC) and by High Speed Solar Wind Streams (HSSWS), on AMI morbidity. Relevant correlation coefficients were calculated. Results revealed statistically significant positive correlation between considered GMA indices and AMI. ANOVA revealed that AMI number was signifi- cantly increased from the day before (-1st) till the day after (+1st) geomagnetic storms with different intensities. Geomagnetic storms caused by MC were related to significant increase of AMI number in comparison with the storms caused by HSSWS. There was a trend for such different effects even on -1st and +1st day.

  18. Intestinal Microbial Metabolites Are Linked to Severity of Myocardial Infarction in Rats

    PubMed Central

    Lam, Vy; Su, Jidong; Hsu, Anna; Gross, Garrett J.; Salzman, Nita H.

    2016-01-01

    Intestinal microbiota determine severity of myocardial infarction in rats. We determined whether low molecular weight metabolites derived from intestinal microbiota and transported to the systemic circulation are linked to severity of myocardial infarction. Plasma from rats treated for seven days with the non-absorbed antibiotic vancomycin or a mixture of streptomycin, neomycin, polymyxin B and bacitracin was analyzed using mass spectrometry-based metabolite profiling platforms. Antibiotic-induced changes in the abundance of individual groups of intestinal microbiota dramatically altered the host’s metabolism. Hierarchical clustering of dissimilarities separated the levels of 284 identified metabolites from treated vs. untreated rats; 193 were altered by the antibiotic treatments with a tendency towards decreased metabolite levels. Catabolism of the aromatic amino acids phenylalanine, tryptophan and tyrosine was the most affected pathway comprising 33 affected metabolites. Both antibiotic treatments decreased the severity of an induced myocardial infarction in vivo by 27% and 29%, respectively. We then determined whether microbial metabolites of the amino acids phenylalanine, tryptophan and tyrosine were linked to decreased severity of myocardial infarction. Vancomycin-treated rats were administered amino acid metabolites prior to ischemia/reperfusion studies. Oral or intravenous pretreatment of rats with these amino acid metabolites abolished the decrease in infarct size conferred by vancomycin. Inhibition of JAK-2 (AG-490, 10 μM), Src kinase (PP1, 20 μM), Akt/PI3 kinase (Wortmannin, 100 nM), p44/42 MAPK (PD98059, 10 μM), p38 MAPK (SB203580, 10 μM), or KATP channels (glibenclamide, 3 μM) abolished cardioprotection by vancomycin, indicating microbial metabolites are interacting with cell surface receptors to transduce their signals through Src kinase, cell survival pathways and KATP channels. These inhibitors have no effect on myocardial infarct size in

  19. 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

  20. [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.

  1. [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.

  2. 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.

  3. Tomato lycopene attenuates myocardial infarction induced by isoproterenol: Electrocardiographic, biochemical and anti-apoptotic study

    PubMed Central

    Aman, Upaganlawar; Vaibhav, Patel; Balaraman, R

    2012-01-01

    Objective To assess the protective effects of lycopene on electrocardiographic, hemodynamic, biochemical and apoptotic changes in isoproterenol induced myocardial infarction. Methods Myocardial infarction was induced in rats by subcutaneous injection of isoproterenol (200 mg/kg) for two consecutive days at an interval of 24 h. Rats were treated with lycopene (10 mg/kg/day, p.o.) for a period of 30 days and isoproterenol (ISO) was injected on the 29th and 30th day. At the end of experiment i.e. on the 31st day electrocardiographic, hemodynamic, biochemical and apoptotic changes were monitored from control and experimental groups. Results ISO injected rats showed a significant alteration in electrocardiograph pattern and hemodynamic changes (i.e. systolic, diastolic and mean arterial pressure). It also showed significant increase in C-reactive protein, myeloperoxidase, nitrite levels and Caspase-3 protease activity. In addition, it also exhibited alteration in the levels of electrolytes (Na+, K+ and Ca2+), vitamin E, uric acid and serum protein. Gel electrophoresis of ISO injected rats showed increase in DNA fragmentation. Triphenyl tetrazolium chloride staining of the heart section shows increase area of infarction in ISO injected rats. Pre-co-treatment with lycopene significantly prevented the ISO induced alteration in ECG, haemodynamic, biochemical and apoptotic changes. Conclusions The present result shows that treatment of lycopene in ISO injected rats significantly attenuates induced myocardial infarction. PMID:23569928

  4. The role of cardiac magnetic resonance imaging (MRI) in acute myocardial infarction (AMI).

    PubMed

    Ahmed, Nadeem; Carrick, David; Layland, Jamie; Oldroyd, Keith G; Berry, Colin

    2013-04-01

    Acute myocardial infarction (AMI) is a leading cause of mortality and morbidity in the world, despite the rate having significantly declined over the past decade. The aim of this review is to consider the emerging diagnostic and clinical utility of cardiac MRI in patients with recent AMI. Cardiac MRI has high reproducibility and accuracy, allowing detailed functional assessment and characterisation of myocardial tissue. In addition to traditional measures including infarct size (IS), transmural extent of necrosis and microvascular obstruction (MVO), other infarct characteristics can now be identified using innovative MRI techniques. These novel pathologies include myocardial oedema and myocardial haemorrhage which also have functional and prognostic implications for patients. In addition to its diagnostic utility in ordinary clinical practice, cardiac MRI has been increasingly used to provide information on surrogate outcome measures, such as left ventricular ejection fraction (LVEF) and volumes, in clinical trials. MRI is becoming more available in secondary care, however, the potential clinical utility and cost effectiveness of MRI in post-MI patients remains uncertain. Cardiac MRI is most likely to be useful in high risk patients with risk factors for heart failure (HF). This includes individuals with early signs of pump failure and risk factors for adverse remodelling, such as MVO. This review focuses on the role of cardiac MRI in the assessment of patients with AMI.

  5. 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

  6. 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

  7. 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.

  8. 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.

  9. 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.

  10. 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.

  11. Effect of pioglitazone on arterial baroreflex sensitivity and sympathetic nerve activity in patients with acute myocardial infarction and type 2 diabetes mellitus.

    PubMed

    Yokoe, Hiroshi; Yuasa, Fumio; Yuyama, Reisuke; Murakawa, Kousuke; Miyasaka, Yoko; Yoshida, Susumu; Tsujimoto, Satoshi; Sugiura, Tetsuro; Iwasaka, Toshiji

    2012-06-01

    Pioglitazone has been shown to reduce the occurrence of fatal and nonfatal myocardial infarction (MI) in type 2 diabetes mellitus (DM). However, the mechanisms of such favorable effects remain speculative. The aim of this study was to investigate the effect of pioglitazone on arterial baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA) in 30 DM patients with recent MI. Patients were randomly assigned to those taking pioglitazone (n = 15) and those not taking pioglitazone (n = 15) at 4 weeks after the onset of MI. BRS, MSNA, calculated homeostasis model assessment of insulin resistance index (HOMA-IR), and plasma adiponectin were measured at baseline and after 12 weeks. Pioglitazone increased plasma adiponectin (from 6.9 ± 3.3 μg/dL to 12.2 ± 7.1 μg/dL) and reduced HOMA-IR (from 4.0 ± 2.2 to 2.1 ± 0.9). In the pioglitazone group, MSNA decreased significantly (from 37 ± 7 bursts/min to 25 ± 8 bursts/min) and BRS increased significantly (from 6.7 ± 3.0 to 9.9 ± 3.2 ms/mm Hg) after 12 weeks. Furthermore, a significant relationship was found between the change in MSNA and HOMA-IR (r = 0.6, P = 0.042). Thus, pioglitazone decreased the sympathetic nerve traffic through the improvement of insulin resistance in DM patients with recent MI, which indicate that the sympathoinhibitory effects of pioglitazone may, at least in part, have contributed to the beneficial effects of pioglitazone.

  12. 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.

  13. Different hemodynamic actions of trinitroglycerin and isosorbide dinitrate in patients with acute myocardial infarction.

    PubMed

    Rezakovic, D; Rutishauser, W; Pavicic, L; Popadic, M; Bloch, A; Imhoff, E W

    1983-10-01

    The hemodynamic effects of intravenously administered trinitroglycerin (TNT) and isosorbide dinitrate (ISDN) in stechiometric equivalent doses were studied in 30 patients with acute myocardial infarction. Both drugs were given over 30 min in every patient, and the stability of the condition of the patient was checked by administering the initial drug again. Measurements were made by right heart catheterization using a balloon tip thermodilution catheter and a catheter in the radial artery. TNT and ISDN have different hemodynamic effects. By multivariate analysis it could be shown that TNT is a venous dilator, lowering mainly pulmonary capillary pressure, while ISDN acts more as a mixed vasodilator, diminishing mainly peripheral vascular resistance and increasing cardiac output. These drugs have, therefore, a different spectrum of indications in patients with acute myocardial infarction.

  14. Bioengineering of injectable encapsulated aggregates of pluripotent stem cells for therapy of myocardial infarction

    PubMed Central

    Zhao, Shuting; Xu, Zhaobin; Wang, Hai; Reese, Benjamin E.; Gushchina, Liubov V.; Jiang, Meng; Agarwal, Pranay; Xu, Jiangsheng; Zhang, Mingjun; Shen, Rulong; Liu, Zhenguo; Weisleder, Noah; He, Xiaoming

    2016-01-01

    It is difficult to achieve minimally invasive injectable cell delivery while maintaining high cell retention and animal survival for in vivo stem cell therapy of myocardial infarction. Here we show that pluripotent stem cell aggregates pre-differentiated into the early cardiac lineage and encapsulated in a biocompatible and biodegradable micromatrix, are suitable for injectable delivery. This method significantly improves the survival of the injected cells by more than six-fold compared with the conventional practice of injecting single cells, and effectively prevents teratoma formation. Moreover, this method significantly enhances cardiac function and survival of animals after myocardial infarction, as a result of a localized immunosuppression effect of the micromatrix and the in situ cardiac regeneration by the injected cells. PMID:27786170

  15. Meteorological factors and the time of onset of chest pain in acute myocardial infarction

    NASA Astrophysics Data System (ADS)

    Thompson, David R.; Pohl, Jurgen E.; Tse, Yiu-Yu S.; Hiorns, Robert W.

    1996-09-01

    Analysis of the time of onset of chest pain in 2254 patients with a myocardial infarction admitted to a coronary care unit in Leicester during a 10-year period shows an association with temperature and humidity. During both the most cold and humid times of the year, the relationship is a strong one. A generalized linear model with a log link was used to fit the data and the backward elimination selection procedure suggested a humid, cold day might help to trigger the occurrence of myocardial infarction. In addition, cold weather was found to have a stronger effect on the male population while those men aged between 50 and 70 years were more sensitive to the effect of high humidity.

  16. Bioengineering of injectable encapsulated aggregates of pluripotent stem cells for therapy of myocardial infarction

    NASA Astrophysics Data System (ADS)

    Zhao, Shuting; Xu, Zhaobin; Wang, Hai; Reese, Benjamin E.; Gushchina, Liubov V.; Jiang, Meng; Agarwal, Pranay; Xu, Jiangsheng; Zhang, Mingjun; Shen, Rulong; Liu, Zhenguo; Weisleder, Noah; He, Xiaoming

    2016-10-01

    It is difficult to achieve minimally invasive injectable cell delivery while maintaining high cell retention and animal survival for in vivo stem cell therapy of myocardial infarction. Here we show that pluripotent stem cell aggregates pre-differentiated into the early cardiac lineage and encapsulated in a biocompatible and biodegradable micromatrix, are suitable for injectable delivery. This method significantly improves the survival of the injected cells by more than six-fold compared with the conventional practice of injecting single cells, and effectively prevents teratoma formation. Moreover, this method significantly enhances cardiac function and survival of animals after myocardial infarction, as a result of a localized immunosuppression effect of the micromatrix and the in situ cardiac regeneration by the injected cells.

  17. Post-infarct sleep disruption and its relation to cardiac remodeling in a rat model of myocardial infarction.

    PubMed

    Aghajani, Marjan; Faghihi, Mahdieh; Imani, Alireza; Vaez Mahdavi, Mohammad Reza; Shakoori, Abbas; Rastegar, Tayebeh; Parsa, Hoda; Mehrabi, Saman; Moradi, Fatemeh; Kazemi Moghaddam, Ehsan

    2017-02-03

    Sleep disruption after myocardial infarction (MI) by affecting ubiquitin-proteasome system (UPS) is thought to contribute to myocardial remodeling and progressive worsening of cardiac function. The aim of current study was to test the hypothesis about the increased risk of developing heart failure due to experience of sleep restriction (SR) after MI. Male Wistar rats (n = 40) were randomly assigned to four experimental groups: (1) Sham, (2) MI, (3) MI and SR (MI + SR) (4) Sham and SR (Sham + SR). MI was induced by permanent ligation of left anterior descending coronary artery. Twenty-four hours after surgery, animals were subjected to chronic SR paradigm. Blood sampling was performed at days 1, 8 and 21 after MI for determination of serum levels of creatine kinase-MB (CK-MB), corticosterone, malondialdehyde (MDA) and nitric oxide (NO). Finally, at 21 days after MI, echocardiographic parameters and expression of MuRF1, MaFBx, A20, eNOS, iNOS and NF-kB in the heart were evaluated. We used H&E staining to detect myocardial hypertrophy. We found out that post infarct SR increased corticosterone levels. Our results highlighted deteriorating effects of post-MI SR on NO production, oxidative stress, and echocardiographic indexes (p < 0.05). Moreover, its detrimental effects on myocardial damage were confirmed by overexpression of MuRF1, MaFBx, iNOS and NF-kB (p < 0.001) in left ventricle and downregulation of A20 and eNOS (p < 0.05). Furthermore, histological examination revealed that experience of SR after MI increased myocardial diameter as compared to Sham subjects (p < 0.05). Our data suggest that SR after MI leads to an enlargement of the heart within 21 days, marked by an increase in oxidative stress and NO production as well as an imbalance in UPS that ultimately results in cardiac dysfunction and heart failure.

  18. [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.

  19. 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

  20. 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

  1. 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.

  2. 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.

  3. Anti‐Inflammatory Peptides From Cardiac Progenitors Ameliorate Dysfunction After Myocardial Infarction

    PubMed Central

    Liu, Mei‐Lan; Nagai, Toshio; Tokunaga, Masakuni; Iwanaga, Koji; Matsuura, Katsuhisa; Takahashi, Toshinao; Kanda, Masato; Kondo, Naomichi; Naito, Atsuhiko T.; Komuro, Issei; Kobayashi, Yoshio

    2014-01-01

    Background Cardiac cell therapy has been proposed as one of the new strategies against myocardial infarction. Although several reports showed improvement of the function of ischemic heart, the effects of cell therapy vary among the studies and the mechanisms of the beneficial effects are still unknown. Previously, we reported that clonal stem cell antigen‐1–positive cardiac progenitor cells exerted a therapeutic effect when transplanted into the ischemic heart. Our aims were to identify the cardiac progenitor‐specific paracrine factor and to elucidate the mechanism of its beneficial effect. Methods and Results By using an antibody array, we found that soluble junctional adhesion molecule‐A (JAM‐A) was abundantly secreted from cardiac progenitor cells. Pretreatment of neutrophils with conditioned medium from cultured cardiac progenitor cells or soluble JAM‐A inhibited transendothelial migration and reduced motility of neutrophils. These inhibitory effects were attenuated by anti–JAM‐A neutralizing antibody. Injection of cardiac progenitor cells into infarct heart attenuated neutrophil infiltration and expression of inflammatory cytokines. Injection of soluble JAM‐A–expressing, but not of JAM‐A siRNA–expressing, cardiac progenitor cells into the infarct heart prevented cardiac remodeling and reduced fibrosis area. Conclusions Soluble JAM‐A secreted from cardiac progenitor cells reduces infiltration of neutrophils after myocardial infarction and ameliorates tissue damage through prevention of excess inflammation. Our finding may lead to a new therapy for cardiovascular disease by using the anti‐inflammatory effect of JAM‐A. PMID:25468657

  4. 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

  5. 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

  6. 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.

  7. 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.

  8. Effects of Combined Phase III and Phase II Cardiac Exercise Therapy for Middle-aged Male Patients with Acute Myocardial Infarction.

    PubMed

    Lee, Chih-Wei; Wang, Ji-Hung; Hsieh, Jen-Che; Hsieh, Tsung-Cheng; Huang, Chien-Hui

    2013-11-01

    [Purpose] To investigate the effects of cardiac exercise therapy (CET) on exercise capacity and coronary risk factors (CRFs) of patients with acute myocardial infarction (AMI). [Methods] Patients who participated in an 8-week supervised, hospital-based phase II and 6-month home-based phase III CET with monthly telephone and/or home visits were defined as the exercise group (EG) (n=20), while those who did not receive phase II or phase III CET were defined as the no-exercise group (NEG) (n=10). CRFs were evaluated pre- and post-phase II and eight months after discharge. One and two-way repeated measures ANOVA were used to perform intra- and inter-group comparisons. [Results] Thirty men with AMI aged 49.3 ± 8.3 years were studied. EG increased their exercise capacity (METs) (6.8 ± 1.6 vs.10.0 ± 1.9) after phase II CET and was able to maintain it at 8-month follow-up. Both groups had significantly fewer persons who kept on smoking compared to the first examination. High density lipoprotein cholesterol (HDL-C) increased from 38.1 ± 11.0 to 43.7 ± 8.7 mg/dl at follow-up in EG while no significant difference was noted in NEG. [Conclusion] After phase III CET subjects had maintained the therapeutic effects of smoking cessation, and increasing exercise capacity obtained in phase II CET. HDL-C in EG continued to improve during phase III CET.

  9. 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.

  10. 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.

  11. 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.

  12. 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.

  13. 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

  14. 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.

  15. 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

  16. [Myocardial infarction associated with oral contraceptive use, smoking and elevated cholesterol level in a young patient].

    PubMed

    Krasznai, Zsuzsa; Tóth, Péter

    2011-09-04

    Oral hormonal contraceptives are the safest methods for young patients to avoid unwanted pregnancy. They are well accepted and have certain beneficial effects; however, physicians should pay attention to risk factors even when applied in young age. Obesity, dyslipidemia, smoking and oral contraceptive pills alone or in combination may lead to serious adverse events. Authors present a young woman who developed acute myocardial infarction in association with several unconsidered risk factors including the use of contraceptive pills.

  17. Testosterone replacement attenuates mitochondrial damage in a rat model of myocardial infarction.

    PubMed

    Wang, Fengyue; Yang, Jing; Sun, Junfeng; Dong, Yanli; Zhao, Hong; Shi, Hui; Fu, Lu

    2015-05-01

    Testosterone can affect cardiovascular disease, but its effects on mitochondrial dynamics in the post-infarct myocardium remain unclear. To observe the effects of testosterone replacement, a rat model of castration-myocardial infarction (MI) was established by ligating the left anterior descending coronary artery 2 weeks after castration with or without testosterone treatment. Expression of mitochondrial fission and fusion proteins was detected by western blot and immunofluorescence 14 days after MI. Cardiac function, myocardial inflammatory infiltration and fibrosis, cardiomyocyte apoptosis, mitochondrial microstructure, and ATP levels were also assessed. Compared with MI rats, castrated rats showed aggravated mitochondrial and myocardial insults, including mitochondrial swelling and disordered arrangement; loss of cristae, reduced mitochondrial length; decreased ATP levels; cardiomyocyte apoptosis; and impaired cardiac function. Results of western blotting analyses indicated that castration downregulated peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1A) and mitofusin 2, but upregulated dynamin-related protein 1. The results were also supported by results obtained using immunofluorescence. However, these detrimental effects were reversed by testosterone supplementation, which also elevated the upstream AMP-activated protein kinase (AMPK) activation of PGC1A. Thus, testosterone can protect mitochondria in the post-infarct myocardium, partly via the AMPK-PGC1A pathway, thereby decreasing mitochondrial dysfunction and cardiomyocyte apoptosis. The effects of testosterone were confirmed by the results of ELISA analyses.

  18. [Enalapril reduces the degree of left ventricular remodeling after acute myocardial infarction and reduces the incidence of arrhythmia in ischemic disease].

    PubMed

    Altieri, P I; González, R; de Mello, W; Escobales, N

    1994-12-01

    The present study shows that enalapril prevents the excessive remodeling of the left ventricle after acute myocardial infarction. This randomized and double blind clinical study analysed 50 patients with an inferior myocardial infarction. The effect of enalapril was evaluated through cardiac volumes, ejection fraction, neurohormonal levels and incidence of the left ventricle disfunction after acute myocardial infarction. The patients treated with enalapril showed a significant reduction on the values of nor-epinefrine, angiotensine II, natriuretic hormone and vasopressine, four weeks after initiation of treatment. The ejection fraction and the level of the wall movement was more favourable, four weeks after infarction, in the group treated with enalapril. The incidence of congestive heart failure and arrhythmias was lower in the group treated with enalapril. So, we conclude that enalapril is a drug that prevents the excessive remodelling of the left ventricle after an acute myocardial infarction.

  19. Relation of Left Ventricular Mass and Infarct Size in Anterior Wall ST-Segment Elevation Acute Myocardial Infarction (from the EMBRACE STEMI Clinical Trial).

    PubMed

    Daaboul, Yazan; Korjian, Serge; Weaver, W Douglas; Kloner, Robert A; Giugliano, Robert P; Carr, Jim; Neal, Brandon J; Chi, Gerald; Cochet, Madeleine; Goodell, Laura; Michalak, Nathan; Rusowicz-Orazem, Luke; Alkathery, Turky; Allaham, Haytham; Routray, Sujit; Szlosek, Donald; Jain, Purva; Gibson, C Michael

    2016-09-01

    Biomarker measures of infarct size and myocardial salvage index (MSI) are important surrogate measures of clinical outcomes after a myocardial infarction. However, there is variability in infarct size unaccounted for by conventional adjustment factors. This post hoc analysis of Evaluation of Myocardial Effects of Bendavia for Reducing Reperfusion Injury in Patients With Acute Coronary Events (EMBRACE) ST-Segment Elevation Myocardial Infarction (STEMI) trial evaluates the association between left ventricular (LV) mass and infarct size as assessed by areas under the curve for creatine kinase-MB (CK-MB) and troponin I release over the first 72 hours (CK-MB area under the curve [AUC] and troponin I [TnI] AUC) and the MSI. Patients with first anterior STEMI, occluded left anterior descending artery, and available LV mass measurement in EMBRACE STEMI trial were included (n = 100) (ClinicalTrials.govNCT01572909). MSI, end-diastolic LV mass on day 4 cardiac magnetic resonance, and CK-MB and troponin I concentrations were evaluated by a core laboratory. After saturated multivariate analysis, dominance analysis was performed to estimate the contribution of each independent variable to the predicted variance of each outcome. In multivariate models that included age, gender, body surface area, lesion location, smoking, and ischemia time, LV mass remained independently associated with biomarker measures of infarct size (CK-MB AUC p = 0.02, TnI AUC p = 0.03) and MSI (p = 0.003). Dominance analysis demonstrated that LV mass accounted for 58%, 47%, and 60% of the predicted variances for CK-MB AUC, TnI AUC, and MSI, respectively. In conclusion, LV mass accounts for approximately half of the predicted variance in biomarker measures of infarct size. It should be considered as an adjustment variable in studies evaluating infarct size.

  20. 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.

  1. 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.

  2. Vane blood-bathed technique reveals the significance of adrenergic reaction in myocardial infarction.

    PubMed

    Herbaczyńska-Cedro, Krystyna; Ceremuzyński, Leszek

    2010-01-01

    Using the blood-bathed technique of Vane we induced acute coronary occlusion in the dog and subsequently detected adrenaline release into the circulatory system, determined the rate of release and documented its significance for induction of cardiac arrhythmias. In the intact anesthetized dog, adrenaline excess of the magnitude released after coronary occlusion was sufficient to injure the healthy myocardium and to induce unfavorable metabolic systemic alterations. Subsequently, clinical research has documented that a serious clinical course of acute myocardial infarction is associated not only with enhanced excretion of catecholamines but also with augmentation of plasma renin activity and aldosterone levels. The positive therapeutic effect of aldosterone antagonists in acute myocardial infarction has been documented. The clinical value of our results, which were obtained in experimental and clinical studies, was later confirmed in multi-center trials.

  3. The impact of winter cold weather on acute myocardial infarctions in Portugal.

    PubMed

    Vasconcelos, João; Freire, Elisabete; Almendra, Ricardo; Silva, Giovani L; Santana, Paula

    2013-12-01

    Mortality due to cardiovascular diseases shows a seasonal trend that can be associated with cold weather. Portugal is the European country with the highest excess winter mortality, but nevertheless, the relationship between cold weather and health is yet to be assessed. The main aim of this study is to identify the contribution of cold weather to cardiovascular diseases within Portugal. Poisson regression analysis based on generalized additive models was applied to estimate the influence of a human-biometeorological index (PET) on daily hospitalizations for myocardial infarction. The main results revealed a negative effect of cold weather on acute myocardial infarctions in Portugal. For every degree fall in PET during winter, there was an increase of up to 2.2% (95% CI = 0.9%; 3.3%) in daily hospital admissions. This paper shows the need for public policies that will help minimize or, indeed, prevent exposure to cold.

  4. Propensity score-matched analysis of effects of clinical characteristics and treatment on gender difference in outcomes after acute myocardial infarction.

    PubMed

    Schiele, François; Meneveau, Nicolas; Seronde, Marie-France; Descotes-Genon, Vincent; Chopard, Romain; Janin, Sebastien; Briand, Florent; Guignier, Alexandre; Ecarnot, Fiona; Bassand, Jean-Pierre

    2011-09-15

    The greater mortality observed in women compared to men after acute myocardial infarction remains unexplained. Using an analysis of pairs, matched on a conditional probability of being male (propensity score), we assessed the effect of the baseline characteristics and management on 30-day mortality. Consecutive patients were included from January 2006 to December 2007. Two propensity scores (for being male) were calculated, 1 from the baseline characteristics and 1 from both the baseline characteristics and treatment. Two matched cohorts were composed using 1:1 matching and computed using the best 8 digits of the propensity score. Paired analyses were performed using conditional regression analysis. During the study period, 3,510 patients were included in the registry; 1,119 (32%) were women. Compared to the men, the women were 10 years older, had more co-morbidities, less often underwent angiography and reperfusion, and received less medical treatment. The 30-day mortality rate was 12.3% (130 of 1,060) for the women and 7.2% (167 of 2,324) for the men (p <0.001). The 2 matched populations represented 1,298 and 1,168 patients. After matching using the baseline characteristics, the only difference in treatment was a lower rate of angiography and reperfusion, with a trend toward greater 30-day mortality in women. After matching using both baseline characteristics and treatment, the 30-day mortality was similar for the men and women, suggesting that the increased use of invasive procedures in women could potentially be beneficial. In conclusion, compared to men, the 30-day mortality is greater in women and explained primarily by differences in baseline characteristics and to a lesser degree by differences in management. The difference in the use of invasive procedures persisted after matching by characteristics. In contrast, after matching using the baseline characteristics and treatment, the 30-day mortality was comparable across the genders.

  5. 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.

  6. 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.

  7. Reperfusion Therapy with Rapamycin Attenuates Myocardial Infarction through Activation of AKT and ERK

    PubMed Central

    Filippone, Scott M.; Samidurai, Arun; Roh, Sean K.; Cain, Chad K.; He, Jun; Salloum, Fadi N.; Kukreja, Rakesh C.

    2017-01-01

    Prompt coronary reperfusion is the gold standard for minimizing injury following acute myocardial infarction. Rapamycin, mammalian target of Rapamycin (mTOR) inhibitor, exerts preconditioning-like cardioprotective effects against ischemia/reperfusion (I/R) injury. We hypothesized that Rapamycin, given at the onset of reperfusion, reduces myocardial infarct size through modulation of mTOR complexes. Adult C57 male mice were subjected to 30 min of myocardial ischemia followed by reperfusion for 1 hour/24 hours. Rapamycin (0.25 mg/kg) or DMSO (7.5%) was injected intracardially at the onset of reperfusion. Post-I/R survival (87%) and cardiac function (fractional shortening, FS: 28.63 ± 3.01%) were improved in Rapamycin-treated mice compared to DMSO (survival: 63%, FS: 17.4 ± 2.6%). Rapamycin caused significant reduction in myocardial infarct size (IS: 26.2 ± 2.2%) and apoptosis (2.87 ± 0.64%) as compared to DMSO-treated mice (IS: 47.0 ± 2.3%; apoptosis: 7.39 ± 0.81%). Rapamycin induced phosphorylation of AKT S473 (target of mTORC2) but abolished ribosomal protein S6 phosphorylation (target of mTORC1) after I/R. Rapamycin induced phosphorylation of ERK1/2 but inhibited p38 phosphorylation. Infarct-limiting effect of Rapamycin was abolished with ERK inhibitor, PD98059. Rapamycin also attenuated Bax and increased Bcl-2/Bax ratio. These results suggest that reperfusion therapy with Rapamycin protects the heart against I/R injury by selective activation of mTORC2 and ERK with concurrent inhibition of mTORC1 and p38. PMID:28373901

  8. Benefits of Intraaortic Balloon Support for Myocardial Infarction Patients in Severe Cardiogenic Shock Undergoing Coronary Revascularization

    PubMed Central

    Chen, Dong-Yi; Tsai, Ming-Lung; Lin, Yu-Sheng; Cherng, Wen-Jin; Wang, Chao-Hung; Wen, Ming-Shien; Hsieh, I-Chang; Hung, Ming-Jui; Chen, Chun-Chi; Chen, Tien-Hsing

    2016-01-01

    Background Prior studies have suggested intraaortic balloon pump (IABP) have a neutral effect on acute myocardial infarction (AMI) patients with cardiogenic shock (CS). However, the effects of IABP on patients with severe CS remain unclear. We therefore investigated the benefits of IABP in AMI patients with severe CS undergoing coronary revascularization. Methods and Results This study identified 14,088 adult patients with AMI and severe CS undergoing coronary revascularization from Taiwan’s National Health Insurance Research Database between January 1, 1997 and December 31, 2011, dividing them into the IABP group (n = 7044) and the Nonusers group (n = 7044) after propensity score matching to equalize confounding variables. The primary outcomes included myocardial infarction(MI), cerebrovascular accidents or cardiovascular death. In-hospital events including dialysis, stroke, pneumonia and sepsis were secondary outcomes. Primary outcomes were worse in the IABP group than in the Nonusers group in 1 month (Hazard ratio (HR) = 1.97, 95% confidence interval (CI) = 1.84–2.12). The MI rate was higher in the IABP group (HR = 1.44, 95% CI = 1.16–1.79), and the cardiovascular death was much higher in the IABP group (HR = 2.07, 95% CI = 1.92–2.23). The IABP users had lower incidence of dialysis (8.5% and 9.5%, P = 0.04), stroke (2.6% and 3.8%, P<0.001), pneumonia (13.9% and 16.5%, P<0.001) and sepsis (13.2% and 16%, P<0.001) during hospitalization than Nonusers. Conclusion The use of IABP in patients with myocardial infarction and severe cardiogenic shock undergoing coronary revascularization did not improve the outcomes of recurrent myocardial infarction and cardiovascular death. However, it did reduce the incidence of dialysis, stroke, pneumonia and sepsis during hospitalization. PMID:27483439

  9. Sustained Release of Engineered Stromal Cell–Derived Factor 1-α From Injectable Hydrogels Effectively Recruits Endothelial Progenitor Cells and Preserves Ventricular Function After Myocardial Infarction

    PubMed Central

    MacArthur, John W.; Purcell, Brendan P.; Shudo, Yasuhiro; Cohen, Jeffrey E.; Fairman, Alex; Trubelja, Alen; Patel, Jay; Hsiao, Philip; Yang, Elaine; Lloyd, Kelsey; Hiesinger, William; Atluri, Pavan; Burdick, Jason A.; Woo, Y. Joseph

    2014-01-01

    Background Exogenously delivered chemokines have enabled neovasculogenic myocardial repair in models of ischemic cardiomyopathy; however, these molecules have short half-lives in vivo. In this study, we hypothesized that the sustained delivery of a synthetic analog of stromal cell–derived factor 1-α (engineered stromal cell–derived factor analog [ESA]) induces continuous homing of endothelial progenitor cells and improves left ventricular function in a rat model of myocardial infarction. Methods and Results Our previously designed ESA peptide was synthesized by the addition of a fluorophore tag for tracking. Hyaluronic acid was chemically modified with hydroxyethyl methacrylate to form hydrolytically degradable hydrogels through free-radical–initiated crosslinking. ESA was encapsulated in hyaluronic acid hydrogels during gel formation, and then ESA release, along with gel degradation, was monitored for more than 4 weeks in vitro. Chemotactic properties of the eluted ESA were assessed at multiple time points using rat endothelial progenitor cells in a transwell migration assay. Finally, adult male Wistar rats (n=33) underwent permanent ligation of the left anterior descending (LAD) coronary artery, and 100 μL of saline, hydrogel alone, or hydrogel+25 μg ESA was injected into the borderzone. ESA fluorescence was monitored in animals for more than 4 weeks, after which vasculogenic, geometric, and functional parameters were assessed to determine the therapeutic benefit of each treatment group. ESA release was sustained for 4 weeks in vitro, remained active, and enhanced endothelial progenitor cell chemotaxis. In addition, ESA was detected in the rat heart >3 weeks when delivered within the hydrogels and significantly improved vascularity, ventricular geometry, ejection fraction, cardiac output, and contractility compared with controls. Conclusions We have developed a hydrogel delivery system that sustains the release of a bioactive endothelial progenitor cell

  10. 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

  11. Depression and the Risk of Myocardial Infarction and Coronary Death

    PubMed Central

    Wu, Qing; Kling, Juliana M.

    2016-01-01

    Abstract Findings regarding the association between depression and risk of coronary heart disease are inconsistent. We aimed to assess the association between depression and risk of myocardial infarction (MI) and coronary death through a meta-analysis. We performed an electronic literature search of MEDLINE, EMBASE, PsycINFO, ISI Web of Science, and Scopus databases through August 1, 2015, and manual search of the references of the eligible papers and related review articles. Two investigators independently conducted study selection and data abstraction. Disagreement was resolved by consensus. Confounder-adjusted hazard ratios (HRs) were pooled using a random-effects model. Heterogeneity was evaluated using the Cochran Q statistic and Higgins index. Publication bias was assessed by funnel plot and Egger test. Study quality was appraised with the Newcastle-Ottawa Scale. Among 19 eligible cohort studies including 323,709 participants, 8447 cases of MI and coronary death were reported during follow-up ranging from 4 to 37 years. The pooled adjusted HRs for patients with depression (vs those without) were 1.22 (95% CI, 1.13–1.32) for combined MI and coronary death, 1.31 (95% CI, 1.09–1.57) for MI alone (9 studies), and 1.36 (95% CI, 1.14–1.63) for coronary death alone (8 studies). The increased risk of MI and coronary death associated with depression was consistent using modified inclusion criteria, across most subgroups, and after adjusting for possible publication bias. Depression is associated with a significantly increased risk of MI and coronary death. Effective prevention and treatment of depression may decrease such risk. PMID:26871852

  12. Geomagnetic Storms and Acute Myocardial Infarctions Morbidity in Middle Latitudes

    NASA Astrophysics Data System (ADS)

    Dimitrova, S.; Babayev, E. S.; Mustafa, F. R.; Stoilova, I.; Taseva, T.; Georgieva, K.

    2009-12-01

    Results of collaborative studies on revealing a possible relationship between solar activity (SA) and geomagnetic activity (GMA) and pre-hospital acute myocardial infarction (AMI) morbidity are presented. Studies were based on medical data from Bulgaria and Azerbaijan. Bulgarian data, covering the period from 01.12.1995 to 31.12.2004, concerned daily distribution of number of patients with AMI diagnose (in total 1192 cases) from Sofia Region on the day of admission at the hospital. Azerbaijani data contained 4479 pre-hospital AMI incidence cases for the period 01.01.2003-31.12.2005 and were collected from 21 emergency and first medical aid stations in Grand Baku Area (including Absheron Economical Region with several millions of inhabitants). Data were "cleaned" as much as possible from social and other factors and were subjected to medical and mathematical/statistical analysis. Medical analysis showed reliability of the used data. Method of ANalysis Of VAriance (ANOVA) was applied to check the significance of GMA intensity effect and the type of geomagnetic storms - those caused by magnetic clouds (MC) and by high speed solar wind streams (HSSWS) - on AMI incidences. Relevant correlation coefficients were calculated. Results were outlined for both considered data. Results obtained for the Sofia data showed statistically significant positive correlation between considered GMA indices and AMI occurrence. ANOVA revealed that AMI incidence number was significantly increased from the day before till the day after geomagnetic storms with different intensities. Geomagnetic storms caused by MC were related to significant increase of AMI number in comparison with the storms caused by HSSWS. There was a trend for such different effects even on -1st and +1st day for the period 1995-2004. Results obtained for the Baku data revealed trends similar to those obtained for Sofia data. AMI morbidity increment was observed on the days with higher GMA intensity and after these days

  13. Reperfusion therapy of myocardial infarction in Mexico: A challenge for modern cardiology.

    PubMed

    Martínez-Sánchez, Carlos; Arias-Mendoza, Alexandra; González-Pacheco, Héctor; Araiza-Garaygordobil, Diego; Marroquín-Donday, Luis Alfonso; Padilla-Ibarra, Jorge; Sierra-Fernández, Carlos; Altamirano-Castillo, Alfredo; Álvarez-Sangabriel, Amada; Azar-Manzur, Francisco Javier; Briseño-de la Cruz, José Luis; Mendoza-García, Salvador; Piña-Reyna, Yigal; Martínez-Ríos, Marco Antonio

    2017-02-03

    Mexico has been positioned as the country with the highest mortality attributed to myocardial infarction among the members of the Organization for Economic Cooperation and Development. This rate responds to multiple factors, including a low rate of reperfusion therapy and the absence of a coordinated system of care. Primary angioplasty is the reperfusion method recommended by the guidelines, but requires multiple conditions that are not reached at all times. Early pharmacological reperfusion of the culprit coronary artery and early coronary angiography (pharmacoinvasive strategy) can be the solution to the logistical problem that primary angioplasty rises. Several studies have demonstrated pharmacoinvasive strategy as effective and safe as primary angioplasty ST-elevation myocardial infarction, which is postulated as the choice to follow in communities where access to PPCI is limited. The Mexico City Government together with the National Institute of Cardiology have developed a pharmaco-invasive reperfusion treatment program to ensure effective and timely reperfusion in STEMI. The model comprises a network of care at all three levels of health, including a system for early pharmacological reperfusion in primary care centers, a digital telemedicine system, an inter-hospital transport network to ensure primary angioplasty or early percutaneous coronary intervention after fibrinolysis and a training program with certification of the health care personal. This program intends to reduce morbidity and mortality associated with myocardial infarction.

  14. 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

  15. Clinical efforts to reduce myocardial infarct size--the next step.