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PubMed1996

Long-term survival after myocardial infarction: relationship with thrombolysis and discharge medication. Results of the Augsburg Myocardial Infarction Follow-up Study 1985 to 1993.

A large number of randomized clinical trials have shown that thrombolysis, long-term treatment with beta-blockers, antiplatelet drugs, and angiotensin converting enzyme inhibitors improve survival after acute myocardial infarction (AMI). However, for calcium channel blockers (nifedipine, diltiazem, and verapamil) there was either no benefit, or positive effects have been reported in subgroups only. Recent studies have raised concern about the safety of this drug class, especially in patients with coronary heart disease. We studied the long-term survival, for a median follow-up time of 4.4 years, of 1197 non-diabetic patients in the population-based AMI registry in Augsburg, Germany, aged 25-74 years, who had survived a first Q wave acute myocardial infarction for at least 28 days. The impact of thrombolysis and prescribed medication at discharge (beta-blockers, antiplatelet drugs, and calcium channel blockers) on long-term survival was analysed using the Cox-Proportional-Hazard model, controlling for age, sex, and concomitant cardiac drug use. Thrombolysis (risk ratio, RR, 0.72; 95% confidence interval, CI, 0.48-1.08), long-term beta-blockade (RR 0.52; 95% CI 0.36-0.74) and antiplatelet drug use (RR 0.69; 95% CI 0.50-0.94) were associated with considerable reductions in total mortality. The use of calcium channel blockers was not associated with a reduction in total mortality (RR 1.23; 95% CI 0.89-1.69). Separate analyses for nifedipine (RR 1.00; 95% CI 0.68-1.48), and diltiazem (RR 1.55; 95% CI 1.04-2.32) showed an increased risk of death associated with the latter. Using patients on beta-blockers only (RR 1.00) as a reference, the prescription of these calcium channel blockers was consistently associated with an increased total mortality (nifedipine, without beta-blockers RR 1.20; 95% CI 1.12-3.57, diltiazem, without beta-blockers RR 2.87; 95% CI 1.75-4.70). These results from an observational study demonstrate a benefit of thrombolysis, beta-adrenergic blockade and antiplatelet drug use on long-term survival in acute myocardial infarction patients. Calcium channel blocker use appears to be associated with an increased risk of death. These data support the need for controlled trials to address this issue specifically.

Adrenergic beta-Antagonists↗
PubMed1996

Effects of insulin treatment on cause-specific one-year mortality and morbidity in diabetic patients with acute myocardial infarction. DIGAMI Study Group. Diabetes Insulin-Glucose in Acute Myocardial Infarction.

Diabetic patients with acute myocardial infarction have a poor prognosis, which has been attributed to a higher incidence of congestive heart failure and fatal reinfarction. This study reports on the one-year morbidity and mortality in a randomized study with the aim of testing whether insulin-glucose infusion initiated as soon as possible after onset of myocardial infarction and followed by long-term subcutaneous insulin treatment may have a beneficial effect on outcome in diabetic patients. In all, 306 patients were recruited to the insulin-treated group, while 314 patients served as controls. The overall mortality after one year was 19% in the insulin group compared to 26% among controls (P < 0.05). The treatment effect was most pronounced in patients without prior insulin medication and at low cardiovascular risk. In this stratum the in-hospital mortality was reduced by 58% (P < 0.05) and the one-year mortality by 52% (P < 0.02). The most frequent cause of death in all patients was congestive heart failure (66%), but cardiovascular mortality (congestive heart failure, fatal reinfarction, sudden death and stroke) tended to be decreased in insulin-treated patients. However, this difference did not reach the level of statistical significance. The number of reinfarctions was 53 (28% fatal) in the insulin group compared to 55 (45% fatal) in the control group. The two groups did not differ as regards need for hospital care or coronary revascularization during the year of follow-up. In summary, left ventricular failure and fatal reinfarctions contribute to increased mortality in diabetic patients following acute myocardial infarction. Intensive insulin treatment lowered this mortality during one year of follow-up.

Adult↗
PubMed1989

Effects of metoprolol on mortality and late infarction in diabetics with suspected acute myocardial infarction. Retrospective data from two large studies.

From two large scale studies in patients with suspected acute myocardial infarction we report the outcome in diabetics after treatment with either metoprolol or placebo. In the Göteborg Metoprolol Trial mortality at 3 months was reduced by metoprolol from 17.9% to 7.5% and late infarction was reduced from 16.4% to 3.8%. In the MIAMI Trial, mortality was decreased by metoprolol from 11.3% to 5.7% and the occurrence of late infarction was decreased from 4.5% to 3.1% during 15-day follow-up. Compared with the overall results, the effect of metoprolol on mortality appears particularly impressive in diabetics.

Diabetes Complications↗
PubMed1992

The significance of myocardial ischaemia and verapamil treatment on the prevalence of supraventricular tachyarrhythmias in patients recovering from acute myocardial infarction. Danish Study Group on Verapamil in Myocardial Infarction.

Twenty-four hour Holter monitoring and symptom-limited exercise testing were carried out prior to discharge in 157 patients recovering from acute myocardial infarction. Supraventricular arrhythmias (SVT) during Holter monitoring were recorded in 15%, and ST segment depression during exercise in 27%. No association between exercise-provoked ischaemia and SVT was found in the late hospital phase of myocardial infarction. After the tests, patients were double-blindly randomized to treatment with verapamil 120 mg t.i.d. or placebo. One month after randomization 24 h Holter monitoring was repeated in 125 patients (verapamil = 63, placebo = 62). At one month a significantly increased incidence of SVT was found in the placebo group (25%) compared to the verapamil-treated patients (9%) (P = 0.04). The increased prevalence in the placebo group was mainly due to an increased incidence of SVT in patients with exercise-induced ischaemia (P = 0.03). This increment was blurred in the verapamil group. In conclusion, the prevalence of SVT increases during the first month after myocardial infarction. The increase is most pronounced in patients with residual myocardial ischaemia and seemed to be prevented by treatment with verapamil.

Double-Blind Method↗
PubMed1994

The prognostic significance of post-infarction angina pectoris and the effect of verapamil on the incidence of angina pectoris and prognosis. The Danish Study Group on Verapamil in Myocardial Infarction.

The prognostic significance of angina pectoris and the effect of intervention with verapamil on the incidence of angina pectoris were studied in patients recovering from myocardial infarction and included in the Danish Verapamil Infarction Trial II. During the second week after admission patients were doubly-blindly randomized to treatment with verapamil 360 mg.day-1 or placebo. Treatment was continued for up to 18 months. At discharge angina pectoris was reported in 11% of 869 patients randomized to verapamil and in 12% of 888 randomized to placebo (ns). One month after discharge a significant increase in the prevalance of angina pectoris was reported in both the verapamil (33%) (P < 0.001) and the placebo groups (39%) (P < 0.001). The one month prevalence of angina pectoris (P = 0.03) and the 18 months overall incidence of angina pectoris (P = 0.002) were both significantly lower in the verapamil group compared with placebo. Stable angina pectoris during the first month of follow-up was a significant predictor of major events (i.e. death or reinfarction) (hazard ratio = 1.45; 95% confidence limits: 1.10, 1.89). As verapamil significantly reduced the incidence of angina pectoris during daily activities, and thereby the number of patients at high risk, the beneficial effect of verapamil in reducing major events in patients recovering from myocardial infarction is likely to be due to abolishing myocardial ischaemia.

Adult↗
PubMed2002

Astrocytic activation and delayed infarct expansion after permanent focal ischemia in rats. Part II: suppression of astrocytic activation by a novel agent (R)-(-)-2-propyloctanoic acid (ONO-2506) leads to mitigation of delayed infarct expansion and early improvement of neurologic deficits.

A novel agent, (R)-(-)-2-propyloctanoic acid (ONO-2506), has a unique property in that it modulates functions of activated cultured astrocytes, including pronounced inhibition of S-100beta synthesis. The present study examined whether administration of this agent would mitigate the delayed expansion of infarct volume and the neurologic deficits after permanent middle cerebral artery occlusion (pMCAO) in rats. Daily intravenous administration of ONO-2506 (10 mg/kg) abolished the delayed infarct expansion between 24 and 168 hours after pMCAO, whereas the acute infarct expansion until 24 hours was unaffected. The agent significantly reduced the expression of S-100beta and glial fibrillary acidic protein in the activated astrocytes and the number of terminal deoxynucleotidyl transferase-mediated 2;-deoxyuridine 5;-triphosphate-biotin nick end labeling-positive cells in the periinfarct area. The neurologic deficits were significantly improved, compared with the vehicle-treated groups, as early as 24 hours after the initial administration of ONO-2506. The agent had a wide therapeutic time window of 0 to 48 hours after pMCAO. These results indicate that because of the pharmacologic modulation of astrocytic activation induced by ONO-2506, symptoms can regress whereas delayed expansion of the lesion is arrested. Pharmacologic modulation of astrocytic activation may confer a novel therapeutic strategy against stroke.

Animals↗
PubMed1997

Treatment with verapamil and trandolapril in patients with congestive heart failure and myocardial infarction. The Danish Verapamil Infarction Trial (DAVIT Study Group).

UNLABELLED: EFFECTS OF VERAPAMIL AND TRANDOLAPRIL: Progression of heart failure, sudden death and death from re-infarction are the major cause of the increased mortality in postinfarct patients with congestive heart failure. Angiotensin converting enzyme (ACE) inhibitors such as trandolapril can prevent the progression of heart failure and thus improve survival. The calcium antagonist verapamil has been shown to prevent sudden death and re-infarction in postinfarct patients without congestive heart failure. HYPOTHESIS: The Danish Verapamil Infarction Trial (DAVIT) study group hypothesized the combined treatment with trandolapril and verapamil might prevent cardiac events in postinfarct patients with coronary heart disease. The first double-blind randomized trial included 100 patients and supported this hypothesis, as the cardiac event rate was significantly lower after 3 months in patients treated with the combination than in those treated with trandolapril alone (14 versus 35%, respectively; P = 0.01, hazard ratio 0.35, 95% confidence interval 0.15-0.85).

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Effects of nisoldipine, a new calcium antagonist, on myocardial infarct size and cardiac dynamics following acute myocardial infarction.

While some calcium antagonists are effective in reducing myocardial infarct size, this beneficial effect may be accompanied by negative inotropic effects. In the following study, a new dihydropyridine calcium antagonist, nisoldipine, was assessed for its effect on infarct size, hemodynamics, and regional function as assessed by percent systolic wall thickening of the left ventricle (SWT) by 2D echocardiography. Open-chest, anesthetized dogs were subjected to 6 h of coronary artery occlusion. After 10 min of coronary artery occlusion, the ischemic area at risk of infarction (AR; % of left ventricle) was determined by left atrial injection of 99mTc-labeled albumin microspheres with subsequent postmortem autoradiography. After 6 h, the hearts were excised, and the area of necrosis (AN) determined by incubation of left ventricular slices in triphenyltetrazolium chloride stain. Treated dogs received 0.005 mg/kg nisoldipine by intravenous infusion at 1.91 ml/min (lasting approximately 8.7 min) during three dosing periods: 15 min, 2 h, and 4 h postocclusion. The AR of eight controls (25.7 +/- 1.8%) was not significantly different from that of 11 treated dogs (25.1 +/- 1.9%). However, the AN/AR X 100 of treated dogs was significantly less than that of controls (62.8 +/- 9.3 vs. 91.6 +/- 7.0%; p less than 0.05). Mean arterial pressure fell in treated dogs by 15.7% (p less than 0.01) at 15 min and by 5.7% (p less than 0.05) at 4 h but not at 2 h postocclusion. Heart rate was not affected by nisoldipine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Adaptive remodeling of the infarct-related artery is associated with recurrent ischemic events after thrombolysis in acute myocardial infarction.

BACKGROUND: Recurrent ischemic events occur during the hospital stay of 7-32% of patients after successful thrombolytic treatment of acute myocardial infarction (AMI). OBJECTIVE: To define the association between postinfarction angina pectoris and the clinical, angiographic, and intravascular ultrasound (IVUS) parameters of the infarct-related artery for consecutive prospectively included patients. METHODS: Clinical, qualitative, and quantitative angiographic and IVUS data for 64 patients (56 men, aged 53+/-12 years) with thrombolysis of AMI were analyzed. All patients underwent coronary angiography and pre-interventional IVUS measurement electively within 1 month of AMI or at the time of the occurrence of postinfarction angina pectoris. Classification as adaptive or constrictive remodeling was according to whether the cross-sectional area of a vessel was larger or smaller than that of the proximal or distal reference segment. RESULTS: Nineteen of the 64 patients (29.7%) suffered from recurrence of ischemic events (group 1), whereas 45 patients (60.3%, group 2) remained free from symptoms. In univariate analyses, multivessel disease (42 versus 24%, P= 0.0236) and adaptive remodeling (63 versus 24%, P= 0.0032) were found to occur more commonly among patients in group 1. The patients in group 1 exhibited larger total vessel cross-sectional areas than did the patients in group 2 (17.5+/-4.2 versus 14.9+/-6.1 mm2, P = 0.0556). In multivariate regression analysis, adaptive remodeling proved to be a significant predictor (P = 0.0145) of the recurrence of ischemic events after thrombolysis of AMI. CONCLUSIONS: Adaptive remodeling of the infarct-related artery is associated with early postinfarction angina pectoris after thrombolysis of AMI.

Adult↗
PubMedDate not supplied

Reperfusion therapy for acute myocardial infarction: observations from the National Registry of Myocardial Infarction 2.

The National Registry of Myocardial Infarction 2 (NRMI-2) provides a unique opportunity to evaluate the practice patterns among participating cardiology and emergency medicine departments involved in the care of patients with acute myocardial infarction. The data from NRMI-2 suggest that almost 1/3 of all non-transfer-in and non-transfer-out patients are eligible for reperfusion therapy. Furthermore, of those patients who are clearly eligible for reperfusion therapy, 24% are not given this proven therapy. Specifically, women, the elderly, patients without chest pain on presentation, and those patients at highest risk for in-hospital mortality were least likely to be treated with reperfusion therapy. The reason for underuse of reperfusion therapy may in part reflect a concern for adverse bleeding events associated with the use of thrombolytic therapy. The data from NRMI-2 also suggest that patients with contraindications to thrombolysis may be very appropriate for primary angioplasty. Realizing the full potential benefits of reperfusion therapy in terms of reduced cardiovascular morbidity and mortality will require that clinical practice patterns be aligned more closely with the recommended national guidelines, which are based on extensive clinical trial data that show the benefit of reperfusion therapy in a wide range of patients with acute myocardial infarction. By using observational databases, such as the NRMI-2, which describe how clinical care is administered in nonclinical trial settings, we can continually monitor our progress and initiate changes to ensure that patients are given access to the many therapies that have been shown to improve their quality of life and survival.

Adult↗
PubMedDate not supplied

Results of recent large myocardial infarction trials, adjunctive therapies, and acute myocardial infarction: improving outcomes.

Despite significant advances in the treatment of myocardial infarction, morbidity and mortality rates remain high. Recently completed, large, randomized trials have evaluated new therapeutic strategies for the management of ST-segment elevation acute myocardial infarction. Third generation fibrinolytic agents may offer advantages over conventional agents, such as more rapid, complete, and sustained reperfusion and greater ease of administration. However, no survival benefit has been observed. Direct thrombin inhibitors and low-molecular-weight heparins are being compared with unfractionated heparin as adjuncts to fibrinolytic therapy, and preliminary data suggest that these agents provide some clinical benefit when combined with streptokinase. More potent antiplatelet agents, such as the glycoprotein IIb/IIIa antagonists, may replace aspirin if they can be safely combined with fibrinolytic agents. These strategies are being tested in ongoing trials. Finally, agents such as adenosine and F2G may prevent reperfusion injury and improve myocardial salvage. The results of these trials have expanded our armamentarium of pharmacotherapy and should lead to improved clinical outcomes after acute myocardial infarction.

Animals↗
PubMedDate not supplied

Recognition and management of inferior wall myocardial infarctions and right ventricular infarcts.

Cardiovascular disease is a predominant health problem in the United States. Annually, more than 6 million people experience an acute myocardial infarction (MI). Right ventricular infarct (RVI) occurs in approximately one third of all patients who present with an inferior wall myocardial infarction (IWMI). The aggressive initial treatment of IWMI with RVI may improve morbidity and mortality. Thus, it is essential to understand the different modalities used to treat a right and left ventricular MI.

Arrhythmias, Cardiac↗
PubMed2005

Tumor necrosis factor alpha, rapid ventricular tachyarrhythmias, and infarct size in canine models of myocardial infarction.

Etanercept (2 mg/kg), a TNFalpha sequestrant, was administered 24 hours and 1 hour before LAD coronary artery ligation to examine the role of TNFalpha on lethal ventricular tachyarrhythmias and myocardial necrosis. Dogs treated with etanercept had decreased very rapid (>360 bpm) ventricular triplets (6 +/- 1/h, n = 8) 2 to 24 hours following coronary artery ligation compared with saline (21 +/- 6/h, n = 10, P < 0.05). This was concordant with 8-fold salvage of beta-adrenergic receptor kinase 1 (betaARK) activity compared with control (33.8 +/- 7.2% versus 4.3 +/- 2.2% of unoperated control tissue, P < 0.01, n = 5). Salvage of betaARK occurred without change in the thickness of the epicardial tissue overlying the infarct. In dogs pretreated with etanercept before a 2-hour occlusion/4-hour reperfusion of the LAD coronary artery, infarct mass decreased by 61% (% area at risk) and 55% (% left ventricular mass) in the etanercept group (n = 8) compared with saline (n = 9, P < 0.05). This was concordant with an etanercept-mediated six-fold decrease in leukocyte accumulation within ischemically injured myocardium. TNFalpha antagonism decreases malignant ventricular tachyarrhythmias and may relate to partial protection of normal betaARK-mediated desensitization of beta-adrenergic receptors. TNFalpha sequestration also decreases infarct size in an occlusion/reperfusion model of myocardial ischemia.

Adrenergic beta-Agonists↗
PubMed2005

Homozygous factor V Leiden mutation in two siblings presenting with acute myocardial infarction: a rare cause of myocardial infarction in the young.

Although factor V Leiden mutation, is the most common established genetic risk factor for venous thrombosis, its effect on the development of myocardial infarction remains unclear. We describe a family case of homozygous factor V Leiden mutation in two siblings presenting with acute myocardial infarction as a rare cause of myocardial infarction in the young.

Adult↗
PubMed1986

Platelet number and volume during myocardial infarction in relation to infarct size.

Platelet number and mean platelet volume (MPV) were measured in 100 patients with acute chest pain, 41 with acute myocardial infarction (AMI), 33 with angina pectoris (AP) and 26 with non-coronary event (NCE), and compared with 21 controls. We found no significant difference in platelet count on admission in the patient groups, but it was lower compared with controls. There were no significant differences in MPV between the patient groups nor between patients and controls. Thirty patients with AMI were followed for 10 days and showed an initial 12% fall in platelet count followed by a 36% increase. Initially there was an increase in MPV (2%) followed by a fall (8%). The fall in platelet count and increase in MPV correlated with infarct size (maximum activity of lactate dehydrogenase (LDH)) and might reflect consumption of platelets. The precise role of platelets in the process of infarction is still unknown.

Aged↗
PubMed1981

Histologic mapping of infarcted myocardium -- a new method for evaluation of myocardial infarct in autopsy cases.

A histologic mapping of myocardium was deviced for the evaluation of myocardial infarction in autopsy cases. By this method, it is possible to understand the three dimensional extension, density and spreading or repairing mode of an infarct in the heart, and should be also possible to estimate the damaged myocardial mass. Furthermore, references of both clinical information and the findings from simultaneously examined coronary arteries gave this technic an efficient means for the clinicopathologic evaluation of myocardial infarction.

Aged↗
PubMed1982

Serum myoglobin, creatine kinase and creatine kinase-MB as mutually supportive indices of myocardial infarction and infarct size.

A comparison was made between the appearance of serum myoglobin and creatine kinase in 22 patients with acute myocardial infarction who were admitted to a coronary-care unit within four hours of onset of chest pain. The MB isoenzyme of creatine kinase was measured in 12 patients. The more rapid appearance and disappearance of myoglobin relative to creatine kinase and creatine kinase-MB was confirmed, as was the correspondence between their respective peak values. A significant correlation was also obtained between the area under the myoglobin time-course and the respective peak levels. Whereas creatine kinase activity declined exponentially from a single peak, myoglobin appeared in multiple episodes inadequately represented by a single peak value and having no clear clinical correlation. The role of myoglobin as a diagnostic aid in myocardial infarction is probably limited to its ability to support creatine kinase and creatine kinase-MB as indices of infarct size.

Creatine Kinase↗
PubMed1988

Pentoxifylline does not reduce infarct size in a canine model of acute myocardial infarction.

1. The effect of the haemorrheological agent pentoxifylline was investigated in a canine model of acute myocardial infarction, induced by occlusion of the left anterior descending coronary for 6 h. Thirty minutes post-occlusion the dogs were randomized to receive either distilled water or pentoxifylline (0.3 mg kg-1 min-1 for 1 h followed by 0.15 mg kg-1 min-1 for 4.5 h) intravenously. 2. At 6 h post-occlusion the in vivo area at risk was determined with monastral blue dye and the area of necrosis was determined with triphenyltetrazolium chloride. The area at risk was 16.5 +/- 1.3% in the control group (n = 10) and 17.2 +/- 1.8% in the pentoxifylline treated group (n = 10; NS). The area of necrosis was 12.3 +/- 1.9% in the control group and 11.9 +/- 2.2% in the pentoxifylline treated group (NS). The area of necrosis expressed as a percentage of the area at risk was 69.3 +/- 7.7% in the control group and 63.6 +/- 7.4% in the pentoxifylline treated group (NS). 3. Pentoxifylline had no significant effects on heart rate, systolic or diastolic blood pressure. Regional myocardial blood flow, measured by the radioactive microsphere technique, was not significantly different between the groups. 4. Thus, pentoxifylline does not reduce infarct size in this model of acute myocardial infarction and does not enhance coronary collateral blood flow.

Animals↗