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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of beta blockade after myocardial infarction is extremely well documented. Close to 50 randomized trials have been performed, involving about 40,000 patients with short- or long-term follow-up. Over 20,000 patients have been included in more than 20 placebo-controlled trials with a follow-up period of 3 months or more. In long-term follow-up studies, about 1 to 2 weeks to 1 year after myocardial infarction, mortality was reduced by 21% and reinfarction by 24% (about 20,000 patients in 24 trials). The trial medication was withdrawn in about 20% in both placebo and beta-blocker groups in the major trials. In addition to reduction of mortality and reinfarction rate, benefits have clearly been demonstrated on severity of chest pain, arrhythmias, and other thromboatherosclerotic complications, as well as on readmissions. Significantly more patients experienced congestive heart failure, hypotension, bradycardia, and cold hands with beta-blocker treatment, whereas no clear-cut difference was found for atrioventricular block, bronchial constriction, and intermittent claudication. Some studies have reported more tiredness, depression, and gastrointestinal disturbances. In the Stockholm metoprolol trial, analyses on quality of life have been performed. In this trial, 3 years of metoprolol treatment after myocardial infarction resulted in a prolongation of both survival and time spent completely asymptomatic, as well as in an optimal functional state. Furthermore, less time was spent disabled after serious atherosclerotic complications. Long-term beta blockade after myocardial infarction reduces mortality and morbidity but causes adverse reactions in some patients. With proper selection of patients and type and dosage of beta blocker, survival without atherosclerotic complications and side effects can be prolonged.
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PMID:Use of beta blockers in postinfarct prophylaxis: aspects on quality of life. 288 38

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore an understanding of factors that influence platelet performance is important. This study was undertaken (1) to characterize during evolving myocardial infarction platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving myocardial infarction were studied. Twenty-two patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 min. In 15 patients with anterior myocardial infarction, transcardiac platelet function and response to PGI2 were studied. Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, were elevated three- and 10-fold. 6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets circulating during evolving myocardial infarction ("ischemic platelets") were hyperaggregable in response to ADP and relatively resistant to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic AMP and the cyclic AMP response to PGI2 were diminished. The platelet hyperreactivity, expressed by plasma beta-TG, platelet aggregation, and PGI2-induced inhibition of aggregation, was most intense early during infarct evolution and decreased with time. The increased platelet performance resulted in "platelet fatigue," indicated by decreased contents of beta-TG of the ischemic platelet and decreased TxA2 production in response to collagen. However, the ischemic platelet produced twice normal TxA2 in response to arachidonic acid (stimulus and substrate), demonstrating a heightened metabolic capacity. TxA2 was produced across the ischemic/infarcting compartment in 10 of 15 patients with anterior myocardial infarction. The antiplatelet effect of PGI2 was greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving myocardial infarction, characterized by a proaggregatory environment, heightened platelet reactivity in both the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequences of the data are that the patient in the acute phase of myocardial infarction may benefit from suppression of platelet function and requires significantly greater doses of PGI2 than normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin. 293 81

During the intervening years since metoprolol was first reviewed in the Journal (1977), it has become widely used in the treatment of mild to moderate hypertension and angina pectoris. Although much data have accumulated, its precise mechanisms of action in these diseases remain largely uncertain. Optimum treatment of hypertension and angina pectoris with metoprolol is achieved through dose titration within the therapeutic range. It has been clearly demonstrated that metoprolol is at least as effective as other beta-blockers, diuretics and certain calcium antagonists in the majority of patients. Although a twice daily dosage regimen is normally used, satisfactory control can be maintained in many patients with single daily doses of conventional or, more frequently, slow release formulations. Addition of a diuretic may improve the overall response rate in hypertension. Several controlled trials have studied the effects of metoprolol administered during the acute phase and after myocardial infarction. In early intervention trials a reduction in total mortality was achieved in one moderately large trial of prolonged treatment, but in another, which excluded patients already being treated with beta-blockers or certain calcium antagonists and where treatment was only short term, mortality was significantly reduced only in 'high risk' patients. Overall results with metoprolol have not demonstrated that early intervention treatment in all patients produces clinically important improvement in short term mortality. Thus, the use of metoprolol during the early stages of myocardial infarction is controversial, largely because of the requirement to treat all patients to save a small number at 'high risk'. This blanket coverage approach to treatment may be more justified during the post-infarction follow-up phase since it has been shown that metoprolol slightly, but significantly, reduces the mortality rate for periods of up to 3 years. Metoprolol is generally well tolerated and its beta 1-selectivity may facilitate its administration to certain patients (e.g. asthmatics and diabetics) in whom non-selective beta-blockers are contraindicated. Temporary fatigue, dizziness and headache are among the most frequently reported side effects. After a decade of use, metoprolol is well established as a first choice drug in mild to moderate hypertension and stable angina, and is beneficial in post-infarction patients. Further study is needed in less well established areas of treatment such as cardiac arrhythmias, idiopathic dilated cardiomyopathy and hypertensive cardiomegaly.
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PMID:Metoprolol. An updated review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy, in hypertension, ischaemic heart disease and related cardiovascular disorders. 294 80

Experimental models of heart failure can be used to address specific questions not easily answered in patients, but no single model can reproduce exactly any of the clinical syndromes of heart failure since these are dominated by fatigue and breathlessness. Heart failure may be induced experimentally by pressure loading, volume loading, myocardial infarction, or by the creation of other disease states within the myocardium. Pressure loading may be especially useful in the study of ventricular hypertrophy, cellular derangements and vascular changes. Volume loading may be useful when examining the pathogenesis of hormone and electrolyte disturbances. Models of myocardial infarction or destruction are likely to be the most suitable for assessing novel therapy provided that peripheral reflexes are maintained. Experimental cardiomyopathy can provide an important means of identifying pathological subcellular mechanisms. They may be of use in the evaluation of vasodilator drugs but caution should be exercised in the study of inotropic agents. Any one model may be useful if it permits study of a single factor or variable in isolation or at a time when information is not obtainable from patients. For greatest clinical relevance, studies should be made in conscious animals with intact reflexes.
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PMID:Experimental models of heart failure. 315 77

Four patients, each with a history of myocardial infarction and diffuse coronary artery disease, underwent application of left latissimus dorsi (LD) muscle with intact neurovascular bundle to the anterolateral wall of the left ventricle. The muscle was conditioned over a six-week period subsequent to operation in 3 patients and was conditioned preoperatively with a burst stimulus in the fourth. Biopsy specimens confirm the experimental data that human skeletal muscle can be electrically conditioned over a six- to ten-week period to contain mainly fatigue-resistant type I fibers. All patients survived the procedure, and 3 showed improvement secondary to aneurysmectomy. In Patient 1, a modified resection was performed, and at 28 months after operation, at the 75-W level of exercise, the ejection fraction was 54% paced versus 45% nonpaced. In Patient 2, at 12 months, the ejection fraction at rest was 44% paced versus 30% nonpaced. Doppler echo studies confirmed the presence of the flap and its function in the paced and nonpaced mode. The third patient died of a sudden ventricular arrhythmia 2 months following operation. An infected, nonfunctioning, degenerated flap was found at autopsy. Patient 4 did not have an aneurysm. She received a bypass graft to the right coronary artery and underwent cardiomyopexy in an attempt to relieve medically refractory incapacitating chronic congestive heart failure. Ten months postoperatively, ejection fraction at rest was 33% paced versus 25% nonpaced. Constrictive myopathy has not been encountered in any of these patients.
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PMID:Paced skeletal muscle for dynamic cardiomyoplasty. 325 62

Twenty two patients with heart failure were studied in a double blind crossover trial to compare amiodarone (200 mg/day) with placebo. Each agent was given for three months. Extrasystoles and complex ventricular arrhythmias were common during ambulatory electrocardiographic monitoring and during exercise testing at entry to the study. Breathlessness and tiredness as assessed by visual analogue scores and duration of treadmill exercise did not become worse during amiodarone treatment. During the placebo and amiodarone phases of the study left ventricular ejection fraction and cardiac index determined by first pass radionuclide ventriculography were similar, both at rest and during upright bicycle exercise. Exercise induced ventricular tachycardia was abolished and simple and complex ventricular arrhythmias observed on 24 hour ambulatory monitoring were greatly diminished during amiodarone treatment. Three patients died, all suddenly, during the placebo phase. In two patients amiodarone was withdrawn after a further myocardial infarction in one and a worsening of symptoms of ventricular arrhythmia in the other. In contrast with other antiarrhythmic agents amiodarone is effective in suppressing ventricular arrhythmias in heart failure without causing adverse haemodynamic effects. Because frequent ventricular arrhythmias are known to be associated with a poor prognosis in heart failure, these data suggest that amiodarone may improve the poor prognosis in patients with heart failure.
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PMID:Clinical, haemodynamic, and antiarrhythmic effects of long term treatment with amiodarone of patients in heart failure. 329 21

Sixty-five patients with ST elevation were retrospectively studied in order to evaluate the clinical significance and underlying mechanisms of ST-segment elevation during exercise. Of these, 50 patients had previous myocardial infarction (Group I) and 15 patients did not (Group II). Exercise thallium-201 imaging was performed on 30 patients, resting gated blood pool imaging was performed on 33 patients, and 23 underwent cardiac catheterization for clinical indications. When the two groups were compared, patients in Group I had more frequent multivessel disease (9/13 vs. 3/10, p less than 0.05), anterior infarctions (33/50 vs. 4/10, p less than 0.02), while Group II patients had more frequent single-vessel disease (7/10 vs. 4/13, p less than 0.05). For Group I patients, the most common reason for termination of exercise was fatigue and/or dyspnea (35/50 vs. 0/15, p less than 0.05), with an irreversible defect noted in both stress and delayed views on thallium imaging (20/24 vs. 1/6, p less than 0.05). In Group II, the most common reason for termination was angina (15/15 vs. 2/50, p less than 0.001), with reversible thallium defects noted more frequently (4/6 vs. 3/24, p less than 0.01). Thus, we conclude that in patients with Q waves, left ventricular dysfunction rather than ischemia is the mechanism for ST elevation. In these patients angina is rare, but fatigue, dyspnea, multivessel disease, and fixed thallium defects are common. In patients with non-Q-wave exertional ST elevation, ischemia is the rule, manifested by frequent chest pain and reversible thallium defects.
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PMID:The role of ischemia and ventricular asynergy in the genesis of exercise-induced ST elevation. 335 73

Seventeen post-myocardial infarction patients experiencing angina on effort performed 6 different exercise tests until they reached symptom-limited maximal level, 3 after placebo and 3 after oral administration of 10 mg of the Calcium antagonist, nifedipine, in a randomized, double blind, cross-over controlled study. Four of the tests were conventional bicycle and treadmill tests with stepwise increasing load. In 2 of the tests an isometric exercise of carrying a weight averaging 6 kg and corresponding to about 30% of maximal grip strength was added to the treadmill walking. When the exercise was stopped because of moderately severe angina, the product of heart rate and systolic blood pressure did not show any statistically significant difference between the tests. However, in the treadmill plus isometric test the work time was shorter and the slope of the treadmill was less than in the treadmill test. The difference was caused partly by non-cardiac factors, namely fatigue of the hand muscles. In routine exercise tests of coronary patients the addition of an isometric to a dynamic load did not give substantially more information than dynamic exercise alone. Nifedipine caused a modest increase of exercise tolerance in all tests, the increase being greatest in the treadmill plus isometric test. The increase in exercise tolerance was seen also in patients receiving beta-blocking agent.
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PMID:Assessment of exercise tolerance of cardiac patients by bicycle, treadmill and treadmill plus isometric exercise with and without nifedipine. 344 98

The effects of regular aerobic exercise are important to an aging society increasingly preoccupied with exercise. Traditionally, most attention has been directed to the relationship between a physically active life-style and cardiovascular mortality. In an aging society, however, active life expectancy and maintenance of independence may be as important as effects of regular exercise on longevity. Regular exercise results in increased maximum aerobic capacity due to peripheral changes in muscle (increased capacity for aerobic metabolism and improved substrate and oxygen extraction with a widened arteriovenous oxygen difference) and also due to cardiovascular changes with increased stroke volume and cardiac output in normal persons. "Therapeutic benefits" of conditioning probably occur at submaximal work loads common to everyday activity, when cardiac work and myocardial oxygen consumption are less for any given work load, muscles are more efficient, and relative oxygen requirements are less. Aging is associated with a linear decline in maximum aerobic capacity. The rate of decline is twofold greater when comparing sedentary with physically active middle-aged men. Thus, regular exercise could conceivably lower functional aerobic age by slowing this functional decline. Exercise, particularly excessive exercise, is also associated with serious hazards, including sudden death, nonfatal myocardial infarction, excessive fatigue, hyperthermia, and significant musculoskeletal problems. Accounts of the health effects of exercise should consider a wide range of risks and benefits, especially those related to improving function, minimizing disability, and prolonging independent living.
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PMID:Health benefits of exercise in an aging society. 354 19

Monitoring for adverse effects in an integral part of controlled clinical trials. Traditionally the results of monitoring are reported as either cumulative percentages at the end of the study or cross-sectional percentages at a given time in the study. These results are likely to underestimate the true number of complaints because participants may be withdrawn (e.g., deaths, losses to follow-up, and refusals) before they ever complain of an adverse effect. However, survival analysis methods can be used to compare the distributions of "time to first complaint" in the active and placebo treatment groups, taking into account withdrawals. Participants in the Beta-Blocker Heart Attack Trial were monitored for possible adverse effects. On each follow-up visit they were asked whether they had had any of four conditions (blacking out, fatigue, depression, and bronchospasm) since their previous visit about 3 months earlier. The patients were followed for up to 30 months. For fatigue and bronchospasm, the complaint-free time was significantly longer in the placebo vs. active (propranolol) treatment group (P less than 0.005).
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PMID:Survival analysis of adverse effects data in the Beta-Blocker Heart Attack Trial. 355 42


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