Search PubMed⌕ Search

Biomedical subjects

S Yusuf

Publications and source records attributed to S Yusuf.

At least 181 records · Page 10Linked to original sources
PubMed1994

Recent advances and future directions in myocardial infarction.

Cardiovascular disease is the leading cause of death in most industrialised countries and is a major source of health care expenditure worldwide. Identification and management of risk factors for the development of coronary heart disease (CHD) have enormous potential for improving health and reducing health care costs. There is evidence that the reduction in deaths from CHD has occurred earlier and to a greater extent in countries with aggressive policies of cardiovascular risk factor intervention. Likewise, the treatment of patients presenting with acute myocardial infarction (MI) should be aimed at both extending event-free survival and improving the quality of life. This review focuses on recent advances and future directions in the understanding of risk factor modification before an MI (prevention), treatment of MI including thrombolysis and primary percutaneous transluminal coronary angioplasty, and the subsequent management of patients after MI.

Angioplasty, Balloon, Coronary↗
PubMed1993

Maximizing benefits of therapies in acute myocardial infarction.

Major advances in the management of acute myocardial infarction have been achieved by a combination of careful experimental work and development of effective pharmacologic and interventional strategies in conjunction with the conduct of large, reliable randomized trials. Current trials indicate that a combination of thrombolytic therapy, aspirin, and intravenous followed by oral beta blockers reduces mortality. There are a number of additional promising interventions, such as intravenous magnesium, nitrates, and the newer antithrombin agents. However, before these agents are used widely in clinical practice, clear proof of benefit and adequate safety should be available from the ongoing randomized trials. Following discharge from the hospital, long-term therapy with aspirin and beta blockers should be considered in all patients. In patients with heart failure and low ejection fraction, angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality, reinfarction, and the need for further hospitalizations for heart failure. Therefore, these therapies, in conjunction with risk factor modification (cessation of cigarette smoking, treatment of hypercholesterolemia, treatment of hypertension), should be considered in all appropriate patients. A number of new strategies for the prevention of atherosclerosis and its complications are currently being evaluated in prospective randomized trials. These include the natural antioxidant vitamins, estrogen replacement therapy, tamoxifen therapy, and ACE inhibitors in patients without evidence of heart failure or left ventricular dysfunction.

Humans↗
PubMed1993

Critical review of the approaches to the prevention of sudden death.

The types of cardiac rhythm in patients with sudden death may vary considerably, depending on the underlying cardiac disease. Although ventricular tachyarrhythmias are likely to be the most common causes, a significant proportion of patients may die suddenly due to asystole, electromechanical dissociation, or cardiac rupture. Therefore, the approaches to preventing sudden death may have to be multifactorial. The classic approach of arrhythmia suppression by empiric antiarrhythmic drugs has not resulted in a decrease in sudden death mortality. Although beta blockers have only a modest effect in suppressing arrhythmias, they have been clearly proven to prevent sudden death. Other promising approaches that require further evaluation include modulation of the autonomic balance between the sympathetic and parasympathetic nervous systems (perhaps by beta blockers, exercise training, or low-dose atropine or scopolamine), relief of ischemia by medical or surgical therapy, magnesium supplementation, and mechanical devices, such as the implantable defibrillator.

Anti-Arrhythmia Agents↗
PubMed1993

Prediction of mortality and morbidity with a 6-minute walk test in patients with left ventricular dysfunction. SOLVD Investigators.

OBJECTIVE: To study the potential usefulness of the 6-minute walk test, a self-paced submaximal exercise test, as a prognostic indicator in patients with left ventricular dysfunction. DESIGN: Data were collected during a prospective cohort study, the Studies of Left Ventricular Dysfunction (SOLVD) Registry Substudy. SETTING: Twenty tertiary care hospitals in the United States, Canada, and Belgium. PARTICIPANTS: A stratified random sample of 898 patients from the SOLVD Registry who had either radiological evidence of congestive heart failure and/or an ejection fraction of 0.45 or less were enrolled in the substudy and underwent a detailed clinical evaluation including a 6-minute walk test. Patients were followed up for a mean of 242 days. OUTCOME MEASURES: Mortality and hospitalization. RESULTS: During follow-up, 52 walk-test participants (6.2%) died and 252 (30.3%) were hospitalized. Hospitalization for congestive heart failure occurred in 78 participants (9.4%), and the combined endpoint of death or hospitalization for congestive heart failure occurred in 114 walk-test participants (13.7%). Compared with the highest performance level, patients in the lowest performance level had a significantly greater chance of dying (10.23% vs 2.99%; P = .01), of being hospitalized (40.91% vs 19.90%; P = .002), and of being hospitalized for heart failure (22.16% vs 1.99%; P < .0001). In a logistic regression model, ejection fraction and distance walked were equally strong and independent predictors of mortality and heart failure hospitalization rates during follow-up. CONCLUSION: The 6-minute walk test is a safe and simple clinical tool that strongly and independently predicts morbidity and mortality in patients with left ventricular dysfunction.

Aged↗
PubMed1993

Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials.

OBJECTIVE: To investigate the effects of prophylactic therapy with antiarrhythmic agents on mortality in patients with myocardial infarction. DATA SOURCES AND STUDY SELECTION: Data were obtained from all completed, published or unpublished, randomized, parallel controlled trials of antiarrhythmic agents, regardless of sample size. Investigators were contacted for data on patients excluded after randomization. DATA EXTRACTION: Data on mortality were extracted by one author and confirmed where necessary by the others. DATA SYNTHESIS: Mortality data from 138 trials on 98,000 patients were combined by the Yusuf-Peto adaptation of the Mantel-Haenszel method. There were 660 deaths among 11,712 patients allocated to receive class I agents and 571 deaths among 11,517 corresponding control patients (51 trials: odds ratio [OR], 1.14; 95% confidence interval [CI], 1.01 to 1.28; P = .03). Of 26,973 patients allocated to receive beta-blockers (class II agents), 1464 died compared with 1727 deaths among 26,295 control patients (55 trials: OR, 0.81; 95% CI, 0.75 to 0.87; P = .00001). Of 778 patients allocated to receive amiodarone (a class III agent), 77 died compared with 101 deaths in 779 control patients (eight trials: OR, 0.71; 95% CI, 0.51 to 0.97; P = .03). There were 982 deaths in 10,154 patients allocated to receive a class IV agent (calcium channel blockers) and 949 deaths in 10,188 control patients (24 trials: OR, 1.04; 95% CI, 0.95 to 1.14; P = .41). CONCLUSIONS: The routine use of class I antiarrhythmic agents after myocardial infarction is associated with increased mortality. beta-Blockers have been conclusively demonstrated to reduce mortality. The limited data on amiodarone appear promising. Data on calcium channel blockers remain unpromising.

Anti-Arrhythmia Agents↗
PubMed1993

Clinical experience in protecting the failing heart.

Several large, carefully randomized studies of pharmaceutical agents in the treatment of patients with congestive heart failure (CHF) and left ventricular dysfunction have demonstrated conclusively that angiotensin-converting enzyme (ACE) inhibitors reduce mortality among patients with CHF, as well as the number of hospitalizations for heart failure, myocardial infarction (MI), and angina. ACE inhibitors also have been shown to prevent the development of heart failure in patients with asymptomatic left ventricular dysfunction. Phosphodiesterase inhibitors and the beta agonists have been shown to increase mortality with no beneficial effect on morbidity. The role of digitalis remains controversial. On the one hand, the limited data available suggest that digoxin prevents clinical deterioration in patients with heart failure, even in the presence of sinus rhythm. On the other hand, when administered after MI, digoxin has been associated with increased mortality. Such conclusions are unreliable, however, since it is impossible to adjust statistically for the fact that digoxin is used in sicker patients. This question will be addressed in a large randomized study currently being conducted by the Digitalis Investigation Group. Pharmacologic approaches to the reduction of sudden death currently being explored include amiodarone, oral magnesium supplements, and beta blockers. According to the Cardiac Arrhythmia Suppression Trial and other studies, the class I antiarrhythmic agents appear unpromising or even harmful. The calcium channel blockers also appear to be contraindicated as routine therapy for CHF.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Natural history and patterns of current practice in heart failure. The Studies of Left Ventricular Dysfunction (SOLVD) Investigators.

A total of 6,273 consecutive relatively unselected patients with heart failure or left ventricular dysfunction, or both (mean age 62 +/- 12 years, mean ejection fraction 31 +/- 9%), were enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) Registry over a period of 14 months. All patients were followed up for vital status and hospital admissions at 1 year. Ischemic heart disease was the underlying cause of failure or dysfunction in approximately 70% of patients, whereas hypertensive heart disease was considered to be primarily involved in only 7%. There were striking differences in the etiology of heart failure among blacks and whites: 73% of whites had an ischemic etiology of failure versus only 36% of blacks; 32% of blacks had a hypertensive condition versus only 4% of whites. The total 1-year mortality rate was 18%; 19% of patients had hospital admissions for heart failure and 27% either died or had a hospital admission for congestive heart failure during the 1st year of follow-up. Factors related to 1-year mortality or hospital admission for congestive heart failure included age, ejection fraction, diabetes mellitus, atrial fibrillation and female gender. There was no difference in mortality associated with congestive heart failure among blacks and whites, but hospital admissions for heart failure were more frequent in blacks. Digitalis and diuretic agents were the drugs most often used in these patients, who were often taking many medications in relation to severity of congestive heart failure symptoms and ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1993

Comparative neurohormonal responses in patients with preserved and impaired left ventricular ejection fraction: results of the Studies of Left Ventricular Dysfunction (SOLVD) Registry. The SOLVD Investigators.

OBJECTIVES: The aim of this study was to determine the differences in neurohumoral responses between patients with pulmonary congestion with and without impaired left ventricular ejection fraction. BACKGROUND: Previous studies have established the presence of neurohumoral activation in patients with congestive heart failure. It is not known whether the activation of these neurohumoral mechanisms is related to the impairment in systolic contractility. METHODS: The 898 patients recruited into the Studies of Left Ventricular Dysfunction (SOLVD) Registry substudy were examined to identify those patients with pulmonary congestion on chest X-ray film who had either impaired (< or = 45%, group I) or preserved (> 45%, group II) left ventricular ejection fraction. Plasma norepinephrine, plasma renin activity, arginine vasopressin and atrial natriuretic peptide levels were measured in these two groups of patients and compared with values in matched control subjects. RESULTS: Distribution of the New York Heart Association symptom classification was the same in the two groups of patients. Compared with control subjects, patients in group II with pulmonary congestion and preserved ejection fraction had no activation of the neurohumoral mechanisms, except for a small but statistically significant increase in arginine vasopressin and plasma renin activity. Compared with patients in group II, those in group I with pulmonary congestion and impaired ejection fraction had significant increases in plasma norepinephrine (p < 0.002), plasma renin activity (p < 0.02) and atrial natriuretic peptide levels (p < 0.0007). When we controlled for baseline differences between groups I and II, the between-group differences in plasma norepinephrine (p < 0.02) and atrial natriuretic peptide (p < 0.002) remained significant. However, plasma renin activity was not significantly different between groups I and II. When the effects of diuretic agents and angiotensin-converting enzyme inhibitors were adjusted, patients with lower ejection fraction were found to have significantly higher plasma norepinephrine and atrial natriuretic peptide levels. CONCLUSIONS: The results point to the importance of the decrease in left ventricular ejection fraction as one of the mechanisms for activation of neurohormones in patients with heart failure.

Adult↗
PubMed1993

Current and ongoing randomized trials in heart failure and left ventricular dysfunction.

Several large randomized trials have been completed recently and provided valuable information on the effects of various interventions in heart failure and left ventricular dysfunction. A review of ongoing randomized trials showed that there were 19 major trials addressing the effect of treatments on exercise tolerance, morbidity or mortality. Although it is hoped that these trials will answer many questions, they will also raise additional questions. Therefore, these remaining questions will need to be answered by future clinical trials.

Adrenergic beta-Antagonists↗
PubMed1993

Effects of beta-blockers and calcium channel blockers in acute myocardial infarction.

beta-blockers and calcium channel blockers have been evaluated extensively during the acute phase and following myocardial infarction. beta-blockers, when administered early and intravenously, reduce early mortality, reinfarction and cardiac arrests by about 16%. The reduction in mortality is likely to be due to multiple mechanisms including reductions in cardiac rupture, reinfarction and ventricular fibrillation. Recent data also suggest a reduction in intracranial haemorrhage when administered in conjunction with thrombolytic therapy. Prolonged use of beta-blockers for a year or two after myocardial infarction leads to significant reductions in total mortality, sudden deaths and reinfarction. The benefits of beta-blockers are probably mediated through a number of mechanisms, including reduction in heart rate and prevention of plaque rupture, in addition to the mechanisms stated above. Calcium channel blockers do not reduce mortality. It appears that some agents that increase heart rate (e.g. dihydropyridines) may increase the risk of death and reinfarction. On the other hand, agents that reduce heart rate (verapamil and diltiazem) appear to have a neutral effect on mortality but may reduce reinfarction rates. The benefits of beta-blockers appear to be consistent in most subgroups of patients examined, whereas the adverse effects of calcium channel blockers are most marked in those with large infarcts or heart failure. In conclusion, beta-blockers are preferable to calcium channel blockers in the acute phase and long-term after myocardial infarction.

Acute Disease↗
PubMed1993

Effect of angiotensin-converting enzyme inhibitors in left ventricular dysfunction: results of the studies of left ventricular dysfunction in the context of other similar trials.

Over 13,000 patients have been randomized in 35 long-term trials of the use of angiotensin-converting enzyme (ACE) inhibitors in patients with heart failure or left ventricular dysfunction. Overall, there is a clear reduction in mortality and hospitalizations for heart failure and myocardial infarction with a trend toward fewer sudden deaths. Furthermore, there is a significant reduction in myocardial infarction in three of the larger trials. These benefits have been demonstrated with several different agents and are consistently seen in various subgroups of patients defined by symptomatic status, etiology of left ventricular dysfunction, age, and gender. However, benefits were greatest among patients with the lowest ejection fraction. In conclusion, ACE inhibitors are of established value in patients with heart failure and/or left ventricular dysfunction.

Angina, Unstable↗
PubMed1993

Primary and secondary prevention of myocardial infarction and strokes: an update of randomly allocated, controlled trials.

AIM: To summarize the risk factors associated with coronary heart disease and strokes and to evaluate measures used in the prevention and treatment of these diseases. METHOD: A review of the results of randomly allocated clinical trials of treatment for both primary and secondary prevention of coronary heart disease and strokes. RESULTS: Reductions in elevated blood pressure and cholesterol and cessation of cigarette smoking have clearly been shown to reduce the incidence of coronary heart disease. A reduction in blood pressure has also been shown to reduce the risk of strokes. In addition to other classical risk factors, such as abnormal serum lipids, diabetes and a genetic predisposition, recent studies have shown that elevated levels of fibrinogen and other clotting factors, elevated levels of renin and decreased levels of anti-oxidant vitamins such as E, C and beta-carotene can predict coronary heart disease and strokes. Thrombolytic therapy, aspirin and beta-blockers have been shown to reduce mortality in patients with myocardial infarction, and the latter two agents reduce mortality, re-infarction and strokes with long-term use. Treatment with intravenous magnesium and nitrates has shown promise but larger trials are required to confirm the results. Both aspirin and heparin have proven value in reducing the incidence of myocardial infarction and death in unstable angina. Following an acute myocardial infarction, long-term therapy with aspirin, beta-blockers, lipid-lowering agents and oral anticoagulants has been shown to reduce mortality and re-infarction. In patients with large infarcts associated with a low ejection fraction or heart failure, the use of angiotensin converting enzyme (ACE) inhibitors reduces mortality, hospitalization for heart failure and re-infarction. The use of diuretics to lower blood pressure reduces strokes. In contrast, calcium antagonists do not appear to consistently reduce mortality or prevent vascular events when used for primary or secondary prevention of either myocardial infarction or strokes. CONCLUSIONS: Myocardial infarction and strokes can be prevented by refraining from smoking and maintaining appropriate blood pressure levels and a favourable balance of lipids. Following a myocardial infarction, further drug treatment should include aspirin, thrombolytic therapy (in acute myocardial infarction), beta-blockers, ACE inhibitors (in patients with a low ejection fraction) and perhaps anticoagulants.

Adrenergic beta-Antagonists↗
PubMed1993

Reduced mortality and morbidity with the use of angiotensin-converting enzyme inhibitors in patients with left ventricular dysfunction and congestive heart failure.

The Studies of Left Ventricular Dysfunction (SOLVD) examined the effect of an angiotensin-converting enzyme (ACE) inhibitor, enalapril on mortality and hospitalization in 6,797 patients with low ejection fraction (EF < 0.35). Patients requiring treatment for heart failure were entered to the treatment trial (n = 2,569) while those patients not receiving pharmacological treatment for heart failure were entered in the prevention trial (n = 4,228). In the treatment trial, there was a 16% (95% confidence interval [CI], 5% to 26%) reduction in mortality with the largest reduction in deaths due to progressive heart failure (22%, 95% CI, 6 to 35%). There was also a 26% (95% CI, 18 to 34%) reduction in mortality or hospitalization for worsening heart failure. In the prevention trial there was an 8% (95% CI, -8 to 21%) reduction in mortality, 12% (95% CI, -3 to 26%) reduction in cardiovascular mortality, and a 29% (95% CI, 21 to 36%) reduction in mortality or development of heart failure. In addition, there was a 20% (95% CI, 9 to 30%) reduction in mortality or hospitalization for heart failure. There were consistent effects among subgroups defined by baseline serum sodium, vasodilator use, etiology and NYHA functional class. The effect of enalapril on mortality and hospitalization for heart failure was significantly greater for patients with the lowest ejection fraction. In both trials, there were highly significant reductions in myocardial infarction (23%, 95% CI, 11 to 34%) and hospitalizations for unstable angina (20%, 95% CI, 9 to 29%).

Adult↗