| Literature DB >> 7903245 |
Abstract
Angina pectoris in patients with severe left ventricular dysfunction (LVD), with or without heart failure, is important clinically and socioeconomically. In the Studies of Left Ventricular Dysfunction (SOLVD), more than 36% of the patients had angina pectoris. Although angiotensin-converting enzyme (ACE) inhibitors improve survival and reduce the incidence of new, acute ischaemic events in these patients, they have no significant impact on the incidence of anginal attacks. Treatment of these patients must, therefore, primarily rely on nitrates, beta-blockers and calcium channel blockers. The beta-blockers, by lowering heart rate, improve the balance between myocardial oxygen supply and demand during exercise, and are among the most effective anti-anginal agents available. In addition, by reducing resting heart rate and by preventing excessive catecholamine stimulation of the myocardium, beta-blockers may slow the progression of ischaemic LVD. This may contribute to the improved survival observed when these agents are used following myocardial infarction. By reducing cardiac sympathetic stimulation, however, beta-blockers may depress right and left ventricular pump function. This depression is generally of no clinical consequence when the ejection fraction remains above 40%, but when the ejection fraction is below 35%, only 30% of patients without heart failure and 10% of those with heart failure seem to tolerate a full dose of beta-blocker. This limits their therapeutic use in angina in this setting. Moreover, beta-blockers do not act on the mechanisms underlying some anginal attacks, namely the vasoconstriction of large coronary vessels at the level of atherosclerotic plaques and the reflex vasoconstriction of small coronary arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)Entities:
Mesh:
Substances:
Year: 1993 PMID: 7903245 DOI: 10.1093/eurheartj/14.suppl_f.26
Source DB: PubMed Journal: Eur Heart J ISSN: 0195-668X Impact factor: 29.983