Abstract
As understanding of the mechanisms of congestive heart failure (CHF) has improved, it has become apparent that the previously applied stepped-care approach (ie, diuretic, digitalis, then vasodilator) is no longer valid. There is compelling evidence that use of vasodilators increases survival in CHF, and angiotensin-converting enzyme (ACE) inhibitors are the vasodilators of choice. Use of an ACE inhibitor in patients with New York Heart Association classes II, III, and IV CHF improves survival over that achieved with use of placebo or direct-acting vasodilators. In patients with asymptomatic left ventricular dysfunction after myocardial infarction, long-term administration of captopril improved survival and reduced morbidity and mortality from major cardiovascular events. Using an ACE inhibitor as preventive therapy in post-myocardial infarction patients without overt CHF but with evidence of muscle dysfunction (ie, left ventricular ejection fraction 40% or less) should be considered. The role of a newer vasodilator (eg, amlodipine besylate [Norvasc]) as an adjunct to therapy remains to be defined. If current theories on the pathophysiology of CHF are correct, continued interest in beta blockers is justified, especially in newer agents that have actual vasodilatory action in addition to their other beneficial properties.
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