Assessing the treatment of congestive heart failure: diuretics, vasodilators, and angiotensin-converting enzyme inhibitors

Abstract

Congestive heart failure (CHF) causes disabling symptoms and increases the likelihood of decreased survival. Diuretics, direct vasodilators, and angiotensin-converting enzyme (ACE) inhibitors can be used to reduce symptoms, prolong life, or both, in these individuals. Diuretics induce sodium and water excretion, leading to decreased cardiac preload and wall tension, and an effective decrease of symptomatic pulmonary and systemic congestion. They have not yet been shown to prolong life in patients with CHF, however. Direct vasodilators, which induce venodilation, arterial dilation, or both (balanced vasodilators), may improve symptoms, and some but not all prolong life. Venodilators, such as nitrates, exert a venous pooling effect, decreasing cardiac preload and symptoms of congestion. Arterial dilators, such as hydralazine, decrease afterload and improve cardiac output. The combination of hydralazine and isosorbide dinitrate provides balanced vasodilation. It also improves survival, but is associated with a relatively high frequency of side effects necessitating discontinuation of one or both agents. The drugs are not approved by the Food and Drug Administration for the treatment of heart failure. Flosequinan, a new orally administered, long-acting, balanced arteriovenous dilator, improves exercise tolerance and symptoms. However, preliminary analysis of data from a large, multicenter trial revealed increased mortality and hospitalization for worsening CHF. The drug has recently been withdrawn from the market. The ACE inhibitors can cause hemodynamic and neurohormonal changes that lead to a reduction of preload and afterload, decreasing symptoms of heart failure. They significantly decrease CHF mortality, and might also deter the development of overt heart failure in some asymptomatic patients with left ventricular dysfunction.