Is the renin-angiotensin system really unnecessary in patients with severe chronic heart failure: The price we pay for interfering with evolution

Abstract

Inhibition of the angiotensin-converting enzyme has become an established approach in the management of patients with severe chronic heart failure (1,2). Both captopril and enalapril produce shortand long-term hemodynamic and clinical improvement in these patients (3), and both drugs have been shown to be more effective than placebo in randomized double-blind clinical trials (4-9). The most recently published trial documenting the efficacy of enalapril in ambulatory patients with heart failure by Creager et al. (9) appears in this issue of the Journal. Other studies (I) suggest that the benefits of long-term treatment with captopril are greater than can be achieved with other vasodilator drugs, particularly hydralazine and prazosin. Furthermore, converting enzyme inhibition may reduce the frequency of ventricular tachyarrhythmias in patients with severe left ventricular dysfunction, perhaps by reducing circulating levels of catecholamines or preserving total body stores of potassium (6). By these favorable hemodynamic and antiarrhythmic actions, long-term therapy with captopril and enalapril may prolong survival in selected patients (10,11). This accumulated evidence creates a compelling case for a direct deleterious effect of the renin-angiotensin system in severe