Immediate effects of captopril in acute left ventricular failure secondary to myocardial infarction

Abstract

In 8 patients with acute left ventricular failure secondary to myocardial infarction, the hemodynamic effects of captopril (25 mg), an orally active converting enzyme inhibitor, were measured. Hemodynamic modifications were maximal at 60 min and lasted for 2-3 h. Pulmonary wedge pressure fell from 23.5 .+-. 4.9 (mean .+-. SD) to 16.8 .+-. 4.7 mm Hg (P < 0.01), cardiac output rose from 3.24 .+-. 1 to 4.05 .+-. 0.91 l/min (P < 0.01). Systemic vascular resistance decreased from 27.34 .+-. 3.81 to 17.52 .+-. 1.65 mm Hg min l-1 (P < 0.01). Mean arterial pressure fell from 89.6 .+-. 13.9 to 75.7 .+-. 16.3 mm Hg (P < 0.001) while heart rate was not significantly modified. Six patients who had high pretreatment plasma renin activity values responded by a decrease in ventricular filling pressure and/or an increase in cardiac output. One patient with normal initial plasma renin activity value showed similar hemodynamic effects. Apparently, in the short term captopril is a vasodilator, with arterial and venous effects, that improves cardiac function in acute left ventricular failure secondary to myocardial infarction.