Effects of a single oral dose of captopril on left ventricular performance in severe mitral regurgitation.

For comparable decreases in systemic resistance, angiotensin-converting enzyme inhibitors produce a lesser increase in cardiac output than do previously used vasodilators. Although the reason for this is not yet clear, the possibility of a negative inotropic effect of angiotensin-converting enzyme inhibitors was demonstrated by intracoronary injection. The effects of an oral dose of captopril on systolic performance were assessed by examining left ventricular (LV) pressure-volume loops obtained with simultaneous cineangiography and micromanometer pressure recordings before and 90 minutes after administration of oral captopril (25 to 50 mg) in 18 patients with chronic, severe mitral regurgitation. Group 1 (n = 9) was given captopril alone, and group 2 (n = 9) was given captopril plus atropine (0.04 mg/kg intravenous) to assess the role of parasympathetic activity in mediating the effects of captopril. Captopril reduced heart rate (90 to 81 beats/min; p less than 0.002) and LV end-diastolic pressure (13 to 10 mm Hg; p = 0.03), despite a slight increase in end-diastolic volume (257 to 264 ml; p = not significant) that suggests improved diastolic properties. Despite a decrease in end-systolic pressure (103 to 90 mm Hg; p less than 0.001), ejection fraction did not increase (0.60 to 0.58; p = not significant) owing to an increase in end-systolic volume (107 to 114 ml; p = 0.008). Contractile performance, estimated from the end-systolic pressure/volume quotient, was consistently depressed by captopril, as was the relation of preload-corrected ejection fraction to end-systolic stress.(ABSTRACT TRUNCATED AT 250 WORDS)