COMPARISON OF SINGLE-DOSE NIFEDIPINE AND CAPTOPRIL FOR CHRONIC SEVEREAORTIC REGURGITATION

The effects of a single dose of either nifedipine 20 mg (n = 10) or ca ptopril 50 mg (n = 10) were compared in 20 patients with symptomatic, chronic severe aortic regurgitation using angiography and micromanomet er left ventricular pressure measurements. At 90 minutes, mean arteria l pressure was reduced comparably after both drugs (86 +/- 15 to 76 +/ - 18 mm Hg for nifedipine vs 95 +/- 19 to 77 +/- 18 mm Hg for captopri l, p = NS between groups by analysis of variance), as was wedge pressu re (11 +/- 5 to 9 +/- 4 mm Hg vs 13 +/- 9 to 9 +/- 5 mm Hg for captopr il). Systemic vascular resistance was reduced more (p = 0.01) after ni fedipine than after captopril (1,549 +/- 468 to 1,067 +/- 291 dynes s cm-5 vs 1,632 +/- 559 to 1,436 +/- 392 dynes s cm-5). Heart rate decli ned after captopril (84 +/- 14/min to 75 +/- 15/min, p = 0.002) but no t after nifedipine (78 +/- 13 min to 80 +/- 14 min). Forward stroke vo lume increased after nifedipine (58 +/- 14 to 70 +/- 16 ml, p < 0.001) but not after captopril (58 +/- 17 to 59 +/- 16 ml). Thus, cardiac ou tput increased after nifedipine (4.4 +/- 0.9 to 5.5 +/- 1.2 liters/min , p < 0.001) but decreased after captopril (4.8 +/- 1.2 to 4.3 +/- 1.0 , p = 0.004). Angiographic ejection fraction did not change significan tly after either drug (0.50 +/- 0.11 to 0.49 +/- 0.12 for nifedipine a nd 0.49 +/- 0.08 to 0.50 +/- 0.08 for captopril), nor did end-systolic wall stress (293 +/- 84 to 260 +/- 67 kdynes/cm2 for nifedipine and 3 03 +/- 62 to 284 +/- 57 kdynes/cm2 for captopril). The ratio of end-sy stolic wall stress to end-systolic volume index was slightly reduced b y both. Thus, although both drugs comparably decrease arterial pressur e in severe aortic regurgitation, only nifedipine increased forward st roke volume and cardiac output and decreased regurgitant fraction thro ugh a more potent vasodilation that offsets its reported negative inot ropic effects.