Beneficial effects of a single dose of Quinapril on left ventricular performance in chronic mitral regurgitation

Abstract

To evaluate the effect of a single dose of the angiotensin-converting enzyme inhibitor quinapril on left ventricular (LV) performance and size in patients with moderate to severe chronic mitral regurgitation (MR), 12 patients with angiographically proven isolated MR grade II to III and no evidence of coronary artery disease were studied. In all patients a baseline right heart catheterization and simultaneous radionuclide angiogram were performed at rest and during supine exercise (maximum 100 W) as well as 2 hours after oral administration of 10 mg of quinapril. Quinapril reduced heart rate slightly and lowered mean blood pressure at rest and during maximal exercise (p < 0.005). Systemic vascular resistance at rest was decreased from 1,484 ± 505 to 1,150 ± 427 dynes s cm −5 and with maximal exercise from 999 ± 455 to 734 ± 395 dynes s cm −5 (p < 0.005). Pulmonary capillary arterial pressure at rest decreased from 13 ± 6 to 10 ± 4 mm Hg (p < 0.01) and during maximal exercise from 29 ± 10 to 29 ± 7 mm Hg (p = 0.001). LV end-diastolic volume at rest (146 ± 26 ml/m 2) decreased after administration of quinapril to 128 ± 24 ml/m 2 (p = 0.001) and was also reduced during exercise (p = 0.001). LV end-systolic volume decreased from 63 ± 43 to 49 ± 35 ml/m 2 at rest (p = 0.001) and with maximal exercise from 56 ± 49 to 44 ± 39 ml/m 2 (p < 0.01). After quinapril administration, LV ejection fraction at rest improved from 0.59 ± 0.20 to 0.62 ± 0.18 (p < 0.05) and during maximal exercise from 0.64 ± 0.21 to 0.67 ± 0.19 (p = 0.06). Furthermore, quinapril decreased regurgitant fraction at rest from 0.43 ± to 0.28 ± 0.11 (p < 0.0010 and during maximal exercise from 0.41 ± 0.12 to 0.27 ± 0.10 (p < 0.001). Concomitantly regurgitant volume decline from 36 ± 17 to 24 ± 11 ml/m 2 at rest and was also reduced during maximal exercise (p < 0.001). The data demonstrate that pre- and afterload reduction with quinapril decreases MR and reduces LV volumes and end-diastolic pressure, thus improving LV performance. If these beneficial effects can be maintained during long-term treatment, LV dysfunction and timing for mitral valve surgery may be markedly delayed in some patients.