Hemodynamic and morphologic changes after long-term angiotensin converting enzyme inhibition in patients with chronic valvular regurgitation

Objective: Angiotensin converting enzyme (ACE) inhibitors decrease preload and afterload and are therefore of potential value in valvular regurgitation. The present study was designed to assess the effects of treatment for 1 year with an ACE inhibitor on myocardial performance. Patients and methods: Twenty-four patients with isolated moderate to severe chronic aortic regurgitation or mitral regurgitation who were free of coronary disease were studied before treatment (control) with the ACE inhibitor quinapril and were then followed for 1 year during quinapril therapy (10–20 mg/day). Results: After 1 year of ACE inhibition, the regurgitant fraction fell by 27 and 42%, compared with control values, in the aortic and mitral regurgitation groups, respectively (P = 0. 0001). The left ventricular end-diastolic volume was reduced from 150 ± 33 to 128 ± 30ml/m² in the aortic regurgitation group, and from 146 ± 26 to 109 ± 24ml/m² in the mitral regurgitation group (P = 0.0001 for each). End-systolic volume decreased from 55 ± 27 to 44 ± 28ml/m2 in the aortic regurgitation group (P = 0.005) and from 63 ± 43 to 47 ± 29ml/m2 in the mitral regurgitation group (P = 0.002). The left ventricular ejection fraction increased slightly at rest and during exercise in patients with aortic regurgitation, but showed no change in the mitral regurgitation patients after 1 year of quinapril treatment. Echocardiographic studies showed that after 1 year of therapy there was a decrease of about 10% in the left ventricular end-diastolic and end-systolic diameter in both patient groups. Moreover, the left ventricular mass was reduced by 35% in the aortic regurgitation group (P = 0.0001), and left ventricular hypertrophy, which was present in all patients, was reversed completely. In the mitral regurgitation group, a mass reduction of 15% was observed after 1 year of quinapril treatment, and the septal wall thickness, which indicated borderline hypertrophy, decreased to normal. Conclusion: These results demonstrate that long-term ACE inhibition in patients with valvular regurgitation reverses left ventricular dilation and reduces left ventricular mass and hypertrophy, thereby improving left ventricular function. Further, they suggest that ACE inhibition may have the potential to delay aortic or mitral valve replacement.