Assessment of hemodynamic effects of angiotensin-converting enzyme inhibitor therapy in chronic aortic regurgitation by using velocity-encoded cine magnetic resonance imaging

Long-term treatment with angiotensin-converting enzyme (ACE) inhibitors has beneficial effects in patients with chronic aortic regurgitation by reducing left ventricular volumes and regurgitant fraction. Velocity-encoded cine magnetic resonance imaging can directly measure antegrade (forward stroke volume) and retrograde blood flow (regurgitant volume) in the ascending aorta. Velocity-encoded cine magnetic resonance imaging was used in 9 patients with moderate to severe aortic regurgitation (regurgitant fraction 49% ± 17%) to measure regurgitant fraction, regurgitant volume, and forward stroke volume at baseline and 3 months after therapy with enalapril (mean dose 29 ± 13 mg). Ten additional patients with aortic regurgitation without any drug therapy served as a control group. In the treatment group, systolic blood pressure slightly decreased from 132 ± 20 mm Hg to 121 ± 14 mm Hg (p = not significant), whereas diastolic blood pressure and heart rate (beats per minute) remained unchanged. Regurgitant fraction decreased in 6 patients (responders) from 49% ± 19% to 39% ± 20% (percentage change 24% ± 14%, p = 0.002) and was unchanged in 3 patients (nonresponder, 49% ± 19% vs 51% ± 16%; p = not significant). In the responder group, forward stroke volume increased from 128 ± 32 ml to 148 ± 57 ml, whereas regurgitant volume remained unchanged (67 ± 40 ml vs 65 ± 51 ml). At baseline, the responder group had a significant higher total vascular resistance than the nonresponder group (998 ± 538 dyne sec•cm−5 vs 625 ± 214 dyne•sec•cm−5; p < 0.05). With enalapril treatment, total vascular resistance in the responder group tended to decrease (891 ± 576 dyne•sec•cm−5), but slightly increased in the nonresponder group (679 ± 276 dyne•sec•cm−5). The control group showed no changes in regurgitant fraction, regurgitant volume, forward stroke volume, and total vascular resistance at follow-up.