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Background: The use of vasodilators to improve long-term outcomes in asymptomatic patients with chronic aortic insufficiency (AI) is controversial., Methods: We reviewed MEDLINE, PREMEDLINE, Current Contents, and Cochrane databases to identify relevant clinical trials on asymptomatic patients with chronic AI of at least moderate severity. We included those studies that involved long-term vasodilator therapy (including hydralazine, calcium-channel blockers, and angiotensin-converting enzyme inhibitors) and assessed either hemodynamic and structural parameters or clinical outcomes. Data on patient demographics, study protocols, and outcomes were abstracted., Results: Ten studies with 544 asymptomatic patients with chronic AI were identified. Treatment duration with vasodilators ranged from 12 weeks to 7 years. Of these, 8 studies compared vasodilators with placebo or no therapy, with 5 demonstrating improvements in at least 1 hemodynamic or structural parameter with vasodilators and 3 showing little or no apparent benefit. The remaining 2 studies directly compared outcomes between 2 different vasodilators. Both of these studies demonstrated greater improvements in hemodynamic and structural parameters with angiotensin-converting enzyme inhibitors compared with hydralazine and nifedipine. Clinical outcomes were primarily reported in only 2 of the 10 studies. Although one study suggested that the use of vasodilators slowed the rate of progression to surgery for aortic valve replacement, another showed no difference., Conclusions: Vasodilators inconsistently improve hemodynamic and structural parameters in asymptomatic patients with chronic AI. In addition, the impact of vasodilators on clinical outcomes is largely uncertain and requires further study.

Background: Afterload reduction decreases volume overload on the left ventricle and may thereby delay the need for valve replacement in chronic asymptomatic aortic regurgitation. The aims of this randomized double-blind, placebo-controlled trial were to examine short- and long-term hemodynamic effects of felodipine in chronic asymptomatic aortic regurgitation., Methods: Sixteen patients were randomly assigned to an intravenous infusion of either felodipine 0. 3 mg or placebo followed by 3 months' treatment with felodipine 10 mg or placebo orally once daily. Magnetic resonance imaging was performed at baseline, immediately after intravenous treatment, and after 3 months of oral treatment., Results: Intravenous felodipine caused a statistically significant reduction in the systemic vascular resistance from (mean +/- SD) 1160 +/- 400 to 970 +/- 320 dynes. s. cm(-5) (P <.05), in the regurgitant volume index from 1.5 +/- 0.8 to 1.3 +/- 0.8 L. min(-1). m(-2) (P <.05), and in the regurgitant fraction from 0.31 +/- 0.15 to 0.26 +/- 0.14 (P <.05). The forward cardiac output index increased significantly from 3.2 +/- 0.9 to 3.5 +/- 0.7 L. min(-1). m(-2) (P <.05). Three months of oral treatment with felodipine caused a corresponding but more pronounced decrease in systemic vascular resistance of 880 +/- 330 dynes. s. cm(-5) (P <.05), regurgitant volume index of 1.2 +/- 0.7 L. min(-1). m(-2) (P <.05), and regurgitant fraction 0.25 +/- 0.11 (P <.05), whereas the forward cardiac output index increased to 3.6 +/- 0.7 L. min(-1). m(-2) (P <.05). No significant changes were found in the placebo group. Left ventricular volumes and ejection fraction remained unaffected by treatment, but compared with the placebo group left ventricular myocardial mass decreased significantly from 137 +/- 24 to 132 +/- 21 g. m(-2) (P <.01)., Conclusion: In chronic asymptomatic aortic regurgitation, felodipine causes beneficial hemodynamic effects that may postpone the need for valve replacement.

Objective: This prospective study was performed to assess the effects of 1 year of angiotensin-converting enzyme inhibition with captopril in 20 children (mean age 14.3+/-2.3 years) with asymptomatic chronic aortic regurgitation., Methods and Results: At 12 months patients receiving captopril had a significant reduction in left ventricular end-diastolic and end-systolic dimensions (57+/-9.3 vs 51+/-9.5 mm, p < 0.001; 35.4+/-6.1 vs 32+/-6.8 mm, p < 0.001), end-diastolic and end-systolic volume indexes (111+/-36 vs 94+/-29 ml/m2, p < 0.001; 35+/-13 vs 30+/-12 ml/m2, p < 0.001, respectively), and mass index (138+/-37 vs 109+/-32 gm/m2, p < 0.0001) determined by two-dimensional echocardiography. Meridian (p < 0.01) and circumferential (p < 0.0001) wall stresses also decreased significantly with therapy. Significant reduction (27.8%, p < 0.0001) was achieved in regurgitant fraction with captopril., Conclusions: These data show that the long-term therapy with angiotensin-converting enzyme inhibitors is able to reverse left ventricular dilation and hypertrophy and suggest that such therapy has the potential to favorably influence the natural history of the disease in children.

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.

Seventeen patients with chronic aortic regurgitation (AR) were examined by echocardiography and left and right heart catheterization. Cardiac output and regurgitation volume were measured by the dye dilution method. Administration of single and four repeated doses of prazosin (PZ) led to reductions of left ventricular (LV) end-diastolic, end-systolic, and left atrial end-systolic diameters, and decrease of left ventricular filling pressure. Regurgitation fraction, regurgitation flow, and volume indexes decreased significantly (p less than 0.01). Total left ventricular output decreased (p less than 0.001) as did derived parameters of left ventricular work and performance. Fractional shortening, ejection fraction, and mean circumferential fiber shortening velocity increased as did LV dP/dt and dP/dt/P. Changes in heart rate and cardiac and stroke indexes after PZ were not significant. Preload reduction (dilation of the venous bed and reduction of regurgitation) seems to be the most important effect of PZ in AR. We found PZ to be a suitable and effective drug for oral treatment of chronic AR.