Theoretically, medical therapy may modify the natural history of aortic regurgitation. Physicians often use vasodilator therapy in patients with chronic asymptomatic aortic regurgitation. However, the safety and efficacy of this strategy is based on a very limited patient experience.

The literature includes just 268 patients treated with hydralazine, nifedipine or angiotensin-converting enzyme inhibitors. Dr. Bonow and others who use angiotensin-converting enzyme inhibitors in these patients base their treatment decision on a total of 61 patients. For nifedipine, the treatment experience includes 107 patients. Most of these studies follow patients for only six months to two years.

However, the results of these studies are consistent. One representative report on nifedipine showed that over a year of treatment, left ventricular end diastolic volume decreased versus placebo. This translated into a reduction in left ventricular mean wall stress. In turn, left ventricular ejection fraction improved. Placebo treated patients experienced an inexorable decline in left ventricular function.

So vasodilator therapy appears effective, but the effect may not be desirable. The improvement may mask the development of symptoms and functional changes that precede irreversible left ventricular dysfunction.

Only one series provides a possible answer to this question. This study compared nifedipine versus a control arm of digoxin. Patients were followed five to six years.

Nifedipine appeared to slow the natural history of disease. Patients receiving nifedipine had a slower rate of symptom progression or left ventricular dysfunction than controls. When patients on nifedipine did have surgery, all did well postoperatively. Left ventricular function returned to normal.

Dr. Bonow described the role for medical therapy in aortic regurgitation. Physicians may consider medical therapy for patients with moderate to severe aortic regurgitation but no symptoms and normal ejection fraction. Patients with severe symptoms and severe depression of left ventricular function are candidates for short-term medical therapy as a bridge to valve replacement.