Improvement of exercise capacity after nifedipine in patients with eisenmenger syndrome complicating ventricular septal defect

We investigated the potential benefit of a preferential pulmonary vasodilatory effect of nifedipine in 4 patients with Eisenmenger syndrome complicating ventricular septal defect. First-pass radionuclide scan was performed at rest to measure intracardiac shunting before and after nifedipine. Two hours after 20 mg sublingual nifedipine, right-to-left shunt increased from 16.3 +/- 1.4 to 20.4 +/- 1.5% (p less than 0.05), but systemic arterial oxygen saturation (SAO2) remained steady. With 4 weeks of maintenance nifedipine therapy, resting intracardiac shunting and SAO2 were unchanged from baseline. Symptom-limited cycle ergometry was performed before and after maintenance nifedipine with placebo control. Exercise duration was prolonged (8.7 +/- 0.6 vs. 6.8 +/- 0.9 min; p less than 0.02) and SAO2 at each stage of exercise was consistently increased in all patients after nifedipine. Cardiac output and the SAO2 at peak exercise were similar. Thus, chronic nifedipine therapy increases SAO2 on exercise and improves maximal exercise capacity in patients with Eisenmenger syndrome, which is not predicted by study of resting intracardiac shunting after acute therapy.