Open AccessImprovement of exercise capacity after nifedipine in patients with eisenmenger syndrome complicating ventricular septal defect
Author(s) -
Wong CheukKit,
Yeung David W. C.,
Lau ChuPak,
Cheng ChunHo,
Leung WingHung
Publication year - 1991
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960141205
Subject(s) - medicine , nifedipine , intracardiac injection , cardiology , anesthesia , shunting , eisenmenger syndrome , placebo , pulmonary hypertension , alternative medicine , pathology , calcium
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<0.05), but systemic arterial oxygen saturation (SAO 2 ) remained steady. With 4 weeks of maintenance nifedipine therapy, resting intracardiac shunting and SAO 2 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<0.02) and SAO 2 at each stage of exercise was consistently increased in all patients after nifedipine. Cardiac output and the SAO 2 at peak exercise were similar. Thus, chronic nifedipine therapy increases SAO 2 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.