Abstract
To investigate the mechanism by which nifedipine improves exercise tolerance in patients with coronary artery disease, we studied 14 patients with stable exertional angina and left anterior descending artery disease by measuring great cardiac vein flow (GCVF) and calculating anterior regional coronary resistance (ARCR) during exercise before and after sublingual administration of 20 mg of nifedipine. After nifedipine seven patients (group I) had no increase in exercise capacity and showed a similar magnitude of ST segment depression at peak exercise, while another seven patients (group II) had prolonged exercise duration (p less than .001) with less ST segment depression at peak exercise (p less than .01). Such effects were achieved despite a significant increase in double product, an indirect index of myocardial oxygen consumption. In group I patients no significant change was induced by nifedipine in GCVF or in ARCR either at rest or at peak exercise. In contrast, in group II patients nifedipine significantly increased GCVF at rest (p less than .05) and at peak exercise (p less than .001). Moreover, resting ARCR was decreased (p less than .01) and remained significantly lower at peak exercise (p less than .01) compared with the prenifedipine values. These data show that nifedipine may increase GCVF and decrease ARCR at rest and at peak exercise in patients with left anterior descending artery disease. Such increase in myocardial oxygen supply seems the most likely mechanism by which nifedipine may improve exercise capacity in patients with stable exertional angina.
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