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 < .001) with less ST segment depression at peak exercise (p < .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 < .05) and at peak exercise (p < .001). Moreover, resting ARCR was decreased (p < .01) and remained significantly lower at peak exercise (p < .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.Circulation 68, No. 5, 1035No. 5, -1043No. 5, , 1983. THE BENEFICIAL EFFECTS of nifedipine, a calcium-channel blocker, in the medical management of angina at rest have been well established, particularly in those patients in whom coronary spasm plays a major role in the pathogenesis of myocardial ischemia.'-3 Several studies have also shown that nifedipine provides substantial benefits to patients with classic exercise-induced angina pectoris. Such salutary action has been ascribed to the reduction in myocardial oxygen consumption that is a result of decreased systemic vascular resistance.9 However, some investigators have demonstrated that intracoronary infusion of nifedipine has the same antianginal efficacy as intravenous administration, despite the absence of significant peripheral hemodynamic effects. '0 Moreover, a druginduced increase in resting myocardial blood flow distal to significant coronary obstructions has been shown in patients with coronary artery disease, suggesting that a direct increase in myocardial oxygen supply could represent a potential alternative mechanism by which nifedipine may exert its antianginal effect.1'The present study was designed to determine whether the increase in coronary flow induced by nifedipine could be of benefit in patients with exertional angina. We examined a homogeneous population of patients with stable exercise-induced angina and left anterior descending artery disease. Great