Nifedipine is a potent coronary vasodilator in the resting state and an effective afterload-reducing agent. This study was undertaken because of the concern that the addition of nifedipine to β-blocker therapy could produce serious untoward hemodynamic consequences. Although this combination is usually well tolerated, occasional reports suggest that the combination of nifedipine and β-blocking agents may increase the likelihood of congestive heart failure, severe hypotension or exacerbation of angina. Further, there is a need to know If the addition of nifedipine to therapy with maximall tolerated doses of long-acting nitrates and β blockers would provide further symptomatic relief without excessive adverse effects. Finally, the effect of adjunctive nifedipine on global left ventricular performance at rest and during exercise was examined. Sixteen patients, all of whom had 3 or more episodes per week of angina pectoris despite therapy with long-acting nitrates and β blockers, were selected. Radionuclide ventriculography was performed at rest and during exercise; global ejection fractions (EFs) were determined by manually tracing the left ventricular end-diastolic perimeter with an electronic cursor. In the first phase, β blockers and nitrates were used; in the second phase nifedipine, 10 mg every 6 hours, was added and titrated to reduce systolic blood pressure at rest by at least 10 mm Hg or until intolerable adverse effects occurred. When nifedipine was added to therapy, the difference between global EF at rest and during exercise was reduced from −0.15 to +0.02 (p <0.00001); exercise duration was increased from 431 seconds to 532 (p <0.001), with only 8 patients limited by angina, compared with 16 during the initial therapy. An improvement in global left ventricular function was noted at comparable workloads and double products in EF at exercise. The exercise-induced ischemia in these patients receiving maximal doses of β blockers and nitrates was significantly reduced when nifedipine was added, without a significant effect on myocardial oxygen demand.