To determine the mechanisms responsible for beneficial effects of nifedipine in pacing‐induced angina pectoris, 20 patients undergoing diagnostic cardiac catheterization were studied. Following left ventriculography and coronary arteriography, right atrial pacing was performed before and 30 min after administration of 20 mg of nifedipine sublingually. Heart rate was increased by 10‐beat‐per‐minute (bpm) increments every 90 sec until angina occurred. Electrocardiogram, central aortic pressure, and pulmonary arterial occlusive pressure were monitored continuously. Mean paced heart rate at the onset of angina was increased from 107 ± 12.6 bpm to 140.6 ± 19.9 (P <.001) after nifedipine. Systolic arterial pressure at the time of angina declined from 143 ± 20 mm Hg to 112 ± 23 mm Hg (P <.001). Consequently, the double product heart rate × systolic blood pressure was not changed significantly at the onset of chest pain (149 ± 28 mm Hg × 10−2 vs. 142 ± 28 mm Hg × 10−2). Pulmonary arterial occlusive pressure also did not change significantly (10.4 ± 4.4 vs. 10.5 ± 5.9 mm Hg). Thus, nifedipine decreased myocardial oxygen demand at a given heart rate by reducing left ventricular afterload, but did not increase the rate pressure product threshold for ischemic pain. These results indicate that peripheral arterial vasodilator effects of nifedipine, with a resultant decrease in myocardial oxygen requirements, account for its antianginal effect in this setting in patients with fixed obstructive coronary artery disease.
- coronary artery disease