A study with nifedipine, given intravenously or into the left coronary artery, was undertaken in an effort to distinguish the peripheral from the central effects of the drug in patients with stable angina. There was a significant antianginal effect 1 hour after intravenous administration of 1.0 mg of nifedipine. Intravenous administration of 0.1 mg of the drug had no antianginal effect, and did not cause hemodynamic alterations or influence coronary sinus oxygen saturation. Intracoronary infusion of 0.1 mg of nifedipine caused a significant increase in coronary sinus oxygen saturation that was abolished 5 minutes after the end of the infusion. A similar increase in oxygen saturation was found after intravenous administration of 1.0 mg of the drug; this effect, quantitatively somewhat smaller, also disappeared after 5 minutes. Infusion of 0.1 mg of nifedipine into the left coronary artery had an antianginal effect during exercise, documented by a reduction in the exercise-induced increase in left ventricular end-diastolic pressure and in the exercise-induced S-T segment depression. A similar antianginal effect, quantitatively slightly more pronounced, was achieved with intravenous administration of 1.0 mg of nifedipine. It is concluded that the antianginal potency of nifedipine cannot be related to its effect on coronary arteriolar resistance because increased flow has returned to normal when the antianginal effect persists. The mechanism of action must include a direct cardiac influence, most likely on myocardial metabolism. No serious side effects were observed after intravenous or intracoronary administration of nifedipine. © 1979.
