In this study it is argued that the clinical manifestations of unstable angina pectoris, with at its extreme end impending myocardial infarction, may be due to increased coronary arterial vasomotion superimposed on a pre-existing obstruction in a coronary artery. As nifedipine, a powerful calcium antagonist, has initially proven its efficacy in relieving the symptoms of Prinzmetal's angina, a condition in which severe spasm of the coronary artery is now proven to be the main cause, the drug was given to two groups of patients in whom abnormal vasomotion was suspected and its effects scrutinized. Twelve patients with symptoms of coronary artery disease (CAD) were studied with repeated arteriograms after injection of 0.15 mg nifedipine in the left coronary artery. Two control cine-angiograms were made prior to drug administration and two cinefilms were repeated 30 s and 5 min after administration of nifedipine. The mean diameter of the normal, stenotic and poststenotic segments showed a statistically significant increase after drug administration. Vasodilalion persisted after coronary O 2 saturation, and presumably coronary flow, had returned to normal. In 52 other patients, who were seen in the coronary care unit for impending myocardial infarction and who had been treated with maximal beta-adrenergic blockade, nitrates and bedrest, but who remained symptomatic, nifedipine 60 mg orally for 24 h was added to the treatment. Within 2 h after administration 42 of the 52 became asymptomatic. In the 10 non-responders, all with extensive multi-vessel disease, two sustained a myocardial infarction and eight received urgent coronary artery bypass grafting in an effort to alleviate their symptoms. All had severe 3 vessel disease in contrast to the responders in whom 1 or 2 vessel disease was predominant. These data show that increased coronary artery vasomotion can be influenced by nifedipine. The excellent clinical response to the drug in this group of patients with unstable angina pectoris indicates that nifedipine may become the preferred agent to be used particularly when the cause of the angina pectoris is suspected to be the result of abnormal coronary vasomotor tone.