Abstract

Coronary artery spasm should now be considered a well-proven clinical entity which may or may not be associated with clinical symptoms and coronary atherosclerosis and may be either “spontaneous” or iatrogenically induced. The most important clinical entity associated with coronary spasm is that of Prinzmetal's angina. In patients with this “variant” form of angina, severe coronary spasm appears to be the cause of the acute reduction of myocardial blood supply leading to their transient ischemic episodes. Recent studies suggest that “spontaneous” coronary spasm may be related to increased parasympathetic activity and stimulation of a-adrenergic receptors and may be possibly associated with inappropriate phasing of circadian rhythms. These observations explain the failures of coronary bypass surgery in cases of Prinzmetal's angina and provide interesting leads for further investigations into the mechanism, significance, and pharmacodynamics of coronary vasomotion. Coronary artery spasm should now be considered a well-proven clinical entity which may or may not be associated with clinical symptoms and coronary atherosclerosis and may be either “spontaneous” or iatrogenically induced. The most important clinical entity associated with coronary spasm is that of Prinzmetal's angina. In patients with this “variant” form of angina, severe coronary spasm appears to be the cause of the acute reduction of myocardial blood supply leading to their transient ischemic episodes. Recent studies suggest that “spontaneous” coronary spasm may be related to increased parasympathetic activity and stimulation of a-adrenergic receptors and may be possibly associated with inappropriate phasing of circadian rhythms. These observations explain the failures of coronary bypass surgery in cases of Prinzmetal's angina and provide interesting leads for further investigations into the mechanism, significance, and pharmacodynamics of coronary vasomotion.

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