Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review.

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.