Clinicians have puzzled over the coronary physiology associated with atypical angina pectoris for the past century. Recent recognition of coronary artery spasm, which has been so thoroughly documented with coronary angiography, has resolved many of these conceptual difficulties. However, several features of coronary artery spasm, both spontaneous and secondary to provocation with ergonovine maleate, remain poorly understood. This paper addresses the management problems associated with spontaneously occurring spasm in the setting of pre-existent atherosclerotic coronary artery disease, angiographically severe spasm unassociated with symptoms of an gina pectoris or signs of myocardial ischemia, and the precipitation of angina pectoris by ergonovine maleate administration unaccompanied by demon strable epicardial coronary artery spasm. The rationale, indications and therapeutic efficacy of a new class of agents known as slow channel inhibitors or calcium antagonists are discussed.
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