Abstract
Prinzmetal's variant angina pectoris is a clinical syndrome characterized by recurrent attacks of anginal discomfort at rest associated with transient ST-segment elevation in the electrocardiogram. Attacks are rarely provoked by stress, and exercise capacity is paradoxically well preserved. Although moderately severe fixed anatomic narrowing is commonly observed in the coronary artery supplying the region of the heart showing ST-segment elevation during attacks, the degree of obstruction seen between attacks is insufficient to account for the attack,1 and frequently there is no organic coronary-artery stenosis at all.2 Since the report of Dhurandhar et al.3 and that of Oliva et al. in . . .
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