After 15 years of relative obscurity, Prinzmetal angina is currently stirring up much interest and a lively controversy. When first described,1 the variant angina, unprovoked by exercise or emotion, unaccompanied by increase in blood pressure and heart rate, and associated with elevated rather than depressed ST segments, was generally viewed as a curiosity rather than an important entity. Furthermore, Prinzmetal's suggestion that the cause of this syndrome was coronary arterial spasm did not fall on receptive ears at a time when spasm was no longer regarded as a factor in the mechanism of anginal pain.
With recent arteriographic demonstration that coronary arteries can undergo spasm and that such spasm has been seen during attacks of variant angina, Prinzmetal's suggestion is inviting a second look.
Having examined 20 patients with variant angina and reviewed 60 other cases reported since Prinzmetal called attention to this condition, MacAlpin and his co-workers2