The unitary facade of angina pectoris was cracked 18 years ago when Prinzmetal et al1 chipped off a "variant" form that departs from the classical pattern of Heberden angina of effort in several respects. The pain occurs at rest and is often accompanied by arrhythmias or heart block; it is associated with electrocardiographic ST-segment elevations; and it carries a grim prognosis.
Prinzmetal ascribed the newly discovered syndrome to spasm in a severely diseased major coronary branch. The explanation did not, however, gain wide acceptance until the advent of angiography, which showed it to be correct.2 Spasm is now acknowledged as the mechanism underlying variant angina. But rather than delineate the syndrome as a single entity, this recognition introduced an element of ambiguity. It soon became apparent that spasm with accompanying pain also occurs in patients with normal coronary arteries.3 It also appeared likely that prolonged spasm with
Vaisrub S. Variants of Variance. JAMA. 1977;237(11):1127. doi:10.1001/jama.1977.03270380071027
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