Abstract
Coronary vasoconstriction has moved in and out of fashion for more than a century. The initial descriptions of angina considered vasomotor instability as a key mechanism,1 but pathologic studies2 and the invention of coronary angiography in the middle of the last century focused attention on structural stenoses and occlusions attributed to atheromatous plaques. When Prinzmetal et al3 described a variant form of angina, which was later confirmed as a coronary spasm,4 vasomotor instability returned to the limelight. Variant angina is characterized by symptoms at rest (not exertion) with ST elevation on ECG (not depression). It usually occurs in the early hours of the morning during depressed vagal tone and is associated with occlusion or near occlusion (>90% stenosis) of a focal proximal coronary segment on angiography.
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