Coronary artery spasm (CAS), also known as variant angina or Prinzmetal angina (named after Dr. Myron Prinzmetal who described it in 1959), is a condition characterized by transient, intense vasoconstriction (spasm) of an epicardial coronary artery that causes significant reduction or complete occlusion of coronary blood flow, producing transmural myocardial ischemia. Unlike typical angina pectoris, which is caused by fixed atherosclerotic plaque limiting coronary blood flow during exertion, variant angina occurs predominantly at REST, typically between midnight and early morning (circadian pattern), and is caused by dynamic vasospasm of coronary smooth muscle rather than fixed obstruction. The coronary artery may appear completely normal on angiography between spasm episodes, or the spasm may occur at the site of a non-obstructive atherosclerotic lesion. The pathogenesis of coronary vasospasm involves hyperreactivity of coronary artery smooth muscle to vasoconstrictive stimuli. Normal coronary artery tone is maintained by a balance between vasodilatory factors (nitric oxide/NO, prostacyclin/PGI2, endothelium-derived hyperpolarizing factor/EDHF) and vasoconstrictive factors (endothelin-1, thromboxane A2, serotonin, acetylcholine). In CAS, this balance is shifted toward vasoconstriction through multiple mechanisms. Endothelial dysfunction is a central mechanism: the...