Spontaneous coronary vasospasm leads to an anginal syndrome (often referred to as Printzmetal angina), occurring at rest or with exertion. Coronary spasm occurs in two broad settings -spasm associated with atherosclerosis or other arterial diseases, and spasm that occurs in the absence of identifiable arteriopathy [1][2][3][4][5] . The former is common, but the latter is not [ 1 ] . Bertrand administered ergonovine, a compound that precipitates spasm in predisposed individuals, to 1,089 patients undergoing coronary arteriography and found that spasm was relatively common in patients with recent coronary thrombosis ( Fig. 20.1 ) [ 3 ] . Vasospasm could be induced in 20% of patients with a recent infarction and 38% of patients with unstable or rest angina, but in only 4.3% of patients with stable, exertional angina. Equally important, only 1.2% of patients with chest pain atypical for angina had inducible spasm, emphasizing that spasm is not a common cause of atypical chest pain.Patients with inducible vasospasm and a significant (>75%) stenotic lesion have a higher incidence of death, infarction, and atherosclerosis progression than patients with isolated stenotic lesions without inducible vasospasm or vasospasm alone [6][7][8] . Harding et al. [ 9 ] retrospectively analyzed ergonovine provocative studies and found that smoking (odds ratio 4.7-7.7:1 compared to nonsmokers) and atherosclerosis were significant risk factors for inducible spasm [ 9,10 ] . More recently, vascular inflammation, polymorphism of eNOS genes, and enhanced phospholipase C activity have been linked to coronary spasm [ 11,12 ] . The diagnosis of coronary vasospasm can be made at the time of angiography by giving drugs that provoke spasm or occasionally by observing spontaneous spasm [ 1,2,[13][14][15][16][17][18] . The most commonly administered agent is an ergot derivative, usually ergonovine maleate or ergometrine, although methacholine was used to induce vasospasm in pioneering studies in the catheterization laboratory. Ergot derivatives are potent constrictors of vascular smooth muscle. Muscarinic receptor agonists (acetylcholine and methacholine) appear to cause vasospasm in a large fraction of patients with ergonovine-induced spasm [ 19 ] . Other agents have also been reported to induce spasm (cold pressor test, histamine, hyperventilation), but not enough information is known to assess the potency and specificity of these agents [ 20,21 ] .Prior to a provocative test for vasospasm, an electrocardiogram should be obtained and a coronary arteriogram should show the absence of severe coronary obstruction. When vasospasm is suspected, acetylcholine or ergonovine generally is given in incremental intravenous doses -starting at 50 m g and increasing doses until a total dose of 350-400 m g intravenously is reached for ergonovine. Although ergonovine appears safe in doses up to 800 m g, the vast majority of patients