Severe Coronary Vasospasm

Coronary artery vasospasm can cause a transient, abrupt, marked decrease in the diameter of an epicardial coronary artery. Various mechanisms have been reported, including endothelial dysfunction, vasoconstrictor substances, pharmacologic stimuli, and neurohormonal effects. Age and also various physiological such as cold, stress, and cigarette smoking are risk factors that could precipitate vasospasm. Patients with variant angina are younger, mostly female and usually do not have common cardiovascular risk factors (other than cigarette smoking). Coronary vasospasm usually occurs most often from midnight to early morning, and usually not induced by exercise in the daytime. Prinzmetal’s angina is a variant angina characterized by episodes of chest pain and transient ST segment elevation caused by coronary vasospasm. The variant angina with normal or near-normal coronary arteries could be found in2%of patients with ST-segment elevation acute coronary syndrome. Various form of arrhythmia often appears during attacks of coronary vasospasm associated with ST-segment elevation, more often when ST segment elevation occurs in the anterior leads. Transmural myocardial ischemia caused by occlusive coronary vasospasm can be complicated by malignant ventricular arrhythmias, especially in patients with multi-vessel coronary spasm, including advance AV block, or even sudden death. The gold standard diagnostic is to perform coronary angiography and an intracoronary provocation test to demonstrate epicardial vasoconstriction. Coronary vasospasm usually responds to conventional medical treatment for coronary vasospasm includes calcium channel blockers alone, or in combination with long acting nitrates. Some cases with severe refractory vasospasm to medical treatment can be resulting in severe cardiac arrhythmia and sudden death. The use of beta-blockers, especially non-selective, can promote attacks or prolong vasospastic state. We presence a case of77-year-old male with recurrent chest pain episodes, that mostly relieved by sublingual nitroglycerin, develop to a refractory vasospasm and cause hemodynamic changes. Immediate coronary angiography showed multi-vessel coronary vasospasm, and responsive to intracoronary nitroglycerin injection.