Although most symptoms of myocardial ischemia result from fixed stenosis of the coronary arteries or intraplaque hemorrhage or thrombosis at the site of lesions, some ischemic events may be precipitated or exacerbated by coronary vasoconstriction.

Spasm of the large coronary arteries with resulting decreased coronary blood flow may occur spontaneously or may be induced by exposure to cold, emotional stress, or vasoconstricting medications, such as ergot derivative drugs. Spasm may occur both in normal and in stenosed coronary arteries and may be silent or result in angina pectoris. Even myocardial infarction may occur as a result of spasm in the absence of visible obstructive coronary heart disease, although most instances of such coronary spasm occur in the presence of coronary stenosis.

Cocaine can induce myocardial ischemia and infarction by causing coronary artery vasoconstriction or by increasing myocardial energy requirements.

Prinzmetal’s (variant) angina is a clinical syndrome in which chest pain occurs without the usual precipitating factors and is associated with ST segment elevation rather than depression. It often affects women under 50 years of age. It characteristically occurs in the early morning, awakening patients from sleep, tends to involve the right coronary artery, and is apt to be associated with arrhythmias or conduction defects. There may be no fixed stenoses. Ischemia usually results from coronary vasoconstriction and may be diagnosed by challenge with ergonovine (a vasoconstrictor).

Patients with this pattern of pain or any chest pain syndrome associated with ST segment elevation should undergo coronary arteriography to determine whether fixed stenotic lesions are present. If they are, aggressive medical therapy or revascularization is indicated, since this may represent an unstable phase of the disease. If significant lesions are not seen and spasm is suspected, ergonovine may be administered intravenously to precipitate vasospasm. This must be done cautiously and with nitroglycerin prepared for intracoronary administration, since irreversible spasm may lead to infarction. Episodes respond well to nitrates or calcium channel blockers, and both drugs are effective prophylactically. By allowing unopposed a1-mediated vasoconstriction, beta-blockers have exacerbated coronary vasospasm, but they may have a role in management of patients in whom spasm is associated with fixed stenoses.

There is a growing consensus that myocardial ischemia may also occur in patients with normal coronary arteries as a result of disease of the coronary microcirculation or abnormal vascular reactivity. This has been termed syndrome X.

Al Suwaidi J et al: Pathophysiology, diagnosis, and current management strategies for chest pain in patients with normal findings on angiography. Mayo Clin Proc 2001;76:813.
Lange RA et al: Cardiovascular complications of cocaine use. N Engl J Med 2001;345:351.