It is caused by a transient, abrupt, marked reduction in the luminal diameter of an epicardial coronary artery leads to myocardial ischemia (decreased blood flow).
Spasm occurs can occur in either normal or diseased vessels. The reduction in diameter is focal and usually at a single site, although spasm in more than one site and diffuse spasm have been described. Spasm typically occurs within 1 cm of an atherosclerotic plaque in a diseased vessel. This process can usually be reversed by nitroglycerin or a calcium channel blocker.
In addition to spasm of large epicardial vessels, a functional abnormality of microvessels may contribute to myocardial ischemia. This occurs predominantly women who had a history of prolonged (>30 min) chest pain.
The clinical presentation and profile of the patient with variant angina are generally different from that of the patient with unstable or chronic stable angina:
- Patients with variant angina are younger and do not exhibit classic cardiovascular risk factors (except for cigarette smoking).
- Variant angina may be associated with other vasospastic disorders, such as Raynaud phenomenon and migraine headache or its treatment.
- Substance abuse (such as cocaine) is an important risk factor; among cocaine users, spasm may be the cause of myocardial infarction in the absence of angiographically documented coronary disease.
- Exercise and hyperventilation can precipitate attacks of vasospastic angina. The majority of patients, however, have normal exercise tolerance.
- There is a circadian variation with an increased prevalence of angina attacks from midnight to early morning.
Although the pathogenesis of coronary vasospastic angina is not well understood, several contributing factors (other than cocaine abuse) have been identified. These include the autonomic nervous system (particularly alpha-adrenergic receptors), endothelial dysfunction, and adhesion molecules.
A variety of factors may contribute to endothelial dysfunction in patients with variant angina, one of these being inflammation.
The key finding for the diagnosis of variant angina is the detection of ST segment elevation during chest discomfort with return of the ST segment to baseline upon resolution of symptoms.
Povocative tests — ergonovine and hyperventilation — can be performed in the catheterization laboratory and have been useful in making the diagnosis of suspected variant angina. These tests are done only when the diagnosis of variant angina is suspected, but not firmly established. At present, provocative testing is less frequently performed.
Medical management of variant angina includes risk factor modification, such as cessation of smoking and lipid lowering, and pharmacologic therapy, which begins with the administration of calcium channel blockers (nifedipine, amlodipine, diltiazem, and verapamil) or nitrates. Both classes of drugs are effective in preventing vasoconstriction and promoting vasodilation in the coronary vasculature.
Statins — Endothelial dysfunction is thought to play a role in the development of variant angina and statins can improve endothelial function.
Estrogen therapy has been recommended in postmenopausal women with variant angina because of its beneficial effects on endothelial function. However, the American Heart Association now recommends against the use of hormone replacement therapy because of the findings from the Women's Health Initiative (WHI) and the Heart and Estrogen/Progestin Replacement Study-II (HERS-II), which suggested that estrogen-progestin therapy might cause harm when used for either primary or secondary prevention of cardiovascular disease.
Patients with variant angina alone (ie, no obstructive coronary disease) generally have a good prognosis
Patients with variant angina who also have obstructive coronary artery disease have a worse prognosis that is, in part, determined by the severity of the underlying disease. T