variant

Variant angina, and less commonly Prinzmetal angina, vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina (cardiac chest pain) in contrast to stable angina which is generally triggered by exertion or intense exercise, commonly occurs in individuals at rest or even asleep and is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the heart's smooth muscle tissue in the vessel walls. In comparison, stable angina is due to the permanent occlusion of these vessels by atherosclerosis (i.e. buildup of fatty plaque and hardening of the arteries).Dr. William Heberden is credited with being the first to describe in a 1768 publication the occurrence of chest pain attacks (i.e. angina pectoris) that appeared due to pathologically occluded coronary arteries. These attacks were triggered by exercise or other forms of exertion and relieved by rest and nitroglycerin. In 1959, Dr. Myron Prinzmetal described a type of angina that differed from the classic cases of Heberden angina in that it commonly occurred in the absence of exercise or exertion. Indeed, it often woke sufferers from their normal sleep. This variant angina differed from the classical angina described by Dr. Heberden in that it appeared due to episodic vasospasm of coronary arteries that were typically not occluded by pathological processes such as atherosclerosis, emboli, or spontaneous dissection (i.e. tears in the walls of coronary arteries). Variant angina had been described twice in the 1930s by other authors and was referred to as cardiac syndrome X (CSX) by Kemp in 1973, in reference to patients with exercise-induced angina who nonetheless had normal coronary angiograms. CSX is now termed microvascular angina, i.e. angina caused by disease of the heart's small arteries.Some key features of variant angina are chest pain that is concurrently associated with elevations in the ST segment on electrocardiography recordings, that often occurs during the late evening or early morning hours in individuals who are at rest, doing non-strenuous activities, or asleep, and that is not associated with permanent occlusions of their coronary vessels. The disorder seems to occur more often in women than men, has a particularly high incidence in Japanese males as well as females, and afflicts individuals who may smoke tobacco products but exhibit few other cardiovascular risk factors. However, individuals exhibiting angina symptoms that are associated with depressions in their electrocardiogram ST segments, that are triggered by exertion, and/or who have atherosclerotic coronary artery disease are still considered to suffer variant angina if their symptoms are caused by coronary artery spasms. Finally, rare cases may exhibit symptom-free coronary artery spasm that is nonetheless associated with cardiac muscle ischemia (i.e. restricted blood flow and poor oxygenation) along with concurrent ischemic electrocardiographic changes. The term vasospastic angina is sometimes used to include all of these atypical cases with the more typical cases of variant angina. Here, variant angina is taken to include typical and atypical cases.
For a portion of patients, variant angina may be a manifestation of a more generalized episodic smooth muscle-contractile disorder such as migraine, Raynaud's phenomenon, or aspirin-induced asthma. Variant angina is also the major complication of eosinophilic coronary periarteritis, an extremely rare disorder caused by extensive eosinophilic infiltration of the adventitia and periadventitia, i.e. the soft tissues, surrounding the coronary arteries. Variant angina also differs from the Kounis syndrome (also termed allergic acute coronary syndrome) in which coronary artery constriction and symptoms are caused by allergic or strong immune reactions to a drug or other substance. Treatment of the Kounis syndrome very much differs from that for variant angina.

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