Vasospastic angina

Variant angina, and less commonly vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina (cardiac chest pain) that unlike classical angina, which is triggered by exertion or exercise, commonly occurs in individuals at rest or even asleep. It is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the smooth muscle tissue in the vessel walls. This contrasts with classical angina which is due to the permanent occlusion of these vessels by atherosclerosis (i.e. buildup of fatty plaque and hardening of the arteries). Variant angina, and less commonly vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina (cardiac chest pain) that unlike classical angina, which is triggered by exertion or exercise, commonly occurs in individuals at rest or even asleep. It is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the smooth muscle tissue in the vessel walls. This contrasts with classical angina which 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. In contrast to patients with angina pectoris secondary to coronary artery atherosclerosis, people with variant angina are generally younger and have fewer risk factors for coronary artery disease except for smoking, which is a common and very significant risk factor for both types of angina. Sufferers usually have repeated episodes of unexplained (e.g., in the absence of exertion and occurring at sleep or in the early morning hours) chest pain, light-headedness, excessive sweating, and/or reduced exercise tolerance that, unlike atherosclerosis-related angina pectoris, typically does not progress to myocardial infarction (i.e. heart attack). Unlike cases of atherosclerosis-related stable angina, these symptoms are often unrelated to exertion and occur in night or early morning hours. (However, individuals with atherosclerosis-related unstable angina may similarly exhibit night to early morning hour symptoms that are unrelated to exertion.) Cardiac examination of individuals with variant angina is usually normal in the absence of current symptoms. Two-thirds of these individuals do have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of their symptoms. Persons who have atherosclerosis-based occlusion that is ≥70% in a single coronary artery or that involves multiple coronary arteries are predisposed to develop a variant angina form that has a poorer prognosis than most other forms of this disorder. In these individuals but also in a small percentage of individuals without appreciable atherosclerosis of their coronary arteries, attacks of coronary artery spasm can have far more serious presentations such as fainting, shock, and cardiac arrest. Typically, these presentations reflect the development of a heart attack and/or a potentially lethal heart arrhythmia; they require immediate medical intervention as well as consideration for the presence of, and specific treatment regimens for, their disorder. Variant angina should be suspected by a cardiologist when a) an individual's symptoms occur at rest or during sleep; b) an individual's symptoms occur in clusters; c) an individual with a history of angina does not develop angina during treadmill stress testing (variant angina is exercise tolerant); d) an individual with a history of angina shows no evidence of other forms of cardiac disease; and/or e) an individual without features of coronary artery atherosclerotic heart disease has a history of unexplained fainting. Patients complaining of chest pain should be immediately checked for an abnormal electrocardiogram (ECG). ECG changes compatible but not indicative of variant angina include elevations rather than depressions of the ST segment or an elevated ST segment plus a widening of the R wave to create a single, broad QRS complex peak termed the 'monophasic curve'. Associated with these ECG changes, there may be small elevations in the blood levels of cardiac damage marker enzymes, especially during long attacks. Some individuals with otherwise typical variant angina may show depressions, rather than elevations in the ST segments of their ECGs during angina pain; they may also show new U waves on ECGs during angina attacks. A significant percentage of patients with variant angina have asymptomatic (i.e. symptom-free) episodes of coronary artery spasm. These episodes may be far more frequent than expected, cause myocardial ischemia (i.e. insufficient blood flow to portions of the heart), and be accompanied by potentially serious abnormalities in the rhythm of heart beats, i.e. arrythmias. The only evidence of the presence of totally asymptomatic variant angina would be detection of diagnostic changes on fortuitously conducted ECGs.