Жұректің тамырларының спазмы: себептері, белгілері және диагностикасы

Variant angina, also known as Prinzmetal angina, vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, is a syndrome typically consisting of angina (cardiac chest pain). Variant angina differs from stable angina in that it commonly occurs in individuals who are at rest or even asleep, whereas stable angina is generally triggered by exertion or intense exercise. Variant angina 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 caused by the permanent occlusion of these vessels by atherosclerosis, which is the buildup of fatty plaque and hardening of the arteries.

In contrast to those with angina secondary to atherosclerosis, people with variant angina are generally younger and have fewer risk factors for coronary artery disease with the exception of smoking, which is a common and significant risk factor for both types of angina. Affected people 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, tightness in throat, chest pressure, light headedness, excessive sweating, and/or reduced exercise tolerance that, unlike atherosclerosis related angina, typically does not progress to myocardial infarction (heart attack). Unlike cases of atherosclerosis related stable angina, these symptoms are often unrelated to exertion and occur in night or early morning hours. Cardiac examination of individuals with variant angina is usually normal in the absence of current symptoms. 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. Acetylcholine is normally released by the parasympathetic nervous system (PSNS) at rest, and causes dilation of the coronary arteries. While acetylcholine induces vasoconstriction of vascular smooth muscle cells through a direct mechanism, acetylcholine also stimulates endothelial cells to produce nitric oxide (NO). NO then diffuses out of the endothelial cells, stimulating relaxation of the nearby smooth muscle cells. In healthy arterial walls, the overall indirect relaxation induced by acetylcholine (via nitric oxide) is of greater effect than any contraction that is induced. When the endothelium is dysfunctional, stimulation with acetylcholine will fail to produce, or produce very little, nitric oxide. Thus, acetylcholine released by the PSNS at rest will simply cause contraction of the vascular smooth muscle. Thromboxane A2, serotonin, histamine, and endothelin are vasoconstrictor which activated platelets release and/or cause to be released. Abnormal platelet activation (e. g. by lipoprotein(a) interference with fibrinolysis by competing with plasminogen to thereby impair fibrinolysis and promote platelet activation) results in the release of these mediators and coronary vasospasm. Other factors thought to be associated with the development of variant angina include: intrinsic hypercontractility of coronary artery smooth muscle; existence of significant atherosclerotic coronary artery disease; and reduced activity of the parasympathetic nervous system (which normally functions to dilate blood vessels). Individuals with variant angina may have many undocumented episodes of symptom free coronary artery spasm that are associated with poor blood flow to portions of the heart and subsequent irregular and potentially serious heart arrhythmias. Accordingly, individuals with variant angina should be intermittently evaluated for this using long term ambulatory cardiac monitoring.

As maintenance therapy, sublingual nitroglycerin tablets can be taken 3 5 min before conducting activity that causes angina by the small percentage of patients who experience angina infrequently and only when doing such activity. or non dihydropyridine class (e. g. verapamil, diltiazem) are regarded as first line drugs to avoid angina attacks. Long acting nitroglycerins such as isosorbide dinitrate or intermittent use of short acting nitroglycerin (to treat acute symptoms) may be added to the calcium channel blocker regimen in individuals responding sub optimally to the channel blockers. However, individuals commonly develop tolerance, or resistance, to the efficacy of continuously used long acting nitroglycerin formulations. One strategy to avoid this is to schedule nitroglycerin free periods of between 12 and 14 hours between doses of long acting nitroglycerin formulations.

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 patients 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. 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 have 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. 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.