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Variant angina, also known as Prinzmetal angina, vasospastic angina, angina inversa, coronary vessel spasm, or coronary artery vasospasm, [2] is a syndrome typically consisting of angina (cardiac chest pain).
Coronary vasospasm refers to when a coronary artery suddenly undergoes either complete or sub-total temporary occlusion. [1]In 1959, Prinzmetal et al. described a type of chest pain resulting from coronary vasospasm, referring to it as a variant form of classical angina pectoris. [2]
Vasospasm is the major cause of Prinzmetal's angina. Cerebral vasospasm may arise in the context of subarachnoid hemorrhage as symptomatic vasospasm (or delayed cerebral ischemia), where it is a major contributor to post-operative stroke and mortality. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage, however the ...
Microvascular angina (MVA), previously known as cardiac syndrome X, [1] also known as coronary microvascular dysfunction (CMD) or microvascular coronary disease is a type of angina (chest pain) with signs associated with decreased blood flow to heart tissue but with normal coronary arteries.
Myron Prinzmetal (February 8, 1908 – January 8, 1987) was an American cardiologist. He studied hypertension and heart arrhythmias among many other topics, and was the first to describe Prinzmetal angina .
Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). [2] It is most commonly a symptom of coronary artery disease. [2] Angina is typically the result of partial obstruction or spasm of the arteries that supply blood to the heart muscle. [3]
The Kounis syndrome is distinguished from two other causes of coronary artery spasms and symptoms viz., the far more common, non-allergic syndrome, Prinzmetal's angina [4] and eosinophilic coronary periarteritis, an extremely rare disorder caused by extensive eosinophilic infiltration of the adventitia and periadventitia, i.e. the soft tissues ...
It is also regarded as responsible for Prinzmetal's angina. Receptors that mediate TXA 2 actions are thromboxane A 2 receptors. The human TXA 2 receptor (TP) is a typical G protein-coupled receptor (GPCR) with seven transmembrane segments. In humans, two TP receptor splice variants – TPα and TPβ – have so far been cloned.