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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. [3]
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 ...
Beta blockers - reduces contractility and automaticity of the heart which reduces irregular rhythms but also lowers blood pressure when symptoms occur, and further reduces perfusion ex: Carvedilol, this will control abnormal heart rhythms, but can precipitate Prinzmetal angina and heart block.
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] Consequently, this angina has come to be reported and referred to in the literature as Prinzmetal angina. [3]
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.
Hypertension, atrial fibrillation and smoking pose a stronger risk for severe stroke, according to a new study. However, lifestyle changes can help prevent stroke.
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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]
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