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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]
Nifedipine, sold under the brand name Procardia among others, is a calcium channel blocker medication used to manage angina, high blood pressure, Raynaud's phenomenon, and premature labor. [2] It is one of the treatments of choice for Prinzmetal angina. [2] It may be used to treat severe high blood pressure in pregnancy. [2]
Amlodipine, sold under the brand name Norvasc among others, is a calcium channel blocker medication used to treat high blood pressure, coronary artery disease (CAD) [10] and variant angina (also called Prinzmetal angina or coronary artery vasospasm, among other names). [11] It is taken orally (swallowed by mouth). [10]
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]
Rest tends to relieve stable angina, whereas unstable angina and vasospastic angina can occur anytime, including at rest. In terms of medications, all three can be treated with Nitroglycerin which is a vasodilator that increases blood vessel diameter to allow more blood flow. In addition, vasospastic angina also responds to calcium channel ...
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 ...
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.
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 ...
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