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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]
This discovery led to this type of angina being referred to in the literature as Prinzmetal angina. [ 3 ] [ 20 ] A following study further distinguished this angina from classical angina pectoris due to the fact that the results showed that the patients with chest pain due to coronary vasospasm lacked evidence of atherosclerosis on cardiac ...
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 ...
All right, as a quick recap…. Angina pectoris is chest pain caused by reduced blood flow resulting in a lack of oxygen in the heart muscle. There are three types: stable angina, unstable angina, and vasospastic angina. Rest tends to relieve stable angina, but not the other two types, and all three can be treated with nitroglycerin.
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.
Prinzmetal authored at least 165 publications over the course of his career. [1] The main focus of his research was hypertension, and he named and described Prinzmetal's angina, a variant of classical angina that occurs at rest. [2] During the Second World War, he focused his research on shock caused by muscle trauma and burns.