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Prinzmetal’s angina, also known as variant angina or angina inversa, is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles. It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than directly by atherosclerosis (buildup of fatty plaque and hardening of the arteries).
It was first described as “A variant form of angina pectoris” in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908–1987).[1]
Symptoms typically occur at rest, rather than on exertion (thus attacks usually occur at night). Two-thirds of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms.
It is associated with specific ECG changes (elevation rather than depression of the ST segment).
The mechanism that causes such intense vasospasm, as to cause a clinically significant narrowing of the coronary arteries is, as of yet, unknown. It is hypothesized, however, to be related to dysfunction of the endothelium of the coronary arteries.
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.
In dysfunctional endothelium, less, or even no, NO is released by the endothelium upon stimulation with acetylcholine. Thus, acetylcholine released by the PSNS at rest will simply cause contraction of the vascular smooth muscle. It is potentially by this mechanism that Prinzmetal’s angina occurs.
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