Prinzmetal's angina
3213678
225329490
2008-07-13T03:17:41Z
200.7.49.221
/* Mechanism */
{{Infobox_Disease |
Name = Prinzmetal's angina |
Image = |
Caption = |
DiseasesDB = 13727 |
ICD10 = {{ICD10|I|20|1|i|20}} |
ICD9 = {{ICD9|413.1}} |
ICDO = |
OMIM = |
MedlinePlus = |
eMedicineSubj = med |
eMedicineTopic = 447 |
MeshID = D000788 |
}}
'''Prinzmetal's angina''', also known as '''variant angina''' or '''angina inversa''', is a syndrome typically consisting of [[Angina pectoris|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).
==Eponym==
It was first described as ''"A variant form of angina pectoris"'' in 1959 by the American cardiologist Dr. [[Myron Prinzmetal]] (1908–1987).<ref>Prinzmetal M, Kennamer R, Merliss R. ''A variant form of angina pectoris.'' Am J Med 1959;27:375–88. PMID 14434946.</ref>
==Features==
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 [[electrocardiography|ECG]] changes (elevation rather than depression of the [[Electrocardiogram#ST_segment|ST segment]]).
==Mechanism==
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 release 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.
==Diagnosis==
Patients who develop cardiac chest pain are generally treated empirically as an "[[Angina pectoris|acute coronary syndrome]]", and are generally tested for cardiac enzymes such as [[creatine kinase]] isoenzymes or [[troponin]] I or T. These may show a degree of positivity, as coronary spasm too can cause myocardial damage. [[Echocardiography]] or thallium scintigraphy is often performed.
The [[gold standard (test)|gold standard]] is [[coronary angiography]] with injection of provocative agents into the coronary artery. Rarely, an active spasm can be documented angiographically (e.g. if the patient receives an angiogram with intent of performing a primary coronary intervention with [[angioplasty]]). Depending on the local protocol, provocation testing may involve substances such as [[ergonovine]], [[methylergonovine]] or [[acetylcholine]]. Exaggerated spasm is diagnostic of Prinzmetal angina.
ECG finding will more often show [[Electrocardiogram#ST segment|ST segment]] elevation than ST depression.
==Treatment==
Prinzmetal angina typically responds to [[nitrate]]s and [[calcium channel blocker]]s.
==References==
<references/>
==External links==
* {{WhoNamedIt|synd|3059}}
* [http://www.prinzmetal.dk www.prinzmetal.dk] A site about Prinzmetal variant angina and cardiac syndrome x
{{Circulatory system pathology}}
[[Category:Ischemic heart diseases]]
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