Prinzmetal's angina: Difference between revisions
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It was first described as a variant form in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).<ref>Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.</ref> | It was first described as a variant form in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).<ref>Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.</ref> | ||
== | ==Signs and Symptoms== | ||
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. | 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. | ||
==Electrocardiographic Changes== | |||
Prinzmetal's angina is associated with transmural injury and [[ST segment elevation]] rather than ST segment depression. | |||
==Diagnosis== | ==Diagnosis== | ||
Revision as of 12:51, 4 September 2009
| Prinzmetal's angina | |
| ICD-10 | I20.1 |
|---|---|
| ICD-9 | 413.1 |
| DiseasesDB | 13727 |
| eMedicine | med/447 |
| MeSH | D000788 |
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Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
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Overview
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).
Eponym
It was first described as a variant form in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).[1]
Signs and Symptoms
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.
Electrocardiographic Changes
Prinzmetal's angina is associated with transmural injury and ST segment elevation rather than ST segment depression.
Diagnosis
Patients who develop cardiac chest pain are generally treated empirically as an "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 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.
EKG finding will more often show ST segment elevation than ST depression.
Treatment
Prinzmetal angina typically responds to nitrates and calcium channel blockers. Patients with multivessel spasm, refractory spasm, spasm that results in sudden death may benefit from dual calcium channel blocker therapy.
References
- ↑ Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.