Prinzmetal's angina

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Prinzmetal angina
Classification and external resources
ICD-10I20.1
ICD-9413.1
DiseasesDB13727
MedlinePlus000159
eMedicinemed/447
MeSHD000788
 
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Prinzmetal angina
Classification and external resources
ICD-10I20.1
ICD-9413.1
DiseasesDB13727
MedlinePlus000159
eMedicinemed/447
MeSHD000788

Prinzmetal's or Prinzmetal angina (/ˈprɪntsmɛtəl/, sounds like "prints metal") (also known as variant angina, angina inversa, or coronary vessel spasm) 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[edit]

It was described as "A variant form of angina pectoris" in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908–1987).[1] However, it had been described twice in the 1930s by other authors.[2][3]

It was first referred to as cardiac syndrome X (CSX) by Kemp in 1973, to describe patients with exercise-induced angina and normal coronary angiograms.[4]

Features[edit]

Symptoms typically occur at rest, rather than on exertion (thus attacks usually occur at night).[5] 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.

Prinzmetal's should be suspected by a cardiologist when the pain occurs at rest and/or in clusters, and in the absence of a positive treadmill stress test, as Prinzmetal's is exercise tolerant and can generally only be diagnosed after other forms of cardiac disease have been ruled out.

It is associated with specific ECG changes (elevation rather than depression of the ST segment). However, in order to be diagnosed, these ECG changes can only be tracked when the electrocardiogram occurs while the patient is experiencing an attack. Therefore, many experts recommend provocative testing during Electrocardiogram testing to attempt to induce an attack when Prinzmetal's is suspected.

Mechanism[edit]

The mechanism that causes such intense vasospasm, as to cause a clinically significant narrowing of the coronary arteries is so far unknown. There are three relevant hypotheses:

Diagnosis[edit]

Although Prinzmetal's Angina has been documented in between 2% to 10% of angina patients, it can be overlooked by cardiologists who stop testing protocol after ruling out typical angina. 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 or may not show a degree of positivity, as coronary spasm too can cause myocardial damage or may leave the arteries undamaged. 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.

Treatment[edit]

Prinzmetal's angina typically responds to nitrates and calcium channel blockers.[10]

Use of a beta blocker such as propranolol is contraindicated in Prinzmetal's angina.[11]

See also[edit]

References[edit]

  1. ^ a b Prinzmetal, Myron; Kennamer, Rexford; Merliss, Reuben; Wada, Takashi; Bor, Naci (1959). "Angina pectoris I. A variant form of angina pectoris". The American Journal of Medicine 27 (3): 375–88. doi:10.1016/0002-9343(59)90003-8. PMID 14434946. 
  2. ^ a b Parkinson, John; Bedford, D.Evan (1931). "Electrocardiographic Changes During Brief Attacks of Angina Pectoris". The Lancet 217 (5601): 15–9. doi:10.1016/S0140-6736(00)40634-3. 
  3. ^ Brown, G.R.; Holman, Delavan V. (1933). "Electrocardiographic study during a paroxysm of angina pectoris". American Heart Journal 9 (2): 259–64. doi:10.1016/S0002-8703(33)90720-6. 
  4. ^ Kemp HG, Jr; Vokonas, PS; Cohn, PF; Gorlin, R (June 1973). "The anginal syndrome associated with normal coronary arteriograms. Report of a six year experience.". The American journal of medicine 54 (6): 735–42. doi:10.1016/0002-9343(73)90060-0. PMID 4196179. 
  5. ^ "Angina Pectoris". Retrieved 2009-02-24. [dead link]
  6. ^ Yoo, Sang-Yong; Kim, Jang-Young (2009). "Recent Insights into the Mechanisms of Vasospastic Angina". Korean Circulation Journal 39 (12): 505–11. doi:10.4070/kcj.2009.39.12.505. PMC 2801457. PMID 20049135. 
  7. ^ Egashira, Kensuke; Katsuda, Yousuke; Mohri, Masahiro; Kuga, Takeshi; Tagawa, Tatuya; Shimokawa, Hiroaki; Takeshita, Akira (1996). "Basal release of endothelium-derived nitric oxide at site of spasm in patients with variant angina". Journal of the American College of Cardiology 27 (6): 1444–9. doi:10.1016/0735-1097(96)00021-6. PMID 8626956. 
  8. ^ Sun, Hongtao; Mohri, Masahiro; Shimokawa, Hiroaki; Usui, Makoto; Urakami, Lemmy; Takeshita, Akira (28 February 2002). "Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina". Journal of the American College of Cardiology 39 (5): 847–851. doi:10.1016/S0735-1097(02)01690-X. PMID 11869851. 
  9. ^ http://www.sciencedirect.com/science/article/pii/S0002870376805686
  10. ^ American Heart Association http://www.americanheart.org/presenter.jhtml?identifier=4496[dead link] "Angina Pectoris Treatments"
  11. ^ British National Formulary, Vol 58, 2009, pg 88.

External links[edit]