Prinzmetal's angina

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and Keywords: Variant angina; angina inversa


Prinzmetal's angina is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in periodic cycles. Prinzmetal's angina is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than fixed narrowings of the coronary arteries due to atherosclerosis (buildup of fatty plaque and hardening of the arteries).

Historical Perspective

Printzmetal's angina was first described as a variant form in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).[1] It was documented by coronary arteriography in 1973.[2]


Classification by Location

Coronary artery spasm can be classified according to the location of vasoconstriction:

Focal coronary spasm

Focal coronary spasm is limited to a localized segment of the coronary artery.

Multifocal coronary spasm

Multifocal coronary spasm involves several localized segments of the same coronary artery.

Multivessel coronary spasm

Multivessel coronary spasm involves several coronary arteries.[3][4]

Classification by Clinical Syndrome

Coronary artery vasospasm can be classified into either spontaneous or iatrogenic.




  • The exact pathogenesis of coronary vasospasm is not well understood, but some causes and contributing factors are known.
  • A significant group of patients with variant angina have underlying obstructive coronary artery disease.[7]

Epidemiology and Demographics

  • Young patients with fewer cardiovascular risk factors (with the exception of smoking) are at a higher risk for coronary vasospasm, as are noncalcified lesions and eccentric plaques.

Risk Factors

Natural History, Complications and Prognosis

History and Symptoms

While the symptoms of chronic stable angina occur with exertion, the symptoms of Prinzmetal's angina typically occur at rest. The symptoms may occur reproducibly at certain times of the day or night. In the classic description, the symptoms often come on at night.


  • Physicians should suspect vasospasm if ST segment elevation is detected in patients experiencing angina, and if the ECG completely returns to baseline upon resolution of symptoms.
  • Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome" patient, and are generally evaluated with serial testing of cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may in some cases be abnormal or positive, as coronary spasm can lead to myocardial necrosis in severe cases.
  • The gold standard test is coronary angiography including the administration of provocative agents, such as acetylcholine or ergonovine, via the intracoronary route. The definitive diagnosis of coronary vasospasm is made angiographically by demonstration of reduction of luminal diameter in a discrete segment of the vessel, which is proven to be reversible. Reversibility may be demonstrated by previous or subsequent enlargement of luminal diameter, often after the administration of intracoronary vasodilators.
  • It should be noted that two-thirds of patients with Prinzmetal's angina have concurrent atherosclerosis of a major coronary artery, but the extent of the atherosclerosis is generally mild, and the symptoms are out of proportion to the extent of disease. Depending on the local protocol, provocative testing may utilize either ergonovine, methylergonovine or acetylcholine. Exaggerated spasm is diagnostic of Prinzmetal's angina. Care should be taken to have nitrates and calcium channel agents readily available to reverse the spasm.


Prinzmetal's angina is associated with transmural injury and ST segment elevation rather than ST segment depression.


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.

  • Calcium channel blockers: Generally, well tolerated and can aid with hypertension control. A combination of dihyropyridine and non-dihydropyridine calcium channel blockers should be used in patients with refractory coronary vasospasm, particularly if it has resulted in ventricular arrhythmia. Multiple calcium channel blockers may be required in patients with refractory or multivessel spasm. A patient who has suffered VT/VF due to spontaneous vasospasm (not due to acute infarction) should also likely undergo ICD placement.
    • Diltiazem 240-360 mg PO qd
    • Verapamil 240-480 mg PO qd
    • Nifedipine XL 60-120 mg PO qd
    • Nicardipine 40-160 mg PO qd
  • Long-acting nitrates: Generally, well tolerated and can aid with hypertension control.
    • Isosorbide mononitrate (Imdur) 60-240 mg PO qd
    • Isosorbide dinitrate (Isordil) 20-40 mg PO tid
  • Statins: May improve endothelial dysfunction and lower inflammation. A small, randomized control trial showed that fluvastatin 30 mg daily reduced rates of vasospasm. Statins also provide benefits of LDL lowering and plaque stabilization.
    • Fluvastatin 30 mg PO qd
  • Hormone replacement therapy: This remains controversial, particularly due to the risk of concern of increased cardiac events.
  • Smoking cessation: Should be emphasized in all patients, as it contains non-cardiac benefits as well. It lowers future event rates of vasospasm and acute coronary syndromes.
  • PTCA/stenting: While resolution occurs following PTCA/stenting in some cases, spasm can propagate to a new location, proximal or distal to the stented site.
  • ICD placement: As described above for patients with VT/VF due to spontaneous coronary vasospasm without other provocation that may be treated.
  • Surgical autonomic denervation/plexectomy: Can be useful in cases that are refractory to medical therapy or percutaneous intervention. It's reserved only for the most refractory cases.

Making a Selection

  • Treatment of chronic vasospasm should be performed in this order (step-wise fashion): medical therapy, percutaneous intervention, and then, surgery.

Medical Therapy

  • Risk factor modification (smoking cessation, lipid control) is recommended for all patients.
  • Begin pharmacologic therapy with oral calcium channel blockers (diltiazem, verapamil, nifedipine) and/or nitrates. If monotherapy is ineffective, begin combination therapy which is generally well tolerated (10% of patients may require 2 calcium channel blockers). If refractory or multi-vessel spasm is present, multiple CCBs are likely necessary, as these patients are at high risk for ventricular arrhythmias. Alpha blockers may also be useful if there is incomplete response to CCB and nitrates.
  • Due to their ability to improve endothelial function, statins should be considered for vasospasm.
  • Certain medications should be avoided: nonselective beta blockers, aspirin, and sumatriptan can exacerbate vasospasm. Hormone replacement therapy (estrogen-progestin) have been associated with an increase in cardiac events (HERS-II and WHI trials) and should also be avoided.

Percutaneous Intervention (PCI)

  • If vasospasm has a clearly definable area that is associated with coronary artery disease and refractory to medical therapy, stenting may be an effective strategy. However, stenting may simply propagate the spasm to a proximal or distal location in the vessel.
  • Following any PCI, adjunctive medical therapy must be continued.
  • Resolution of symptoms, ECG changes, and angiographic vasospasm is usually apparent within one minute post-procedure.
  • Refractory spasm occurring during PCI is likely secondary to dissection, which requires stenting unless the artery is small and the patient is clinically stable.
  • The role of revascularization in the setting of multivessel vasospasm is uncertain.


  • In the rare circumstance that a patient is refractory to pharmacologic and percutaneous therapy, surgical denervation and plexectomy have been effective.

2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes (DO NOT EDIT) [8]

Recommendations for Prizmental's angina

Class I
"1.CCBs alone or in combination with long-acting nitrates are useful to treat and reduce the frequency of vasospastic angina.(Level of Evidence: B)"
"2.Treatment with HMG-CoA reductase inhibitor, cessation of tobacco use, and additional atherosclerosis risk factor modification and are useful in patients with vasospastic angina. (Level of Evidence: B)"
"3.Coronary angiography (invasive or noninvasive) is recommended in patients with episodic chest pain accompanied by transient ST-elevation to rule out severe obstructive CAD. (Level of Evidence: C)"
Class IIb
"1. Provocative testing during invasive coronary angiography†† may be considered in patients with suspected vasospastic angina when clinical criteria and noninvasive testing fail to establish the diagnosis (Level of Evidence: B)"

ESC Guidelines for Diagnostic Tests in Suspected Vasospastic Angina (DO NOT EDIT)[9]

Class I
"1. ECG during angina if possible. (Level of Evidence: B)"
"2. Coronary arteriography in patients with characteristic episodic chest pain and ST-segment changes that resolve with nitrates and/or calcium channel blockers to determine the extent of underlying coronary disease. (Level of Evidence: B)"
Class IIa
"1. Intracoronary provocative testing to identify coronary spasm in patients with normal findings or nonobstructive lesions on coronary arteriography and the clinical picture of coronary spasm. (Level of Evidence: B)"
"2. Ambulatory ST Segment Monitoring to identify ST-deviation. (Level of Evidence: C)"

ESC Guidelines for Pharmacological Therapy of Vasospastic Angina (DO NOT EDIT)[9]

Class I
"1. Treatment with calcium channel blocker and if necessary nitrates in patients whose coronary arteriogram is normal or shows only non-obstructive lesions. (Level of Evidence: B)"


  1. Prinzmetal M, Kennamer R, Merliss R. of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.
  2. Oliva PB, Potts DE, Pluss RG (1973). "Coronary arterial spasm in Prinzmetal angina. Documentation by coronary arteriography". N Engl J Med. 288 (15): 745–51. doi:10.1056/NEJM197304122881501. PMID 4688712.
  3. Ahooja V, Thatai D (2007). "Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease". J Invasive Cardiol. 19 (7): E178–81. PMID 17620681. Unknown parameter |month= ignored (help)
  4. Miwa K, Ishii K, Makita T, Okuda N (2004). "Diagnosis of multivessel coronary vasospasm by detecting postischemic regional left ventricular delayed relaxation on echocardiography using color kinesis". Circ. J. 68 (5): 483–7. PMID 15118293. Unknown parameter |month= ignored (help)
  5. Lanza GA, Careri G, Crea F (2011). "Mechanisms of coronary artery spasm". Circulation. 124 (16): 1774–82. doi:10.1161/CIRCULATIONAHA.111.037283. PMID 22007100.
  6. Mahemuti A, Abudureheman K, Schiele F, Ecarnot F, Abudureyimu S, Tang B; et al. (2014). "Association between inflammatory markers, hemostatic markers, and traditional risk factors on coronary artery spasm in patients with normal coronary angiography". J Interv Cardiol. 27 (1): 29–35. doi:10.1111/joic.12086. PMID 24345233.
  7. Maseri A, Severi S, Nes MD, L'Abbate A, Chierchia S, Marzilli M et al. (1978) "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol 42 (6):1019-35. PMID: 727129
  8. Ezra A. Amsterdam, MD, FACC; Nanette K. Wenger, MD et al.2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. JACC. September 2014 (ahead of print)
  9. 9.0 9.1 Fox K, Garcia MA, Ardissino D, Buszman P, Camici PG, Crea F; et al. (2006). "Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology". Eur Heart J. 27 (11): 1341–81. doi:10.1093/eurheartj/ehl001. PMID 16735367.


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