Coronary artery vasospasm

(Redirected from Prinzmetal's angina)


  • Commonly referred to as Prinzmetal Angina or Variant Angina
  • Typically affects patients <50 yo
  • Associated with transient ST elevation in local distribution
  • Often occurs in early morning [1]
  • Mechanism is likely vagal withdrawal
  • Tobacco use a major risk factor (up to 75% of cases)[2]
  • May be associated with migraines [3]
  • Vfib, tachycardia, and complete AV block may be associated with ischemic episodes

Clinical Features

  • Chest discomfort/tightness/pressure
    • Gradual onset/resolution
    • No respirophasic component to pain
    • Poorly localized; radiation of pain is common
    • Often no exertional component to chest pain
      • Exertion results in variable symptoms, including increase, decreased, or no change in chest pain
        • Makes exertional symptoms unreliable
  • Associated with nausea, diaphoresis, and palpitations
  • Attacks may be precipitated by hyperventilation

Differential Diagnosis

Chest pain





  • ECG
    • Characteristically demonstrates transient ST elevation during spasm
    • May be followed by ST depression or T-wave inversion[4]
  • Labs
    • Troponin(often negative)
    • Toxicology screen (if cocaine suspected as etiology)
  • Imaging
    • CXR (R/O other etiologies)
  • Other
    • Holter monitor (helpful in identifying dysrhythmia or silent cases)
    • Stress testing
      • Typically done to evaluate for fixed CAD; often yields negative results[5]
    • Coronary angiography considered in following patients:[6]
      • ECG with STE
      • History strongly indicative and stress testing/ambulatory monitoring are normal


  • Sublingual nitroglycerin
  • Counsel on smoking cessation
  • For chronic management
    • Diltiazem 240-360mg/day
    • Isosorbide mononitrate considered 2nd line due to adverse effect profile
  • Avoid nonselective β-blockers as they may exacerbate vasospasm [7]
  • ASA used with caution and at low dose in patients without history of CAD [8]


  • Admission
    • Consider admission for serial cardiac enzymes and provocative testing
      • Sometimes spasm occurs around an already existing plaque
  • Discharge
    • Discharge hemodynamically stable patients who have a negative ischemic workup
    • Provide smoking cessation education
    • Follow up w/ cardiology within one week

See Also

External Links


  1. Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris. I. A variant form of angina pectoris; preliminary report. Am J Med. 1959;27:375-88.
  2. Takaoka K. Comparison of the risk factors for coronary artery spasm with those for organic stenosis in a Japanese population: role of cigarette smoking. Int J Cardiol. 2000;72:121–126.
  3. Rosamond W. Are migraine and coronary heart disease associated? An epidemiologic review. Headache. 2004;44 Suppl 1:S5-12.
  4. Miwa K. Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks
  5. Stern SS. Coronary artery spasm: a 2009 update.. Circulation (New York, N.Y.). 2009-05;119:2531-2534.
  6. Montalescot G, Sechtem U, Achenbach S, et al. 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J. 2013;34(38):2949-3003.
  7. Robertson RM, Wood AJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation. 1982;65(2):281-5.
  8. Miwa K, Kambara H, Kawai C. Effect of aspirin in large doses on attacks of variant angina. Am Heart J. 1983;105(2):351-5.