Coronary artery vasospasm: Difference between revisions

 
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==Background==
==Background==
*Commonly referred to as ''Prinzmetal Angina'' or ''Variant Angina''
*Typically affects patients <50 yo
*Typically affects patients <50 yo
*Associated with transient ST deviation in local distribution
*Associated with transient [[ST elevation]] in local distribution
*Often occurs in early morning <ref> 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.</ref>
*Often occurs in early morning <ref> 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.</ref>
*Mechanism is likely vagal withdrawal
*Mechanism is likely vagal withdrawal
*Tobacco use a major risk factor<ref> 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.</ref>
*Tobacco use a major risk factor (up to 75% of cases)<ref> 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.</ref>
*May be associated with migraines <ref> Rosamond W. Are migraine and coronary heart disease associated? An epidemiologic review. Headache. 2004;44 Suppl 1:S5-12. </ref>
*May be associated with migraines <ref> Rosamond W. Are migraine and coronary heart disease associated? An epidemiologic review. Headache. 2004;44 Suppl 1:S5-12. </ref>
*Vfib, tachycardia, and complete AV block may be associated with ischemic episodes
*Vfib, tachycardia, and complete AV block may be associated with ischemic episodes


==Clinical Features==
==Clinical Features==
*Chest discomfort/tightness/pressure
*[[Chest pain|Chest discomfort]]/tightness/pressure
*Gradual onset/resolution
**Gradual onset/resolution
*Often no exertional component to chest pain
**No respirophasic component to pain
*No respirophasic component to pain
**Poorly localized; radiation of pain is common
*Poorly localized; radiation of pain is common
**Often no exertional component to chest pain
*Associated with nausea, diaphroesis, and palpations
***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
*Attacks may be precipitated by hyperventilation


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{{Chest Pain DDX}}
{{Chest Pain DDX}}


==Diagnosis==
==Evaluation==
*ECG and troponin
*'''[[ECG]]'''
**May demonstrate ST elevation during spasm, but troponin often negative
**Characteristically demonstrates transient ST elevation during spasm
*CXR
**May be followed by ST depression or T-wave inversion<ref>Miwa K. Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks</ref>
*Holter monitor
*'''Labs'''
*Stress testing typically done to evaluate for fixed CAD
**[[Troponin]](often negative)
**Often yields negative results <ref>Stern SS. Coronary artery spasm: a 2009 update.. Circulation (New York, N.Y.). 2009-05;119:2531-2534.</ref>
**Toxicology screen (if cocaine suspected as etiology)
*Coronary angiography considered in following patients:<ref> 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.</ref>
*'''Imaging'''
**ECG with STE
**[[CXR]] (R/O other etiologies)
**History strongly indicative and stress testing/ambulatory monitoring are normal
*'''Other'''
**Holter monitor (helpful in identifying dysrhythmia or silent cases)
**Stress testing  
***Typically done to evaluate for fixed CAD; often yields negative results<ref>Stern SS. Coronary artery spasm: a 2009 update.. Circulation (New York, N.Y.). 2009-05;119:2531-2534.</ref>
**Coronary angiography considered in following patients:<ref> 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.</ref>
***[[ECG]] with STE
***History strongly indicative and stress testing/ambulatory monitoring are normal


==Management==
==Management==
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*Counsel on smoking cessation
*Counsel on smoking cessation
*For chronic management
*For chronic management
**[[Diltiazem]] 240-360 mg/day
**[[Diltiazem]] 240-360mg/day
**Isosorbide mononitrate considered 2nd line due to adverse effect profile
**Isosorbide mononitrate considered 2nd line due to adverse effect profile
*Avoid nonselective [[beta blockers]] as they may exacerbate vasospasm <ref>Robertson RM, Wood AJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation. 1982;65(2):281-5. </ref>
*Avoid nonselective [[β-blockers]] as they may exacerbate vasospasm <ref>Robertson RM, Wood AJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation. 1982;65(2):281-5. </ref>
*ASA used with caution and at low dose in patients without h/o CAD <ref>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.</ref>
*[[ASA]] used with caution and at low dose in patients without history of CAD <ref>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.</ref>


==Disposition==
==Disposition==
*Consider admission for serial cardiac enzymes and provocative testing
*'''Admission'''
*Sometimes spasm occurs around an already existing plaque
**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==
==See Also==
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==External Links==
==External Links==
 
*[https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/variant-angina?query=prinzmetal%20angina| Merk Manual: Variant Angina (Prinzmetal Angina)]


==References==
==References==

Latest revision as of 19:24, 15 July 2021

Background

  • 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

Critical

Emergent

Nonemergent

Evaluation

  • 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

Management

  • 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]

Disposition

  • 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

References

  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.