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 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 | *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 | *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 | ||
* | **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 | ||
* | ***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}} | ||
== | ==Evaluation== | ||
* | *'''[[ECG]]''' | ||
**May | **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 | **[[Troponin]](often negative) | ||
**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== | ||
* | *Sublingual [[nitroglycerin]] | ||
*Counsel on smoking cessation | *Counsel on smoking cessation | ||
*For chronic management | *For chronic management | ||
**Diltiazem 240- | **[[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 | *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 | *[[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''' | ||
**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== | ||
| Line 48: | Line 63: | ||
==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
- Exertion results in variable symptoms, including increase, decreased, or no change in chest pain
- Associated with nausea, diaphoresis, and palpitations
- Attacks may be precipitated by hyperventilation
Differential Diagnosis
Chest pain
Critical
- Acute coronary syndromes (ACS)
- Aortic dissection
- Cardiac tamponade
- Coronary artery dissection
- Esophageal perforation (Boerhhaave's syndrome)
- Pulmonary embolism
- Tension pneumothorax
Emergent
- Cholecystitis
- Cocaine-associated chest pain
- Mediastinitis
- Myocardial rupture
- Myocarditis
- Pancreatitis
- Pericarditis
- Pneumothorax
Nonemergent
- Aortic stenosis
- Arthritis
- Asthma exacerbation
- Biliary colic
- Costochondritis
- Esophageal spasm
- Gastroesophageal reflux disease
- Herpes zoster / Postherpetic Neuralgia
- Hypertrophic cardiomyopathy
- Hyperventilation
- Mitral valve prolapse
- Panic attack
- Peptic ulcer disease
- Pleuritis
- Pneumomediastinum
- Pneumonia
- Rib fracture
- Stable angina
- Thoracic outlet syndrome
- Valvular heart disease
- Muscle sprain
- Psychologic / Somatic Chest Pain
- Spinal Root Compression
- Tumor
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
- Consider admission for serial cardiac enzymes and provocative testing
- 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
- ↑ 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.
- ↑ 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.
- ↑ Rosamond W. Are migraine and coronary heart disease associated? An epidemiologic review. Headache. 2004;44 Suppl 1:S5-12.
- ↑ Miwa K. Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks
- ↑ Stern SS. Coronary artery spasm: a 2009 update.. Circulation (New York, N.Y.). 2009-05;119:2531-2534.
- ↑ 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.
- ↑ Robertson RM, Wood AJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation. 1982;65(2):281-5.
- ↑ 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.
