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Coronary Artery Vasospasm Workup

  • Author: Stanley S Wang, MD, JD, MPH; Chief Editor: Eric H Yang, MD  more...
 
Updated: Nov 21, 2015
 

Laboratory Studies

Evaluation of the standard hematology, serum chemistry, and lipid profiles is appropriate for excluding anemia, infection, primary platelet disorders, renal failure, hyperglycemia, electrolyte abnormalities, and dyslipidemia. Serial measurement of cardiac enzyme and troponin levels should be performed to assess for evidence of ischemia.

Magnesium levels may be checked; magnesium deficiency can heighten sensitivity to acetylcholine- and hyperventilation-induced spasm. Magnesium supplementation may be a potentially useful therapy.[5]

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Perfusion Imaging and Echocardiography

Myocardial perfusion imaging may be helpful in ruling out obstructive atherosclerotic disease between episodes of coronary artery vasospasm. During episodes, myocardial perfusion imaging may help identify and quantify ischemia and localize it to the culprit artery.

Standard transthoracic echocardiography should be considered to evaluate for stigmata of other causes of nonexertional chest pain (eg, pericarditis or abnormalities of the aorta). Preliminary data suggest a potential role for hyperventilation and cold-pressor stress echocardiography as a noninvasive means for detecting coronary artery vasospasm, though this method may not be as sensitive as using intracoronary acetylcholine as the provocative agent.[34]

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Electrocardiography and Monitoring

Transient ST-segment elevation on electrocardiography (ECG) is a characteristic finding in patients with variant angina,[5] but it may only be present during symptomatic episodes and typically resolves completely within minutes. However, in more severe cases, ST elevation may be followed by T-wave inversions for hours to days.[35] During recovery, U-wave inversions may be present, particularly in lead V5.[36]

Many episodes of coronary artery vasospasm are brief and may be asymptomatic; however, ST-segment changes may be detected by ambulatory electrocardiography, which may allow for more accurate characterization of the frequency and duration of attacks.

Severe vasospastic angina may result in heart block or potentially fatal ventricular arrhythmias. Inpatient telemetry monitoring serves an important role in acutely ill patients. In outpatients, Holter monitoring may facilitate detection of nonsustained arrhythmias.

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Angiography

Coronary angiography may reveal focal spasm of a coronary artery; when coupled with typical symptoms, ECG changes, and even ventricular dysfunction, this spasm may be pathognomonic for the condition.

Most patients with variant angina and documented coronary artery vasospasm have some angiographic evidence of atherosclerotic coronary artery disease (CAD), which is typically mild. Focal spasm more commonly occurs within 1 cm of an angiographically apparent obstruction. If minimal or no angiographic evidence of CAD is found in a patient who has recently had angina at rest with transient ST-segment elevation, variant angina is the more likely diagnosis, and further testing is unnecessary.

The angiographic demonstration of a myocardial bridge may have prognostic implications as well. Not only are myocardial bridges associated with a higher likelihood of more severe coronary artery vasospasm in response to an intracoronary acetylcholine challenge, but a 2012 study suggested that these patients may have greater related morbidity and mortality.[37]

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Provocative Testing

Provocative testing is infrequently used in clinical practice but may facilitate identification of patients with coronary artery vasospasm.

The most commonly used provocative agent is ergonovine maleate, an ergot alkaloid that stimulates both alpha-adrenergic and serotonergic receptors, exerting a direct constrictive effect on vascular smooth muscle. Normal coronary arteries respond to ergonovine maleate with a mild diffuse spasm, whereas abnormal arteries may respond with an intense focal spasm. Acetylcholine and hyperventilation have also been used to provoke spasm.

Intravenous (IV) administration of incremental doses of methylergonovine, starting at 0.05 mg and increasing to a maximum of 0.40 mg, is both sensitive and specific, and there is an inverse relation between the dose required to provoke spasm in the laboratory and the frequency of spontaneous episodes experienced by the patient.

To ensure a valid test, nitrates and calcium antagonists must be withdrawn for at least 48 hours before testing. The intracoronary route of administering methylergonovine is preferable for provocation of spasm and affords the opportunity to evaluate the left and right coronary circulations separately. Small dosing increments (ie, 5-10 µg) are used, with the total dose not to exceed 50 µg.

Intracoronary nitrates should be readily available. Complication rates during provocative testing are relatively low with either ergonovine or acetylcholine, provided that intracoronary nitrates are on hand for use to relieve induced spasms.[38] A 2012 study showed that use of beta blockers during the intracoronary acetylcholine provocation test in patients with vasospastic angina is not associated with a worsening of clinical and angiographic parameters.[39]

A 2015 study suggests that left-ventricular end diastolic pressure (LVEDP) may be effective in identifying myocardial ischemia during ergonovine provocation testing.[40]  

Absolute contraindications to provocative testing with methylergonovine include the following:

  • Pregnancy
  • Severe hypertension
  • Severe left ventricular dysfunction
  • Moderate-to-severe aortic stenosis
  • High-grade left main coronary stenosis
  • Significant stenoses in epicardial coronary vessels

Relative contraindications include the following:

  • Uncontrolled or unstable angina
  • Uncontrolled ventricular arrhythmia
  • Recent MI
  • Advanced coronary disease
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Contributor Information and Disclosures
Author

Stanley S Wang, MD, JD, MPH Clinical Cardiologist, Austin Heart South; Director of Legislative Affairs, Austin Heart; Director, Sleep Disorders Center at Heart Hospital of Austin; Assistant Professor of Medicine (Adjunct), University of North Carolina School of Medicine

Stanley S Wang, MD, JD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, American Society of Echocardiography, Texas Medical Association, American Academy of Sleep Medicine, American Stroke Association, American Society of Nuclear Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Acknowledgements

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Gregory J Dehmer, MD Director, Division of Cardiology, Scott & White Healthcare; Professor of Medicine, Texas A&M Health Science Center College of Medicine

Gregory J Dehmer, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Society for Cardiac Angiography and Interventions, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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This electrocardiogram (ECG) is from a patient who underwent urgent cardiac catheterization, which revealed diffuse severe coronary spasm (most marked in the left circumflex system) without any fixed obstructive lesions. Severe left ventricular wall motion abnormalities were present, involving the anterior and inferior segments. A question of so-called takotsubo cardiomyopathy (left ventricular apical ballooning syndrome) is also raised (see Bybee et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Int Med 2004:141:858-65). The latter is most often reported in postmenopausal, middle-aged to elderly women in the context of acute emotional stress and may cause ST elevations acutely with subsequent T wave inversions. A cocaine-induced cardiomyopathy (possibly related to coronary vasospasm) is a consideration but was excluded here. Myocarditis may also be associated with this type of ECG and the cardiomyopathic findings shown here. No fixed obstructive epicardial coronary lesions were detected by coronary arteriography. The findings in this ECG include low-amplitude QRS complexes in the limb leads (with an indeterminate QRS axis), loss of normal precordial R wave progression (leads V1-V3), and prominent anterior/lateral T wave inversions. Image courtesy of http://ecg.bidmc.harvard.edu .
 
 
 
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