eMedicine Specialties > Cardiology > Coronary Artery Disease

Coronary Artery Vasospasm: Differential Diagnoses & Workup

Author: Andrew P Selwyn, MD, MA, FACC, FRCP, Professor of Medicine, Harvard Medical School; Senior Physician and Cardiologist, Associate Chief of the Cardiovascular Division(Academic Affairs), Brigham and Women's Hospital
Coauthor(s): James L Orford, MBChB, Clinical and Research Fellow in Cardiovascular Diseases, Department of Internal Medicine, Brigham and Women's Hospital, Harvard Medical School
Contributor Information and Disclosures

Updated: Jul 14, 2009

Differential Diagnoses

Angina Pectoris
Myocardial Infarction
Anxiety Disorders
Myocardial Ischemia
Aortic Dissection
Panic Disorder
Coronary Artery Atherosclerosis
Pericarditis, Acute
Esophageal Motility Disorders
Toxicity, Cocaine
Esophageal Spasm
Unstable Angina
Gastroesophageal Reflux Disease
Isolated Coronary Artery Anomalies

Workup

Laboratory Studies

  • Evaluation of the standard hematology, serum chemistry, and lipid profiles to exclude anemia, infection, primary platelet disorder, renal failure, hyperglycemia, electrolyte abnormality, and dyslipidemia is appropriate. Serial cardiac enzyme determination is appropriate if MI is suspected.

Imaging Studies

  • Thallium scintigraphy has been used to localize the myocardial perfusion defect to an area perfused by a coronary artery in which spasm can be demonstrated by angiography. This was a valuable research tool and helped define the syndromes of coronary artery vasospasm; however, the routine clinical utility of this test is uncertain.
  • Coronary angiography is the criterion standard for the diagnosis of variant angina when coupled with the clinical syndrome of angina pectoris at rest with transient ST-segment elevation. Focal spasm of the proximal portion of a major coronary artery not preceded by an increase in heart rate or blood pressure that is followed by chest pain, ST-segment elevation, and ventricular dysfunction is pathognomonic.
    • Most patients with variant angina and documented coronary artery vasospasm have some angiographic evidence of atherosclerotic coronary artery disease, although evidence is mild in many patients. Spasm typically occurs within 1 cm of an angiographically apparent obstruction. If minimal or no angiographic evidence of coronary artery disease is found in a patient who has recently had angina at rest with transient ST-segment elevation, variant angina is the likely diagnosis, and further testing is unnecessary. In some patients, it may be necessary to perform provocative testing to induce coronary artery spasm.
    • Ergonovine maleate is an ergot alkaloid that stimulates both alpha-adrenergic and serotonergic receptors and thus exerts a direct constrictive effect on vascular smooth muscle. Coronary arteries, which constrict spontaneously, appear to be abnormally sensitive to this agent. The response of normal coronary arteries to ergonovine maleate is a mild, diffuse spasm.
    • Of the provocative test agents shown to induce coronary artery spasm in susceptible patients, ergonovine maleate, methylergonovine maleate, acetylcholine, or hyperventilation are the most useful. Ergonovine maleate for injection is no longer available, and the availability of methylergonovine is limited. The intravenous administration of incremental doses of methylergonovine starting at 0.05 mg to a maximum of 0.40 mg is both sensitive and specific, and there is an inverse relationship between the dose required to provoke spasm in the laboratory and the frequency or 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. Women are more sensitive than men to methylergonovine. The intracoronary route of administration of methylergonovine for provocation of spasm is relatively safe, sensitive, and specific, but rarely used today. This route is preferable in hypertensive patients and affords the opportunity to evaluate the left and right coronary circulations separately. Small dosing increments of 5-10 mcg are used, with a total dose not to exceed 50 mcg and with intracoronary nitroglycerine available.
    • Absolute contraindications to methylergonovine include pregnancy, severe hypertension, severe left ventricular dysfunction, moderate-to-severe aortic stenosis, high-grade left main coronary stenosis, and significant stenoses in epicardial coronary vessels. Relative contraindications include uncontrolled or unstable angina, uncontrolled ventricular arrhythmia, recent MI, and advanced coronary disease. Alternatively, intracoronary acetylcholine can be used as a provocative test for spasm, and its effectiveness is comparable to methylergonovine. In patients with more than 1 episode of variant angina per day, the hyperventilation provocative test is nearly as effective as methylergonovine in causing vasospasm. In patients with less frequent attacks, hyperventilation is less sensitive.

Other Tests

  • Electrocardiography: Transient ST-segment elevation is the characteristic finding in patients with variant angina. If the patient is fortunate, this is detected during the initial evaluation of a patient with chest pain. Until the diagnosis is firmly established, a 12-lead electrocardiograph should be performed during each and every episode of chest pain. As previously noted, ST-segment elevation and depression and T-wave inversion or pseudonormalization may follow episodes of ST-elevation.
    • Ambulatory electrocardiography: Many episodes of coronary artery vasospasm are brief and may be asymptomatic; however, ST-segment changes may be detected by ambulatory electrocardiography and may better characterize the frequency and duration of myocardial ischemia.
    • Holter monitoring: Variant angina, which is associated with ventricular dysrhythmia and sudden cardiac death, may be detected during inpatient telemetry observation or ambulatory Holter monitoring.
  • Exercise tolerance testing is controversial and of questionable utility. Prinzmetal originally described patients who had chest pain at rest and preserved exercise tolerance. However, we now know that many patients with coronary artery vasospasm experience exertional angina pectoris due to fixed coronary artery stenoses; furthermore, we know that exercise may precipitate coronary artery vasospasm in some patients. The results of exercise testing in patients with variant angina therefore are highly variable, and approximately equal numbers of patients show ST-segment depression, elevation, or no change during exercise testing.

Histologic Findings

In one report, increased numbers of mast cells were found in the adventitial layer of the coronary artery in a patient who died from coronary artery spasm.

More on Coronary Artery Vasospasm

Overview: Coronary Artery Vasospasm
Differential Diagnoses & Workup: Coronary Artery Vasospasm
Treatment & Medication: Coronary Artery Vasospasm
Follow-up: Coronary Artery Vasospasm
References
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References

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Further Reading

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Keywords

coronary artery vasospasm, vasospastic angina, variant angina, Prinzmetal angina, Prinzmetal's angina, focal coronary artery vasospasm, acute myocardial infarction, myocardial ischemia, coronary vasoconstriction, dynamic coronary obstruction, myocardial infarction, MI, dyslipidemia, platelet aggregation, atherosclerotic coronary artery disease, stable angina pectoris, unstable angina pectoris, focal coronary artery vasospasm, normal vasodilator function abnormality, subclinical atherosclerosis, clinical atherosclerosis

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Contributor Information and Disclosures

Author

Andrew P Selwyn, MD, MA, FACC, FRCP, Professor of Medicine, Harvard Medical School; Senior Physician and Cardiologist, Associate Chief of the Cardiovascular Division(Academic Affairs), Brigham and Women's Hospital
Disclosure: Nothing to disclose.

Coauthor(s)

James L Orford, MBChB, Clinical and Research Fellow in Cardiovascular Diseases, Department of Internal Medicine, Brigham and Women's Hospital, Harvard Medical School
Disclosure: Nothing to disclose.

Medical Editor

Gregory Joseph Dehmer, MD, Director, Division of Cardiology, Professor, Department of Medicine, Scott & White Clinic, Texas A&M University School of Medicine
Gregory Joseph 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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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, and American College of Physicians
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

 
 
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