eMedicine Specialties > Cardiology > Coronary Artery Disease

Coronary Artery Vasospasm: Follow-up

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

Follow-up

Complications

  • MI is a complication of variant angina. It typically develops in the region corresponding to the location of the electrocardiographic changes during prior anginal attacks, which supports the theory that coronary artery vasospasm is the primary mechanism. Incidence depends on the relevant diagnostic criteria, but it is as high as 30% in some series. The incidence and prognosis of MI in patients with variant angina appears to be associated with the extent and severity of any underlying fixed atherosclerotic coronary stenoses.
  • Arrhythmias: Syncope and presyncope are recognized symptoms that are not infrequently associated with variant angina and are likely due to significant arrhythmias, which cause hemodynamic deterioration. An increased incidence of sudden cardiac death, ventricular tachycardia, ventricular fibrillation, and complete atrioventricular block have been observed during episodes of variant angina and myocardial ischemia. The risk of sudden death is approximately 2% and is most common in patients with multivessel spasm and prior serious arrhythmia during anginal attacks.

Patient Education

  • For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Chest Pain.

Miscellaneous

Medicolegal Pitfalls

  • The absence of obstructive atherosclerotic coronary artery disease (stenosis of 70% or more) should not lead the physician to conclude that the patient is at no risk of future morbidity and mortality.
  • Technical limitations of the 2-dimensional coronary angiogram, operator and interpreter error, variant angina, and rupture of a nonobstructive atherosclerotic plaque with endogenous fibrinolysis of the endovascular thrombus may render the results of this apparently objective test of coronary artery anatomy misleading.
  • A full reevaluation of the clinical syndrome should follow an unexpected angiographic result, and consideration of the aforementioned entities, including variant angina, is appropriate.
  • Addressing risk factors for future coronary heart disease events, including the lowering of cholesterol, almost invariably is appropriate. Full and accurate documentation of this decision-making process is essential.
 


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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