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Analytic Review: Treatment of Coronary Artery Spasm and Variant Angina

Department of Medicine, Division of Cardiovascular Medicine, University of Florida, College of Medicine, Veterans Administration Medical Center, Gainesville, FL

James A. Hill, MD

Department of Medicine, Division of Cardiovascular Medicine, University of Florida, College of Medicine, Veterans Administration Medical Center, Gainesville, FL

Robert L. Feldman, MD

Department of Medicine, Division of Cardiovascular Medicine, University of Florida, College of Medicine, Veterans Administration Medical Center, Gainesville, FL

Jawahar L. Mehta, MD

Department of Medicine, Division of Cardiovascular Medicine, University of Florida, College of Medicine, Veterans Administration Medical Center, Gainesville, FL

Carl J. Pepine, MD

Department of Medicine, Division of Cardiovascular Medicine, University of Florida, College of Medicine, Veterans Administration Medical Center, Gainesville, FL

Coronary artery spasm is an abnormal constriction of the conductive arteries that produces myocardial ischemia in the absence of any marked increase in heart rate or blood pressure. Ischemia is a transient phenomenon and is promptly reversed spontaneously or by nitroglycerine. The so-called "hallmark of spasm"—ST segment elevation—is evidence for severe myocardial ischemia rather than conclusive evidence for coronary artery spasm. Any process that transiently or permanently restricts coronary blood flow (e.g., transient occlusion by thrombus) will produce similar electrocardiogram (EKG) abnormalities.

Most patients with symptoms and EKG changes related to coronary artery spasm respond to sublingual nitrates. Thus, their use for relief of the acute ischemic episode remains the initial treatment of choice. When symptoms are moderate in severity or unacceptably controlled in frequency using nitrates alone, other pharmacologic measures are needed.

When spasm is superimposed upon hemodynamically important atherosclerotic obstruction, the favorable response to calcium antagonist may not be as great as that seen when spasm occurs alone. One possible explanation is that spasm is not really occurring. The ST segment elevation may be related to transient total occlusion from platelet aggregation or thrombosis. Thus, aspirin may be the drug of choice. However, if spasm is the culprit, recommendations for surgery and angioplasty require proof that spasm is occurring in and around the area of fixed atherosclerotic obstruction and not in other vessels or over the entire course of the distal vessel.

Journal of Intensive Care Medicine, Vol. 1, No. 2, 66-74 (1986)
DOI: 10.1177/088506668600100203


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