Editor’s Corner: Barcelona Farewell

By Alfred A. Bove, MD, PhD

For many of us who were in the cath lab in the 1970s and 1980s, the diagnosis of coronary artery spasm was not rare. For patients with angina unrelated to effort, we had a high suspicion that spasm may be playing a significant role.

In the cath lab, the finding of no fixed coronary obstruction often led to a provocative test for spasm using ergonovine. I became convinced of the importance of coronary spasm in 1972, when a patient with recurrent episodes of chest pain, ST segment elevation, and ventricular fibrillation was referred to me. No fixed luminal narrowing was seen, but marked constriction of the dominant circumflex artery, ST elevation, and pain occurred during catheterization. Nitroglycerin reversed the syndrome; however, therapy for this life-threatening condition was, at that time, lacking. Calcium channel blockers were not yet available and continued episodes led us to perform bypass surgery to the involved artery.

Relief was only temporary, and when the graft occluded (likely due to competitive flow) everything resumed. I had a hard time selling this as spasm without significant fixed obstruction. Luminaries such as Thomas James and Mason Sones thought I was just missing severe coronary narrowing due to atherosclerosis. The controversy led to delays in publication,1 and others beat us to the journals, preventing our claim of first demonstration of angiographically-proven mechanism of prinzmetal angina.

With the major attention of Attilio Maseri, MD, many of us became interested in making the diagnosis of spasm in patients without evidence of fixed stenosis. Ergonovine became the provocateur of choice, and the diagnosis was common. Now the diagnosis is almost extinct in Western countries. Yes, we do receive images of coronary spasm submitted to JACC: Cardiovascular Interventions, but even that may speak to the perception that it is rare. The ergonovine test went away in the United States with the unavailability of the drug and some occasional adverse events with its utilization.

An excellent review of various causes of angina pectoris without angiographic obstructive disease can be found in the May issue of JACC: Cardiovascular Interventions.2  This state-of-the-art paper points out that the acetylcholine test has largely replaced ergot testing in North America, but ergonovine testing remains in the European guidelines. These authors think we should look more carefully for these causes of angina pectoris in patients without fixed disease.

If spasm has met its demise in the West, it is alive and well in the East. A research fellow in our group at Emory who has had extensive clinical experience in Korea estimates that spasm is associated with up to 20-25% of acute coronary syndromes. Most of these angiographically-documented spasms are revealed with provocative ergonovine testing, but about 1.5% occurs spontaneously during catheterization. When I poll my clinical colleagues at Emory about their impression about how many acute angina presentations are due to spasm, the answer they give is less than 1%. In Japan, the high prevalence of coronary spasm is also found. Is this a genetic difference? There may be other explanations such as environmental factors or variation in medication usage. Do we know anything about East Asian patients residing outside those countries? Are we ignoring the “out-of-date” diagnosis of coronary spasm in Western countries, or is it simply a case of “if you look you will find, and if you don’t look, you will seldom see?”


  1. King SB, Mansour KA, Hatcher CR, Silverman ME, Hart NC.  Ann Thorac Surg. 1973;16:337-43.
  2. Redico F, Cicchitti V, Zimarino M, DeCaterina R. JACC Cardiovasc Interv. 2014;7:453-63.

Alfred A. Bove, MD, PhD, is professor emeritus of medicine at Temple University School of Medicine in Philadelphia, and former president of the ACC.

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