[Skip to Navigation]
Comment & Response
June 5, 2019

A Myocardial Bridge or Not?

Author Affiliations
  • 1The Carl and Edyth Lindner Center for Research and Education, The Christ Hospital, Cincinnati, Ohio
  • 2Minneapolis Heart Institute Foundation, Abbott Northwestern Hospital, Minneapolis, Minnesota
  • 3Barbra Streisand Women’s Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, California
JAMA Cardiol. 2019;4(7):713-714. doi:10.1001/jamacardio.2019.1658

To the Editor We read with interest and carefully reviewed the article entitled “A Woman in her 40s With Non–ST-Elevation Myocardial Infarction.”1 In summary, a 40-year-old woman presented with rest chest pain and troponin level increase (0.38 ng/mL to 51.0 ng/mL), consistent with acute non–ST-elevation myocardial infarction. Apparently, echocardiography revealed normal left ventricular function and normal wall motion, unusual for a troponin peak of that magnitude. In addition, based on the albeit limited angiographic images, we wonder whether the authors considered spontaneous coronary artery dissection (SCAD). In particular, the proximal arrow in the Figure, B,1 points to an epicardial segment of the vessel, which is not typical for myocardial bridging, the included video does not appear to show significant bridging, and the still images appear to show a linear density in the left anterior descending coronary artery raising concern for SCAD. It seems implausible to propose a myocardial bridge as the cause of myocardial infarction in a patient at rest and with this magnitude of troponin elevation. The history, age, and sex are more typical of SCAD.

Add or change institution