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April 10, 2019

The Evidence on Estrogen, Progesterone, and Spontaneous Coronary Artery Dissection

Author Affiliations
  • 1Department of Cardiovascular Diseases, Mayo Clinic College of Medicine and Science, Rochester, Minnesota
  • 2Department of Surgery, Mayo Clinic College of Medicine and Science, Rochester, Minnesota
  • 3Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota
JAMA Cardiol. 2019;4(5):403-404. doi:10.1001/jamacardio.2019.0774

Spontaneous coronary artery dissection (SCAD) is a noteworthy causative mechanism of acute coronary syndrome (ACS), owing to a tear and/or hematoma formation within the coronary artery wall that reduces myocardial perfusion. Cases of SCAD are diagnosed by coronary angiography and, in equivocal cases, confirmed with intracoronary imaging. Female patients from as young as 14 years to older than 80 years (mean age, 43-53 years) constitute the largest percentage (in most samples, >80%) of those affected by SCAD. The condition causes 1% to 4% of all cases of ACS and as much as 35% of all myocardial infarctions in women younger than 50 years.1,2 Fibromuscular dysplasia, a female-predominant noninflammatory arteriopathy, is a frequent comorbidity, occurring in over 40% of patients with SCAD.1,2 Other relevant associations with SCAD include a history of hypertension, migraine headache, extreme exertion or emotional stress, and pregnancy or postpartum status.1-3 Furthermore, SCAD is a common causative mechanism of pregnancy-associated myocardial infarction.1,2 The association of SCAD with female sex and pregnancy suggests that sex hormones may contribute to its pathophysiology.

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