[Skip to Navigation]
Invited Commentary
March 13, 2019

Comparing the Risk Factors of Plaque Rupture and Failed Plaque Healing in Acute Coronary Syndrome

Author Affiliations
  • 1Brigham and Women’s Hospital, Boston, Massachusetts
  • 2Harvard Medical School, Boston, Massachusetts
  • 3College of Osteopathic Medicine, University of New England, Biddeford, Maine
  • 4Massachusetts Institute of Technology, Cambridge
JAMA Cardiol. 2019;4(4):329-331. doi:10.1001/jamacardio.2019.0312

The article by Vergallo et al1 in this issue of JAMA Cardiology supports a hypothesis that healed plaques are a marker for reduced acute coronary syndrome (ACS) risk. This commentary expands on this idea by examining a mechanistic hypothesis of their results beyond looking at healing just as a marker. Specifically, failed healing, which correlated in the study by Vergallo et al1 with long core axial extent, predisposes plaque ruptures to progress to ACS. Acute coronary syndrome may require a double hit of both rupture and impaired healing. This is somewhat analogous to the situation in oncology, where after studying oncogenes for decades, it was discovered that 50% of all human cancers also have a mutation in the p53 tumor suppressor gene.

Add or change institution