The Combination of Systemic Evidence of Inflammation and OCT Findings in the Culprit Plaque Identifies Very High-Risk ACS?
CBSMD

For many years, we thought of coronary artery disease (CAD) as a disease of deposition of atherosclerotic plaque in arteries that ultimately became occluded and caused either ischemia or an acute myocardial infarction. Therapy for CAD focused on lipid lowering to reduce atherosclerosis, and initially bypass surgery and then PCI to restore blood flow to arteries occluded by atherosclerotic plaque. Logic dictates that the opened artery would cure CAD if all the occluded arteries were opened. But alternate facts would occasionally appear that did not fit this open artery hypothesis.

The observation that a population of patients exists with ischemic heart disease who show no evidence of proximally occluded arteries has been a focus of interest for over 50 years. These patients showed clear evidence of microvascular narrowing that produced ischemia and infarction. Other clinical studies indicated that patients with inflammatory disorders like rheumatoid arthritis had an increased incidence of CAD — and with these observations the word “inflammation” began to appear in the cardiology literature.

The literature linked on the right side are the references of the above contents and the relevant research progress regarding the "inflammation hypothesis" by the end of January 2019.