Understanding Vulnerable Plaques: Current Status and Future Directions

Author: Kwan Yong LEE ¹ ; Kiyuk CHANG
Author Information

1. Cardiovascular Center and Cardiology Division, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Publication Type:Review
Keywords: Atherosclerotic plaque; Fibroatheroma; Coronary atherosclerosis; Microcalcification
MeSH: Apoptosis; Cholesterol; Coronary Artery Disease; Coronary Thrombosis; Hemodynamics; Hydrodynamics; Inflammasomes; Macrophages; Molecular Imaging; Myocardial Infarction; Plaque, Atherosclerotic; Rupture
From:Korean Circulation Journal 2019;49(12):1115-1122
CountryRepublic of Korea
Language:English
Abstract: The main cause of acute myocardial infarction is plaque rupture accompanied by superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested as a type of lesion with a vulnerability that can cause plaque rupture. However, not only the existence of a TCFA but also the fine and complex interactions of other anatomical and hemodynamic factors, such as microcalcification in the fibrous cap, cholesterol crystal-induced inflammasome activation, the apoptosis of intraplaque macrophages, and endothelial shear stress distribution should precede a clinical event caused by plaque rupture. Recent studies are being conducted to identify these mechanisms through molecular imaging and hemodynamic assessment using computational fluid dynamics, which will result in better clinical results through selective coronary interventions.