Why the study?
Thin-cap fibroatheromas cause acute myocardial infarction, but complex interactions of anatomical and hemodynamic factors preceding plaque rupture require identification to improve selective coronary interventions.
Key points are not available for this paper at this time.
Design
Review
May guide integrated plaque research; leaves open whether advanced imaging alters clinical intervention thresholds.
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.
No takes yet. Share an insight, caveat, or question.
Lee et al. (2019) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: