ABSTRACT

Local endothelial shear stress (ESS) triggers vascular phenomena which synergistically exacerbate atherosclerosis toward an unstable phenotype. Specifi cally, low ESS augments lipid uptake and catabolism, induces plaque infl ammation and oxidation, downregulates the production and upregulates the degradation of extracellular matrix, and increases cellular apoptosis ultimately leading to thin-cap fi broatheromas and/or endothelial erosions. Increases in blood thrombogenicity that result from either high or low ESS, also contribute to plaque destabilization. A destabilized plaque manifests clinically as either abrupt luminal occlusion and acute coronary syndrome, or accelerated atherosclerosis progression via repeated cycles of subclinical partial luminal occlusion and healing which causes worsening ischemia.