Endothelial Shear Stress Metrics Associate With Proinflammatory Pathways at the Culprit Site of Coronary Erosion

Abstract

Low endothelial shear stress (ESS) and associated adverse biomechanical features stimulate inflammation, contribute to atherogenesis, and predispose to coronary plaque disruption. The mechanistic links between adverse flow-related hemodynamics and inflammatory mediators implicated in plaque erosion, however, remain little explored. We investigated the relationship of high-risk ESS metrics to culprit lesion proinflammatory/proatherogenic cells and cytokines/chemokines implicated in coronary plaque erosion in patients with acute coronary syndromes. In eroded plaques, low ESS, high ESS gradient, and steepness of plaque topographical slope associated with increased numbers of local T cells and subsets (CD4⁺, CD8⁺, natural killer T cells) as well as inflammatory mediators (interleukin [IL]-6, macrophage inflammatory protein-1β, IL-1β, IL-2).