Figure 1.

Relationship Between Local Adverse Plaque Biomechanics and Inflammatory Mediators

Schematic drawing showing the proposed mechanisms involved in the pathobiology of coronary plaque erosion. Flow-related hemodynamics modify local shear stress patterns on the endothelial monolayer and trigger inflammatory processes. CD4⁺ = CD4+ T cells; ESSG = endothelial shear stress gradient; HA = hyaluronic acid; IL = interleukin; maxESS = maximum endothelial shear stress; minESS = minimum endothelial shear stress; MIP = macrophage inflammatory protein; MLA = minimal lumen area; Mono = monocyte; NK = natural killer; NKT = natural killer T (cells); T cells = T lymphocytes.