Early intimal thickening (IT) in the carotid artery bifurcation has been associated with multiple hemodynamic and biophysical factors including low wall shear stress (WSS) and high oscillatory shear index (OSI) (Ku et al., 1995), as well as abnormal intramural stress and strain. While WSS conditions have been widely shown to affect vascular biology and arterial wall self-regulation, the near-wall localization of critical blood particles, such as monocytes and platelets, also plays a significant role in atherosclerotic lesion formation and general IT (Ross, 1993). In this study, we hypothesize that locations of elevated monocyte and platelet interactions with reactive or activated vascular surfaces, due to injury or endothelial dysfunction, are highly susceptible to IT initialization and progression in the carotid artery bifurcation (CAB). To assess the potential role of platelet-and monocyte-wall interactions, as well as other WSS-based hemodynamic wall parameters (HWPs), experimentally validated particle-hemodynamic simulations have been conducted for a representative CAB geometry. Areas of significant particle interactions with the vascular surface have been identified by a validated near-wall residence time (NWRT) model for monocytes and platelets, which encapsulates regions of near-wall particle stasis and/or elevated concentrations. Actual early intimal thickening has been assumed consistent with the observations of Masawa et al. (1994a & b) (Fig. 1).

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