There are two major hemodynamic stresses imposed at the blood-arterial wall interface by flowing blood: the wall shear stress (WSS) acting tangentially to the wall, and the wall pressure (WP) acting vertically to the wall. These forces influence the artery wall metabolism and correspond to the local modifications of artery wall thickness, composition, microarchitecture, and compliance [2]. The role of flow wall shear stress in atherosclerosis progression has been under intensive investigation [4], while the impact of local blood pressure on plaque progression has been under-studied.

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