Abstract

Non-uniform hemodynamic factors are believed to play important roles in the onset and development of atherosclerotic lesions in branching blood vessels and intimal hyperplasia at graft-artery bypass junctions. At present, a variety of theories regarding the hemodynamic aspects of atherogenesis have been proposed, which include almost all hemodynamic factors, such as high and low shear stresses, oscillatory shear index (OSI), temporal and spatial variations of wall shear stresses, flow separation, long particle residence time, and secondary flow, etc.[1–4] However, the underlying mechanism of endothelial cell (EC) response to hemodynamic forces leading to atherosclerosis is still not well understood.

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