Asymmetrical stenoses are typical in atherosclerosis (1), and it is expected that 3-D flow field effects in the poststenotic region may be significant. Wall shear stress (WSS) which oscillates in direction about a low mean value has been shown to increase the expression of adhesion molecules (VCAM-1, ICAM-1) in cultured endothelial cells, with a consequent increase in monocyte adhesion (2). Thus, the flow field in the vicinity of a raised atherosclerotic lesion may be favorable to monocyte infiltration with subsequent release of matrix-degrading substances (3), leading to plaque rupture.

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