Wall shear stress temporal gradient and anastomotic intimal hyperplasia.

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Abstract
Unusual wall shear stress patterns on the bed of end-to-side arterial anastomoses appear to be the primary factor in the development of intimal hyperplasia that often leads to arterial bypass graft failure. In this in vitro study using the photochromic tracer technique, the shear stress variation on the bed of a 30 degrees anastomosis was examined before and after the development of hyperplasia. With the disease-free model, a rapid downstream shift in the stagnation point was seen on the bed during the systolic phase of the flow cycle, which led to sharp temporal changes in the shear stress from positive to negative values, ie, rapid changes in the direction of the shearing force. The resulting negative temporal gradients were roughly eight times larger than those seen in a straight tube, and it is suggested that this may lead to endothelial deformation or injury and eventually to intimal thickening. With the diseased model, the simulated tissue overgrowth on the bed appeared to act as a flow divider that restricted the motion of the stagnation point, and this drastically reduced the rapid changes in the direction of the shearing forces. Thus, it seems that the development of bed anastomotic intimal hyperplasia may be a response designed to reduce shear-induced endothelial deformation or injury.