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Hemodynamics and the development of anastomotic intimal hyperplasia of the polytetrafluoroethylene graft in dogs.

To clarify whether or not changes in wall shear stress play a determinant role in the induction of anastomotic intimal hyperplasia of polytetrafluoroethylene (PTFE) grafts, two experimental models were devised. Based on our previous study (J Vasc Surg, 1985), wall shear stress was defined by variation of wall shear stress (tau-variation) in one cardiac cycle. In experiment I, PTFE grafts were implanted into dogs under conditions of 85.2 +/- 36.2 ml/min of low flow rate with 66.7 +/- 31.1 dyne/cm2 of low tau-variation. In experiment II PTFE grafts were implanted under conditions of 10.1 +/- 4.6 ml/min of low flow rate with 120.4 +/- 37.2 dyne/cm2 of moderate tau-variation. The intimal thickness of 581 +/- 127 microns at one month and 1230 +/- 260 microns at three months implantation at the distal anastomosis under an abnormal flow condition in experiment I was statistically significant compared with findings in the case of 124 +/- 36 microns at 1 month and 171 +/- 74 microns at 3 months at the proximal anastomosis under an abnormal flow condition in experiment I, and with those of 164 +/- 68 microns at 1 month and 195 +/- 57 microns at three months at the distal anastomosis in experiment II (p less than 0.01). Under a normal flow condition, there was no evident intimal hyperplasia at proximal and distal anastomotic sites in experiment I. These observations are pertinent evidence that change in wall shear stress and not the rate of blood flow is the determinant factor related to development of intimal hyperplasia of PTFE grafts at the distal anastomosis.