Interposition vein cuff anastomosis alters wall shear stress distribution in the recipient artery

Objective: Interposition of a vein cuff between a prosthetic infrainguinal bypass graft and a recipient infrageniculate artery can improve graft paten cy. There is evidence that the improved performance may be explained by a r edistribution of myointimal hyperplasia (MIH) away from the critical areas at the heel and toe of the cuff-artery anastomosis. It is widely accepted t hat there is an association between hemodynamic forces, more specifically l ow wall sheer stress (WSS), and the development of MIH. The aim of this stu dy was to determine whether the reported redistribution of MPH in the inter position vein cuff (IVC) may be explained by differences in magnitude and d istribution of WSS. Design of study and method: Detailed flow velocity measurements were made i n life-size models of conventional end-to-side (ETS) and IVC anastomoses us ing a two-component laser Doppler anemometer under pulsatile flow condition s. Velocity vectors were determined in the plane of symmetry of the anastom osis, and the variation of WSS was estimated from near-wall velocity measur ements on the floor and upper wall of the artery Results: The main flow features in the ETS anastomosis were flow separation at the graft hood, strong radial velocity at the heel, and a stagnation po int on the floor of the artery that moved slightly during the flow cycle. I n the IVC anastomosis, a coherent vortex that occupied most of the cuff vol ume was present from the systolic deceleration phase to end diastole. A sta gnation point on the anastomosis floor was found to oscillate by about 4 mm . Critical regions of low mean WSS tie, below 0.5 N/m(2)) were identified. In the ETS anastomosis, they were found at the heel and along the floor In the IVC anastomosis, low mean WSS was found only on the floor, and it was g enerally less extensive than in the ETS anastomosis. Conclusion: The vein cuff anastomosis alters the mean WSS distribution with in the recipient artery and removes the area of low WSS at the heel. This m ay explain the redistribution of MIH away from important sites in the recip ient artery.