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

Interposition of a vein cuff between a prosthetic infrainguinal bypass graft and a recipient infrageniculate artery can improve graft patency. There is evidence that the improved performance may be explained by a redistribution of myointimal hyperplasia (MIH) away from the critical areas at the heel and toe of the cuff-artery anastomosis. It is widely accepted that there is an association between hemodynamic forces, more specifically, low wall shear stress (WSS), and the development of MIH. The aim of this study was to determine whether the reported redistribution of MIH in the interposition vein cuff (IVC) may be explained by differences in magnitude and distribution of WSS. Design of Study and Method: Detailed flow velocity measurements were made in life-size models of conventional end-to-side (ETS) and IVC anastomoses using a two-component laser Doppler anemometer under pulsatile flow conditions. Velocity vectors were determined in the plane of symmetry of the anastomosis, and the variation of WSS was estimated from near-wall velocity measurements on the floor and upper wall of the artery.

The main flow features in the ETS anastomosis were flow separation at the graft hood, strong radial velocity at the heel, and a stagnation point on the floor of the artery that moved slightly during the flow cycle. In the IVC anastomosis, a coherent vortex that occupied most of the cuff volume was present from the systolic deceleration phase to end diastole. A stagnation point on the anastomosis floor was found to oscillate by about 4 mm. Critical regions of low mean WSS (ie, 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 generally less extensive than in the ETS anastomosis.

The vein cuff anastomosis alters the mean WSS distribution within the recipient artery and removes the area of low WSS at the heel. This may explain the redistribution of MIH away from important sites in the recipient artery.