Flow patterns and preferred sites of intimal thickening in diameter-mismatched vein graft interpositions.

It is suspected that blood flow and flow-induced shear stress play an important role in the pathogenesis and localization of intimal hyperplasia in anastomosed vessels. However, experimental data that demonstrate the correlation between the flow and the sites of intimal thickening obtained in the same vessel are scarce. For this reason, we have studied the relationship between the flow and precise locations of wall thickening specific to the particular vessel by performing diameter-mismatched vein graft interpositions. This method created more flow disturbances than those found in our previous study, which was carried out by dividing an artery and simply suturing its ends back to their original positions. In the current study, grafting procedures consisting of 26 saphenous vein interpositions and 10 jugular vein interpositions were carried out on the femoral arteries of 22 adult mongrel dogs. The vessels were harvested at 3 months after operation, perfusion-fixed, and rendered transparent. The precise location and the size of intimal thickening and characteristics of the flow, such as flow patterns, distributions of fluid velocity, and wall shear stress, were studied in detail by means of flow visualization and cinemicrographic techniques. It was found that the diameters of interposed saphenous vein grafts, which were about one-half the diameter of host arteries, increased drastically and became almost the same as those of the host arteries. Intimal thickening was found distal to the distal anastomotic junction in smaller diameter saphenous vein-interposed vessels and distal to the proximal anastomotic junction in larger diameter jugular vein-interposed vessels. In both cases, flow was disturbed with the formation of a slow recirculation flow due to a sudden enlargement of vessel diameter caused by a mismatch of vessel diameters at the anastomotic junction and at the location where the wall shear stress was low. The results suggest that the key hemodynamic factors involved in the localization of intimal thickening are the low velocity of flowing blood and the resultant low shear stress acting on the vessel wall.