ANASTOMOTIC INTIMAL HYPERPLASIA - MECHANICAL INJURY OR FLOW INDUCED

All anastomotic intimal thickening may not be the same, and the underlying mechanism(s) regulating the different types may vary. We investigated the localization of experimental anastomotic intimal thickening in relation to known biomechanical and hemodynamic factors. Bilateral iliofemoral saphenous vein and polytetrafluoroethylene grafts were implanted in 13 mongrel dogs. The distal end-to-side anastomotic geometry was standardized, and the flow parameters were measured. After 8 weeks, seven of 10 animals (group 1) with patent grafts were killed and the anastomoses fixed by perfusion. Histologic sections from each anastomosis were studied with light microscopy; and regions of intimal thickening were identified and quantitated with use of oculomicrometry. To characterize the anastomotic flow patterns, transparent silicone models were constructed from castings of the distal anastomosis of three animals (group 11), and flow was visualized with use of helium-neon laser-illuminated particles under conditions simulating the in vivo pulsatile flow parameters. Histologic sections revealed two separate and distinct regions of anastomotic intimal thickening. The first, suture line intimal thickening, was greater in polytetrafluoroethylene anastomoses (0.35 +/- 0.23-mu-m) than in vein anastomoses (0. 15 +/- 0.03-mu-m, p < 0.05). The second distinct type of intimal thickening developed on the arterial floor and was the same in polytetrafluoroethylene (0.11 +/- 0.11-mu-m) and vein anastomoses (0.12 +/- 0.03-mu-m). Model flow visualization studies revealed a flow stagnation point along the arterial floor resulting in a region of low and oscillating shear where the second type of intimal thickening developed. High shear and short particle residence time were observed along the hood of the graft, an area devoid of intimal thickening. Regions of relatively low shear and long particle residence time formed along the lateral walls and heel of the anastomoses and were not specifically related to intimal thickening at the suture line. We conclude that at least two different types of anastomotic intimal thickening exist. Suture line intimal thickening represents vascular healing; greater prominence with prosthetic grafts may be related to compliance mismatch. Arterial floor intimal thickening is unrelated to graft type and develops in regions of flow oscillation and relatively low shear. In either situation the response is associated with altered flow conditions. Prevention of graft failure caused by occlusive intimal hyperplasia requires precise understanding of the hemodynamically modulated mechanisms that control each different type.