BIOMECHANICAL FACTORS IN ANASTOMOTIC INTIMAL HYPERPLASIA

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Intimal thickening is a feature of the normal healing response at graft anastomoses. Yet, in grafts to peripheral arteries, intimal hyperplasia at the distal anastomosis is the major cause of prosthetic vascular graft failure. Pharmacologic efforts to minimize intimal hyperplasia in small vessel anastomoses have thus far been unsuccesful. This approach does not directly address the biomechanical factors which prevail at distal anastomoses to small vessels or the nature of the changes in the flow field at anastomotic sites. Hemodynamic factors associated with branch geometry and with the mechanical properties of the artery wall correlate closely with the localization of intimal thickening and atherosclerosis. Vascular anastomoses affect near-wall flow properties by altering geometry, wall compliance and motion, and flow velocities about the anastomotic junction. It is our working hypothesis that the distribution of anastomotic intimal thickening or hyperplasia corresponds to the distribution of shear stress acting on the wall at the fluid-wall interface and occurs principally in regions of lowered and oscillartory shear stress, i.e., where local particle residence time is increased. We therefore propose to construct vascular bypass grafts in dogs under conditions of differing anastomotic geometry, flow conditions an wall characteristics such as those which occur in patients undergoing lower extremity arterial bypass surgery and to assess the effects of the associated mechanical and configurational factors on the localization and degree of anastomotic intimal thickening during the course of the healing process. To accomplish this we will quantify the spatial distribution of anastomotic intimal thickening using computer- assisted three dimensional reconstruction techniques and correlate these findings with the spatial distribution in scale models of wall shear stress and particle residence time in relation to geometry, to graft versus artery compliance and to the distribution of flow velocities in the perianastomatic vessels. The findings would be expected to define clearly and quantitatively, for the first time, the actual localization of perianastomotic intimal thickening and the corresponding flow field conditions, and to identify the optimal biomechanical conditions for minimizing anastomotic intimal hyperplasia.