Distal Anastomotic Intimal Hyperplasia: Histopathologic Character and Biogenesis

Although thrombogenicity of the prosthetic graft, progression of the atherosclerotic disease and distal anastomotic intimal hyperplasia are known etiologic factors of late graft failure, its occurrence is frequently encountered in late graft occlusion. Forty-two canine PTFE iliofemoral grafts (all with end-to-side distal anastomosis) were studied. Computer digitization revealed that distal anastomotic intimal hyperplasia occurred exclusively at the heel and the toe of the graft and the floor of the host artery. The distal anastomotic intimal hyperplasia was 80–130 cells thick. Light microscopy and transmission electron microscopy revealed a similar architecture of interlamination of cellular elements and extracellular matrix in the hyperplastic cells. Transmission electron microscopy further defined a gradual cell transformation and orientation from the graft to the lumen. The cells near the graft were characterized by a gradual reduction of rough endoplasmic reticulum with a concomitant acquisition of myofilaments, transforming ovoid mesenchymoid cells to slender myofibroblasts. The orientation of cells in distal anastomotic intimal hyperplasia was embodied by random cell distribution at the periphery to a well-organized interlamination of myofibroblasts and extracellular matrix near the lumen. Distal anastomotic intimal hyperplasia is a biologic entity with active cellular and subcellular events. Its biogenesis appears to be influenced by the hemodynamics of blood flow at the distal anastomosis.