Distal anastomotic intimal hyperplasia: biogenesis and etiology

Abstract

Anastomotic intimal hyperplasia occurred exclusively at the heel and the toe plus the floor of the distal end-to-side anastomosis of canine autologous femoro-femoral bypass (n = 14) and not in the end-to-end carotid or femoral interposition graft (n = 14). The occurrence of anastomotic intimal hyperplasia in the absence of compliance mismatch in an autologous bypass suggests that the geometry of the end-to-side anastomosis is primarily responsible for intimal hyperplasia formation. It is believed that because an end-to-side distal anastomosis is not a natural occurrence it is conductive to turbulent flow. The latter causes endothelial injury which in turn allows platelet growth factor to incite subendothelial myoblasts in extracellular matrix synthesis and intimal hyperplasia formation. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) identify myofibroblasts and fibrocollagenous matrix as the dominant cellular and extracellular substances in anastomotic intimal hyperplasia.