Mechanisms of venous graft failure

Abstract

Venous graft failure is a complex pathology of surgical revascularization that comprises many physiopathologic mechanisms, some of them still unclear until the present moment. Arterialization of the venous graft produces structural modifi cations in the graft wall, including all anatomic layers: intima, media, and adventitia. Of these, the most important aspect of graft dysfunction is intimal destructuration by various mechanisms: endothelial cell separation and cell loss, intimal edema, exposed basement membrane, subendothelial collagen and elastin, intimal tears and fl aps, fi brointimal hyperplasia, neointimal hyperplasia, and thrombus formation. Some of these pathogenic processes are exacerbated while others are diminished, but, overall, they lead to graft restenosis. Intimal edema extends toward the superjacent layer, producing myocite necrosis, fi brosis, and eventually aneurysm formation. Adventitial ischemia produced by graft harvesting determines vasa vasorum loss and vein sclerosis. Under these circumstances, neoangiogenesis occurs without oxygenation importance criteria, which leads to augmentation of neointimal hyperplasia and intimal and medial fi brosis. Therefore, graft restenosis is a complex process with many pathologic mechanisms, in general without sequentiality, but which taken together lead toward what is designated as "venous graft disease."