Intimal Hyperplasia in Vascular Grafts: Surgery-induced Arteriosclerosis

ABSTRACT

Intimal hyperplasia is a feature of the normal adaptive response of vessels to hemodynamic stresses as well as a characteristic of the healing of vessel injuries. The events leading to intimal hyperplasia formation involve numerous cellular and molecular components. Various cellular elements of the vessel wall are involved as are leucocyte-endothelial interactions that trigger the coagulation cascade leading to localized thrombus formation. Subsequent phenotypic modification of the medial smooth muscle cells and their intimal migration is the basis of the lesion formation that is thought to be propagated by an immune-mediated reaction. Intimal hyperplasia in the region of endarterectomy, balloon angioplasty, and vascular bypass graft anastomosis is a major problem of long-term failure of vascular reconstruction. The underlying causes of intimal hyperplasia are proliferation and migration of vascular smooth muscle cells provoked by injury, inflammation, and stretch. This review discusses the cellular and molecular mechanisms in the pathophysiology of intimal hyperplasia, and the different anastomosing techniques to improve the patency of peripheral arterial bypass.