During and after the harvesting,<unk> s go through a period of ischemia and reperfusion after engraftment, which causes damage to endothelial and smooth muscle cells (SMC). The<unk> ing exposes the<unk>  to arterial pressure and flow that causes increased shear stress and wall tension, which further damages the endothelial layer and SMC. The damage causes local release of tissue factors and reduced bioavailability of prostacyclin and nitric oxide (NO), all of which contribute to platelet activation, deposition of fibrin, which promotes thrombosis. Growth factors that released from macrophages and platelets lead to increased proliferation and migration of SMCs to the intima. The migrated SMC release extracellular matrix resulting in reduced intimal cellularity. Low levels of endothelial nitric oxide, adenosine and prostaglandins, further contribute to SMC proliferation. Over time continued SMC migration and proliferation cause extracellular matrix deposition and fibrotic change that lead to development of intimal hyperplasia, which results in luminal loss that makes the<unk>  more susceptible to atherosclerosis. Progressive atherosclerosis is the primarily cause of late<unk> .<unk><unk>  atherosclerotic lesions are more diffuse and concentric, yet less calcified, compared to native atherosclerotic lesions, and are more susceptible to thrombosis formation and rupture.
Vein graft failure
Arterial insufficiency ulcer
Vascular access steal syndrome
Gas gangrene
Diabetic foot infection
Chronic venous insufficiency
Arteriovenous fistula
Diabetic foot ulcer