In medicine, vein graft failure (VGF) is a condition in which vein grafts, which are used as alternative conduits in bypass surgeries (e.g. CABG), get occluded. Veins, mainly the great saphenous vein (GSV) are the most frequently used conduits in bypass surgeries (CABG or PABG), due to their ease of use and availability. Some structural changes of intima thickening and vein wall remodeling are necessary for vein graft adaptation to the arterial environment. The reasons why some of the grafts progress to clinical stenosis is unknown. The patency rates of saphenous vein grafts after CABG at 1 year is approximately 80%. After 5 years the patency rate drops to 65% and at 10 years GSV patency rates are approximately 50%, with only half of the veins are atherosclerosis free. VGF may be identified in asymptomatic patients, but can also produce symptoms of ischemia, depending on the area of the supplied territory of the heart, and the function of native arteries and other grafts. VGF has been closely correlated with revascularization, myocardial infarction and death. Treatment of occluded GSVs can be performed by percutaneous coronary intervention or redo CABG and is considered to be challenging, and thus preventing their obstruction is of great importance. Mechanism During and after the harvesting, veins go through a period of ischemia and reperfusion after engraftment, which causes damage to endothelial and smooth muscle cells (SMC). The grafting exposes the vein 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 graft more susceptible to atherosclerosis. Progressive atherosclerosis is the primarily cause of late vein graft failure. Vein graft atherosclerotic lesions are more diffuse and concentric, yet less calcified, compared to native atherosclerotic lesions, and are more susceptible to thrombosis formation and