Long-term patency of infrainguinal arterial reconstructions for lower-leg ischemia is altered by changes in the anatomic and hemodynamic characteristics of the inflow artery, the outflow artery, and the bypass conduit. The two disease processes that primarily affect long-term patency are the progression of atherosclerosis and the development of fibrointimal hyperplasia. These changes generally occur after the first postoperative month. Factors that limit the patency that occur within the first postoperative month are primarily due to errors in patient selection, technical errors in constructing the bypass, problems with the conduit, in terms of viability when using autogenous material, and finally, hypercoagulable states. The progression of atherosclerosis in inflow and outflow arteries can result in diameter-reducing stenosis that threatens bypass patency. The occurrence and progression of fibrointimal hyperplasia to diameter-reducing lesions resulting in bypass failure are related to the injurious effects of modifying the poor quality venous conduit, correcting technical errors, handling of the vein, and performing the anastomosis. Superior long-term patency rates in recent series of vein bypasses (in situ and reversed) have been attributed to improved surgical technique, increasing the experience of the vascular surgeon, and aggressive postoperative follow up to detect stenotic lesions.

The emphasis for improving graft patency of infrainguinal autogenous vein bypass grafts has evolved over the past two decades. Initially attempts were made to improve operative results by developing better surgical techniques and improving patient selection with improved angiographic imaging. More recently, the emphasis was to attempt to prevent patent grafts from failing in the follow-up period by detecting graft-threatening lesions with prospective ongoing graft surveillance protocols. Up to one third of grafts will require intervention to prevent failure in the follow-up period because of the development of lesions that threaten patency in the conduit, anastomotic sites, and inflow and outflow vessels. Because the autogenous vein is living tissue, secondary patency rates are better if lesions that lead to graft failure can be detected before thrombosis, preventing transmural injury to segments of the vein and reducing the chances of salvaging the conduit.

Understanding the biology of the autogenous vein conduit is essential in attempting to maximize patency of these vascular reconstructions. The location and natural history of particular lesions that are likely to threaten patency of the bypass graft can be predicted. In the first 30 days, problems related to the operative procedure and patient selection are most likely to cause problems. These include technical errors in the construction of the anastomosis and when the in situ technique is used, residual competent valves, and persistent and/or developing arteriovenous (AV) fistulae. In the interval between 1 and 24 months, the primary etiology of graft failure is fibrointimal hyperplasia. This is manifested as a stricture of either the proximal or distal anastomosis or, more commonly, as a stenosis of the conduit at the site of valve leaflets or traumatic injury to the vein from intraluminal instrumentation required for valve disruption. Long strictures of the vein can occur and are related to damage during vein harvest or abnormal veins where a fibrotic process may have been initiated prior to the bypass by previous episodes of phlebitis. After 24 months the vein graft is most likely to be placed at risk due to progression of atherosclerotic disease in the inflow and outflow vessels, as well as the development of atherosclerosis in the autogenous vein graft itself. Inflow obstruction occurs at a median of 15 months after bypass construction, and outflow obstruction develops at a mean of 29 months into the life of the bypass. These lesions in the native arterial system develop later than lesions in the conduit, which occur at a median of 8.5 months.