Duplex Surveillance of Infrainguinal Bypass Grafts

Vascular laboratory surveillance using duplex ultrasound is recommended after infrainguinal bypass grafting as it benefits patient outcome by improving graft patency.1,2 Ideally, duplex testing should begin in the operating room to survey the graft and anastomotic sites for stenosis and to document augmented flow in the runoff arteries and foot. Color duplex imaging is more sensitive than arteriography for intraoperative assessment and detects unrecognized graft abnormalities in 5–10% of reconstructions, permitting immediate correction.3 The application of duplex graft surveillance has been shown to reduce the incidence of both early (<30 days) and late bypass failure.1,2,4 Infrainguinal arterial bypasses, constructed of either autologous vein or a prosthetic graft, are prone to develop intrinsic stenotic lesions, which when progressive to cause thrombosis if graft flow is reduced below the “thrombotic threshold velocity.”5–9 Myointimal hyperplasia producing lumen reduction is the most common etiology for graft stenosis, but its temporal occurrence and site(s) of development differ between vein and prosthetic grafts. The occurrence of vein graft stenosis is highest in the 6 months following the procedure, and decreases thereafter. Myointimal stenosis is most common at vein valve and anastomotic sites, and has anatomic features of a smooth, typically focal (<2 cm) stricture. This acquired lesion has been implicated in nearly 80% of vein bypass failures, with other graft failures caused by technical errors, intrinsic graft lesions, or hypercoagulable states.1,2,6,10 Following prosthetic grafting, intragraft abnormalities are rare (<10% of all stenoses) with graft stenosis developing most commonly at the distal anastomosis and the adjacent runoff artery. The failure rate of prosthetic grafts (10–15%/year) is higher than autologous vein grafts (2–5%/year) and has been attributed to differences in “thrombotic threshold velocity,” myointimal hyperplasia development, and atherosclerotic disease progression.8,9