Incidentally detected stenoses proximal to grafts originating below the common femoral artery: do they affect graft patency or warrant repair in asymptomatic patients?

Abstract Objective: Stenoses in infrainguinal arteries proximal to a lower extremity vein graft may reduce flow velocity through the bypass graft and are thought to predispose to graft occlusion. Repair of these lesions has been recommended to preserve graft function. This study was undertaken to better define the natural history of grafts below inflow lesions and to evaluate the necessity of repair to preserve graft patency. Methods: From 1994 through 1999, patients undergoing lower extremity vein grafts by a single surgeon at a university hospital and an affiliated teaching hospital were placed in a prospective protocol for proximal infrainguinal native artery and graft surveillance through use of duplex scanning. The records of those patients with grafts originating distal to the common femoral artery were evaluated; they form the basis for this report. Arteriograms were obtained before bypass grafting, and no patient had a stenosis greater than 50% diameter reduction proximal to the graft origin. Follow-up scans were obtained from the common femoral artery through the graft and outflow artery. The peak systolic velocity and velocity ratio in an infrainguinal native artery proximal to the graft origin were recorded, as were the location and the time interval since the bypass graft. Repair of these proximal lesions was not performed during the course of this study. Revision of the bypass graft or its anastomoses was undertaken according to preestablished duplex scan criteria. Results: During this time, 288 autogenous infrainguinal bypass grafts were performed, of which 159 originated below the common femoral artery; of these, 74 were from the superficial femoral artery, 29 from the profunda femoris artery, 49 from the popliteal artery, and 7 from a tibial artery. The maximum peak systolic velocity proximal to the graft origin was more than 250 in 38 arteries (25%) and more than 300 in 26 arteries (16%). The velocity ratio was 3.0 or more in 32 arteries at the same location as the peak systolic velocity and 3.5 or more in 23 arteries (15%), confirming hemodynamically significant stenoses at these sites. The location of peak systolic velocity was the common femoral artery in 81 patients (51%), the superficial femoral artery in 50 (31%), the popliteal artery in 22 (14%), and a tibial artery in 6 (4%). Follow-up ranged from 8 to 60 months (mean, 35 months). During follow-up, 19 patients died, 18 with patent grafts. Overall, nine grafts occluded. One of the occluded grafts had a velocity ratio greater than 3.0; this may have contributed to graft thrombosis. The other occlusions resulted from an unrepaired graft lesion in 2 patients, graft infection in 2 patients, and graft ligation necessitated by below-knee amputation in 2 patients. No cause for the occlusion could be identified in two of the grafts (neither had evidence of proximal arterial stenosis). Assisted primary patency rates were 95% and 91% at 3 and 5 years, respectively. Conclusions: For grafts originating distal to the common femoral artery, stenoses proximal to the graft do not affect bypass graft patency and do not require repair to prevent graft occlusion. Surveillance of these lesions may therefore be unnecessary, inasmuch as the repair of proximal lesions should not be undertaken to preserve graft function. (J Vasc Surg 2000;32:1180-9.)