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progression of atherosclerosis as a contributing factor to these problems. Because atherosclerosis as a cause of graft failure usually occurs more than 24 months after surgery, we have arbitrarily decided to examine those grafts that fail within the period of 1 month to 24 months in an attempt to try to determine the relative incidence of problems of fibromuscular hyperplasia. Since we rarely excise the involved diseased segment in the secondary procedures, we are therefore unable to give microscopic evidence as to the definitive cause. However, the findings of fibrointimal hyperplasia are generally so distinctive and different from those seen in progressive atherosclerosis that these findings can be reliably made on gross evaluation. In a more recent updating of this series, which now has grown to 215 in situ bypass graftings to the popliteal or tibial arteries, 70 grafts were identified to have correctable anatomic lesions and underwent a total of 95 revisions (28%). No lesion was identified in three grafts that had thrombectomy alone. Thirteen bypasses had multiple revisions, with one graft being revised four times over a period of 3 years. Correction of vein conduit or anastomotic abnormalities comprised 79% of the revisions, whereas corrections of atherosclerotic lesions identified in the iliac or infrapopliteal artery, which accounted for 10% and 11% of the revisions respectively. Graft revision rate was highest in the perioperative period, 10% at 30 days, and decreased to 7% per 6-month interval until 18 months after operation, and was at 3% per year thereafter. Ten bypass grafts were thrombosed at the time of graft revision. Graft thrombectomy alone restored patency in only one graft. Occasionally the secondary operative procedures were unsuccessful. Late failure of secondary repairs involved restenosis of vein patch anastomotic sites or occlusion of cephalic vein sequential grafts performed for anastomotic myointimal hyperplasia. The value of the rigorous surveillance and secondary procedures is documented in the secondary patency of 70 revised in situ bypass graftings 4 years after operation, which is similar to the primary patency of 180 bypass graftings that did not require revision (81% vs 86%, respectively). If remedial technical problems are identified throughout the life of the graft and corrected, the resultant, most common mechanism for late failure is the development of low flow states not amendable by revision. In the last 3 years of the study unexpected failure of grafts judged to have normal blood flow rates occurred in only one of approximately 100 to 120 patients routinely followed within the guidelines of the surveillance protocol. This patient had previously undergone a vein patch angioplasty of the valve site stenosis and probably had restenosis at this location. When the site and morphologic characteristics of the 92 lesions revised after in situ saphenous vein grafting were evaluted, 39 (42%) were totally or partially caused by fibrointimal hyperplasia. These included 20 patients with stenoses at the valve site, which in our experience are exclusively fibrointimal hyperplasia. Nineteen other patients had stricture and hyperplasia at anastomotic sites, which is partially a result of fibromuscular hyperplasia. All of these occurred in the time interval 1 month to 24 months after surgery. Fibromuscular hyperplasia is a significant factor in the development of problems in the vein conduit and anastomosis. If pharmacologic therapy or surgical techniques can be developed to control its development or limit its progression, significant advances in vein graft patency will result. In the meantime vigilant surveillance will identify grafts in need of revision to prolong patency and to assure continued limb salvage. Postoperative surveillance of femorodistal he goal of this study was to
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