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PURPOSE: Provision of lifelong angioaccess for hemodialysis generally requires multiple procedures. To extend the availability of each extremity as an access site, we have used the transposed basilic vein for fistula construction since 1988. Our purpose is to present our initial experience, with follow-up of 30 months. METHODS: We have used the transposed proximal basilic vein in 65 procedures to construct an autogenous arteriovenous fistula (AVF) to the brachial artery in 58 patients without suitable superficial venous anatomy. There were 25 males and 33 females, with a mean age of 47 years (range 10 to 77). The basilic vein transposition was the initial angioaccess procedure in only 25% of cases and secondary in 75%. Three additional patients underwent exploration of an inadequate basilic vein with subsequent prosthetic grafting. RESULTS: There were no operative deaths. Two postoperative complications included a wound infection and a transient steal syndrome. The actuarial life-table patency rate for all successfully completed AVFs was 49% at 30 months. Late revisions with continued patency were required in 11 cases, including repair of a focal stenosis in six, pseudoaneurysm resection in two, and thrombectomy in one. Sixty-seven percent of patients who required subsequent prosthetic grafting for a failed basilic vein AVF had an ipsilateral procedure. Patient preference for the opposite arm was the usual indication for contralateral grafting in the remainder. CONCLUSIONS: The transposed basilic vein AVF was technically feasible in 95% of cases, can frequently be performed in patients with multiple previous access procedures, does not compromise the arm for future prosthetic grafting, and has a long-term patency rate that is comparable to more traditional autologous AVFs. This underused procedure should be considered before placement of polytetrafluoroethylene graft for long-term angioaccess

PURPOSE: To determine why some vein grafts fail, we prospectively studied the relationship between the histologic condition of the greater saphenous vein (GSV) at the time of grafting and subsequent stenosis of the vein graft. METHODS: Ninety-four remnant segments of GSVs were obtained at the time of infrainguinal bypass in 91 patients and were perfusion fixed before histologic and ultrastructural examination. All bypass grafts were evaluated clinically and by duplex ultrasonography at regular intervals from 1 to 30 months after operation. All 24 grafts that developed lesions that caused thrombosis (failed grafts) or flow reduction (failing grafts) underwent arteriography and appropriate operative or other interventional correction of the causative lesion. RESULTS: There was no significant difference in the incidence of coronary artery disease, kidney disease, hypertension, or history of smoking in patients with normally functioning and failed or failing grafts. Diabetes occurred with an increased frequency in failed or failing grafts (p = 0.056). At the time of their insertion, GSVs that subsequently developed significant lesions had thicker walls (0.72 +/- 0.33 mm) compared with normally functioning grafts (0.58 +/- 21 mm; p < 0.02). Most of this difference was related to a significantly thicker intima (0.27 +/- 0.17 vs 0.11 +/- 0.7 mm; p < 0.0001). Another significant finding was the presence of subendothelial spindle-shaped cells greater than five cell layers thick. This occurred more often in pregraft biopsies from grafts that developed significant lesions (70.4% vs 7.5%, p < 0.0001). Electron microscopic examination of these cells demonstrated a subpopulation of poorly differentiated cells with few fibers and many vesicles. Four of 24 (17%) failed or failing grafts had evidence of vein wall calcification at the time of vein grafting. This was seen in only one (1.4%) of 70 normally functioning grafts without lesions (p < 0.005). CONCLUSIONS: We conclude that GSVs with thick and calcified walls or hypercellular intima at the time of grafting are at increased risk of developing intragraft lesions that may lead to graft failure. Frequent duplex ultrasonography surveillance is particularly warranted for such high-risk grafts

PURPOSE: Smooth muscle cell (SMC) proliferation is a central event in the development of arteriosclerotic plaque. Regulation of this proliferative process is controlled in part by the action of specific peptide growth factors that may influence early cell-cycle regulatory gene expression. Such 'early' response genes include the protooncogene c-myc, which has been implicated in the induction of cell proliferation and differentiation. We compared the distribution of the c-myc protooncogene product in healthy and atherosclerotic human carotid arteries to determine its cellular and tissue localization. METHODS: Samples of six carotid artery plaques from six patients were rapidly frozen in liquid nitrogen at the time of carotid endarterectomy. Three nondiseased human carotid arteries obtained at organ harvest from brain-dead organ donors were similarly prepared. Frozen sections were labeled with a polyclonal rabbit anti-c-myc antibody that recognizes the 64 kd c-myc human protein. The percentages of cells positive for c-myc (c-myc index) and the intensity of antibody labeling were determined. RESULTS: Normal human carotid artery demonstrated minimal, isolated cell staining, with single scattered grains of immunocytochemical staining product seen in SMC nuclei. The myc index was 14.7% +/- 3.5% positive cells. In comparison, SMCs from carotid plaque showed a significant predominance of c-myc immunoreactive cells (89.8% +/- 4%; p < 0.001). The intensity of c-myc staining was greater in plaque SMCs, with many of the cells demonstrating confluence of immunocytochemical precipitate throughout 50% of SMC nuclei. CONCLUSIONS: Although the exact role of enhanced expression of the c-myc protooncogene in atherosclerosis is unclear, a cooperative influence of abnormal early cell-cycle gene expression and humoral factors may initiate the atherogenic process. The c-myc gene and other protooncogenes are early molecular markers of cell-cycle activity, which may be important in the development of atherosclerosis and occlusive vascular disease

PURPOSE: The presence of preexisting saphenous vein lesions adversely affects graft patency. Despite careful preoperative venous duplex examination and meticulous intraoperative evaluation, clinically significant saphenous vein disease may remain undetected. We evaluated angioscopy as a means to better detect these vein lesions. METHODS: Ninety saphenous vein remnants, obtained at bypass surgery, were perfusion fixed for subsequent angioscopic and histologic evaluation. The specimens were categorized by independent examiners on the basis of the angioscopic or light microscopic findings. Of the 90 vein remnants, 66 were normal by angioscopic criteria. Fifty-three (80%) of these angioscopically normal vein segments were normal histologically, and all 24 angioscopically abnormal saphenous vein remnants showed disease on microscopic examination. RESULTS: Angioscopy correctly identified sclerotic vein segments (n = 20) by irregular white plaques, whereas postphlebitic veins (n = 3) demonstrated multiple lumens, fibrous strands, and thickened opaque valve cusps on angioscopic evaluation. Absence of an angioscopic lumen was confirmed histologically in occluded veins (n = 2). Angioscopy failed to identify thick-walled (n = 10) and varicose (n = 2) vein segments as abnormal; one sclerotic segment was normal angioscopically, thereby lowering the sensitivity of angioscopy. CONCLUSIONS: Angioscopy detected unsuspected preexisting saphenous vein disease in five patients undergoing arterial reconstruction with saphenous vein. Because the use of angioscopy is a reliable means of prospectively assessing the vein for most preexisting lesions, its routine use may ultimately improve graft patency

This case report describes a new approach to repair a femoral arteriovenous fistula with a transluminally placed intraarterial graft-covered stent. A balloon-expandable stented polytetrafluoroethylene graft was inserted percutaneously to obliterate an arteriovenous fistula after a bullet injured the left superficial femoral artery and vein of an 18-year-old man. Follow-up duplex ultrasonography at 5 months demonstrated patency and luminal integrity of the involved artery and vein, with resolution of the associated pseudoaneurysm. Additional follow-up will be needed to further substantiate the utility of this minimally invasive procedure in the treatment of traumatic arterial injuries

Completion arteriography is widely regarded as an essential component of infrainguinal bypasses. However, the significance of various intraluminal filling defects is poorly defined, and strategies for managing these defects are unclear. Completion arteriography was performed by a standard technique in 78 infrapopliteal bypasses and were evaluated prospectively for the presence of angiographic defects. Thirty-nine arteriograms (50%) had no visible abnormality (grade O). Six arteriograms (8%) had minimal (grade I) defects, i.e., round lucencies (bubbles) or valve leaflets. Eighteen arteriograms (23%) had moderate (grade II) defects, i.e., uniform smooth tapering (up to 90% of luminal diameter) of the graft or outflow artery, irregular intraluminal filling defect (less than 60% of luminal diameter) within the distal graft or its adjacent outflow artery, or incomplete or faint graft opacification. Fifteen arteriograms (19%) had severe (grade III) defects, i.e., total cutoff of graft or outflow artery opacification or irregular intraluminal filling defect (greater than 60%) in the distal graft or adjacent outflow artery. Completion arteriograms were further stratified for type of bypass and outflow characteristics. All 24 bypasses with grade I or grade II defects on completion arteriography had no further surgical treatment. However, the 18 bypasses with grade II defects on completion arteriography had minimal nonsurgical manipulations consisting of repeat arteriography without or with papaverine infusion or urokinase instillation. In all 18, repeat arteriography showed improvement in the defect. The 15 bypasses with grade III defects had further surgical intervention (graftotomy, thrombectomy, vein patching, interposition graft, or graft extension). One-month and 1-year patency rates for grafts with grade I and grade II defects (87% and 79%, respectively) were not significantly worse than those for the 39 grafts with no arteriographic abnormalities (87% and 82%, respectively). In contrast, grafts with grade III defects had significantly worse (p < 0.01) 1-month and 1-year patency rates (33% and 20%, respectively) despite aggressive surgical correction of the arteriographic defects. These results emphasize the value of repeat completion arteriography and minimal interventional strategies when grade I or II defects are seen on arteriography. The poor outcome with surgical correction of grade III defects suggests that completion arteriography may not always define the full extent of the problem or that the corrective surgical maneuvers were either incomplete or detrimental

The application of duplex ultrasonography to the diagnosis of venous thrombosis requires validation by comparison of the duplex findings with the results of ascending contrast venography. In this study, 2534 veins were examined by both methods with contrast venography results serving as the standard for comparison. In this setting, duplex ultrasonography proved to be 100% sensitive and 99% specific for venous thrombosis. Duplex ultrasonography is as reliable as venography in the diagnosis of venous thrombosis and has no associated risks or known complication. In addition, duplex ultrasonography provides information regarding pathologic anatomy that is comparable to the detail provided by high-quality venography. The authors conclude that duplex ultrasonography should be the diagnostic method of choice for evaluating patients with suspected venous thrombosis. $$:

BACKGROUND. A significant number of vascular injuries occur with the use of percutaneous diagnostic and therapeutic procedures. This study was done to indicate the types of these injuries and their management. METHODS. Over a 30-month period, 55 patients required operation for vascular complications after percutaneous femoral procedures including infrarenal arteriography (six patients) and angioplasty (22 patients), coronary angiography (16 patients) and angioplasty (five patients), and aortic balloon pump insertion (six patients). RESULTS. The 14 iliac and 41 femoral artery injuries included 29 pseudoaneurysms, six lacerations with persistent bleeding, seven dissections, six occlusions, three ruptures, two arteriovenous fistulas, and two large hematomas. Control for all femoral and distal external iliac artery lesions was obtained solely through a groin incision in 45 (82%) patients. Our technique for exposure of the external iliac artery through the groin is described. A separate retroperitoneal incision was necessary in 10 patients because of proximal injury, massive pseudoaneurysm, morbid obesity, or heavily scarred groins. In this series 34 lateral suture repairs, 11 interposition or bypass grafts, four patch angioplasties, one endarterectomy, three thrombectomies, and two hematoma evacuations were performed. Although no limb loss occurred, we encountered nine wound complications, five myocardial infarctions, and two deaths. CONCLUSIONS. This experience shows the wide variety of vascular complications caused by percutaneous procedures and the different techniques necessary for their management