James S.T. Yao

Six-year prospective multicenter randomized comparison of autologous saphenous vein and expanded polytetrafluoroethylene grafts in infrainguinal arterial reconstructions

Autologous saphenous vein (ASV) and polytetrafluoroethylene (PTFE) grafts were compared in 845 infrainguinal bypass operations, 485 to the popliteal artery and 360 to infrapopliteal arteries. Life-table primary patency rates for randomized PTFE grafts to the popliteal artery paralleled those for randomized ASV grafts to the same level for 2 years and then became significantly different (4-year patency rate of 68% +/- 8% [SE] for ASV vs. 47% +/- 9% for PTFE, p less than 0.025). Four-year patency differences for randomized above-knee grafts were not statistically significant (61% +/- 12% for ASV vs. 38% +/- 13% for PTFE, p greater than 0.25) but were for randomized below-knee grafts (76% +/- 9% for ASV vs. 54% +/- 11% for PTFE, p less than 0.05). Four-year limb salvage rates after bypasses to the popliteal artery to control critical ischemia did not differ for the two types of randomized grafts (75% +/- 10% for ASV vs. 70% +/- 10% for PTFE, p greater than 0.25). Although primary patency rates for randomized and obligatory PTFE grafts to the popliteal artery were significantly different (p less than 0.025), 4-year limb salvage rates were not (70% +/- 10% vs. 68% +/- 20%, p greater than 0.25). Primary patency rates at 4 years for infrapopliteal bypasses with randomized ASV were significantly better than those with randomized PTFE (49% +/- 10% vs. 12% +/- 7%, p less than 0.001). Limb salvage rates at 3 1/2 years for infrapopliteal bypasses with both randomized grafts (57% +/- 10% for ASV and 61% +/- 10% for PTFE) were better than those for obligatory infrapopliteal PTFE grafts (38% +/- 11%, p less than 0.01). These results fail to support the routine preferential use of PTFE grafts for either femoropopliteal or more distal bypasses. However, this graft may be used preferentially in selected poor-risk patients for femoropopliteal bypasses, particularly those that do not cross the knee. Although every effort should be made to use ASV for infrapopliteal bypasses, a PTFE distal bypass is a better option than a primary major amputation.

Atherosclerotic plaque rupture in symptomatic carotid artery stenosis

PURPOSE Plaque rupture is often the precipitating event in acute coronary syndromes. We hypothesized that a similar process occurs in stenotic carotid plaques in association with ischemic neurologic symptoms. Our purpose was to examine several morphologic features of stenotic carotid plaques and to determine which characteristics are more commonly associated with plaques obtained from patients with symptomatic carotid artery disease than with those from patients with asymptomatic carotid artery disease. METHODS Forty-four carotid endarterectomy specimens (from 25 asymptomatic and 19 symptomatic patients) were analyzed with pentachrome staining and light microscopy. The asymptomatic patients and symptomatic patients had similar mean percent stenosis (77% vs 74%). Other risk factors, including hypertension, diabetes mellitus, coronary artery disease, smoking history, serum cholesterol, and triglyceride levels, were similar between groups. RESULTS Patients with symptomatic carotid artery disease were found to have more frequent plaque rupture, fibrous cap thinning, and fibrous cap foam-cell infiltration when compared with the asymptomatic group. Plaque rupture was seen in 74% of symptomatic plaques and in only 32% of plaques from asymptomatic patients (p = 0.004). Fibrous cap thinning was noted in 95% of symptomatic plaques and in 48% of asymptomatic plaques (p = 0.003). Infiltration of the fibrous cap with foam cells was also significantly more common in the symptomatic plaques (84% vs 44% of asymptomatic plaques; p = 0.006). In addition, intraplaque fibrin was more common in symptomatic plaques than in asymptomatic (100% vs 68%; p = 0.008). No significant differences were found between the two groups with respect to plaque hemorrhage, the presence of a necrotic core, luminal thrombus, smooth muscle cell infiltration, eccentric shape, and plaque type (fibrous, necrotic, or calcified). CONCLUSIONS As in the coronary artery system, rupture of the atherosclerotic plaque may play an important role in the pathogenesis of ischemic stroke caused by carotid artery stenosis. The process of inflammation, involving foam-cell infiltration of the fibrous cap, may contribute to rupture of the atherosclerotic plaque.

Collagen types and matrix protein content in human abdominal aortic aneurysms

Deficiencies of total collagen, type III collagen, and elastin have been proposed to explain aneurysm formation. Infrarenal aortas were collected from 19 patients (age 70 +/- 7 years) undergoing operative repair of abdominal aortic aneurysms (diameter 7 +/- 2 cm) and from 13 autopsies (age 63 +/- 17 years) of patients without aneurysm disease (controls). Wall thickness and collagen and elastin concentration were determined in full-thickness aorta. Collagen types I and III were measured after digestion with cyanogen bromide, which solubilized nearly 90% of total collagen for typing. Cyanogen bromide peptides were separated by sequential carboxymethylcellulose and agarose chromatography and quantified by peak area measurement with computerized image analysis. Histologic examination revealed prominent inflammatory cell infiltration and deficient, fragmented elastin in the aneurysms. Aortic wall thickness was similar in aneurysms and in control specimens. In the aneurysms, collagen was increased (37% +/- 16% vs 24% +/- 5%; p less than 0.05) and elastin was decreased (1% +/- 1% vs 12% +/- 7%; p less than 0.001), expressed as a percentage of delipidized, decalcified dry weight. Collagen type I accounted for 74% +/- 4% of aneurysm and 73% +/- 4% of control collagen solubilized for typing, and collagen type III accounted for 26% +/- 4% of aneurysm and 27% +/- 4% of control collagen solubilized for typing. Neither patients with a family history of aneurysms nor those without a history of aneurysms had collagen type III deficiency. Atherosclerotic abdominal aortic aneurysms are associated with an inflammatory process and may result from elastin degradation and not a deficiency of type III collagen.

Current management of visceral artery aneurysms

BACKGROUND Visceral artery aneurysms are an uncommon but important form of abdominal vascular disease. This study reviews a contemporary experience with special emphasis on newer methods of diagnosis and treatment. METHODS From 1980 to 1994, 37 patients were diagnosed with 46 visceral artery aneurysms. These consisted of 22 splenic, 10 hepatic, 4 superior mesenteric, 2 gastroduodenal, 3 celiac, 2 left gastric, 1 pancreatoduodenal, 1 jejunal-ileal, and 1 inferior mesenteric artery aneurysms. Follow-up was complete for 28 patients, average of 37.7 months. There were 17 asymptomatic and 29 symptomatic aneurysms, including 11 presenting with rupture. RESULTS Seventeen patients were treated surgically, with no surgical deaths. Surgical complications included splenic abscess (two) and failure to thrombose (one). Transcatheter embolization was used in 12 patients. Complications included splenic infarction (one) and recurrence (two), successfully treated with repeat embolization. Nine patients were treated with observation. Eight experienced no complications during follow-up; one died of a ruptured splenic artery aneurysm before treatment was initiated. CONCLUSIONS The widespread use of computed tomography has led to increased detection of asymptomatic visceral artery aneurysms. Although surgery remains necessary in many patients, transcatheter embolization is effective in the treatment of selected visceral artery aneurysms with few complications and low recurrence.

Reduction in aortic aneurysm size: Early results after endovascular graft placement

PURPOSE Previous reports demonstrate initial technical success with transluminally placed endovascular grafts (TPEG) for the treatment of abdominal aortic aneurysms. However, long-term changes in the size of the aorta and aneurysmal segments are unknown. The purpose of this study was to determine aortic dimensions at several levels by computed tomographic (CT) scans 1 year after TPEG. METHODS Thirty-four patients underwent TPEG with 1-year CT scans. Patients were divided into three groups: group I, no perigraft leak; group II, early perigraft leak that sealed during the first year; and group III, persistent perigraft leak. Aortic minor and major diameters, perimeter, and area were measured at four locations: the celiac aorta, proximal neck, maximal aneurysm size, and distal neck. RESULTS There were 32 men and two women, with a mean age of 73 +/- 8 years. In group I there were 20 patients (58%), and groups II and III had seven patients (21%) each. The overall mean aneurysm minor diameter decreased from 4.79 +/- 0.68 cm at implantation to 4.39 +/- 0.86 cm at 1 year (p < 0.0001). The aneurysm sac decreased by 0.63 +/- 0.58 cm in group I, and by 0.34 +/- 0.24 cm in group II. In group III, however, the aneurysm sac increased by 0.19 +/- 0.21 cm. Aneurysm size change did not correlate with inferior mesenteric or lumbar artery patency. The dimensions of the celiac aorta and proximal neck did not change significantly. However, diameter of the distal neck enlarged by 0.12 +/- 0.27 cm (p < 0.01). CONCLUSIONS TPEG exclusion is associated with reduction of aneurysm size 1 year after implantation. Expansion of the aneurysms occurred with persistent perigraft leak. The aortic size at the celiac artery and proximal neck did not change. Dilation of the distal neck was minor but requires further long-term follow-up to determine clinical significance.

Mesenteric venous thrombosis

Sixteen patients with mesenteric venous thrombosis were reviewed retrospectively during a period from 1983 to 1987. Twelve patients had progressive abdominal pain, three had gastrointestinal bleeding, and one had general malaise. Seven of these 16 patients had previous deep-vein thrombosis. After negative routine gastrointestinal and hepatobiliary evaluation, 11 patients underwent an infusion computerized tomographic scan. Of these, 10 had superior mesenteric vein thrombosis; three of these 10 patients had portal vein thrombosis. Selective arteriography was done in two patients because of gastrointestinal bleeding, and a diagnosis of mesenteric vein thrombosis was made on the venous phase of the examination. The remaining four patients developed acute abdominal symptoms requiring surgical exploration, at which time mesenteric venous thrombosis was discovered. An identifiable coagulopathy was detected in nine patients (protein C deficiency in six, protein S deficiency in two, and factor IX deficiency treated with factor IX concentrate in one). No case of congenital antithrombin-III deficiency was identified. Six of these nine patients had a past history of deep venous thrombosis. Of five patients who underwent surgical exploration, all required bowel resection. In follow-up, two patients died of intestinal necrosis and a third died of associated pancreatic cancer. Thirteen patients were discharged from the hospital. Treatment of coagulopathy was by heparin in three patients and sodium warfarin (Coumadin) in four patients. Long-term anticoagulation was not instituted because of gastrointestinal bleeding in three and cirrhosis in three patients. Mesenteric venous thrombosis can occur without gangrenous bowel. Diagnosis should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes and a coagulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Mesenteric artery bypass: Objective patency determination

PURPOSE Many authors have reported extended relief of intestinal ischemia by use of a variety of reconstructive techniques, but all have relied on symptomatic follow-up. None have objectively measured patency rates. The purpose of this study was to determine the primary patency rates of bypass grafts placed for acute and chronic splanchnic atherosclerotic occlusive disease with use of objective follow-up with mesenteric duplex ultrasound scanning or arteriography. METHODS Twenty-five consecutive patients (mean age 61, female/male ratio of 2.7:1) who underwent placement of 38 splanchnic bypass grafts (29 saphenous vein grafts, 9 polytetrafluoroethylene) (22 retrograde, 16 antegrade) for ischemic symptoms (9 acute ischemia: 16 chronic ischemia) between 1984 and 1994 were monitored with either duplex scanning (30 grafts) or arteriography. Life-table and log rank analysis were used to determine and compare graft patency. RESULTS Three patients (12%, 2 acute ischemia and 1 chronic ischemia) died after operation. Six patients (30%) had significant morbidity (4 acute ischemia and 2 chronic ischemia). During follow-up from 1 to 136 months (mean 35 months), no patient died of bowel infarction or required revision for recurrent symptoms. Objective testing revealed three graft occlusions. Symptomatic follow-up had a sensitivity of only 33% for graft occlusion when compared with objective measurement. The life-table primary patency rate was 89% at 72 months. Life-table survival for the same patients was 75% at 36 months. Patency rates for antegrade (93% at 36 months) versus retrograde (95% at 36 months) bypass and saphenous vein grafts (95% at 36 months) versus polytetrafluoroethylene (89% at 36 months) were not significantly different (p = 0.47 and 0.43, respectively). Late patency rates of grafts placed for acute ischemia (92% at 36 months) versus chronic ischemia (89% at 36 months) were not significantly different (p = 0.77). CONCLUSION Splanchnic bypass for mesenteric ischemia, with a primary patency rate of 89% at 72 months, is an extremely durable form of revascularization. Long-term patency of grafts placed for acute ischemia does not differ significantly from that of bypasses for chronic occlusion. Duplex scanning allows standardized objective periodic follow-up of splanchnic reconstruction. Objective assessment is critical to accurately measure visceral revascularization patency rates.

Arterial injuries in the thoracic outlet syndrome

PURPOSE This article reviews experience with arterial injury caused by thoracic outlet syndrome. Special emphasis is placed on the influence of athletic or work activities on the axillary-subclavian artery system and the mechanism by which the humeral head compresses the axillary artery and the circumflex humeral arterial branches. METHODS Retrospective review identified 34 patients (age range 13 to 67 years) treated for upper extremity symptoms or ischemic complications of thoracic outlet syndrome from 1983 to 1993. Evaluation included assessment of occupational and recreational activities plus duplex ultrasonography and contrast arteriography with positional maneuvers. RESULTS Twenty-two patients (27 arms) had subclavian artery injury, which was most commonly caused by compression by a bony abnormality (cervical rib, 16; anomalous first rib, two; cervical rib and anomalous first rib, two). Fourteen of the 27 arms had distal embolization. All 27 had surgical decompression of the subclavian artery; 15 required concomitant arterial reconstruction. Twelve additional patients (nine athletes) had axillary artery involvement, all from arterial compression by the head of the humerus during abduction maneuvers; all had concomitant compression of the posterior circumflex humeral artery. Axillary arterial injury included thrombosis (one), aneurysm (two), and symptomatic extrinsic compression only (nine). Five patients with axillary artery involvement were treated without a surgical procedure; of the remainder, three underwent decompression procedures only, and four had direct arterial repair. In both groups all subclavian and axillary artery reconstructions were patent at last follow-up examination (mean 31 months). CONCLUSION Most patients with thoracic outlet syndrome who have arterial involvement have a bony anomaly causing subclavian artery compression. This study demonstrates that humeral head compression of the axillary artery and its circumflex branches is a surprisingly common pathologic mechanism. Awareness of this condition affords a better therapeutic approach to arterial injuries caused by thoracic outlet syndrome.

Carotid plaque morphology correlates with presenting symptomatology

PURPOSE In carotid artery disease, correlation of carotid plaque morphology with the patients presenting symptoms has drawn conflicting conclusions. The purpose of this series was to correlate carotid plaque characteristics with the presenting symptoms from a large cohort of patients who underwent operation for carotid artery disease. METHODS From a series of 1252 consecutive patients who underwent carotid endarterectomy, presenting symptoms were divided into three groups: transiently symptomatic (transient ischemic attack [TIA] or amaurosis fugax), prior stroke, and asymptomatic. Plaque characteristics, including ulceration, intraplaque hemorrhage, and degree of stenosis, were recorded prospectively for 1008 procedures. All endarterectomy specimens were inspected during the procedure, and plaque characteristics were recorded immediately after operation. RESULTS There was a higher incidence of plaque ulceration in the transiently symptomatic and prior stroke groups (391 of 508 [77%] and 91 of 115 [79%]) than in the asymptomatic cohort (231 of 385 [60%]; p < 0.0001, chi2 test). There was no significant difference in the incidence of plaque hemorrhage between the transiently symptomatic and prior stroke patients compared with the asymptomatic patients. There was no statistical difference for ulcerated plaque or plaque hemorrhage between the transiently symptomatic and prior stroke group. Intraplaque hemorrhage occurred more frequently in patients with high-grade stenosis (90% to 99%) than in those with less than 90% stenosis (202 of 299 [68%] versus 97 of 299 [32%]; p = 0.01, chi2 test). CONCLUSIONS On gross examination of the carotid specimen in the operating room, plaque ulceration correlates with an initial presentation of amaurosis fugax, TIA, or prior stroke compared with patients operated on for asymptomatic disease. The presence of intraplaque hemorrhage is associated with more advanced stenosis of the internal carotid artery. These findings suggest that plaque morphology does play an important role in the presentation of carotid artery disease.

Guidelines for development and use of transluminally placed endovascular prosthetic grafts in the arterial system

THE feasibility of placing prosthetic grafts within the arterial tree by inserting them via a remote site, guiding them intraluminally to the appropriate location, and fixing them there with attachment systems, such as a variety of expandable stents, has been demonstrated in animals and human subjects (1–3). There is a potential for these transluminally placed endovascular grafts (TPEGs) to provide improved treatment for a variety of arterial lesions including aneurysms, traumatic injuries, and arteriosclerotic occlusions. TPEG repairs of all three kinds of lesions have been carried out at various levels of the arterial tree with short-term success (1,4–17). Because TPEG repairs can be performed less invasively, their risks and costs may be less than those of standard vascular graft operations. They will, therefore, be extremely attractive to both patients and physicians, and consequently there will be enormous pressures to develop and use these devices rapidly. The purpose of this document is to foster the development of safe, effective devices for performing TPEG repairs of various arterial lesions at all levels of the arterial tree. To this end, it will provide guidelines for the careful and structured evaluation and monitoring that is necessary to document the safety, efficacy, and effectiveness of these devices in various settings before they undergo widespread clinical use. Although these guidelines are not a regulatory document, they are intended to help avoid premature and potentially harmful usage of TPEGs.