Improving longevity of prosthetic dialysis grafts in patients with disadvantaged venous outflow.

OBJECTIVE: Angioaccess for hemodialysis in an extremity with disadvantaged venous outflow has reduced long-term patency. We hypothesized that arteriovenous bridge graft patency could be improved in patients with disadvantaged venous outflow by preoperative venous duplex mapping. METHODS: The charts of 114 patients who underwent 115 prosthetic arteriovenous bridge grafts were reviewed. Disadvantaged venous outflow was defined on the basis of any combination of prior arteriovenous bridge graft, multiple venipunctures, and clinical examination. Patients were grouped according to the presence or absence of disadvantaged venous outflow. Three groups were analyzed: those with normal venous outflow who had an initial arteriovenous bridge graft (NML), those with disadvantaged venous outflow who had only a clinical examination before redo arteriovenous bridge graft (REDO/DVO), and those with disadvantaged venous outflow who underwent preoperative duplex scanning venous evaluation (MAP/DVO). Life table primary and secondary 12-month patency rates were compared by means of log-rank analysis. RESULTS: Life table analysis yielded 6-month primary patency rates of 65.9% +/- 5.7%, 66.4% +/- 7.3%, and 43.8% +/- 10.9% for NML, MAP/DVO, and REDO/DVO, respectively. The secondary patency rates at 6 months for NML (91.9% +/- 3.4%) and MAP/DVO (91.1% +/- 4. 9%) were statistically equivalent, and both were significantly better than the patency for REDO/DVO (75.0% +/- 10.0%; P =.004 and P =.04, respectively). This trend persisted beyond 12 months. CONCLUSION: Preoperative evaluation of venous anatomy in patients with disadvantaged venous outflow results in an arteriovenous bridge graft patency comparable to that seen in patients undergoing initial arteriovenous bridge grafts. Vein mapping improves arteriovenous bridge graft durability in the patient with disadvantaged venous outflow by allowing the surgeon to select venous return that is in direct continuity with the central venous system.

Coronary bypass in vascular patients: a relatively high-risk procedure.

A premise of cardiac risk stratification is that the added risk of coronary artery bypass grafting (CABG) is offset by the improved safety of subsequent vascular reconstruction (VR). We questioned if elective CABG is patients with severe peripheral vascular disease (PVD) is a relatively high-risk procedure. A cohort study of 680 elective CABG patients from January 1993 to December 1994 was performed using three mutually exclusive outcomes of complication-free survival, morbidity, and mortality. Patient characteristic, operative, and outcome data were prospectively collected. Retrospective review determined that 58 patients had either a standard indication for or a history of VR. Overall CABG mortality was 2.5%, with statistically similar but relatively higher rates for PVD as compared to non-PVD patients. In contrast, major morbidity occurred at rates 3.6-fold higher in PVD patients (39.7%) than in disease-free patients (16.7%) after adjustment for the effects of patient and operative variables (odds ratio [OR] 3.67, 95% confidence interval [CI] 1.93-6.99). CABG morbidity in the PVD patient was most likely in those patients with aortoiliac (OR 9.51, CI 3.20-28.27) and aortic aneurysmal (OR 5.24, CI 1.28-21.41) disease types. CABG in PVD patients is associated with significant major morbidity. Such morbidity may preclude or alter the timing of subsequent VR.

Graft smooth muscle cells specifically synthesize increased collagen.

PURPOSE: Anastomotic intimal hyperplasia is characterized by smooth muscle cell (SMC) proliferation, but its final form is predominantly extracellular matrix. The purpose of this study was to compare collagen synthesis from graft SMC to that from adjacent native arterial SMC. METHODS: Thoracoabdominal bypass grafts were excised 20 weeks after implantation into canine models. SMC harvested from six anastomotic graft segments and adjacent native aorta were passaged twice, grown to near-confluence, and then assayed for collagen synthesis and total protein synthesis. In four of these sites type I alpha-1 procollagen mRNA levels were measured and normalized to glyceraldehyde-3-phosphate dehydrogenase. To control for increases in collagen synthesis associated with proliferation, SMC were plated at equal densities and tritium-thymidine incorporation and DNA concentration were determined. Data (mean +/- SE) were analyzed with two-factor ANOVA for repeated measures and paired Student t test and were considered significant if p < 0.05. RESULTS: There was no difference in thymidine incorporation and total protein synthesis between groups, but collagen synthesis (graft: 52.9 +/- 1.6 disintegrations per minute/ng DNA versus native: 42.6 +/- 1.9 dpm/ng DNA; p = 0.03) and collagen synthesis as a percentage of total protein synthesis (graft: 7.16% +/- 0.11% versus native: 5.8% +/- 0.14%; p = 0.001) increased significantly in graft SMC as compared to native SMC. Type I alpha-1 procollagen mRNA levels were higher in graft SMC, but this difference was not significant. CONCLUSIONS: Graft SMC specifically produce more collagen than SMC from adjacent native artery. This change does not simply reflect increases in either total protein synthesis or proliferation and may, in part, be due to increased collagen gene expression.

Upper extremity bypass grafting. A 15-year experience.

OBJECTIVE: To analyze the perioperative morbidity and mortality, long-term patient survival, and patency characteristics of arterial bypass related to upper extremity ischemia. DESIGN: This is a retrospective review of sequential patients undergoing upper extremity arterial bypass during a 15-year period at a single tertiary-care teaching hospital. Data are expressed in a 5-year life-table format and interpreted using log-rank analysis. PATIENTS: Seventy-four patients with upper extremity ischemia undergoing arterial bypass, which included 95 separate operations. MAIN OUTCOME MEASURES: Operative morbidity and mortality, life-table survival, life-table bypass graft patency, and limb salvage are reported. RESULTS: There was no operative mortality, and there was a single major amputation. Survival rate was 86% at 5 years, and overall patency rate was 61.2% at 5 years, with autogenous conduits superior at all sites compared with prosthesis (70.9% vs 37.7%). Secondary operation was inferior to primary bypass (66% vs 48%) and associated with higher morbidity (22% vs 5%). All far distal forearm prosthetic bypass grafts failed within 1 year. CONCLUSIONS: Primary upper extremity bypass with venous conduit is a safe, durable procedure, after which prolonged patient survival can be expected.

Descending thoracic aorta-to-femoral artery bypass: ten years' experience with a durable procedure.

PURPOSE: Arterial bypass from the descending thoracic aorta to the femoral system provides successful perfusion when an approach to the abdominal aorta is undesirable. This review of a large series with a decade of experience was conducted to better define patency data and the natural history of patients after this operation. METHODS: During a 10-year period, 21 patients, 18 men and 3 women (mean age 57 years), underwent descending thoracic aorta to left femoral artery bypass with femorofemoral bypass. These were placed to convert axillopopliteal or axillofemoral grafts (12 patients) to a more permanent inflow source. The axillary bypasses had been previously placed to allow removal of infected aortic grafts and had undergone a total of 14 revisions or thrombectomies before conversion. In addition, patients had this procedure after multiple failed attempts (at least two) at intraabdominal aortic repair (five patients) or to avoid exploration of the abdomen after extensive retroperitoneal dissection or radiation (four patients). Surgical technique involved a seventh interspace thoracotomy with a transdiaphragmatic retroperitoneal anterior axillary line tunnel to the left groin. RESULTS: There was no perioperative mortality. The mean hospital visit was 15.1 days and intensive care stay 4.3 days. There was no perioperative myocardial infarction, stroke, or renal failure that necessitated dialysis. With a follow-up period of 1 to 121 months (mean 44), the 4-year patency rate was 100%. A single graft failed at 49 months but was renewed by thrombectomy and femorofemoral bypass. Thus the extended patency rate was 86%, but the secondary patency rate remained 100% throughout. Since the thoracic operations, patients have required five femoropopliteal, three femorotibial, two profunda, and two femorofemoral operations. CONCLUSIONS: Descending thoracic aorta-to-femoral artery grafting is a safe, extremely durable arterial bypass configuration. It is an excellent reconstruction for survivors of aortic graft infection, those who have had multiple failures of aortic grafts, and patients for whom abdominal exploration would be hazardous.

Limb-threatening ischemia complicated by perigenicular infection.

When graft infection or infection of the medial leg or popliteal fossa precludes a standard approach to revascularization of the ischemic leg, the literature suggests amputation may be the most prudent course because of excessive perioperative mortality and morbidity of attempts to reestablish axial flow. The purpose of this study is to define the outcome of revascularization when limb-threatening ischemia is complicated by perigenicular infection. Of 1020 infrainguinal reconstructions performed since 1984, nine (0.9%) presented with limb-threatening ischemia and graft or wound infections involving the popliteal fossa (6) or medial thigh or calf wounds (3) which precluded standard revascularization in the five women and four men. Risk factors for infection included diabetes mellitus (5/9), wound hematoma at initial operation (2/9), and intravenous drug abuse (1/9); Staphylococcus aureus was the predominant organism in all infected wounds and two popliteal fossa infections. The other deep infections grew group D streptococci, Enterococcus, and Salmonella. Extra-anatomic reconstruction was performed from the femoral (7) and iliac vessels (2) extending to the below-knee popliteal (2), the anterior tibial (4) and the peroneal (3) arteries using vein (5), and PTFE (4) in a lateral tunnel which avoiding the plane of the infection. Postoperative complications included MI (1), early graft thrombosis (2), and osteomyelitis of the femur (1); there were no deaths. With a mean follow-up of 19 months (3-57 months), primary graft patency was 66% and secondary patency was 78%, resulting in salvage of 66% of extremities at risk. These data demonstrate the safety and efficacy of extra-anatomic reconstruction for maintaining axial flow when limb-threatening ischemia is complicated by perigenicular infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Collagen and elastin gene expression in aortic aneurysms.

BACKGROUND: The decreased elastin concentration found in abdominal aortic aneurysms (AAAs) may result from a differential synthetic response wherein elastin gene expression fails to increase in parallel with type I procollagen (COL I) gene expression. The purpose of this study is to determine tissue mRNA levels for elastin and COL I in AAAs compared with levels in normal, age-matched aorta and to determine the relationship between aging and COL I gene expression. METHODS: Total RNA exacted from normal infrarenal aortic tissue (n = 7) and AAA (n = 10) tissue was subjected to Northern analysis. Mean values for COL I, elastin, and alpha-tubulin mRNA levels were compared by use of the Student t test. Age and COL I mRNA levels were analyzed by regression analysis. RESULTS: COL I mRNA was increased significantly in AAAs (1.18 +/- 0.13) compared with normal aortas (0.14 +/- 0.05). A commensurate increase in elastin mRNA (AAAs, 0.11 +/- 0.02, vs normal aortas, 0.39 +/- 0.2) was absent. There was no correlation between age and COL gene expression. CONCLUSIONS: The decreased elastin concentration relative to collagen in AAAs may be explained, in part, by the changes in message level of elastin and collagen. The enhanced COL I gene expression in AAAs is unrelated to age.

Hepatic oxidant and antioxidant systems in portacaval-shunted rats.

The purpose of the present study was to determine the effects of chronic portal diversion on antioxidant levels in the rat liver. Male Sprague-Dawley rats (n = 32) were used for these studies. An end-to-side portacaval anastomosis was constructed in 17 of the rats. Sham-operated rats (n = 15) served as controls. Two weeks later, hepatic blood flow was measured by the radioactive microsphere technique and the liver was harvested for biochemical measurement of catalase, manganese superoxide dismutase, copper-zinc superoxide dismutase, selenium glutathione peroxidase, xanthine oxidase, xanthine dehydrogenase and reduced glutathione (acid soluble sulfhydryls). Total hepatic blood flow was approx. 40% lower in portacaval-shunted rats when compared to sham-operated control rats. Total superoxide dismutase (SOD) and xanthine dehydrogenase (XD) levels were significantly reduced in the liver of shunted rats when compared to controls. Xanthine oxidase activity was unaltered. The decreased superoxide dismutase levels were exclusively due to reductions in the cytosolic Ca/Zn SOD; Mn SOD levels were unaltered. These data are consistent with oxidant stress and suggest that the liver of subjects with conditions characterized by decreased portal blood flow may be more susceptible to oxidant-induced liver injury.

Intestinal vascular sensitivity to vasopressin in portal hypertensive rats.

The intestinal vascular responsiveness to arginine vasopressin was evaluated in rats with chronic portal hypertension. Male Sprague-Dawley rats were made portal hypertensive by stenosis of the portal vein. Ten to twelve days after the induction of chronic portal hypertension, the responsiveness of the small intestinal circulation to cumulative doses of vasopressin was evaluated using an isolated pump-perfused small intestinal preparation. The ED50 for maximal vasoconstriction was increased twofold in portal hypertensive rats compared with control rats. To determine if the impaired responsiveness to arginine vasopressin was related to the hyperglucagonemia of chronic portal hypertension, plasma glucagon levels were elevated in normal rats to levels previously measured in portal hypertensive rats (i.e. approximately 450 pg/mL), and the dose response studies were repeated. Glucagon significantly attenuated the responsiveness of the intestinal vasculature to vasopressin. Equipotent doses of nitroprusside also attenuated intestinal vascular responsiveness to vasopressin. The results indicate that there is a reduced vascular sensitivity to vasopressin in the intestine of portal hypertensive animals and suggest that elevations in circulating vasodilators in portal hypertensive conditions may partially explain this altered vascular responsiveness.

The effect of hemodilution on blood flow regulation in normal and postischemic intestine.

We investigated the effect of hemodilution on intestinal blood flow and oxygen consumption (VO2) in denervated rat small intestinal preparations. In one series of experiments, intestinal blood flow (IBF) and intestinal oxygen extraction (A-VO2) were measured during graded decreases in perfusion pressure. Control animals underwent consecutive studies without hemodilution; experimental animals were studied before and after isovolemic hemodilution. In a second series of experiments, normovolemic hemodilution was performed in experimental animals NH while hematocrit was maintained in controls, C. Preparations were then subjected to 30 min of complete ischemia followed by 30 min of reperfusion. Hemodilution (40.5 +/- 0.8% to 17.2 +/- 2.5%) decreased A-VO2 (3.9 +/- 0.5 to 2.1 +/- 0.4 ml/dl; P less than 0.05) but increased IBF (77.5 +/- 9.8 to 132.1 +/- 15.0 ml/min/100 gm; P less than 0.01). IBF was maintained to the limit of pressure:flow autoregulation (69 mmHg). Below this point, decreases in IBF were accompanied by increases in A-VO2 thus maintaining VO2. At a much lower "critical pressure" (42 mmHg) maximal oxygen extraction was reached and VO2 decreased with IBF. In the second series of experiments, hemodiluted animals (hematocrit 25 +/- 1%) studied during the reperfusion period maintained higher O2 consumption [30 min values (ml/min/100 gm): 4.8 +/- 0.9 NH vs 1.6 +/- 0.2 C, P less than 0.01] and A-VO2 difference [30 min values (vol%): 3.9 +/- 0.4 NH vs 2.1 +/- 0.4 C, P less than 0.005] than control animals (hct 33 +/- 2%). Hemodilution does not impair the intestine's ability to maintain O2 consumption during hypotension and hypoperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative effects of aspartate and glutamate during myocardial ischemia.

The effects of amino acids aspartate (Asp) and glutamate (Glu) on recovery of contractile function and preservation of compliance were studied in globally ischemic, isolated, blood-perfused cat hearts. Ischemia-induced declines in contractility and compliance were measured with an intraventricular fluid-filled balloon. Asp and Glu were delivered to isolated hearts in physiological salt solution (PSS) containing 10 mM glucose, just prior to, and intermittently during (every 15 min for 1 min) 1 h of normothermic ischemia. Isolated hearts which received Asp and Glu showed recoveries of left ventricular (LV) developed pressure of 79 +/- 8 and 50 +/- 7% of their preischemic values, respectively, compared to 34 +/- 7% in hearts perfused only with PSS. These alterations of contractile function were paralleled by changes in LV compliance. The addition of amino-oxyacetate, and aminotransferase inhibitor, to Asp- containing PSS markedly attenuated the beneficial effects of this amino acid. The results indicate that certain amino acids can protect the ischemic myocardium, presumably through effects on intermediary metabolism.