Search

Background Although evidence suggests that end-stage renal disease is associated with poor limb salvage and patient survival after arterial revascularization, little is known about the effect of renal transplantation. We analyzed the outcome in patients with renal transplants who underwent infrainguinal bypass procedures. Methods Data prospectively entered into our vascular registry were reviewed for all patients who underwent lower extremity bypass procedures from January 1, 1990, through January 31, 2002. Sixty patients were identified who had a functioning renal allograft at infrainguinal revascularization. Kaplan-Meier survival curves were generated for limb salvage, patency, and patient survival and were compared with the Mantel-Cox log- rank test. Results Sixty patients (40 men, 20 women; mean age, 47.1 years) underwent 76 bypass procedures in 71 limbs. Preoperative demographic data included diabetes (59 of 60 patients, 98.3%), coronary artery disease (26 of 60 patients, 43.3%), and preoperative serum creatinine concentration (SCr) greater than 2.0 mg/dL (9 of 60 patients, 11.7%). Mean follow-up was 25.1 months. Overall major complication rate was 11.8%, and 30-day mortality rate was 1.3%. Survival was 93.3% at 1 year and 66.6% at 5 years. Limb salvage was 87% at 1 year and 78% at 5 years. Primary graft patency was 78% at 1 year and 44% at 5 years. Preoperative SCr less than or equal to 2.0 mg/dL was associated with improved overall patient survival (5-year survival, 73.4% vs 37.5%; P = .01, log-rank test). Limb salvage and patency rates were not significantly affected by preoperative SCr greater than 2.0 mg/dL. Conclusions Lower extremity bypass can be performed safely and effectively in patients who have undergone renal transplantation. However, the importance of a well-functioning renal allograft at surgery is demonstrated by marked improvement in patient survival.

Background: Research with animal models has demonstrated tissue healing of endovascular grafts in both native arte-rial segments and in experimentally created arterial aneurysms. Fundamental to the successful clinical use of endovascular grafts for the treatment of aneurysmal disease is the creation of a permanent hemostatic seal between the graft ends and the arterial wall. Characteristics of this healing process in patients with aneurysmal disease have not been fully studied. In this study, we analyzed the macroscopic and histopathologic changes of the arterial wall after endovascular repair of aortic aneurysms. Methods: Over a 7-year period, 313 patients were treated with endovascular grafts to exclude arterial aneurysms of the thoracic and abdominal aorta. Of these patients, 11 had their endovascular grafts recovered for analysis. Five graft specimens were recovered during subsequent open aortic surgery. Six grafts were recovered at autopsy after the death of the patient of causes unrelated to the patient's endovascular graft. All specimens were fixed in formalin. Histologic analysis included light microscopy with hematoxylin and eosin and trichrome stains. Well-preserved specimens were selected after light microscopic examination and postfixed in 3% buffered glutaraldehyde for electron microscopy. The aortas from autopsy specimens were removed en bloc and fixed in formalin; representative regions of each graft were sectioned for analysis. Adherence of the graft to the vessel wall was categorized as densely adherent or easily separated after graft explantation. Traction applied to the graft-aortic anastomosis was equal to traction generated by suspending a standardized 2-kg weight. Infrarenal graft specimens were obtained with supraceliac aortic clamping, longitudinal aortotomy, and graft sampling before endograft revision. Results: In eight patients, endograft fixation was found to be firmly adherent to the arterial wall. A translucent film of fibrinous material was consistently seen across the entire luminal surface of the endograft. Light and electron microscopy failed to demonstrate an endothelial layer or organized pseudointima at the graft-artery interface. Conclusion: Despite suggestive experimental data regarding endograft healing in animals, minimal graft incorporation was apparent in the stent grafts recovered in this study. A greater emphasis on the construction and mechanism of fixation of endograft attachment systems will be important for long-term device function. (J Vasc Surg 2001;33:733-8.)

An endothelium-derived factor with the properties of nitric oxide (NO) has recently been implicated in the regulation of basal Na(+)-K(+)-adenosinetriphosphatase (ATPase) activity in vascular smooth muscle. To determine whether this factor also plays a role in the stimulation of ouabain-sensitive (OS) 86Rb uptake by specific agonists, studies were carried out using rabbit aortic rings. In endothelium-intact rings incubated for 3 h with Krebs-Henseleit solution containing 5.5 mM glucose, endothelin (ET) caused a concentration-dependent increase in OS 86Rb uptake (maximal increase = 205%, with 100 nM ET). Incubation with phenylephrine (Phe; 0.1 and 1 microM) or phorbol 12,13-dibutyrate (PDBu; 0.1 microM), under the same conditions, increased OS 86Rb uptake by 128, 144, and 140%, respectively. Removal of endothelium before incubation decreased the ability of ET to stimulate OS 86Rb uptake by 38–45%, but it did not diminish the stimulation of OS 86Rb uptake by Phe or PDBu. An increase in the concentration of glucose from 5.5 to 44 mM diminished ET-stimulated OS 86Rb uptake by 50% in endothelium-intact rings but had no effect on Phe- or PDBu-induced increases in OS 86Rb uptake. Addition of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 0.3 mM) to the medium decreased ET-stimulated OS 86Rb uptake by 40%. Guanosine 3',5'-cyclic monophophate (cGMP) formation in endothelium-intact rings was also increased (65%) by ET but not by Phe or PDBu. The increase in cGMP by ET was totally inhibited by L-NMMA or endothelium denudation.(ABSTRACT TRUNCATED AT 250 WORDS)

IntroductionDespite the frequent performance of minor foot amputations in patients with lower extremity vascular disease, little is known regarding the rate of conversion to major amputations and the role of bypass graft timing in relation to amputation.MethodsBetween January 1990 and December 2001, 670 patients underwent 920 minor amputations (interphalangeal, ray, or transmetatarsal) on 747 limbs.ResultsOf 670 patients, 468 were men (69.9%), 616 had diabetes mellitus (91.9%), and 137 (19.7%) had a serum creatinine level >2.0 mg/dL, of whom 92 were on dialysis (end-stage renal disease) (11.5%). Ipsilateral revascularization was performed ≤30 days before the initial amputation in 64.9% (485 of 747), whereas 9.8% (73 of 747) had a bypass ≤30 days postamputation. The initial amputation levels were 466 interphalangeal (62.4%), 159 transmetatarsal (21.3%), and 122 ray (16.3%). Operative 30-day mortality was 0.7% (6 of 920). Limb salvage was 89.8% at 1 year and 82.3% at 5 years. Diabetes mellitus had no impact on limb salvage (P = .61). Limb loss predictors included end-stage renal disease (odds ratio [OR], 1.72, 95% confidence interval [CI], 1.12 to 2.83, P < .01) and the need for transmetatarsal amputation as the initial procedure (OR, 1.62; 95% CI, 1.15 to 1.93; P < .01). Patients with revascularizations subsequent to an initial amputation had a significant increase in limb loss (OR, 2.11; 95% CI, 1.39 to 4.21, P < .005). Patient survival was 83.9% at 1 year and 43.5% at 5 years. Neither gender nor diabetes mellitus impacted survival; however, serum creatinine levels >2.0 mg/dL (5 years, 48.8% ± 2.3% vs 23.9% ± 4.2%, P < .0001) and the need for a major amputation ≤30 days (3 years, 60.8% ± 2.1% vs 40.1% ± 7.8%, P < .01) adversely affected survival.ConclusionsAlthough minor amputations can lead to limb preservation in most patients, the performance of a revascularization subsequent to amputation, transmetatarsal as the initial amputation, and end-stage renal disease are poor prognostic indicators. Inferior long-term patient survival is most closely associated with renal insufficiency and conversion to major amputation early after the initial procedure.

Several factors may limit the success of conventional operative therapy for traumatic arterial injuries. In particular, the inaccessibility of the vascular lesion, anatomic distortion, and the inherent problems associated with operating in a traumatized and often contaminated field are among these limiting factors. As a result, endovascular therapy has emerged as an important potential alternative. This paper focuses on the application of endovascular therapy to the trauma patient, based on our experience and those previously published by other groups. Injuries to the carotid, femoral, axillary/subclavian and iliac arteries, as well as to the abdominal and thoracic aorta, have been successfully managed by stent-grafting. Despite the potential benefits of this mode of therapy, its long-term utility will depend on our ability to overcome certain limitations associated with the technique, and on careful patient selection.

Purpose: Standard surgical repair of para-anastamotic aneurysms (PAAs) of the abdominal and thoracic aorta and the iliac arteries has been associated with high morbidity and mortality rates. We reviewed our continuing experience with endovascular repair of these lesions to determine whether this approach is favorable and durable. Methods: All patients with PAAs of the aorta or iliac arteries who underwent endovascular treatment of their lesions between August 1993 and July 1999 were prospectively followed up, and data on age, previous aortic pathology and surgery, size of PAA, time to diagnosis, and symptoms at presentation were recorded. Preoperative, intraoperative, and postoperative imaging studies were analyzed. All patients had endovascular stent-grafts placed under digital fluoroscopic guidance in the operating room. Data on intraoperative and postoperative complications, mortality, and endoleaks were reviewed. Results: From August 1993 to July 1999, 28 patients (20 men, 8 women) had 35 PAAs of the aorta or iliac arteries. There were 5 thoracic aortic, 12 abdominal aortic, and 18 iliac artery PAAs. Three patients had a contained rupture of their PAA. All patients who had originally undergone reconstruction for occlusive disease had lesions consistent with false aneurysms, whereas 73% of the aortic or iliac PAAs in patients originally treated for aneurysm disease appeared to be true aneurysms. Thirty-four of 35 PAAs were successfully excluded with stent-grafts (97%). There was one death at 30 days (3.6%) in a patient who was successfully treated endovascularly for a contained rupture of a thoracic PAA. There were four major postoperative complications (14.2%) in the 28 patients who were treated. One patient had continued perfusion of a thoracic aortic PAA (type I endoleak). The in-hospital length of stay after endovascular repair of PAA was 4 days (range, 1-18 days). The mean follow-up period was 21 months (range, 1-68 months). Conclusion: Endovascular repair of aortic and iliac artery PAAs is technically feasible and provides a high rate of lesion exclusion. Morbidity and mortality rates appear lower than those reported for open surgical repair. These patients can typically be discharged by the second postoperative day. Endovascular therapy for stable ruptured PAAs can be successfully performed and should be considered as an option only when appropriate devices and expertise are available. For uncomplicated PAAs of the aorta and iliac arteries, endovascular therapy may be more favorable than surgical repair. (J Vasc Surg 2001;33:503-12.)

An endothelium-derived factor with the properties of nitric oxide (NO) has been implicated in the regulation of Na(+)-K(+)-adenosinetriphosphatase (ATPase) activity in vascular smooth muscle. To examine this phenomenon further and to explore its modulation by guanosine 3',5'-cyclic monophosphate (cGMP), studies were carried out in the isolated rabbit aorta. Incubation of endothelium-denuded rings with NO (1 microM) or sodium nitroprusside (SNP, 10 microM) caused a time-dependent increase in ouabain-sensitive (OS) 86Rb uptake with the maximal stimulation (approximately 170%) seen after 20 min. In contrast, increases in cGMP concentration caused by NO and SNP (40- and 20-fold increases, respectively) were transient, with peak values observed after 2 min and significantly lower values by 10 min. The ability of NO or SNP to increase OS Rb uptake in endothelium-denuded rings was not mimicked by incubation with 8-bromo- or dibutyryl-cGMP or increases in cGMP caused by treatment with the phosphodiesterase inhibitor isobutylmethylxanthine. Depletion of intracellular cGMP levels by the guanylate cyclase inhibitor LY83583 also did not alter OS Rb uptake. SNP-stimulated OS Rb uptake was not inhibited by LY83583 in endothelium-denuded rings; however, it was completely prevented by the Na(+)-H+ exchange inhibitors amiloride and ethylisopropylamiloride. The results suggest that NO stimulates Na(+)-K(+)-ATPase activity in rabbit aorta by a mechanism independent of its ability to increase the intracellular cGMP concentration. They also suggest that NO may stimulate Na(+)-K(+)-ATPase activity secondary to increases in Na(+)-H+ exchange.

Hyperglycemia has been shown to diminish Na(+)-K+ ATPase activity in rabbit aorta. To examine the basis for this effect, aortic rings were incubated for 3 h in Krebs-Henseleit solution containing 5.5 or 44 mM glucose, and Na(+)-K+ ATPase activity was then quantified on the basis of ouabain-sensitive (OS) 86Rb-uptake. Incubation with 44 mM glucose medium caused a 60% decrease in Na(+)-K+ ATPase activity in rings with intact endothelium (from 0.22 +/- 0.01 to 0.091 +/- 0.006 nmol/min per mg dry wt; P less than 0.01). Similar decreases (45%; P less than 0.01) in Na(+)-K+ ATPase activity were seen when rings incubated with 5.5 mM glucose were exposed to NG-monomethyl L-arginine (300 microM), an inhibitor of endothelium-derived nitric oxide (EDNO) synthesis or when the endothelium was removed (43% decrease). The decrease in Na(+)-K+ ATPase activity induced by hyperglycemia was totally reversed upon adding to the medium either L-arginine, a precursor of EDNO biosynthesis or sodium nitroprusside, which bypasses endothelium and directly activates the soluble guanylate cyclase in vascular smooth muscle. A decrease in Na(+)-K+ ATPase activity (42%; P less than 0.05), only seen in the presence of endothelium, was also observed in aortas taken directly from alloxan-induced diabetic rabbits. These studies suggest that the decrease in vascular Na(+)-K+ ATPase activity induced by hyperglycemia is related, at least in part, to a decrease in the basal release of EDNO. They also suggest that alterations in basal EDNO release and possibly Na(+)-K+ ATPase activity contribute to the impairment in vascular relaxation caused by hyperglycemia and diabetes.