Comparison of outcomes after endovascular and open repair of abdominal aortic aneurysms in low-risk patients.

BACKGROUND: In randomized trials endovascular aortic aneurysm repair (EVAR) has been shown to have superior perioperative outcomes compared with open aneurysm repair (OAR). However, outcomes in patients at low risk of complications are unclear and many surgeons still prefer OAR in this cohort. The objective was to analyse perioperative and longer-term outcomes of OAR and EVAR in this low-risk group of patients. METHODS: All elective infrarenal EVARs and OARs in the Vascular Study Group of New England database were reviewed from 2003 to 2014. The Medicare scoring system was used to identity patients at low risk of perioperative complications and death. Perioperative and longer-term outcomes were analysed in this cohort. A Kaplan-Meier plot was constructed for evaluation of longer-term survival. Further propensity matching and multivariable analysis were performed to analyse additional differences between the two groups. RESULTS: Some 1070 patients who underwent EVAR and 476 who had OAR were identified. Mean(s.d.) age was 67·3(5·7) and 65·1(6·3) years respectively (P < 0·001). EVAR was associated with a lower overall perioperative complication rate (4·2 versus 26·5 per cent; P < 0·001). There was no difference in 30-day mortality (0·4 versus 0·6 per cent; P = 0·446). Overall survival at 3 years was similar after EVAR and OAR (92·5 versus 92·1 per cent respectively; P = 0·592). In multivariable analyses there was no difference in freedom from reintervention (odds ratio 1·69, 95 per cent c.i. 0·73 to 3·90; P = 0·220) or survival (hazard ratio 0·85, 0·61 to 1·20; P = 0·353). CONCLUSION: In patients predicted to be at low risk of perioperative death following aneurysm repair, EVAR resulted in fewer perioperative complications than OAR. However, perioperative mortality, reinterventions and survival rates in the longer term appeared similar between endovascular and open repair.

Outcomes of Endovascular Aortic Aneurysm Repair in Kidney Transplant Recipients: Results From a National Quality Initiative.

Contrast-induced nephropathy after endovascular aortic aneurysm repair (EVAR) in kidney transplant recipients (KTRs) can have devastating consequences. The Vascular Quality Initiative (VQI) database was queried to select all KTRs who underwent EVAR between January 2003 and December 2014. Our primary outcome was renal dysfunction, defined as acute kidney injury (AKI; elevation of serum creatinine >0.5 mg/dL from baseline) or new postoperative hemodialysis requirement. Within the EVAR VQI dataset, 40 patients were KTRs (40 of 17 213, or 0.2%). Renal dysfunction occurred in five of 40 patients in the KTR group in comparison to 779 of 17 173 patients in the nontransplanted group (12.5% versus 4.5%, p < 0.01). Emergent EVAR was required in 2 (5%) patients, one of whom required dialysis after surgery and subsequently died. One-year survival after EVAR was similar in the two groups (92.9% versus 93.1%, p = 0.73). KTRs who developed renal dysfunction had significantly lower preoperative estimated glomerular filtration rates (eGFRs) (29.5 versus 54.7, p = 0.007) and a significantly higher iodine:eGFR ratio (0.78 versus 0.39, p = 0.02) despite receiving a similar volume of contrast (70.0 versus 68.8, p = 0.97). Renal dysfunction is 3 times more frequent in KTRs treated with EVAR, though overall survival did not differ between the groups. Decreased preoperative eGFR and a higher iodine:eGFR ratio are associated with postoperative renal dysfunction.

Monocyte adhesion to human vein grafts: a marker for occult intraoperative injury?

OBJECTIVE: Monocyte adhesion to the vessel wall is believed to be an important initiating event in atherosclerosis and intimal hyperplasia. We hypothesized that occult intraoperative vein injury induces an immediate increase in monocyte adhesion that may be critical to the development of vein graft disease. METHODS: Vein segments were obtained from patients (n = 23) undergoing lower extremity bypass. The initial segment (V1, n = 17) was excised immediately at the time of conduit harvest. A second segment (V2, n = 23) was obtained from the distal conduit just before performing the distal anastomosis. Segments were incubated with radiolabeled THP-1 cells (monocytoid cell line) for 1 hour at 37 degrees C, then rinsed and solubilized for determination of bound radioactivity. In a subset of grafts (n = 4), THP-1 cells were preincubated with monoclonal antibody (mAB) 7E3 (which binds to the monocyte integrin Mac-1 at its fibrinogen [Fg]-binding site) or control (mAB 14E11). Fg deposition and endothelial coverage were evaluated by immunohistochemistry (n = 10). Statistical analysis was performed using the paired t test and analysis of variance. Follow-up graft patency data were obtained and correlated with adhesion values using an exact test (StatXact, Cytel Software, Cambridge, Mass). RESULTS: Monocyte adhesion was significantly increased after surgical manipulation (V1, 2400 +/- 770 versus V2, 7343 +/- 1555 cells/cm(2); P <.02). Fg deposition was abundant in V2 sections and not seen in V1. Monocyte adhesion to V2 segments was significantly reduced (58% of control, P <.01) by 7E3 treatment. Graft follow-up was complete with a mean interval of 11 months. Higher V2 adhesion values were associated with occluded grafts (P =.07). The median value for the six occluded grafts was 6234 cells/cm(2) versus 3892 cells/cm(2) for the 17 patent grafts. CONCLUSIONS: Monocyte adhesion to the vein wall is immediately increased after surgical manipulation and is inhibited by mAB 7E3. Early monocyte adhesion to vein grafts is likely to involve interactions between Mac-1 and Fg. Heightened levels of monocyte adhesion at implantation may be a marker for subsequent vein graft failure.

Monocyte adhesion to balloon-injured arteries: the influence of endothelial cell seeding.

OBJECTIVE: Deendothelialization of injuries of the artery disrupts normal vascular homeostasis, affecting both the structural integrity of the blood vessel wall, as well as the interaction of the arterial surface with blood components such as platelets, leukocytes, and circulating proteins. Leukocyte and, in particular, monocyte recruitment to damaged vessels has been implicated in the pathogenesis of intimal hyperplasia. We hypothesize that reendothelialization is an important modulator of monocyte adhesion to healing arterial surfaces. METHODS: New Zealand white rabbits (n = 20) were subjected to bilateral iliofemoral artery balloon injury. Cultured, autologous venous endothelial cells (ECs) were immediately seeded onto one vessel, whereas the contralateral artery received medium alone, to accelerate endothelial relining. Vessels were harvested (5-9 days after injury) for analysis of permeability (Evans Blue dye exclusion), endothelial coverage (anti-CD31 immunohistochemistry), monocyte adhesion (ex vivo binding of 51Na2CrO4-labeled monocytic THP-1 cells), and monocyte recruitment (RAM-11 immunohistochemistry). RESULTS: Improved EC coverage was evidenced by positive staining for CD31 in the seeded vessels. Vessel wall permeability was markedly reduced in EC-seeded arteries (29% +/- 10% vs 99% +/- 0% surface Evans blue staining, P <.005), consistent with restoration of a functional endothelial barrier. EC seeding significantly reduced ex vivo THP-1 binding to vessels explanted at a mean of 8 days after injury (45,170 +/- 8939 vs 85,994 +/- 16,500 cells/cm2, P <.05). However, RAM-11 staining revealed no significant difference in overall macrophage accumulation between seeded and control vessels 1 week after injury (111 +/- 22 vs 95 +/- 14 cells/section, P =.36). CONCLUSIONS: Immediate seeding of a balloon-injured rabbit artery with cultured ECs results in accelerated restoration of the endothelial lining. At 1 week, barrier function is improved, and the seeded vessel surface is less adhesive to activated monocytes ex vivo, as compared with injured controls. Nonetheless, EC-seeded and nonseeded arteries demonstrate similar total macrophage accumulation over 1 week. These data suggest that after mechanical arterial injury, endothelial coverage may be one important variable influencing leukocyte adhesion.

Operation for acute peripheral arterial occlusion: is it still the gold standard?

Acute arterial ischemia secondary to peripheral arterial occlusion has been shown to cause severe morbidity and mortality. Debate continues about the best mode for initial therapy of patients presenting with acute limb ischemia (ALI). Surgery traditionally has been used as the sole mode of therapy. Since the introduction of catheter-directed thrombolysis (CDT), role of surgery as the "gold standard" has been questioned. In this report the authors review the role of surgery compared with CDT. They discuss the role of prompt diagnosis on the outcome of the intervention and the results of CDT compared with the surgical standard. The best therapy for ALI is the one that is instituted early; intervention should be tailored based on the initial clinical presentation, and surgery remains the gold standard with CDT, an adjunctive tool for the vascular surgeon dealing with acute peripheral arterial occlusion (PAO).

Gene delivery to in situ veins: differential effects of adenovirus and adeno-associated viral vectors.

PURPOSE: Gene transfer offers the potential to modify vein graft biology at the time of surgical implantation. Efficiency of gene delivery, stability of expression, and host responses are critical parameters for candidate vectors. We compared the effects of intraluminal exposure with adenovirus (AD) and adeno-associated virus (AAV) vectors on transgene expression and monocyte adhesion (MA) in treated vein segments. METHODS: Adult New Zealand white rabbits (N = 51) were anesthetized, and the jugular veins were cannulated bilaterally. Veins were gently distended with either vector (2.10(8) to 1.10(10) infective particles/mL) or vehicle (control) for 30 minutes, after which venous flow was restored. AD and AAV vectors encoding for the marker genes beta-galactosidase (LacZ) and green fluorescent protein (GFP) were used. Vessels were explanted 2 to 40 days postinfection for analysis of gene expression (X-gal staining, reverse transcriptase-polymerase chain reaction), MA, and immunohistochemistry. Ex vivo adhesion assays used (51)Cr-labeled THP-1 cells. Statistical significance was tested by using analysis of variance with a P value less than.05. RESULTS: All animals survived, and all treated veins were patent at sacrifice. Intraluminal exposure to AD at a titer of 1.10(9) resulted in near complete transduction of the endothelium at 2 days, with no detectable expression by day 14. At an equal titer of infectious particles, transgene expression was markedly less for AAV at 2 to 7 days, but improved at 2 weeks and persisted to 40 days. MA was significantly increased 2 days after AD exposure (2.7-fold vs control, *P <.002); AAV treatment had no discernible effect on MA. CONCLUSION: AD-mediated gene transfer to vein segments resulted in robust, transient gene expression that disappeared after 2 weeks. In comparison, AAV-mediated gene delivery was less efficient, but resulted in delayed onset, persistent expression beyond 30 days. AD exposure induced an early increase in MA to the vein surface that was not seen with AAV treatment. Current generations of both AD and AAV vectors have significant, albeit different, limitations for vascular gene therapy.

Optimal methods for autogenous bypass to the anterior tibial artery.

BACKGROUND: Autogenous bypass to the anterior tibial artery (AT) has been increasingly used for infrageniculate revascularization. The conduit may be routed through the interosseous membrane, a pretibial tunnel, or through a lateral thigh and calf tunnel. This study reviewed results of AT bypass to determine the optimal routing method. METHODS: One hundred thirty consecutive vein grafts to the AT were analyzed retrospectively to compare the experience with the interosseous (group I; n = 50), pretibial (group II; n = 51), and lateral (group III; n = 29) routing alternatives. RESULTS: Indications were claudication in 16 (12.3%) and critical ischemia in 114 (87.8%) procedures with no differences among routing subgroups. Ectopic nonreversed and composite conduits were more common in group III. Major operative morbidity occurred after 7 procedures (5.4%) with no differences in early graft failure (7.7% overall) among the three routing subgroups. Wound infections were more common among group I patients, but without predilection to the interosseous tunnel. During a mean follow-up of 24.9 months (0 to 111.2) overall 5-year secondary patency was 70% with no difference among routing technique. CONCLUSION: Optimal routing choice depends on the location of suitable AT, the length of adequate vein conduit, and the surgeon's preference rather than on factors inherent to the method used.

Esophageal physiology.

Esophageal peristalsis and sphincter function involve coordinated neuromuscular processes the nature of which differs according to regional muscular anatomy and, to a degree, according to whether motility is initiated by swallowing or esophageal distension. The physical characteristics of the bolus and the conditions of testing may alter the speed and force of the propulsive contraction. Neural control of these processes and their modulation involves parasympathetic, sympathetic and enteric innervation of the organ. In smooth muscle regions, myogenic mechanisms may also play a role.