Role of Anticoagulation in Nonagenarian Patients with Acute Limb Ischemia.

BACKGROUND: Preoperative anticoagulant therapy is known to have a positive impact on the prognosis of patients with acute limb ischemia (ALI). However, little is known about its efficacy in elderly patients. We aimed to investigate the potential effect of anticoagulation in nonagenarian patients managed for ALI. METHODS: Between January 2015 and December 2021, we identified all nonagenarian patients managed for ALI at a single center. Long-term anticoagulation and hemostasis parameters (prothrombin rate, activated partial thromboplastin time [APTT], platelet count) measured on admission were reviewed. The primary end point was mortality at 30-day mortality (D30) in patients with or without long-term anticoagulation therapy. We also studied the effect of these factors on the occurrence of revascularization failure in operated patients (initial failure, ischemic recurrence during hospitalization, necrosis requiring major amputation). RESULTS: A total of 68 nonagenarian patients were managed for ALI, with a mean age of 93.8 years (from 90-107 years), 76.5% of whom were women. Of these patients, 47 (69%) were managed surgically. Long-term anticoagulation therapy was associated with better survival at D30, both in nonoperated (P < 0.01) and operated (P < 0.05) patients. In operated patients, the absence of long-term anticoagulation therapy was associated with the occurrence of revascularization failure (P < 0.05). In operated patients, survival to D30 and successful revascularization were associated with a longer APTT (P < 0,05). We were able to observe the survival of 4 patients contraindicated for surgery and treated with a single medical therapy (intravenous unfractionated heparin). CONCLUSIONS: Anticoagulation appears to have an impact on the survival and postoperative prognosis of nonagenarian patients with ALI. In addition, curative anticoagulation therapy may be an alternative treatment when surgery is contraindicated in this frail population.

Late Outcomes of Carotid Artery Stenting for Radiation Therapy-Induced Carotid Stenosis.

PURPOSE: Carotid artery stenting (CAS) appears as a promising alternative treatment to carotid endarterectomy for radiation therapy (RT)-induced carotid stenosis. However, this is based on a poor level of evidence studies (small sample size, primarily single institution reports, few long-term data). The purpose of this study was to report the long-term outcomes of a multicentric series of CAS for RT-induced stenosis. METHODS: All CAS for RT-induced stenosis performed in 11 French academic institutions from 2005 to 2017 were collected in this retrospective study. Patient demographics, clinical risk factors, elapsed time from RT, clinical presentation and imaging parameters of carotid stenosis were preoperatively gathered. Long-term outcomes were determined by clinical follow-up and duplex ultrasound. The primary endpoint was the occurrence of cerebrovascular events during follow-up. Secondary endpoints included perioperative morbidity and mortality rate, long-term mortality rate, primary patency, and target lesion revascularization. RESULTS: One hundred and twenty-one CAS procedures were performed in 112 patients. The mean interval between irradiation and CAS was 15 ± 12 years. In 31.4% of cases, the lesion was symptomatic. Mean follow-up was 42.5 ± 32.6 months (range 1-141 months). The mortality rate at 5 years was 23%. The neurologic event-free survival and the in-stent restenosis rates at 5 years were 87.8% and 38.9%, respectively. Diabetes mellitus (p=0.02) and single postoperative antiplatelet therapy (p=0.001) were found to be significant predictors of in-stent restenosis. Freedom from target lesion revascularization was 91.9% at 5 years. CONCLUSION: This study showed that CAS is an effective option for RT-induced stenosis in patients not favorable to carotid endarterectomy. The CAS was associated with a low rate of neurological events and reinterventions at long-term follow-up.

Hypoxia and hypoxia-inducible factors promote the development of neointimal hyperplasia in arteriovenous fistula.

KEY POINTS: Patients with end-stage renal failure need arteriovenous fistulas (AVF) to undergo dialysis. However, AVFs present a high rate of failure as a result of excessive venous thickness. Excessive venous thickness may be a consequence of surgical dissection and change in oxygen concentration within the venous wall. We show that venous cells adapt their metabolism and growth depending on oxygen concentration, and drugs targeting the hypoxic response pathway modulate this response in vitro. We used the same drugs on a mouse model of AVF and show that direct or indirect inhibition of the hypoxia-inducible factors (HIFs) help decrease excessive venous thickness. Hypoxia and HIFs can be targets of therapeutic drugs to prevent excessive venous thickness in patients undergoing AVF surgical creation. ABSTRACT: Because the oxygen concentration changes in the venous wall, surrounding tissue and the blood during surgical creation of arteriovenous fistula (AVF), we hypothesized that hypoxia could contribute to AVF failure as a result of neointimal hyperplasia. We postulated that modulation of the hypoxia-inducible factors (HIF) with pharmacological compounds could promote AVF maturation. Fibroblasts [normal human fibroblasts (NHF)], smooth muscle cells [human umbilical vein smooth muscle cells (HUVSMC)] and endothelial cells [human umbilical vein endothelial cells (HUVEC)], representing the three layers of the venous wall, were tested in vitro for proliferation, cell death, metabolism, reactive oxygen species production and migration after silencing of HIF1/2-α or after treatment with deferioxamine (DFO), everolimus (Eve), metformin (Met), N-acetyl-l-cysteine (NAC) and topoisomerase I (TOPO), which modulate HIF-α stability or activity. Compounds that were considered to most probably modify intimal hyperplasia were applied locally to the vessels in a mouse model of aortocaval fistula. We showed, in vitro, that NHF and HUVSMC can adapt their metabolism and thus their growth depending on oxygen concentration, whereas HUVEC appears to be less flexible. siHIF1/2α, DFO, Eve, Met, NAC and TOPO can modulate metabolism and proliferation depending on the cell type and the oxygen concentration. In vivo, siHIF1/2α, Eve and TOPO decreased neointimal hyperplasia by 32%-50%, 7 days after treatment. Within the vascular wall, hypoxia and HIF-1/2 mediate early failure of AVF. Local delivery of drugs targeting HIF-1/2 could inhibit neointimal hyperplasia in a mouse model of AVF. Such compounds may be delivered during the surgical procedure for AVF creation to prevent early AVF failure.

Co-culture of human fibroblasts, smooth muscle and endothelial cells promotes osteopontin induction in hypoxia.

Arteriovenous fistulas (AVFs) are the preferred vascular access for haemodialysis of patients suffering from end-stage renal disease, a worldwide public health problem. However, they are prone to a high rate of failure due to neointimal hyperplasia and stenosis. This study aimed to determine if osteopontin (OPN) was induced in hypoxia and if OPN could be responsible for driving AVF failure. Identification of new factors that participate in remodelling of AVFs is a challenge. Three cell lines representing the cells of the three layers of the walls of arteries and veins, fibroblasts, smooth muscle cells and endothelial cells, were tested in mono- and co-culture in vitro for OPN expression and secretion in normoxia compared to hypoxia after silencing the hypoxia-inducible factors (HIF-1α, HIF-2α and HIF-1/2α) with siRNA or after treatment with an inhibitor of NF-kB. None of the cells in mono-culture showed OPN induction in hypoxia, whereas cells in co-culture secreted OPN in hypoxia. The changes in oxygenation that occur during AVF maturation up-regulate secretion of OPN through cell-cell interactions between the different cell layers that form AVF, and in turn, these promote endothelial cell proliferation and could participate in neointimal hyperplasia.

Comparison of Cryopreserved Arterial Allografts Versus Heparin-bonded Vascular Grafts in Infragenicular Bypass for Chronic Limb Threatening Ischemia.

BACKGROUND: The purpose of this study was to compare cryopreserved arterial allograft (CAA) to heparin-bonded prosthesis (HBP) in infragenicular bypasses for patients with chronic limb-threatening ischemia (CLTI). METHODS: This retrospective study took place in 2 university hospitals and included 41 consecutive patients treated for CLTI. In the absence of a suitable saphenous vein, an infragenicular bypass was performed using either CAA (24 cases) or HBP (17 cases). Kaplan-Meyer analysis compared primary and secondary patency and amputation-free survival rates. Binomial logistic regression analyzed risk factors for major amputation and thrombosis. RESULTS: The mean followup was 18.5 months (±14.3) in the CAA group, 17.6 (±6.1) in the HBP group. In the CAA group, primary and secondary patency rates at 12 months were 52% (±10.6) and 61% (±10.3), compared to 88% (±7.8) and 94% (±5.7) in the HBP group, respectively. The difference in patency rates was not statistically different (P = 0.27 and P = 0.28, respectively). The statistically significant factors of graft thrombosis were, a stage 4 from the WIfI classification (Wound Ischemia foot Infection) with a 6 times higher risk (P = 0.04), and a distal anastomosis on a leg artery with a 9 times higher risk of thrombosis (P = 0.03). Amputation-free survival rates at 18 months were similar between the groups (CCA: 75% (±9) versus HBP: 94% (±6), P = 0.11). Patients classified as WIfI stage 4 had 13 times higher odds to undergo major amputation than patients with WIfI stage 2 or 3 (95% CI, 1.16-160.93; P = 0.04). The intervention was longer in the CCA group of 74 min (278 min ± 86) compared to the HBP group (203 min ± 69). This difference was statistically significant (95% CI, 17.86-132.98), t(35) = 2.671, P = 0.01. CONCLUSIONS: CCA is not superior to HBP in infragenicular bypasses for CLTI, and may not be worth the extra cost and the longer operative duration.

Pseudoaneurysm of the Brachial Artery after Reduction and Fixation of a Displaced Supracondylar Elbow Fracture in a Child.

About 10% of supracondylar humerus fractures in children are associated with distal ischemia. In case of acute limb ischemia after reduction and fixation, it is recommended to explore the brachial artery surgically without delay. However, there is no consensus on the management of intermediate situations, like a perfused hand with a weak pulse after fracture fixation. A 6-year-old boy presented a displaced Gartland type III supracondylar humerus fracture with no radial or ulnar pulse and hand ischemia. Immediately after closed reduction and internal fixation, the pulses were still missing. A duplex ultrasound of the radial artery showed an arterial flow, although diminished compared to the contralateral limb. Ten minutes later, a weak radial pulse was noticed and the hand perfusion was progressively increasing. Therefore, we suspected an arterial spasm. At 48 hr, distal pulse was present and the saturometer showed 98% of O2. The patient was discharged. At day 11, the patient complained about a painful tumefaction above the elbow. An injected computed tomography scan showed a pseudoaneurysm of the brachial artery surrounded by an hematoma. Forearm arteries were patent. The injured segment of the brachial artery was resected and replaced by a venous graft. At 2-month follow up, there were no vascular or cutaneous complications, duplex ultrasound examination was normal and the fracture was healed. This case highlights a "gray zone" between complete ischemia and complete recovery after supracondylar fracture fixation with initial ischemia. In such situations, a full duplex ultrasound examination, or a contrast computed tomography scan of the upper limb arteries seem appropriate.

Role of Hypoxia and Metabolism in the Development of Neointimal Hyperplasia in Arteriovenous Fistulas.

For patients with end-stage renal disease requiring hemodialysis, their vascular access is both their lifeline and their Achilles heel. Despite being recommended as primary vascular access, the arteriovenous fistula (AVF) shows sub-optimal results, with about 50% of patients needing a revision during the year following creation. After the AVF is created, the venous wall must adapt to new environment. While hemodynamic changes are responsible for the adaptation of the extracellular matrix and activation of the endothelium, surgical dissection and mobilization of the vein disrupt the vasa vasorum, causing wall ischemia and oxidative stress. As a consequence, migration and proliferation of vascular cells participate in venous wall thickening by a mechanism of neointimal hyperplasia (NH). When aggressive, NH causes stenosis and AVF dysfunction. In this review we show how hypoxia, metabolism, and flow parameters are intricate mechanisms responsible for the development of NH and stenosis during AVF maturation.

Large-vessel vasculitis in human immunodeficiency virus-infected patients.

OBJECTIVE: The objective of this study was to describe large-vessel vasculitis (LVV) in patients with human immunodeficiency virus (HIV) infection. It is a retrospective single-center study conducted between 2000 and 2015 through a university hospital of 11 HIV-infected patients with LVV. METHODS: The characteristics and outcome of 11 HIV-infected patients with LVV (7 patients fulfilled international criteria for Takayasu arteritis, 5 patients had histologic findings of vasculitis, and 5 patients had imaging features of aortitis) were analyzed and compared with those of 82 patients with LVV but without HIV infection. RESULTS: Concerning the HIV-infected patients with LVV (n = 11), the mean age was 40 years (range, 36-56 years), and 55% of patients were female. At diagnosis of LLV, the mean initial CD4 cell count was 455 cells/mm3 (range, 166-837 cells/mm3), and the median HIV viral load was 9241 copies. Vascular lesions were located in the aorta (n = 7), in supra-aortic trunks (n = 7), and in digestive arteries (n = 3). Inflammatory aorta infiltrates showed a strong expression of interferon-γ and interleukin 6. In HIV-negative LVV patients (n = 82), the median age was 42 years, and 88% of the patients were women. Thirty patients had an inflammatory syndrome. Seventy patients had been treated with glucocorticosteroids and 57 with immunosuppressive treatments. Compared with their negative counterparts, HIV-positive patients with LVV were more frequently male (P = .014), had more vascular complications (ie, Ishikawa score; P = .017), and had more frequent revascularization (P = .047). After a mean follow-up of 96 months, four relapses of vasculitis were reported, and one patient died. Regardless of the HIV virologic response, antiretroviral therapy improved LVV in only one case. CONCLUSIONS: LVV in HIV-infected patients is a rare and severe entity.

Increased Oxidative Stress and Hypoxia Inducible Factor-1 Expression during Arteriovenous Fistula Maturation.

BACKGROUND: The poor clinical results that are frequently reported for arteriovenous fistulae (AVF) for hemodialysis are typically due to failure of AVF maturation. We hypothesized that early AVF maturation is associated with generation of reactive oxygen species and activation of the hypoxia-inducible factor-1 (HIF-1) pathway, potentially promoting neointimal hyperplasia. We tested this hypothesis using a previously reported mouse AVF model that recapitulates human AVF maturation. METHODS: Aortocaval fistulae were created in C57Bl/6 mice and compared with sham-operated mice. AVFs or inferior vena cavas were analyzed using a microarray, Amplex Red for extracellular H2O2, quantitative polymerase chain reaction, immunohistochemistry, and immunoblotting for HIF-1α and immunofluorescence for NOX-2, nitrotyrosine, heme oxygenase-1 (HO-1), and vascular endothelial growth factor (VEGF)-A. RESULTS: Oxidative stress was higher in AVF than that in control veins, with more H2O2 (P = 0.007) and enhanced nitrotyrosine immunostaining (P = 0.005). Immunohistochemistry and immunoblot showed increased HIF-1α immunoreactivity in the AVF endothelium; HIF-1 targets NOX-2, HO-1 and VEGF-A were overexpressed in the AVF (P < 0.01). AVF expressed increased numbers of HIF-1α (P < 0.0001) and HO-1 (P < 0.0001) messenger RNA transcripts. CONCLUSIONS: Oxidative stress increases in mouse AVF during early maturation, with increased expression of HIF-1α and its target genes NOX-2, HO-1, and VEGF-A. These results suggest that clinical strategies to improve AVF maturation could target the HIF-1 pathway.

Radial artery deviation and reimplantation inhibits venous juxta-anastomotic stenosis and increases primary patency of radial-cephalic fistulas for hemodialysis.

OBJECTIVE: Although the end cephalic vein-to-side radial artery arteriovenous fistula is the "gold standard" procedure for primary hemodialysis access, it is associated with high rates of primary failure because of the development of neointimal hyperplasia and juxta-anastomotic stenosis. We report initial results of a new approach to perform radial-cephalic fistulas, radial artery deviation and reimplantation (RADAR), designed to avoid juxta-anastomotic stenosis. METHODS: RADAR patients' data were prospectively maintained and retrospectively reviewed and compared with a historical control group of traditional radial-cephalic fistulas created in the same center. Duplex ultrasound was used to monitor maturation (flow ≥500 mL/min and venous diameter ≥5 mm) and to diagnose juxta-anastomotic stenosis. Study end points were rates of maturation, juxta-anastomotic stenosis, reintervention, and primary and secondary patency. RESULTS: There were 53 RADAR fistulas performed (follow-up, 10.5 ± 2.6 months) and compared with 73 control fistulas (follow-up, 12.0 ± 6.6 months). RADAR fistulas had increased rates of maturation compared with control fistulas (75% vs 45% at 6 weeks, P = .001; 92% vs 71% at 3 months, P = .003) and decreased incidence of juxta-anastomotic venous stenoses (2% vs 41%; P = .001). At 6 months, RADAR fistulas had increased primary patency (93% vs 53%; P < .0001) and secondary patency (100% vs 89%; P = .0003) and decreased incidence of reinterventions (10% vs 74%; P = .001) compared with control fistulas. No RADAR fistulas caused ischemic symptoms. CONCLUSIONS: The RADAR technique is associated with less juxta-anastomotic stenosis, increased maturation and patency, and fewer secondary interventions. These improved outcomes suggest that RADAR may be the preferred surgical technique to perform radial-cephalic arteriovenous fistula.

Ephrin type-B receptor 4 activation reduces neointimal hyperplasia in human saphenous vein in vitro.

BACKGROUND: Vein bypass is an essential therapy for patients with advanced peripheral and coronary artery disease despite development of neointimal hyperplasia. We have shown that stimulation of the receptor tyrosine kinase ephrin type-B receptor 4 (Eph-B4) with its ligand ephrin-B2 prevents neointimal hyperplasia in murine vein grafts. This study determines whether Eph-B4 in adult human veins is capable of phosphorylation and activation of downstream signaling pathways, as well as functional to release nitric oxide (NO) and prevent neointimal hyperplasia in vitro. METHODS: Discarded human saphenous veins were taken from the operating room and placed in organ culture without or with ephrin-B2/Fc (2 µg/mL) for 14 days, and the neointima/media ratio was measured in matched veins. Primary human umbilical vein endothelial cells were treated with ephrin-B2/Fc (2 µg/mL) and examined with quantitative polymerase chain reaction, Western blot, immunoassays, and for release of NO. Ephrin-B2/Fc (2 µg/mL) was placed on the adventitia of saphenous veins treated with arterial shear stress for 24 hours in a bioreactor and activated Eph-B4 examined with immunofluorescence. RESULTS: The baseline intima/media ratio in saphenous vein rings was 0.456 ± 0.097, which increased to 0.726 ± 0.142 in untreated veins after 14 days in organ culture but only to 0.630 ± 0.132 in veins treated with ephrin-B2/Fc (n = 19, P = .017). Ephrin-B2/Fc stimulated Akt, endothelial NO synthase and caveolin-1 phosphorylation, and NO release (P = .007) from human umbilical vein endothelial cells (n = 6). Ephrin-B2/Fc delivered to the adventitia stimulated endothelial Eph-B4 phosphorylation after 24 hours of arterial stress in a bioreactor (n = 3). CONCLUSIONS: Eph-B4 is present and functional in adult human saphenous veins, with intact downstream signaling pathways capable of NO release and prevention of neointimal hyperplasia in vitro. Adventitial delivery of ephrin-B2/Fc activates endothelial Eph-B4 in saphenous veins treated with arterial shear stress in vitro. These results suggest that stimulation of Eph-B4 function may be a candidate strategy for translation to human clinical trials designed to inhibit venous neointimal hyperplasia.

Increased reintervention in radial-cephalic arteriovenous fistulas with anastomotic angles of less than 30 degrees.

OBJECTIVE: Although radial-cephalic (RC) and brachial-cephalic (BC) fistulas are the recommended primary accesses for hemodialysis, access failure is frequently due to juxta-anastomotic stenosis (JAS). Because increased turbulence at the anastomosis may lead to JAS, we hypothesized that an acute angle at the arteriovenous anastomosis is associated with JAS, reduced fistula patency, and increased reinterventions. METHODS: Between February 2013 and September 2014, the anastomotic angle and vessel diameters were prospectively collected for all patients who underwent RC or BC fistula creation. The primary end point was reintervention on the juxta-anastomotic segment. Secondary end points were primary and secondary patency of the fistula. RESULTS: A total of 149 patients (median age, 72 years) received 73 RC and 76 BC fistulas; the median follow-up was 7 months (range, 1-22 months) for RC and 12 months (range, 2-24 months) for BC fistulas. The median anastomotic angle in RC fistulas, was 30°. Anastomotic angles of <30° were associated with reduced primary patency (38% vs 66%, P = .003) and secondary patency (84% vs 97%, P = .02) and increased numbers of reinterventions (67% vs 34%, P = .001). Cox analysis showed that an anastomotic angle of <30° was an independent factor predicting decreased primary patency (P = .009) and secondary patency (P = .03) as well as increased reinterventions (P = .004). In BC fistulas, the median anastomotic angle was 90°. Patients with anastomotic angles <90° and ≥90° had similar rates of primary patency (67% vs 67%, P = .39) and secondary patency (93% vs 94%, P = .89) at 6 months, with a similar reintervention rate at 12 months (31% vs 32%, P = .56). Vein diameter was the only factor that predicted reintervention (P < .0001). CONCLUSIONS: RC fistulas with anastomotic angles of <30° have reduced primary and secondary patency and increased numbers of reinterventions, suggesting that, if possible, surgeons should avoid an anastomotic angle of <30° when creating RC fistulas. Anastomotic angles of <90° or ≥90° may not play a role in outcome of BC fistulas.

Surgical repair of descending thoracic and thoracoabdominal aortic aneurysms in patients with human immunodeficiency virus infection: a 10-patient series.

BACKGROUND: Major surgery in patients with human immunodeficiency virus (HIV) infection increases the risk of complications such as cardiovascular morbidity and opportunistic infections. METHODS: This study reports our experience with open surgical repair of 10 descending thoracic and thoracoabdominal aortic aneurysms in patients with HIV. RESULTS: Seven were men, and their median age was 49 years. All patients were controlled with highly active antiretroviral therapy (mean CD4+: 613/mm(3)). Three patients died (1 preoperatively, 1 after rupture, and 1 after elective surgery). No patient had spinal cord ischemia or infectious complications, either early or after a median follow-up of 29 months. Bacteriologic and histologic analyses did not determine any specific etiology for the aneurysms. CONCLUSIONS: Surgical repair of descending thoracic and thoracoabdominal aortic aneurysms in patients with HIV infection is feasible and may not lead to remote infectious complications.

Vascular access thrombosis in France: incidence and treatment patterns.

BACKGROUND: Vascular access thrombosis lacks the implementation of a treatment algorithm at large scale, involving all the actors. We aimed to determine a better understanding of the current practice patterns around vascular access thrombosis in France, with 4 axes: incidence, surveillance protocol, treatment, and time to treatment. METHODS: A comprehensive survey of all the nephrologists staffing all hemodialysis centers in France during April 2013 included 266 of 269 (99%) centers, treating 27,798 patients with arteriovenous fistula or graft. RESULTS: In 104 centers treating 11,088 patients, there were 905 documented episodes of vascular access thrombosis (8.8%) in 1 year; in the other 162 centers that supplied a range of events, the mean incidence was 8.4%. Use of in-line access flow monitoring as part of surveillance program was not correlated with better outcome compared with Doppler ultrasound (thrombosis: 7.9% vs. 10%, respectively, P = 0.09). Fifty-three percent of centers referred the patients to a vascular surgeon and 32% to an interventional radiologist (2% to urologist and 13% variable referral depending on the case complexity). Time to treatment was <24 hr in 58% and <48 hr in 91% of the centers; treatment >48 hr (9%) occurred mainly in rural zones (P = 0.04). The specialty of the treating physician did not influence time to treatment (P > 0.05). CONCLUSIONS: In France, vascular access thrombosis rate is low and not influenced by surveillance protocol type. Most patients can receive timely treatment by vascular surgeons or interventional radiologists.

Salvage of Early-Failing Radiocephalic Fistulae with Techniques that Minimize Venous Dissection.

Although radiocephalic fistulae are the preferred hemodialysis access, juxta-anastomotic stenosis is often responsible for early fistula failure. We hypothesized that wall ischemia from surgical manipulation leads to early juxta-anastomotic neointimal hyperplasia and failure of maturation and that minimal venous dissection will improve surgical salvage, increasing fistula maturation rates. For failing-to-mature radiocephalic fistulae that develop early juxta-anastomotic stenosis, we describe 3 variations to perform a new proximal anastomosis with a minimal dissection technique on the forearm cephalic vein: (1) side-to-side anastomosis, (2) radial artery deviation and reimplantation, or (3) radial artery deviation and loop reimplantation. Minimal dissection of the cephalic vein achieves fistula salvage without needing a more proximal site for access.

Early surgical thrombectomy improves salvage of thrombosed vascular accesses.

OBJECTIVE: The timing and urgency of salvage attempts for acutely thrombosed hemodialysis vascular accesses remain poorly defined. We examined the outcome of early surgical thrombectomy after acute access thrombosis to assess the influence of expedited timing on access salvage. METHODS: Between January 2007 and October 2012, 114 surgical thrombectomy attempts were performed on 82 patients to salvage 89 accesses. The time between the diagnosis of thrombosis and admission to the operative suite (T1), the time between diagnosis and the following dialysis session (T2), and clinical and biologic parameters were collected prospectively. Data were retrospectively compared between the early (T1 <6 hours) and later (T1 >6 hours) treatment groups. The main outcome measure was technical success. Kaplan-Meier survival analysis was used to estimate functional patency rates. RESULTS: Mean patient follow-up was 22 ± 18 months. The mean time from referral to procedure (T1) was 5.7 ± 4.5 hours. The mean time T1 was 3.6 ± 1.2 hours in the early group and 10.3 ± 5.4 hours in the later group. The mean time to dialysis (T2) was 14.3 ± 6.5 hours in the early group and 23.9 ± 9.4 hours in the later group. Thrombectomy performed ≤ 6 hours after diagnosis (T1 <6 hours) had significantly higher technical success of 86% compared with 69% for thrombectomy performed later (T1 >6 hours; P = .04). The two groups did not differ significantly in patient comorbidities, type of access, or adjunctive procedures performed (P ≥ .1). At 12 months, the primary patency rate for all index cases, including technical failures, was 55% ± 7.1% in the early group and 33% ± 9.7% in the later group (P = .13). The secondary patency rate was 67% ± 6.8% in the early group and 50% ± 9.9% in the later group (P = .05). CONCLUSIONS: After acute access thrombosis, early surgical thrombectomy was associated with higher technical success and potentially improved midterm patency.

Pelvic ischemia and quality of life scores after interventional occlusion of the hypogastric artery in patients undergoing endovascular aortic aneurysm repair.

OBJECTIVE: The aim of this study was to analyze the pelvic ischemic complications and their impact on quality of life after interventional occlusion of the hypogastric artery (IOHA) in patients undergoing endovascular aortic aneurysm repair (EVAR). METHODS: Between January 2004 and April 2012, 638 consecutive patients with aortoiliac aneurysm treated by EVAR were prospectively registered in two teaching hospitals. We identified all EVAR patients who underwent IOHA. Demographic, clinical, and radiologic data were extracted from electronic databases and patient records as requested. All patients who survived the postoperative period took part in a quality of life survey, the Walking Impairment Questionnaire (WIQ), which included four items: pain, distance, walking speed, and stair climbing. Outcome measures included the 30-day rate of pelvic ischemic complications, the buttock claudication (BC) rate at 30 days and during follow-up, and the comparative WIQ scores between patients with persistent BC, those with regressive BC, and those who never had BC after the IOHA procedure. RESULTS: A total of 71 patients (97% men; mean age, 76 years ± 7.69) required 75 IOHA procedures. These were deemed proximal in 44 cases and distal in 31, with use of coil embolization in 64%, Amplatzer plug in 24%, or a combination of coils and plugs in 12%. The technical success rate was 100%. Two patients (2.8%) experienced fatal acute pelvic ischemic complications in the postoperative period after EVAR. Another patient died of iliac rupture during EVAR, leading to an operative mortality rate of 4.3%. Eighteen patients (25.3%) suffered BC, among whom 11 cases resolved at a median follow-up of 42 months. Young age (odds ratio, 0.92; 95% confidence interval, 0.85-0.99; P = .03) and distal IOHA (odds ratio, 3.5; 95% confidence interval, 1.01-11.51; P = .04) were independent predictors of BC occurrence. The actuarial rate of persistent BC was 85% at 18 months. The WIQ scores were lower for patients with persistent BC (median score, 35.04; interquartile range, 16.36; P = .001) compared with patients with regressive BC (median score, 76.5; interquartile range, 36.66; P = .02) or those who never experienced BC after the IOHA procedure (median score, 65.34; interquartile range, 10.94; P < .0003). CONCLUSIONS: Pelvic ischemia associated with IOHA may be severe and lead to fatality after EVAR. Our data show that BC may lead to severe quality of life impairment when it does not regress during follow-up.

Vein graft adaptation and fistula maturation in the arterial environment.

Veins are exposed to the arterial environment during two common surgical procedures, creation of vein grafts and arteriovenous fistulae (AVF). In both cases, veins adapt to the arterial environment that is characterized by different hemodynamic conditions and increased oxygen tension compared with the venous environment. Successful venous adaptation to the arterial environment is critical for long-term success of the vein graft or AVF and, in both cases, is generally characterized by venous dilation and wall thickening. However, AVF are exposed to a high flow, high shear stress, low-pressure arterial environment and adapt mainly via outward dilation with less intimal thickening. Vein grafts are exposed to a moderate flow, moderate shear stress, high-pressure arterial environment and adapt mainly via increased wall thickening with less outward dilation. We review the data that describe these differences, as well as the underlying molecular mechanisms that mediate these processes. Despite extensive research, there are few differences in the molecular pathways that regulate cell proliferation and migration or matrix synthesis, secretion, or degradation currently identified between vein graft adaptation and AVF maturation that account for the different types of venous adaptation to arterial environments.

The mouse aortocaval fistula recapitulates human arteriovenous fistula maturation.

Several models of arteriovenous fistula (AVF) have excellent patency and help in understanding the mechanisms of venous adaptation to the arterial environment. However, these models fail to exhibit either maturation failure or fail to develop stenoses, both of which are critical modes of AVF failure in human patients. We used high-resolution Doppler ultrasound to serially follow mice with AVFs created by direct 25-gauge needle puncture. By day 21, 75% of AVFs dilate, thicken, and increase flow, i.e., mature, and 25% fail due to immediate thrombosis or maturation failure. Mature AVF thicken due to increased amounts of smooth muscle cells. By day 42, 67% of mature AVFs remain patent, but 33% of AVFs fail due to perianastomotic thickening. These results show that the mouse aortocaval model has an easily detectable maturation phase in the first 21 days followed by a potential failure phase in the subsequent 21 days. This model is the first animal model of AVF to show a course that recapitulates aspects of human AVF maturation.