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.

Standardized Methodology for Duplex Ultrasound Examination of Arteriovenous Access for Hemodialysis: A Proposal of the French Society of Vascular Medicine and the French-Speaking Society of Vascular Access.

Duplex ultrasound (DUS) is an essential tool for characterizing and monitoring arteriovenous (AV) access for hemodialysis. The aim of the work described here, requested by the French Society of Vascular Medicine in collaboration with the French-Speaking Vascular Access Society, is to propose a standardized methodology for performing and documenting DUS, taking into account the variety of AV access techniques and the problems routinely encountered. A steering committee reviewed the literature and selected the relevant references. A draft was prepared, and all items with missing or conflicting data were submitted to a Delphi consensus. The final document was discussed and approved by all participants. The principles of DUS evaluation of AV access consist of examination of the afferent artery, the anastomosis and the entire venous drainage system. DUS uses B-mode ultrasound, color flow, pulsed wave and power Doppler analysis. DUS can be used in a variety of clinical situations, which can directly influence the methodology of the examination and the interpretation of the results. Blood flow should be assessed as it correlates with the risk of thrombosis. The measurement should be adapted to the different anatomical and hemodynamic conditions encountered. Characterization of stenosis should take into account the residual diameter of the drainage vein and its hemodynamic consequences. Other complications can be assessed with a standardized DUS examination. When performed according to a rigorous methodology, DUS of the AV access allows a comprehensive assessment of its functionality and eliminates the need for further invasive diagnostic procedures.

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.

Plasmatic osteopontin and vascular access dysfunction in hemodialysis patients: a cross-sectional, case-control study (The OSMOSIS Study).

BACKGROUND AND AIMS: Despite close follow-up of patients with native arteriovenous fistulas (AVFs), up to 10% experience thrombosis each year. The OSMOSIS Study (Osteopontin as a Marker of Stenosis) tested the hypothesis that the systemic osteopontin level, a pro-inflammatory mediator related to vascular remodelling and intimal hyperplasia, increases in AVF stenosis, and may be used in clinical surveillance. METHODS: Our cross-sectional study compared the level of plasmatic osteopontin (pOPN) between patients with a well-functioning AVF (control group) and patients who required revision of their AVF due to stenosis (stenosis group). Blood samples were collected before dialysis (control group) or before intervention (stenosis group) from the AVF arm, and from the opposite arm as a within-subject control. pOPN level was measured by enzyme-linked immunosorbent assay. RESULTS: A total of 76 patients were included in the study. Baseline characteristics were similar between the groups (mean age, 70 years; men, 63%; AVF duration, 39 months), apart from prevalence of type 2 diabetes (T2D) (control group, 33%; stenosis group, 57%; p = 0.04). pOPN levels were similar between the AVF arm and the contralateral arm (551 ± 42 ng/mL vs. 521 ± 41 ng/mL, respectively, p = 0.11, paired t-test). Patients in the stenosis group displayed a higher pOPN level than patients in the control group (650.2 ± 59.8 ng/mL vs. 460.5 ± 61.2, respectively, p = 0.03; two-way ANOVA). T2D was not identified as an associated factor in a multivariate analysis (p = 0.50). CONCLUSIONS: The level of pOPN in hemodialysis patients was associated with the presence of AVF stenosis requiring intervention. Thus, its potential as a diagnostic biomarker should be assessed in a vascular access surveillance program.

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.

Evidences of a Direct Relationship between Cellular Fuel Supply and Ciliogenesis Regulated by Hypoxic VDAC1-ΔC.

Metabolic flexibility is the ability of a cell to adapt its metabolism to changes in its surrounding environment. Such adaptability, combined with apoptosis resistance provides cancer cells with a survival advantage. Mitochondrial voltage-dependent anion channel 1 (VDAC1) has been defined as a metabolic checkpoint at the crossroad of these two processes. Here, we show that the hypoxia-induced cleaved form of VDAC1 (VDAC1-ΔC) is implicated in both the up-regulation of glycolysis and the mitochondrial respiration. We demonstrate that VDAC1-ΔC, due to the loss of the putative phosphorylation site at serine 215, concomitantly with the loss of interaction with tubulin and microtubules, reprograms the cell to utilize more metabolites, favoring cell growth in hypoxic microenvironment. We further found that VDAC1-ΔC represses ciliogenesis and thus participates in ciliopathy, a group of genetic disorders involving dysfunctional primary cilium. Cancer, although not representing a ciliopathy, is tightly linked to cilia. Moreover, we highlight, for the first time, a direct relationship between the cilium and cancer cell metabolism. Our study provides the first new comprehensive molecular-level model centered on VDAC1-ΔC integrating metabolic flexibility, ciliogenesis, and enhanced survival in a hypoxic microenvironment.

Artery to vein configuration of arteriovenous fistula improves hemodynamics to increase maturation and patency.

Arteriovenous fistulae (AVF) are the preferred mode of hemodialysis access, but 60% of conventional [vein-to-artery (V-A)] AVF fail to mature, and only 50% remain patent at 1 year. We previously showed improved maturation and patency in a pilot study of the radial artery deviation and reimplantation (RADAR) technique that uses an artery-to-vein (A-V) configuration. Here, we show that RADAR exhibits higher rates of maturation, as well as increased primary and secondary long-term patencies. RADAR is also protective in female patients, where it is associated with decreased reintervention rates and improved secondary patency. RADAR and conventional geometries were compared further in a rat bilateral carotid artery-internal jugular vein fistula model. There was decreased cell proliferation and neointimal hyperplasia in the A-V configuration in male and female animals, but no difference in hypoxia between the A-V and V-A configurations. Similar trends were seen in uremic male rats. The A-V configuration also associated with increased peak systolic velocity and expression of Kruppel-like factor 2 and phosphorylated endothelial nitric oxide synthase, consistent with improved hemodynamics. Computed tomography and ultrasound-informed computational modeling showed different hemodynamics in the A-V and V-A configurations, and improving the hemodynamics in the V-A configuration was protective against neointimal hyperplasia. These findings collectively demonstrate that RADAR is a durable surgical option for patients requiring radial-cephalic AVF for hemodialysis access.

Identification of a new aggressive axis driven by ciliogenesis and absence of VDAC1-ΔC in clear cell Renal Cell Carcinoma patients.

Rationale: Renal cell carcinoma (RCC) accounts for about 2% of all adult cancers, and clear cell RCC (ccRCC) is the most common RCC histologic subtype. A hallmark of ccRCC is the loss of the primary cilium, a cellular antenna that senses a wide variety of signals. Loss of this key organelle in ccRCC is associated with the loss of the von Hippel-Lindau protein (VHL). However, not all mechanisms of ciliopathy have been clearly elucidated. Methods: By using RCC4 renal cancer cells and patient samples, we examined the regulation of ciliogenesis via the presence or absence of the hypoxic form of the voltage-dependent anion channel (VDAC1-ΔC) and its impact on tumor aggressiveness. Three independent cohorts were analyzed. Cohort A was from PREDIR and included 12 patients with hereditary pVHL mutations and 22 sporadic patients presenting tumors with wild-type pVHL or mutated pVHL; Cohort B included tissue samples from 43 patients with non-metastatic ccRCC who had undergone surgery; and Cohort C was composed of 375 non-metastatic ccRCC tumor samples from The Cancer Genome Atlas (TCGA) and was used for validation. The presence of VDAC1-ΔC and legumain was determined by immunoblot. Transcriptional regulation of IFT20/GLI1 expression was evaluated by qPCR. Ciliogenesis was detected using both mouse anti-acetylated α-tubulin and rabbit polyclonal ARL13B antibodies for immunofluorescence. Results: Our study defines, for the first time, a group of ccRCC patients in which the hypoxia-cleaved form of VDAC1 (VDAC1-ΔC) induces resorption of the primary cilium in a Hypoxia-Inducible Factor-1 (HIF-1)-dependent manner. An additional novel group, in which the primary cilium is re-expressed or maintained, lacked VDAC1-ΔC yet maintained glycolysis, a signature of epithelial-mesenchymal transition (EMT) and more aggressive tumor progression, but was independent to VHL. Moreover, these patients were less sensitive to sunitinib, the first-line treatment for ccRCC, but were potentially suitable for immunotherapy, as indicated by the immunophenoscore and the presence of PDL1 expression. Conclusion: This study provides a new way to classify ccRCC patients and proposes potential therapeutic targets linked to metabolism and immunotherapy.

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.

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.

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.

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.

Long-term functional outcomes and subclavian vein patency in patients undergoing thoracic outlet surgery for Paget-Schroetter Syndrome.

BACKGROUND: To assess subclavian vein (SCV) patency and long-term functional outcomes following surgical decompression of the thoracic outlet (SDTO) for Paget-Schroetter Syndrome (PSS). METHODS: Between January 1978 and January 2013, we identified 33 patients with PSS who underwent SDTO. Demographic, clinical and radiological data were extracted from electronic databases and patient records. All patients were invited to update their follow-up data during dedicated outpatient visits between October and December 2013. Outcome measures included long-term SCV patency and clinical success rates during follow-up. Clinical success was defined as the combined absence of functional symptoms and patient's ability to maintain normal professional activities at final follow-up. The QuickDASH score was also determined. RESULTS: The study population comprised 17 men and 16 women (mean age 34 years; range: 14-53 years) with PSS. Diagnosis was reached by venography (29 cases) or duplex scan (4 cases). SDTO was performed via the transaxillary route (25 cases) or using the combined supra-infraclavicular approach (8 cases). The procedure was carried out within 10 days in 13 patients (early-group), and between 30 to 120 days in the remaining 20 patients (late-group). The former had SCV recanalization obtained actively by thrombolysis (3 cases), thrombectomy (9 cases) or endovenectomy followed by patch venoplasty (1 case). The latter were maintained under chronic oral anticoagulation to allow SCV recanalization. There was neither postoperative death nor major bleeding complications. At a median follow-up of 240 months, 11 SCV remained patent in the early group, while in the other there was 3 re-occlusions, 4 residual stenoses and 5 chronic SCV occlusions. Clinical success was achieved in 73% of patients for the whole cohort, but was significantly better in patients operated on in the early stages (100% vs. 55%; P=0.005). The mean Quick Disabilities of the Arm, Shoulder, and Hand Score was 3.5 (95% CI: 1.5-5.4) in the early-group and 17.3 (95% CI: 8.4-26.2) in the late-group (P=0.01). CONCLUSIONS: Our data shows that long-term functional outcomes and SCV patency remained better in PSS patients who underwent early SDTO and active SCV recanalization techniques.

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.