Background: We reviewed the results of endovascular aneurysm repair in patients from the Japanese Committee for Stentgraft Management registry to determine the significance of persistent type II endoleak (p-T2EL) and the risk of late adverse events, including aneurysm sac enlargement. Methods: The prospectively captured medical records of 17 099 patients <75 years of age who underwent endovascular aneurysm repair for abdominal aortic aneurysm from 2006 to 2015 were reviewed. Patients were divided into 2 groups (with or without p-T2EL) and compared to examine the correlation between p-T2EL and the occurrence of aneurysm sac enlargement after endovascular aneurysm repair. Results: Of the patients, 4957 (29.0%) had p-T2EL and 12 142 (71.0%) had no p-T2EL (non-T2EL). Mean age was significantly higher ( P <0.001), and there were fewer men ( P <0.001) in the p-T2EL group. Among comorbidities, hypertension ( P =0.019) and chronic kidney disease ( P =0.040) were more prevalent and respiratory disorders were less prevalent ( P <0.001) in the p-T2EL group. From each group, 4957 patients were matched according to propensity score to adjust for differences in patient characteristics. The cumulative incidence rates of abdominal aortic aneurysm–related mortality (p-T2EL: 52 of 4957 [1.0%] versus non-T2EL: 21 of 12 142 [0.2%]), rupture (p-T2EL: 38 of 4957 [0.8%] versus non-T2EL: 13 of 12 142 [0.1%]), sac enlargement (≥5 mm; p-T2EL: 1359 of 4957 [27.4%] versus non-T2EL: 332 of 12 142 [2.7%]), and reintervention (p-T2EL: 739 of 4957 [14.9%] versus non-T2EL: 91 of 12 142 [0.7%]) were significantly higher in the p-T2EL than the nonpT2EL group ( P <0.001). Propensity score matching yielded higher estimated incremental risk, including abdominal aortic aneurysm–related mortality, rupture, sac enlargement (≥5 mm), and reintervention for p-T2EL ( P <0.001). Cox regression analysis revealed older age ( P =0.010), proximal neck diameter ( P =0.003), and chronic kidney disease ( P <0.001) as independent positive predictors and male sex as an independent negative predictor ( P =0.015) of sac enlargement. Conclusions: The Japanese Committee for Stentgraft Management registry data show a correlation between p-T2EL and late adverse events, including aneurysm sac enlargement, reintervention, rupture, and abdominal aortic aneurysm–related mortality after endovascular aneurysm repair. Besides p-T2EL, older age, female sex, chronic kidney disease, and dilated proximal neck were associated with sac enlargement.

Background: Arteriovenous fistulae (AVF) are the gold standard for vascular access for hemodialysis. Although the vein must thicken and dilate for successful hemodialysis, excessive wall thickness leads to stenosis causing AVF failure. Since TGF-β (transforming growth factor-beta) regulates ECM (extracellular matrix) deposition and smooth muscle cell (SMC) proliferation—critical components of wall thickness—we hypothesized that disruption of TGF-β signaling prevents excessive wall thickening during venous remodeling. Methods: A mouse aortocaval fistula model was used. SB431542—an inhibitor of TGF-β receptor I—was encapsulated in nanoparticles and applied to the AVF adventitia in C57BL/6J mice. Alternatively, AVFs were created in mice with conditional disruption of TGF-β receptors in either SMCs or endothelial cells. Doppler ultrasound was performed serially to confirm patency and to measure vessel diameters. AVFs were harvested at predetermined time points for histological and immunofluorescence analyses. Results: Inhibition of TGF-β signaling with SB431542-containing nanoparticles significantly reduced p-Smad2–positive cells in the AVF wall during the early maturation phase (days 7–21) and was associated with decreased AVF wall thickness that showed both decreased collagen density and decreased SMC proliferation. SMC-specific TGF-β signaling disruption decreased collagen density but not SMC proliferation or wall thickness. Endothelial cell–specific TGF-β signaling disruption decreased both collagen density and SMC proliferation in the AVF wall and was associated with reduced wall thickness, increased outward remodeling, and improved AVF patency. Conclusions: Endothelial cell–targeted TGF-β inhibition may be a translational strategy to improve AVF patency.

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The object of the study is to determine the long-term outcomes of surgical treatment of patients with popliteal artery entrapment syndrome at a single institute. We retrospectively reviewed 19 limbs of 16 consecutive patients who underwent surgery for popliteal artery entrapment syndrome at our hospital over the past 36 years. The popliteal artery was stenotic in 11 limbs, occlusive in 7 limbs, and compressed and deviated by the medial head of the gastrocnemius muscle but not damaged in 1 limb. Six limbs were treated with autologous saphenous vein bypass, 10 with bypass or venous patch graft concomitant with musculotendinous section, and 3 limbs underwent musculotendinous section alone. The 10-year cumulative patency of the 13 limbs treated with bypass was 100%, although two of them showed occlusion at 23 and 12 years after surgery. One patient who received a venous patch graft showed occlusion 15 years after surgery. Additionally, one asymptomatic patient with an apparently non-damaged popliteal artery who received preventive musculotendinous section alone showed stenosis of the artery 2 years after musculotendinous section. In conclusion, the bypass patency observed in this study was excellent in the long term. Careful examination of popliteal artery anatomy using imaging studies is essential for selecting the appropriate surgical procedure for popliteal artery entrapment syndrome.