Objective: This study aimed to evaluate the effect of inferior mesenteric artery (IMA) embolization during endovascular aneurysm repair (EVAR) in patients at high risk of type II endoleak (T2EL) in randomized controlled trial (RCT). Summary Background Data: Several studies have demonstrated a reduction of T2EL by IMA embolization before EVAR. However, there have been no RCT confirming the efficacy of IMA embolization. Methods: Patients scheduled for elective EVAR between April 2014 and March 2018 were eligible. Patients at high risk of T2EL (IMA patency with IMA ≥3 mm, LAs ≥2 mm, or an aortoiliac-type aneurysm) were prospectively randomized to receive EVAR with or without IMA embolization. The primary endpoint was occurrence of T2EL during follow-up. Secondary endpoints included aneurysmal sac changes, adverse events from IMA embolization, and reintervention rate due to T2EL. This trial is registered with the University Hospital Medical Information Network, number UMIN000022147. Results: One hundred thirteen patients had high risk and 106 were randomized. In the intention-to-treat analysis, the incidence of T2EL was significantly lower in the embolization group [24.5% vs 49.1%; P = 0.009, absolute risk reduction = 24.5%; 95% confidence interval (CI), 6.2–40.5, number needed to treat = 4.1; 95% CI, 2.5–16.1]. The aneurysmal sac shrunk significantly more in the embolization group (−5.7 ± 7.3 mm vs −2.8 ± 6.6 mm; P = 0.037), and the incidence of aneurysmal sac growth related to T2EL was significantly lower in the embolization group (3.8% vs 17.0%; P = 0.030). There were no complications related to IMA embolization or reinterventions associated with T2EL. Conclusions: Our results demonstrated the effectiveness of IMA embolization during EVAR in high-risk patients for the prevention of T2EL, which is suggested for avoiding aneurysmal sac enlargement related to T2EL.

Patients with these risk factors are the candidates for undergoing treatment of preoperative IMA occlusion to reduce ELII.

Objective: We aimed to study venous leg ulcer (VLU) healing and recurrence rates of VLU using a self-care-based treatment strategy. Methods: The study included 36 patients (43 legs) who visited our clinic between April 2009 and June 2015 because of non-healing VLUs and who had been treated by us for more than a year (until June 2016). Patients or their caregivers were first provided instructions for performing the no-intentional-stretch bandaging technique using ordinary elastic bandages. Wounds were cleansed with tepid water daily, and bandages were re-applied by patients or their caregivers; this was continued until VLUs were healed. Compression was discontinued after healing, but was restarted if persistent swelling and/or dermatitis was noticed on their legs. Results: The median ulcer size was 6.5 cm 2 (range, 1-105 cm 2 ). The median number of clinic visits until healing was six (range, 3-35). The 6-and 12-month healing rates were 67% and 86%, respectively. Twenty (44%) legs required compression therapy after VLU healing. The cumulative recurrence-free rate at 60 months was 86%. Conclusion: Reasonable healing and recurrence rates were achieved by applying a self-care-based VLU treatment strategy.

Objective— Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease that is associated with persistent inflammation and extracellular matrix degradation. The molecular mechanisms underlying the macrophage-mediated progression of AAA remain largely unclear. Approach and Results— We show that focal adhesion kinase (FAK) expression and activity are enhanced in macrophages that are recruited to AAA tissue. FAK potentiates tumor necrosis factor-α–induced secretion of matrix-degrading enzymes and chemokines by cultured macrophages. FAK also promotes macrophage chemotaxis. In mice, the administration of a FAK inhibitor that tempers local macrophage accumulation markedly suppresses the development and progression of chemically induced AAA. Conclusions— FAK plays a key role in macrophage behavior, which underlies the chronic progression of AAA. These findings provide insights into AAA progression and identify FAK as a novel therapeutic target.

Objectives To investigate the adherence to and efficacy of different compression methods in elderly patients. Methods A retrospective review of compression therapy in 120 elderly patients (≥65 years) with chronic venous insufficiency was performed to study the initially preferred compression method, adherence to each method, and its efficacy. Results Initially, an oversize strong stocking (24%), an appropriate size moderate stocking (19%), and bandages (37%) were equally preferred. Adherence at 1 month was 69%, 96%, and 91%, respectively, and they reduced ankle circumferences in C3 patients by 1.8 ± 1.9 cm, 0.3 ± 1.7 cm, and 2.9 ± 1.7 cm, respectively. The improvement rates of C4 symptoms were 79%, 60%, and 91%, respectively. Only three patients (2%) preferred an appropriate size strong stocking. Conclusions In elderly patients, an appropriate size strong stocking was not preferred. The best adherence was achieved by using a moderate stocking, while the best efficacy was achieved by using bandages.

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Celiac stenosis may result in a pancreaticoduodenal artery aneurysm (PDAA). Celiac stenosis with a PDAA is rare and treatment guidelines are absent. Here, we report 4 cases of celiac stenosis treated using different methods. Of these, 3 involved PDAAs. The PDAAs were successfully treated with coil embolization. For celiac stenosis, we performed open surgery for decompression in 1 patient, stenting in 2 patients, and bypass grafting in 1 patient. In the patients who underwent stenting, stent-associated thrombosis occurred. PDAAs can be treated with coil embolization; however, treatment of celiac stenosis with the endovascular approach might be difficult.

Abdominal aortic aneurysm (AAA) is characterized by chronic inflammation, which leads to pathological remodeling of the extracellular matrix. Decorin, a small leucine-rich repeat proteoglycan, has been suggested to regulate inflammation and stabilize the extracellular matrix. Therefore, the present study investigated the role of decorin in the pathogenesis of AAA. Decorin was localized in the aortic adventitia under normal conditions in both mice and humans. AAA was induced in mice using CaCl2 treatment. Initially, decorin protein levels decreased, but as AAA progressed decorin levels increased in all layers. Local administration of exogenous decorin prevented the development of CaCl2-induced AAA. However, decorin was highly expressed in the degenerative lesions of human AAA walls, and this expression positively correlated with matrix metalloproteinase (MMP)-9 expression. In cell culture experiments, the addition of decorin inhibited secretion of MMP-9 in vascular smooth muscle cells, but had the opposite effect in macrophages. The results suggest that decorin plays a dual role in AAA. Adventitial decorin in normal aorta may protect against the development of AAA, but macrophages expressing decorin in AAA walls may facilitate the progression of AAA by up-regulating MMP-9 secretion.