Outcomes of open and endovascular repair of inflammatory abdominal aortic aneurysms.

Objective Reports on inflammatory aortic abdominal aneurysm treatment are scarce. Traditionally, open surgery has been validated as the gold standard of treatment; however, high technical skills are required. Endovascular aortic repair has been suggested as a less invasive treatment by some authors offering good results. The purpose of our study was to report our experience and outcomes in the treatment of inflammatory aortic abdominal aneurysm using both approaches. Material and methods A retrospective review and data collection of all patients treated for inflammatory aortic abdominal aneurysm between 2000 and 2015 was done in one academic center. Diagnosis of inflammatory aortic abdominal aneurysm was based on preoperative CT-scan imaging. Type of treatment, postoperative and long-term morbidity and mortality are described. Abdominal compressive symptoms (hydronephrosis) severity and relief after treatment are described. Results Thirty-four patients with intact inflammatory aortic abdominal aneurysm were included. Twenty-nine (85.3%) patients were treated by open means and the remaining five (14.7%) with endovascular aortic repair. Nearly 90% were considered high-risk patients. Median follow-up was 46 months (range 24-112). The two groups were comparable, except for the age and preoperative hydronephrosis. There was no statistical significance in blood transfusion requirements, intensive care hospitalization, 30-day and long-term mortality between the two groups. Preoperative hydronephrosis was diagnosed in four (13.8%) patients in the open surgery group and three (60%) patients in the endovascular aortic repair group. Improvement of hydronephrosis was recognized in three out of the four patients in the open repair group and two out of the three in the endovascular aortic repair group. Renal function remained stable in both groups during follow-up. Conclusions Open surgery remains a safe and valid option for the treatment of inflammatory aortic abdominal aneurysm. Although our study included a small number of patients with endovascular aortic repair treatment, results are promising. Further randomized controlled studies may be necessary to assess long-term effectiveness of endovascular aortic repair treatment in this disease.

Cardiotrophin-1 Regulates Adipokine Production in 3T3-L1 Adipocytes and Adipose Tissue From Obese Mice.

Cardiotrophin-1 (CT-1) belongs to the IL-6 family of cytokines. Previous studies of our group revealed that CT-1 is a key regulator of glucose and lipid metabolism. The aim of the present study was to analyze the in vitro and in vivo effects of CT-1 on the production of several adipokines involved in body weight regulation, nutrient metabolism, and inflammation. For this purpose, 3T3-L1 adipocytes were incubated with recombinant protein CT-1 (rCT-1) (1-40 ng/ml) for 1 and 18 h. Moreover, the acute effects of rCT-1 administration (0.2 mg/kg, i.v.) for 30 min and 3 h on adipokines levels were also evaluated in high-fat fed obese mice. In 3T3-L1 adipocytes, rCT-1 treatment downregulated the expression and secretion of leptin, resistin, and visfatin. However, rCT-1 significantly stimulated apelin mRNA and secretion. rCT-1 (18 h) also promoted the activation by phosphorylation of AKT, ERK 1/2, and STAT3. Interestingly, pre-treatment with the PI3K inhibitor LY294002 reversed the stimulatory effects of rCT-1 on apelin expression, suggesting that this pathway could be mediating the effects of rCT-1 on apelin production. In contrast, acute administration of rCT-1 (30 min and 3 h) to diet-induced obese mice downregulated leptin and resistin, without significantly modifying apelin or visfatin mRNA in adipose tissue. Furthermore, CT-1 null mice exhibited altered expression of adipokines in adipose tissue. The present study demonstrates that rCT-1 modulates the production of adipokines in vitro and in vivo, suggesting that the regulation of the secretory function of adipocytes could be involved in the metabolic actions of this cytokine. J. Cell. Physiol. 232: 2469-2477, 2017. © 2016 Wiley Periodicals, Inc.