No abstract

Smoking is a major risk factor for abdominal aortic aneurysm (AAA). Among the components of smoke, nicotine is known to exert pro-atherosclerotic, prothrombotic, and proangiogenic effects on vascular smooth muscle cells (VSMCs). The current study was designed to investigate the mechanisms through which nicotine induces vascular wall dysfunction and to examine whether melatonin protects against nicotine-related AAA. Methods: In this study, an enzyme-linked immunosorbent assay (ELISA) was used to measure melatonin and TNF-α levels, as well as total antioxidant status (TAS), in patients with AAA. We established a nicotine-related AAA model and explored the mechanisms underlying the therapeutic effects of melatonin. Tissue histopathology was used to assess vascular function, while western blotting (WB) and immunofluorescence staining were performed to detect protein expression. Results: We observed melatonin insufficiency in the serum from patients with AAA, particularly smokers. Moreover, melatonin level was positively correlated with antioxidant capacity. In the in vivo model, nicotine accelerated AAA expansion and destroyed vascular structure. Furthermore, OPN, LC3II, p62, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), NF-κB p65, TNF-α, phosphorylated AKT, and phosphorylated mTOR levels were increased, in vivo, following nicotine treatment, while SM22α and α-SMA levels were reduced. Additionally, melatonin attenuated the effects of nicotine on AAA and reversed changes in protein expression. Moreover, melatonin lost its protective effects following bafilomycin A1-mediated inhibition of autophagy. Conclusion: Based on our data, melatonin exerts a beneficial effect on rats with nicotine-related AAA by downregulating the AKT-mTOR signaling pathway, improving autophagy dysfunction, and restoring the VSMC phenotype.

BackgroundEndovascular aneurysm repair (EVAR) is often seen as the first choice treatment for patients with abdominal aortic aneurysm (AAA), particularly high-risk patients, yet the long-term survival rate and improvement in quality of life are still unclear. In order to seek the value of EVAR to the entire healthcare field, we conducted a retrospective study to evaluate whether the improvement EVAR can truly bring to the quality of medical care in the era of value-based healthcare.MethodsWe included AAA patients who underwent surgical treatment in the Department of Vascular Surgery, First Hospital of China Medical University, from January 1, 2004, to December 31, 2019 and evaluated surgery procedure data, short-term and long-term mortality, complications, prognoses, and medical costs.ResultsWe analyzed 507 patients with AAA who underwent open repair (n = 232) or EVAR (n = 275) over a 15-year period. The operative time, blood loss, blood transfusion rate, and postoperative length of hospital stay of the EVAR group is significantly lower than which of the open repair group. Meanwhile, neither short-term nor long-term mortality rates shows significant differences between the two groups. On the other hand, the complication rate of the EVAR group was significantly higher than that of the open repair group. Lastly, the total cost of EVAR was significantly higher than that of open repair.ConclusionExisting evidence suggests that EVAR improves neither short-term nor long-term survival rate compared with open surgery. In contrast, the complication rate and the reintervention rate in the EVAR group were higher than those in the open surgery group. Moreover, the cost of EVAR and that paid by medical insurance were higher than those for open surgery. For patients with a long-life expectancy, in order to ensure that patients receive appropriate and effective care, surgeons should choose a suitable method that considers both the quality of medical care as well as the expense accordingly.