Objective To update available evidence on safety and efficacy of carotid endarterectomy (CEA) versus carotid artery stenting (CAS) in treatment of carotid artery stenosis by a meta-analysis of randomized controlled trials (RCTs). Methods A comprehensive search was performed of PubMed, EMBASE, Cochrane Library, Web of science, WanFang, and CNKI databases (from January 1990 to July 2015), to collect articles and past systematic reviews, and then abstraced lists of recent scientific conferences which were related with safety and efficacy of CEA versus CAS in treatment of carotid artery stenosis. At last, Meta analysis was performed by RevMan 5.1 software. Results Fifteen RCTs enrolling 9 828 patients were included in the Meta-analysis. Compared with CAS, CEA was associated with a significantly lower incidences of any stroke or death within 30 days after surgery (OR=0.63, 95% CI: 0.51-0.77, P＜0.05) and any stroke or death during follow-up, or ipsilateral stroke after 30 days of operation (OR=0.61, 95% CI: 0.48-0.76, P＜0.05）, but associated with a significantly greater incidences of myocardial infarction (OR=1.81, 95% CI: 1.14-2.87, P=0.01) and cranial neuropathy (OR=18.28, 95% CI: 7.99-41.82, P＜0.05) within 30 days after surgery. Conclusion In comparison with CAS, CEA is associated with a lower incidences of stroke or death and a greater incidence of myocardial infarction and cranial neuropathy within 30 days after surgery, and was associated with a significantly lower incidence of any stroke or death during follow-up, or ipsilateral stroke after 30 days of operation. So the results of Meta-analysis support continued use of CEA as the standard method in treatment of carotid artery stenosis.
ObjectiveTo investigate the pivotal role and key molecular mechanisms of aortic dissection (AD) pathogenesis, providing novel perspectives for early diagnosis and treatment. Methods The relevant literature on domestic and foreign research in recent years was summarized. ResultsVascular aging constitutes a fundamental pathological basis for AD, genic abnormalities (e.g., Gene 33, CEBPB, IGFBP-3) and signal pathway dysregulation(e.g., Notch, ferroptosis) are important to genesis of AD. ConclusionAD pathogenesis is intimately linked to vascular aging. Targeting aging-associated genes or pathways may emerge as innovative strategies for AD prevention and management. Further clinical translational research is warranted to establish the safety and therapeutic efficacy.