ABSTRACT
@#Objective To analyze the short-term and long-term efficacy of staged coronary artery bypass grafting (CABG) and carotid artery stenting (CAS) compared with CABG alone in patients with coronary heart disease with preoperative history of stroke and carotid stenosis. Methods We reviewed the clinical data of 55 patients (48 males, 7 females, aged 67.62±7.06 years) with coronary heart disease and carotid stenosis who had a history of stroke and underwent CABG+CAS or CABG alone in Zhongshan Hospital from 2008 to 2017. There were 13 patients in the staged CABG+CAS group and 42 patients in the CABG alone group. The differences in the incidence of perioperative adverse events and long-term survival between the two groups were studied, and univariate and multivariate analyses were carried out to determine the independent risk factors of long-term adverse events. Results Perioperative adverse events occurred in 1 (7.69%) patient of the staged CABG+CAS group, and 4 (9.52%) patients of the CABG alone group (P=0.84). During the follow-up period (67.84±37.99 months), the long-term survival rate of patients in the staged CABG+CAS group was significantly higher than that in the CABG alone group (P=0.02). The risk of long-term adverse events in the staged CABG+CAS group was 0.22 times higher than that in the CABG alone group (95%CI 0.05-0.92, P=0.04). Conclusion Staged CABG+CAS can significantly improve the long-term survival prognosis without increasing the perioperative risk. It is a safe and effective treatment, but prospective randomized studies are still needed to further confirm this finding.
ABSTRACT
FSTL3 as adipokine takes part in dyslipidemia and inflammatory response, but the association of FSTL3 with atherosclerosis is unclear. This study indicated that FSTL3 showed significantly higher level (control: 7.68 ± 3.10 vs. AS: 9.29 ± 2.37 ng/mL; P < 0.001) in atherosclerosis, and FSTL3 expressed higher in plaque of ApoE knockout mice and located in macrophages. Oxidized low-density lipoproteins induced expression and secretion of FSTL3, meanwhile FSTL3 promoted lipid accumulation in macrophages. The advanced study found that FSTL3 upregulated CD36 and LOX-1 expression in a dose-dependent manner; however, FSTL3 also evoked interleukin 1-ß (IL1-ß), monocyte chemoattractant protein 1 (MCP-1), tumor necrosis factor-α, and matrix metalloproteinase-9 (MMP-9) secretion in macrophages. On the contrary, that downregulated FSTL3 attenuated expression of oxidized low-density lipoproteins induced CD36, LOX-1, and inflammatory cytokines expressing. All of these results demonstrated that FSTL3 as a novelty cytokine takes part in the process of atherosclerosis through increasing lipid accumulation and inflammation through regulating CD36 and LOX-1 expression.