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血管内皮功能对颈动脉支架植入术后再狭窄的影响
Effect of vascular endothelial function on restenosis after carotid artery stenting
收稿日期:  
DOI:10.3969/j.issn.1673-9701.2024.19.009
关键词:  颈动脉狭窄  颈动脉支架植入术  血管内皮功能  炎症反应  氧化应激反应
Key Words:
基金项目:浙江省金华市公益性技术应用研究项目(2022-4-162)
作者单位
王晓光 金华市人民医院影像科浙江金华 321000 
叶芳余 金华市人民医院影像科浙江金华 321000 
唐建红 金华市人民医院介入与血管外科浙江金华 321000 
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摘要:目的 探讨血管内皮功能对颈动脉支架植入(carotid artery stenting,CAS)术后再狭窄的影响。方法 选取2019年1月至2022年12月金华市人民医院接受CAS的236例颈动脉狭窄患者为研究对象,根据随访过程是否发生支架内再狭窄(in-stent restenosis,ISR)将其分为ISR组(n=41)和non-ISR组(n=195)。收集并比较两组患者的血脂指标[低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)、总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、高密度脂蛋白胆固醇(high-density lipoprotein cholesterol,HDL-C)]、血管内皮指标[血清内皮素(endothelin-1,ET-1)、血管性血友病因子(von Willebrand factor,vWF)、血管内皮生长因子(vascular endothelial growth factor,VEGF)、血管细胞黏附分子1(vascular cell adhesion molecule 1,VCAM-1)、血栓素B2(thromboxane B2,TXB2)、内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)及一氧化氮(nitric oxide,NO)]、炎症因子[肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、C反应蛋白(C-reactive protein,CRP)]和氧化应激指标[丙二醛(malondialdehyde,MDA)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、超氧化物歧化酶(superoxide dismutase,SOD)]。对ISR组和non-ISR组患者外周血进行转录组测序。采用多因素Logistic回归分析CAS术后发生ISR的独立影响因素。结果 ISR组患者的TC、TNF-、CRP、IL-6、MDA、ET-1、vWF、TXB2、VCAM-1均显著高于non-ISR组(P<0.01),HDL-C、SOD、GSH-Px、NO、eNOS和VEGF水平均显著低于non-ISR组(P<0.01)。转录组差异基因富集分析显示炎症反应激活、氧化应激反应、内皮细胞功能障碍等信号通路在ISR组显著增强;多因素Logistic回归分析结果显示,TNF-、IL-6、ET-1、vWF、VEGF、SOD、GSH-Px均是CAS术后发生ISR的独立影响因素(P<0.05)。结论 炎症因子、氧化应激指标和血管内皮功能三者共同促进颈动脉狭窄患者CAS术后ISR的发生发展;TNF-α、IL-6、ET-1、vWF、VEGF、SOD、GSH-Px均是CAS术后发生ISR的独立影响因素。
Abstract:Objective To investigate the effect of vascular endothelial function on restenosis after carotid artery stenting (CAS). Methods A total of 236 patients with carotid artery stenosis who received CAS in Jinhua People’s Hospital from January 2019 to December 2022 were selected as study objects. According to whether in-stent restenosis (ISR) occurred during follow-up, they were divided into ISR group (n=41) and non-ISR group (n=195). Blood lipid indexes [low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C)], vascular endothelial indexes [endothelin-1 (ET-1), von Willebrand factor (vWF), vascular endothelial growth factor (VEGF), vascular cell adhesion molecule 1 (VCAM-1), thromboxane B2 (TXB2), endothelial nitric oxide synthase (eNOS), nitric oxide (NO)], inflammatory factors [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP)] and oxidative stress indexes [malondialdehyde (MDA), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD)] were collected and compared between two groups. Transcriptome sequencing was performed on peripheral blood of ISR group and non-ISR group. Multivariate Logistic regression was used to analyze the independent influencing factors of ISR after CAS. Results The levels of TC, TNF-, CRP, IL-6, MDA, ET-1, vWF, TXB2 and VCAM-1 in ISR group were significantly higher than those in non-ISR group (P<0.01), and the levels of HDL-C, SOD, GSH-Px, NO, eNOS and VEGF in ISR group were significantly lower than those in non-ISR group (P<0.01). Transcriptome differential gene enrichment analysis showed that the signaling pathways such as inflammatory response activation, oxidative stress response, and endothelial cell dysfunction were significantly enhanced in ISR group. Multivariate Logistic regression analysis showed that TNF-, IL-6, ET-1, vWF, VEGF, SOD, and GSH-Px were independent influencing factors for ISR after CAS (P<0.05). Conclusion Inflammatory factors, oxidative stress indexes and vascular endothelial function jointly promoted the occurrence and development of ISR after CAS in patients with carotid artery stenosis. TNF-α, IL-6, ET-1, vWF, VEGF, SOD, GSH-Px were independent risk factors for ISR after CAS.
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