第一部分 外科辅助原位针刺开窗技术治疗复杂主动脉弓部病变

目的 评估原位针刺开窗技术治疗复杂主动脉弓部病变的中期疗效。方法 回顾性分析2017年10月至2019年9月应用原位针刺开窗技术治疗的13例主动脉夹层患者的临床资料。结果 13例患者均采用主动脉覆膜支架进行原位开窗，其中8例患者行弓上二分支重建，5患者行弓上三分支重建，技术成功率100%（13/13）；1例患者术后4个月突发脑出血死亡，其余12例患者获得随访 至2020年12月，平均随访时间23.3±0.7个月；手术后再发夹层并发症发生率 15.4%（2/13），其中 1例患者6个月出现逆撕，行升主动脉置换术；1例患者术后1个月出现颈动脉夹层，无不适表现，未做特殊处理。 结论 需重建多分支的复杂主动脉弓部病变，经颈部切口原位开窗技术进行重建可以取得良好的中期效果。

第二部分 外翻式颈动脉内膜剥脱术与补片式颈动脉内膜剥脱术10年随访结果比较

目的 比较补片式颈动脉内膜剥脱术（patch carotid endarterectomy，p-CEA）与外翻式颈动脉内膜剥脱术（eversion carotid endarterectomy，e-CEA）的长期疗效。方法 回顾性分析2009年10月至2015年10月在北京协和医院血管外科接受颈动脉内膜剥脱手术治疗的372例次颈动脉狭窄患者的临床资料（p-CEA=193例，e-CEA=179例），重点比较两种手术方式远期的全因死亡、心梗、所用卒中及手术同侧卒中发生率，以及症状复发率。结果 共纳入340例患者372例次手术，两组基线结果比较显示p-CEA组患者高脂血症比例高于e-CEA组（46.1%比34.6%，P=0.032）。在133个月的随访期间，p-CEA组与e-CEA组的死亡率为17.8%比13.8%（P=0.4855），心梗发生率7.8%比5.9%（P=0.360），所有卒中率12.8%比15.6%（P=0.228），手术同侧卒中率4.3%比5.9%（P=0.282），以及术后症状复发（P=0.85）均无统计差异。Kaplan-Meier分析显示，在第6年，两组之间术后再狭窄和术后死亡无显著差异（分别为P=0.87和P=0.18）；在第8年，两组之间术后死亡和卒中无显著差异（分别为P=0.34和P=0.24）。结论 p-CEA组和e-CEA组的远期死亡、心梗、所有的卒中和手术同侧卒中，以及术后症状复发上无显著差异。p-CEA和e-CEA均是治疗颈动脉狭窄的有效方法。

第三部分 通过基因集合富集分析鉴定ITGAX和CCR1等作为动脉粥样硬化的潜在生物标志物

目的 动脉粥样硬化(AS)是世界范围内老年人口中一种危及生命的疾病。然而，AS的分子和基因调控机制尚不清楚。本研究旨在确定人类动脉粥样硬化斑块与正常组织之间的基因表达差异。方法 表达谱数据集GSE43292来自基因表达综合数据库(GEO)数据集。通过GEO2R鉴定了动脉粥样硬化斑块与正常组织之间的差异表达基因(DEGs)，并通过GSEA对DEGs进行了功能注释。利用细胞景观的字符串和MCODE插件构建蛋白相互作用(PPP)网络，分析核心基因。最后，采用定量聚合酶链反应(qPCR)对核心基因进行验证。结果 共筛选134例。功能注释表明，这些DEGs主要富集于鞘脂代谢、细胞凋亡、溶酶体等方面。从PPI网络中鉴定出6个核心基因：ITGAX、CCR1、IL1RN、CXCL10、CD163和MMP9。qPCR分析显示，6个核心基因的相对表达水平显著升高。结论 我们利用生物信息学技术鉴定了6 个核心基因： ITGAX 、CCR1 、IL1RN 、CXCL10、CD163和MMP9。这些核心基因是AS潜在的有前途的诊断和治疗靶点。

Part I

Objective: To evaluate the mid-term results of surgery-assisted in-situ needle fenestration technique in complicated aortic arch lesion. Methods: Clinical data were retrospectively collected and analyzed from 13 patients who were diagnosed with complicated aortic dissection (AD) between October 2017 and September 2019. All the patients underwent endovascular repair by the surgery-assisted in-situ needle fenestration technique. Results: The technical success rates were 100% (13/13). The postoperative complication rate was 15.4% (2/13). One patient was performed with ascending aortic replacement due to the retrograde tear of the AD in the 6th month. Another patient suffered carotid artery dissection in the first postoperative month but was treated with conservative observation. Endovascular repair of two supra-arch branches were performed in 8 patients while the other 5 patients underwent three supra-arch branches reconstruction. The average follow-up period were 23.3±0.7 months, during which one patient died of cerebral hemorrhage in the 4th month. Conclusion: For complex multiple branches lesions in aortic arch, promising prognosis were shown with the treatment of surgery-assisted in-situ needle fenestration technique.

Part II  

Objective: To compare the long-term effects of patch carotid endarterectomy (p-CEA) and eversion carotid endarterectomy (e-CEA). Methods: A retrospective analysis of the clinical data of 372 patients with carotid artery stenosis who underwent carotid endarterectomy at the Department of Vascular Surgery of Peking Union Medical College Hospital from October 2009 to October 2015 (p-CEA=193 cases, e-CEA) =179 cases), focusing on the comparison of the long-term all-cause mortality, myocardial infarction, the incidence of stroke used and the stroke on the same side of the operation, and the rate of symptom recurrence between the two surgical methods.Results: A total of 340 patients with 372 operations were included. The baseline results of the two groups showed that the proportion of patients with hyperlipidemia in the p-CEA group was higher than that in the e-CEA group (46.1% vs. 34.6%, P=0.032). During the 133-month follow-up period, the mortality rate of the p-CEA group and the e-CEA group was 17.8% vs. 13.8% (P=0.4855), and the incidence of myocardial infarction was 7.8% vs. 5.9% (P=0.360). All stroke rates There was no statistical difference between 12.8% and 15.6% (P=0.228), 4.3% and 5.9% (P=0.282) of stroke on the same side of surgery (P=0.282), and ratio of postoperative symptom recurrence（P=0.85）. Kaplan-meier analysis showed no significant difference in postoperative restenosis and postoperative death between the two groups at year 6 [(P=0.87 and P=0.18, respectively); and no significant difference in postoperative death and stroke between the two groups at year 8 (P=0.34 and P=0.24, respectively). Conclusion: There were no significant differences in the long-term death, myocardial infarction, all strokes and strokes on the same side of the operation, and the recurrence of postoperative symptoms between the p-CEA group and the e-CEA group. Both p-CEA and e-CEA are effective methods to treat carotid artery stenosis.

Part III  

of atherosclerosis via Gene Set Enrichment Analysis

Objective: Atherosclerosis (AS) is a life-threatening disease in aging populations worldwide. However, the molecular and gene regulation mechanisms of AS are still unclear. This study aimed to identify gene expression differences between atheroma plaques and normal tissues in humans. Methods: The expression profiling dataset GSE43292 was obtained from the Gene Expression Omnibus (GEO) dataset. The differentially expressed genes (DEGs) were identified between the atheroma plaques and normal tissues via GEO2R, and functional annotation of the DEGs was performed by GSEA. STRING and MCODE plug-in of Cytoscape were used to construct a protein–protein interaction (PPI) network and analyze hub genes. Finally, quantitative polymerase chain reaction (qPCR) was performed to verify the hub genes. Results: Overall, 134 DEGs were screened. Functional annotation demonstrated that these DEGs were mainly enriched in sphingolipid metabolism, apoptosis, lysosome, and more. Six hub genes were identified from the PPI network: ITGAX, CCR1, IL1RN, CXCL10, CD163, and MMP9. qPCR analysis suggested that the relative expression levels of the six hub genes were significantly higher in AS samples.Conclusions: We used bioinformatics to identify six hub genes: ITGAX, CCR1, IL1RN, CXCL10, CD163, and MMP9. These hub genes are potential promising diagnostic and therapeutic targets for AS.