Endovascular therapy has become the first choice for the treatment of aortoiliac occlusive disease due to its characteristics of minimally invasive, easy to tolerate, and satisfactory medium- and long-term patency rates. However, to improve the technical success rate and efficacy of endovascular surgery, attention must be paid to treatment strategies and technical details such as the approach selection, the recanalization of lesions, the vessel preparation, the reconstruction of the arteries, the protection of important branches, and the prevention of serious complications. The author has made a relatively comprehensive exposition based on the latest technological progress and personal experience, in order to provide reference and benefit to my young colleagues.

Background In patients with acute aortic dissection (AAD), increased vascular smooth muscle cell (VSMC) apoptosis has been found. Human cytomegalovirus (HCMV)-miR-US33-5p was significantly increased in the plasma of patients with AAD. However, the roles of miR-US33-5p in human aortic VSMC (HA-VSMC) apoptosis remain to be elucidated. Methods In the current study, cell apoptosis was analyzed by flow cytometry, cell proliferation by CCK-8 assay, and differentially expressed genes by RNA sequencing. Luciferase reporter assay was used for binding analysis between miR-US33-5p and endothelial PAS domain protein 1 (EPAS1), and EPAS1 and amino acid transporter heavy chain, member 2 (SLC3A2). The enrichment degree of SLC3A2 promoter DNA was analyzed by chromatin immunoprecipitation assay. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and immunoblotting were performed for measuring messenger RNA (mRNA) and protein levels, respectively. Results It was found that HCMV infection inhibited proliferation but promoted HA-VSMC apoptosis by upregulating HCMV-miR-US33-5p. Transfection of HCMV-miR-US33-5p mimics the significant effect on several signaling pathways including integrin signaling as shown in the RNA sequencing data. Western blotting analysis confirmed that HCMV-miR-US33-5p mimics suppression of the activity of key factors of the integrin signal pathway including FAK, AKT, CAS, and Rac. Mechanistic study showed that HCMV-miR-US33-5p bound to the 3′-untranslated region of EPAS1 to suppress its expression, leading to suppression of SLC3A2 expression, which ultimately promoted cell apoptosis and inhibited cell proliferation. This was confirmed by the findings that silencing EPAS1 significantly reduced the SLC3A2 expression and inhibited proliferation and key factors of integrin signal pathway. Conclusions HCMV-miR-US33-5p suppressed proliferation, key factors of integrin signal pathway, and EPAS1/SLC3A2 expression, but promoted HA-VSMC apoptosis. These findings highlighted the importance of HCMV-miR-US33-5p/EPAS1/SCL3A2 signaling and may provide new insights into therapeutic strategies for AAD.

目的 评估自主研发的Castor分支型主动脉覆膜支架（简称Castor支架）治疗累及左锁骨下动脉（LSA）的Stanford B型主动脉夹层的中期治疗效果。方法 选择2018年12月—2020年6月间在海军军医大学第一附属医院使用Castor支架行胸主动脉腔内修复术（TEVAR）的Stanford B型主动脉夹层患者70例，其中男64例、女6例，年龄为（60.02±13.03）岁。所有患者均于全身麻醉下行TEVAR。记录围手术期和随访期间主要观察指标和次要观察指标。主要观察指标为患者全因死亡及夹层逆撕、脑梗死等主动脉夹层相关不良事件。次要观察指标：术前测量主动脉夹层近端锚定区主动脉直径、LSA开口与主动脉夹层近端裂口距离、LSA开口与主动脉夹层近端边缘距离、LSA起始部直径、左颈总动脉（LCA）开口远端与LSA开口近端距离，手术完成情况、手术时间、术中对比剂使用量，住院时间、随访时间，内漏、支架闭塞等并发症情况，Castor支架主体近端及远端直径、分支支架直径，主动脉主体支架近端和远端放大率。结果 主要观察指标：围手术期3例患者发生主动脉夹层相关不良事件（夹层逆撕1例，脑梗死2例）,随访期间5例患者死亡（夹层逆撕破裂1例，呼吸衰竭1例，心力衰竭1例，脑出血2例）。次要观察指标：主动脉夹层近端锚定区主动脉直径为（31.63±3.16） mm, LSA开口与主动脉夹层近端裂口距离为（45.79±19.60）mm, LSA开口与主动脉夹层近端边缘距离为（8.14±14.37） mm, LSA起始部直径为（11.35±1.45） mm, LCA开口远端与LSA开口近端距离为（8.44±2.44） mm。所有患者均顺利完成手术。手术时间为（109.63±44.65） min,术中对比剂使用量为（200.79±35.11） mL,住院时间为（8.57±3.22） d,随访时间为（11.64±6.77）个月，6例患者失访。随访期间发生Ⅰb型内漏1例，分支支架闭塞1例。Castor支架主体近端直径为（32.43±3.45）mm、远端直径为（26.46±3.40）mm,分支支架直径为（10.92±4.08） mm。主动脉主体支架近端放大率为2.48%（0,3.45%）,主动脉主体支架远端放大率为0（-7.14%,4.35%）。结论 Castor分支型主动脉覆膜支架能够安全、有效地用于累及LSA的Stanford B型主动脉夹层的腔内治疗。

Objective: PGC-1 alpha achieves the protective effect of TNF-alpha-induced injury to human umbilical vein endothelial cells by inhibiting the Ca2+/NFAT pathway.Methods: Human umbilical vein endothelial cells were treated with 20, 40, and 80 ng/mL TNF-alpha to create three models with different degrees of cell injury. The human umbilical vein endothelial cells were cultured in vitro and transfected by interfering with the PGC-1 alpha RNA lentivirus. The silencing of the PGC-1 alpha gene was divided into two groups: the control group and the down-regulation of the PGC-1 alpha gene group. The effects of different concentrations of TNF-alpha on apoptosis of human umbilical vein endothelial cells were determined by flow cytometry. The expression of intracellular genes was detected by real-time quantitative PCR, and the expression of intracellular protein was measured by western blot assay. The concentrations of mtROS and Ca2+ were measured.Results: After human vein endothelial cells were treated for 24 h with different concentrations of TNF-alpha, the apoptosis rate gradually increased with the increase of TNF-alpha concentration, and the difference was statistically significant compared with the control group (P<0.05). The expression of PGC-1 alpha mRNA in each group was significantly lower than that of the control group after human venous endothelial cells were treated for 24 h of with different concentrations of TNF-alpha (P<0.05). After treatment with different concentrations of TNF-alpha, the relative expression rate of PGC-1 alpha protein in each group was remarkably lower than that in the control group (P<0.05). The expression of NFAT1 mRNA in the TNF-alpha 40 and 80 ng/mL treatment groups was significantly higher than that in the control group (P<0.05), and the expression of NFAT2 mRNA in different concentrations of the TNF-alpha treatment groups was markedly higher than that in the control group (P<0.05). The expression of NFAT1 protein in the TNF-alpha 40 and 80 ng/mL treatment groups was significantly higher than that in the control group (P<0.05), and the expression level of NFAT2 protein in different concentrations of TNF-alpha treatment group was clearly higher than that in the control group (P<0.05). The intracellular mROS and Ca2+ concentrations were significantly higher than that in the control group after the down-regulation of the PGC-1 alpha gene expression (P<0.05). After down-regulating the expression of the PGC-1 alpha gene, the levels of NFAT1, NFAT2, mRNA, and protein in the cells were significantly higher than those in the control group (P<0.05).Conclusion: 20, 40, and 80 ng/mL of TNF-alpha can induce different degrees of human umbilical vein endothelial cell injury. PGC-1 alpha has a protective effect on this kind of cell injury, and its related mechanism may be to inhibit the Ca2+/NFAT signalling pathway by reducing the intracellular mtROS concentration, and thus to protect damaged cells.

Objective To observe the long-term efficacy of human fibrin sealant (FS) in the treatment of proximal type Ⅰ endoleak after endovascular aneurysm repair (EVAR) in abdominal aortic aneurysm (AAA).Methods The clinical data of 104 AAA patients with proximal type Ⅰ endoleak receiving EVAR + FS in Changhai Hospital from 2003 to 2012 was retrospectively analyzed,among those 77 cases were with less than 15 mm proximal neck,21 cases with greater than 60 degrees proximal neck angulation,37 cases with severe calcification or thrombosis in proximal neck.After failure of conventional endoleak therapy FS was injected through AAA catheter and long-term efficacy was evaluated by CTA during the follow-up.Results Intra-sac pressure decreased significantly after FS injection.Three patients (2.9％)died perioperatively.Postoperative 1'-,3' and 5 year survival rate was 91.8％,80.6％ and 60.2％respectively.Maximum diameter of AAA decreased from (58.78 ± 13.41) mm to (52.6-± 12.2) mm.There was no FS injection related complications.Conclusion Intra-sac injection of FS is an effective,economical and safe method for treating post-EVAR endoleak,especially for AAA with relatively short and twisted aneurysm neck.

住院患者静脉血栓栓塞症(VTE)可以有效预防.上海长海医院在原有基础上,根据国内外学术进展、实践经验、专家共识和临床需求,修订为指导院内各科室应用的新版《院内VTE预防指南》,包含上海长海医院院内VTE综合防治管理体系,住院患者VTE防治管理制度,VTE防治流程及具体做法,住院患者VTE风险评估及评分表,出血风险评估,VTE预防措施及注意事项等,为有效减少院内住院患者VTE的发生起到重要作用.有助于各类医院进行标准化推广及信息化应用.

下肢静脉曲张是血管外科常见病,传统的高位结扎+剥脱术虽然疗效确切,但该术式具有创伤大、术中出血量多、恢复慢等缺陷[1].随着外科手术技术的不断发展更新,创伤更小的手术方式如泡沫硬化剂、激光等[2],使大隐静脉曲张的治疗不断趋向微创化.近年来采用硬化剂注射治疗下肢静脉曲张,逐渐成为静脉曲张主要手术方式之一,硬化剂注射治疗具有经济、微创、恢复快、疗效较好、并发症发生率低等优点,但在临床实际工作中仍会遇到相关并发症的发生,现将长海医院血管科收治的1例硬化剂注射治疗致下肢动脉栓塞的病例报告如下.

目的 探讨3D打印技术在血管外科主动脉扩张性疾病临床教学中的应用.方法 将2015年6月-2016年5月在我科学习的73名住院医师分为传统方法教学组(传统教学组)和3D打印辅助教学组(3D打印教学组),结合本院住院医师规范化培训和研究生临床教学大纲的要求,选取5例典型的主动脉扩张性疾病病例,根据术前CT影像数据,应用3D打印技术制作出主动脉病变部位的三维模型,并据此同时打印出腔内支架移植物,进而模拟腔内隔绝手术.结果 3D打印教学组在对血管系统解剖结构的了解、对主动脉扩张性疾病特征的了解、对腔内手术器具和过程的了解、学习的主动性和自信心方面均优于传统教学组(P<0.05),在平均手术时间方面短于传统教学组(P<0.05),在模拟手术的效果方面优于传统教学组(P<0.01).结论 3D打印技术对于主动脉扩张性疾病腔内治疗的临床教学具有重要的促进意义,有良好的应用前景.

Objective To evaluate popliteal artery local technique in superficial femoral artery antegrade subintimal recanalization.Methods From January 2009 to Dec 2011,550 limbs in 476 TASC (Trans-Atlantic Inter-Society Consensus) Ⅱ C/D cases underwent endo-therapy at our department.The success rate、operation time、symptom progress and follow up were analyzed retrospectively.Results In the 550 limbs,62 limbs received popliteal artery local technique directly.There was 9 technical failures.Procedures succeeded in 53 limbs(85.5％ ).The average operation time was (69 ±24) min,(1.8 ±0.6) stents were used and the main covered length was ( 33 ± 6) cm.Symptoms of 46 limbs was improved and unchanged in 6,amputation needed to be done in one limb.One year follow up accomplished for 39 limb.The 6 and 12 months patence rate was 87.1％ and 69.2％.For 488 limbs using traditional approach 378 achieved anti-grade recanalization,the average operation time was ( 89 ± 30) min,average (2.1 ± 0.6) stents were used and the main covered length is (31 ± 13) cm.Symptom in 300 limbs improved.The half and one year patence rate in 292 limbs was 92.1％ and 61.0％.Conclusions The popliteal artery local technique is as effective as with traditional approach and is time saving.