老年Stanford A 型主动脉夹层外科治疗*

目的:总结老年Stanford A型主动脉夹层外科治疗经验,探讨手术方式的选择,以提高手术疗效。方法:2008年9月至2011年5月对31例老年Stanford A型主动脉夹层行手术治疗,根据夹层破口位置、累及范围、主动脉根部病变情况采取相应术式,W-heat手术2例,David+全弓置换+支架象鼻术3例,Bentall+全弓置换+支架象鼻术9例,改良Wheat+全弓置换+支架象鼻术1例,升主动脉+全弓置换+支架象鼻术16例。同时行冠状动脉旁路移植术4例,心包剥脱术1例。结果:全组体外循环(221±43)min,平均心肌阻断(132±41)min,深低温停循环(47±12)min。术后并发症12例(38.7%),其中2例死亡,8例治愈(66.7%),2例术后出现肾功能衰竭家属放弃治疗。全组病人出院前复查主动脉CTA,见升主动脉、弓部人工血管血流通畅,支架位置正常,无明显移位。支架远端降主动脉假腔闭合率87.1%。随访2~35个月,术后近期死亡1例(3.2%),无再次手术者。结论:对老年StanfordA型主动脉夹层这一高危人群,术中根据其病变部位施行最佳的外科手术方式,可明显降低死亡率,改善患者预后。     

覆膜支架腔内修复术对Stanford B型主动脉夹层动脉瘤患者术后血清血管内皮生长因子、核因子-κB水平的影响

目的:分析覆膜支架腔内修复术对Stanford B型主动脉夹层动脉瘤患者术后血清血管内皮生长因子(VEGF)、核因子-κB(NF-κB)水平的影响。方法:选取2015年6月～2017年6月空军军医大学第一附属医院收治的150例Stanford B型主动脉夹层动脉瘤患者,根据治疗方法不同分为两组。对照组(75例)采用药物治疗,观察组(75例)采用覆膜支架腔内修复术治疗,对比两组治疗前后血清血管内皮生长因子(VEGF)、核因子-KB(NF-κB)、白细胞介素-1β(IL-1β)、干扰素-γ(IFN-γ)、急性生理和慢性健康状况(Acute physiology and chronic health evaluation,APACHEⅡ)评分、SF-36量表评分的变化,并发症(内漏、动脉栓塞、左上肢乏力、支架后移等)发生情况,再次手术或介入治疗发生率及病死率。结果:治疗后,观察组血清VEGF、NF-κB、IL-1β、IFN-γ水平显著低于对照组(P0.05);两组治疗后APACHEⅡ评分均较治疗前降低,SF-36量表评分均较治疗前升高,且观察组APACHEⅡ与SF-36量表评分改善程度大于对照组(P0.05);观察组并发症总发生率4%、再次手术或介入治疗发生率为5.33%,病死率为1.33%,均显著低于对照组(17.33%、21.33%、10.67%,P0.05)。结论:覆膜支架腔内修复术能显著提高Stanford B型主动脉夹层动脉瘤患者生活质量与生存率,并发症与再治疗发生率,改善其病情,可能降低VEGF、NF-κB水平有关。     

Stanford B型主动脉夹层撕破口局部计算流体力学研究

目的:探索Stanford B型主动脉夹层局部血流动力学改变对主动脉夹层发生、发展以及临床预后评估的作用,为临床治疗方案选择提供理论依据。方法:通过CT扫描获取临床常见典型形态的Stanford B型主动脉夹层断层序列,重建出三维主动脉夹层计算流体力学分析模型,对主动脉夹层真假腔内血液流场进行数值模拟计算。结果:血液流经Stanford B型主动脉夹层撕破口时会对血管局部壁面产生冲击,造成动脉管壁局部压强升高,此种"冲击效应"不但会出现在近端夹层撕破口附近管腔壁面,也会出现在中间段及远端夹层撕破口附近,当入口血流压强升高时,夹层撕破口附近局部壁面压强差值也会增加。在心动周期内,Stanford B型主动脉夹层壁面剪切应力异常升高区也主要集中在撕破口区附近的动脉壁面上。结论:对于Stanford B型主动脉夹层而言,撕破口的位置相对于撕破口直径而言似乎更有临床意义。对B型夹层患者采用降低血压治疗,可减低局部动脉管壁上的壁面压强差值,但无法消除此壁面压强差,即主动脉夹层管壁上的局部危险区始终存在。此现象揭示主动脉夹层中远端撕破口也可能是造成夹层局部危险因素的原因,采用手术治疗方法封闭撕破口,以消除局部壁面压强增高区,降低破裂风险,可能是更理想的治疗方法。     

构建基于患者个体化的Stanford B型主动脉夹层计算流体力学数值模拟分析模型

目的:探索简便、高效、精确的构建基于真实人体解剖形态结构的Stanford B型主动脉夹层计算流体力学数值模拟分析模型的方法.方法:利用Siemens Sensation Cardiac 64层螺旋CT薄层扫描技术,基于1mm层厚获取6例Stanford B型主动脉夹层连续断层DICOM格式图像,导入Materialise MIMICS v12.11软件,界定目标区域后生成三维动脉模型,经网格优化处理去除低质量及相交面网格,保存结果输出,导入TGrid 5.0软件,对主动脉面网格模型进行几何修复,使面网格扭曲率<0.75,采用自由分网方式生成Stanford B型主动脉夹层计算流体力学分析体网格模型,并对所构建模型进行血流属性、流场边界等界定,初步验证模型的有效性.结果:通过初步计算求解,确定所构建的6例Stanford B型主动脉夹层计算流体力学分析模型分别包含1857030,1820501,1844181,1849651,1858246及1814914个四面体单元.结论:利用64层螺旋CT薄层扫描技术获取DICOM格式连续断层CT图像可快速、准确地构建Stanford B型主动脉夹层计算流体力学数值模拟分析模型,为进一步的计算流体力学分析奠定了良好的基础.     

91例主动脉夹层动脉瘤的临床治疗体会

目的:依据临床经验,熟练运用开放手术、腔内修复术及杂交手术方法治疗各类主动脉夹层动脉瘤。方法:收集2009年7月~2013年1月在我院手术治疗的主动脉夹层动脉瘤患者共91例,StanfordB型夹层动脉瘤36例(其中21例降主动脉瘤、9例腹主动脉及双髂动脉瘤行腔内覆膜支架隔绝术,6例行腹主动脉人工血管置换术),StanfordA型夹层动脉瘤55例(其中单纯Sun,s手术12例伴Bentall术6例,Bentall术伴部分主动脉弓人工血管置换36例,1例行Ⅱ型的主干与分支动脉人工血管转流+介入腔内隔绝降主动脉及左半弓杂交术),分别以不同的手术方法给予治疗。结果:顺利治愈出院85例,死亡6例,4例因全弓置换术后出现难以控制的大出血、肠坏死、肾功能不全、少尿等并发症而死亡,2例死于Bentall术后严重多功能脏器急性衰竭,1例杂交手术术后出现高血压伴神经系统并发症,1例伴肺部感染及低心排综合征,给予对症治疗后效果不佳,有2例出现肾功能不全,经过透析治愈。腔内修复术后有神经系统的并发症2例,下肢的功能障碍2例,少量内漏4例,以上并发症均经对症治疗后痊愈。术后随访76例,时间3~12个月,除2例于术后第9个月死亡、1例因脑梗塞、脑血管意外等与手术无关的疾病而死亡,2例因吻合口动脉瘤或动脉瘤破裂大出血死亡外,余患者生活状态良好,心功能在I~Ⅱ级。结论:根据主动脉瘤疾病的临床特点和定位诊断,合理选择和运用治疗方法使手术操作变得更为迅速、安全和方便,同时能够取得良好的临床治疗效果。     

构建基于患者个体化的Stanford B型主动脉夹层计算流体力学数值模拟分析模型（英文）

目的：探索简便、高效、精确的构建基于真实人体解剖形态结构的Stanford B型主动脉夹层计算流体力学数值模拟分析模型的方法。方法：利用Siemens Sensation Cardiac64层螺旋CT薄层扫描技术,基于1mm层厚获取6例Stanford B型主动脉夹层连续断层DICOM格式图像,导入Materialise MIMICS v12.11软件,界定目标区域后生成三维动脉模型,经网格优化处理去除低质量及相交面网格,保存结果输出,导入TGrid5.0软件,对主动脉面网格模型进行几何修复,使面网格扭曲率〈0.75,采用自由分网方式生成Stanford B型主动脉夹层计算流体力学分析体网格模型,并对所构建模型进行血流属性、流场边界等界定,初步验证模型的有效性。结果：通过初步计算求解,确定所构建的6例Stanford B型主动脉夹层计算流体力学分析模型分别包含1857030,1820501,1844181,1849651,1858246及1814914个四面体单元。结论：利用64层螺旋CT薄层扫描技术获取DICOM格式连续断层CT图像可快速、准确地构建Stanford B型主动脉夹层计算流体力学数值模拟分析模型,为进一步的计算流体力学分析奠定了良好的基础。     

支架置入术治疗DebakeyⅢ型主动脉夹层患者的护理

目的探讨经皮血管腔内覆膜支架置入术治疗DebakeyⅢ型主动脉夹层患者的术前、术后护理措施。方法总结21例DebakeyⅢ型主动脉夹层患者覆膜支架置入术术前、术后的疗效及护理。结果 21例患者均成功置入覆膜支架,均在术后2~3周康复出院,跟踪随访6个月~1年,未出现病情恶化或死亡病例。结论覆膜支架置入术术前、术后给予积极、细致、有效的护理是DebakeyⅢ型主动脉夹层患者康复的重要保证。     

胸主动脉腔内修复术对亚急性期Standford B型主动脉重塑的影响

为了探讨胸主动脉腔内修复术(thoracic endovascular aortic repair, TEVAR)治疗亚急性期Standford B型主动脉夹层术中远端破口特点对术后主动脉重塑的影响,本研究分析了本院2011年7月至2015年4月期间Stanford B型主动脉夹层TEVAR术中支架置入封闭近端破口后,所有支架都植入成功,远端破口仍有明显造影剂返流的43例,随访跟踪术后3~24月主动脉真、假腔面积变化及血栓化情况,同时分析破口血流方向及假腔造影剂充填所需心搏数对主动脉假腔血栓的影响。结果表明:不同假腔造影剂充填所需心搏(2和≥2)、患者术前和术后的真假腔面积变化及假腔形成率方面存在统计学差异(p0.05),同时单因素分析显示远端破口血流溢入假腔方向对TEVAR对术后主动脉重塑无影响,但术后血压控制不佳(≥140/90 mmHg),不利于术后主动脉重塑。本研究初步结论表明,TEVAR术中支架置入封闭近端破口远端仍有破口且流速较快的患者,术后需严格控制血压并密切随访。     

经胸超声胸骨右缘切面对Stanford A型主动脉夹层诊断价值的研究

目的:通过经胸超声心动图获取胸骨右缘升主动脉长短轴切面观察Stanford A型主动脉夹层患者的升主动脉结构,探讨对该类患者进行检查时该切面的应用价值。方法:31例经CTA或手术证实为A型主动脉夹层的连续性患者,超声心动图检查除常规通过胸骨左缘切面观察升主动脉结构外,均做胸骨右缘切面以进一步观察升主动脉结构,包括最大内径,有无撕脱内膜及内膜活动情况,同时应用常规胸骨左缘切面和胸骨右缘切面对A型主动脉夹层能够清晰显示出的病例比例加以比较。结果:胸骨左缘切面能够清晰显示升主动脉结构9例,占比例29%。胸骨右缘切面能够清晰显示升主动脉结构20例,比例65%。将两种切面结合能够清晰显示升主动脉结构的比例升高到74%。胸骨右缘肋间切面测得的升主动脉最大径线数值与CTA结果的一致性更好。结论:胸骨右缘肋间切面对A型主动脉夹层显示的清晰度更好,有助于临床诊断,具有重要的参考价值,值得临床广泛推广。     

孤立性肠系膜上动脉夹层介入血管腔内治疗的初步体会

目的:评价介入血管腔内治疗孤立性肠系膜上动脉夹层(ISMAD)的安全性和疗效.方法:5例患者均通过腹部CT及血管造影明确诊断ISMAD,本组病例确诊后行介入血管腔内治疗,术后继予抗凝抗血小板治疗,并术后1、3、6个月进行CTA或血管造影随访.结果:5例患者手术成功率100％,其中支架联合弹簧圈栓塞2例,双支架重叠技术3例,无并发症发生.全部患者术后3周内症状逐渐消失;术后3～6个月时肠系膜上动脉CTA及血管造影显示动脉瘤腔不显影,支架腔内血流通畅;随访3～12个月(平均7.8个月)夹层动脉瘤无复发.结论:介入血管腔内治疗是治疗ISMAD的安全有效的方法.     

Computed Tomography of Aortic Wall Calcifications in Aortic Dissection Patients

Objectives

To investigate the frequency of aortic calcifications at the outer edge of the false lumen and the frequency of fully circular aortic calcifications in a consecutive series of patients with aortic dissection who underwent contrast-enhanced CT.

Methods

The study population compromised of 69 consecutive subjects aged 60 years and older with a contrast-enhanced CT scan demonstrating an aortic dissection. All CT scans were evaluated for the frequency of aortic calcifications at the outer edge of the false lumen and the frequency of fully circular aortic calcifications by two experienced observers. Between observer reliability was evaluated by using Cohen’s Kappa. Differences between groups were tested using unpaired T test and Chi-square test.

Results

Presumed media calcifications were observed in 22 (32%) patients of 60 years and older and were found more frequently in chronic aortic dissection (N = 12/23, 52%) than in acute aortic dissection (N = 10/46, 22%).

Conclusion

As the intima has been torn away by the aortic dissection it is highly likely that CT scans can visualize the calcifications in the tunica media of the aorta.     

MMP-2 Isoforms in Aortic Tissue and Serum of Patients with Ascending Aortic Aneurysms and Aortic Root Aneurysms

ObjectiveThe need for biological markers of aortic wall stress and risk of rupture or dissection of ascending aortic aneurysms is obvious. To date, wall stress cannot be related to a certain biological marker. We analyzed aortic tissue and serum for the presence of different MMP-2 isoforms to find a connection between serum and tissue MMP-2 and to evaluate the potential of different MMP-2 isoforms as markers of high wall stress.MethodsSerum and aortic tissue from n = 24 patients and serum from n = 19 healthy controls was analyzed by ELISA and gelatin zymography. 24 patients had ascending aortic aneurysms, 10 of them also had aortic root aneurysms. Three patients had normally functioning valves, 12 had regurgitation alone, eight had regurgitation and stenosis and one had only stenosis. Patients had bicuspid and tricuspid aortic valves (9/15). Serum samples were taken preoperatively, and the aortic wall specimen collected during surgical aortic repair.ResultsPro-MMP-2 was identified in all serum and tissue samples. Pro-MMP-2 was detected in all tissue and serum samples from patients with ascending aortic/aortic root aneurysms, irrespective of valve morphology or other clinical parameters and in serum from healthy controls. We also identified active MMP-2 in all tissue samples from patients with ascending aortic/aortic root aneurysms. None of the analyzed serum samples revealed signals relatable to active MMP-2. No correlation between aortic tissue total MMP-2 or tissue pro-MMP-2 or tissue active MMP-2 and serum MMP-2 was found and tissue MMP-2/pro-MMP-2/active MMP-2 did not correlate with aortic diameter. This evidence shows that pro-MMP-2 is the predominant MMP-2 species in serum of patients and healthy individuals and in aneurysmatic aortic tissue, irrespective of aortic valve configuration. Active MMP-2 species are either not released into systemic circulation or not detectable in serum. There is no reliable connection between aortic tissue—and serum MMP-2 isoforms, nor any indication that pro-MMP-2 functions as a common marker of high aortic wall stress.