老年人升主动脉夹层五例临床与病理分析

目的 探讨老年人升主动脉夹层的临床表现与病理特点及其相互关系，并对该病的病因及发病机制进行简略探讨。方法 分析5例老年人升主动脉夹层病例尸检切片，对其临床表现、病理特点、组织化学及免疫组织化学检测状况进行分析。结果 老年人升主动脉夹层临床表现复杂多样。病理特点为夹层壁内平滑肌细胞明显退行性变，弹力纤维减少或断裂，胶原纤维增生等改变。结论 升主动脉夹层是一种严重威胁老年人生命的急性血管疾病。诊断该病时要根据临床特点并配合MRI等辅助检查综合考虑。     

老年高血压伴主动脉夹层患者临床及病理分析

目的探讨老年高血压伴主动脉夹层临床表现与病理特点。方法选择15例老年高血压伴主动脉夹层患者为夹层组,同期选择高血压未伴主动脉夹层15例患者为对照组,取入选患者的尸体解剖病理切片,回顾性分析2组临床表现、病理特点及免疫组织化学检测状况。结果与对照组比较,夹层组患者临床表现复杂多样,病理特点为夹层壁内平滑肌细胞明显退行性变,弹力纤维减少或断裂,胶原纤维增生,夹层壁内血管第八因子相关抗原表达增强,平滑肌肌动蛋白表达降低。结论高血压伴主动脉夹层是严重威胁老年人生命的一种并发症。严格控制血压,是预防老年人主动脉夹层发生的重要手段。     

组织蛋白酶B及其抑制剂Cystatin C在人腹主动脉瘤平滑肌细胞中的表达

目的 观察组织蛋白酶B及其抑制剂Cystatin C在人腹主动脉瘤平滑肌细胞中的表达情况,以探讨其在腹主动脉瘤发生发展中的作用.方法 对21例腹主动脉瘤患者和8例正常腹主动脉尸检者的腹主动脉血管标本行苏木精-伊红染色和免疫组织化学染色,观察组织蛋白酶B及其抑制剂Cystatin C对血管中膜的影响.结果 免疫组织化学染色可见组织蛋白酶B和Cystatin C分别在腹主动脉瘤、正常腹主动脉中免疫反应阳性,阳性定位于平滑肌细胞质;腹主动脉瘤平滑肌细胞中组织蛋白酶B阳性细胞平均光密度值明显增高,Cystatin C明显降低,与正常腹主动脉之间有显著差异(P<0.01).结论 腹主动脉瘤平滑肌细胞中组织蛋白酶B表达增强,Cystatin C表达下降,组织蛋白酶及其抑制剂Cystatin C间的不平衡可能引起动脉瘤壁细胞外基质广泛降解,从而导致腹主动脉瘤的发生和破裂.     

Bentall术治疗儿童马凡氏综合征合并巨大升主动脉瘤1例

马凡氏综合征（Marfan syndrome,MFS）是一种常染色体显性遗传的先天性结缔组织疾病,可累及骨骼肌肉、眼部及心血管。心血管病变主要表现为大动脉中层弹力纤维发育不全,主动脉扩张,形成主动脉瘤。患者主动脉瘤壁均匀菲薄,瘤内可能产生急性或慢性的内膜剥离而形成主动脉夹层。有报道指近90%的患者死于心血管并发症,其中的80%是因为主动脉根部病变引起。     

老年人腹主动脉瘤血管平滑肌细胞相关蛋白表达及巨噬细胞浸润的病理学特点

目的 观察血管平滑肌细胞(VSMC)表达变化及巨噬细胞浸润在老年人腹主动脉瘤中的病理学特点. 方法 对15例老年人腹主动脉瘤与6例正常腹主动脉组织行HE染色、VanGieson法染色和免疫组织化学染色.用免疫组织化学染色检测α-平滑肌肌动蛋白(α-SMA)、组织蛋白酶B及CD68蛋白表达. 结果 老年人腹主动脉瘤病变处胶原容积百分比(9.3±1.9)%,较正常主动脉的(5.3±1.8)%增高(P＜0.05).老年人腹主动脉瘤中组织蛋白酶B和CD68的表达增强分别为0.38+0.07和0.51±0.12,α-SMA表达减弱为0.23±0.05,与正常腹主动脉(分别为0.13±0.06和0.01±0.01,0.33±0.05)比较.差异有统计学意义(P＜0.05). 结论 VSMC相关蛋白表达水平改变及巨噬细胞浸润可能参与了老年人腹主动脉瘤血管壁的破坏.     

胸主动脉瘤/主动脉夹层的基因组学研究进展

胸主动脉瘤/主动脉夹层是一种极其凶险、有极高病死率的大血管疾病。目前发病机制尚不明确,除了原发性高血压(高血压)、动脉粥样硬化、外伤、吸烟、嗜铬细胞瘤、炎性改变等常见危险因素外,基因突变也会引起主动脉的病理改变。胸主动脉瘤/主动脉夹层是涉及FBN1、TGFBR1、TGFBR2、SMAD3、ACTA2等的多基因疾病,随着分子生物学技术的发展,在精准医学的指导下,通过基因检测可以提高主动脉疾病的风险预知性。本文主要综述胸主动脉瘤/主动脉夹层的基因组学研究进展。     

退行性变升主动脉瘤中骨桥蛋白的表达与细胞表型转化

目的观察骨桥蛋白(osteopontin,OPN)在退行性变升主动脉瘤(Degenerative ATAA,DATAA)中的表达,初步探讨OPN及平滑肌细胞表型转化在DATAA发病中的作用。方法升主动脉瘤术中切除标本18例为DATAA组,冠状动脉搭桥患者术中主动脉标本18例为对照组。应用实时定量PCR的方法检测所有标本中OPN的mRNA表达水平,免疫组化方法检测主动脉壁中OPN的表达情况,H-E染色和Masson染色分别检测主动脉壁的一般情况及胶原的含量。结果 DATAA组OPN的免疫组化半定量结果与对照组相比表达增加(P<0.01),与主动脉直径显著相关(r=0.737,P<0.01),主要位于中膜及外膜;实时PCR结果与免疫组化结果一致(P<0.01)。胶原纤维在DATAA中表达增加(P<0.01),与OPN表达量正相关(r=0.694,P<0.01)。组织学结果显示DATAA组标本弹力蛋白降解明显,平滑肌细胞增生及排列紊乱。结论 OPN在DATAA主动脉壁中高表达,胶原含量在DATAA中表达增强。合成型平滑肌细胞增多可能导致了胶原分泌增加,参与了升主动脉瘤壁的重塑过程,在DATAA的发病中具有重要的作用...     

内质网应激通路相关蛋白ATF4及CHOP在主动脉夹层中的表达以及意义

目的探讨主动脉夹层(AD)患者环磷酸腺苷反应元件结合转录因子同源蛋白(CHOP和活性转录因子4(ATF4)的表达及其意义。方法选取2017年3月至2018年4月于武汉大学人民医院确诊为StanfordⅠ型夹层并行胸主动脉夹层全弓置换患者为AD组(n=13),另选取5例于武汉大学人民医院接受心脏移植的患者作为Donor组(此5例患者均无大血管疾病,其在心脏移植术中取下的主动脉血管可作为相对正常主动脉血管组织)。通过Masson染色、间苯二酚染色研究两组患者主动脉血管结构变化,通过TUNEL染色明确主动脉夹层发病后平滑肌细胞凋亡情况;通过RT-PCR及Western-blot分别在mRNA水平及蛋白水平检测ATF4及CHOP的变化情况。在动物实验方面,20只SD大鼠随机分为两组:Control组(n=10)及AD组(n=10)。Control组给予大鼠维持饲料,AD组给予含0.3%的β-异氨基丙腈酯(BAPN)的大鼠维持饲料进行主动脉夹层动物模型构建。动物模型构建成功后,取两组大鼠主动脉组织做石蜡包埋,标本切片后处理步骤及检测指标同人体标本。结果在人体标本中,Masson染色及间苯二酚染色发现,AD组患者主动脉血管标本胶原沉积较Donor组明显增多,弹力纤维断裂程度也更加严重;TUNEL凋亡染色发现,AD组患者主动脉血管组织较Donor组正常血管组织细胞凋亡明显增多,差异有统计学意义(P0.01);RT-PCR及Western-blot实验发现,AD组患者主动脉血管ATF4、CHOP的表达在RNA水平及蛋白水平均较Donor组正常主动脉血管明显增高,差异均有统计学意义(P0.05)。在动物实验中,Masson染色发现,AD组大鼠主动脉血管较Control组胶原沉积明显增多;间苯二酚染色发现,AD组大鼠主动脉血管较Control组弹力纤维断裂程度明显加重,Control组基本无弹力纤维断裂;TUNEL凋亡染色发现,AD组大鼠主动脉血管较Control组细胞凋亡明显增多,差异有统计学意义(P0.05)。RT-PCR及Western-blot实验亦发现,AD组大鼠主动脉血管ATF4、CHOP的表达在RNA水平及蛋白水平均较Control组明显增高,差异均有统计学意义(P0.05)。结论 CHOP和ATF4与内质网应激关系密切,CHOP及ATF4在人主动脉夹层标本及主动脉夹层动物模型标本中均显著升高,说明在主动脉夹层中内质网应激水平较高,这或许是主动脉血管平滑肌细胞发生凋亡的重要原因之一,进而在一定程度上参与主动脉夹层的发生发展。     

主动脉夹层患者主动脉壁中载脂蛋白D的表达分析及潜在临床价值

目的 检测载脂蛋白D（APOD）在主动脉夹层患者主动脉壁组织中的表达水平,并探讨其与主动脉夹层发生的潜在关系。方法 收集2020年1月至2021年12月华中科技大学同济医学院附属同济医院心脏大血管外科行手术治疗的9例主动脉夹层患者（夹层组）和5例心脏移植患者（对照组）的主动脉壁组织,通过苏木精-伊红（HE）染色和弹性纤维（EVG）染色检测两组主动脉壁的形态学差异,进一步通过蛋白质免疫印迹实验和组织免疫荧光染色检测APOD在主动脉壁组织中的蛋白表达水平及亚细胞定位。结果HE和EVG染色显示,与对照组比较,夹层组的主动脉壁结构紊乱、炎性细胞广泛浸润、弹性纤维大量断裂且减少;蛋白免疫印迹实验与组织免疫荧光染色显示,与对照组比较,主动脉夹层患者主动脉壁组织中的APOD蛋白表达水平显著降低（P<0.05）;组织免疫荧光染色显示APOD主要分布在血管平滑肌细胞外基质和细胞质中。结论 主动脉夹层患者主动脉壁中APOD的蛋白水平降低,提示APOD可能参与主动脉夹层的发生发展,作为分泌蛋白APOD有望成为诊断主动脉夹层的新型标志物,亦有望成为治疗主动脉夹层的新靶点。     

Hippo-YAP信号通路调控升主动脉瘤发病机制的研究进展

<正>升主动脉瘤(aortic aneurysm,AA)是指:由于多种原因导致主动脉壁结构破坏、强度减弱,主动脉壁在血流压力下发生瘤样扩张或膨出的一种高危性疾病,最终可因主动脉瘤壁无法承受血流冲击而发生破裂[1]。目前,主动脉瘤的发病机制及病理生理学变化过程尚不完全明确,但研究者一致认为中层血管平滑肌细胞(vascular smooth muscle cells,VSMCs)的变化是胸主动脉瘤发生、发展中的重要环节[1-2]。Hippo-     

Short term outcome of thoracic endovascular aortic repair in patients with thoracic aortic diseases

Aim and background

Open surgical repair for thoracic aortic diseases is associated with a high perioperative mortality and morbidity. Most of type B aortic dissections are uncomplicated and are medically treated which carries a high mortality rate. Thoracic endovascular aortic repair is the first-line therapy for isolated aneurysms of the descending aorta and complicated type B aortic dissection. The aim of this study is to test the safety of early thoracic endovascular aortic repair in patients with uncomplicated type B aortic dissection and patients with thoracic aortic aneurysms.

Ultrafast computed tomography in the diagnosis of aortic aneurysms and dissections

UFCT, by virtue of its 50 to 400 millisecond acquisition times, 0.75 to 1.5 mm resolution, and excellent vascular opacification, provides a rapid, minimally invasive method for assessing aortic aneurysms and dissections. During a 3.5-year period, 50 patients with suspected thoracic, thoracoabdominal, and abdominal aortic aneurysms or dissections were evaluated using the Imatron C-100 UFCT scanner. Eighteen patients had thoracic or thoracoabdominal aneurysms. 17 had thoracic or thoracoabdominal dissections, 7 had abdominal aneurysms, and in 8 no aneurysms or dissections were found. In 23 of the 35 patients with thoracic or thoracoabdominal aneurysms or dissections, the UFCT findings accurately reflected the findings at aortography, surgery, or autopsy. There was one false-positive examination. The remaining 11 patients with UFCT findings of aneurysm or dissection were followed clinically. In the 7 patients with abdominal aneurysms, 4 were confirmed by angiography or surgery, and 3 were followed clinically. Of the 8 patients with negative UFCT examinations, 2 had subsequent angiography that failed to show an aneurysm, and 6 were followed from 6 to 30 months without developing findings suggestive of aneurysm. UFCT appears to be a useful, minimally invasive technique for detecting and following aortic aneurysms and dissections.     

主动脉瘤/夹层手术远端吻合方法的改良及其效果比较

目的 总结主动脉瘤及主动脉夹层手术远端吻合口吻合方法改良的经验.方法 2006年6月至2011年6月,对10例主动脉瘤/夹层手术患者的主动脉远端吻合口应用了单纯腔内覆膜支架置入、血管箍加残端全层翻转和血管箍加腔内覆膜支架置入三种改良吻合方法.患者年龄36～69（52.2±12.0）岁.Bentall手术5例、Bentall手术＋全主动脉弓置换2例、Bentall手术＋二尖瓣置换1例、单纯升主动脉置换＋二尖瓣及主动脉瓣置换1例、Cabrol手术1例.结果 应用单纯腔内覆膜支架置入后吻合法1例,恢复循环后吻合口出血部位较多,止血极其困难,术后患者死于大量失血.应用血管箍加残端全层翻转吻合法7例,恢复循环后吻合口少量出血3例,补针后均顺利止血.应用血管箍加腔内覆膜支架置入法2例,恢复循环后吻合口未见明显出血.结论 血管箍加主动脉残端全层翻转吻合法有较好的预防主动脉远端吻合口出血的效果,出血时补针亦易成功.血管箍加腔内覆膜支架置入法预防主动脉吻合口出血效果最为可靠,适合于各种类型主动脉瘤或主动脉夹层主动脉壁菲薄、脆弱者.     

主动脉夹层CTA的诊断及介入治疗

目的对主动脉夹层CTA的诊断及介入治疗进行探讨与分析。方法本研究共纳入研究对象60例,均为2012年6月到2014年1月我院收治的主动脉夹层患者,所有患者均经DSA抑或MR T1-FS确诊。对患者的内膜瓣、管壁增厚、夹层动脉瘤和双腔征等影像学征象进行回顾性分析。结果 60例患者中出现主动脉夹层病变的70处,其中30例前循环,40例后循环。在70处主动脉夹层病变当中,有27处内膜瓣,7处双腔征,36处血管狭窄。相比DSA诊断,通过CTA可以把23处内膜瓣显示出来,占85.2%(23/27),可把5处双腔征显示出来,占71.4%(5/7),可把34处血管狭窄显示出来,占94.4%(34/36)。而在显示主动脉夹层脉瘤和血管闭塞上差异不显著。CTA比MR T1-FS更容易把血管内膜增厚给显示出来。结论通过CTA诊断主动脉夹层,能够把多种影像学征象给清晰显示出来,包括管壁和血管腔在内的主动脉夹层,是一种有效的影像学方式,对临床上运用适当的介入治疗有着重要的指导作用。     

Stenting Versus Surgery of the Thoracic Aorta

Aneurysms and dissections of the aorta represent a potentially life-threating situation. Surgical resection and interposition of vascular prostheses (Gortex or Dacron) has long been considered the only treatment option. Although there have been great strides during the past decades in the management of patients with thoracic aortic aneurysms and dissections by new surgical techniques, postoperative morbidity and mortality remain high. The afflicted population is usually of older age and present with a variety of comorbidities and significant impact on postsurgical outcome. Postoperative complications, such as paraplegia and renal insufficiency, contribute to prolonged hospital stays and higher medical costs. Conversely, interventional stent-graft placement may be a promising nonsurgical strategy for the treatment of thoracic aortic aneurysms and dissections. The endovascular stent-graft prostheses is based on the concept of a metal grid covered with vessel graft material. The initiation of the natural healing process by exclusion of an aneurysm or sealing of the proximal entry in dissection induces remodeling of the aortic wall and consolidation of the false lumen. Although the initial results of stent-graft treatment of thoracic aortic aneurysms and dissections are promising, the concept of nonsurgical reconstruction must be subjected to a randomized long-term study.     

孙氏手术与联合三分支支架血管术中置入治疗急性Stanford A型主动脉夹层对比

目的 探讨孙氏手术、联合三分支支架血管术中置入两手术方式治疗急性Stanford A型主动脉夹层的疗效.方法 2011年1月至2013年1月我院收治的急性Stanford A型主动脉夹层患者,以孙立忠教授主动脉细化分型中AC型为入选标准,选取患者24例.孙氏手术组患者12例,单纯行升主动脉及全弓替换加支架“象鼻”手术9例,同期主动脉根部替换手术（Bentall术）2例,主动脉瓣成形1例.联合三分支支架血管术中置入组患者12例,单纯三分支支架术中置入3例,同期升主动脉替换8例,主动脉根部替换手术（Bentall术）1例.出院前、术后3个月、术后每年复查主动脉全程重建CT.结果 孙氏手术组：平均手术时间（10.00±1.60）h,平均体外循环时间（253.33±49.33）min,平均心肌阻断时间（141.41±27.58）min,选择性脑灌注时间（39.67±10.28）min.住院死亡4例,死亡原因：多脏器衰竭2例,术后肾功能衰竭1例,术后呼吸功能衰竭1例.联合三分支支架血管术中置入组：平均手术时间（7.77±2.06）h,平均体外循环时间（168.25±32.05）min,平均心肌阻断时间（79.75±29.54）min,选择性脑灌注时间（24.33±6.53）min.住院死亡2例,死亡原因：术后呼吸功能衰竭死亡1例,1例术后一直未醒,术后第5天少尿,家属放弃治疗.孙氏手术组随访（11.09±6.87）个月,无死亡及需再次手术者.联合三分支支架术中置入组随访（18.40±8.03）个月,术后死亡2例,1例术后1年胸痛发作,心脏彩超提示升主动脉明显增宽,主动脉后壁分离为两层,当即死亡;1例术后2年随访主动脉全程重建CT提示无名动脉近端内漏.结论 孙氏手术和联合三分支支架血管术中置入术是治疗大多数急性Stanford A型主动脉夹层安全有效的方法.作为一种崭新的技术手段,联合三分支支架血管术中置入简化了手术步骤,术后内漏是高危因素,对该种手术方式患者选取应有一定针对性,根据患者信息订制更加个体化支架,并且需要长期随访.     

Transcatheter Inoue endovascular graft for treatment of canine aortic dissection

Summary We examined whether the Inoue endovascular graft could be used as a device for the treatment of aortic dissection. This graft consists of a cylinder made from a thin Dacron sheet suspended by several extra-flexible wire rings. Aortic dissections were experimentally created in 11 dogs. Using aortography and intravascular ultrasound imaging (IVUS), we selected the size of the graft diameter according to the diameter of the normal descending aorta (distal to aortic dissection) in 5 dogs (group I) and according to the diameter of the true lumen of the aorta within the aneurysm in 6 dogs (group II). The graft was deployed transfemorally through a 15-F long sheath into the aneurysm to close the entry site, immediately after creation of the aortic dissection. The entry was completely closed in all dogs after immediate implantation. All 5 dogs in group I died within 11 days (mean, 7 days) after graft deployment. However, all grafts in group II were tolerated very well and followed up for as long as 5 months. After the follow up, IVUS and aortography showed no rupture of the aortic aneurysmal wall and no migration, leakage, or damage to the graft in any of the 6 dogs. These 6 dogs were sacrificed and autopsy showed that the graft was covered by a thin, translucent, neointima, effectively recreating a new aortic lumen and completely closing the entry of the aneurysm. The Inoue endovascular graft proved to be effective in the long-term treatment of aortic dissection without surgery, when the size of the graft was selected according to the diameter of the true lumen of the aorta within the aneurysm.     

Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections

The natural history of thoracic aortic aneurysms and dissections is diverse, reflecting a broad spectrum of etiologies which include increasing aortic size, hypertension, and genetic factors. The pathogenesis is related to defects or degeneration in structural integrity of the adventitia, not the media, which is required for aneurysm formation. The ascending and descending aorta appear to have separate underlying disease processor that lead to a weakened vessel wall and an increased susceptibility for dissection. Etiologic factors for aortic aneurysms and dissections are multifactorial, reflecting genetic, environmental, and physiologic influences.     

Endovascular stent grafting of descending thoracic aortic aneurysms

The treatment of descending thoracic aortic aneurysms using endovascular stents is one of the more recent advances in treatment and is receiving increasing attention as it is a less invasive alternative to open surgical repair. Although the technology is still primitive, significant improvements have lately been made in the design and deployment of the endovascular stent-grafts. Aortic stent-grafts were used initially to exclude abdominal, and later thoracic, aortic true and false aneurysms. These prostheses have been increasingly used to treat aneurysms, dissections, and traumatic ruptures of the descending thoracic aorta with good early and mid-term outcomes. Although the long-term outcome of patients with aneurysms of the descending thoracic aorta after stent graft implantation has not been investigated, continued refinement of the endovascular approaches has decreased the need for conventional open thoracic aortic aneurysm repair, especially in patients who are at a high risk for standard surgery because of advanced age or the presence of comorbid diseases. The placement of endoluminal stent-grafts to exclude the dissected or ruptured site of thoracic aortic aneurysms is a technically feasible and relatively safe procedure. With the rapid development of endovascular approaches, the treatment of the descending thoracic aortic aneurysms might alter even more, but an extended follow-up is necessary to determine the longer term outcome. Historical perspectives, advantages, device considerations, complications, and current perspectives of the endovascular stent grafting of the descending thoracic aortic aneurysms are elaborated on.     

False aneurysm formation at proximal and distal ends of a stent graft: a rare complication in the repair of endovascular thoracic aortic aneurysm.

This case report demonstrates a rare complication of false aneurysm formation at the proximal and distal ends of a stent graft that was placed in the descending thoracic aorta to repair an atherosclerotic aneurysm with a fibrotic, solid aortic wall. This complication can develop not only in penetrating aortic ulcers and aortic dissections but also in atherosclerotic aneurysms.