颈动脉粥样硬化性狭窄的基础与临床研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
缺血性脑卒中是人类常见多发病,我国缺血性脑卒中年发病率为120~180/10万,年病死率80~120/10万,而动脉狭窄是主要因素之一。颈动脉粥样硬化是缺血性脑血管病重要的危险因素,20%~30%的卒中是颈动脉狭窄性病变进行性发展所致,因此,颈动脉狭窄多年来一直是神经科学者关注的热点。
     人类对于颅外颈动脉与脑功能的关系、颈动脉病变在TIA和中风发病中的作用以及手术消除病变和预防缺血症状等方面知识经过近3000年的探索才得以确立。1684年,Thomas Willis最早在尸检时发现颈动脉完全闭塞,并将颅内血管循环网以自已的名字命名;1905年,Chiari强调了颅外颈动脉闭塞性病变和动脉斑块栓子是致病的直接原因;上个世纪50年代,Fish对颈动脉狭窄的病理进行了研究,提出:对颈动脉分叉处病变进行外科干预可能有效地预防中风;1951年,三位阿根廷医生为一位患有失语和右侧偏瘫的41岁男性患者进行了颈内动脉狭窄病变的切除及MCA-STA吻合手术;1953年DeBakey成功的为一名53岁反复TIA发作的患者行颈动脉粥样斑块剥脱手术(CEA),病人3年后才死于其他疾病;此后大批学者报道了不少的手术病例,但到了20世纪80年代,一些疗效较差的手术治疗结果相继报道使得长期应用抗血小板药物的医生对CEA的疗效充满了怀疑,特别在80年代后期有关CEA并发症报道的不断出现,更使一些怀疑者对以前非随机对照的结果表示怀疑,疗效较好的报告甚至被认为是赞成手术的的外科医生不严密选择病例的结果。这种争论使80年代后期全世界CEA手术的病例数急剧下降。
     为了解答针对CEA手术有效性的疑问,一些大规模的前瞻随机对照临床试验应运而生,到上个世纪90年代中期,试验结果相继发表,代表性的有:①北美有症状性颈动脉内膜切除术试验协作组(NASCET,1988~1991)②欧洲颈动脉外科试验协作组(ECSTCG,1981~1991)③无症状性颈动脉硬化性狭窄研究(ACAS,1987~1993)。得出重要结论:①CEA对治疗近期大脑半球缺血和TIA以及致残性中风的同侧颈动脉重度狭窄非常有效;②对伴有脑缺血症状的重度颈动脉狭窄,CEA是最佳的治疗手段;③CEA对无手术禁忌的无症状性颈动脉狭窄>86%的病例有明显的预防中风的疗效。
     受上述试验报告的鼓舞,90年代以来全世界CEA病例数急剧增加,文献报道数量亦成倍增加,随着研究的深入和不断的积累经验,CEA手术本身的操作已日趋成熟。技术的不断改进使得CEA的并发症越来越少,到八十年代末期美国每年约有10万人接受CEA手术。九十年代初,几项大规模、多中心的临床试验相继对CEA的有效性进行了客观评价,认为CEA治疗颈动脉狭窄优于内科药物疗法,一些学者甚至称之为治疗颈动脉狭窄的“金标准”。
     CEA毕竟是一种手术,有一定的创伤和危险性,随着时代的进步,临床医生们又在思索着能否有更为微创的方法来解决颈动脉狭窄的问题,Dotter于1964年首先描述经皮腔内动脉成形术(PTA),Kerber等于1980年由颈总动脉分叉处远端切开血管行颈总动脉近端球囊扩张术治疗颈总动脉狭窄。20世纪80年代到90年代初,介入治疗颈动脉狭窄多限于球囊血管腔内成形术。单纯球囊扩张后可发生内膜撕裂、斑块移位和栓子脱落以及血管壁弹性回缩,引起动脉夹层,甚至闭塞。脑栓塞以及再狭窄成为影响其疗效的主要因素。球囊导管的出现使PTA技术得到飞跃发展。Mathias是这一方面的先驱,在经过对动物进行实验后他于1979年为1例女性颈动脉肌纤维发育不良患者行PTA手术,1980年又首先报道一例颈内动脉硬化性狭窄的PTA术,于1989年成功进行世界首例颈动脉支架成形术(CASS),随之世界范围内CASS的病例不断出现。随着支架置入技术上成功率的提高(98%~99%)和并发症发生率的下降,CASS有逐步取代CEA的趋势。以国内为例,据统计,从1994年到2005年9月,国内全文报道了297篇关于颈动脉狭窄研究的文献,其中CEA治疗有1578例,而CASS治疗有4165例之多。
     颈动脉支架术的合并症:①过度灌注损伤是最早发现的CASS术后的一种合并症,它是由于闭塞、狭窄的颈动脉开通后,脑组织血供骤然增加,超过脑血管的自主调节能力,造成脑水肿、毛细血管破裂、血管旁出血以及脑内血肿等。②脑栓塞是颈动脉支架术的主要合并症。③动脉穿刺部位血肿。④颈动脉痉挛、夹层及闭塞。⑤心律过缓和低血压。⑥支架再狭窄和支架变形。
     本实验着重进行了颈动脉粥样硬化性狭窄的动物实验研究,并在临床中对颈动脉粥样硬化性狭窄病人的支架植入进行了初步的观察总结。
     第一部分猪颈动脉粥样硬化性狭窄模型的建立
     目的:建立稳定可靠切实符合人类颈动脉粥样硬化性狭窄治疗研究的动物模型。
     方法:普通猪10头,采用血管内膜热空气损伤法在猪的颈总动脉上造成特定条件的损伤,实验程序:动物麻醉→取耳血查血脂→行双侧颈总动脉热空气损伤→高脂喂养二月→取耳血查血脂→颈动脉彩超、DSA及CTA检查→切取病变处颈动脉行病理学检查,评价猪血管狭窄程度和病理改变特点。颈动脉内膜热空气损伤法:以无菌技术显露并游离一侧颈总动脉,长约5cm。远近两端用动脉瘤夹阻断,纵向切开血管,翻转后,电吹风中档,距20cm处,3分钟;生理盐水冲洗,原位缝合,置换盐水后再通。缝合全程软组织。术后即刻肌注青霉素80万单位,以后在饲料中加入氟哌酸,0.4g~*3/日,共5天。颈动脉狭窄程度的判定:以DSA机器上自带软件精确测量每根颈动脉最狭窄处的最小残腔直径(DMS)和狭窄远端正常颈动脉直径(DCC)。狭窄率=(DCC-DMS)/DCC~*100%。狭窄程度的判定:狭窄率<70%为不能满足实验需要,狭窄率≥70%为满足需要。
     结果:实验用猪无死亡,20根颈动脉1根狭窄率<70%,19根狭窄率≥70%,建模成功率95%,无完全血管闭塞。高脂喂养不同时间猪血脂测定结果:高脂喂养二月后可见LDL-C比基础值增长了近15倍,而在TC中,LDL-C易于造成内皮损伤并易进入内膜下参与粥样硬化,与之相对应,具有抗粥样硬化作用的TC成分HDL-C仅增加了9倍。损伤前与损伤后二月颈动脉彩超显示损伤处血流速度明显加快,峰值增高,DSA及CTA均显示颈动脉明显狭窄。猪颈动脉粥样硬化性狭窄形成后病变病理特点:内膜明显增厚,细胞数目减少但细胞体积增大,胞内脂质成分增多,中膜变薄,内中膜之间常见断裂现象,偶见胆固醇结晶。
     结论:既往有关颈动脉狭窄动物模型均建立在鼠、兔及犬的基础上,然而,上述实验动物的颈动脉在形态学上与人体差异较大,评价狭窄程度上在依赖DSA这个“金标准”时操作困难程度高。猪的颈动脉与人类近似,且行DSA时操作也与人体相似,成功率显然也高,按本实验方法,损伤后喂养二月的猪颈动脉粥样硬化性狭窄程度和病理改变均较好符合颈动脉狭窄治疗研究之实验需要。
     第二部分猪颈动脉狭窄前后血流动力学的改变
     目的:研究猪颈动脉狭窄前后颈动脉及颅内动脉的血流动力学变化。
     方法:采用第一部分所述方法,建立猪的颈动脉狭窄模型,模型建立前后,采用美国Acuson公司生产的3D彩超仪,经颈部用6MHz探头检测颈总动脉血流特征;各血管血流动力学参数包括:收缩期峰值流速(Vs)、舒张期末流速(Vd)、平均流速(Vm)及搏动指数(PI)。测量部位和内容与术前相同。
     记录其狭窄处残余管腔内径(d)、附近正常管腔内径(D)、斑块性质和最狭窄处收缩期峰值血流速度(PSV),并根据以下公式计算血管内径狭窄程度和每分钟血流量(Q)。
     内径狭窄程度=(D-d)÷D×100%Q=Vm×S×60其中S为血管面积,Vm为时间平均血流速度。计算Q时,应在靶血管管腔相对规则处测量S和Vm,声束与血流方向之间夹角均<60°。
     应用彩超探测动物大脑中动脉(MCA)血流的变化。术后二月内分别行、彩超和DSA检查,其结果与术前进行对比分析。对10例动物手术前后术侧颈内动脉PSV、血流量和双侧MCA的PSV进行自身对照和显著性检验,全部数据均以均数±标准差表示,应用SPSS 10.0软件,P<0.05为有统计学意义。
     结果:猪的颈动脉粥样硬化性狭窄模型建立后,大脑中动脉PSV均有所变慢[术后(95.78±9.86))cm/s,术前(72.04±12.24)cm/s,P<0.05]。术后二月颈内动脉PSV较术前显著增快[术后(244.76±52.30)cm/s,术前(113.09±19.92)cm/s,P<0.05];血流量均有显著减少[术后(215.18±41.55)ml/min,术前(382.68±33.26)ml/min,P<0.05],与术前相比差异均有显著性意义(P<0.05)。术后高脂喂养二月,猪的颈动脉彩超检查发现颈动脉管腔明显狭窄,内膜增厚,并有不同程度的粥样斑块附壁。模型建立后,猪的颈内动脉血流速度明显增快,最高速度达(104.9±12.0)cm/s,而术前最高速度仅为(54.7±7.4)cm/s,彩超显示高脂喂养二月后,猪的颈动脉搏动呈现高阻力型,阻力指数RI明显上升[术后(0.91±0.09),术前(0.28±0.07),P<0.05]。
     结论:
     ①彩色多普勒超声对颈动脉的检查方法,简单、迅速、准确,能够直接清晰显示动脉内膜的改变,了解斑块的大小、部位及对血管血流的影响。
     ②猪颈动脉严重狭窄后,颅内动脉灌注压下降,出现血流速度降低,即双侧半球、前后循环动脉的血流速度和血管搏动指数的不对称性改变,而颅外动脉出现血流速度增快,彩超显示峰值增高,血流量较狭窄前明显减少。
     ③脑血管造影虽然是诊断、评价血管病变的“金标准”,但鉴于该技术的有创性、费用高及不易接受等原因,不可能作为筛选或反复检测的手段。彩超检测技术具有简便、可重复、经济等特点,是诊断颅内和颈部大血管狭窄的可靠指标。
     第三部分颈动脉粥样硬化性狭窄病人血管内支架植入治疗的初步观察
     目的:总结32例颈动脉粥样硬化性狭窄血管内支架治疗的经验。
     方法:自2002年5月至2005年11月,经门诊筛选的脑缺血病患者,其临床表现和神经影像学检查符合NASCET的纳入标准,其中,男23例,女9例,年龄55~79岁,平均64.3岁。24例表现为反复发作的脑缺血发作(TIA),2例为严重不能缓解的头晕,6例为陈旧性脑梗死,无严重神经功能障碍。伴有高血压病者23例,高血脂者15例,糖尿病者7例。
     影像学资料:病人术前均行脑MR扫描,部份病人术前及术后还行DWI及PWI加权成像检查,以了解有无新的脑梗死,所有病人行颈动脉彩超检查,发现颈动脉不同程度狭窄及动脉内斑块,DSA检查示:颈动脉分叉部并延伸到颈内动脉狭窄23例,另9例狭窄主要位于近端的颈内动脉。利用血管机上自带软件测量所选病例颈动脉狭窄程度均超过70%,其中有8例病人超过90%,平均狭窄程度(76±20)%,狭窄长度为1.6~4.2cm。
     术前3~5天给予抗血小板准备,(氯吡格雷75mg,1次/日,加用阿斯匹林300mg,1次/日)。术中常规监护,视情采用局麻或全麻,一般情况下均采用局麻,右股动脉穿刺成功后置入9F鞘,全身肝素化后行主动脉弓上造影及颈动脉,锁骨下或椎动脉造影,评估造影结果,确认所要进行治疗的血管是病人症状的责任血管,撤出造影管,将导引管放入患侧颈总动脉,在Roadmap下将过滤伞通过狭窄处到达远端正常血管,至少距离正常血管处4cm,释放保护伞后在过滤伞微导丝的同一轨道上将所选定的支架跨过狭窄部位,透视下将支架安放在选定部分,如支架扩张不满意,可选取合适球囊行后扩张,使支架能充分扩张到和狭窄远端正常血管直径接近(大致即可,因支架术后还有自膨功能),回收保护伞,术后常规给予低分子肝素钠0.4ml肌注,1/12h,3天。同时口服氯吡格雷及阿斯匹林抗血小板治疗。术后3月任选一种抗血小板治疗至少6月以上,严密随访。
     结果:病人原有症状明显缓解或消失,无操作技术失败,8例病人狭窄程度超过90%患者考虑保护伞通过困难先选取Amii球囊行预扩张,其余患者均直接放入保护伞后进行了支架植入,支架植入到位情况满意,有2例病人因颈动脉狭窄位置过高而将保护伞放置在颈内动脉岩骨段水平,20例病人支架植入后发现狭窄改善不满意而行后扩张,残余狭窄率均小于30%,术后颈动脉平均狭窄率从(76±20)%降低至(15±18)%。
     本组病人无围手术期死亡及严重神经系统并发症,20例病人在颈动脉分叉处行球囊扩张时(不论是预扩还是后扩),出现心率减慢,12例出现血压下降,经注射阿托品及多巴胺后好转,未引起不良反应。所有病人均行彩超随访,16例患者行DSA复查,随访最长时间18月,7例支架植入后3月发现支架有不同程度狭窄,但狭窄率未超过50%,支架内光滑,考虑有血管内皮形成,且病人无脑缺血症状,故未行进一步处理。
     结论:血管内治疗是治疗颈动脉粥样硬化性狭窄的安全有效手段。选择合适的病例是CASS成功的前提和重要条件,CASS手术最常见的并发症是脑栓塞,使用保护伞可以有效降低中风的发生,严格血管内支架成形术的围手术期处理,术中精细操作及术后的密切观察处理是防止手术失败的根本措施。
Cerebral arterial thrombosis is common frequently-occurring disease in mankind,the incidence of cerebral arterial thrombosis a year in China is 0.12~0.18%, casefatality is 0.08~0.12%, arterial stenosis is the main cause in these factor.
     Carotid artery atherosclerotic is an important risk factor of cerebral arterialdisease, 20%~30%apoplexy results from carotid artery atherosclerotic stenosis, as aresult, carotid artery atherosclerotic stenosis is the hot spot for pay close attention toin neuroscientist. Thomas Willis founded early total obstruct of carotid artery inautopsy in 1684, Chiar emphasized external skull carotid artery obstruct was theimmediate cause of stroke,
     Fish researched the pathology of carotid artery stenosis in 50's last century andsuggested: it might be effective to prevent stroke for surgical process in carotid arterycrotch; 3 Argentina doctors finished a resects of carotid artery stenosis and MCA-STAbypass for a 41 years man with anemia and right hemiplegics; DeBakey successfulfinished a carotid endarterectomy (CEA) for a 53 years old people with repeatedlytransient ischemic attack (TIA) in 1953; After this, a large number of scholar reportedmany operations, but in 80's, 20 century, some poor curative effect made physiciansto suspect the effect of CEA, This suspect and controversy resulted sharp descend ofthe number for CEA surgery.
     To solute the question of the effect of CEA, some large-scale to look up and tocompare random clinical trial has been done by the end of 90's last century, representative were:①North American Symptomatic Carotid Endarterectomy Trial(NASCET, 1988~1991),②European Carotid Surgery Trialists' CollaborativeGroup(ECSTCG; 1981~1991),③Asymptomatic Carotid Arthrosclerosis Study(ACAS,1987~1993). They draw some important conclusion:①CEA is extremely utility forhomonymy carotid artery weight stenosis with near time hemisphere ischemic andTIA;②to carotid artery weight stenosis with cerebral ischemia symptom, CEA is thebest therapeutic tool;③CEA has apparent curative effect in prevent stroke for nosymptom carotid artery stenosis without operation contraindicated people.
     To suffer from the test report enhearten above-mentioned, the case of particularCEA in the world improved rapidly since 1990's, literature number report improvedmultiplication, too. The technical improvement made the complication of CEA lessand less, as a result, there were about 100 thousand people received CEA per year bythe end of 1980's.
     But CEA as an operation still has determinate trauma and chanciness, clinicaldoctors begun to find a more micro-injury way to solve the question of carotid arterystenosis. Dotter firstly described percutem intracavity arterioplasty (PTA), Kerber cutopen blood vessel with sacculus dilatation to treat carotid stenosis in 1980, Mathiasfinished PTA for a woman with carotid artery fibrodysplasia in 1979 afterexperimentize on animal, successfully finished the first carotid artery stenosisstenting in 1989, then, the cases of CASS appeared unceasing in the world. PTA cancause endomembrane tear apart、plaque shifting and embolus desquamate and vesselwall elasticity recovery, this can result vessel secret compartment even block up.Cerebral embolism and restenosis became chief factor of effecting curative effect.With the improvement of technically achievement ratio in stentt insertion (98%-99%)and descend of complication, CASS appear a tendency to replace CEA gradually. InChina, from 1994 to September 2005, there were 297 articles about carotid arterystenosis research, in these articles; there were 1578 cases with CEA but 4165 cases
     In spite of these, the CASS still has determinate complications:①hyperperfusion injury. Which is a complication founded first after CAS.②cerebralinfarction. It is the main complication after CAS.③The place of arteriorpuncturehaematoma.④carotid arteriospasm, secret compartment and obstruction.⑤cardiac rhythm Brady and hyperpiesia.⑥stem restenosis and stentdeformation.
     This research undertakes the animal experiment of carotid artery atheroscleroticstenosis emphasize, observed and summarize the preliminary experiment of CASS inthe cases with carotid artery atherosclerotic stenosis.
     PartⅠThe establishment of pig model of carotid atherosclerotic stenosis
     Objective: To establishes the methods and factors affecting the development ofa stable and reliable animal model suitable for experimental studies of surgicaltreatments of carotid atherosclerotic stenosis (CASS).
     Methods: Using 10 normal pigs, lesions were created by hot air-drying isolatedsegments of carotid arteries. Empirical procedure: pig to anesthetize→recipe blood ofear to check blood-fat→to lesions double common carotid artery by hotair-drying→feeding the pigs a diet of 6%cholesterol, 12%peanut oil for 2months→recipe blood of ear to check blood-fat→inspected by Doppler color flowimaging, DSA and CTA→reset pathological changes ICA to pathological exam.Evaluated the stenosis of carotid arteries and observed the character of pathologicalchanges. The method of ICA endarterium lesions by hot air-drying: to reveal anddissociation one side CCA for 8 cm by aseptic technique, to obstruct by aneurysmclip in distant and near place, discussion blood engthways, aerates it by electricityaerate for 3 minutes spur 20cm after turnover; rinsed by saline water, sutured innatural position, recanalization after replaced by saline water. To sew up whole rangesoft tissue. Intramuscular penicillinu 80 pan- unit after method at once, afterwardsadds norfloxacin in animal feed, 0.4g~*3/D, for 5 days. Determination extent of ICA:using the software in DSA to precision measurement the diameter of most stenosis ineach ICA (DMS) and the diameter of distal end of normal ICA (DCC). The ratio ofstenosis=(DCC-DMS)/DCC~*100%. The judgement of external stenosiss: stenosisratio<70%were unable to satisfied the requirement for test, stenosis rati≥70%wereable to satisfied the requirement.
     Results: No animal dead. In 20 vasculars, 19 with severe stenosis were all morethan 70%, the ratio of success is 95%. No completely vascular occlusion.Determination of Pig blood-fat: LDL-C increased about 15 times than foundation after feed by high lip foods for 2 months, otherwise, the HDL-C in TC which haveresist scleratheroma function increased about 9 times. The Doppler color flowimaging indicates that blood flow rate in injured place accelerates obviously after 2months feeding than before, peak amplitude raise up, both DSA and CTA demonstrateobviously stenosis in ICA. The pathological studies suggested that the atheroscleroticlessions were belong to the mature fibrous plaque period as fed the atherogenic diedfor 2 months.
     Conculsion: The carotid arteries of pig have a well same as mankind inantatimical and physiology. Injured and fed as described by the authors, thepercentage of stenosis and pathological changes of the animal model is stable andreliable, and it meets the demand of experimental studies of surgical treatment ofCASS.
     PartⅡPestenotic and poststenotic hemodynamic alter in the ICA of pit model
     Objective: To study the prestenotic and poststenotic hemodynamic alter of ICAand Intracal arterial in pig.
     Methods: To adopt the method stated by partⅠ, to establish the pig model ofcarotid atherosclerotic stenosis, before and after modeling, using 3D Doppler colorflow imaging made by Acuson company(USA), with 6MHz scarching unit toexamine the characteristic of blood flow via the neck area of the body; hemodynamicparameter in each blood vessel include: peak systolic velocity (PSV), ending diastolicvelocity(EDV), mean glow velocity(MVF) and pulsatility index(PI)。Location andcontent for detect were same as preparation.
     To record the diameter of stenosis (d), the diameter of distal end of normalICA(D), character of plaque and PSV in most stenosis place, to calculate the stenosisextent of blood vessel and volume of blood flow per minute (Q) by below formula。stenosis extent of inner diameter=(D-d)÷D×100%Q=Vm×S×60 Among the total, S is blood vessel's areas, Vm is time average blood flow rate.
     Results: After the establishment of pig model of carotid atherosclerotic stenos,all MCA's PSV have negative acceleration [post operation (95.78±9.86)cm/s, preoperation (72.04±12.24)cm/s, P<0.05]. ICA's PSV after 2 months post operationincrease significantly than preparation [post operation (244.76±52.30)cm/s, preoperation (l13.09±19.92)cm/s, P<0.05]; all volume of blood flow decreasesignificantly than pre operation [post operation (215.18±41.55)ml/min, pre operation(382.68±33.26)ml/min, P<0.05]. After feed by high lip foods for 2 months postoperation, The Doppler color flow imaging indicates that pig's ICA lumina becameobviously stenosis, endomembrane thickening and different degree atheromatousplaque adnexal wall. after founding model, velocity of ICA was (104.9±12.0)cm/s,but the velocity pre operation was (54.7±7.4)cm/s, The Doppler color flow imagingindicates feed by high lip foods for 2 months post operation, carotid artery pulse ofpig present a type of high resistance, RI rise obviously[post operation (0.91±0.09),pre operation (0.28±0.07), P<0.05].
     Conculsion:①The Doppler color flow imaging is simple, quickly andaccurately, which can clear display the changes of endarterium, understand the size ofplaque, position and influence to blood flow.
     ②While ICA of pig become severe stenosis, intracal arterial perfusion descend,appears depress of blood flow rate: arterial perfusion of double hemisphere and circacirculation changes asymmetry, otherwise outside cranium artery appears increase ofblood flow rate, Doppler color flow imaging indicates peak value raise up, blood flowrate obviously decreases obviously.
     ③Although DSA is the "gold standard" of diagnose and evaluation to vascularlesion, but respecting it's injury、expensive and uneasy to accept, it can't to a screenand repeatedly detect way. Doppler color flow imaging has simply, repeatedly andeconomical, as a result, it is a reliable indicator to diagnose intracal and cervix bigvessel stenosis.
     PartⅢInitial follow-up of Endovascular stenting for stenosis of internalcarotid artery
     Objective: To conclude the initial experience of percutaneous transluminalstenting for stenosis of internal carotid artery (ICA).
     Methods: From May, 2002 to November, 2005, 32 CEVD patients wereidentification by outpatient because of repeated transient ischemic attacks (TIA) orcerebral infarction. Which clinical manifestation and neuroimagings correspondedstand of NASCET, 23 males, 9 females, 55~79 years old, average age is 64.3 yearsold. 24 cases display TIA, 2 display severity dizzy, 6 were old cerebral infarction,without severity nerve functional disturbance. In these patients, 23 cases withhypertensive disease, 15 cases with hyperlipemia, and 7 with diabetes.
     Imaging data: all cases received MR scanning Preoperative, partly received DWIand PWI weighted imaging to understand if there was new infarction, all patientsreceived Doppler color flow imaging, DSA results shows: 23 cases had stenosis infurcation of CCA, 9 stenosis situated with sub terminal ICA. The stenosis degreewere all over 70%, The mean degree of stenosis was (76±20)%, 8 cases were over90%, mean length of stenosis was 1.6~4.2cm
     Antiplatelet prepare should be adopt 3~5 days pre operation, routine monitoringin operation, with local anesthesia or total anesthesia, then DSA of cerebral finished,to evaluate the result of DSA, confirm the responsibility vessel, Under the guaid ofRoadmap of DSA, self-expandable stents were placed into the stenosis.Post-expanded was selected to execution. Retrieve protective umbrella, intramuscular0.4 ml Low Molecular Heparin, 1/12h, 3 days. At the same times, take orallyclopidogrel and aspermin, one kind of antiplatelet treated more than 6 months postoperation and follow-up.
     Results: The symptoms of patients were relieve and vanished, 8 patients withstenosis degree over 90%received Amii sacculus expanding, No operative failure, thestents were placed in the exact place of stenosis. Among 41 stenosis in 32 patientswere successfully treated with self-expansion stents. The mean degree of stenosisreduced from(76±20)%to (15±8)%. No other complications occurred except a frontallobe cerebral infarction occurring in 1 patient during operation. All cases received follow-up with Doppler color flow imaging, 16 received DSA follow-up, No TIA orinfarction happened in the 5-18months (mean 10.7 months) of follow-up. Clinicalsymptoms were significant improved than pre-operation. 7 cases after stenting for 3months founded stenosis but less than 50%, smooth and glossy in stent, thinking therewere blood vessel endothelium formed and patients without the symptom ofinfarction, as a result, no further treatment to adept.
     Conclusion: Endovascular stenting is a safe and effective way in the treatmentof carotid artery stenosis. Suitable cases are the precondition and important conditionto success of CASS. The most complication of CASS is infarction; adoptingprotective umbrella can decrees the take place of stroke. Strictly process aroundoperative, fineness procedure and closely observe, handle are fundamentalmeasurements to avoid failed.
引文
[1] Lastas A, Graziene V, Barkauskas E, etal. Carotid artery ather osclerotic plaque: clinical and morphological immuno histo chemical correlation. Med Sci Monit, 2004, 10(11): 606 6014.
    
    [2] Hennerici MG. The unstable plaque. Cerebrovasc Dis, 2004, 17(13): 17-22
    [3] De Jahromi AS, Cina CS, Liu Y, etal. Sensitivity and specificity ty of color duplex ultrasound measurement in the estimation of internal carotid artery stenosis: a systematic review and meta analysis. J VascSurg, 2005, 41(6): 962 972.
    [4] Soma, Maurizio R, Donetti, Elena, etal. Recombinant Apoli poprotein A IsubMilanoDimer Inhibits Carotid Intimal Thickening Induced by Perivascular Manipulation in Rabbits. Circles, 1995, 76(3): 405-411.
    [5] Pozo M, Castilla V, Gutierrez C, etal. Ursolicacid inhibits neo intimaformation in the rat carotid artery injury model. Athero sclerosis, 2005, 24(3): 576-583.
    [6] Nanobashvili J, Prager M, Jozkowicz A, etal. Positive effect of treatment with synthetic steroid hormonetibolon on intimal hyper plasia and rest enosis after experimental end authorial injury of rabbit carotid artery. EurSurgRes, 2004, 36(2): 74 82.
    
    [7] Meyer, Guido RY, Van Put, etal. Possible Mechanisms of Collar Induced Initial Thickening. Arteriosclerosis Thromb Vasc Biol, 1997, 17(10): 1924 1930.
    [8] Betz E, Schlote W. Responses of vessel wallsto chronically lyap plied electrical stimuli. Basic Res Cardiol, 1979,74(1): 10 20.
    [9] Khurana R, Zhuang Z, Bhardwaj S, etal. Angiogenesis dependent and independent phases of initial hyperplasia. Circulation, 2004, 110(16): 2436 2443.
    [10] Dietrich G, Tepe T, Grafen F, etal. Reduction of initial hyper plasia with Re 188 labeled stents in a rabbit model at 7 and 26 weeks: an experimental study. Card iovasc Intervent Radiol, 2005,28(5): 632 -637.
    [11] Gordon AA, Ferns AL, Stewart L, etal. Arterial response to mechanical injure: balloon catheter deendothelialization. Athero sclesis, 1992, 3(2): 89-104.
    [12] Chekanov VS, Mortada ME, Tchekanov GV, etal. Pathologic And histological results of electrical impulses in a rabbit model of atherosclerosis. J Vasc Surg, 2002,35(3): 554-562
    [13] Booth RF, Martin JF, Honey AC, etal. Rapid development of atherosclerotic lesions in the rabbit carotid artery induced by perivascularman. Atherosclerosis, 1989,76(23): 257-268
    [14] VanPut DJ, Va nOsselaer N, De Meyer GR, etal. Role of Poly morphs nuclear Leukocytes in Collar Induced Initial Thickening in the Rabbit Carotid Artery. Arterioscler Thromb VascBiol, 1998,18(6): 915-921.
    [15] Chiesa G, Rigamonti E, Monteggia E, etal. Evaluation of a soft atherosclerotic lesion in the rabbit aorta by an invasive IVUSmeth odversusanon invasive MRI technology. Atherosclerosis, 2004, 174(1): 25-33.
    [16] Kumar A, Lindner V. Remodeling with neointima formation in the mouse carotid artery after cession of blood flow. Arterioscler ThrombVascBiol, 1997,2238-2244.
    [17] Mousa SA, Kapil R, Mu DX. Intravenous and oral antithrombotic efficacy of the novel platelet GPⅡb/Ⅲ aantagonistroxifiban (DMP754) and its free acid form, XV459. Arterioscler Thromb VascBiol, 1999, 19(10): 25-35.
    [18] Holm J, Hansson GK. Cellular and immunologic features of carot id artery disease in man and experimental animal models. Eur J VascSurg, 1990, 4(1): 49-55.
    [19] 王启弘,马廉亭,周志红,等.改进手术技术制作的犬囊状动脉瘤模型.中华实验外科杂志,2005,22(9):1107-1108.
    [20] LeVeen RF, Wolf GL, Villanerva TG; etal. New rabbit atherosclerosis model for the investigation of Tran luminal angioplasty. Invest Radiol, 1982, 17: 470-475.
    [21] 高奋,李静梅,肖传实,等.高同型半胱氨酸血症兔模型动脉粥样硬化的形成.中国动脉硬化杂志,2002,10(2):348-349.
    [22] 张磊,陈国荣,郑荣远,等.高脂加空气干燥法建立兔颈动脉粥样硬化模型.中国动脉硬化杂志,2001,9(2):155-158.
    [23] 徐永革,周定标,王自正,等.颈动脉粥样硬化性动物模型的建立.中华神经外科杂志,2003,19(4):255-258.
    [24] Neaton JD, Blackburn H, Jacobs D, etal. Serum cholesterol level and mortality findings for men screened in the Multiple Risk Factor Intervention Trial [J]. Arch Intern Med, 1992, 152: 1490-1500.
    [25] Fagot Campagna A, Hanson RL, Narayan KM, etal. Serum cholesterol and mortality rates in a native American population with low cholesterol concentrations: a U shaped association [J]. Circulation, 1997, 96: 1408-1415.
    [26] Lepala JM, Virtamo J, Fogelholm R, etal. Different risk factors for different stroke subtypes; association of blood pressure, cholesterol, and antioxidants [J]. Stroke, 1999, 30:2535-2540
    [27] LIPIDS Study Group. Long term effectiveness and safety of pravastatin in 9014 patients with coron a ryheard disease and average cholesterol concentrations: the LIPID trial follow up [J]. Lancet, 2002, 359:1379-1387
    [28] Ohtani K, Egashira K, Hiasa K, et al. Blockade of vascular endothelial growth factor suppresses experimental rest enosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells [J], Circulation, 2004, 110: 2444-2452.
    [29] 王春喜,蔡相军,梁发启,等.髂股动脉粥样硬化闭塞症家兔模型的制作.中华实验外科杂志.2000,17(3):259.
    [1] North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high grade carotid stenosis. N Engl JMed, 1991, 325: 445-453.
    [2] European Carotid Surgery Trialists' Collaborative Group. MRC European Carotid Surgery Trial: Interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet, 1991, 337:1235-1243.
    [3] Executive Committee for the A symptomatic Carotid Athero sclerosis Study. Endarterectomy for a symptomatic carotid artery stenosis. JAMA, 1995, 273: 1421-1428.
    [4] Carpenter JP, Lexa FJ, Davis JT. Determination of six type center greater carotid artery stenosis by duplex Doppler ultrasonography. J VascSurg, 1995, 22: 697 -703.
    [5] Blackshear WM, Phillips DJ, Thiele BL, etal. Detection of carotid occlusive disease by ultrasonic imaging and pulsed Doppler spectrum analysis. Surgery, 1979, 86: 698-706.
    [6] Bluth EI, Stavros AT, Marich KW, etal. Carotid duplex monograph: A multi center recommendation for standardized imaging and Doppler criteria. Radio graphics, 1988, 8: 487-506.
    [7] Zierler RE, Kohler TR, Strand ness DE Jr. Duplex scanning of normal or minimally diseased carotid arteries: Correlation with autobiography and clinical outcome. J Vasc Surg, 1990, 12: 447-455.
    [8] Zbornikova V, Lassvik C, Johansson I. Prospective evaluation of the accuracy of duplex scanning with spectral analysis in carotid artery disease. Clin Physiol, 1985,5: 257-269.
    [9] Corriveau MM, Johnston KW. Inter observer varies ability of carotid Doppler peak velocity measurements among technologists Nan ICAVL an accredited vascular laboratory. J Vasc Surg, 2004, 39: 735-741.
    [10] Moneta GL, Edwards JM, Chitwood RW, etal. Correlation of North American Symptomatic Carotid Endarterectomy Trial (NASCET) angiographic definition of 70% to 99% internal carotid artery stenosis with duplex scanning. J Vasc Surg, 1993, 17: 152-159.
    [11] Carpenter JP, Lexa FJ, Davis JT. Determination of duplex Doppler ultrasound criteria appropriate to the North America cans Symptomatic Carotid Endarterectomy Trial. Stroke, 1996, 27: 695-699.
    [12] 华扬编著.实用颈动脉与颅脑血管超声诊断学.北京:科学出版社,2002.185.
    [13] 华扬,凌晨,段春,等.双功能彩超与经颅多普勒超声对颈内动脉重度狭窄或闭塞的诊断价值.中华超声影像杂志,2000,9:413-415.
    [14] Grant EG, Benson CB, Moneta GL, etal. Carotid artery stenosis: gray scale and Doppler ultrasound diagnosis—society of radiologists in ultrasound consensus conference. Ultrasound Q, 2003, 19: 190-198.
    [15] 周勤.超声评价颈动脉硬化斑块与脑梗塞的关系[J].临床超声医学杂志,2002,4(6):336~338.
    [16] Ringelstein EB, Weiller C, Weckesser S. Cerebral vasomotor reactivity is significantly reduced in low flow as compared to thrombi embolic infarctions:the key role or circle of Willis [J].J Neural Sic, 1994,121: 103-109.
    [17] 华扬.实用颈动脉与颅脑血管超声诊断学[M].北京:科学出版社,2002.69-74.
    [18] Muller M, Hermes M, Bruckmann H, etal. Trans cranial Doppler ultrasound in the evaluation of collateral blood flow in patients with internal carotid artery occlusion: Correlation with cerebral angiography [J]. Am J Neuroradial, 1995, 16(1): 195-202.
    [19] 郑宇,华扬,凌晨,等.颈动脉严重狭窄或闭塞对颅内循环的影响[J].中国医学影像技术,2004,20(6):901-903.
    [1] Kerber CW, Cromwell LD, Loehden OL. Catheter dilatation of proximal carotids enosis during distal bifurcation darterectomy [J]. AJNR, 1980, 1:348-349
    [2] Mathias K, Jger H, Gissler M. Carotid angioplasty and stent placement: A 20 year experienence [M]. Paris, ETC 99: Tenth International Course Book of Peripheral Vascular Intervention, 1999.729-737
    [3] Athanasoulis CA, Plomaritoglou A. Preoperative imaging of the carotid bifurcation. Currenttrends. IntAngiol, 2000, 19: 1-7.5
    [4] Norris JW, Morriello F, Rowed DW, etal. Vascular imaging before Carotid endarterectomy. Stroke, 2003, 34: 16
    [5] Streifler JY, Eliaziw M, Fox AJ, etal. Angiographic detection of carotid plaque ulceration. Comparison with surgical observations in a multicenter study. North American Symptomatic Carotid Endarterectomy Trial. Stroke, 1994, 25: 1130-1132
    [6] Nederkoorn PJ, vanderGraaf Y, Hunink MG. Duplex ultrasound and magnetic resonance angiography compared with digital subtraction angiography in carotid artery stenosis: a systematic review. Stroke, 2003, 34:1324-1332
    [7] AbuRahma AF, Thiele SP, Wulu JTJr. Prospective controlled study of the natural history of a symptomatic 60% to 69% carotid stenosis according to ultrasonic plaque morphology. J VascSurg, 2002, 36:437-442
    [8] Moore WS. For severe carotid stenosis found on ultrasound, further arterial evaluation is unnecessary. Stroke, 2003, 34:1816-1817
    [9] Rothwell PM. For severe carotid stenosis found on ultrasound, fur the arterial evaluate on prior to carotid endarterectomy is unnecessary: the argument against. Stroke, 2003, 34: 1817-1819
    [10] Arnold JAC, Modaresi KB, Thomas N, etal. Carotid plaque char cauterization by duplex scanning: observer error may undermine cur rent clinical trials. Stroke, 1999,30:61-65
    [11] U-King-Im JM, Trivedi RA, Graves MJ, etal. Contrast enhanced MR angiography for carotid disease: diagnostic and potential clinical impact. Neurology, 2004, 62:1282-1290
    [12] Hollingworth W, Nathens AB, Kanne JP, etal. The diagnostic curacy of computed tomography angiography for traumatic or atherosclerotic lesions of the carotid and vertebral arteries: a systematic view. Eur J Radiol, 2003, 48:88-102
    [13] McKinney AM, Casey SO, Teksam M, etal. Carotid bifurcation calcium and correlation with percent stenosis of the internal carotid artery on CT angiography. Neuroradiology, 2005, 47:1-9
    [14] Nandalur KR, Baskurt E, Hagspiel KD, etal. Calcified carotid atherosclerotic plaques associated less with ischemic symptoms than is nonqualified plaque on MDCT. A JR AmJ Roentgenol. 2005, 184:295-298
    [15] Walker LJ, Ismail A, McMeekin W, etal. Computed tomography angiography for the evaluation of carotid atherosclerotic plaque: correlation with histopathology of endarterectomy specimens. Stroke, 2002, 33:977-981
    [16] Castriota F, Cremonesi A, Manetti R, etal. Impact of cerebral protection device on early outcome of carotid stenting. J Endovasc Ther, 2002, 9:786-792
    [17] Qureshi AI, Luft AR, Mudist Sharma BS, etal. Frequency and determinants of post procedural homodynamic in stability after carotid angioplasty and stenting [J] Stroke, 1999, 30:2086-2093
    [18] Mubarak N, Roubin GS, Vitek JJ, etal. Effect of the distal-balloon protection system on micro remobilization during carotid stenting [J].Circulation, 2001, 104:1999-2002
    [19] Li SM, Dong ZJ. Wu J, etal. The application of percutaneous trunsluninal stent in angioplasty to high degree stenosis of internal carotid artery. China J Radiol, 2000, 34: 817-819.李慎茂,董宗俊,武剑,等.血管内支架在治疗颈内动脉高度狭窄疾病中的 应用.中华放射学杂志,2000,34:817-819
    [20] Li SM, Miao ZR, Ling F, etal. Percutaneoustrunsluminal stenting for stenosis of internal carotid artery: A report of 83 cases. Chin J GenSurg, 2002,17:325-328.李慎茂,缪中荣,凌锋,等.颈内动脉狭窄83例的血管内支架治疗.中华普通外科杂志,2002,17:325-328
    [21] Mc Carthy WJ, Wang R, Pearce WH, etal. Carotid endarterectomy with an occluded contral ateral carotid artery. Am J Surg, 1993,166:168-172
    [22] Riles TS, Imparato AM, Jacobo witz GR, etal. The cause of preoperative stroke after carotid endarterectomy. J Vasc Surg, 1994,19:206-216
    [23] Appleberg MC, Cottier D, Crozier J, etal. Carotid endarterectomy for a symptomatic carotid artery stenosis: patients with sever bilateral disease a high risk subgroup. Aust NZJ Surg, 1995, 65: 160, 165
    [24] Wholey MH, Wholey M, Berggeron P, etal. Current global stature of carotid artery stent placement. Cathet Cardiovase Diagn, 1998,44:16
    [25] Yadav J Sk, Roubin CS, Vitek J, etal. Elective stenging of the extra cranial carotid arteries. Circulation, 1997, 95:367-381
    [26] Wholey MH, Wholey MH, Jarmoloski CR, etal. Endovascular stents for carotid artery occlusive disease [J]. Endvasc Surg, 1997, 4:326-338
    [27] Wholey MH. Global experience in cervix cal carotid artery stent placement [J]. Catheter cardiovasl Interments, 2000, 50:160-167
    [28] 马廉亭.介入神经外科学.武汉:湖北科学出版社,2003(1),第1版:402
    [29] 吴中学.脑血管疾病的支架应用展望[J].中华神经外科杂志.2005.21(2):65-66
    [30] Kerber CW, Cromwell LD, Loehden OL. Catheter dilatation of proximal carotids enosis during distal bifurcation darterectomy [J]. AJNR, 1980, ⅰ: 348-349
    [31] 缪中荣,李玉芳,武一平.颈动脉支架成形术中少见并发症的预防和处理技巧[J].中国脑血管病杂志.2006.3(1):9-14
    [32] 洪波,刘建民,许奕.过滤伞保护下的颈动脉狭窄支架成形术[J].中华放射 学杂志,2004,38(1):45-47.
    [33] 李光,林曙光,陈纪言.支架置入后局部内膜增生以及血管紧张素ILAT1受体的演变[J].第一军医大学学报,2005,25(1):96-98
    [34] He shihua, Wang yan etal. Safety and efficacy of carotid artery stenting.Wang yiqing[J]. 南方医科大学学报,2006,26(1):6-10
    [35] 林爱龙,马廉亭,李俊,等.颈动脉粥样硬化狭窄的血管内支架治疗[J].南方医科大学学报,2006,26(12):1731-1732.
    [36] Wholey MH. Global results of Carotid stenting trials [J]. JVIR, 2002, 13(2) Part2: 183.
    [1] 马廉亭.介入神经外科学.武汉:湖北科学出版社,2003,1第1版:402.
    [2] Debakey MH. Carotid endarterectomy revisited [J]. J En dovasular Surg, 1996, 3:4.
    [3] Kerber CW, Cromwell LD, Loehden OL. Catheter dilatation of proximal carotids enosis during distal bifurcation darterectomy. [J]. AJNR, 1980, 1: 48-349.
    [4] Mathias K, Jger H, Gissler M. Carotid angioplasty and stent placement: A 20 year experienence [M]. Paris, ETC 99: Tenth International Course Book of Peripheral Vascular Intervention, 1999. 729, 737
    [5] Hurst RW. Carotid angioplasty [J]. Radiology, 1996, 201: 613-616.
    [6] The North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in Symptomatic patients with high-grade carotid Stenosis [J]. N Engl J Med, 1991, 325: 445-453.
    [7] European Carotid Surgery Titlist's Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70%-99%) or with mild (0%-29%) carotid stenosis [J]. Lancet, 1991, 337(8752): 1235-1243.
    [8] Endarterectomy for asymptomatic carotid artery stenosis. Executive committee for the Asymptomatic Carotid Arthrosclerosis Study [J]. AMA, 1995, 273(18): 1421-1428.
    [9] 周定标主编.颈动脉内膜剥脱术.北京:人民军医出版社,2005年1月第1版,第1页.
    [10] Paciaroni M, Eliasziw M, Sharpe B L, etal. Long-term clinical and angiographic out comes in symptomatic patients with 70% to 99% carotid artery stenosis. Stroke, 2000, 31:2037-2042.
    [11] European Carotid Surgery Titlist's Collaborative Group. Endarterectomy for moderate symptomatic carotids enosis: interim results from the MRC European Carotid Surgery Trial [J]. Lancet, 1996, 347; 1591-1593.
    [12] Billet J, Feinberg WM, Castaldo JE, etal. Guidelines for carotid endarteritis-my [J]. Circulation, 1998, 97(5): 501-509
    [13] Wholey MH. Global results of Carotid stenting trials [J]. JVIR, 2002, 13(2) Part2: 183.
    [14] Mubarak N, Roubin GS, Vitek JJ, etal. Effect of the distal-balloon protection system on micro embolization during carotid stenting [J]. Circulation, 2001, 104: 1999-2002.
    [15] Qureshi AI, Luft AR, Mudist Sharma BS, etal. Frequency and determinants of post proceed dual homodynamic in stability after carotid angioplasty and stenting [J] Stroke, 1999, 30: 2086-2093.
    [16] Wholey MH, Wholey MH, Jarmoloski CR, etal. Endovascular stents for carotid artery occlusive disease[J]. Endvasc Surg, 1997,4:326-338.
    [17] Wholey MH. Global experience in cervix cal carotid artery stent placement [J]. Catheter cardiovasl Interments, 2000, 50:160-167.
    [18] Castriota F, Cremonesi A, Manetti R, etal. Impact of cerebral protection device on early outcome of carotid stenting. J Endovasc Ther, 2002, 9:786-792.
    [19] Golledge J, Mitchell A, Greenhalgh RM, etal. Systematic comparison of the early outcome of angioplasty and end arterectomy for symptomatic carotid artery disease [J]. Stroke, 2000, 31:1439-1443.
    [20] Brooks WH, McClure RR, Jones MR, etal. Carotid angioplasty and stenting versus carotid endarterectomy: randomized trial in a community hospital. [J]AmColl Cardiol, 2001,38:1589-1595.
    [21] Brooks WH, McClure RR, Jones MR, etal. Carotid angioplasty and stenting versus carotid endarterectomy for treatment of a symptomatic carotid stenosis: a randomized trial in a community hospital. Neurosurgery, 2004, 54:318-325.
    [22] Roubin GS, Yadav JS, Lyer SS, etal. Carotids tent-supported angioplasty: a euro vascular intervention to prevent stroke [J]. Am J Cardiol, 1996,78(suppl3A):8-12
    [23] 凌锋,管凤增.颈动脉狭窄:支架植入术还是颈动脉内膜切除术?中华医学信息导报,2005,20(1):1.
    [24] 吴中学.脑血管疾病的支架应用展望.中华神经外科杂志,2005,21(2):65-66
    [25] 介入神经放射诊断治疗规范.第七届全国神经外科血管内治疗研讨会,2005年8月,重庆.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700