血管内支架成形术治疗基底动脉狭窄

目的 探讨血管内支架成形术治疗基底动脉狭窄的近期疗效。方法 20例症状性基底动脉狭窄应用球囊膨胀支架行血管内成形术治疗。结果 12例基底动脉恢复正常管径，8例狭窄程度减小80％以上，无手术相关并发症。无短暂性脑缺血发作(Transient ischemic sttack，TIA)或卒中再发作。脑血管造影随访13例，均无血管再狭窄。结论 血管内支架成形术治疗基底动脉狭窄的近期疗效令人满意。     

颈动脉支架成形术中脑保护伞释放鞘断裂1例

颈动脉支架成形术(CAS)是当今治疗颈动脉狭窄性病变的主要方法之一。我院血管外科于2007年2月治疗1例一侧颈内动脉高度狭窄,对侧颈内动脉闭塞的高危病人过程中,遇到脑保护伞释放鞘部分断裂的少见情况。本文就其处理技巧及经验总结如下。1病历简介病人男,73岁。因“反复发作右上肢无力”入院,术前诊断为颈动脉狭窄、一过性脑缺血发作及高血压病。术前头颅CT提示双侧基底节区腔梗死灶。颈动脉血管造影显示右颈内动脉起始段85%狭窄,斑块内未见明显龛影;左颈内动脉闭塞;右侧大脑中动脉及大脑前动脉显影良好,部分代偿左侧大脑血供;左椎动脉代偿…     

支架成形术治疗颅内血管狭窄的安全性及短期疗效分析

目的　评价血管内支架成形术治疗颅内动脉狭窄的安全性及短期疗效。方法　对 4 6例患者 5 0处颅内动脉狭窄病变行血管内支架成形术 ,其中基底动脉狭窄 16处 ,椎动脉颅内段狭窄12处 ,颈内动脉颅内段狭窄 13处 ,大脑中动脉狭窄 9处。结果　 5 0处狭窄中有 4 9处成功地进行了支架成形术 (98% ) ,动脉狭窄程度从治疗前的 (72 4± 12 3) %降为 (10 6± 7 8) %。本组患者无手术死亡及缺血性脑卒中 ;4例出现和操作有关的并发症 ,其中 1例发生近端颅外段颈内动脉夹层 ,1例微导丝引起颅内出血 ,2例穿刺部位出现皮下血肿。 37例患者临床随访超过 6个月 (平均 8 5个月 ) ,无缺血性脑卒中发生。结论　血管内支架成形术治疗颅内动脉狭窄的成功率高 ,具有一定的安全性 ,但长期疗效有待于进一步随访     

症状性大脑中动脉狭窄的血管内干预治疗

目的 探讨经皮腔内血管成形术及血管成形支架置入术治疗症状性大脑中动脉狭窄的可行性、安全性及有效性.方法 回顾性分析39例患者经药物治疗无效、反复短暂性脑缺血发作(TIA)或有明显脑缺血症状的大脑中动脉狭窄,经皮腔内血管成形或支架置入术的治疗及术后随访结果.结果 39例大脑中动脉狭窄(左侧23例,右侧13例,双侧3例,合并颈动脉狭窄5例)患者经皮腔内血管成形术9例、血管成形支架置入术30例(术后残余狭窄程度均<10%)均获成功,术后给予抗血小板聚集治疗,临床脑缺血症状和体征明显改善.2例患者术中见对比剂外泄,但无明显临床症状,且恢复良好;1例在术后1 h出现意识变化、对侧肢体活动障碍,CT提示支架侧底节区脑出血,经手术治疗后患者遗留语言障碍及右侧肢体不全偏瘫.其余患者无并发症发生.临床随访5～60个月,仅1例在支架置入7个月后右上肢无力症状复发,但较前轻微.经颅多普勒复查26例,显示原病变侧大脑中动脉血流速度增快2例;行数字减影血管造影复查14例,2例支架内发生再狭窄,均行药物治疗观察.结论 经皮腔内血管成形术及血管成形支架置入术治疗大脑中动脉狭窄是可行、安全、有效的;大样本的长期疗效有待于进一步观察.     

支架成形术治疗症状性脑供血动脉狭窄及其并发症分析

目的探讨应用颈动脉支架成形术治疗症状性脑供血动脉狭窄的安全性、临床疗效及其并发症的防治。方法对经彩色多普勒超声检查筛选,并经脑血管造影确诊的104例症状性脑供血动脉狭窄患者实施支架成形术治疗。分析围手术期及术后随访期相关并发症的发生情况。结果 1例术中出现严重血管痉挛,致手术失败,全组技术成功率99.04%(103/104)。术前平均狭窄率为82.23%,术后残余狭窄率均20.00%。术后1周内患者症状及神经功能缺损体征均有不同程度改善。24例术后3天发生心率减慢,其中20例出现血压下降;1例介入术后第9天脑出血死亡,1例术后10天靶病变部位急性血栓形成。随访2个月～3年,死亡2例,其中82例复查经颅多普勒(TCD)示血流速度正常,12例复查DSA未发现再狭窄、支架移位及缺血性脑卒中。结论颈动脉支架成形术是治疗症状性脑供血动脉狭窄较为安全、有效的方法,严格掌握适应证和熟练操作并规律服药可降低术中及术后风险。     

血管内支架成形术治疗颅外颈动脉狭窄

目的　评价颅外颈动脉狭窄支架成形术的安全性及近期疗效。　方法　 2 0 0 0年 10月～ 2 0 0 2年 12月共收治颈动脉狭窄 16 4例 ,其中颅外分叉部颈内动脉狭窄 14 6例 ,单纯颅外段颈内动脉狭窄 13例 ,单纯颈总动脉狭窄 5例 ,采用自膨胀支架进行血管成形治疗。　结果　 16 4例支架植入均获得成功 ,血管狭窄程度从治疗前 (78 8± 13 6 ) %降低到 (10 2± 7 5 ) % ,围手术期无死亡及大卒中发生 ,1例出现短暂性脑缺血发作 (Transientischemicattack ,TIA) (0 6 % ) ,1例出现小卒中 (0 6 % )。14 5例获得随访 ,时间 3月～ 30月 (平均 8 9月 ) ,随访期间无TIA及卒中发生 ,无死亡。术后 6月数字减影脑血管造影随访 4 5例 ,再狭窄 1例 (2 2 % ) ,但无临床症状。　结论　血管内支架成形术是治疗颈动脉狭窄安全而有效的方法 ,短中期结果令人满意。     

定向斑块切除联合药物涂层球囊治疗同侧锁骨下、椎动脉重度狭窄1例报告

<正>随着腔内技术的迅猛发展,支架成形术已成为动脉狭窄及闭塞性病变的重要治疗手段。椎动脉开口合并锁骨下动脉狭窄是较常见的颅外供血血管阻塞性疾病,也是引起椎-基底动脉短暂性脑缺血发作、患侧上肢缺血和后循环脑梗死的重要原因~([1,2])。我科曾成功应用定向斑块切除联合药物涂层球囊治疗椎动脉硬化所致重度狭窄患者~([3]),2018年7月我     

短暂性脑缺血发作与脑动脉狭窄的脑血管造影研究

目的探讨TIA与颅内外血管狭窄的关系,研究DSA对短暂性脑缺血发作(TIA)血管病变的诊断价值。方法选择符合TIA诊断标准的患者54例行颈部血管B超、经颅多普勒(TCD)、心脏超声以及DSA检查,观察TIA患者颈内动脉和椎动脉颅内、外血管有无狭窄及粥样硬化斑块。结果54例患者中发现46例有血管狭窄,其中颈总动脉狭窄2例,颈内动脉狭窄13例,大脑中动脉狭窄5例,锁骨下动脉狭窄3例,椎动脉狭窄18例,基底动脉狭窄5例。狭窄部位斑块31例。其中大动脉狭窄性TIA 36例,栓塞性TIA 13例,腔隙性TIA 3例,血管痉挛性TIA 2例。结论TIA患者大多存在颅内外动脉狭窄及粥样硬化斑块,颅内外动脉狭窄程度及粥样硬化斑块稳定性决定TIA类型。     

应用脑保护装置实施颈动脉支架成形术的临床经验

目的探讨脑保护装置在颈动脉支架成形术中的价值。方法自2000年10月至2006年8月对65例颈动脉狭窄患者实施了颈动脉支架成形术。共植入支架75个,其中颈内动脉支架68个,颈总动脉支架2个,同时植入锁骨下动脉支架2个,椎动脉支架3个,4例术前安装了临时起搏器。结果65例中2例脑保护装置置放失败,63例成功。63例脑保护装置中26例可见斑块碎片,1例术中出现一过性脑缺血,1例同时置入椎动脉支架后发生椎动脉血栓形成;9例术中出现一过性低血压、心动过缓,4例术前安装临时起搏器者未发生术中低血压。5例出现术后低血压,1例术后原有神经系统症状加重。1例双颈动脉支架成形术后出现高血压。结论颈动脉支架成形术是治疗颈动脉狭窄的有效手段,在有脑保护装置的条件下,正规熟练的操作和严格的预防措施能有效提高安全性,减少并发症。     

右侧肱动脉入路左颈动脉支架成形术治疗颈内动脉狭窄合并牛型主动脉弓1例报告

2013年10月我科收治1例63岁女性左颈动脉狭窄,有左侧脑梗死病史并频繁出现一过性脑缺血发作（transient ischemic attack,TIA）。术前CTA检查为牛型主动脉弓,左侧颈内动脉起始部重度狭窄,但位于C2水平不适合行颈动脉内膜切除术。采用全麻下经右侧肱动脉人路穿刺,造影导管选人左颈外动脉,加硬导丝引导F6长鞘选人左颈总动脉建立手术通路,然后常规进行保护伞下的颈动脉球囊扩张和支架成形术。手术成功,未发生任何并发症。术后1个月随访,TIA症状完全消失,颈动脉超声提示左颈内动脉支架术后血流通畅。我们认为经右侧肱动脉人路行支架成形术治疗牛型主动脉弓变异的左侧颈内动脉狭窄是安全、可行的。     

Surgical results of two cases of simultaneous surgery of carotid and coronary occlusive disease]

Two cases of symptomatic extracranial carotid artery stenosis associated with ischemic heart disease are reported. The first case was 72-year-old male, who was admitted because of transient ischemic attack due to the stenosis of left internal carotid artery. He had a history of myocardial infarction and coronary angiography revealed three vessel disease. The second case was 74-year-old female with diabetes mellitus. She was admitted because of cerebral infarction. The carotid angiography revealed critical stenosis of bilateral internal carotid arteries. Her coronary angiography revealed three vessel disease. Her chest symptom became unstable after her admission. In both cases, simultaneous carotid endarterectomy and coronary bypass grafting were performed with successful outcome. In the patients with symptomatic extracranial carotid occlusive disease associated with severe ischemic heart diseases, we advocate simultaneous operation both for carotid and coronary artery occlusive disease.     

颈动脉狭窄的外科手术治疗

目的探讨颈动脉内膜切除术(CEA)治疗颈动脉狭窄的疗效。方法对2001年1月—2011年5月90例颈动脉狭窄患者行颈动脉内膜切除术93次,其中男78例,女15例;年龄50～78(平均65.6岁)。术前有短暂性脑缺血发作62例(TIA),31例术前患过脑梗死。所有患者术前均行脑血管造影和\或CTA明确颈动脉狭窄,狭窄程度均>80%。对侧颈动脉狭窄或闭塞者22例。结果 90例术后临床症状改善,包括TIA消失,记忆力明显好转,语言障碍恢复等。术后80例获得随访1～36个月。15例发现有手术部位再狭窄,狭窄率小于25%,其中1例脑卒中,1例TIA保守治疗好转。其余13例无临床症状。结论颈动脉内膜切除术是治疗颈动脉狭窄的安全、有效的方法。     

Temporal profile of de novo development of moyamoya vasculopathy in an adult: case report

A 46-year-old woman developed transient ischemic attack (TIA) caused by progressive moyamoya vasculopathy in the right hemisphere. She had presented with minor cerebellar infarction due to left vertebral artery dissection 7 years prior to the onset of TIA. Initial carotid angiography at the onset of vertebral artery dissection demonstrated absence of steno-occlusive changes in the anterior circulation. During the next 7 years, she had been strictly followed up with magnetic resonance angiography every 6 months, which demonstrated the asymptomatic development of steno-occlusive change in the proximal right middle cerebral artery, finally involving the terminal internal carotid artery. Carotid angiography at the onset of TIA showed terminal internal carotid artery stenosis with abnormal vascular network at the right base of the brain, indicating a definitive diagnosis of moyamoya vasculopathy with unilateral involvement. She underwent right superficial temporal artery-middle cerebral artery anastomosis without complication one month later. TIA completely disappeared after surgery, and no cerebrovascular events occurred during the follow-up period of 6 months. De novo formation of moyamoya vasculopathy is extremely rare in adulthood. The present case demonstrated the entire temporal profile of the development of this rare entity in adulthood. The previous presentation of vertebral artery dissection before the development of moyamoya vasculopathy as well as the initiation of steno-occlusive change at the middle cerebral artery is apparently unique.     

Intracerebral haemorrhage after internal carotid endarterectomy

This paper reports three fatal cases of intracerebral haemorrhage after internal carotid artery thrombendarterectomy, one in a patient operated on four weeks after a cerebral infarction and two in patients operated after a transient ischemic attack. Two other late intracerebral haemorrhagic events are reported in patients submitted to internal carotid artery surgery, one from a ruptured intracerebral aneurysm and another probably due to anticoagulation medication. It is emphasized to make a clear distinction between haemorrhagic and ischemic events when reporting stroke frequency in patient materials after internal carotid artery surgery.     

颅外段颈动脉狭窄的治疗策略

目的：探讨颅外段颈动脉粥样硬化性狭窄的治疗方法。方法回顾性分析上海中山医院血管外科2012年1～6月51例颅外段颈动脉粥样硬化性狭窄患者的临床资料,16例行颈动脉内膜剥脱术（carotid endarterectomy,CEA）,35例行颈动脉支架置入术（ carotid artery stenting ,CAS）。结果51例手术均获成功,1例CAS术后即刻脑卒中,1例CEA术后第3天短暂性脑缺血发作（transient ischemic attack,TIA）,1例CAS术后颈动脉窦压迫。全组术后随访9～15个月,平均13．6月,复查颈动脉B超,无严重再狭窄。结论根据颅外段颈动脉粥样硬化性狭窄患者的相关医学资料,对于有下列情况之一的患者我们倾向于行CEA：①6个月内1次或多次TIA,且颈动脉狭窄度≥70％;②6个月内1次或多次轻度非致残性卒中发作,症状或体征持续超过24小时且颈动脉狭窄度≥70％;③对于经颈部血管CTA和颈动脉全脑血管造影发现的颈动脉狭窄段≥2 cm。对于有下列情况之一的患者我们倾向于行CAS：①无症状性颈动脉狭窄度≥70％;②有症状性狭窄度范围50％～69％;③无症状性颈动脉狭窄度＜70％,但血管造影或其他检查提示狭窄病变处于不稳定状态。     

Spontaneous intracerebral hemorrhage following carotid endarterectomy. Experience of 328 operations from 1983-1988.

In a consecutive series of 328 carotid endarterectomies there were two cases of postoperative intracerebral hemorrhage. The patients with transient ischemic attacks and subsequent major cerebral infarction had repair of their very tight carotid stenosis. Each developed intracerebral hemorrhage after a symptom free interval and hypertension was uncontrolled during the postoperative period. Hypertension is a significant complication of carotid endarterectomy and may be a prominent factor in the development of intracerebral hemorrhage after carotid endarterectomy. Also defective cerebrovascular autoregulation in chronic ischemic brain regions may predispose patients to intracerebral hemorrhage.     

Early carotid endarterectomy after cerebral infarction

The objective of the study was to review our recent experience with carotid endarterectomy performed within 30 days of completed cerebral infarction and to evaluate the role of computed tomographic (CT) scanning in the decision-making process. Twenty-seven of 302 operations (9%) were carried out during the 30-day time period. The mean interval between cerebral infarction and surgery was 14 days. Angiography revealed severe stenosis (greater than 75%) of the internal carotid artery in 19 patients. Severe stenosis with deep ulceration found in 6 patients and moderate stenosis (i.e., 50-75%) with deep ulceration was found in 2 patients. CT scans showed recent infarction in 4 patients and an old subcortical lacune in 2 patients. Twenty-two patients were neurologically stable with mild deficits and showed normal results on a CT scan performed 24 hours or more after the ischemic event. These patients underwent early cerebral angiography and carotid endarterectomy without permanent morbidity or mortality. Two patients with moderate stable neurological deficits and findings of recent infarction on CT scans had uneventful postoperative courses. Five patients who were neurologically unstable underwent surgery. The 2 patients with repeated transient ischemic attacks and normal findings on CT scans had uneventful postoperative courses. Two of the three patients with progressive neurological deficits and CT findings of recent cerebral infarction experienced extension of their infarcts after surgery. One of these patients died. Our personal experience, together with a review of previous reports, indicated that patients who have minimal residual neurological deficits and whose CT scans show normal findings are at low surgical risk, perhaps approaching that of patients with transient ischemic attacks.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term follow-up study of 93 patients with TIA

Long-term outcome and recurrence rate were discussed in 96 patients of TIA out of 792 of cerebral ischemic disease who were admitted to our hospital during the past 11 years. They all had had attacks in the territory of internal carotid artery. Ninety-three patients could be interviewed finally. They included 63 males and 30 females and the age ranged from 36 to 88 years with an average of 60.5 years. The follow-up period ranged from 4 months to 8 years and 10 months with an average of 3 years and 1 month. Cerebral angiography was performed in 88 patients of them and revealed 16 patients of internal carotid artery stenosis, 12 patients of middle cerebral artery stenosis, 19 patients of severe cerebral arteriosclerosis and 41 patients of normal findings. CT scan was performed in 88 patients and showed abnormal findings in 12 patients. Eleven patients of them had lacunar infarction. Twenty-four patients of arterial stenosis (14 patients of internal carotid artery stenosis and 10 patients of middle cerebral artery stenosis) had surgical treatment of STA-MCA anastomosis (the superficial temporal artery-the middle cerebral artery) and carotid endarterectomy because they were considered to be cause of TIA. The other 69 patients were treated conservatively mainly with antiplatelet therapy. Four of 24 surgical treated patients developed another attack of cerebral ischemia thereafter, 2 patients had TIA of the contra-lateral hemisphere, one had cerebral infarction in the territory of posterior cerebral artery and the rest had lacunar infarction in the contra-lateral basal ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)