中青年急性脑梗死的危险因素分析

目的分析中青年急性脑梗死(ACI)的危险因素,为早期预防及干预提供临床依据。方法选取2017年1月-2017年12月于本院住院治疗的136例中青年ACI患者作为观察组,同时选取106例中青年非ACI住院患者作为对照组,对比分析两组高血压、糖尿病、高脂血症、吸烟、饮酒、白细胞(WBC)计数、同型半胱氨酸(Hcy)等指标的差异性,应用Logistic回归方程分析中青年罹患ACI的危险因素。结果通过单因素分析发现,观察组高血压、吸烟、饮酒、男性、WBC计数、血尿酸(BUA)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、Hcy,均显著高于对照组(P0.05);多因素分析提示高血压、吸烟、LDL-C是中青年ACI的独立危险因素。结论高血压、吸烟、饮酒、男性、WBC、BUA、TC、LDL-C、Hcy是引发中青年ACI的危险因素;其中高血压、吸烟、LDL-C是其独立危险因素。     

进展性脑卒中与血脂、颈内动脉斑块和狭窄的关系

目的探讨进展性脑卒中(PS)与血脂、颈内动脉斑块和狭窄的关系。方法对85例PS及85例非PS(NPS)患者进行血总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平检测,以及颈内动脉彩色超声多普勒检查,采用多因素Logistic回归分析其对PS的影响。结果 PS组患者LDL-C水平明显高于NPS组(P<0.01),PS组颈内动脉斑块和狭窄的比率(81.2%)显著高于NPS组(22.4%)(P<0.01)。Logistic回归分析显示,LDL-C(OR=5.035)颈内动脉斑块和狭窄(OR=3.224)为PS的危险因素。结论血LDL-C水平高及颈内动脉斑块和狭窄为PS发病的危险因素。     

进展性脑卒中与血脂、颈内动脉斑块和狭窄及降脂治疗的关系

目的 探讨进展性脑卒中(PS)与血脂、颈内动脉斑块和狭窄及降脂治疗的关系.方法 对45例PS及45例非PS(NPS)患者进行血总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平检测,以及颈内动脉彩色超声多普勒检查.采用多因素Logistic回归分析其对PS的影响.结果 PS组患者LDL-C水平明显高于NPS组(P＜0.01).PS组有颈内动脉斑块和狭窄的比率(75.6％)显著高于NPS组(42.2％)(P＜0.01)；而降血脂治疗的比率(51.1％)显著低于NPS组(80.0％)(P＜0.05).Logistic回归分析显示,LDL-C(OR=5.035)、颈内动脉斑块和狭窄(OR=3.224)为PS的危险因素,降血脂治疗(OR =0.175)为PS的保护因素(P ＜0.05 ～0.01).结论 血LDL-C水平高及颈内动脉斑块和狭窄为PS发病的危险因素,降血脂治疗对PS具有预防作用.     

急性脑梗死患者血清尿酸水平与颅内动脉重度狭窄或闭塞的侧支循环关系分析

目的探讨伴颅内动脉重度狭窄或闭塞的急性脑梗死(ACI)患者血清尿酸水平与侧支循环及病情恢复的关系。方法采用数字减影脑血管造影技术(DSA),根据颅内动脉狭窄程度将297例ACI患者分为轻度或无狭窄组、中度狭窄组和重度狭窄或闭塞组;收集患者临床资料,检测血清总胆固醇、三酰甘油、低密度脂蛋白、高密度脂蛋白及尿酸水平,进行比较;评估重度狭窄或闭塞患者颅内侧支循环代偿情况,分析与血尿酸水平的关系;根据入院及出院时进行NIHSS评分,将重度狭窄或闭塞患者分为恢复良好组(分值减少≥4)和恢复不良组(分值减少<4)。结果与轻度或无狭窄组相比,重度狭窄或闭塞组患者高血压、糖尿病病史及吸烟史比例较高,血清尿酸、总胆固醇及低密度脂蛋白水平也显著较高;侧支循环开放组血尿酸水平显著低于未开放组;恢复良好组尿酸水平低于恢复不良组。结论血清尿酸水平与ACI患者颅内动脉狭窄程度有关,并且重度颅内动脉狭窄或闭塞患者中,尿酸水平与侧支循环代偿相关,而且是影响ACI病情恢复的因素。     

脑梗死患者伴脑白质疏松症的相关危险因素及与脂蛋白相关磷脂酶A2相关性的研究

目的 探讨脑梗死患者伴脑白质疏松症(LA)的相关危险因素及与脂蛋白相关磷脂酶A2( LP - PLA2)的相关性.方法 选取178例脑梗死患者,依其影像学表现将其分为脑梗死合并LA组(83例)和脑梗死不合并LA组(95例),对比分析两组的Lp-PLA2含量以及临床、辅助检查指标.结果 (1)脑梗死患者共178例,LA的发病率46.63％.(2)单因素分析结果显示:在LA例组和无LA组年龄、Lp-PLA2、高血压病史及腔隙性脑梗死之间的差异具有统计学意义;多因素Logistic回归分析结果筛选出3个具有统计学意义的指标:Lp-PLA2、年龄和腔隙性脑梗死.(3)性别、糖尿病史、高脂血症、吸烟史、饮酒史、冠心病史及脑血管狭窄发生率在LA组和无LA组的差异无统计学意义.(4)两组高脂血症患者的LDL、甘油三脂、胆固醇水平及两组糖尿病患者的空腹血糖值差异无统计学意义,脑血管狭窄分为单纯前循环病变、单纯后循环病变及前后循环均有病变后,两组间构成比差异无统计学意义.结论 年龄、Lp-PLA2、腔隙性脑梗死是LA独立的危险因素.颅内外大血管狭窄与LA无确切的相关性.高血压是LA重要的危险因素.糖尿病、高血脂、吸烟史、饮酒史、冠心病史是LA和缺血性脑卒中的共同危险因素.     

颈动脉狭窄斑块性质与缺血性脑血管事件关系的研究

目的应用超声造影技术(CEUS)探讨颈动脉狭窄斑块性质与缺血性脑血管事件的关系。方法选择颈内动脉狭窄(70%)的患者24例,其中纳入狭窄处斑块45个作为研究对象。超声造影检测斑块内新生血管化情况,行头部MRI检查明确诊断,检测患者血清中甘油三酯、低密度脂蛋白等化验指标,并对其治疗前后的状态行NIHSS评分。分析颈内动脉狭窄处斑块内新生血管的增强程度与患者的临床症状、同侧脑梗死灶、血脂及预后等情况的关系。结果(1)有临床症状和无临床症状两组斑块内新生血管造影剂的增强强度比较(42.61±13.63VS 18.29±6.68,P0.05),差异有显著统计学意义;(2)ICA狭窄同侧脑梗死组与非脑梗死组狭窄处斑块内的新生血管增强强度比较(34.66±13.67 VS 20.36±6.53,P0.05),差异有显著统计学意义;(3)ICA狭窄处斑块内新生血管增强强度与并发高血压、糖尿病及血脂水平无统计学意义;(4)ICA狭窄处斑块内新生血管增强强度与治疗前NIHSS评分及治疗前后的NIHSS评分差值无明显相关性。结论 (1)有临床症状组ICA狭窄处斑块的新生血管增强强度明显高于无临床症状组;(2)ICA狭窄同侧的缺血性脑血管事件的发生与其狭窄处斑块内新生血管增强强度有相关性;(3)ICA狭窄处斑块内的新生血管增强强度与其高血压病病史、2型糖尿病病史、LDL和TG水平无明显相关性;(4)ICA狭窄处斑块内新生血管增强强度与治疗前NIHSS评分及治疗前后的NIHSS评分差值无明显相关性。     

400例缺血性脑梗死患者数字减影全脑血管造影分析

目的 分析缺血性脑梗死患者的脑血管病因和病变血管的分布情况.方法 回顾性分析400例缺血性脑梗死数字减影全脑血管造影(DSA)结果,分析脑梗死的血管病因,并对动脉粥样硬化脑梗死者总结分析动脉病变的部位、分布及血管狭窄形态.结果 脑血管造影结果提示88.25％缺血性脑梗死患者为不同程度的动脉粥样硬化引起血管狭窄或闭塞(353例),此外11.75％缺血性脑梗死患者病因是由于动脉夹层、Moyamoya病、椎基底动脉扩张延长症、鼻咽癌放疗后脑动脉病变、血管迂曲、微血管病变等原因引起.353例动脉粥样硬化性脑梗死中单纯前循环血管受累(45.61％)明显多于单纯后循环血管受累(34.27％),P＜0.01;前循环脑梗死中以颈内动脉(56.6％)和大脑中动脉(26.4％)受累最常见;后循环脑梗死中以椎动脉病变(33.0％)最多见.结论 脑血管造影显示缺血性脑梗死患者有最常见病因是动脉粥样硬化脑血管狭窄或闭塞,占88.25％.前循环脑梗死患者血管病变以颈内动脉起始部病变和大脑中动脉病变多见,后循环脑梗死中以椎动脉动脉病变多见.颅外血管狭窄以颈内动脉颅起始部和椎动脉起始部多见,颅内血管狭窄以大脑中动脉和椎动脉颅内段多见.     

低密度脂蛋白胆固醇水平与非溶栓性脑梗死出血转化的关系分析

目的探讨低密度脂蛋白胆固醇(LDL-C)水平与非溶栓性脑梗死出血转化(HT)的关系。方法分析2013年1月至2016年7月在本院住院的637例非溶栓性脑梗死(ACI)患者,发病后14d内复查头颅CT或MRI发现是否有出血,分为脑梗死出血转化组(HT组)及非脑梗死出血转化组患者(NHT组);以LDL-C 2.6mmol·L~(-1)为临界点,LDL-C2.6mmol·L~(-1)为Ⅰ组,LDL-C≥2.6mmol·L~(-1)为Ⅱ组,将发生HT和NHT患者的LDL-C水平进行差异统计学分析。结果 LDL-C组与HT组及NHT组,存在明显差异(P0.05)。结论 LDL-C是HT的危险因素之一,LDL-C水平与HT呈负相关关系。在临床中严格掌握脑血管疾病的一级预防、心源性脑梗死二级预防的降脂治疗指南十分关键。     

颈动脉迂曲与前循环动脉瘤形成的相关性研究

目的 探讨颈动脉迂曲与前循环动脉瘤形成的相关性。 方法 采用头颈部CTA检查测量2018年1-6月100例前循环动脉瘤住院患者与同期100例无颅内动 脉瘤住院患者的颈总动脉（common carotid artery,CCA）迂曲指数（tortuosity index,TI）、颈内动脉 （internal carotid artery,ICA）TI、颈动脉夹角（ICA角）等指标,来衡量颈动脉的迂曲程度。Pearson相关 分析CCA TI、ICA TI、ICA角与一般危险因素的关系,使用单因素及多因素逐步Logistic回归分析颈动脉 迂曲与前循环动脉瘤形成的关系。 结果 前循环动脉瘤组高脂血症病史（43% vs 58%,P =0.034）、缺血性卒中病史（39% vs 58%, P =0.007）比例低于对照组,而C CA TI（1.409±0.135 vs 1.352±0.137,P =0.004）、I CA TI （1.592±0.186 vs 1.523±0.149,P =0.005）、ICA角（46.450°±6.465°vs 44.303°±6.409°,P =0.016） 均高于对照组。前循环动脉瘤组CCA TI与冠心病病史正相关（r =0.220,P =0.027）,ICA TI与男性正相 关（r =0.244,P =0.025）。I CA TI（OR 4.694,95%CI 0.999～1.099,P =0.018）、I CA角（OR 1.052,95%CI 1.389～23.308,P =0.039）是前循环动脉瘤的独立危险因素,而缺血性卒中史患者较少发生动脉瘤 （OR 0.569,95%CI 0.313～1.017,P =0.045）。 结论 颈内动脉迂曲程度与男性相关,颈总动脉迂曲程度与冠心病病史相关,颈动脉迂曲程度是前 循环动脉瘤形成的独立危险因素,而缺血性卒中史患者较少发生动脉瘤。     

无脑动脉狭窄急性脑梗死患者的临床特点

目的 探讨无脑动脉狭窄急性脑梗死(ACI)患者的临床特点.方法 对352例ACI患者进行数字减影全脑血管造影(DSA),根据检查结果分为无动脉狭窄组和动脉狭窄组,比较两组患者临床神经功能缺损评分、卒中危险因素和预后;并比较无动脉狭窄组中前循环梗死亚组与后循环梗死亚组的病情和预后.结果 根据DSA结果,无动脉狭窄组70例,动脉狭窄组282例.无动脉狭窄组患者合并高血压、糖尿病以及既往腩卒中、冠心病史者的比率明显低于动脉狭窄组(P<0.05～0.01);入院时及发病3个月时美国国立卫生研究院卒中鼍表(NIHSS)评分均明显低于动脉狭窄组,改良Rankin量表(mRS)评分及3个月卒中复发或死亡率明显低于动脉狭窄组(P<0.05～0.01);无动脉狭窄组中后循环梗死亚组患者入院时及发病3个月时NIHSS、mRS评分及死亡率明显高于前循环梗死亚组(P<0.05～0.01).结论 无明显脑动脉狭窄ACI患者的病情较轻,预后较好;但其中后循环梗死患者预后较差.     

Ophthalmic artery fed by posterior communicating artery after trapping of the internal carotid artery

The authors report a 50-year-old man with a ruptured large carotid-ophthalmic aneurysm on the right side and an unruptured anterior communicating artery (A Com) aneurysm. The A Comm aneurysm was clipped and the carotid-ophthalmic aneurysm was managed by combining internal carotid artery (ICA) trapping with an interposed radial artery graft from the external carotid artery (ECA) to the middle cerebral artery (MCA). The patient had an uncomplicated postoperative recovery. Postoperative carotid angiography demonstrated no aneurysms and excellent flow through the bypass graft. Postoperative vertebral angiography showed the right ophthalmic artery to be fed by the posterior communicating artery. It is speculated that collateral circulation from the angular artery of the ECA to the ophthalmic artery did not develop because of high flow graft from the ECA to MCA and ICA trapping.     

Superior cerebellar artery infarction and vertebral artery dissection

Isolated superior cerebellar artery infarction is rare, and the mechanism is often not readily apparent. We describe a patient with an isolated superior cerebellar artery infarction resulting from an ipsilateral vertebral artery dissection. Angiography demonstrated intraluminal clot in the superior cerebellar artery, suggesting artery-to-artery embolus as a mechanism of this uncommon stroke syndrome.     

Embolic internal auditory artery infarction from vertebral artery dissection

A 51-year-old man developed sudden vertigo, right hearing loss and dysphagia. Examination revealed right Horner syndrome, spontaneous torsional-horizontal nystagmus, right central type facial palsy, dysarthria, reduced soft palate elevation without gag reflex, left hypesthesia, right dysmetria and imbalance. Audiometry and bithermal caloric tests documented right sensorineural hearing loss and canal paresis. Brain MRI and cerebral angiography documented right lateral medullary infarction from vertebral artery dissection, without involvement of other parts of the brainstem supplied by the anterior inferior cerebellar artery (AICA). This case suggests artery-to-artery embolism as a possible mechanism of isolated vertigo or hearing loss from labyrinthine infarction.     

支架成形术治疗椎动脉颅内段和基底动脉狭窄17例临床观察

目的评估症状性椎动脉颅内段、基底动脉狭窄患者经皮血管内支架成形术(PTAS)治疗的安全性和有效性。方法17例症状性椎动脉颅内段及基底动脉狭窄患者,狭窄程度在50%以上且规范的内科药物治疗无效,给予PTAS治疗,术后常规给予抗凝、抗血小板聚集、降脂药物。结果17例患者20处狭窄行PTAS,所有的病例手术均取得成功,没有严重并发症,术后即刻造影残存狭窄平均在10%以下,病人平均随访6.8个月(3～10个月),有1例患者出现再狭窄(狭窄程度>50%),所有患者均无缺血症状发作。结论PTAS治疗椎动脉颅内段及基底动脉狭窄是安全和有效的。     

Posterior cerebral artery infarction from middle cerebral artery infarction

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.     

Management of coexistent carotid artery and coronary artery disease

At the present time staged carotid reconstruction several days before elective coronary artery bypass surgery seems to be the safest and most logical approach for patients with neurological symptoms, stable cardiac symptoms, and acceptable coronary anatomy. Combined procedures may well be necessary for those who have active neurological symptoms or bilateral carotid lesions in conjunction with diffuse or unstable coronary artery disease, but the incidence of neurological complications at the time of simultaneous operations could exceed the stroke risk for either carotid endarterectomy or coronary bypass alone. The asymptomatic patient with unilateral carotid stenosis who presents for coronary artery bypass might be best managed by myocardial revascularization followed by medical or surgical management of the carotid disease. In order to obtain optimal long-term results, both coronary disease and associated carotid disease require appropriate evaluation and medical and surgical management.     

External carotid artery stenting in symptomatic internal carotid artery occlusion

We report the case of a patient with an anterior ischemic stroke due to tandem occlusion of the left M2 segment and ipsilateral internal carotid artery (ICA), with concomitant severe stenosis of the ipsilateral external carotid artery (ECA) and contralateral ICA, and moderate stenosis of the left vertebral artery (VA); as thrombectomy was not possible, stenting of the right ICA was performed. Two days after significant recovery, the patient showed neurological deterioration when in upright position, and brain magnetic resonance imaging confirmed decreased cerebral blood flow on the left hemisphere. Stenting of the left ECA and balloon angioplasty of the ipsilateral VA were performed in order to increase collateral flow, with an almost complete resolution of symptoms. This case highlights the importance of assessing the collateralization pattern when an ICA occlusion is present, and the potential need to revascularize an ipsilateral stenotic ECA.     

The relation of retinal artery occlusion and carotid artery stenosis

We retrospectively studied 46 patients with symptomatic retinal artery occlusion and assessed the pattern and extent of carotid artery disease ipsilateral to the retinal artery occlusion. Ipsilateral internal carotid artery atherosclerotic lesions were virtually limited to the cervical arterial segment; 50% of such lesions were plaques or stenoses of less than or equal to 60%, whereas 15% of the angiograms were normal. No clinical features were significantly associated with a flow-limiting carotid stenosis of greater than 60%. Contrary to previous reports, the type of retinal artery occlusion, whether branch or central artery occlusion, was not predictive of severe underlying carotid stenosis or occlusion. Likely mechanisms of retinal artery occlusion include in situ thrombosis and emboli from carotid, and possibly cardiac, sources. Extension of thrombus from an occluded carotid artery into the ophthalmic artery did not appear to be a mechanism of retinal artery occlusion.