外周血白细胞端粒长度与初发卒中患者心脑血管死亡风险的关系

目的 探讨外周血白细胞端粒长度缩短对初发卒中患者心脑血管死亡风险的影响。 方法 本研究为前瞻性随访研究,纳入2000年12月至2001年12月全国7家临床中心的急性起病的发病3周内的1662例初发卒中患者,根据国际疾病分类第9版标准分为动脉粥样硬化性脑梗死（725例）、腔隙性脑梗死（481例）和脑出血（456例）,患者发病后4～5周抽取外周静脉血,通过实时荧光定量聚合酶链反应法（polymerase chain reaction,PCR）检测外周白细胞端粒长度。通过Cox生存回归模型分析端粒长度与卒中后全因死亡和心脑血管死亡风险的关系。 结果 所有研究对象随访中［随访时间4.5年（中位数）］,312例死亡,其中181例死于心脑血管疾病。校正年龄、性别、体重指数、吸烟、饮酒、血脂、血糖、糖尿病、高血压、卒中家族史后,发现在动脉粥样硬化性脑梗死患者中,端粒较短时发生全因死亡的风险增加69%［校正相对风险（adjusted relative risk,adj.RR）1.69,95%可信区间（confidence interval,CI）1.07～2.67;P=0.02］,心脑血管死亡风险增加是长端粒组的2.57倍（adj.RR 2.57,95%CI 1.24～5.31;P=0.01）。腔隙性脑梗死和脑出血患者中,未发现端粒缩短与全因死亡（adj.RR 1.14,95%CI 0.59～2.18,P=0.35;adj.RR 0.92,95%CI 0.57～1.50,P=0.59）、心脑血管死亡风险（adj.RR 1.95,95%CI 0.76～4.97,P=0.24;adj.RR 1.06,95%CI 0.59～1.89,P=0.56）的关系。 结论 外周血白细胞端粒缩短有可能作为评估动脉粥样硬化性脑梗死患者发生全因死亡和心脑血管死亡风险的重要因素。     

在脑梗死二级预防中阿司匹林抵抗的危险因素分析

目的探讨脑梗死二级预防患者的阿司匹林(ASA)抵抗可能的影响因素,为脑梗死的二级预防提供新的资料和参考指标。方法选取120例脑梗死患者和正常对照组56例,采用比浊法(LPT),以"ADP诱导和花生四烯酸诱导"相结合的方法测定血小板聚集率,判定阿司匹林抵抗,并按血小板聚集率水平分为阿司匹林抵抗组(AR)、半抵抗组(ASR)、敏感组(AS)和正常组。分别记录患者性别、年龄、血糖、总胆固醇、甘油三酯、低密度脂蛋白胆固醇等及糖尿病、既往脑梗死史。结果单因素分析显示,脑梗死各亚组的性别、年龄、糖尿病、短暂性脑缺血发作(TIA)、大动脉闭塞性脑梗死或腔隙性梗死(LAA)较正常组有差异,其中糖尿病(OR=13.297,95%CI 2.422~72.984,P=0.003)、既往有TIA史(OR=5.019,95%CI1.026~24.538,P=0.046),为AR发生的独立危险因素。结论 AR与糖尿病、既往有TIA史有关,其中糖尿病与AR关系最密切。     

脑微出血与脑白质高信号及服用阿司匹林相关性分析

目的探讨脑微出血与脑白质高信号和服用阿司匹林的关联性,并筛查脑微出血相关危险因素。方法纳入2016年6月至2021年2月首都医科大学附属北京朝阳医院收治的2654例缺血性脑血管病患者,记录入院时收缩压和舒张压、是否服用阿司匹林和服药时间,以及入院24 h内测定血清高密度脂蛋白胆固醇、低密度脂蛋白胆固醇(LDL-C)和血浆糖化血红蛋白(Hb A1c)、同型半胱氨酸(Hcy)、纤维蛋白原、D-二聚体;头部MRI评估脑白质高信号严重程度(Fazekas评分)并计数脑微出血灶数目[脑微出血解剖评分量表(MARS)]。单因素和多因素逐步法Logistic回归分析筛查脑微出血及其严重程度相关危险因素。结果 2654例患者根据Fazekas评分分为对照组(1315例)、轻度脑白质高信号组(461例)、中度脑白质高信号组(440例)和重度脑白质高信号组(438例),各组年龄(H=353.837,P=0.000),合并高血压(χ~2=79.818,P=0.000)、冠心病(χ~2=56.768,P=0.000)和糖尿病(χ~2=8.936,P=0.030)比例,入院时收缩压(H=47.979,P=0.000),服用阿司匹林比例(χ~2=161.576,P=0.000)和服药时间(H=4.766,P=0.000),血清LDL-C(H=16.533,P=0.002),血浆Hb A1c(H=22.127,P=0.000)和Hcy(H=83.558,P=0.002),脑微出血比例(χ~2=642.054,P=0.000)差异有统计学意义。Logistic回归分析显示,入院时舒张压高(OR=1.017,95%CI:1.007～1.026,P=0.001;OR=1.020,95%CI:1.011～1.029,P=0.000)和Fazekas评分高(OR=1.673,95%CI:1.590～1.761,P=0.000;OR=1.754,95%CI:1.669～1.844,P=0.000)是存在脑微出血及其严重程度的危险因素,血清LDL-C是存在脑微出血及其严重程度的保护因素(OR=0.856,95%CI:0.765～0.957,P=0.006;OR=0.860,95%CI:0.774～0.956,P=0.005);而服用阿司匹林和服药时间与存在脑微出血及其严重程度无明显关联性。结论脑白质高信号严重程度(Fazekas评分)是存在脑微出血及其严重程度的危险因素。     

阿司匹林对脑室旁脑白质疏松患者新发脑卒中的影响

目的探讨阿司匹林对脑室旁脑白质疏松患者新发脑卒中的影响。方法选取伴腔隙性梗死的脑室旁脑白质疏松患者400例,随机分为阿司匹林组(200例)和对照组(200例)。阿司匹林组服用阿司匹林肠溶片100mg,1次/d,持续1a。对照组不服用任何抗血小板药或抗凝药。记录1a内患者发生急性脑血管疾病和神经功能缺损情况。记录入组时及1a后受试者的认知功能(MoCA评分)、白质疏松的严重程度及脑微出血。结果阿司匹林组1a后脑微出血的数量明显大于对照组,阿司匹林组急性脑梗死的发生率明显小于对照组(P0.05),脑出血发生率差异无统计学意义(P0.05)。脑卒中患者1a后神经功能缺损程度(NIHSS评分)阿司匹林组和对照组差异无统计学意义(P0.05),2组白质疏松程度评、认知功能差异无统计学意义(P0.05)。结论采用阿司匹林对伴脑室旁白质疏松的腔隙性梗死患者缺血性卒中的一级或二级预防可使新发脑梗死疾病显著减少,且不加快白质疏松进程及增加颅内出血。     

成都卒中登记方法及3123例患者基本特征和功能结局

目的 探讨卒中登记方法、了解卒中患者基本特征和功能结局.方法 前瞻性、连续性登记自2002年3月1日起在四川大学华西医院神经内科住院的卒中患者.由统一培训的专科医师填写卒中登记表,登记患者临床特点、住院诊治情况,并随访各时点结局(发病后7d,1、3、6和12个月末的死亡和残疾).结果 纳入自2002年3月1日至2006年8月31日连续性登记的卒中患者共3123例.其中65.5％来自城区,34.5％来自农村.年龄14～98(63.05±17.98)岁,男性占60.3％,住院期间完成头颅CT和(或)MRI者占97％(3028/3123).2002年3月至2004年9月纳入各类卒中患者共1804例.其中缺血性卒中62.1％ (1120/1804),脑出血 28.4％(513/1804),蛛网膜下腔出血4.0％ (72/1804),TIA 5.5％ (99/1804).2004年10月后未纳入蛛网膜下腔出血和TIA患者.入院时中位NIHSS评分脑出血患者8(3 ～ 15)分,脑梗死5(2 ～10)分.糖尿病(OR=2.427,95％ CI1.811 ～3.253,P=0.000)、房颤(OR =6.121,95％ CI3.535 ～ 10.60,P=0.000)、冠心病(OR=4.144,95％ CI2.944～5.832,P=0.000)、TIA史(OR =4.342,95％ CI1.726 ～ 10.92,P=0.001)发生比例脑梗死组高于脑出血组,而饮酒史脑梗死组低于脑出血组(OR=0.740,95％ CI0.611 ～0.896,P=0.002).缺血性卒中患者溶栓占0.9％(20例),抗血小板治疗83.0％,甘露醇23.5％,神经保护剂(胞二磷胆碱)68.1％,中成药89.7％.7d和1个月病死率脑出血组分别为10.7％和13.9％,脑梗死组分别为3.0％和5.2％.3、6及12个月死亡或残疾率脑出血组分别为40.4％、40.3％和38.9％;脑梗死组分别为37.1％、35.0％和33.4％.结论 本研究是国内目前报告的最大样本、最长时间的前瞻性连续性单中心卒中登记项目,提供了深入研究卒中临床特点的重要平台;本组患者病情偏轻,近期病死率及远期病死或残疾率低于国外,中国卒中防治的干预性临床试验设计应注意考虑这些特点.     

血清炎性标志物与缺血性脑血管病的关系

目的 比较急性脑梗死、短暂性脑缺血发作(TIA)、陈旧脑梗死患者和健康对照者血清炎性标志物白细胞介素-6(IL-6)、高敏C反应蛋白(hsCRP)、基质金属蛋白酶-9(MMP-9)和组织金属蛋白酶抑制物-1(TIMP-1)水平.方法 收集作者医院急性脑梗死患者56例,TIA患者46例,陈旧脑梗死患者56例,对照组30名,采用ELISA法测定其血IL-6、MMP-9和TIMP-1水平,采用免疫比浊法测定其血hsCRP水平.结果 急性脑梗死和TIA组IL-6水平均高于陈旧脑梗死和对照组 (P<0.05).各组间hsCRP水平比较差异均有统计学意义(P<0.05),水平由高至低依次为急性脑梗死组、TIA组、对照组和陈旧脑梗死组.急性脑梗死组和TIA组MMP-9水平高于陈旧脑梗死和对照组(P<0.05).TIA、急性脑梗死和陈旧脑梗死组TIMP-1水平均高于对照组(P<0.05).IL-6水平(OR=20.525,95%CI:2.623～160.58,P=0.004)和hsCRP(OR=1.878, 95%CI:1.138～3.100, P=0.014)是脑卒中患者预后不佳的独立危险因素.结论 TIA与急性脑梗死患者炎性标志物水平升高,其中IL-6和hsCRP水平升高是患者预后不佳的独立危险因素.     

缺血性卒中患者服用阿司匹林后再发脑梗死的危险因素分析

目的 探讨缺血性卒中患者服用阿司匹林进行二级预防后再发脑梗死的危险因素.方法 收集我院缺血性卒中265例患者的资料:年龄、性别、高血压病、冠心病、糖尿病、高脂血症、高同型半胱氨酸血症病史、吸烟史等情况,并对在服药期间患者各项卒中危险因素的控制情况进行随访:包括血压、血脂、血糖、同型半胱氨酸水平,并依据调查结果筛选出水平高于正常的患者.随访3年,患者分为缺血性卒中再发组和缺血性卒中无再发组两组,分析以上因素在两组间的差异.结果 265例患者入选,5例因其他系统疾病死亡失访,8例因出现胃肠道并发症停用阿司匹林,252例参加随访的缺血性卒中病例中54例再发,再发率21.4%.单因素分析显示,缺血性卒中再发组中合并高脂血症、糖尿病或高同型半胱氨酸血症的患者比例显著高于缺血性卒中无再发组;缺血性再发组在服用阿司匹林期间血浆总胆固醇(TC)及低密度脂蛋白(LDL)水平高于正常或血脂3项都高于正常、血糖水平高于正常、同型半胱氨酸(Hcy)水平高于正常的患者比例明显高于缺血性卒中无再发组.多因素分析显示,服用阿司匹林期间,TC及LDL高于正常或血脂3项都高于正常[比值比(odds ratio,OR)=2.54;95%置信区间(confidenceinterval,CI)1.33～5.36,P=0.007]、血糖水平高于正常(OR=2.83;95%CI 1.49～5.61,P=0.003)、血浆HCY水平高于正常(OR=2.44;95%CI 1.29～5.28,P=0.009)与服用阿司匹林进行缺血性卒中二级预防患者的脑梗死再发独立相关.结论 服用阿司匹林期间,TC及LDL高于正常或血脂3项都高于正常、空腹血糖水平高于正常以及同型半胱氨酸水平高于正常是服用阿司匹林预防进行二级预防患者缺血性卒中再发的独立危险因素.     

水蛭素合用阿司匹林与单用阿司匹林或氯吡格雷治疗短暂性脑缺血发作的随机对照研究

目的：探讨水蛭素合用阿司匹林治疗短暂性脑缺血发作（TIA）的疗效和安全性。方法：89例TIA患者随机分为3组：（1）氯吡格雷组（n=29），口服氯吡格雷75mg／d：（2）阿司匹林组（n=30），口服阿司匹林100mg／d；（3）水蛭素合用阿司匹林组（n=30），口服水蛭素0．32g，3次／d，阿司匹林100mg／d。观察治疗后90d内TIA复发或进展为脑梗死的病例数，观察出血等不良事件发生率。结果：治疗后90d内总的脑梗死发生率为4．5％，3组之间无显著差异。水蛭素合用阿司匹林组和氯吡格雷组90d内的TIA复发风险分别较单用阿司匹林降低69％（P=0．0078）和65％（P=0．0170）。总的出血发生率为2．25％，均发生在水蛭素合用阿司匹林组。结论：水蛭素合用阿司匹林可降低90d内TIA复发率的效果优于单用阿司匹林，与单用氯吡格雷相似，但出血风险增高。     

短暂性脑缺血发作后缺血性脑卒中的危险因素

目的探讨TIA后缺血性脑卒中的危险因素。方法收集184例TIA患者的临床资料,分析TIA后缺血性脑卒中的危险因素。结果与无缺血性脑梗死组比较,缺血性脑梗死组高龄(≥60岁)、高血压、糖尿病以及有吸烟、饮酒史的比率显著升高(P0.05~0.01),性别及高血脂比率差异无统计学意义(均P0.05)。与无缺血性脑梗死组比较,缺血性脑梗死组发作时间≥30 min、发作次数≥3次、病程≥24 h(P0.05~0.01),而TIA类型差异无统计学意义(均P0.05)。Logistic回归分析显示,高龄、高血压、糖尿病以及吸烟、饮酒史与TIA进展为缺血性脑卒中呈正相关(OR=29.799,95%CI:2.189~405.569,P=0.011;OR=0.649,95%CI:0.038~6.850,P=0.005;OR=8.569,95%CI:1.314~55.862,P=0.025;OR=0.158,95%CI:0.025~0.980,P=0.048)。结论高龄、高血压、糖尿病、有吸烟饮酒史是TIA发展为缺血性脑卒中的独立危险因素。     

CT显示无症状腔隙性与有症状非腔隙性脑梗死的影响因素差异分析

目的 通过对无症状腔隙性脑梗死的患者以及有症状非腔隙性脑梗死的患者的危险因素进行比较分析,初步探讨这两类疾病的发病机制异同. 方法 选取郑州大学第二附属医院体检中心进行健康检查的年龄在50岁以上的体检者共1989例,检查出48例无症状腔隙性脑梗死(A组)以及51例有症状非腔隙性脑梗死(B组)分别与1862例非脑血管病对照组进行危险因素的单因素分析,然后进行多因素分析,再在两病例组间进行危险因素分布的比较以及数量的比较分析.结果 经过单因素及多因素分析后得到年龄、高血压及吸烟是无症状腔隙性脑梗死的独立危险因素(P＜0.05),而有症状非腔隙性脑梗死的独立危险因素是年龄、性别、糖尿病、酗酒、卒中家族史及颅内动脉狭窄(P＜0.05).组间比较显示糖尿病和颅内动脉动脉狭窄在两组间的分布差异具有统计学意义(糖尿病x2=17.603,P=0.008;颅内动脉狭窄:,x2=19.319,P=0.005).有症状非腔隙性脑梗死的危险因素数量明显多于无症状腔隙性脑梗死,差异具有统计学意义(Z=2598,P=0.009). 结论 无症状腔隙性脑梗死和有症状非腔隙性脑梗死的危险因素存在差异,而血管机制有所不同,糖尿病及颅内动脉狭窄在有症状非腔隙性脑梗死中更多见.     

Low-dose warfarin in atrial fibrillation leads to more thromboembolic events without reducing major bleeding when compared to adjusted-dose--a meta-analysis

The use of warfarin with a range INR of 2.0-3.0 is recommended in prevention of stroke for nonvalvular atrial fibrillation (AF) patients, in particular those older than 75 years. The risk of bleeding that is associated with this range of INR has led to evaluate lower ranges (low-dose or fixed minidose) in terms of risks and benefits. A meta-analysis of all randomized controlled trials evaluating 'low-intensity' 'minidose' or 'low-dose anticoagulant' treatment for prevention of thromboembolic events in AF was conducted by two independent reviewers. Study quality was evaluated in a blinded fashion. Four original studies were retrieved. Outcome events were determined in various treatment groups: ischemic stroke, systemic embolism, thromboses (ischemic stroke, systemic embolism or myocardial infarction), vascular death, major hemorrhage and hemorrhagic death. Results obtained with a random effects model were expressed as a common relative risk. Adjusted-dose warfarin compared with lower dose warfarin (INR < or = 1.6) in 2108 randomised patients significantly reduced the risk of any thrombosis: Relative risk (RR): 0.50 (95% CI; 0.25 to 0.97). The RR was 0.46 (95%CI; 0.2 to 1.07) for ischemic stroke. Inversely lower dose did not statistically decrease the risk for major hemorrhage compared to adjusted-dose: RR adjusted-dose vs lower dose: 1.23 (95% CI; 0.67-2.27). The RR was 0.97 (95 % CI 0.27-3.54) for hemorrhagic death. Our meta-analysis showed that adjusted-dose compared with low-dose or minidose warfarin therapy (INR < or =1.6) was more effective to prevent ischemic thromboembolic events in patients with atrial fibrillation.     

脑微出血与脑卒中

目的探讨脑微出血与脑卒中发生、发展的联系。方法卒中患者83例，分为脑缺血组（43例）和脑出血组（40例），以同期住院的50岁以上非脑卒中患者设立对照组（32例）。采用T2加权梯度回波MRI观察各病例脑微出血、卒中病灶、腔隙性梗塞以及白质疏松情况，同时记录卒中患者的高血压、糖尿病、高脂血症、卒中病史以及阿司匹林使用史。结果微出血在缺血组和出血组的发生率分别为34．9％、75．0％，对照组9．4％。各组微出血均最常见于基底节区。微出血与高血压、卒中病史相关（P〈0．01），与高脂血症、糖尿病病史及使用阿司匹林无关（P〉0．05）。微出血的严重程度与腔隙性梗塞、白质疏松的严重程度相关（P〈0．01）．．微出血在卒中病灶区域同侧或对侧分布无显著性差异（P〉0．05）。出血组微出血在卒中病灶区域的分布率明显高于缺血组。结论微出血与脑卒中．特别是与出血性脑卒中有密切关系，对卒中患者出血性转化具有预测意义。     

阿司匹林抵抗的危险因素分析和临床干预

目的探讨脑梗死患者阿司匹林抵抗的危险因素,研究阿司匹林抵抗者抗血小板药物调整后阿司匹林抵抗的发生情况及预后。方法选取269例新发脑梗死患者,口服阿司匹林100 mg/d,经血栓弹力图筛选出阿司匹林抵抗者90例,分析其危险因素,并将其随机分为3组:A组口服阿司匹林200 mg/d;B组口服阿司匹林100 mg/d+氯吡格雷75 mg/d;C组口服阿司匹林100 mg/d。1 m后复测血栓弹力图,比较血小板抑制率的变化。随访12 m观察血管事件和死亡的发生情况。结果阿司匹林抵抗的发生率为33.5%。单因素分析显示,阿司匹林抵抗组(AR)与阿司匹林敏感组(AS)年龄比较差异有统计学意义(P=0.029);Logistic回归分析显示,年龄是脑梗死患者阿司匹林抵抗的危险因素(OR=1.026,95%CI 1.002 1.049,P=0.030)。A组和B组患者AA诱导的血小板抑制率明显升高(P0.05),且B组患者血小板抑制率升高更明显;C组患者AA诱导的血小板抑制率较前无明显改变(P0.05)。随访12 m后3组患者总体缺血性事件发生率比较差异有统计学意义(P=0.002),C组总体缺血性事件发生率明显高于A组和B组;3组患者出血性事件发生率比较差异无统计学意义(P0.05)。结论年龄是脑梗死患者阿司匹林抵抗的危险因素;阿司匹林加量或联合氯吡格雷治疗可以有效改善阿司匹林抵抗现象,并可减少或避免缺血性事件发生。     

Combined clopidogrel–aspirin treatment for high risk TIA or minor stroke does not increase cerebral microbleeds

Abstract

Objectives:

To study whether Clopidogrel–Aspirin combined treatment for high risk transient ischaemic attack (TIA) or minor stroke results in increased number of lesions associated with anti-thrombotic cerebral haemorrhage or cerebral micro-bleeds (CMB) than aspirin alone treatment.

Methods:

The patients recruited in CHANCE test in our hospital participated in this study. We made a comparison between treatments Aspirin–Clopidogrel combined group and the Aspirin alone group in the numbers of CMB and subsequent cerebral haemorrhages. In addition, we analysed the association between the increased numbers of CMB and subsequent intracerebral haemorrhages. All 129 patients with high risk TIA with microbleeds or minor stroke within 24?hours after the onset (average age 65.9?±?9.3, 48.7% were male patients) were divided randomly into two groups: (1) 67 patients were given combination therapy with clopidogrel and aspirin (clopidogrel at an initial dose of 300?mg, then 75?mg per day for 90?days, plus aspirin at a dose of 75?mg per day for the first 21?days);(2) the rest patients were given aspirin treatment (75?mg per day for 90?days). All participants received open-label aspirin at a clinician-determined dose of 75–300?mg on the first day.

Results:

The CMB were found in 52.7% of all patients in both groups. There was no siginificant difference between the Aspirin group and the Aspirin–clopidogrel treated group, though the latter showed some slight increase in CMB (Odds ratios (OR)?=?1.16, 95% confidence intervals (CI) =?0.54–2.47, P?=?0.71). But the numbers of CMB were remarkably associated with the number of primary existing CMB (OR?=?6.46, 95%CI 2.57–16.23, P?<?0.001), especially that of primary existing CMB ≥?3.In addition, the increasing numbers of CMB associated with primary CMB lesions, which located in corticosubcortical area (CSC) (OR?=?4.69, 95%CI 1.51–14.53, P?=?0.007).

Conclusions:

For the treatment of high-risk TIA or minor stroke patients, the clopidogrel–aspirin treatment did not increase the number of CMB than Aspirin alone. It appears that the extent of CMB was associated with the extent of existing CMB occurred in previous stroke, which was mostly located in cortical, subcortical zone.     

影响急性脑梗死出血性转化的危险因素

目的 探讨急性脑梗死的出血性转化的危险因素。方法 收集2012年1月～2015年1月在湖北省恩施州利川市人民医院神经内科住院的急性脑梗死患者的临床及实验室检查资料,并在入院后10 d内行头颅CT复查,采用多变量logistic回归分析确定出血性转化的独立危险因素。结果 共纳入345例急性脑梗死患者,其中男205例,女140例,101例发生出血性转化。出血性转化组的年龄、脑梗死体积、脑卒中史或TIA史、高血压病、糖尿病、抗凝药和房颤的比例均显著高于非出血性转化组(P<0.05),而2组抗血小板聚集药、他汀类、高脂血症史、吸烟或饮酒史无明显差异(P>0.05)。多变量logistic回归分析显示年龄(OR=1.168,95%,CI=1.059～3.412; P=0.021)、梗死体积(OR=3.461,95%C1=1.317～6.270; P=0.044)和房颤(OR=1.284,95%C1= 1.117～2.903; P=0.015)为出血性转化的独立危险因素。结论 急性脑梗死患者出血性转化的发生率为29.3%,年龄、脑梗死体积和房颤为出血性转化的独立危险因素,绝大多数出血性转化不会加重临床症状,临床症状加重的患者主要是脑实质血肿型。     

巴曲酶联合阿斯匹林治疗短暂性脑缺血发作的临床观察

目的:研究巴曲酶联合阿斯匹林治疗短暂性脑缺血发作(TIA)的有效性和安全性.方法:将112例TIA患者随机分为巴曲酶联合阿斯匹林组(治疗组),低分子肝素钙联合阿斯匹林(对照组),结果:巴曲酶联合阿斯匹林组有效率为83.33%;低分子肝素钙联合阿斯匹林组总有效率为57.69%.两组间比较有显著差异性(P<0.05).结论:巴曲酶联合阿斯匹林治疗短暂性脑缺血发作,疗效显著,可广泛应用于临床.     

青年烟雾病患者的卒中类型及危险因素分析

目的 探索青年烟雾病患者的卒中类型及临床特征,分析青年烟雾病患者发生卒中的危险因素。 方法 回顾性纳入2020年1月-2021年12月解放军总医院第五医学中心收治的青年（18～45岁）卒中型烟雾病患者,将患者分为出血性卒中组和缺血性卒中组进行亚型分析,对比不同卒中类型患者的临床及影像学特征。并以同期未发生卒中的烟雾病患者作为对照组,应用多因素logistic回归分析青年烟雾病患者发生出血性或缺血性卒中的危险因素。 结果 共入组108例卒中型烟雾病患者,其中出血性卒中22例（20.4%）,缺血性卒中86例（79.6%）。出血性卒中组中脑室出血12例（54.5%）,脑实质出血7例（31.8%）,蛛网膜下腔出血3例（13.6%）。缺血性卒中组中大动脉梗死型21例（24.4%）,血流动力学梗死36例（41.9%）,穿支动脉梗死29例（33.7%）。出血性卒中组与缺血性卒中组性别和合并动脉瘤者比例的差异有统计学意义。无卒中对照组共104例,多因素logistic回归分析结果显示,合并动脉瘤（OR?10.569,95%CI?1.524～73.274,P=0.017）为青年烟雾病患者发生出血性卒中的独立危险因素;增龄（OR?1.058,95%CI?1.004～1.115,P=0.034）、合并糖尿病（OR?4.005,95%CI?1.766～9.080,P=0.001）、高铃木分期（OR?1.363,95%CI 1.037～1.793,P=0.027）为青年烟雾病患者发生缺血性卒中的独立危险因素。 结论 青年烟雾病患者的卒中类型以缺血性卒中为主。血流动力学梗死和脑室出血分别是缺血性卒中和出血性卒中的主要类型。增龄、高铃木分期、合并糖尿病和颅内动脉瘤是引起青年烟雾病患者卒中的独立危险因素。     

Prospective study of aspirin use and risk of stroke in women.

BACKGROUND AND PURPOSE: In secondary prevention, aspirin reduces risk of ischemic stroke. In primary prevention of stroke, however, the role of aspirin is uncertain, especially in women. METHODS: In 1980, 79 319 women in the Nurses' Health Study cohort, 34 to 59 years of age and free of diagnosed cardiovascular disease, cancer, and rheumatoid arthritis, completed questionnaires that included information on aspirin use. Data on aspirin use were updated in 1982, 1984, and 1988. By 1994, after 994 231 person-years of follow-up, 503 incident strokes (295 ischemic strokes, 100 subarachnoid hemorrhages, 52 intraparenchymal hemorrhages, and 56 strokes of undetermined type) were documented. RESULTS: There was no clear relationship between aspirin use and risk of total stroke; risk was slightly reduced among women who took 1 to 6 aspirin per week and slightly increased among women who took 7 or more aspirin per week. Women who took 1 to 6 aspirin per week had a lower risk of large-artery occlusive infarction compared with women who reported no aspirin use; after simultaneous adjustment for other cardiovascular risk factors and selected nutrients, the multivariate relative risk was 0.50 (95% CI 0.29 to 0.85, P=0.01). Women who took 15 or more aspirin per week had an excess risk of subarachnoid hemorrhage; the multivariate relative risk was 2.02 (95% CI 1.04 to 3.91, P for trend=0.02). The reduction in large-artery occlusive infarction with aspirin was of greater magnitude for older, hypertensive, or smoking women than for younger, nonhypertensive, or nonsmoking women; the elevation in subarachnoid hemorrhage with aspirin was also more apparent for older or hypertensive women than for younger or nonhypertensive women. Aspirin use was not associated with risk of other subtypes of stroke. CONCLUSIONS:These prospective data indicate that women who take 1 to 6 aspirin per week have a reduced risk of large-artery occlusive infarction, but those who use 15 or more aspirin per week have an increased risk of subarachnoid hemorrhage. This observational study suggests benefits of aspirin for ischemic stroke with low frequency of use and hazards for hemorrhagic stroke with high frequency of use, particularly among older or hypertensive women. Thus, the effect on total stroke will depend on the dose of aspirin and the distribution of stroke subtypes and risk factors in the population.     

Observation of plasma levels of antithrombin-III and plasminogen in acute cerebrovascular disease

In 75 patients with acute cerebral vascular disease (infarction 43, TIA 4, cerebral hemorrhage 25, subarachnoid hemorrhage 3), the plasma levels of Antithrombin-III (AT-III) and plasminogen (Plg) were measured within one week stroke patient and with 27 non-stroke patient as controls. The results showed: the plasma AT-III level was of no significant difference between the patients with hemorrhagic or ischemic cerebral vascular disease group and control group; the plasma plg level was a significant decrease in ischemic cerebral vascular disease groups (cerebral infarction. TIA), and it was of significant difference between the cerebral infarction group, or the TIA group and those of the control group (P less than 0.001 and P less than 0.01) respectively. In view of these results suggest that measuring of Plasma Plg level is a valuable unspecific assays indicator for ischemic cerebral vascular diseases. Finally, the relationship between high coagulation and acute cerebral vascular disease was discussed.