脑梗死二级预防中阿司匹林抵抗及其与血管事件的关系

目的 探讨脑梗死二级预防中阿司匹林抵抗(AR)发生率.随访期AR与脑梗死复发及其他血管事件发生的关系.方法 600例脑梗死患者,入院当Et开始服用阿司匹林,服用7～10 d后检测血小板聚集率,筛选出AR患者及敏感患者,并对患者进行6～24个月随访,观察脑梗死复发及其他血管事件发生情况,采用Logistic回归分析AR及血管事件发生的危险因素和预后.结果 600例脑梗死患者中有AR者150例(25.0%),敏感者450例(75.0%);AR组女性、糖尿病患者比例及血低密度脂蛋白(LDL)胆固醇水平均高于阿司匹林敏感组;糖尿病(OR=2.58,95% CI 1.37～4.85,P=0.003)、高LDL血症(OR=1.89,95% CI 1.21～2.93,P=0.005)为AR发生的独立危险因素;AR组随访期脑梗死复发率、心肌梗死发生率以及全因死亡率均高于阿司匹林敏感组;糖尿病(OR=2.47,95% CI 1.36～4.65,P=0.003)、动脉粥样硬化血栓型脑梗死(OR=2.13,95% CI 1.24～3.95,P=0.023)及AR(OR=3.86,95% CI 1.79～5.87,P=0.002)是随访期血管事件发生的独立危险因素,有AR者血管事件发生的风险增加3.86倍.结论 脑梗死二级预防中AR发生率高,AR与脑梗死复发及其他血管事件的发生密切相关.

Abstract：

Objective To investigate the incidence of the aspirin resistance in secondary prevention of cerebral infarction, and the relationship between the aspirin resistance and the cerebral infarction recurrence or other vascular events during the follow-up periods.Methods Aspirin were taken from the first day of admission in 600 patients with cerebral infarction.The platelet aggregation rate was measured after 7-10 days to screen the patients with aspirin resistance or aspirin sensitivity.All patients were followed up for 6 to 24 months and the cerebral infarction recurrence and other vascular events were recorded.Logistic regression model was used to estimate the risk factors of aspirin resistance, vascular events and prognosis.Results Of 600 patients, 150 (25.0% ) patients were resistant to aspirin and 450 (75.0% ) patients were sensitive to aspirin.The proportion of female and diabetes patients, and the level of low density lipoproteins (LDL) in the aspirin resistance group were higher than those in the aspirin sensitivity group.Diabetes (OR = 2.58, 95% CI 1.37-4.85, P=0.003) and high LDL level (OR = 1.89, 95% CI 1.21-2.93, P = 0.005 ) were independent risk factors of aspirin resistance.The incidence of cerebral infarction recurrence and myocardial infarction and all-cause mortality in the aspirin resistance group were all higher than those in the aspirin sensitivity group.Diabetes ( OR = 2.47, 95% CI 1.36-4.65, P = 0.003 ) , atherothrombosis cerebral infarction (OR = 2.13, 95% CI 1.24-3.95, P = 0.023) and aspirin resistance (OR = 3.86,95% CI 1.79-5.87, P = 0.002) were independent risk factors of vascular events during the following-up period.In the patients with aspirin resistance, the risk of the recurrence of vascular events increased 3.86 times.Conclusions The incidence of aspirin resistance is high in secondary prevention of cerebral infarction.Aspirin resistance is closely correlated with cerebral infarction recurrence and other vascular events.     

脑梗死二级预防中阿司匹林抵抗及其与血管事件的关系

目的 探讨脑梗死二级预防中阿司匹林抵抗(AR)发生率.随访期AR与脑梗死复发及其他血管事件发生的关系.方法 600例脑梗死患者,入院当Et开始服用阿司匹林,服用7～10 d后检测血小板聚集率,筛选出AR患者及敏感患者,并对患者进行6～24个月随访,观察脑梗死复发及其他血管事件发生情况,采用Logistic回归分析AR及血管事件发生的危险因素和预后.结果 600例脑梗死患者中有AR者150例(25.0%),敏感者450例(75.0%);AR组女性、糖尿病患者比例及血低密度脂蛋白(LDL)胆固醇水平均高于阿司匹林敏感组;糖尿病(OR=2.58,95% CI 1.37～4.85,P=0.003)、高LDL血症(OR=1.89,95% CI 1.21～2.93,P=0.005)为AR发生的独立危险因素;AR组随访期脑梗死复发率、心肌梗死发生率以及全因死亡率均高于阿司匹林敏感组;糖尿病(OR=2.47,95% CI 1.36～4.65,P=0.003)、动脉粥样硬化血栓型脑梗死(OR=2.13,95% CI 1.24～3.95,P=0.023)及AR(OR=3.86,95% CI 1.79～5.87,P=0.002)是随访期血管事件发生的独立危险因素,有AR者血管事件发生的风险增加3.86倍.结论 脑梗死二级预防中AR发生率高,AR与脑梗死复发及其他血管事件的发生密切相关.     

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。     

脑梗死患者阿司匹林抵抗与复发缺血性血管事件风险

目的探讨急性脑梗死患者阿司匹林抵抗(AR)的发生与复发缺血性血管事件风险的关系。方法选择2013年7月~2014年6月在北京大学深圳医院神经内科住院的急性脑梗死患者110例,其中男64例,女56例;年龄40~82岁,平均年龄(64.7±12.1)岁。患者口服阿司匹林肠溶片7~10 d后采集外周静脉血,运用全血阻抗法测定血小板聚集程度,0.5 mmol/L花生四烯酸诱导的血小板聚集程度大于0欧姆即定义为AR,根据上述标准将患者分为AR及AS(aspirin sensitive,AS)组,对患者进行为期6个月的随访,终点事件包括短暂性脑缺血发作(TIA)、脑梗死、心肌梗死、死亡。结果 110例患者中31例患者为AR,AR的发生率为28.2%;AR组2型糖尿病患者的比例大于AS组(P0.05);AR组复发缺血性血管事件的发生率大于AS组(22.6%vs 7.9%,P0.05)。多元Logistic回归分析显示,AR是急性脑梗死患者缺血性血管事件复发的独立危险因素(OR=4.091,95%CI=0.024~0.946,P0.05)。结论脑梗死患者存在一定比例的AR;2型糖尿病可能是AR发生的危险因素;AR可增加急性脑梗死患者复发缺血性血管事件的风险。     

生化阿司匹林抵抗与脑梗死的关系

目的分析脑梗死患者中生化阿司匹林抵抗的发生率,探讨其与脑梗死以及与其他危险因素的关系。方法 75例脑梗死患者以及46例对照组人群,均服用阿司匹林100mg,1次/d。10d后采用比浊法以及尿11-脱氢-血栓素B2的检测,确定阿司匹林抵抗的发生率。结果阿司匹林抵抗者共7例,均出现于脑梗死组,对照组未见。阿司匹林半抵抗者病例组22例,对照组6例,两组间比较有统计学差异(P0.05)。相对而言,女性中阿司匹林抵抗者更多见。结论阿司匹林抵抗是脑梗死的一个危险因素,而且在女性中更常见。如果脑梗死患者存在阿司匹林抵抗,应该改换其他药物治疗及预防脑梗死。     

阿司匹林抵抗与大动脉粥样硬化型脑梗死复发的相关性研究

目的 探讨大动脉粥样硬化型脑梗死(LAA)复发的影响因素,并分析其与阿司匹林抵抗(AR)的相关性.方法 选取漯河市中心医院2019-01—08收治的200例大动脉粥样硬化型脑梗死患者为研究对象,根据脑梗死有无复发分为LAA未复发组(158例)和LAA复发组(42例).所有患者口服阿司匹林治疗,采用阿司匹林药物基因检测,...     

阿司匹林在不同年龄段脑梗死病人中的二级预防

目的 探讨阿司匹林在不同年龄段脑梗死病人中二级预防的效果。方法 以2008年1月至2015年6月诊断为急性脑梗死的住院病人3 300例为研究对象,根据是否长期服用阿司匹林分为暴露组（1 800例）和非暴露组（1 500例）;每组按照年龄分为3个年龄段:41~60 岁,61~80岁,81岁及以上。前瞻性追踪调查6个月,分别记录其终点事件（脑梗死复发、症状性颅内出血及上消化道出血）,分析评价阿司匹林在二级预防中的获益与风险。结果 与非暴露组比较,暴露组各个年龄段脑梗死复发率明显降低（P<0.05）,上消化道出血率明显增高（P<0.05）;在61岁之上的两个年龄段,暴露组脑出血和蛛网膜下腔出血发生率明显降低（P<0.05）。ROC曲线显示:81岁以上年龄段,阿司匹林的服药时间对终点事件的预测度有统计学意义（AUC=0.813）。结论 阿司匹林在不同年龄段脑梗死病人中二级预防效果存在差异,41~60岁应用阿司匹林进行二级预防获益最大,风险最小。     

蚓激酶联合阿司匹林在脑梗死二级预防中的应用效果

目的探讨蚓激酶联合阿司匹林在脑梗死二级预防中的应用效果。方法 82例急性脑梗死患者随机分为观察组和对照组。除给予对症处理外,对照组给予阿司匹林治疗,观察组给予阿司匹林联合蚓激酶治疗。观察2组复发情况,检测2组患者治疗前后血液相关指标。结果观察组脑梗死复发率低于对照组,差异有统计学意义(P0.05)。观察组治疗后血浆纤维蛋白原水平、血浆比黏度及全血比黏度水平与对照组治疗后比较,差异有统计学意义(P0.05)。观察组治疗后6个月和12个月的NIHSS评分分别低于同期对照组,差异有统计学意义(P0.05)。结论蚓激酶联合阿司匹林在脑梗死二级预防中应用效果显著,能够减少脑梗死复发,改善患者的血液流变学指标,值得借鉴。     

阿司匹林用于脑梗死二级预防中发生抵抗的原因分析及氯吡格雷干预效果研究

目的分析阿司匹林用于脑梗死二级预防中发生抵抗的原因及氯吡格雷干预效果。方法选择2014年1月—2015年9月256例脑梗死患者纳入研究对象,所有患者均于入院当日开始服用阿司匹林,服用7d后检测血小板聚集率,筛选出阿司匹林抵抗(AR)及阿司匹林半抵抗(ASR)患者共62例,分析引起AR相关因素。采用随机数字表法将62例AR患者分为观察组和对照组各31例,对照组继续服用阿司匹林治疗,观察组服用氯吡格雷联合阿司匹林治疗,观察两组患者血小板聚集率变化、再发脑梗死及出血情况。结果 256例脑梗死患者中,发生AR 62例,发生率24.22%。AR+ASR组患者女性、合并糖尿病、低密度脂蛋白(LDL)水平均明显高于阿司匹林敏感(AS)组(t/χ~2=4.396,4.083,11.191,P<0.05);治疗7d、14d后,观察组血小板聚集率均明显低于对照组(t=10.578,10.466,P<0.05);随访6个月(2014年7月—2016年3月)和12个月(2014年12月-2016年8月),观察组再发梗死率均明显低于对照组(3.23%vs19.38%,3.23%vs22.58%)(χ~2=4.026,5.167,P<0.05)。结论女性、糖尿病、高低密度脂蛋白是脑梗死二级预防中发生AR的高危因素,氯吡格雷联合阿司匹林治疗能降低血小板聚集率,预防脑梗死复发。     

急性脑梗死患者阿司匹林抵抗及相关因素分析

目的观察急性脑梗死患者阿司匹林抵抗发生情况及影响急性脑梗死患者阿司匹林抵抗的相关因素。方法 2010年10月-2011年11月在我院神经内科住院治疗的176例急性脑梗死患者作为研究对象,根据入院前是否服用阿司匹林分为两组:已服组32例,未服组144例。入院后两组均服拜阿司匹林100mg·d-1,连服1w后用全血电阻法监测两组阿司匹林抵抗发生情况,,分为阿司匹林抵抗组和阿司匹林敏感组,分析两组在性别、年龄、血常规、生化指标、心电图、超声心动图、颈动脉彩超及基础疾病等方面的差异。结果 176例脑梗死患者中发生阿司匹林抵抗27例,发生率为15.3%,发生阿司匹林半抵抗97例,发生率为55.1%。阿司匹林抵抗发生情况与入院前是否服用阿司匹林无明显关系(P>0.05)。阿司匹林抵抗组在性别、血小板计数、白细胞计数、糖化血红蛋白与阿司匹林敏感组比较差异有统计学意义(P<0.05)。结论服用阿司匹林的急性脑梗死患者阿司匹林抵抗是完全存在的。发生阿司匹林抵抗可能与性别、血小板数、白细胞数及糖化血红蛋白等因素有关。     

Aspirin resistance in secondary stroke prevention

BACKGROUND: We investigated the platelet function in stroke patients treated with aspirin [acetylsalicylic acid (ASA)] for secondary stroke prevention during a follow-up period of 1 year. METHODS: In this prospective study 291 patients with first initiated aspirin therapy (300 mg/day) for secondary stroke prevention were included. Platelet aggregation measurements were performed 24 h, 3, 6, and 12 months after starting medication. RESULTS: Twenty-one of 291 patients (7.2%) were identified as primary ASA-non-responders (initial insufficient platelet inhibition) and 4.1% as secondary ASA-non-responders (insufficient platelet inhibition during follow-up). There were no significant differences between ASA-responders and ASA-non-responders concerning age, gender, risk factors, and stroke characteristics. CONCLUSION: Aspirin resistance in stroke patients is not uncommon. The clinical usefulness of routine platelet function tests needs to be proved by further trials.     

影响脑梗死患者阿司匹林抵抗的随访研究

目的观察患者依从性与阿司匹林抵抗的关系,并探讨影响患者依从性的相关因素。方法纳入2014年-2015年于青岛大学附属医院出院的首发脑梗死患者451例,且住院时血栓弹力图(TEG)结果显示AA抑制率≥50%,随访12个月,终点事件为脑梗死复发或者死亡,复测患者AA抑制率结果,并运用Morisky-8服药依从性量表对患者进行服药依从性评估。结果共有429例患者纳入分析,AR患者为52例占12.12%,依从性差是AR发生的独立危险因素(P=0.027,OR=3.147,95%CI 1.004~9.834)。依从性较好比例只有35.89%,文化程度低、月收入低、医疗费用支付方式-自费、疾病了解少是依从性差的危险因素(P0.05)。结论依从性差是阿司匹林抵抗发生的独立危险因素;文化程度低、月收入低、医疗费用支付方式-自费、疾病了解少是依从性差的危险因素。     

蚓激酶对动脉粥样硬化性脑梗死二级预防作用探讨

目的探讨蚓激酶药物对动脉粥样硬化性脑梗死二级预防的作用。方法在我院住院和急诊观察的动脉粥样硬化性脑梗死和短暂性脑缺血发作患者268例,随即分为对照组134例,治疗组134例,2组均应用阿司匹林100mg qd,并且对其他危险因素均给与干预。治疗组加用蚓激酶40万U tid 4w为1疗程,服用3个疗程。通过到院随诊1年,以脑卒中复发、心血管事件为研究终点。结果治疗组缺血性脑卒中1年复发率7.8%,心血管事件发生率7.0%分别明显低于对照组16.5%和13.8%,P0.05有统计学意义。结论蚓激酶对动脉粥样硬化性脑梗死的二级预防是有效的。     

急性中重型颅脑损伤患者继发脑梗死的危险因素分析

目的探讨急性中重型颅脑损伤患者继发脑梗死的危险因素,并依据探讨结果制定相应的预防措施。方法选取我院2012-04-2014-01收治并确诊为急性中重型颅脑损伤的患者298例,根据患者有无继发脑梗死,将其分为观察组与对照组。观察组39例为继发脑梗死患者,对照组259例为无继发脑梗死患者,分析各危险因素对急性中重型颅脑损伤患者继发脑梗死的影响。结果单因素分析,继发脑梗死发生的重要相关危险因素有:年龄、格拉斯哥昏迷评分(GCS)、脑疝、创伤性蛛网膜下腔出血、糖尿病和低血压或休克;性别与颅底骨折不是导致继发脑梗死发生的危险因素;导致继发脑梗死发生的独立危险因素是脑疝和低血压。急性中重型颅脑损伤患者继发脑梗死预后恢复良好11例,轻度残疾8例,重度残疾4例,植物生存2例,死亡13例,病死率33.33%,总有效率为48.72%。结论临床应高度重视急性中重型颅脑损伤患者继发脑梗死的相关危险因素,避免血液高黏状态,控制血压及颅内压,注意呼吸道卫生及顺畅,保持出入量平衡,及时补充血容量,降低继发脑梗死的发生率,提高患者生活质量。     

Aspirin for the primary prevention of stroke and other major vascular events: meta-analysis and hypotheses

BACKGROUND: Aspirin therapy reduces stroke by about 25% for persons with atherosclerotic vascular disease, but the effect in those without clinically apparent vascular disease is distinctly different. OBJECTIVE: To define the effect of aspirin use on stroke and other major vascular events when given for primary prevention to persons without clinically recognized vascular disease. DATA SOURCES AND EXTRACTION: Systematic review of randomized clinical trials and large prospective observational cohort studies examining the relation between aspirin use and stroke in persons at low intrinsic risk. Studies were identified by a computerized search of the English-language literature. DATA SYNTHESIS: Five randomized trials of primary prevention included 52 251 participants randomized to aspirin doses ranging from 75 to 650 mg/d; the mean overall stroke rate was 0.3% per year during an average follow-up of 4.6 years. Meta-analysis revealed no significant effect on stroke (relative risk = 1.08; 95% confidence interval, 0.95-1.24) contrasting with a decrease in myocardial infarction (relative risk = 0.74; 95% confidence interval, 0.68-0.82). The lack of reduction of stroke by aspirin for primary prevention was incompatible with its protective effect against stroke in patients with manifest vascular disease (P = .001). Intracranial hemorrhage was increased by the regular use of aspirin (relative risk = 1.35; P = .03), similarly for both primary and secondary prevention. In 4 large observational studies, self-selected use of aspirin was consistently associated with higher rates of stroke. CONCLUSIONS: The effect of aspirin therapy on stroke differs between individuals based on the presence or absence of overt vascular disease, in contrast with the consistent reduction in myocardial infarction by aspirin therapy observed in all populations. We hypothesize that the effect of aspirin therapy on stroke for persons with major risk factors for vascular disease may be intermediate between a substantial decrease for those with manifest vascular disease and a possible small increase for healthy persons due to accentuated intracranial hemorrhage. When aspirin is given for primary prevention of vascular events, available data support using 75 to 81 mg/d.