高龄老年冠心病患者抗血小板药物使用及效果

目的分析高龄老年冠状动脉粥样硬化性心脏病(冠心病)患者服用抗血小板药物情况及治疗效果。方法回顾性纳入2013年6月至2014年12月间在北京军区总医院干四科住院治疗的高龄老年(年龄≥75岁)冠心病患者75例,分为双联抗血小板组(n=32)、单用阿司匹林组(n=16)、单用氯吡格雷组(n=12)及未服用抗血小板药物组(n=15)。比较双联抗血小板组、阿司匹林组、氯吡格雷组患者凝血功能及血栓弹力图指标。结果 75例高龄老年冠心病患者中双联抗血小板占42.7%,单用阿司匹林占21.3%,单用氯吡格雷占16.0%,未服用抗血小板药物占20.0%。双联抗血小板组、阿司匹林组、氯吡格雷组3组患者在年龄、性别构成、常规凝血指标及血小板计数方面无统计学差异(P0.05)。97.9%服用阿司匹林治疗者花生四烯酸(AA)诱导的血小板聚集抑制率(IRAA)50%,70.5%服用氯吡格雷治疗者二磷酸腺苷(ADP)诱导的血小板聚集抑制率(IRADP)≥30%。双联抗血小板组、阿司匹林组、氯吡格雷组3组患者R、K、Angle、MA值水平无统计学差异(P0.05),MAADP、IRADP、IRAA存在统计学差异(P0.05),双联抗血小板组MAADP显著低于阿司匹林组及氯吡格雷组(P0.05),IRADP显著高于阿司匹林组及氯吡格雷组(P0.05),氯吡格雷组IRAA显著低于双联抗血小板组及阿司匹林组(P0.05)。结论高龄老年冠心病患者抗血小板药物使用率较高,阿司匹林与氯吡格雷均获得较好的抗血小板疗效,但阿司匹林反应低下的发生率明显低于氯吡格雷。     

GBE50对应用抗血小板药物的老年人血液流变学影响的临床研究

目的 探讨银杏叶提取物GBE50对应用抗血小板药物的老年人血液流变学的影响.方法 将64例老年患者按抗血小板药物使用情况分为四组:A组未使用抗血小板药物;B组使用阿司匹林100 mg/d;C组使用氯吡格雷75 mg/d;D组使用阿司匹林100 mg/d加氯吡格雷75 mg/d.各组每日均口服2片GBE50,于用药前及连续用药后第30 d分别测定各组患者血黏度和血小板聚集率水平.结果 用药后各组血黏度、红细胞聚集指数、血小板聚集率较用药前下降,差异有统计学意义(P＜0.05).结论 患者使用GBE50后同阿司匹林及氯吡格雷在抗血小板治疗上存在协同作用,可降低血黏度、血小板聚集率,改善老年人的血液流变学.     

阿司匹林、氯吡格雷、西洛他唑抗血栓形成作用及其机制的研究

目的观察常用抗血小板药物阿司匹林、氯吡格雷、西洛他唑的抗血栓形成作用,并探讨其机制。方法将70只SD大鼠随机分成7组各10只,其中对照组不做特殊处理;模型组、阿司匹林组、氯吡格雷组、西洛他唑组、三联组均制备冠状动脉微栓塞模型,建模成功后分别灌服安慰剂、阿司匹林、氯吡格雷、西洛他唑及阿司匹林＋氯吡格雷＋西洛他唑,连续7 d;假手术组在冠状动脉微栓塞模型制作中以生理盐水代替血栓微粒注入左心室,术后灌服安慰剂。实验期间各组均经腹主动脉取血,用自动血凝分析仪分别测定凝血参数凝血酶原时间（PT）、活化部分凝血活酶时间（APTT）和凝血酶时间（TT）,采用血小板聚集率检测仪在6μmol/L的腺苷二磷酸（ADP）诱导下测量最大血小板聚集率,采用ELISA法测定环腺苷酸（c AMP）、血栓素A2（TXA2）和Ⅲ型磷酸二酯酶（PDEⅢ）水平;实验结束后,将各组大鼠仰卧固定消毒、麻醉,采用左颈外静脉、右颈总动脉置入聚乙烯管法检测血栓形成抑制率。结果与模型组比较,4个用药组PT、APTT及TT均明显延长,血小板聚集率明显降低,血栓形成抑制率显著升高,血浆c AMP显著升高、TXA2及PDEⅢ显著降低,尤以三联组为著（P均〈0.01）。实验第3～7天假手术组、阿司匹林组、氯吡格雷组和三联组上述凝血参数均无统计学差异。结论阿司匹林、氯吡格雷、西诺他唑均可抑制血栓形成,三者联用具有协同增效作用;主要作用机制包括减少血小板聚集、上调血浆c AMP及下调TXA2及PDEⅢ水平。     

泮托拉唑对氯吡格雷抗血小板功能的影响研究

目的观察泮托拉唑对氯吡格雷抗血小板功能的影响。方法选取240例急性冠状动脉综合征患者,随机分为两组,对照组（120例）给予氯匹格雷和阿司匹林治疗,泮托拉唑组（120例）在对照组治疗基础上给予泮托拉唑治疗。用药前及用药7d后检测ADP诱导的血小板聚集率。比较前后的血小板聚集率、住院期间及1个月内的主要心血管事件。结果泮托拉唑组和对照组用药前后血小板聚集率及1个月内的主要心血管事件差异无统计学意义（P〉0.05）。结论 泮托拉唑不影响氯吡格雷的抗血小板聚集作用。     

氯吡格雷联合阿司匹林对心绞痛患者血小板功能的影响

目的:观察氯吡格雷联合阿司匹林对心绞痛患者血小板功能的影响。方法:将168例心绞痛患者随机分为对照组和观察组,在常规治疗的基础上,对照组给予口服阿司匹林,观察组给予口服阿司匹林联合氯吡格雷。比较两组患者治疗前后血小板和凝血功能指标。结果:治疗前,两组患者的血小板和凝血功能指标无明显差异;治疗后,两组患者的血小板颗粒膜蛋白140(GMP-140)水平和血小板聚集率均较治疗前降低,且观察组的降低程度较对照组更显著;部分凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)均较前延长,凝血酶原活动度(PTA)均降低,且观察组改变的程度高于对照组(P均0.05)。结论:氯吡格雷联合阿司匹林能有效抗血小板聚集,改善患者凝血功能。     

氯吡格雷与阿司匹林治疗急性脑梗死患者疗效比较

目的比较观察氯吡格雷和阿司匹林治疗急性脑梗死的疗效及安全性。方法 120例急性脑梗死患者随机分为氯吡格雷组(60例)和阿司匹林组(60例),分别服用氯吡格雷(50mg/d)及肠溶阿司匹林(100mg/d),治疗同时,两组均给予相同的抗高血压、降颅压、营养神经及对症支持治疗,疗程为14d,测定治疗前后血浆高敏C反应蛋白(hs-CRP)和血小板聚集率的变化,并评定临床疗效和观察不良反应。结果氯吡格雷组与阿司匹林组对hs-CRP和血小板聚集率均有明确的抑制作用(P0.05),但氯吡格雷组优于阿司匹林组(P0.05);同时氯吡格雷组的临床有效率明显高于阿司匹林组,而阿司匹林组出现不良反应的发生率高于氯吡格雷组,但无严重事件发生。结论服用氯吡格雷治疗急性脑梗死较阿司匹林治疗的临床疗效确切,且较安全可靠,值得临床应用。     

精准医疗在经皮冠状动脉介入术后抗血小板药物选择中的作用

目的:探讨精准医疗、个体化给药在经皮冠状动脉介入术(PCI)后抗血小板药物选择中的作用。方法:入选PCI后服用常规剂量阿司匹林(100 mg/d)和氯吡格雷(75 mg/d)且疗程在3个月左右的患者,根据CYP2C19基因多态性检测结果,将患者分为快代谢组、中代谢组和低代谢组,并给予个体化干预治疗。快代谢组继续服用常规剂量的阿司匹林和氯吡格雷;中代谢组将氯吡格雷调整为1.5倍剂量;低代谢组分为两组,氯吡格雷组将氯吡格雷调整为2倍剂量,替格瑞洛组将氯吡格雷改换为替格瑞洛(90 mg、2次/d)。检测各组个体化干预治疗前后凝血指标和血小板聚集率的变化及干预治疗后的出血事件。结果:各组患者干预治疗前后组间和组内比较,凝血指标差异均无统计学意义(P均0.05)。干预治疗前,血小板聚集率为快代谢组中代谢组低代谢组,3组间差异均有统计学意义(P均0.05);干预治疗后,中代谢组患者血小板聚集率较干预治疗前明显下降(P0.05),低代谢组中氯吡格雷组血小板聚集率与干预治疗前比较差异无统计学意义,替格瑞洛组血小板聚集率较干预治疗前明显下降(P0.05)。干预治疗后快代谢组、中代谢组血小板聚集率差异无统计学意义;低代谢组中替格瑞洛组血小板聚集率明显低于快/中代谢组,氯吡格雷组仍明显高于快/中代谢组(P均0.05)。干预治疗后,中代谢组、低代谢组与快代谢组比较出血风险均未增加(P均0.05)。结论:根据CYP2C19基因多态性检测结果个体化给药,可提高抗血小板治疗效果,且不增加出血风险。对于CYP2C19基因型为低代谢型的患者建议改用替格瑞洛治疗。     

氯吡格雷联合应用他汀类药物药效及副反应观察

目的观察氯吡格雷药效及副反应是否因为合用他汀药物而受到影响。方法124例临床诊断不稳定型心绞痛（UA）患者均给予氯吡格雷300 mg顿服,继75 mg/d,随机分为合用氟伐他汀80 mg/d组、合用阿托伐他汀10mg/d组和对照组,给药前及治疗2周后分别测定其血小板聚集率和血常规。结果患者血小板聚集率均明显降低,与治疗前比较,差异有显著性,3组血小板聚集率降低幅度无显著性差异,3组均未发现中性粒细胞及血小板计数减少患者。结论联合应用氟伐他汀或阿托伐他汀后,氯吡格雷药效及副反应未受影响。     

血栓弹力图评价急性冠状动脉综合征患者氯吡格雷反应低下的研究

目的 通过血栓弹力图(TEG)检测血小板聚集率,观察接受双联抗血小板药物治疗的急性冠状动脉综合征患者发生氯吡格雷反应低下的情况.方法 选取住院的急性冠状动脉综合征患者167例,在常规口服阿司匹林(100 mg/d)的基础上,随机给予氯吡格雷75 mg/d或顿服300 mg后继续75 mg/d.常规剂量组在连续用药5天后、负荷组在顿服300 mg后次日采血,通过TEG方法测定血小板聚集率,以二磷酸腺苷诱导的血小板聚集率≥70％为氯吡格雷反应低下,花生四烯酸诱导的血小板聚集率＞50％为阿司匹林反应低下.结果 总计50例患者出现氯吡格雷反应低下,发生率为29.9％,常规剂量组和负荷组比较差异无统计学意义(P＞0.05);16例(9.6％)患者发生阿司匹林和氯吡格雷反应双低下;氯吡格雷反应低下组与非低下组间阿司匹林反应低下的发生率比较差异有显著统计学意义(P＜0.01).氯吡格雷反应低下组与非低下组患者的年龄、高血压、糖尿病、合并用药等方面比较差异无统计学意义(P＞0.05),但两组性别、吸烟史、入院时总胆固醇水平比较差异具有统计学意义(P＜0.05).结论 接受标准抗血小板治疗的急性冠状动脉综合征患者存在氯吡格雷反应低下的现象,这一现象不受年龄、合并用药及氯吡格雷给药方式的影响,而女性、无吸烟史或烟龄短、年支数少、存在高总胆固醇血症或阿司匹林反应低下的患者更易发生氯吡格雷反应低下.     

阿司匹林联合氯吡格雷在老年冠心病患者中的治疗效果分析

目的研究阿司匹林联合氯吡格雷在老年冠心病患者中的治疗效果分析。方法选取2016年4月到2017年7月来我院就诊的老年冠心病患者共74例,随机均分为两组,对照组老年冠心病患者采取阿司匹林单纯药物治疗方法,观察组基于对照组用药方案加用氯吡格雷,观察联合用药方案与单纯采取阿司匹林药物治疗的效果差异。结果观察组总有效率达到了94.59%,而对照组总有效率为78.38%,明显低于观察组;且治疗后观察组老年冠心病患者的血小板计数、血小板聚集率较对照组患者明显要低,另外观察组与对照组不良反应发生率分别为2.70%、16.22%,相比对照组,观察组发生率更低,两组差异具有统计学意义(P0.05)。结论采用阿司匹林联合氯吡格雷用药在治疗老年冠心病方面有较为确切的效果,且不良反应少,具有较高推广应用价值。     

血栓弹力图检测老年冠心病患者经皮冠状动脉介入治疗后血小板反应性

目的探讨经皮冠状动脉介入治疗术后,经血栓弹力图检测的氯吡格雷药物抵抗患者,不同药物剂量治疗下血小板反应性。方法筛选120例阿司匹林抑制良好而氯吡格雷抑制不敏感的患者,随机分为试验组(60例)和对照组(60例),对照组每天服用100 mg阿司匹林及75 mg氯吡格雷,试验组服用100 mg阿司匹林及150 mg氯吡格雷,检测6个月后氯吡格雷的作用效果,观察2组间6个月内心血管事件及出血事件的发生率。结果试验组心血管死亡、支架内血栓形成、不稳定性心绞痛、心肌梗死发生率分别为0,8.3%,21.7%,8.3%;对照组分别为3.3%,18.3%,35.0%,15.0%,试验组患者氯吡格雷药物抑制率较对照组明显升高(65.6±5.1)% vs (40.9±7.3)%,差异有统计学意义(P0.01)。结论对于血小板高反应性老年患者,每天75 mg氯吡格雷不能满足血小板抑制效果,长期加倍剂量服用能够在一定程度上有效减低药物抵抗发生率,改善血小板抑制效果,从而降低心血管缺血事件的发生率。     

The effects of laropiprant on the antiplatelet activity of co-administered clopidogrel and aspirin

Abstract

Laropiprant is an antagonist of the prostaglandin PGD₂ receptor DP1. Laropiprant has a weak affinity for the thromboxane A₂ receptor TP. Two double-blinded, randomized, placebo-controlled, crossover studies evaluated the effects of multiple-dose laropiprant at steady state on the antiplatelet effects of multiple-dose aspirin and clopidogrel. Study 1 had two treatment periods, in which each healthy subject received laropiprant 40?mg, clopidogrel 75?mg, and aspirin 80?mg (Treatment A), or placebo, clopidogrel 75?mg, and aspirin 80?mg (Treatment B) once daily for 7 days. Study 2 consisted of three treatment periods. In the first two, each patient with hypercholesterolemia or mixed dyslipidemia received laropiprant 40?mg, clopidogrel 75?mg, and aspirin 81?mg (Treatment A), or placebo, clopidogrel 75?mg, and aspirin 81?mg (Treatment B) once daily for 7?days. In period 3, patients received a single dose of two tablets of extended release nicotinic acid 1?g/laropiprant 20?mg (Treatment C). In both studies, pharmacodynamic endpoints included bleeding time at 24 (primary) and 4 hours (secondary) post-dose following 7 days of once-daily laropiprant in combination with clopidogrel and aspirin, and platelet aggregation in platelet-rich plasma at 4 and 24 hours post-dose on day 7 (secondary). After 7 days, increased bleeding time of 27% (Study 1) and 23% (Study 2) at 24 hours post-dose was observed with laropiprant compared to placebo (both combined with clopidogrel and aspirin), with corresponding upper bounds of the 90% CI marginally exceeding the prespecified upper comparability bound of 1.50 in both studies. The GMR and 90% CI for bleeding time of laropiprant compared to placebo (both combined with clopidogrel and aspirin) at 4 hours post-dose on day 7 was 0.92 (0.70, 1.21) in Study 1, and 1.46 (1.20, 1.78) in Study 2. Compared with placebo, laropiprant (both combined with clopidogrel and aspirin) increased the inhibition of collagen- and ADP-induced platelet aggregation, respectively, by ～2.4% and ～8.1% in Study 1 and by ～4% and ～5.4% in Study 2, at 24 hours post-dose on day 7. The inhibition of collagen- and ADP-induced platelet aggregation, respectively, was increased by ～0.1% and ～5.0% in Study 1, and by ～5% and ～12% in Study 2, at 4 hours post-dose on day 7. In conclusion, co-administration of multiple doses of laropiprant with aspirin and clopidogrel induced a prolongation of bleeding time and an inhibitory effect on platelet aggregation ex vivo in healthy subjects and patients with dyslipidemia.     

Effects of triple antiplatelet therapy (aspirin, clopidogrel, and cilostazol) on platelet aggregation and P-selectin expression in patients undergoing coronary artery stent implantation

The purpose of this study was to determine the effect of the addition of cilostazol to aspirin plus clopidogrel on platelet aggregation after intracoronary stent implantation. Twenty patients who underwent coronary stent placement were randomly assigned to therapy with aspirin plus clopidogrel (dual-therapy group, n = 10) or aspirin plus clopidogrel plus cilostazol (triple-therapy group, n = 10). A loading dose of clopidogrel (300 mg) and cilostazol (200 mg) was administered immediately after stent placement, and clopidogrel (75 mg/day) and cilostazol (100 mg twice daily) were given for 1 month. Platelet aggregation in response to adenosine diphosphate (ADP; 5 and 20 micromol/L) or collagen and P-selectin (CD-62P) expression was assayed at baseline, 2 hours, 24 hours, 1 week, and 1 month after stent placement. Inhibition of ADP-induced platelet aggregation was significantly higher in patients receiving triple therapy than those receiving dual therapy from 24 hours after stent placement, and inhibition of collagen-induced platelet aggregation was significantly higher in the triple-therapy group beginning 1 week after stent placement. P-Selectin expression was significantly lower in the triple-therapy than dual-therapy group at 1 week and 30 days. In conclusion, compared with dual antiplatelet therapy, triple therapy after coronary stent placement resulted in more potent inhibition of platelet aggregation induced by ADP and collagen. These findings suggest that triple therapy may be used clinically to prevent thrombotic complications after coronary stent placement.     

Dynamic platelet adhesion in patients with an acute coronary syndrome: The effect of antiplatelet therapy

Platelet adhesion and aggregation are key functions leading to thrombus formation. The effect of aspirin, clopidogrel, and ticagrelor on platelet aggregation has been well established, however, there is limited data on the effect of these drugs on platelet adhesion. We therefore evaluated the effect of these drugs on platelet adhesion in acute coronary syndrome (ACS) patients. Citrated blood was collected from 50 ACS patients loaded with 325 mg of aspirin (baseline) and at 5 days after the administration of aspirin 100 mg/day and clopidogrel (600 mg loading dose, 75 mg/day) (n = 26) or ticagrelor (180 mg loading dose, 90 mg × 2/day) (n = 24). High on-treatment platelet reactivity (HTPR) to clopidogrel was estimated by vasodilator stimulated phosphoprotein (VASP) phosphorylation assay. Platelet adhesion to collagen was studied for 6 min under high shear stress and was evaluated using the time to platelet recruitment (TPR), the perimeter and average area of each adherent object, number of adherent objects, and the total percent of surface coverage (SC%). Six ACS patients exhibited HTPR to clopidogrel and excluded from the platelet adhesion assays. TPR and SC% values were similar among patient groups at baseline and controls. However, all other adhesion parameters were different in ACS patients, indicating the formation of more aggregates in regard to controls. At 5 days post-treatment with either clopidogrel or ticagrelor, the TPR values were increased and the SC% values were reduced to a similar extent compared with baseline. However, significant differences were observed in the ticagrelor group in the perimeter, number of adherent objects, and the average area of each adherent object indicating a more potent inhibition of adherence-induced platelet aggregation than clopidogrel. In conclusion, aspirin does not affect platelet adherence to collagen, whereas clopidogrel and ticagrelor inhibit to a similar extent dynamic platelet adhesion at 5 days post-treatment in ACS patients. However, ticagrelor exhibits a greater inhibitory effect on reducing adhesion-induced platelet aggregation.     

长期负荷量硫酸氢氯吡格雷显著降低血小板高反应性患者PCI术后心血管缺血事件发生率

目的 观察长期负荷量使用硫酸氢氯吡格雷对血小板高反应性患者PCI术后心血管缺血事件发生率的影响。方法 采用血栓弹力仪检测硫酸氢氯吡格雷的药物效果,筛选PCI术后对硫酸氢氯吡格雷药物不敏感患者（血小板高反应性患者）作为研究对象,随机分为对照组及试药组,每组患者各60例,对照组每天服用100 mg阿司匹林及75 mg硫酸氢氯吡格雷,试药组服用100 mg阿司匹林以及150 mg硫酸氢氯吡格雷,检测6个月后硫酸氢氯吡格雷的药物效果,同时观察两组6个月内心血管事件的发生率。结果 6个月内试药组心血管病病死率、支架内血栓再形成率、再发心肌梗死和再发不稳定心绞痛发生率分别为0%、10%、23%以及6%,对照组为3%、20%、36%以及17%,试药组显著低于对照组,试药组硫酸氢氯吡格雷所致血小板抑制率明显高于对照组,两组患者出血风险无显著性差异。结论对于血小板高反应性患者,长期加倍剂量服用硫酸氢氯吡格雷可降低心血管缺血事件发生率。     

Comparison of increased aspirin dose versus combined aspirin plus clopidogrel therapy in patients with diabetes mellitus and coronary heart disease and impaired antiplatelet response to low-dose aspirin

The effects of therapy with aspirin 300 mg/day and with combined aspirin 100 mg/day plus clopidogrel 75 mg/day on platelet function were compared in patients with diabetes mellitus and coronary artery disease and impaired antiplatelet responses to aspirin 100 mg/day. The study population consisted of 151 outpatients with type II diabetes mellitus and coronary artery disease who were taking aspirin 100 mg/day. Of the 151 patients, a subgroup of subjects with impaired aspirin response were selected on the basis of the results of platelet aggregometry. Nonresponsiveness to aspirin was defined as mean aggregation > or =69% with 3 micromol/L adenosine diphosphate and mean aggregation > or =70% with 2 micromol/L collagen. Aspirin semiresponders were defined as meeting 1 but not both of these criteria. Nonresponders and semiresponders were randomized equally to aspirin 300 mg/day and aspirin 100 mg/day plus clopidogrel 75 mg/day, and aggregation tests were repeated after 2 weeks. Sixty of the 151 patients with diabetes (40%) were found to respond to aspirin inadequately. Platelet aggregation induced by adenosine diphosphate and collagen decreased significantly after aspirin 300 mg/day or combined therapy. Combined treatment was found to have a stronger inhibitory effect on platelet aggregation induced by adenosine diphosphate than aspirin 300 mg/day (p = 0.002). Impaired aspirin response was resolved by increasing the aspirin dose or adding clopidogrel to aspirin (p <0.0001 for each). However, desired platelet inhibition was achieved in significantly more patients by combined treatment than by aspirin 300 mg/day (p <0.05). In conclusion, aspirin 100 mg/day does not inhibit platelet function adequately in a significant number of patients with diabetes mellitus and coronary artery disease. Increasing the aspirin dose to 300 mg/day or adding clopidogrel to aspirin can provide adequate platelet inhibition in a significant number of those patients with impaired responses to low-dose aspirin.     

Effect of Ginkgo biloba (EGb 761) and aspirin on platelet aggregation and platelet function analysis among older adults at risk of cardiovascular disease: a randomized clinical trial.

Several case reports have implicated Ginkgo biloba in clinically adverse bleeding disorders. Ginkgo biloba has been reported to increase pain-free walking distance among patients with peripheral artery disease (PAD). Standard PAD therapy includes 325 mg/day aspirin. The objective of this study was to examine potential adverse effects of concomitant aspirin and Ginkgo biloba on platelet function. Ginkgo biloba (EGb 761, 300 mg/day) was compared with placebo for effects on measures of platelet aggregation among adults consuming 325 mg/day aspirin in a randomized, double-blind, placebo-controlled, parallel design trial of 4-week duration. Participants were adults, age 69 +/- 10 years, with PAD or risk factors for cardiovascular disease. Outcome measures included platelet function analysis (PFA-100 analyzer) using ADP as an agonist (n = 26 placebo; n = 29 ginkgo), and platelet aggregation using ADP, epinephrine, collagen and ristocetin as agonists (n = 21 placebo; n = 23 ginkgo). Participants kept daily logs of bleeding or bruising episodes. There were no clinically or statistically significant differences between treatment groups for any agonists, for either PFA-100 analysis or platelet aggregation. Reports of bleeding or bruising were infrequent and similar for both study groups. In conclusion, in older adults with PAD or cardiovascular disease risk, a relatively high dose of Ginkgo biloba combined with 325 mg/day daily aspirin did not have a clinically or statistically detectable impact on indices of coagulation examined over 4 weeks, compared with the effect of aspirin alone. No adverse bleeding events were observed, although the trial was limited to a small sample size.     

Response to aspirin and clopidogrel monitored with different platelet function methods

Laboratory non-response to aspirin or clopidogrel is defined as an inability to cause in vitro detectable platelet function inhibition. It would be beneficial to monitor response to aspirin or clopidogrel with widely available and routinely used platelet function methods, like the platelet function analyzer (PFA-100) or the fully automated coagulation analyzer BCT. The aim of this study was to assess the potential of the coagulation analyzer BCT and the platelet function analyzer PFA-100 in monitoring the response of aspirin and clopidogrel. A group of 125 consecutive patients with arterial occlusive disease treated either with aspirin 100 mg/day (82 patients) or clopidogrel 75 mg/day (43 patients) as only antiplatelet drug were investigated. For the first time platelet-enriched plasma (PRP), not adjusted to a fixed predetermined concentration of platelets, was used for aggregation studies and the effect of clopidogrel alone without combination of aspirin treatment on platelet function was investigated. Response to aspirin was observed in 85% (70/82) of patients using PFA-100, while performing the arachidonic acid-induced aggregation on the BCT showed an inhibitory effect to aspirin in 91% (75/82) of patients. Non-response to aspirin was assessed with both platelet function methods in 7% (6/82) of patients. Clopidogrel response was observed in 58% (25/43) of patients when performing ADP-induced aggregation on the BCT. On the PFA-100 the antiplatelet effect of clopidogrel could not be detected. In conclusion, measurement of platelet aggregation on the BCT using native platelet-enriched plasma allows the quantification of individual inhibitory effects to aspirin as well as to clopidogrel, while the PFA-100 seems only suitable to investigate the degree of platelet inhibition induced by aspirin but not by clopidogrel.     

替格瑞洛用于经皮冠状动脉介入治疗术后患者抗血小板治疗短期内的有效性和安全性研究

目的：观察替格瑞洛用于经皮冠状动脉介入治疗（PCI）患者抗血小板治疗的有效性和安全性。方法选择50例冠心病PCI术后应用氯吡格雷抗血小板,因血小板聚集率不达标且CYP2C19基因异常而改用替格瑞洛的患者。所有入选患者应用阿司匹林首次负荷剂量300 mg,维持剂量100 mg,每日一次;替格瑞洛维持剂量90 mg,每日二次,持续1年。研究主要终点为随访1个月的主要不良心血管事件（包括死亡、支架内血栓形成、支架内再狭窄、非致死性心肌梗死、靶血管血运重建）和脑卒中的发生率;次要终点为一般不良事件（包括轻微出血、过敏、呼吸困难）的发生率及血小板计数的变化情况。结果患者应用替格瑞洛后随访1个月未出现主要不良心血管事件和脑卒中;一般不良事件的发生率较低,2例（4%）出现呼吸困难,2例（4%）发生轻微出血,其中1例鼻出血,1例皮下淤血。应用替格瑞洛后血小板聚集率明显低于氯吡格雷,血小板计数未明显下降。结论替格瑞洛用于存在氯吡格雷抵抗的PCI患者抗血小板治疗,短期内安全有效。