等剂量国产氯吡格雷与进口氯吡格雷的等效性及安全性比较
|
摘要
背景：心血管疾病,尤其是冠状动脉粥样硬化性心脏病(coronary atherosclerotic heart disease, CAD)是严重威胁人类健康的主要疾病。冠心病的发病率和死亡率逐年上升,我国冠心病的负担越来越大。冠状动脉介入治疗(percutaneous coronary interventions, PCI)已经成为治疗冠心病的重要有效方法,我国PCI的患者数量越来越多。但是,伴随的相关血栓并发症也是越来越多。双联抗血小板(阿司匹林+氯吡格雷)已经成为PCI术后的标准方案。然而,进口氯吡格雷价格昂贵,国产非专利氯吡格雷价格便宜,其对血小板聚集的抑制和对PCI术后的疗效及安全性尚无大样本资料证实。
目的：1、探讨等剂量国产和进口氯吡格雷对血小板聚集率影响效果是否相同；2、等剂量国产和进口氯吡格雷对凝血系统影响效果是否相同；3、等剂量国产和进口氯吡格雷对血细胞计数代表的血液系统的影响效果是否相同；4、等剂量国产和进口氯吡格雷对PCI术后疗效及安全性是否相同5、等剂量国产和进口氯吡格雷对急诊PCI术后疗效及安全性是否相同。
方法：1、连续入选199例不稳定性心绞痛患者,随机分为国产氯吡格雷(泰嘉组,89例)和进口氯吡格雷(波立维组,110例),按照相同的应用剂量及应用方法,并应用电阻法在用药前、用药后8-12小时、24～36小时、48～60小时测定二磷酸腺苷(ADP)诱导的血小板聚集率,在用药前和用药后48-60小时测定白细胞计数、红细胞计数、血小板计数、D—二聚体(D-dimer)、凝血系统[包括凝血酶原时间(PT)、凝血酶原时间国际标准化比值(INR)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、纤维蛋白原(FIB)]等指标。2、入选1798例接受PCI治疗的冠心病患者,随机分为泰嘉组(1104例)及波立维组(694例),在PCI术前给予300mg负荷剂量,序贯75mg/d,随访3-28个月,观察急性、亚急性、晚期、极晚期支架内血栓和心肌梗死、心源性死亡、脑卒中的联合终点MACE事件的影响以及出血等相关副作用的影响。3、入选204例接受急诊PCI治疗的急性心肌梗死患者,随机分为泰嘉组(123例)及波立维组(81例),在急诊室给予300mg负荷剂量,序贯75mg/d,随访3-28个月,观察急性、亚急性、晚期、极晚期支架内血栓和心肌梗死、心源性死亡、脑卒中的联合终点MACE事件的影响以及出血等相关副作用的影响。
结果：1、泰嘉组及波立维组血小板聚集率均随用药时间延长而降低,在负荷量后降低最明显,泰嘉组与波立维组用药前、用药后8～12小时、24～36小时、48～60小时的血小板聚集率电阻值分别为7.67±3.48欧姆(ohm),4.67±3.84ohm,3.46±3.93 ohm,3.36±3.86 ohm和6.84±3.25ohm,4.25±3.94ohm,2.63±3.27ohm,2.59±3.50ohm,经单个重复测量因素的方差分析,两组间差异无统计学意义(F=3.092,P=0.080),4次重复测量的血小板聚集率之间差异具有统计学意义(F=117.101,P=0.000);而凝血系统PT、INR、APTT、TT、FIB、D-dimer治疗前无显著差异(t值分别为0.825、1.260、1.448、0.299、1.112、0.388,P值分别为0.411、0.209、0.149、0.765、0.267、0.699)；治疗后PT、INR、APTT、TT、FIB、D-dimer治疗前无显著差异(t值分别为1.350、1.159、1.406、0.915、1.810、0.372,P值分别为0.179、0.248、0.161、0.361、0.072、0.710)；血常规的各项血细胞计数WBC、RBC、HGB、PLT治疗前比较无差异(t值分别为1.840、0.101、0.664、2.027,P值分别为0.067、0.920、0.507、0.054)；治疗后WBC、RBC、HGB、PLT比较无差异(t值分别为1.404、0.083、0.565、1.581,P值分别为0.162、0.934、0.574、0.116)。泰嘉组和波立维组治疗前后PT、INR、APTT、TT、D-dimer经自身配对t检验无显著差异(t值分别为1.198和1.016、0.989和0.697、0.872和0.981、0.368和1.225、0.051和0.032,P值分别为0.234和0.311、0.325和0.487、0.385和0.328、0.714和0.223、0.959和0.975)；而泰嘉组和波立维组FIB均较前升高(t值分别为3.389和2.074,P值分别为0.001和0.040)；泰嘉组和波立维组治疗前后WBC及PLT计数经自身配对t检验无明显变化(t值分别为0.248和0.808、1.654和1.618,P值分别为0.804和0.421、0.102和0.109)；而泰嘉组和波立维组治疗后RBC计数及HGB定量均较治疗前明显下降,经自身配对t检验,有显著性差异(t值分别为7.539和9.562、9.224和10.856,P值分别为0.000和0.000、0.000和0.000)。2、泰嘉组和波立维组靶血管重建、联合终点事件发生率,经统计学检验,差异无显著性意义(X2值分别为2.176、3.287,P值分别为0.140、0.070)；支架内血栓及心源性死亡经Fisher's精确概率计算,无显著性差异(P值分别为0.440、0.149)；出血和大出血事件发生率,经统计学检验,差异无显著性意义(P值分别为0.072和0.380)；两组之间无事件生存情况经Kaplan-Meier生存分析,Log Rank (Mantel-Cox)比较,无显著差异(X2值=3.438,P值=0.064)；累积MACE事件经Kaplan-Meier生存分析,Log Rank (Mantel-Cox)比较,无显著差异(X2值=1.076,P值=0.300)。
3、泰嘉组和波立维组均无支架内血栓和出血事件；波立维组有2例心源性死亡,分别为心源性休克及心脏破裂；两组靶血管重建及联合终点事件发生率,经统计学检验,差异无显著性意义(X2分别为0.000和0.921,P值分别为0.989和0.337)；两组之间累积MACE事件经Kaplan-Meier生存分析计算,绘制K-M曲线见图3.1,经Log Rank (Mantel-Cox)比较,无显著差异(X2值=0.679,P值=0.410)。
结论：1、大样本、随机、阳性对照比较同剂量、同方案国产氯吡格雷和进口氯吡格雷对电阻法测定的血小板聚集率的影响,进行了“头对头”的疗效比较,以及对凝血系统、血液系统的影响,发现二者具有等同影响,疗效及安全性类似。2、国内最大样本量(应用国产氯吡格雷超过1000例)、随机、阳性对照比较同剂量、同方案国产氯吡格雷和进口氯吡格雷对PCI术后疗效及安全性的比较,发现二者对PCI术后的疗效及安全性相似,发现在白细胞下降副作用方面,国产氯吡格雷(泰嘉)优于进口氯吡格雷(波立维)。3、大样本、随机、阳性对照比较同剂量、同方案国产氯吡格雷和进口氯吡格雷对AMI患者急诊PCI术后疗效及安全性的比较,发现二者对急诊PCI术后的疗效及安全性相似。
Background:Over the past two centuries, the Industrial and Technological Revolutions and their associated economic and social transformations have resulted in dramatic shifts in the diseases responsible for illness and death. Cardiovascular disease (CVD) has emerged as the dominant chronic disease in many parts of the world, and early in the 21st century it is predicted to become the main cause of disability and death worldwide. CVD is a major disease threaten human health, especially coronary atherosclerotic heart disease (CAD). Morbidity and mortality of CAD rises year by year and the burden of CAD is more and more accelerating in China. Percutaneous coronary interventions has been the major and effect therapy and there were more and more CAD patients to underwent CAG and PCI, however, there were more and more stent thrombus complication correlation PCI. Dual antiplatelet therapy (aspirin and clopidogrel) has been the standard proposal after PCI, however, the cost of imported clopidogrel (PlavixTM) is expensive and the domestic generic clopidogrel (TalcomTM) is cheap relative PlavixTM. There are not large sample data to confirm the effect to inhibit platelet aggregation and the effect and safety after PCI of TalcomTM.
Objective:1.To explore whether the effects of isodose domestic clopidogrel (TalcomTM) and imported clopidogrel (PlavixTM) on platelet function in patients with unstable angina (UAP).2. To explore whether the effects of isodose TalcomTM and PlavixTM on parameters of blood clot system in patients with unstable angina (UAP). 3. To explore whether the safety of isodose TalcomTM and PlavixTM on parameters of blood routin test in patients with unstable angina (UAP).4. To compare the efficacy and safety of TalcomTM and PlavixTM on PCI.5. To compare the efficacy and safety of TalcomTM and PlavixTM on directed PCI in AMI patients.
Methods:1.199 patients with UAP were randomized to two groups, including TalcomTM group (n=89), PlavixTM group (n=110). Venous blood samples were obtained before taking orally clopidogrel,8-12 hours after taking loading dose clopidogrel 300 mg, and after 75 mg/day for 24 hours,48 hours in two clopidogrel groups in order to test platelet aggregation rate induced by adenosine diphosphate (ADP) detected by electric resistance method and before taking orally clopidogrel and after 75 mg/day for 48 hours in two clopidogrel groups in order to test lencocyte count, red blood cell count, blood platelets count, D-dimer, prothrombin time (PT), international normalized ratio of prothrombin time (INR), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen.2.1798 patients with CAD to undergo CAG+PCI were randomized to two groups, including TalcomTM group (n=1104), PlavixTM group (n=694).300mg loading dose clopidogrel was oral before PCI and 75mg/d foreword one year. There were follow-up 3-28 month to survey the incidence rate of MACE of combination end point of acute, subacute, late stage, very late stage stent thrombus and AMI, cardiac death, stroke and correlated adverse reaction of bleed, major bleed, gastrointestinal complaint, and etc. 3.204 patients with AMI to undergo directed CAG+PCI were randomized to two groups, including TalcomTM group (n=123), PlavixTM group (n=81).300mg loading dose clopidogrel was oral before PCI in emergency room and 75mg/d foreword one year. There were follow-up 3-28 month to survey the incidence rate of MACE of combination end point of acute, subacute, late stage, very late stage stent thrombus and AMI, cardiac death, stroke and correlated adverse reaction of bleed, major bleed, gastrointestinal complaint, and etc.
Results:There were no significant differences in the platelet aggregation rate and blood cell count and the item of blood clot system between Talcom group and Plavix group before treatment. There were no significant differences in the aforementioned markers between TalcomTM group and PlavixTM group after treatment. With the time, platelet aggregation rate of TalcomTM group and PlavixTM group was degrading, and there was the most obviously after orally loading dose, and resistance value of TalcomTM group and PlavixTM group in before taking orally, after orally 8～12 hour, 24～36 hour,48～60 hour was 7.67±3.48ohm,4.67±3.84 ohm,3.46±3.93 ohm, 3.36±3.86 ohm and 6.84±3.25ohm,4.25±3.94ohm,2.63±3.27ohm,2.59±3.50ohm, respectively. There were significant differences in 4 repeated detected platelet aggretion rate by one way repeated measure factor ANOVA, (F=117.101, P=0.000). There were no significant differences in the parameters (PT, INR, APTT, TT, FIB, D-dimer) of blood clot system between TalcomTM group and PlavixTM group before treatment (t value 0.825,1.260,1.448,0.299,1.112,0.388, P value 0.411, 0.209,0.149,0.765,0.267,0.699, respectively); There were no significant differences in the parameters (PT, INR, APTT, TT, FIB, D-dimer) of blood clot system between TalcomTM group and PlavixTM group after treatment (t value 1.350、1.159、1.406、0.915、1.810、0.372, P value 0.179、0.248、0.161、0.361、0.072、 0.710, respectively); There were no significant differences in the parameters (WBC, RBC, HGB, PLT) of blood routin test between TalcomTM group and PlavixTM group before treatment (t value 1.840,0.101,0.664,2.027, P value 0.067,0.920,0.507, 0.054, respectively); There were no significant differences in the parameters (WBC, RBC, HGB, PLT) of blood routin test between TalcomTM group and PlavixTM group after treatment (t value 1.404,0.083,0.565,1.581, P value 0.162,0.934,0.574,0.116, respectively). There were no significant differences in the parameters (PT, INR, APTT, TT, FIB, D-dimer) of blood clot system between before and after treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 1.198 and 1.016,0.989 and 0.697,0.872 and 0.981,0.368 and 1.225,0.051 and 0.032, P value 0.234 and 0.311,0.325 and 0.487,0.385 and 0.328,0.714 and 0.223,0.959 and 0.975, respectively); but the level of FIB of after treatment is increase to compare to before treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 3.389 and 2.074, P value 0.001 and 0.040, respectively); There were no significant differences in the parameters (WBC and PLT) of blood routin test to compare to before treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 0.248 and 0.808,1.654 and 1.618, P value 0.804 and 0.421,0.102 and 0.109, respectively); but the level of the count of RBC and the quantitation of HGB of after treatment is decrease to compare to before treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 7.539 and 9.562,9.224 and 10.856, P value 0.000 and 0.000,0.000 and 0.000, respectively).2. There were no significant differences in the incidence of target vessel revascularization and combination end point between TalcomTM group and PlavixTM group (X2 value 2.176,3.287, P value 0.140,0.070). There were no significant differences in the incidence of stent thrombus and cardiac death between TalcomTM group and PlavixTM group by Fisher's exact probability (P value 0.440,0.149). There were no significant differences in the incidence of bleed and major bleed between TalcomTM group and PlavixTM group (P value 0.072 and 0.380). There were no significant differences in survival without event and accumulation MACE hazard analysised by Kaplan-Meier survival analysis (X2 3.438 and 1.076, P=0.064 and 0.300).3. There were not stent thrombus and bleed event both TalcomTM group and PlavixTM group. There are two patients death of cardiac shock and heart rupture in PlavixTM group. There were no significant differences in the incidence of target vessel revascularization and combination end point between TalcomTM group and PlavixTM group (X2 value 0.000 and 0.921, P value 0.989 and 0.337). There were no significant differences in accumulation MACE hazard analysised by Kaplan-Meier survival analysis(X20.679, P=0.410).
Conclusions:1.The anti-platelet aggregation and antiplatelet activation effects of isodose TalcomTM are similar to those of PlavixTM. The two drugs have good anti-platelet effects. Furthermore, the two drugs have no significant adverse drug reaction.2. Effects and safety of isodose TalcomTM used in underwent PCI patients are similar to those of PlavixTM.3. Effects and safety of isodose TalcomTM used in AMI patients that underwent directed PCI are similar to those of PlavixTM.
目的：1、探讨等剂量国产和进口氯吡格雷对血小板聚集率影响效果是否相同；2、等剂量国产和进口氯吡格雷对凝血系统影响效果是否相同；3、等剂量国产和进口氯吡格雷对血细胞计数代表的血液系统的影响效果是否相同；4、等剂量国产和进口氯吡格雷对PCI术后疗效及安全性是否相同5、等剂量国产和进口氯吡格雷对急诊PCI术后疗效及安全性是否相同。
方法：1、连续入选199例不稳定性心绞痛患者,随机分为国产氯吡格雷(泰嘉组,89例)和进口氯吡格雷(波立维组,110例),按照相同的应用剂量及应用方法,并应用电阻法在用药前、用药后8-12小时、24～36小时、48～60小时测定二磷酸腺苷(ADP)诱导的血小板聚集率,在用药前和用药后48-60小时测定白细胞计数、红细胞计数、血小板计数、D—二聚体(D-dimer)、凝血系统[包括凝血酶原时间(PT)、凝血酶原时间国际标准化比值(INR)、活化部分凝血活酶时间(APTT)、凝血酶时间(TT)、纤维蛋白原(FIB)]等指标。2、入选1798例接受PCI治疗的冠心病患者,随机分为泰嘉组(1104例)及波立维组(694例),在PCI术前给予300mg负荷剂量,序贯75mg/d,随访3-28个月,观察急性、亚急性、晚期、极晚期支架内血栓和心肌梗死、心源性死亡、脑卒中的联合终点MACE事件的影响以及出血等相关副作用的影响。3、入选204例接受急诊PCI治疗的急性心肌梗死患者,随机分为泰嘉组(123例)及波立维组(81例),在急诊室给予300mg负荷剂量,序贯75mg/d,随访3-28个月,观察急性、亚急性、晚期、极晚期支架内血栓和心肌梗死、心源性死亡、脑卒中的联合终点MACE事件的影响以及出血等相关副作用的影响。
结果：1、泰嘉组及波立维组血小板聚集率均随用药时间延长而降低,在负荷量后降低最明显,泰嘉组与波立维组用药前、用药后8～12小时、24～36小时、48～60小时的血小板聚集率电阻值分别为7.67±3.48欧姆(ohm),4.67±3.84ohm,3.46±3.93 ohm,3.36±3.86 ohm和6.84±3.25ohm,4.25±3.94ohm,2.63±3.27ohm,2.59±3.50ohm,经单个重复测量因素的方差分析,两组间差异无统计学意义(F=3.092,P=0.080),4次重复测量的血小板聚集率之间差异具有统计学意义(F=117.101,P=0.000);而凝血系统PT、INR、APTT、TT、FIB、D-dimer治疗前无显著差异(t值分别为0.825、1.260、1.448、0.299、1.112、0.388,P值分别为0.411、0.209、0.149、0.765、0.267、0.699)；治疗后PT、INR、APTT、TT、FIB、D-dimer治疗前无显著差异(t值分别为1.350、1.159、1.406、0.915、1.810、0.372,P值分别为0.179、0.248、0.161、0.361、0.072、0.710)；血常规的各项血细胞计数WBC、RBC、HGB、PLT治疗前比较无差异(t值分别为1.840、0.101、0.664、2.027,P值分别为0.067、0.920、0.507、0.054)；治疗后WBC、RBC、HGB、PLT比较无差异(t值分别为1.404、0.083、0.565、1.581,P值分别为0.162、0.934、0.574、0.116)。泰嘉组和波立维组治疗前后PT、INR、APTT、TT、D-dimer经自身配对t检验无显著差异(t值分别为1.198和1.016、0.989和0.697、0.872和0.981、0.368和1.225、0.051和0.032,P值分别为0.234和0.311、0.325和0.487、0.385和0.328、0.714和0.223、0.959和0.975)；而泰嘉组和波立维组FIB均较前升高(t值分别为3.389和2.074,P值分别为0.001和0.040)；泰嘉组和波立维组治疗前后WBC及PLT计数经自身配对t检验无明显变化(t值分别为0.248和0.808、1.654和1.618,P值分别为0.804和0.421、0.102和0.109)；而泰嘉组和波立维组治疗后RBC计数及HGB定量均较治疗前明显下降,经自身配对t检验,有显著性差异(t值分别为7.539和9.562、9.224和10.856,P值分别为0.000和0.000、0.000和0.000)。2、泰嘉组和波立维组靶血管重建、联合终点事件发生率,经统计学检验,差异无显著性意义(X2值分别为2.176、3.287,P值分别为0.140、0.070)；支架内血栓及心源性死亡经Fisher's精确概率计算,无显著性差异(P值分别为0.440、0.149)；出血和大出血事件发生率,经统计学检验,差异无显著性意义(P值分别为0.072和0.380)；两组之间无事件生存情况经Kaplan-Meier生存分析,Log Rank (Mantel-Cox)比较,无显著差异(X2值=3.438,P值=0.064)；累积MACE事件经Kaplan-Meier生存分析,Log Rank (Mantel-Cox)比较,无显著差异(X2值=1.076,P值=0.300)。
3、泰嘉组和波立维组均无支架内血栓和出血事件；波立维组有2例心源性死亡,分别为心源性休克及心脏破裂；两组靶血管重建及联合终点事件发生率,经统计学检验,差异无显著性意义(X2分别为0.000和0.921,P值分别为0.989和0.337)；两组之间累积MACE事件经Kaplan-Meier生存分析计算,绘制K-M曲线见图3.1,经Log Rank (Mantel-Cox)比较,无显著差异(X2值=0.679,P值=0.410)。
结论：1、大样本、随机、阳性对照比较同剂量、同方案国产氯吡格雷和进口氯吡格雷对电阻法测定的血小板聚集率的影响,进行了“头对头”的疗效比较,以及对凝血系统、血液系统的影响,发现二者具有等同影响,疗效及安全性类似。2、国内最大样本量(应用国产氯吡格雷超过1000例)、随机、阳性对照比较同剂量、同方案国产氯吡格雷和进口氯吡格雷对PCI术后疗效及安全性的比较,发现二者对PCI术后的疗效及安全性相似,发现在白细胞下降副作用方面,国产氯吡格雷(泰嘉)优于进口氯吡格雷(波立维)。3、大样本、随机、阳性对照比较同剂量、同方案国产氯吡格雷和进口氯吡格雷对AMI患者急诊PCI术后疗效及安全性的比较,发现二者对急诊PCI术后的疗效及安全性相似。
Background:Over the past two centuries, the Industrial and Technological Revolutions and their associated economic and social transformations have resulted in dramatic shifts in the diseases responsible for illness and death. Cardiovascular disease (CVD) has emerged as the dominant chronic disease in many parts of the world, and early in the 21st century it is predicted to become the main cause of disability and death worldwide. CVD is a major disease threaten human health, especially coronary atherosclerotic heart disease (CAD). Morbidity and mortality of CAD rises year by year and the burden of CAD is more and more accelerating in China. Percutaneous coronary interventions has been the major and effect therapy and there were more and more CAD patients to underwent CAG and PCI, however, there were more and more stent thrombus complication correlation PCI. Dual antiplatelet therapy (aspirin and clopidogrel) has been the standard proposal after PCI, however, the cost of imported clopidogrel (PlavixTM) is expensive and the domestic generic clopidogrel (TalcomTM) is cheap relative PlavixTM. There are not large sample data to confirm the effect to inhibit platelet aggregation and the effect and safety after PCI of TalcomTM.
Objective:1.To explore whether the effects of isodose domestic clopidogrel (TalcomTM) and imported clopidogrel (PlavixTM) on platelet function in patients with unstable angina (UAP).2. To explore whether the effects of isodose TalcomTM and PlavixTM on parameters of blood clot system in patients with unstable angina (UAP). 3. To explore whether the safety of isodose TalcomTM and PlavixTM on parameters of blood routin test in patients with unstable angina (UAP).4. To compare the efficacy and safety of TalcomTM and PlavixTM on PCI.5. To compare the efficacy and safety of TalcomTM and PlavixTM on directed PCI in AMI patients.
Methods:1.199 patients with UAP were randomized to two groups, including TalcomTM group (n=89), PlavixTM group (n=110). Venous blood samples were obtained before taking orally clopidogrel,8-12 hours after taking loading dose clopidogrel 300 mg, and after 75 mg/day for 24 hours,48 hours in two clopidogrel groups in order to test platelet aggregation rate induced by adenosine diphosphate (ADP) detected by electric resistance method and before taking orally clopidogrel and after 75 mg/day for 48 hours in two clopidogrel groups in order to test lencocyte count, red blood cell count, blood platelets count, D-dimer, prothrombin time (PT), international normalized ratio of prothrombin time (INR), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen.2.1798 patients with CAD to undergo CAG+PCI were randomized to two groups, including TalcomTM group (n=1104), PlavixTM group (n=694).300mg loading dose clopidogrel was oral before PCI and 75mg/d foreword one year. There were follow-up 3-28 month to survey the incidence rate of MACE of combination end point of acute, subacute, late stage, very late stage stent thrombus and AMI, cardiac death, stroke and correlated adverse reaction of bleed, major bleed, gastrointestinal complaint, and etc. 3.204 patients with AMI to undergo directed CAG+PCI were randomized to two groups, including TalcomTM group (n=123), PlavixTM group (n=81).300mg loading dose clopidogrel was oral before PCI in emergency room and 75mg/d foreword one year. There were follow-up 3-28 month to survey the incidence rate of MACE of combination end point of acute, subacute, late stage, very late stage stent thrombus and AMI, cardiac death, stroke and correlated adverse reaction of bleed, major bleed, gastrointestinal complaint, and etc.
Results:There were no significant differences in the platelet aggregation rate and blood cell count and the item of blood clot system between Talcom group and Plavix group before treatment. There were no significant differences in the aforementioned markers between TalcomTM group and PlavixTM group after treatment. With the time, platelet aggregation rate of TalcomTM group and PlavixTM group was degrading, and there was the most obviously after orally loading dose, and resistance value of TalcomTM group and PlavixTM group in before taking orally, after orally 8～12 hour, 24～36 hour,48～60 hour was 7.67±3.48ohm,4.67±3.84 ohm,3.46±3.93 ohm, 3.36±3.86 ohm and 6.84±3.25ohm,4.25±3.94ohm,2.63±3.27ohm,2.59±3.50ohm, respectively. There were significant differences in 4 repeated detected platelet aggretion rate by one way repeated measure factor ANOVA, (F=117.101, P=0.000). There were no significant differences in the parameters (PT, INR, APTT, TT, FIB, D-dimer) of blood clot system between TalcomTM group and PlavixTM group before treatment (t value 0.825,1.260,1.448,0.299,1.112,0.388, P value 0.411, 0.209,0.149,0.765,0.267,0.699, respectively); There were no significant differences in the parameters (PT, INR, APTT, TT, FIB, D-dimer) of blood clot system between TalcomTM group and PlavixTM group after treatment (t value 1.350、1.159、1.406、0.915、1.810、0.372, P value 0.179、0.248、0.161、0.361、0.072、 0.710, respectively); There were no significant differences in the parameters (WBC, RBC, HGB, PLT) of blood routin test between TalcomTM group and PlavixTM group before treatment (t value 1.840,0.101,0.664,2.027, P value 0.067,0.920,0.507, 0.054, respectively); There were no significant differences in the parameters (WBC, RBC, HGB, PLT) of blood routin test between TalcomTM group and PlavixTM group after treatment (t value 1.404,0.083,0.565,1.581, P value 0.162,0.934,0.574,0.116, respectively). There were no significant differences in the parameters (PT, INR, APTT, TT, FIB, D-dimer) of blood clot system between before and after treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 1.198 and 1.016,0.989 and 0.697,0.872 and 0.981,0.368 and 1.225,0.051 and 0.032, P value 0.234 and 0.311,0.325 and 0.487,0.385 and 0.328,0.714 and 0.223,0.959 and 0.975, respectively); but the level of FIB of after treatment is increase to compare to before treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 3.389 and 2.074, P value 0.001 and 0.040, respectively); There were no significant differences in the parameters (WBC and PLT) of blood routin test to compare to before treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 0.248 and 0.808,1.654 and 1.618, P value 0.804 and 0.421,0.102 and 0.109, respectively); but the level of the count of RBC and the quantitation of HGB of after treatment is decrease to compare to before treatment both TalcomTM group and PlavixTM group by paired sample t test (t value 7.539 and 9.562,9.224 and 10.856, P value 0.000 and 0.000,0.000 and 0.000, respectively).2. There were no significant differences in the incidence of target vessel revascularization and combination end point between TalcomTM group and PlavixTM group (X2 value 2.176,3.287, P value 0.140,0.070). There were no significant differences in the incidence of stent thrombus and cardiac death between TalcomTM group and PlavixTM group by Fisher's exact probability (P value 0.440,0.149). There were no significant differences in the incidence of bleed and major bleed between TalcomTM group and PlavixTM group (P value 0.072 and 0.380). There were no significant differences in survival without event and accumulation MACE hazard analysised by Kaplan-Meier survival analysis (X2 3.438 and 1.076, P=0.064 and 0.300).3. There were not stent thrombus and bleed event both TalcomTM group and PlavixTM group. There are two patients death of cardiac shock and heart rupture in PlavixTM group. There were no significant differences in the incidence of target vessel revascularization and combination end point between TalcomTM group and PlavixTM group (X2 value 0.000 and 0.921, P value 0.989 and 0.337). There were no significant differences in accumulation MACE hazard analysised by Kaplan-Meier survival analysis(X20.679, P=0.410).
Conclusions:1.The anti-platelet aggregation and antiplatelet activation effects of isodose TalcomTM are similar to those of PlavixTM. The two drugs have good anti-platelet effects. Furthermore, the two drugs have no significant adverse drug reaction.2. Effects and safety of isodose TalcomTM used in underwent PCI patients are similar to those of PlavixTM.3. Effects and safety of isodose TalcomTM used in AMI patients that underwent directed PCI are similar to those of PlavixTM.
引文
[1]吴兆苏,姚崇华,赵冬,等.我国多省市心血管病趋势及决定因素的人群监测(中国MONICA方案)I.发病率和死亡率监测结果[J].中华心血管病杂志,1997,25(1)：6-11
[2]中华医学会心血管病分会介入心脏病学组中华心血管病杂志编辑部.全国首次冠心病介入性治疗病例注册登记资料分析[J].中华心血管病杂志,1998,26(1)：25-29
[3]中华医学会心血管病分会介入心脏病学组中华心血管病杂志编辑部.全国第二次冠心病介入性治疗病例注册登记资料分析[J].中华心血管病杂志,2000,28(1)：10-13
[4]中华医学会心血管病分会介入心脏病学组中华心血管病杂志编辑部.全国第三次冠心病介入治疗病例注册登记资料分析[J].中华心血管病杂志,2002,30(12)：719-723
[5]吕树铮,宋现涛,陈韵岱,等.代表中国经皮冠状动脉介入治疗登记调查研究协作组.中国大陆2005年度经皮冠状动脉介入治疗登记调查研究结果初步分析[J].中华心血管病杂志,2006,34(11)：966-970
[6]胡大一.健康中国2020-从心血管疾病预防抓起[A].见：胡大一,马长生.心脏病学实践20100——规范化治疗[M].北京：人民卫生出版社,2010,1-4
[7]柏瑾,李志善,戚文航,等.国产硫酸氯吡格雷片降低血小板聚集率的临床观察[J].中国临床药学杂志,2001,10(2)：67-69
[8]陈凌,李志善,戚文航,等.硫酸氯吡格雷的抗血小板聚集临床研究[J].中国新药杂志2000,9(10)：715-717
[9]李志娟,董平栓,杨旭明,等.国产和进口氯吡格雷对经皮冠状动脉介入术后血小板功能的影响[J].中国介入心脏病学杂志,2006,14(4)：208-210
[10]顾俊,胡伟,肖红兵,等.国产和进口氯吡格雷对PCI近中期预后的影响[J].上海交通大学学报(医学版),2008,28(5)：608-609
[11]CAPRIE Steering Committee. A randomized, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE) [J]. Lancet,1996,348(9038): 1329-1339
[12]Yusuf S, Mehta SR, Zhao F, et al. Clopidogrel in Unstable angina to prevent Recurrent Events Trial (CURE) investigators. Early and late effects of clopidogrel in patients with acute coronary syndromes[J]. Circulation,2003,107(7):966-972
[13]Chen ZM, Jiang LX, Chen YP, et al. COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction:randomised placebo-controlled trial [J]. Lancet,2005,366(9497):1607-1621
[14]Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation[J]. N Engl J Med,2005,352(12):1179-1189
[15]Sabatine MS, Cannon CP, Gibson CM, et al. Clopidogrel as Adjunctive Reperfusion Therapy (CLARITY)-Thrombolysis in Myocardial Infarction (TIMI) 28 Investigators. Effect of clopidogrel pretreatment before percutaneous coronary intervention in patients with ST-elevation myocardial infarction treated with fibrinolytics:the PCI-CLARITY study[J]. JAMA,2005,294(10):1224-1232
[16]Verheugt FW, Montalescot G, Sabatine MS, et al. Prehospital fibrinolysis with dual antiplatelet therapy in ST-elevation acute myocardial infarction:a substudy of the randomized double blind CLARITY-TIMI 28 trial [J]. J Thromb Thrombolysis, 2007,23(3):173-179
[17]Bertrand ME, Rupprecht HJ, Urban P, et al. CLASSICS Investigators. Double-blind study of the safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in combination with aspirin after coronary stenting:the clopidogrel aspirin stent international cooperative study (CLASSICS)[J]. Circulation,2000,102(6):624-629
[18]Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention:the PCI-CURE study [J]. Lancet,2001,358(9281):527-533
[19]Steinhubl SR, Berger PB, Mann JT 3rd, et al. CREDO Investigators. Clopidogrel for the Reduction of Events During Observation. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention:a randomized controlled trial[J]. JAMA,2002,288(19):2411-2420
[20]Mehta SR, Bassand JP, Chrolavicius S, et al. CURRENT-OASIS 7 Investigators. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes [J]. N Engl J Med,2010,363(10):930-942
[21]刘倩竹,洪涛,刘兆平,等.不同负荷剂量氯毗格雷对血小板聚集率的影响[J].中华内科杂志,2007,46(2)：107-110
[22]卢春山,周志强,柳景华,等.冠状动脉支架术后进口氯吡格雷(波立维)与国产氯吡格雷(泰嘉)抗血小板治疗的对照研究[J].中国介入心脏病学杂志,2009,17(2)：67-70
[23]李鹏,王文红,刘勇.国产氯吡格雷(泰嘉)与进口氯吡格雷(波立维)PCI术后应用的有效性和安全性对照研究[J].中国心血管病研究,2010,8(7)：506-508
[24]阴赪茜,李志忠,张京梅,等.国产与进口氯吡格雷在冠状动脉介入治疗中的疗效对比分析.中国新药杂志,2010,19(10)：849-852
[25]中华医学会心血管病学分会中华心血管病杂志编辑委员会.经皮冠状动脉介人治疗指南(2009)[J].中华心血管病杂志,2009,37(1)：4-25
[26]陈凌,郭若冰,戴军.氯吡格雷在缺血性心血管疾病防治中的作用[J].中国新药杂志,2009,9(10)：718-721
[27]中华医学会心血管病学分会中华心血管病杂志编辑委员会.经皮冠状动脉介人治疗指南[J].中华心血管病杂志,2002,30(12)：707-718
[28]Bovill EG, Terrin ML, Stump DC, et al. Hemorrhagic events during therapy with recombinant tissue-type plasminogen activator, heparin, and aspirin for acute myocardial infarction. Results of the Thrombolysis in Myocardial Infarction (TIMI), Phase Ⅱ Trial [J]. Ann Intern Med,1991,115(4):256-265
[29]Kushner FG, Hand M, Smith SC Jr, et al.2009 Focused Updates:ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the 2005 Guideline and 2007 Focused Update):a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [J]. Circulation,2009,120(22):2271-2306
[30]Silber S, Albertsson P, Aviles FF, et al. Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology [J]. Eur Heart J,2005,26(8):804-847
[31]Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction):developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons:endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine [J]. Circulation,2007,116(7):e148-304
[32]Holmes DR, Kereiakes DJ, Kleiman NS, et al. Combining antiplatelet and anticoagulant therapies [J]. J Am Coll Cardiol,2009,54(2):95-109
[33]段罡.进口和国产氯毗格雷对PCI术后的血小板功能及预后的影响[J].临床合理用药,2009,2(7)：6-7
[34]冯克福,马礼坤,余华,等.国产氯吡格雷在冠心病合并糖尿病患者冠状动脉支架术后的临床应用[J].中国临床保健杂志,2009,12(3)：233-234
[35]王禹,盖鲁粤,沈洪,等.国产氯吡格雷在急性心肌梗死急诊冠脉介入治疗过程中的有效性及对血小板聚集功能的影响[J].中国急救医学,2006,26(7)：512-514
[36]李纲,李玉东,牛桂林.冠状动脉支架植入术后相同剂量国产和进口氯吡格雷的防治效果比较[J].中国保健(医学研究版),2007,15(15)：53
[37]张晓玲,陈方,朱小玲,等.国产硫酸氯吡格雷在PTCA及支架植入术中的临床应用[J].中国医刊,2003,38(11)：55-56
[38]Meng Kang, Lu Shu-zheng, Zhu Hua-gang, et al. Use of tailored loading-dose clopidogrel in patients undergoing selected percutaneous coronary intervention based on adenosine diphosphate-mediated platelet aggregation [J]. Chin Med J,2010, 123(24):3578-3582
[39]雷鸣,刘志辉,徐惠琳,等.冠状动脉支架术后国产(泰嘉)与进口氯吡格雷(波立维)疗效及安全性的对照研究[J].中国实用医药,2010,5(7)：148-149
[40]钱利华.国产和进口氯吡格雷对PCI术治疗中的效果比较[J].中国现代医生,2010,48(3)：49-50
[41]周利民,李开如,陶春明,等.国产和进口氯吡格雷对经皮冠状动脉介入治疗术近中期预后的影响[J].中国医药指南,2010,8(35)：27-28
[42]孙裕华,陶秀彬,倪芳,等。国产氯吡格雷治疗冠心病疗效及安全性的M eta分析[J].中国循证心血管医学杂志,2010,2,(4)：214-218
[43]Hartzler GO, Rutherford BD, McConahay DR, et al. Percutaneous transluminal coronary angioplasty with and without thrombolytic therapy for treatment of actute myocardial infarction [J]. Am Heart J,1983,106(5 pt 1):965-973
[1]李家增,侯明,包承鑫.血小板疾病[M].北京：科学技术文献出版社,2009：9-23
[2]Bearer EL. Platelet membrane skeleton revealed by quick-freeze deep-etch [J]. Anat Rec,1990,227(1):1-11
[3]Allen RD, Zacharski LR, Widirstky ST, et al. Transformation and motility of human platlets:details of the shape change and release reaction observed by optical and electron microscopy [J]. J Cell Biol,1979,83(1):126-142
[4]周玉杰,葛均波,韩雅玲.防栓抗栓现代治疗策略[M].北京：人民卫生出版社,2006：31-44
[5]Savage B, Saldivar E, Ruggeri ZM. Initiation of platelet adhesion by arrest onto fibrinogen or translocation on von Willebrand factor [J]. Cell,1996,84(2):289-297
[6]Savage B, Almus-Jacobs F, Ruggeri ZM. Specific synergy of multiple subsrate-receptor interactions in platelet thrombus formation under flow [J]. Cell,1998,94(5): 657-666
[7]Kroll MH, Hellums JD, McIntire LV, et al. Platelets and shear stress [J]. Blood, 1996,88(5):1525-1541
[8]Goto S, Ikeda Y, Saldivar E, et al. Distinct mechanisms of platelet aggregation as a consequence of different shearing flow conditions [J]. J Clin Invest,1998,101(2): 479-486
[9]Ruggeri ZM. Old concepts and new developments in the study of platelet aggregation [J]. J Clin Invest,2000,105(6):699-701
[10]Ruggeri ZM, Dent JA, Saldivar E. Contribution of distinct adhesive interactions to platelet aggregation in flowing blood [J]. Blood,1999,94(1):172-178
[11]Wu YP, Vink T, Schiphorst M, et al. Platelet thrombus formation on collagen at high shear rates is mediated by von Willebrand factor-glycoprotein I b interaction and inhibited by von Willebrand factor-glycoprotein Ⅱb/Ⅲa interaction [J]. Arterioscler Thromb Vasc Biol,2000,20(6):1661-1667
[12]Tsuji S, Sugimoto M, Miyata S, et al. Real-time analysis of mural thrombus formation in various platelet aggregation disorders:distinct shear-dependent roles of platelet receptors and adhesive proteins under flow [J]. Blood,1999,94(3):968-975
[13]Simon DI, Chen Z, Xu H, et al. Platelet glycoprotein Ibalpha is a counterreceptor for the leukocyte integrin Mac-1(CD11b/CD 18) [J]. J Exp Med,2000,192(2): 193-204
[14]Mazzucato M, Marco LD, Masotti A, et al. Characterization of the initial a-thrombin interaction with glycoprotein I b a in relation to platelet activation [J]. J Biol Chem,1998,273(4):1880-1887
[15]Bradford HN, Dela Cadena RA, Kunapuli SP, et al. Human kininogens regulate thrombin binding to platelets through the glycoprotein Ib-IX-V complex [J]. Blood, 1997,90(4):1508-1515
[16]Baglia FA, Badellino KO, Li CQ, et al. Factor XI bingding to the platelet glycoprotein Ib/IX/V complex promotes factor XI activation by thrombin [J]. J Biol Chem,2002,277(3):1662-1668
[17]Bradford HN, Pixley RA, Colman RW. Human factor XII binding to the glycoprotein Ib-IX-V complex inhibits thrombin-induced platelet aggregation [J]. J Biol Chem,2000,275(30):22756-22763
[18]Jackson SP, Mistry N, Yuan Y. Platelets and the injured vessel wall-"rolling into action". Focus on glycoprotein Ⅰb/Ⅴ/Ⅸ and the platelet cytoskeleton [J]. Trends Cardiovasc Med,2000,10(5):192-197
[19]Ware J. Molecular analyses of the platelet glycoprotein Ⅰb/Ⅸ/Ⅴ receptor [J]. Thromb Haemost,1998,79(3):466-478
[20]Mazzucato M, Pradella P, Cozzi R, et al. Sequential cytoplasmic calcium signals in a two stage platelet activation process induced by the glycoprotein I b a mechanoreceotor [J]. Blood,2002,100(8):2793-2800
[21]Yap CL, Anderson KF, Hughan SC, et al. Essential role for phosphoinositide 3-kinase in shear-dependent signaling between platelet glycoprotein Ⅰb/Ⅴ/Ⅳ and integrin αⅡbβ3 [J]. Blood,2002,99(1):151-158
[22]Andrews RK, Shen Y, Gardiner EE, et al. The glycoprotein Ib-IX-V complex in platelet adhesion and signaling [J]. Thromb Haemost,1999,82(2):357-364
[23]Berndt MC, Shen Y, Dopheide SM, et al. The vascular biology of the glycoprotein Ⅰb-Ⅸ-Ⅴ complex [J]. Thromb Haemost,2001,86(1):178-188
[24]Gardiner EE, Arthur JF, Shen Y, et al. GPIbalpha-selective activation of platelets induces platelet signaling events comparable to GPVI activation events [J]. Platelets, 2010,21(4):244-252
[25]van Zanten GH, Heijnen HF, Wu Y, et al. A fifty percent reduction of platelet surface glycoprotein Ib does not affect platelet adhesion under flow conditions [J]. Blood,1998,91(7):2353-2359
[26]Michelson AD, Benoit SE, Furman MI, et al. The platelet surface expression of glycoprotein V is regulated by two independent mechanisms:proteolysis and a reversible cytoskeletal-mediated redistribution to the surface-connected canalicular system [J]. Blood,1996,87(4):1396-1408
[27]Uff S, Clemetson JM, Harrison T, et al. Crystal structure of the platelet glycoprotein Ib(alpha) N-terminal domain reveals an unmasking mechanism for receptor activation [J]. J Biol Chem,2002,277(38):35657-35663
[28]Huizinga EG, Tsuji S, Romijn RA, et al. Structures of glycoprotein Ibalpha and its complex with von Willebrand factor Al domain [J]. Science,2002,297(5584): 1176-1179
[29]Dong JF, Li CQ, Lopez JA. Tyrosine sulfation of the glycoprotein Ib-IX complex: identification of sulfated residues and effect on ligand binding [J]. Biochemistry,1994, 33(46):13946-13953
[30]Bodnar RJ, Gu M, Li Z, et al. The cytoplasmic domain of the platelet glycoprotein Ibalpha is phosphorylated at serine 609 [J]. J Biol Chem,1999,274(47): 33474-33479
[31]Munday AD, Berndt MC, Mitchell CA. Phosphoinositide 3-kinase forms a complex with platelet membrane glycoprotein Ib-IX-V complex and 14-3-3zeta [J]. Blood,2000,96(2):577-584
[32]Ramakrishnan V, DeGuzman F, Bao M, et al. A thrombin receptor function for platelet glycoprotein Ⅰb-Ⅸ unmasked by cleavage of glycoprotein V [J]. Proc Natl Acad Sci USA,2001,98(4):1823-1828
[33]Kasirer-Friede A, Ware J, Leng L, et al. Lateral clustering of platelet GP Ib-IX complexes leads to up-regulation of the adhesive function of integrin alpha Ⅱbbeta 3 [J]. J Biol Chem,2002,277(14):11949-11956
[34]Satoh K, Asazuma N, Yatomi Y, et al. Activation of protein-tyrosine kinase pathways in human platelets stimulated with the Al domain of von Willebrand factor [J]. Platelets,2000,11(3):171-176
[35]Falati S, Edmead CE, Poole AW. Glycoprotein Ib-V-IX, a receptor for von Willebrand factor, couples physically and functionally to the Fc receptor gamma-chain, Fyn, and Lyn to activate human platelets [J]. Blood,1999,94(5):1648-1656
[36]Torti M, Bertoni A, Canobbio I, et al. Rap 1B and Rap2B translocation to the cytoskeleton by von Willebrand factor involves FcgammaⅡ receptor-mediated protein tyrosine phosphorylation [J]. J Biol Chem,1999,274(19):13690-13697
[37]Sullam PM, Hyun WC, Szollosi J, et al. Physical proximity and functional interplay of the glycoprotein Ib-IX-V complex and the Fc receptor FcgammaRIIA on the platelet plasma membrane [J]. J Biol Chem,1998,273(9):5331-5336
[38]Watson SP, Asazuma N, Atkinson B, et al. The role of ITAM-and ITIM-coupled receptors in platelet activation by collagen [J]. Thromb Haemost,2001,86(1): 276-288
[39]Gu M, Xi X, Englund GD, et al. Analysis of the roles of 14-3-3 in the platelet glycoprotein Ib-IX-mediated activation of integrin alpha(IIb)beta(3) using a reconstituted mammalian cell expression model [J]. J Cell Biol,1999,147(5): 1085-1096
[40]Clemetson JM, Polgar J, Magnenat E, et al. The platelet collagen receptor glycoprotein VI is a member of the immunoglobulin superfamily closely related to FcalphaR and the natural killer receptors [J]. J Biol Chem,1999,274(41): 29019-29024
[41]Clemetson KJ, Clemetson JM. Platelet collagen receptors [J]. Thromb Haemost, 2001,86(1):189-197
[42]Moog S, Mangin P, Lenain N, et al. Platelet glycoprotein V binds to collagen and participates in platelet adhesion and aggregation [J]. Blood,2001,98(4):1038-1046
[43]Ramakrishnan V, Reeves PS, DeGuzman F, et al. Increased thrombin responsiveness in platelets from mice lacking glycoprotein V [J]. Proc Natl Acad Sci USA,1999,96(23):13336-13341
[44]Kunicki TJ. The role of platelet collagen receptor (glycoprotein Ia/IIa; integrin alpha2 betal) polymorphisms in thrombotic disease [J]. Curr Opin Hematol,2001, 8(5):277-285
[45]Moshfegh K, Wuillemin WA, Redondo M, et al. Association of two silent polymorphisms of platelet glycoprotein Ⅰa/Ⅱa receptor with risk of myocardial infarction:a case-control study [J]. Lancet,1999,353(9150):351-354
[46]Santoso S, Kunicki TJ, Kroll H, et al. Association of the platelet glycoprotein la C807T gene polymorphism with nonfatal myocardial infarction in younger patients [J]. Blood,1999,93(8):2449-2453
[47]Takada Y, Hemler ME. The primary structure of the VLA-2/collagen receptor alpha 2 subunit (platelet GPIa):homology to other integrins and the presence of a possible collagen-binding domain [J]. J Cell Biol,1989,109(1):397-407
[48]Emsley J, Knight CG, Farndale RW, et al. Structure of the integrin alpha2betal-binding collagen peptide [J]. J Mol Biol,2004,335(4):1019-1028
[49]Savage B, Ginsberg MH, Ruggeri ZM. Influence of fibrillar collagen structure on the mechanisms of platelet thrombus formation under flow [J]. Blood,1999,94(8): 2704-2715
[50]Verkleij MW, Morton LF, Knight CG, et al. Simple collagen-like peptides support platelet adhesion under static but not under flow conditions:interaction via alpha2 betal and von Willebrand factor with specific sequences in native collagen is a requirement to resist shear forces [J]. Blood,1998,91(10):3808-3816
[51]Wang R, Kini RM, Chung MC. Rhodocetin, a novel platelet aggregation inhibitor from the venom of Calloselasma rhodostoma (Malayan pit viper):synergistic and noncovalent interaction between its subunits [J]. Biochemistry,1999,38(23): 7584-7593
[52]Marcinkiewicz C, Lobb RR, Marcinkiewicz MM, et al. Isolation and characterization of EMS 16, a C-lectin type protein from Echis multisquamatus venom, a potent and selective inhibitor of the alpha2betal integrin [J]. Biochemistry,2000, 39(32):9859-9867
[53]Kamiguti AS, Theakston RD, Watson SP, et al. Distinct contributions of glycoprotein VI and alpha(2)beta(1) integrin to the induction of platelet protein tyrosine phosphorylation and aggregation [J]. Arch Biochem Biophys,2000,374(2): 356-362
[54]Chung CH, Au LC, Huang TF. Molecular cloning and sequence analysis of aggretin, a collagen-like platelet aggregation inducer [J]. Biochem Biophys Res Commun,1999,263(3):723-727
[55]Nakamura T, Kambayashi J, Okuma M, et al. Activation of the GP Ⅱb-Ⅲa complex induced by platelet adhesion to collagen is mediated by both alpha2betal integrin and GP Ⅵ [J]. J Biol Chem,1999,274(17):11897-11903
[56]Jung SM, Sonoda M, Tsuji K, et al. Are integrin alpha(2)beta(1), glycoprotein Ib and vWf levels correlated with their contributions to platelet adhesion on collagen under high-shear flow? [J]. Platelets,2010,21(2):101-111
[57]Sugiyama T, Okuma M, Ushikubi F, et al. A novel platelet aggregating factor found in a patient with defective collagen-induced platelet aggregation and autoimmune thrombocytopenia [J]. Blood,1987,69(6):1712-1720
[58]Jandrot-Perrus M, Busfield S, Lagrue AH, et al. Cloning, characterization, and functional studies of human and mouse glycoprotein VI:a platelet-specific collagen receptor from the immunoglobulin superfamily [J]. Blood,2000,96(5):1798-1807
[59]Nieswandt B, Bergmeier W, Schulte V, et al. Expression and function of the mouse collagen receptor glycoprotein Ⅵ is strictly dependent on its association with the FcR gamma chain [J]. J Biol Chem,2000,275(31):23998-24002
[60]Gross BS, Lee JR, Clements JL, et al. Tyrosine phosphorylation of SLP-76 is downstream of Syk following stimulation of the collagen receptor in platelets [J]. J Biol Chem,1999,274(9):5963-5971
[61]Clements JL, Lee JR, Gross B, et al. Fetal hemorrhage and platelet dysfunction in SLP-76-deficient mice [J]. J Clin Invest,1999,103(1):19-25
[62]Berridge MJ. Inositol trisphosphate and calcium signalling mechanisms [J]. Biochim Biophys Acta,2009,1793(6):933-940
[63]Falet H, Barkalow KL, Pivniouk VI, et al. Roles of SLP-76, phosphoinositide 3-kinase, and gelsolin in the platelet shape changes initiated by the collagen receptor GPVI/FcR gamma-chain complex [J]. Blood,2000,96(12):3786-3792
[64]Quek LS, Pasquet JM, Hers I, et al. Fyn and Lyn phosphorylate the Fc receptor gamma chain downstream of glycoprotein VI in murine platelets, and Lyn regulates a novel feedback pathway [J]. Blood,2000,96(13):4246-4253
[65]Judd BA, Koretzky GA. The role of the adapter molecule SLP-76 in platelet function [J]. Oncogene,2001,20(44):6291-6299
[66]Pasquet JM, Bobe R, Gross B, et al. A collagen-related peptide regulates phospholipase Cgamma2 via phosphatidylinositol 3-kinase in human platelets [J]. Biochem J,1999,342(Pt 1):171-177
[67]Lagrue AH, Francischetti IM, Guimaraes JA, et al. Phosphatidylinositol 3'-kinase and tyrosine-phosphatase activation positively modulate Convulxin-induced platelet activation. Comparison with collagen [J]. FEBS Lett,1999,448(1):95-100
[68]Schulz C, Penz S, Hoffmann C, et al. Platelet GPVI binds to collagenous structures in the core region of human atheromatous plaque and is critical for atheroprogression in vivo [J]. Basic Res Cardiol,2008,103(4):356-367
[69]Kato K, Kanaji T, Russell S, et al. The contribution of glycoprotein VI to stable platelet adhesion and thrombus formation illustrated by targeted gene deletion [J]. Blood,2003,102(5):1701-1707
[70]Daniel JL, Dangelmaier C, Jin J, et al. Molecular basis for ADP-induced platelet activation. I. Evidence for three distinct ADP receptors on human platelets [J]. J Biol Chem,1998,273(4):2024-2029
[71]Cattaneo M, Gachet C. ADP receptors and clinical bleeding disorders [J]. ArteriosclerThromb Vasc Biol,1999,19(10):2281-2285
[72]Jin J, Daniel JL, Kunapuli SP. Molecular basis for ADP-induced platelet activation. Ⅱ. The P2Y1 receptor mediates ADP-induced intracellular calcium mobilization and shape change in platelets [J]. J Biol Chem,1998,273(4):2030-2034
[73]Hollopeter G, Jantzen HM, Vincent D, et al. Identification of the platelet ADP receptor targeted by antithrombotic drugs [J]. Nature,2001,409(6817):202-207
[74]Zhang FL, Luo L, Gustafson E, et al. ADP is the cognate ligand for the orphan G protein-coupled receptor SP1999 [J]. J Biol Chem,2001,276(11):8608-8615
[75]Shankar H, Murugappan S, Kim S, et al. Role of G protein-gated inwardly rectifying potassium channels in P2Y12 receptor-mediated platelet functional responses [J]. Blood,2004,104(5):1335-1343
[76]Hechler B, Leon C, Vial C, et al. The P2Y1 receptor is necessary for adenosine 5'-diphosphate-induced platelet aggregation [J]. Blood,1998,92(1):152-159
[77]Bauer M, Retzer M, Wilde JI, et al. Dichotomous regulation of myosin phosphorylation and shape change by Rho-kinase and calcium in intact human platelets [J]. Blood,1999,94(5):1665-1672
[78]Wilde JI, Retzer M, Siess W, et al. ADP-induced platelet shape change:an investigation of the signalling pathways involved and their dependence on the method of platelet preparation [J]. Platelets,2000,11(5):286-295
[79]Fabre JE, Nguyen M, Latour A, et al. Decreased platelet aggregation, increased bleeding time and resistance to thromboembolism in P2Y1-deficient mice [J]. Nat Med,1999,5(10):1199-1202
[80]Gachet C. ADP receptors of platelets and their inhibition [J]. Thromb Haemost, 2001,86(1):222-232
[81]Leon C, Hechler B, Freund M, et al. Defective platelet aggregation and increased resistance to thrombosis in purinergic P2Y(1) receptor-null mice [J]. J Clin Invest, 1999,104(12):1731-1737
[82]Savi P, Herbert JM. Clopidogrel and ticlopidine:P2Y12 adenosine diphosphate-receptor antagonists for the prevention of atherothrombosis [J]. Semin Thromb Hemost,2005,31(2):174-183
[83]Savi P, Labouret C, Delesque N, et al. P2y(12), a new platelet ADP receptor, target of clopidogrel [J]. Biochem Biophys Res Commun,2001,283(2):379-383
[84]Daniel NG, Goulet J, Bergeron M, et al. Antiplatelet drugs:is there a surgical risk? [J]. J Can Dent Assoc,2002,68(11):683-687
[85]Sharis PJ, Cannon CP, Loscalzo J. The antiplatelet effects of ticlopidine and clopidogrel [J]. Ann Intern Med,1998,129(5):394-405
[86]Vu TK, Wheaton VI, Hung DT, et al. Domains specifying thrombin-receptor interaction [J]. Nature,1991,353(6345):674-677
[87]Faruqi TR, Weiss EJ, Shapiro MJ, et al. Structure-function analysis of protease-activated receptor 4 tethered ligand peptides. Determinants of specificity and utility in assays of receptor function [J]. J Biol Chem,2000,275(26):19728-19734
[88]Ishihara H, Connolly AJ, Zeng D, et al. Protease-activated receptor 3 is a second thrombin receptor in humans [J]. Nature,1997,386(6624):502-506
[89]Xu WF, Andersen H, Whitmore TE, et al. Cloning and characterization of human protease-activated receptor 4 [J]. Proc Natl Acad Sci USA,1998,95(12):6642-6646
[90]Camerer E, Huang W, Coughlin SR. Tissue factor- and factor X-dependent activation of protease-activated receptor 2 by factor Ⅶa [J]. Proc Natl Acad Sci USA, 2000,97(10):5255-5260
[91]Kahn ML, Nakanishi-Matsui M, Shapiro MJ, et al. Protease-activated receptors 1 and 4 mediate activation of human platelets by thrombin [J]. J Clin Invest,1999, 103(6):879-887
[92]Covic L, Gresser AL, Kuliopulos A. Biphasic kinetics of activation and signaling for PAR1 and PAR4 thrombin receptors in platelets [J]. Biochemistry,2000,39(18): 5458-5467
[93]Brass LF, Manning DR, Cichowski K, et al. Signaling through G proteins in platelets:to the integrins and beyond [J]. Thromb Haemost,1997,78(1):581-589
[94]Kramer RM, Roberts EF, Um SL, et al. p38 mitogen-activated protein kinase phosphorylates cytosolic phospholipase A2 (cPLA2) in thrombin-stimulated platelets. Evidence that proline-directed phosphorylation is not required for mobilization of arachidonic acid by cPLA2 [J]. J Biol Chem,1996,271(44):27723-27729
[95]O'Brien PJ, Prevost N, Molino M, et al. Thrombin responses in human endothelial cells. Contributions from receptors other than PAR1 include the transactivation of PAR2 by thrombin-cleaved PAR1 [J]. J Biol Chem,2000,275(18): 13502-13509
[96]Andrade-Gordon P, Maryanoff BE, Derian CK, et al. Design, synthesis, and biological characterization of a peptide-mimetic antagonist for a tethered-ligand receptor [J]. Proc Natl Acad Sci USA,1999,96(22):12257-12262
[97]Maeda H, Inazu T, Nagai K, et al. Possible involvement of protein-tyrosine kinases such as p72syk in the disc-sphere change response of porcine platelets [J]. J Biochem,1995,117(6):1201-1208
[98]Hermand P, Gane P, Huet M, et al. Red cell ICAM-4 is a novel ligand for platelet-activated alpha Ⅱbbeta 3 integrin [J]. J Biol Chem,2003,278(7):4892-4898
[99]Shattil SJ, Hoxie JA, Cunningham M, et al. Changes in the platelet membrane glycoprotein Ⅱb.Ⅲa complex during platelet activation [J]. J Biol Chem,1985, 260(20):11107-11114
[100]Stephens G, O'Luanaigh N, Reilly D, et al. A sequence within the cytoplasmic tail of GpⅡb independently activates platelet aggregation and thromboxane synthesis [J]. J Biol Chem,1998,273(32):20317-20322
[101]Leisner TM, Wencel-Drake JD, Wang W, et al. Bidirectional transmembrane modulation of integrin alphaⅡbbeta3 conformations [J]. J Biol Chem,1999,274(18): 12945-12949
[102]Naik UP, Naik MU. Association of CIB with GPIIb/IIIa during outside-in signaling is required for platelet spreading on fibrinogen [J]. Blood,2003,102(4): 1355-1362
[103]Tsuboi S. Calcium integrin-binding protein activates platelet integrin alpha Ilbbeta 3 [J]. J Biol Chem,2002,277(3):1919-1923
[104]Bertoni A, Tadokoro S, Eto K, et al. Relationships between Raplb, affinity modulation of integrin alpha Ⅱbbeta 3, and the actin cytoskeleton [J]. J Biol Chem, 2002,277(28):25715-25721
[105]Haataja L, Kaartinen V, Groffen J, et al. The small GTPase Rac3 interacts with the integrin-binding protein CIB and promotes integrin alpha(IIb)beta(3)-mediated adhesion and spreading [J]. J Biol Chem,2002,277(10):8321-8328
[106]Wagner CL, Mascelli MA, Neblock DS, et al. Analysis of GPⅡb/Ⅲa receptor number by quantification of 7E3 binding to human platelets [J]. Blood,1996,88(3): 907-914
[107]Hynes RO. Integrins:a family of cell surface receptors [J]. Cell,1987,48(4): 549-554
[108]Rosa JP, Bray PF, Gayet O, et al. Cloning of glycoprotein Ⅲa cDNA from human erythroleukemia cells and localization of the gene to chromosome 17 [J]. Blood,1988,72(2):593-600
[109]Weisel JW, Nagaswami C, Vilaire G, et al. Examination of the platelet membrane glycoprotein Ⅱb-Ⅲa complex and its interaction with fibrinogen and other ligands by electron microscopy [J]. J Biol Chem,1992,267(23):16637-16643
[110]D'Souza SE, Ginsberg MH, Burke TA, et al. The ligand binding site of the platelet integrin receptor GPⅡb-Ⅲa is proximal to the second calcium binding domain of its alpha subunit [J]. J Biol Chem,1990,265(6):3440-3446
[111]Cierniewski CS, Byzova T, Papierak M, et al. Peptide ligands can bind to distinct sites in integrin alphaⅡbbeta3 and elicit different functional responses [J]. J Biol Chem,1999,274(24):16923-16932
[112]Loftus JC, O'Toole TE, Plow EF, et al. A beta 3 integrin mutation abolishes ligand binding and alters divalent cation-dependent conformation [J]. Science,1990, 249(4971):915-918
[113]Tozer EC, Liddington RC, Sutcliffe MJ, et al. Ligand binding to integrin alphaⅡbbeta3 is dependent on a MIDAS-like domain in the beta3 subunit [J]. J Biol Chem,1996,271(36):21978-21984
[114]Obergfell A, Eto K, Mocsai A, et al. Coordinate interactions of Csk, Src, and Syk kinases with [alpha] Ⅱb [beta] 3 initiate integrin signaling to the cytoskeleton [J]. J Cell Biol,2002,157(2):265-275
[115]Coburn LA, Damaraju VS, Dozic S, et al. GPIba-vWF rolling under shear stress shows differences between type 2B and 2M von Willebrand disease [J]. Biophys J, 2011,100(2):304-312
[116]Locke D, Chen H, Liu Y, et al. Lipid rafts orchestrate signaling by the platelet receptor glycoprotein VI [J]. J Biol Chem,2002,277(21):18801-18809
[117]Ezumi Y, Kodama K, Uchiyama T, et al. Constitutive and functional association of the platelet collagen receptor glycoprotein VI-Fc receptor gamma-chain complex with membrane rafts[J]. Blood,2002,99(9):3250-3255
[118]Cicmil M, Thomas JM, Leduc M, et al. Platelet endothelial cell adhesion molecule-1 signaling inhibits the activation of human platelets [J]. Blood,2002,99(1): 137-144
[119]Larson MK, Chen H, Kahn ML, et al. Identification of P2Y12-dependent and-independent mechanisms of glycoprotein Ⅵ-mediated Rapl activation in platelets [J]. Blood,2003,101(4):1409-1415
[120]Cho MJ, Liu J, Pestina TI, et al. The roles of alpha Ⅱb beta 3-mediated outside-in signal transduction, thromboxane A2, and adenosine diphosphate in collagen-induced platelet aggregation [J]. Blood,2003,101(7):2646-2651
[121]Funk CD, FitzGerald GA. COX-2 inhibitors and cardiovascular risk [J]. J Cardiovasc Pharmacol,2007,50(5):470-479
[122]Furuyashiki T, Narumiya S. Stress responses:the contribution of prostaglandin E(2) and its receptors [J]. Nat Rev Endocrinol,2011,7(3):163-175
[123]Halushka PV, Allan CJ, Davis-Bruno KL. Thromboxane A2 receptors [J]. J Lipid Mediat Cell Signal,1995,12(2-3):361-378
[124]Li Z, Xi X, Du X. A mitogen-activated protein kinase-dependent signaling pathway in the activation of platelet integrin alpha IIbbeta3 [J]. J Biol Chem,2001, 276(45):42226-42232
[125]Dorsam RT, Kim S, Jin J, et al. Coordinated signaling through both G12/13 and G(i) pathways is sufficient to activate GPⅡb/Ⅲa in human platelets [J]. J Biol Chem, 2002,277(49):47588-47595
[126]Nieswandt B, Schulte V, Zywietz A, et al. Costimulation of Gi- and G12/G13-mediated signaling pathways induces integrin alpha Ilbbeta 3 activation in platelets [J]. J Biol Chem,2002,277(42):39493-39498.
[127]Nadal-Wollbold F, Pawlowski M, Levy-Toledano S, et al. Platelet ERK2 activation by thrombin is dependent on calcium and conventional protein kinases C but not Raf-1 or B-Raf [J]. FEBS Lett,2002,531(3):475-82
[128]Fujimoto TT, Katsutani S, Shimomura T, et al. Thrombospondin-bound integrin-associated protein (CD47) physically and functionally modifies integrin alphaⅡbbeta3 by its extracellular domain [J]. J Biol Chem,2003,278(29): 26655-26665
[129]Lagadec P, Dejoux O, Ticchioni M, et al. Involvement of a CD47-dependent pathway in platelet adhesion on inflamed vascular endothelium under flow [J]. Blood, 2003,101(12):4836-4843
[130]Dale GL, Friese P, Batar P, et al. Stimulated platelets use serotonin to enhance their retention of procoagulant proteins on the cell surface [J]. Nature,2002, 415(6868):175-179
[131]Polgar J, Chung SH, Reed GL. Vesicle-associated membrane protein 3 (VAMP-3) and VAMP-8 are present in human platelets and are required for granule secretion [J]. Blood,2002,100(3):1081-1083
[132]Barry OP, Kazanietz MG, Pratico D, et al. Arachidonic acid in platelet microparticles up-regulates cyclooxygenase-2-dependent prostaglandin formation via a protein kinase C/mitogen-activated protein kinase-dependent pathway [J]. J Biol Chem,1999,274(11):7545-7556
[133]Coller BS, Lang D, Scudder LE. Rapid and simple platelet function assay to assess glycoprotein Ⅱb/Ⅲa receptor blockade [J]. Circulation,1997,95(4):860-867
[134]Despotis GJ, Levine V, Filos KS, et al. Evaluation of a new point-of-care test that measures PAF-mediated acceleration of coagulation in cardiac surgical patients [J]. Anesthesiology,1996,85(6):1311-1323
[135]Kundu SK, Heilmann EJ, Sio R, et al. Description of an in vitro platelet function analyzer－-PFA-100 [J]. Semin Thromb Hemost,1995,21 (Suppl 2):106-112
[136]Nicholson NS, Panzer-Knodle SG, Haas NF, et al. Assessment of platelet function assays [J]. Am Heart J,1998,135(5 Pt 2 Su):S170-S178
[137]Li CK, Hoffmann TJ, Hsieh PY, et al. Xylum CSA:automated system for assessing hemostasis in simulated vascular flow [J]. Clin Chem,1997,43(9): 1788-1790
[138]Mancuso A, Fung K, Cox D, et al. Assessment of blood coagulation in severe liver disease using thromboelastography:use of citrate storage versus native blood [J]. Blood Coagul Fibrinolysis,2003,14(2):211-216
[139]Lewis HD Jr, Davis JW, Archibald DG, et al. Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study [J]. N Engl J Med,1983,309(7):396-403
[140]Cairns JA, Gent M, Singer J, et al. Aspirin, sulfinpyrazone, or both in unstable angina. Results of a Canadian multicenter trial [J]. N Engl J Med,1985,313(22): 1369-1375
[141]The RISC Group. Risk of myocardial infarction and death during treatment with low dose aspirin and intravenous heparin in men with unstable coronary artery disease [J]. Lancet,1990,336(8719):827-830
[142]Juul-Moller S, Edvardsson N, Jahnmatz B, et al. Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable chronic angina pectoris. The Swedish Angina Pectoris Aspirin Trial (SAPAT) Group[J]. Lancet,1992, 340(8833):1421-1425
[143]Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy--Ⅲ:Reduction in venous thrombosis and pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients [J]. BMJ,1994, 308(6923):235-246
[144]ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction:ISIS-2 [J]. Lancet,1988, 2(8607):349-360
[145]The SALT Collaborative Group. Swedish Aspirin Low-Dose Trial (SALT) of 75 mg aspirin as secondary prophylaxis after cerebrovascular ischaemic events [J]. Lancet,1991,338(8779):1345-1349
[146]The Dutch TIA Trial Study Group. A comparison of two doses of aspirin (30 mg vs.283 mg a day) in patients after a transient ischemic attack or minor ischemic stroke [J]. N Engl J Med,1991,325(18):1261-1266
[147]Farrell B, Godwin J, Richards S, et al. The United Kingdom transient ischaemic attack (UK-TIA) aspirin trial:final results [J]. J Neurol Neurosurg Psychiatry,1991, 54(12):1044-1054
[148]The ESPS Group. The European Stroke Prevention Study (ESPS). Principal end-points [J]. Lancet,1987,2(8572):1351-1354
[149]Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention Study.2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke [J]. J Neurol Sci,1996,143(1-2):1-13
[150]ETDRS Investigators. Aspirin effects on mortality and morbidity in patients with diabetes mellitus. Early Treatment Diabetic Retinopathy Study report 14 [J]. JAMA,1992,268(10):1292-1300
[151]Hansson L, Zanchetti A, Carruthers SG, et al. HOT Study Group. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. HOT Study Group [J]. Lancet,1998,351(9118):1755-1762
[152]Steering Committee of the Physicians' Health Study Research Group. Final report on the aspirin component of the ongoing Physicians'Health Study [J]. N Engl J Med,1989,321(3):129-135
[153]de Gaetano G, Collaborative Group of the Primary Prevention Project. Low-dose aspirin and vitamin E in people at cardiovascular risk:a randomised trial in general practice [J]. Lancet,2001,357(9250):89-95
[154]Peto R, Gray R, Collins R, et al. Randomised trial of prophylactic daily aspirin in British male doctors [J]. Br Med J (Clin Res Ed),1988,296(6618):313-316
[155]Ridker PM, Cook NR, Lee IM, et al. A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women [J]. N Engl J Med,2005, 352(13):1293-1304
[156]Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events [J]. N Engl J Med,2006,354(16): 1706-1717
[157]International Stroke Trial Collaborative Group. The International Stroke Trial (IST):a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke [J]. Lancet,1997,349(9065):1569-1581
[158]CAST (Chinese Acute Stroke Trial) Collaborative Group. CAST:randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke [J]. Lancet,1997,349(9066):1641-1649
[159]中华医学会心血管病学分会中华心血管病杂志编辑委员会.阿司匹林在动脉硬化性心血管疾病中的临床应用：中国专家共识(2005)[J].中华心血管病杂志,2006,34(3)：281-284
[160]中华内科杂志编辑部.规范应用阿司匹林治疗缺血性脑血管病的专家共识[J].中华内科杂志,2006,45(1)：81-82
[161]急性ST段抬高心肌梗死溶栓治疗中国专家共识组.急性ST段抬高心肌梗死溶栓治疗的中国专家共识(修订版)[J].中华内科杂志,2008,47(2)：170-174
[162]中华医学会心血管病学分会中华心血管病杂志编辑委员会.不稳定性心绞痛和非ST段抬高心肌梗死诊断与治疗指南[J].中华心血管病杂志,2007,35(4)： 295-304
[163]中华医学会心血管病学分会中华心血管病杂志编辑委员会中国循环杂志编辑委员会.急性心肌梗死诊断和治疗指南[J].中华心血管病杂志,2001,29(12)：710-725
[164]中华医学会心血管病学分会中华心血管病杂志编辑委员会.慢性稳定性心绞痛诊断与治疗指南[J].中华心血管病杂志,2007,35(3)：195-206
[165]中华医学会心血管病学分会中华心血管病杂志编辑委员会.经皮冠状动脉介人治疗指南(2009)[J].中华心血管病杂志,2009,37(1)：4-25
[166]澳大利亚国家卒中基金会专家工作组.急性卒中临床处理指南[J].国际脑血管病杂志,2008,16(9)：641-689
[167]欧洲卒中组织(ESO)执行委员会和ESO写作委员会.缺血性卒中和短暂性脑缺血发作处理指南2008[J].国际脑血管病杂志,2008,16(6)：401-440
[168]Kushner FG, Hand M, Smith SC Jr, et al.2009 Focused Updates:ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the 2005 Guideline and 2007 Focused Update):a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [J]. Circulation,2009,120(22):2271-2306
[169]Antman EM, Hand M, Armstrong PW, et al.2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines:developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians:2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee [J]. Circulation,2008, 117(2):296-329
[170]Fraker TD Jr, Fihn SD, Gibbons RJ, et al.2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina [J]. Circulation,2007,116(23):2762-2772
[171]Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction):developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons:endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine [J]. Circulation,2007,116(7):e148-304
[172]Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation:the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology [J]. Eur Heart J,2008,29(23):2909-2945
[173]Adams H, Adams R, Del Zoppo G, et al. Guidelines for the early management of patients with ischemic stroke:2005 guidelines update a scientific statement from the Stroke Council of the American Heart Association/American Stroke Association [J]. Stroke,2005,36(4):916-923
[174]Bertrand ME, Simoons ML, Fox KA, et al. Task Force on the Management of Acute Coronary Syndromes of the European Society of Cardiology. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [J]. Eur Heart J,2002 Dec;23(23):1809-1840
[175]Fox K, Garcia MA, Ardissino D, et al. Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology; ESC Committee for Practice Guidelines (CPG). Guidelines on the management of stable angina pectoris:executive summary:The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology [J]. Eur Heart J,2006,27(11):1341-1381
[176]Silber S, Albertsson P, Aviles FF, et al. Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology [J]. Eur Heart J,2005,26(8):804-847
[177]Balsano F, Rizzon P, Violi F, et al. The Studio della Ticlopidina nell'Angina Instabile Group. Antiplatelet treatment with ticlopidine in unstable angina. A controlled multicenter clinical trial [J]. Circulation,1990,82(1):17-26
[178]Cutlip DE, Leon MB, Ho KK, et al. Acute and nine-month clinical outcomes after "suboptimal" coronary stenting:results from the STent Anti-thrombotic Regimen Study (STARS) registry [J]. J Am Coll Cardiol,1999,34(3):698-706
[179]Urban P, Macaya C, Rupprecht HJ, et al. Randomized evaluation of anticoagulation versus antiplatelet therapy after coronary stent implantation in high-risk patients:the multicenter aspirin and ticlopidine trial after intracoronary stenting (MATTIS) [J]. Circulation,1998,98(20):2126-2132
[180]Hass WK, Easton JD, Adams HP Jr, et al. Ticlopidine Aspirin Stroke Study Group. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients[J]. N Engl J Med,1989,321(8):501-507
[181]Gent M, Blakely JA, Easton JD, et al. The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke [J]. Lancet,1989,1(8649):1215-1220
[182]CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE) [J]. Lancet,1996, 348(9038):1329-1339
[183]Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation [J]. N Engl J Med,2001,345(7):494-502
[184]Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation [J]. N Engl J Med,2005,352(12):1179-1189
[185]Chen ZM, Jiang LX, Chen YP, et al. COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction:randomised placebo-controlled trial [J]. Lancet,2005,366(9497):1607-1621
[186]Bertrand ME, Rupprecht HJ, Urban P, et al. CLASSICS Investigators. Double-blind study of the safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in combination with aspirin after coronary stenting:the clopidogrel aspirin stent international cooperative study (CLASSICS) [J]. Circulation,2000,102(6):624-629
[187]Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention:the PCI-CURE study [J]. Lancet,2001,358(9281):527-533
[188]Steinhubl SR, Berger PB, Mann JT 3rd, et al. CREDO Investigators. Clopidogrel for the Reduction of Events During Observation. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention:a randomized controlled trial [J]. JAMA,2002,288(19):2411-2420
[189]Mehta SR, Bassand JP, Chrolavicius S, et al. CURRENT-OASIS 7 Investigators. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes [J]. N Engl J Med,2010,363(10):930-942
[190]Park SW, Lee CW, Kim HS, et al. Comparison of cilostazol versus ticlopidine therapy after stent implantation [J]. Am J Cardiol,1999,84(5):511-514
[191]Park SW, Lee CW, Kim HS, et al. Effects of cilostazol on angiographic restenosis after coronary stent placement [J]. Am J Cardiol,2000,86(5):499-503
[192]Ge J, Han Y, Jiang H, et al. RACTS (Randomized Prospective Antiplatelet Trial of Cilostazol Versus Ticlopidine in Patients Undergoing Coronary Stenting) Trial Investigators. RACTS:a prospective randomized antiplatelet trial of cilostazol versus ticlopidine in patients undergoing coronary stenting:long-term clinical and angiographic outcome [J]. J Cardiovasc Pharmacol,2005,46(2):162-166
[193]Lee SW, Park SW, Hong MK, et al. Comparison of cilostazol and clopidogrel after successful coronary stenting [J]. Am J Cardiol,2005,95(7):859-862
[194]Douglas JS, Weintraub WS, Holmes D. Rationale and design of the randomized, multicenter, cilostazol for RESTenosis (CREST) trial [J]. Clin Cardiol,2003,26(10): 451-454
[195]The EPIC Investigation. Use of a monoclonal antibody directed against the platelet glycoprotein Ⅱb/Ⅲa receptor in high-risk coronary angioplasty [J]. N Engl J Med,1994,330(14):956-961
[196]Simoons ML. GUSTO IV-ACS Investigators. Effect of glycoprotein Ⅱb/Ⅲa receptor blocker abciximab on outcome in patients with acute coronary syndromes without early coronary revascularisation:the GUSTO IV-ACS randomised trial [J]. Lancet,2001,357(9272):1915-1924
[197]The EPILOG Investigators. Platelet glycoprotein Ⅱb/Ⅲa receptor blockade and low-dose heparin during percutaneous coronary revascularization [J]. N Engl J Med, 1997,336(24):1689-1696
[198]EPISTENT Investigators. Randomised placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-Ⅱb/Ⅲa blockade [J]. Lancet,1998,352(9122):87-92
[199]The CAPTURE Investigators. Randomised placebo-controlled trial of abciximab before and during coronary intervention in refractory unstable angina:the CAPTURE Study[J]. Lancet,1997,349(9063):1429-1435
[200]Montalescot G, Barragan P, Wittenberg O, et al. ADMIRAL Investigators. Abciximab before Direct Angioplasty and Stenting in Myocardial Infarction Regarding Acute and Long-Term Follow-up. Platelet glycoprotein Ⅱb/Ⅲa inhibition with coronary stenting for acute myocardial infarction [J]. N Engl J Med,2001, 344(25):1895-1903
[201]Stone GW, Grines CL, Cox DA, et al. Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) Investigators. Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction [J]. N Engl J Med,2002,346(13):957-966
[202]Brener SJ, Barr LA, Burchenal JE, et al. ReoPro and Primary PTCA Organization and Randomized Trial (RAPPORT) Investigators. Randomized, placebo-controlled trial of platelet glycoprotein Ⅱb/Ⅲa blockade with primary angioplasty for acute myocardial infarction [J]. Circulation,1998,98(8):734-741
[203]Ndrepepa G, Kastrati A, Neumann FJ, et al. Five-year outcome of patients with acute myocardial infarction enrolled in a randomised trial assessing the value of abciximab during coronary artery stenting [J]. Eur Heart J,2004,25(18):1635-1640
[204]Gibson CM, de Lemos JA, Murphy SA, et al. Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: a TIMI 14 substudy [J]. Circulation,2001,103(21):2550-2554
[205]Strategies for Patency Enhancement in the Emergency Department (SPEED) Group. Trial of abciximab with and without low-dose reteplase for acute myocardial infarction[J]. Circulation,2000,101(24):2788-2794
[206]Topol EJ. GUSTO V Investigators. Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein Ⅱb/Ⅲa inhibition:the GUSTO V randomised trial [J]. Lancet, 2001,357(9272):1905-1914
[207]Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT)-3 Investigators. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin:the ASSENT-3 randomised trial in acute myocardial infarction [J]. Lancet,2001,358(9282):605-613
[208]The PURSUIT Trial Investigators. Platelet Glycoprotein Ⅱb/Ⅲa in Unstable Angina:Receptor Suppression Using Integrilin Therapy. Inhibition of platelet glycoprotein Ⅱb/Ⅲa with eptifibatide in patients with acute coronary syndromes [J]. N Engl J Med,1998,339(7):436-443
[209]The IMPACT-Ⅱ Investigators.Integrilin to Minimise Platelet Aggregation and Coronary Thrombosis-Ⅱ. Randomised placebo-controlled trial of effect of eptifibatide on complications of percutaneous coronary intervention:IMPACT-Ⅱ[J]. Lancet,1997, 349(9063):1422-1428
[210]ESPRIT Investigators. Enhanced Suppression of the Platelet Ⅱb/Ⅲa Receptor with Integrilin Therapy. Novel dosing regimen of eptifibatide in planned coronary stent implantation (ESPRIT):a randomised, placebo-controlled trial [J]. Lancet,2000, 356(9247):2037-2044
[211]Ohman EM, Kleiman NS, Gacioch G, et al. IMPACT-AMI Investigators. Combined accelerated tissue-plasminogen activator and platelet glycoprotein Ilb/IIIa integrin receptor blockade with Integrilin in acute myocardial infarction. Results of a randomized, placebo-controlled, dose-ranging trial [J]. Circulation,1997,95(4): 846-854
[212]Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) Study Investigators. A comparison of aspirin plus tirofiban with aspirin plus heparin for unstable angina [J]. N Engl J Med,1998,338(21):1498-1505
[213]Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) Study Investigators. Inhibition of the platelet glycoprotein Ⅱb/Ⅲa receptor with tirofiban in unstable angina and non-Q-wave myocardial infarction [J]. N Engl J Med,1998,338(21): 1488-1497
[214]The RESTORE Investigators. Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis. Effects of platelet glycoprotein Ⅱb/Ⅲa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty [J]. Circulation,1997,96(5): 1445-1453
[215]Cohen M, Theroux P, Borzak S, et al. For the ACUTE II Investigators. The Antithrombotic Combination Using Tirofiban and Enoxaparin. Randomized double-blind safety study of enoxaparin versus unfractionated heparin in patients with non-ST-segment elevation acute coronary syndromes treated with tirofiban and aspirin: the ACUTE II study [J]. Am Heart J,2002,144(3):470-477
[216]Ferguson JJ, Antman EM, Bates ER, et al. For the NICE-3 Investigators. Combining enoxaparin and glycoprotein Ⅱb/Ⅲa antagonists for the treatment of acute coronary syndromes:final results of the National Investigators Collaborating on Enoxaparin-3(NICE-3) study [J]. Am Heart J,2003,146(4):628-634
[217]黄春艳,买苏木.不同剂量替罗非班对急性心肌梗死行经皮冠状动脉介入治疗术的疗效分析[J].临床荟萃,2010,25(3)：248-250
[218]何兴娜.冠脉支架置入术后患者半剂量替罗非班治疗的疗效和安全性分析[J].山东医药,2009,49(37)：63-64
[219]张孝忠,张军,王红,等.国产替罗非班在急性冠脉综合症介入治疗中应用的安全性及长期疗效观察[J].中国全科医学,2010,13(2B)：535-536
[220]姜玉蓉,曾秋棠,杨俊,等.替罗非班在急性ST段抬高型心肌梗死非介入 治疗中的应用[J].临床心血管病杂志,2010,26(5)：356-359
[221]张红雨,王佩显,曹艳君,等.替罗非班在急性心肌梗死经皮冠状动脉介入治疗中的应用[J].临床荟萃,2010,25(1)：70-72
[222]陈雪斌,马利平,王秋芬.小剂量替罗非班治疗老年急性冠脉综合症的临床研究[J].中国心血管病研究,2009,7(9)：672-674
[223]崔晓琼,李彤,王怀祯,等.盐酸替罗非班在急性心肌梗死患者急诊冠状动脉介入治疗中的有效性和安全性评价[J].临床心血管病杂志,2010,26(5)：332-335
[2]中华医学会心血管病分会介入心脏病学组中华心血管病杂志编辑部.全国首次冠心病介入性治疗病例注册登记资料分析[J].中华心血管病杂志,1998,26(1)：25-29
[3]中华医学会心血管病分会介入心脏病学组中华心血管病杂志编辑部.全国第二次冠心病介入性治疗病例注册登记资料分析[J].中华心血管病杂志,2000,28(1)：10-13
[4]中华医学会心血管病分会介入心脏病学组中华心血管病杂志编辑部.全国第三次冠心病介入治疗病例注册登记资料分析[J].中华心血管病杂志,2002,30(12)：719-723
[5]吕树铮,宋现涛,陈韵岱,等.代表中国经皮冠状动脉介入治疗登记调查研究协作组.中国大陆2005年度经皮冠状动脉介入治疗登记调查研究结果初步分析[J].中华心血管病杂志,2006,34(11)：966-970
[6]胡大一.健康中国2020-从心血管疾病预防抓起[A].见：胡大一,马长生.心脏病学实践20100——规范化治疗[M].北京：人民卫生出版社,2010,1-4
[7]柏瑾,李志善,戚文航,等.国产硫酸氯吡格雷片降低血小板聚集率的临床观察[J].中国临床药学杂志,2001,10(2)：67-69
[8]陈凌,李志善,戚文航,等.硫酸氯吡格雷的抗血小板聚集临床研究[J].中国新药杂志2000,9(10)：715-717
[9]李志娟,董平栓,杨旭明,等.国产和进口氯吡格雷对经皮冠状动脉介入术后血小板功能的影响[J].中国介入心脏病学杂志,2006,14(4)：208-210
[10]顾俊,胡伟,肖红兵,等.国产和进口氯吡格雷对PCI近中期预后的影响[J].上海交通大学学报(医学版),2008,28(5)：608-609
[11]CAPRIE Steering Committee. A randomized, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE) [J]. Lancet,1996,348(9038): 1329-1339
[12]Yusuf S, Mehta SR, Zhao F, et al. Clopidogrel in Unstable angina to prevent Recurrent Events Trial (CURE) investigators. Early and late effects of clopidogrel in patients with acute coronary syndromes[J]. Circulation,2003,107(7):966-972
[13]Chen ZM, Jiang LX, Chen YP, et al. COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction:randomised placebo-controlled trial [J]. Lancet,2005,366(9497):1607-1621
[14]Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation[J]. N Engl J Med,2005,352(12):1179-1189
[15]Sabatine MS, Cannon CP, Gibson CM, et al. Clopidogrel as Adjunctive Reperfusion Therapy (CLARITY)-Thrombolysis in Myocardial Infarction (TIMI) 28 Investigators. Effect of clopidogrel pretreatment before percutaneous coronary intervention in patients with ST-elevation myocardial infarction treated with fibrinolytics:the PCI-CLARITY study[J]. JAMA,2005,294(10):1224-1232
[16]Verheugt FW, Montalescot G, Sabatine MS, et al. Prehospital fibrinolysis with dual antiplatelet therapy in ST-elevation acute myocardial infarction:a substudy of the randomized double blind CLARITY-TIMI 28 trial [J]. J Thromb Thrombolysis, 2007,23(3):173-179
[17]Bertrand ME, Rupprecht HJ, Urban P, et al. CLASSICS Investigators. Double-blind study of the safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in combination with aspirin after coronary stenting:the clopidogrel aspirin stent international cooperative study (CLASSICS)[J]. Circulation,2000,102(6):624-629
[18]Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention:the PCI-CURE study [J]. Lancet,2001,358(9281):527-533
[19]Steinhubl SR, Berger PB, Mann JT 3rd, et al. CREDO Investigators. Clopidogrel for the Reduction of Events During Observation. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention:a randomized controlled trial[J]. JAMA,2002,288(19):2411-2420
[20]Mehta SR, Bassand JP, Chrolavicius S, et al. CURRENT-OASIS 7 Investigators. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes [J]. N Engl J Med,2010,363(10):930-942
[21]刘倩竹,洪涛,刘兆平,等.不同负荷剂量氯毗格雷对血小板聚集率的影响[J].中华内科杂志,2007,46(2)：107-110
[22]卢春山,周志强,柳景华,等.冠状动脉支架术后进口氯吡格雷(波立维)与国产氯吡格雷(泰嘉)抗血小板治疗的对照研究[J].中国介入心脏病学杂志,2009,17(2)：67-70
[23]李鹏,王文红,刘勇.国产氯吡格雷(泰嘉)与进口氯吡格雷(波立维)PCI术后应用的有效性和安全性对照研究[J].中国心血管病研究,2010,8(7)：506-508
[24]阴赪茜,李志忠,张京梅,等.国产与进口氯吡格雷在冠状动脉介入治疗中的疗效对比分析.中国新药杂志,2010,19(10)：849-852
[25]中华医学会心血管病学分会中华心血管病杂志编辑委员会.经皮冠状动脉介人治疗指南(2009)[J].中华心血管病杂志,2009,37(1)：4-25
[26]陈凌,郭若冰,戴军.氯吡格雷在缺血性心血管疾病防治中的作用[J].中国新药杂志,2009,9(10)：718-721
[27]中华医学会心血管病学分会中华心血管病杂志编辑委员会.经皮冠状动脉介人治疗指南[J].中华心血管病杂志,2002,30(12)：707-718
[28]Bovill EG, Terrin ML, Stump DC, et al. Hemorrhagic events during therapy with recombinant tissue-type plasminogen activator, heparin, and aspirin for acute myocardial infarction. Results of the Thrombolysis in Myocardial Infarction (TIMI), Phase Ⅱ Trial [J]. Ann Intern Med,1991,115(4):256-265
[29]Kushner FG, Hand M, Smith SC Jr, et al.2009 Focused Updates:ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the 2005 Guideline and 2007 Focused Update):a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [J]. Circulation,2009,120(22):2271-2306
[30]Silber S, Albertsson P, Aviles FF, et al. Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology [J]. Eur Heart J,2005,26(8):804-847
[31]Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction):developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons:endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine [J]. Circulation,2007,116(7):e148-304
[32]Holmes DR, Kereiakes DJ, Kleiman NS, et al. Combining antiplatelet and anticoagulant therapies [J]. J Am Coll Cardiol,2009,54(2):95-109
[33]段罡.进口和国产氯毗格雷对PCI术后的血小板功能及预后的影响[J].临床合理用药,2009,2(7)：6-7
[34]冯克福,马礼坤,余华,等.国产氯吡格雷在冠心病合并糖尿病患者冠状动脉支架术后的临床应用[J].中国临床保健杂志,2009,12(3)：233-234
[35]王禹,盖鲁粤,沈洪,等.国产氯吡格雷在急性心肌梗死急诊冠脉介入治疗过程中的有效性及对血小板聚集功能的影响[J].中国急救医学,2006,26(7)：512-514
[36]李纲,李玉东,牛桂林.冠状动脉支架植入术后相同剂量国产和进口氯吡格雷的防治效果比较[J].中国保健(医学研究版),2007,15(15)：53
[37]张晓玲,陈方,朱小玲,等.国产硫酸氯吡格雷在PTCA及支架植入术中的临床应用[J].中国医刊,2003,38(11)：55-56
[38]Meng Kang, Lu Shu-zheng, Zhu Hua-gang, et al. Use of tailored loading-dose clopidogrel in patients undergoing selected percutaneous coronary intervention based on adenosine diphosphate-mediated platelet aggregation [J]. Chin Med J,2010, 123(24):3578-3582
[39]雷鸣,刘志辉,徐惠琳,等.冠状动脉支架术后国产(泰嘉)与进口氯吡格雷(波立维)疗效及安全性的对照研究[J].中国实用医药,2010,5(7)：148-149
[40]钱利华.国产和进口氯吡格雷对PCI术治疗中的效果比较[J].中国现代医生,2010,48(3)：49-50
[41]周利民,李开如,陶春明,等.国产和进口氯吡格雷对经皮冠状动脉介入治疗术近中期预后的影响[J].中国医药指南,2010,8(35)：27-28
[42]孙裕华,陶秀彬,倪芳,等。国产氯吡格雷治疗冠心病疗效及安全性的M eta分析[J].中国循证心血管医学杂志,2010,2,(4)：214-218
[43]Hartzler GO, Rutherford BD, McConahay DR, et al. Percutaneous transluminal coronary angioplasty with and without thrombolytic therapy for treatment of actute myocardial infarction [J]. Am Heart J,1983,106(5 pt 1):965-973
[1]李家增,侯明,包承鑫.血小板疾病[M].北京：科学技术文献出版社,2009：9-23
[2]Bearer EL. Platelet membrane skeleton revealed by quick-freeze deep-etch [J]. Anat Rec,1990,227(1):1-11
[3]Allen RD, Zacharski LR, Widirstky ST, et al. Transformation and motility of human platlets:details of the shape change and release reaction observed by optical and electron microscopy [J]. J Cell Biol,1979,83(1):126-142
[4]周玉杰,葛均波,韩雅玲.防栓抗栓现代治疗策略[M].北京：人民卫生出版社,2006：31-44
[5]Savage B, Saldivar E, Ruggeri ZM. Initiation of platelet adhesion by arrest onto fibrinogen or translocation on von Willebrand factor [J]. Cell,1996,84(2):289-297
[6]Savage B, Almus-Jacobs F, Ruggeri ZM. Specific synergy of multiple subsrate-receptor interactions in platelet thrombus formation under flow [J]. Cell,1998,94(5): 657-666
[7]Kroll MH, Hellums JD, McIntire LV, et al. Platelets and shear stress [J]. Blood, 1996,88(5):1525-1541
[8]Goto S, Ikeda Y, Saldivar E, et al. Distinct mechanisms of platelet aggregation as a consequence of different shearing flow conditions [J]. J Clin Invest,1998,101(2): 479-486
[9]Ruggeri ZM. Old concepts and new developments in the study of platelet aggregation [J]. J Clin Invest,2000,105(6):699-701
[10]Ruggeri ZM, Dent JA, Saldivar E. Contribution of distinct adhesive interactions to platelet aggregation in flowing blood [J]. Blood,1999,94(1):172-178
[11]Wu YP, Vink T, Schiphorst M, et al. Platelet thrombus formation on collagen at high shear rates is mediated by von Willebrand factor-glycoprotein I b interaction and inhibited by von Willebrand factor-glycoprotein Ⅱb/Ⅲa interaction [J]. Arterioscler Thromb Vasc Biol,2000,20(6):1661-1667
[12]Tsuji S, Sugimoto M, Miyata S, et al. Real-time analysis of mural thrombus formation in various platelet aggregation disorders:distinct shear-dependent roles of platelet receptors and adhesive proteins under flow [J]. Blood,1999,94(3):968-975
[13]Simon DI, Chen Z, Xu H, et al. Platelet glycoprotein Ibalpha is a counterreceptor for the leukocyte integrin Mac-1(CD11b/CD 18) [J]. J Exp Med,2000,192(2): 193-204
[14]Mazzucato M, Marco LD, Masotti A, et al. Characterization of the initial a-thrombin interaction with glycoprotein I b a in relation to platelet activation [J]. J Biol Chem,1998,273(4):1880-1887
[15]Bradford HN, Dela Cadena RA, Kunapuli SP, et al. Human kininogens regulate thrombin binding to platelets through the glycoprotein Ib-IX-V complex [J]. Blood, 1997,90(4):1508-1515
[16]Baglia FA, Badellino KO, Li CQ, et al. Factor XI bingding to the platelet glycoprotein Ib/IX/V complex promotes factor XI activation by thrombin [J]. J Biol Chem,2002,277(3):1662-1668
[17]Bradford HN, Pixley RA, Colman RW. Human factor XII binding to the glycoprotein Ib-IX-V complex inhibits thrombin-induced platelet aggregation [J]. J Biol Chem,2000,275(30):22756-22763
[18]Jackson SP, Mistry N, Yuan Y. Platelets and the injured vessel wall-"rolling into action". Focus on glycoprotein Ⅰb/Ⅴ/Ⅸ and the platelet cytoskeleton [J]. Trends Cardiovasc Med,2000,10(5):192-197
[19]Ware J. Molecular analyses of the platelet glycoprotein Ⅰb/Ⅸ/Ⅴ receptor [J]. Thromb Haemost,1998,79(3):466-478
[20]Mazzucato M, Pradella P, Cozzi R, et al. Sequential cytoplasmic calcium signals in a two stage platelet activation process induced by the glycoprotein I b a mechanoreceotor [J]. Blood,2002,100(8):2793-2800
[21]Yap CL, Anderson KF, Hughan SC, et al. Essential role for phosphoinositide 3-kinase in shear-dependent signaling between platelet glycoprotein Ⅰb/Ⅴ/Ⅳ and integrin αⅡbβ3 [J]. Blood,2002,99(1):151-158
[22]Andrews RK, Shen Y, Gardiner EE, et al. The glycoprotein Ib-IX-V complex in platelet adhesion and signaling [J]. Thromb Haemost,1999,82(2):357-364
[23]Berndt MC, Shen Y, Dopheide SM, et al. The vascular biology of the glycoprotein Ⅰb-Ⅸ-Ⅴ complex [J]. Thromb Haemost,2001,86(1):178-188
[24]Gardiner EE, Arthur JF, Shen Y, et al. GPIbalpha-selective activation of platelets induces platelet signaling events comparable to GPVI activation events [J]. Platelets, 2010,21(4):244-252
[25]van Zanten GH, Heijnen HF, Wu Y, et al. A fifty percent reduction of platelet surface glycoprotein Ib does not affect platelet adhesion under flow conditions [J]. Blood,1998,91(7):2353-2359
[26]Michelson AD, Benoit SE, Furman MI, et al. The platelet surface expression of glycoprotein V is regulated by two independent mechanisms:proteolysis and a reversible cytoskeletal-mediated redistribution to the surface-connected canalicular system [J]. Blood,1996,87(4):1396-1408
[27]Uff S, Clemetson JM, Harrison T, et al. Crystal structure of the platelet glycoprotein Ib(alpha) N-terminal domain reveals an unmasking mechanism for receptor activation [J]. J Biol Chem,2002,277(38):35657-35663
[28]Huizinga EG, Tsuji S, Romijn RA, et al. Structures of glycoprotein Ibalpha and its complex with von Willebrand factor Al domain [J]. Science,2002,297(5584): 1176-1179
[29]Dong JF, Li CQ, Lopez JA. Tyrosine sulfation of the glycoprotein Ib-IX complex: identification of sulfated residues and effect on ligand binding [J]. Biochemistry,1994, 33(46):13946-13953
[30]Bodnar RJ, Gu M, Li Z, et al. The cytoplasmic domain of the platelet glycoprotein Ibalpha is phosphorylated at serine 609 [J]. J Biol Chem,1999,274(47): 33474-33479
[31]Munday AD, Berndt MC, Mitchell CA. Phosphoinositide 3-kinase forms a complex with platelet membrane glycoprotein Ib-IX-V complex and 14-3-3zeta [J]. Blood,2000,96(2):577-584
[32]Ramakrishnan V, DeGuzman F, Bao M, et al. A thrombin receptor function for platelet glycoprotein Ⅰb-Ⅸ unmasked by cleavage of glycoprotein V [J]. Proc Natl Acad Sci USA,2001,98(4):1823-1828
[33]Kasirer-Friede A, Ware J, Leng L, et al. Lateral clustering of platelet GP Ib-IX complexes leads to up-regulation of the adhesive function of integrin alpha Ⅱbbeta 3 [J]. J Biol Chem,2002,277(14):11949-11956
[34]Satoh K, Asazuma N, Yatomi Y, et al. Activation of protein-tyrosine kinase pathways in human platelets stimulated with the Al domain of von Willebrand factor [J]. Platelets,2000,11(3):171-176
[35]Falati S, Edmead CE, Poole AW. Glycoprotein Ib-V-IX, a receptor for von Willebrand factor, couples physically and functionally to the Fc receptor gamma-chain, Fyn, and Lyn to activate human platelets [J]. Blood,1999,94(5):1648-1656
[36]Torti M, Bertoni A, Canobbio I, et al. Rap 1B and Rap2B translocation to the cytoskeleton by von Willebrand factor involves FcgammaⅡ receptor-mediated protein tyrosine phosphorylation [J]. J Biol Chem,1999,274(19):13690-13697
[37]Sullam PM, Hyun WC, Szollosi J, et al. Physical proximity and functional interplay of the glycoprotein Ib-IX-V complex and the Fc receptor FcgammaRIIA on the platelet plasma membrane [J]. J Biol Chem,1998,273(9):5331-5336
[38]Watson SP, Asazuma N, Atkinson B, et al. The role of ITAM-and ITIM-coupled receptors in platelet activation by collagen [J]. Thromb Haemost,2001,86(1): 276-288
[39]Gu M, Xi X, Englund GD, et al. Analysis of the roles of 14-3-3 in the platelet glycoprotein Ib-IX-mediated activation of integrin alpha(IIb)beta(3) using a reconstituted mammalian cell expression model [J]. J Cell Biol,1999,147(5): 1085-1096
[40]Clemetson JM, Polgar J, Magnenat E, et al. The platelet collagen receptor glycoprotein VI is a member of the immunoglobulin superfamily closely related to FcalphaR and the natural killer receptors [J]. J Biol Chem,1999,274(41): 29019-29024
[41]Clemetson KJ, Clemetson JM. Platelet collagen receptors [J]. Thromb Haemost, 2001,86(1):189-197
[42]Moog S, Mangin P, Lenain N, et al. Platelet glycoprotein V binds to collagen and participates in platelet adhesion and aggregation [J]. Blood,2001,98(4):1038-1046
[43]Ramakrishnan V, Reeves PS, DeGuzman F, et al. Increased thrombin responsiveness in platelets from mice lacking glycoprotein V [J]. Proc Natl Acad Sci USA,1999,96(23):13336-13341
[44]Kunicki TJ. The role of platelet collagen receptor (glycoprotein Ia/IIa; integrin alpha2 betal) polymorphisms in thrombotic disease [J]. Curr Opin Hematol,2001, 8(5):277-285
[45]Moshfegh K, Wuillemin WA, Redondo M, et al. Association of two silent polymorphisms of platelet glycoprotein Ⅰa/Ⅱa receptor with risk of myocardial infarction:a case-control study [J]. Lancet,1999,353(9150):351-354
[46]Santoso S, Kunicki TJ, Kroll H, et al. Association of the platelet glycoprotein la C807T gene polymorphism with nonfatal myocardial infarction in younger patients [J]. Blood,1999,93(8):2449-2453
[47]Takada Y, Hemler ME. The primary structure of the VLA-2/collagen receptor alpha 2 subunit (platelet GPIa):homology to other integrins and the presence of a possible collagen-binding domain [J]. J Cell Biol,1989,109(1):397-407
[48]Emsley J, Knight CG, Farndale RW, et al. Structure of the integrin alpha2betal-binding collagen peptide [J]. J Mol Biol,2004,335(4):1019-1028
[49]Savage B, Ginsberg MH, Ruggeri ZM. Influence of fibrillar collagen structure on the mechanisms of platelet thrombus formation under flow [J]. Blood,1999,94(8): 2704-2715
[50]Verkleij MW, Morton LF, Knight CG, et al. Simple collagen-like peptides support platelet adhesion under static but not under flow conditions:interaction via alpha2 betal and von Willebrand factor with specific sequences in native collagen is a requirement to resist shear forces [J]. Blood,1998,91(10):3808-3816
[51]Wang R, Kini RM, Chung MC. Rhodocetin, a novel platelet aggregation inhibitor from the venom of Calloselasma rhodostoma (Malayan pit viper):synergistic and noncovalent interaction between its subunits [J]. Biochemistry,1999,38(23): 7584-7593
[52]Marcinkiewicz C, Lobb RR, Marcinkiewicz MM, et al. Isolation and characterization of EMS 16, a C-lectin type protein from Echis multisquamatus venom, a potent and selective inhibitor of the alpha2betal integrin [J]. Biochemistry,2000, 39(32):9859-9867
[53]Kamiguti AS, Theakston RD, Watson SP, et al. Distinct contributions of glycoprotein VI and alpha(2)beta(1) integrin to the induction of platelet protein tyrosine phosphorylation and aggregation [J]. Arch Biochem Biophys,2000,374(2): 356-362
[54]Chung CH, Au LC, Huang TF. Molecular cloning and sequence analysis of aggretin, a collagen-like platelet aggregation inducer [J]. Biochem Biophys Res Commun,1999,263(3):723-727
[55]Nakamura T, Kambayashi J, Okuma M, et al. Activation of the GP Ⅱb-Ⅲa complex induced by platelet adhesion to collagen is mediated by both alpha2betal integrin and GP Ⅵ [J]. J Biol Chem,1999,274(17):11897-11903
[56]Jung SM, Sonoda M, Tsuji K, et al. Are integrin alpha(2)beta(1), glycoprotein Ib and vWf levels correlated with their contributions to platelet adhesion on collagen under high-shear flow? [J]. Platelets,2010,21(2):101-111
[57]Sugiyama T, Okuma M, Ushikubi F, et al. A novel platelet aggregating factor found in a patient with defective collagen-induced platelet aggregation and autoimmune thrombocytopenia [J]. Blood,1987,69(6):1712-1720
[58]Jandrot-Perrus M, Busfield S, Lagrue AH, et al. Cloning, characterization, and functional studies of human and mouse glycoprotein VI:a platelet-specific collagen receptor from the immunoglobulin superfamily [J]. Blood,2000,96(5):1798-1807
[59]Nieswandt B, Bergmeier W, Schulte V, et al. Expression and function of the mouse collagen receptor glycoprotein Ⅵ is strictly dependent on its association with the FcR gamma chain [J]. J Biol Chem,2000,275(31):23998-24002
[60]Gross BS, Lee JR, Clements JL, et al. Tyrosine phosphorylation of SLP-76 is downstream of Syk following stimulation of the collagen receptor in platelets [J]. J Biol Chem,1999,274(9):5963-5971
[61]Clements JL, Lee JR, Gross B, et al. Fetal hemorrhage and platelet dysfunction in SLP-76-deficient mice [J]. J Clin Invest,1999,103(1):19-25
[62]Berridge MJ. Inositol trisphosphate and calcium signalling mechanisms [J]. Biochim Biophys Acta,2009,1793(6):933-940
[63]Falet H, Barkalow KL, Pivniouk VI, et al. Roles of SLP-76, phosphoinositide 3-kinase, and gelsolin in the platelet shape changes initiated by the collagen receptor GPVI/FcR gamma-chain complex [J]. Blood,2000,96(12):3786-3792
[64]Quek LS, Pasquet JM, Hers I, et al. Fyn and Lyn phosphorylate the Fc receptor gamma chain downstream of glycoprotein VI in murine platelets, and Lyn regulates a novel feedback pathway [J]. Blood,2000,96(13):4246-4253
[65]Judd BA, Koretzky GA. The role of the adapter molecule SLP-76 in platelet function [J]. Oncogene,2001,20(44):6291-6299
[66]Pasquet JM, Bobe R, Gross B, et al. A collagen-related peptide regulates phospholipase Cgamma2 via phosphatidylinositol 3-kinase in human platelets [J]. Biochem J,1999,342(Pt 1):171-177
[67]Lagrue AH, Francischetti IM, Guimaraes JA, et al. Phosphatidylinositol 3'-kinase and tyrosine-phosphatase activation positively modulate Convulxin-induced platelet activation. Comparison with collagen [J]. FEBS Lett,1999,448(1):95-100
[68]Schulz C, Penz S, Hoffmann C, et al. Platelet GPVI binds to collagenous structures in the core region of human atheromatous plaque and is critical for atheroprogression in vivo [J]. Basic Res Cardiol,2008,103(4):356-367
[69]Kato K, Kanaji T, Russell S, et al. The contribution of glycoprotein VI to stable platelet adhesion and thrombus formation illustrated by targeted gene deletion [J]. Blood,2003,102(5):1701-1707
[70]Daniel JL, Dangelmaier C, Jin J, et al. Molecular basis for ADP-induced platelet activation. I. Evidence for three distinct ADP receptors on human platelets [J]. J Biol Chem,1998,273(4):2024-2029
[71]Cattaneo M, Gachet C. ADP receptors and clinical bleeding disorders [J]. ArteriosclerThromb Vasc Biol,1999,19(10):2281-2285
[72]Jin J, Daniel JL, Kunapuli SP. Molecular basis for ADP-induced platelet activation. Ⅱ. The P2Y1 receptor mediates ADP-induced intracellular calcium mobilization and shape change in platelets [J]. J Biol Chem,1998,273(4):2030-2034
[73]Hollopeter G, Jantzen HM, Vincent D, et al. Identification of the platelet ADP receptor targeted by antithrombotic drugs [J]. Nature,2001,409(6817):202-207
[74]Zhang FL, Luo L, Gustafson E, et al. ADP is the cognate ligand for the orphan G protein-coupled receptor SP1999 [J]. J Biol Chem,2001,276(11):8608-8615
[75]Shankar H, Murugappan S, Kim S, et al. Role of G protein-gated inwardly rectifying potassium channels in P2Y12 receptor-mediated platelet functional responses [J]. Blood,2004,104(5):1335-1343
[76]Hechler B, Leon C, Vial C, et al. The P2Y1 receptor is necessary for adenosine 5'-diphosphate-induced platelet aggregation [J]. Blood,1998,92(1):152-159
[77]Bauer M, Retzer M, Wilde JI, et al. Dichotomous regulation of myosin phosphorylation and shape change by Rho-kinase and calcium in intact human platelets [J]. Blood,1999,94(5):1665-1672
[78]Wilde JI, Retzer M, Siess W, et al. ADP-induced platelet shape change:an investigation of the signalling pathways involved and their dependence on the method of platelet preparation [J]. Platelets,2000,11(5):286-295
[79]Fabre JE, Nguyen M, Latour A, et al. Decreased platelet aggregation, increased bleeding time and resistance to thromboembolism in P2Y1-deficient mice [J]. Nat Med,1999,5(10):1199-1202
[80]Gachet C. ADP receptors of platelets and their inhibition [J]. Thromb Haemost, 2001,86(1):222-232
[81]Leon C, Hechler B, Freund M, et al. Defective platelet aggregation and increased resistance to thrombosis in purinergic P2Y(1) receptor-null mice [J]. J Clin Invest, 1999,104(12):1731-1737
[82]Savi P, Herbert JM. Clopidogrel and ticlopidine:P2Y12 adenosine diphosphate-receptor antagonists for the prevention of atherothrombosis [J]. Semin Thromb Hemost,2005,31(2):174-183
[83]Savi P, Labouret C, Delesque N, et al. P2y(12), a new platelet ADP receptor, target of clopidogrel [J]. Biochem Biophys Res Commun,2001,283(2):379-383
[84]Daniel NG, Goulet J, Bergeron M, et al. Antiplatelet drugs:is there a surgical risk? [J]. J Can Dent Assoc,2002,68(11):683-687
[85]Sharis PJ, Cannon CP, Loscalzo J. The antiplatelet effects of ticlopidine and clopidogrel [J]. Ann Intern Med,1998,129(5):394-405
[86]Vu TK, Wheaton VI, Hung DT, et al. Domains specifying thrombin-receptor interaction [J]. Nature,1991,353(6345):674-677
[87]Faruqi TR, Weiss EJ, Shapiro MJ, et al. Structure-function analysis of protease-activated receptor 4 tethered ligand peptides. Determinants of specificity and utility in assays of receptor function [J]. J Biol Chem,2000,275(26):19728-19734
[88]Ishihara H, Connolly AJ, Zeng D, et al. Protease-activated receptor 3 is a second thrombin receptor in humans [J]. Nature,1997,386(6624):502-506
[89]Xu WF, Andersen H, Whitmore TE, et al. Cloning and characterization of human protease-activated receptor 4 [J]. Proc Natl Acad Sci USA,1998,95(12):6642-6646
[90]Camerer E, Huang W, Coughlin SR. Tissue factor- and factor X-dependent activation of protease-activated receptor 2 by factor Ⅶa [J]. Proc Natl Acad Sci USA, 2000,97(10):5255-5260
[91]Kahn ML, Nakanishi-Matsui M, Shapiro MJ, et al. Protease-activated receptors 1 and 4 mediate activation of human platelets by thrombin [J]. J Clin Invest,1999, 103(6):879-887
[92]Covic L, Gresser AL, Kuliopulos A. Biphasic kinetics of activation and signaling for PAR1 and PAR4 thrombin receptors in platelets [J]. Biochemistry,2000,39(18): 5458-5467
[93]Brass LF, Manning DR, Cichowski K, et al. Signaling through G proteins in platelets:to the integrins and beyond [J]. Thromb Haemost,1997,78(1):581-589
[94]Kramer RM, Roberts EF, Um SL, et al. p38 mitogen-activated protein kinase phosphorylates cytosolic phospholipase A2 (cPLA2) in thrombin-stimulated platelets. Evidence that proline-directed phosphorylation is not required for mobilization of arachidonic acid by cPLA2 [J]. J Biol Chem,1996,271(44):27723-27729
[95]O'Brien PJ, Prevost N, Molino M, et al. Thrombin responses in human endothelial cells. Contributions from receptors other than PAR1 include the transactivation of PAR2 by thrombin-cleaved PAR1 [J]. J Biol Chem,2000,275(18): 13502-13509
[96]Andrade-Gordon P, Maryanoff BE, Derian CK, et al. Design, synthesis, and biological characterization of a peptide-mimetic antagonist for a tethered-ligand receptor [J]. Proc Natl Acad Sci USA,1999,96(22):12257-12262
[97]Maeda H, Inazu T, Nagai K, et al. Possible involvement of protein-tyrosine kinases such as p72syk in the disc-sphere change response of porcine platelets [J]. J Biochem,1995,117(6):1201-1208
[98]Hermand P, Gane P, Huet M, et al. Red cell ICAM-4 is a novel ligand for platelet-activated alpha Ⅱbbeta 3 integrin [J]. J Biol Chem,2003,278(7):4892-4898
[99]Shattil SJ, Hoxie JA, Cunningham M, et al. Changes in the platelet membrane glycoprotein Ⅱb.Ⅲa complex during platelet activation [J]. J Biol Chem,1985, 260(20):11107-11114
[100]Stephens G, O'Luanaigh N, Reilly D, et al. A sequence within the cytoplasmic tail of GpⅡb independently activates platelet aggregation and thromboxane synthesis [J]. J Biol Chem,1998,273(32):20317-20322
[101]Leisner TM, Wencel-Drake JD, Wang W, et al. Bidirectional transmembrane modulation of integrin alphaⅡbbeta3 conformations [J]. J Biol Chem,1999,274(18): 12945-12949
[102]Naik UP, Naik MU. Association of CIB with GPIIb/IIIa during outside-in signaling is required for platelet spreading on fibrinogen [J]. Blood,2003,102(4): 1355-1362
[103]Tsuboi S. Calcium integrin-binding protein activates platelet integrin alpha Ilbbeta 3 [J]. J Biol Chem,2002,277(3):1919-1923
[104]Bertoni A, Tadokoro S, Eto K, et al. Relationships between Raplb, affinity modulation of integrin alpha Ⅱbbeta 3, and the actin cytoskeleton [J]. J Biol Chem, 2002,277(28):25715-25721
[105]Haataja L, Kaartinen V, Groffen J, et al. The small GTPase Rac3 interacts with the integrin-binding protein CIB and promotes integrin alpha(IIb)beta(3)-mediated adhesion and spreading [J]. J Biol Chem,2002,277(10):8321-8328
[106]Wagner CL, Mascelli MA, Neblock DS, et al. Analysis of GPⅡb/Ⅲa receptor number by quantification of 7E3 binding to human platelets [J]. Blood,1996,88(3): 907-914
[107]Hynes RO. Integrins:a family of cell surface receptors [J]. Cell,1987,48(4): 549-554
[108]Rosa JP, Bray PF, Gayet O, et al. Cloning of glycoprotein Ⅲa cDNA from human erythroleukemia cells and localization of the gene to chromosome 17 [J]. Blood,1988,72(2):593-600
[109]Weisel JW, Nagaswami C, Vilaire G, et al. Examination of the platelet membrane glycoprotein Ⅱb-Ⅲa complex and its interaction with fibrinogen and other ligands by electron microscopy [J]. J Biol Chem,1992,267(23):16637-16643
[110]D'Souza SE, Ginsberg MH, Burke TA, et al. The ligand binding site of the platelet integrin receptor GPⅡb-Ⅲa is proximal to the second calcium binding domain of its alpha subunit [J]. J Biol Chem,1990,265(6):3440-3446
[111]Cierniewski CS, Byzova T, Papierak M, et al. Peptide ligands can bind to distinct sites in integrin alphaⅡbbeta3 and elicit different functional responses [J]. J Biol Chem,1999,274(24):16923-16932
[112]Loftus JC, O'Toole TE, Plow EF, et al. A beta 3 integrin mutation abolishes ligand binding and alters divalent cation-dependent conformation [J]. Science,1990, 249(4971):915-918
[113]Tozer EC, Liddington RC, Sutcliffe MJ, et al. Ligand binding to integrin alphaⅡbbeta3 is dependent on a MIDAS-like domain in the beta3 subunit [J]. J Biol Chem,1996,271(36):21978-21984
[114]Obergfell A, Eto K, Mocsai A, et al. Coordinate interactions of Csk, Src, and Syk kinases with [alpha] Ⅱb [beta] 3 initiate integrin signaling to the cytoskeleton [J]. J Cell Biol,2002,157(2):265-275
[115]Coburn LA, Damaraju VS, Dozic S, et al. GPIba-vWF rolling under shear stress shows differences between type 2B and 2M von Willebrand disease [J]. Biophys J, 2011,100(2):304-312
[116]Locke D, Chen H, Liu Y, et al. Lipid rafts orchestrate signaling by the platelet receptor glycoprotein VI [J]. J Biol Chem,2002,277(21):18801-18809
[117]Ezumi Y, Kodama K, Uchiyama T, et al. Constitutive and functional association of the platelet collagen receptor glycoprotein VI-Fc receptor gamma-chain complex with membrane rafts[J]. Blood,2002,99(9):3250-3255
[118]Cicmil M, Thomas JM, Leduc M, et al. Platelet endothelial cell adhesion molecule-1 signaling inhibits the activation of human platelets [J]. Blood,2002,99(1): 137-144
[119]Larson MK, Chen H, Kahn ML, et al. Identification of P2Y12-dependent and-independent mechanisms of glycoprotein Ⅵ-mediated Rapl activation in platelets [J]. Blood,2003,101(4):1409-1415
[120]Cho MJ, Liu J, Pestina TI, et al. The roles of alpha Ⅱb beta 3-mediated outside-in signal transduction, thromboxane A2, and adenosine diphosphate in collagen-induced platelet aggregation [J]. Blood,2003,101(7):2646-2651
[121]Funk CD, FitzGerald GA. COX-2 inhibitors and cardiovascular risk [J]. J Cardiovasc Pharmacol,2007,50(5):470-479
[122]Furuyashiki T, Narumiya S. Stress responses:the contribution of prostaglandin E(2) and its receptors [J]. Nat Rev Endocrinol,2011,7(3):163-175
[123]Halushka PV, Allan CJ, Davis-Bruno KL. Thromboxane A2 receptors [J]. J Lipid Mediat Cell Signal,1995,12(2-3):361-378
[124]Li Z, Xi X, Du X. A mitogen-activated protein kinase-dependent signaling pathway in the activation of platelet integrin alpha IIbbeta3 [J]. J Biol Chem,2001, 276(45):42226-42232
[125]Dorsam RT, Kim S, Jin J, et al. Coordinated signaling through both G12/13 and G(i) pathways is sufficient to activate GPⅡb/Ⅲa in human platelets [J]. J Biol Chem, 2002,277(49):47588-47595
[126]Nieswandt B, Schulte V, Zywietz A, et al. Costimulation of Gi- and G12/G13-mediated signaling pathways induces integrin alpha Ilbbeta 3 activation in platelets [J]. J Biol Chem,2002,277(42):39493-39498.
[127]Nadal-Wollbold F, Pawlowski M, Levy-Toledano S, et al. Platelet ERK2 activation by thrombin is dependent on calcium and conventional protein kinases C but not Raf-1 or B-Raf [J]. FEBS Lett,2002,531(3):475-82
[128]Fujimoto TT, Katsutani S, Shimomura T, et al. Thrombospondin-bound integrin-associated protein (CD47) physically and functionally modifies integrin alphaⅡbbeta3 by its extracellular domain [J]. J Biol Chem,2003,278(29): 26655-26665
[129]Lagadec P, Dejoux O, Ticchioni M, et al. Involvement of a CD47-dependent pathway in platelet adhesion on inflamed vascular endothelium under flow [J]. Blood, 2003,101(12):4836-4843
[130]Dale GL, Friese P, Batar P, et al. Stimulated platelets use serotonin to enhance their retention of procoagulant proteins on the cell surface [J]. Nature,2002, 415(6868):175-179
[131]Polgar J, Chung SH, Reed GL. Vesicle-associated membrane protein 3 (VAMP-3) and VAMP-8 are present in human platelets and are required for granule secretion [J]. Blood,2002,100(3):1081-1083
[132]Barry OP, Kazanietz MG, Pratico D, et al. Arachidonic acid in platelet microparticles up-regulates cyclooxygenase-2-dependent prostaglandin formation via a protein kinase C/mitogen-activated protein kinase-dependent pathway [J]. J Biol Chem,1999,274(11):7545-7556
[133]Coller BS, Lang D, Scudder LE. Rapid and simple platelet function assay to assess glycoprotein Ⅱb/Ⅲa receptor blockade [J]. Circulation,1997,95(4):860-867
[134]Despotis GJ, Levine V, Filos KS, et al. Evaluation of a new point-of-care test that measures PAF-mediated acceleration of coagulation in cardiac surgical patients [J]. Anesthesiology,1996,85(6):1311-1323
[135]Kundu SK, Heilmann EJ, Sio R, et al. Description of an in vitro platelet function analyzer－-PFA-100 [J]. Semin Thromb Hemost,1995,21 (Suppl 2):106-112
[136]Nicholson NS, Panzer-Knodle SG, Haas NF, et al. Assessment of platelet function assays [J]. Am Heart J,1998,135(5 Pt 2 Su):S170-S178
[137]Li CK, Hoffmann TJ, Hsieh PY, et al. Xylum CSA:automated system for assessing hemostasis in simulated vascular flow [J]. Clin Chem,1997,43(9): 1788-1790
[138]Mancuso A, Fung K, Cox D, et al. Assessment of blood coagulation in severe liver disease using thromboelastography:use of citrate storage versus native blood [J]. Blood Coagul Fibrinolysis,2003,14(2):211-216
[139]Lewis HD Jr, Davis JW, Archibald DG, et al. Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study [J]. N Engl J Med,1983,309(7):396-403
[140]Cairns JA, Gent M, Singer J, et al. Aspirin, sulfinpyrazone, or both in unstable angina. Results of a Canadian multicenter trial [J]. N Engl J Med,1985,313(22): 1369-1375
[141]The RISC Group. Risk of myocardial infarction and death during treatment with low dose aspirin and intravenous heparin in men with unstable coronary artery disease [J]. Lancet,1990,336(8719):827-830
[142]Juul-Moller S, Edvardsson N, Jahnmatz B, et al. Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable chronic angina pectoris. The Swedish Angina Pectoris Aspirin Trial (SAPAT) Group[J]. Lancet,1992, 340(8833):1421-1425
[143]Antiplatelet Trialists' Collaboration. Collaborative overview of randomised trials of antiplatelet therapy--Ⅲ:Reduction in venous thrombosis and pulmonary embolism by antiplatelet prophylaxis among surgical and medical patients [J]. BMJ,1994, 308(6923):235-246
[144]ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction:ISIS-2 [J]. Lancet,1988, 2(8607):349-360
[145]The SALT Collaborative Group. Swedish Aspirin Low-Dose Trial (SALT) of 75 mg aspirin as secondary prophylaxis after cerebrovascular ischaemic events [J]. Lancet,1991,338(8779):1345-1349
[146]The Dutch TIA Trial Study Group. A comparison of two doses of aspirin (30 mg vs.283 mg a day) in patients after a transient ischemic attack or minor ischemic stroke [J]. N Engl J Med,1991,325(18):1261-1266
[147]Farrell B, Godwin J, Richards S, et al. The United Kingdom transient ischaemic attack (UK-TIA) aspirin trial:final results [J]. J Neurol Neurosurg Psychiatry,1991, 54(12):1044-1054
[148]The ESPS Group. The European Stroke Prevention Study (ESPS). Principal end-points [J]. Lancet,1987,2(8572):1351-1354
[149]Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention Study.2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke [J]. J Neurol Sci,1996,143(1-2):1-13
[150]ETDRS Investigators. Aspirin effects on mortality and morbidity in patients with diabetes mellitus. Early Treatment Diabetic Retinopathy Study report 14 [J]. JAMA,1992,268(10):1292-1300
[151]Hansson L, Zanchetti A, Carruthers SG, et al. HOT Study Group. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. HOT Study Group [J]. Lancet,1998,351(9118):1755-1762
[152]Steering Committee of the Physicians' Health Study Research Group. Final report on the aspirin component of the ongoing Physicians'Health Study [J]. N Engl J Med,1989,321(3):129-135
[153]de Gaetano G, Collaborative Group of the Primary Prevention Project. Low-dose aspirin and vitamin E in people at cardiovascular risk:a randomised trial in general practice [J]. Lancet,2001,357(9250):89-95
[154]Peto R, Gray R, Collins R, et al. Randomised trial of prophylactic daily aspirin in British male doctors [J]. Br Med J (Clin Res Ed),1988,296(6618):313-316
[155]Ridker PM, Cook NR, Lee IM, et al. A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women [J]. N Engl J Med,2005, 352(13):1293-1304
[156]Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events [J]. N Engl J Med,2006,354(16): 1706-1717
[157]International Stroke Trial Collaborative Group. The International Stroke Trial (IST):a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19435 patients with acute ischaemic stroke [J]. Lancet,1997,349(9065):1569-1581
[158]CAST (Chinese Acute Stroke Trial) Collaborative Group. CAST:randomised placebo-controlled trial of early aspirin use in 20,000 patients with acute ischaemic stroke [J]. Lancet,1997,349(9066):1641-1649
[159]中华医学会心血管病学分会中华心血管病杂志编辑委员会.阿司匹林在动脉硬化性心血管疾病中的临床应用：中国专家共识(2005)[J].中华心血管病杂志,2006,34(3)：281-284
[160]中华内科杂志编辑部.规范应用阿司匹林治疗缺血性脑血管病的专家共识[J].中华内科杂志,2006,45(1)：81-82
[161]急性ST段抬高心肌梗死溶栓治疗中国专家共识组.急性ST段抬高心肌梗死溶栓治疗的中国专家共识(修订版)[J].中华内科杂志,2008,47(2)：170-174
[162]中华医学会心血管病学分会中华心血管病杂志编辑委员会.不稳定性心绞痛和非ST段抬高心肌梗死诊断与治疗指南[J].中华心血管病杂志,2007,35(4)： 295-304
[163]中华医学会心血管病学分会中华心血管病杂志编辑委员会中国循环杂志编辑委员会.急性心肌梗死诊断和治疗指南[J].中华心血管病杂志,2001,29(12)：710-725
[164]中华医学会心血管病学分会中华心血管病杂志编辑委员会.慢性稳定性心绞痛诊断与治疗指南[J].中华心血管病杂志,2007,35(3)：195-206
[165]中华医学会心血管病学分会中华心血管病杂志编辑委员会.经皮冠状动脉介人治疗指南(2009)[J].中华心血管病杂志,2009,37(1)：4-25
[166]澳大利亚国家卒中基金会专家工作组.急性卒中临床处理指南[J].国际脑血管病杂志,2008,16(9)：641-689
[167]欧洲卒中组织(ESO)执行委员会和ESO写作委员会.缺血性卒中和短暂性脑缺血发作处理指南2008[J].国际脑血管病杂志,2008,16(6)：401-440
[168]Kushner FG, Hand M, Smith SC Jr, et al.2009 Focused Updates:ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction (updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on Percutaneous Coronary Intervention (updating the 2005 Guideline and 2007 Focused Update):a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [J]. Circulation,2009,120(22):2271-2306
[169]Antman EM, Hand M, Armstrong PW, et al.2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines:developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians:2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee [J]. Circulation,2008, 117(2):296-329
[170]Fraker TD Jr, Fihn SD, Gibbons RJ, et al.2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina [J]. Circulation,2007,116(23):2762-2772
[171]Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction):developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons:endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine [J]. Circulation,2007,116(7):e148-304
[172]Van de Werf F, Bax J, Betriu A, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation:the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology [J]. Eur Heart J,2008,29(23):2909-2945
[173]Adams H, Adams R, Del Zoppo G, et al. Guidelines for the early management of patients with ischemic stroke:2005 guidelines update a scientific statement from the Stroke Council of the American Heart Association/American Stroke Association [J]. Stroke,2005,36(4):916-923
[174]Bertrand ME, Simoons ML, Fox KA, et al. Task Force on the Management of Acute Coronary Syndromes of the European Society of Cardiology. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [J]. Eur Heart J,2002 Dec;23(23):1809-1840
[175]Fox K, Garcia MA, Ardissino D, et al. Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology; ESC Committee for Practice Guidelines (CPG). Guidelines on the management of stable angina pectoris:executive summary:The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology [J]. Eur Heart J,2006,27(11):1341-1381
[176]Silber S, Albertsson P, Aviles FF, et al. Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology. Guidelines for percutaneous coronary interventions. The Task Force for Percutaneous Coronary Interventions of the European Society of Cardiology [J]. Eur Heart J,2005,26(8):804-847
[177]Balsano F, Rizzon P, Violi F, et al. The Studio della Ticlopidina nell'Angina Instabile Group. Antiplatelet treatment with ticlopidine in unstable angina. A controlled multicenter clinical trial [J]. Circulation,1990,82(1):17-26
[178]Cutlip DE, Leon MB, Ho KK, et al. Acute and nine-month clinical outcomes after "suboptimal" coronary stenting:results from the STent Anti-thrombotic Regimen Study (STARS) registry [J]. J Am Coll Cardiol,1999,34(3):698-706
[179]Urban P, Macaya C, Rupprecht HJ, et al. Randomized evaluation of anticoagulation versus antiplatelet therapy after coronary stent implantation in high-risk patients:the multicenter aspirin and ticlopidine trial after intracoronary stenting (MATTIS) [J]. Circulation,1998,98(20):2126-2132
[180]Hass WK, Easton JD, Adams HP Jr, et al. Ticlopidine Aspirin Stroke Study Group. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients[J]. N Engl J Med,1989,321(8):501-507
[181]Gent M, Blakely JA, Easton JD, et al. The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke [J]. Lancet,1989,1(8649):1215-1220
[182]CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE) [J]. Lancet,1996, 348(9038):1329-1339
[183]Yusuf S, Zhao F, Mehta SR, et al. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation [J]. N Engl J Med,2001,345(7):494-502
[184]Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation [J]. N Engl J Med,2005,352(12):1179-1189
[185]Chen ZM, Jiang LX, Chen YP, et al. COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Addition of clopidogrel to aspirin in 45,852 patients with acute myocardial infarction:randomised placebo-controlled trial [J]. Lancet,2005,366(9497):1607-1621
[186]Bertrand ME, Rupprecht HJ, Urban P, et al. CLASSICS Investigators. Double-blind study of the safety of clopidogrel with and without a loading dose in combination with aspirin compared with ticlopidine in combination with aspirin after coronary stenting:the clopidogrel aspirin stent international cooperative study (CLASSICS) [J]. Circulation,2000,102(6):624-629
[187]Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention:the PCI-CURE study [J]. Lancet,2001,358(9281):527-533
[188]Steinhubl SR, Berger PB, Mann JT 3rd, et al. CREDO Investigators. Clopidogrel for the Reduction of Events During Observation. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention:a randomized controlled trial [J]. JAMA,2002,288(19):2411-2420
[189]Mehta SR, Bassand JP, Chrolavicius S, et al. CURRENT-OASIS 7 Investigators. Dose comparisons of clopidogrel and aspirin in acute coronary syndromes [J]. N Engl J Med,2010,363(10):930-942
[190]Park SW, Lee CW, Kim HS, et al. Comparison of cilostazol versus ticlopidine therapy after stent implantation [J]. Am J Cardiol,1999,84(5):511-514
[191]Park SW, Lee CW, Kim HS, et al. Effects of cilostazol on angiographic restenosis after coronary stent placement [J]. Am J Cardiol,2000,86(5):499-503
[192]Ge J, Han Y, Jiang H, et al. RACTS (Randomized Prospective Antiplatelet Trial of Cilostazol Versus Ticlopidine in Patients Undergoing Coronary Stenting) Trial Investigators. RACTS:a prospective randomized antiplatelet trial of cilostazol versus ticlopidine in patients undergoing coronary stenting:long-term clinical and angiographic outcome [J]. J Cardiovasc Pharmacol,2005,46(2):162-166
[193]Lee SW, Park SW, Hong MK, et al. Comparison of cilostazol and clopidogrel after successful coronary stenting [J]. Am J Cardiol,2005,95(7):859-862
[194]Douglas JS, Weintraub WS, Holmes D. Rationale and design of the randomized, multicenter, cilostazol for RESTenosis (CREST) trial [J]. Clin Cardiol,2003,26(10): 451-454
[195]The EPIC Investigation. Use of a monoclonal antibody directed against the platelet glycoprotein Ⅱb/Ⅲa receptor in high-risk coronary angioplasty [J]. N Engl J Med,1994,330(14):956-961
[196]Simoons ML. GUSTO IV-ACS Investigators. Effect of glycoprotein Ⅱb/Ⅲa receptor blocker abciximab on outcome in patients with acute coronary syndromes without early coronary revascularisation:the GUSTO IV-ACS randomised trial [J]. Lancet,2001,357(9272):1915-1924
[197]The EPILOG Investigators. Platelet glycoprotein Ⅱb/Ⅲa receptor blockade and low-dose heparin during percutaneous coronary revascularization [J]. N Engl J Med, 1997,336(24):1689-1696
[198]EPISTENT Investigators. Randomised placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-Ⅱb/Ⅲa blockade [J]. Lancet,1998,352(9122):87-92
[199]The CAPTURE Investigators. Randomised placebo-controlled trial of abciximab before and during coronary intervention in refractory unstable angina:the CAPTURE Study[J]. Lancet,1997,349(9063):1429-1435
[200]Montalescot G, Barragan P, Wittenberg O, et al. ADMIRAL Investigators. Abciximab before Direct Angioplasty and Stenting in Myocardial Infarction Regarding Acute and Long-Term Follow-up. Platelet glycoprotein Ⅱb/Ⅲa inhibition with coronary stenting for acute myocardial infarction [J]. N Engl J Med,2001, 344(25):1895-1903
[201]Stone GW, Grines CL, Cox DA, et al. Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) Investigators. Comparison of angioplasty with stenting, with or without abciximab, in acute myocardial infarction [J]. N Engl J Med,2002,346(13):957-966
[202]Brener SJ, Barr LA, Burchenal JE, et al. ReoPro and Primary PTCA Organization and Randomized Trial (RAPPORT) Investigators. Randomized, placebo-controlled trial of platelet glycoprotein Ⅱb/Ⅲa blockade with primary angioplasty for acute myocardial infarction [J]. Circulation,1998,98(8):734-741
[203]Ndrepepa G, Kastrati A, Neumann FJ, et al. Five-year outcome of patients with acute myocardial infarction enrolled in a randomised trial assessing the value of abciximab during coronary artery stenting [J]. Eur Heart J,2004,25(18):1635-1640
[204]Gibson CM, de Lemos JA, Murphy SA, et al. Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: a TIMI 14 substudy [J]. Circulation,2001,103(21):2550-2554
[205]Strategies for Patency Enhancement in the Emergency Department (SPEED) Group. Trial of abciximab with and without low-dose reteplase for acute myocardial infarction[J]. Circulation,2000,101(24):2788-2794
[206]Topol EJ. GUSTO V Investigators. Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein Ⅱb/Ⅲa inhibition:the GUSTO V randomised trial [J]. Lancet, 2001,357(9272):1905-1914
[207]Assessment of the Safety and Efficacy of a New Thrombolytic Regimen (ASSENT)-3 Investigators. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin:the ASSENT-3 randomised trial in acute myocardial infarction [J]. Lancet,2001,358(9282):605-613
[208]The PURSUIT Trial Investigators. Platelet Glycoprotein Ⅱb/Ⅲa in Unstable Angina:Receptor Suppression Using Integrilin Therapy. Inhibition of platelet glycoprotein Ⅱb/Ⅲa with eptifibatide in patients with acute coronary syndromes [J]. N Engl J Med,1998,339(7):436-443
[209]The IMPACT-Ⅱ Investigators.Integrilin to Minimise Platelet Aggregation and Coronary Thrombosis-Ⅱ. Randomised placebo-controlled trial of effect of eptifibatide on complications of percutaneous coronary intervention:IMPACT-Ⅱ[J]. Lancet,1997, 349(9063):1422-1428
[210]ESPRIT Investigators. Enhanced Suppression of the Platelet Ⅱb/Ⅲa Receptor with Integrilin Therapy. Novel dosing regimen of eptifibatide in planned coronary stent implantation (ESPRIT):a randomised, placebo-controlled trial [J]. Lancet,2000, 356(9247):2037-2044
[211]Ohman EM, Kleiman NS, Gacioch G, et al. IMPACT-AMI Investigators. Combined accelerated tissue-plasminogen activator and platelet glycoprotein Ilb/IIIa integrin receptor blockade with Integrilin in acute myocardial infarction. Results of a randomized, placebo-controlled, dose-ranging trial [J]. Circulation,1997,95(4): 846-854
[212]Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) Study Investigators. A comparison of aspirin plus tirofiban with aspirin plus heparin for unstable angina [J]. N Engl J Med,1998,338(21):1498-1505
[213]Platelet Receptor Inhibition in Ischemic Syndrome Management in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS) Study Investigators. Inhibition of the platelet glycoprotein Ⅱb/Ⅲa receptor with tirofiban in unstable angina and non-Q-wave myocardial infarction [J]. N Engl J Med,1998,338(21): 1488-1497
[214]The RESTORE Investigators. Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis. Effects of platelet glycoprotein Ⅱb/Ⅲa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty [J]. Circulation,1997,96(5): 1445-1453
[215]Cohen M, Theroux P, Borzak S, et al. For the ACUTE II Investigators. The Antithrombotic Combination Using Tirofiban and Enoxaparin. Randomized double-blind safety study of enoxaparin versus unfractionated heparin in patients with non-ST-segment elevation acute coronary syndromes treated with tirofiban and aspirin: the ACUTE II study [J]. Am Heart J,2002,144(3):470-477
[216]Ferguson JJ, Antman EM, Bates ER, et al. For the NICE-3 Investigators. Combining enoxaparin and glycoprotein Ⅱb/Ⅲa antagonists for the treatment of acute coronary syndromes:final results of the National Investigators Collaborating on Enoxaparin-3(NICE-3) study [J]. Am Heart J,2003,146(4):628-634
[217]黄春艳,买苏木.不同剂量替罗非班对急性心肌梗死行经皮冠状动脉介入治疗术的疗效分析[J].临床荟萃,2010,25(3)：248-250
[218]何兴娜.冠脉支架置入术后患者半剂量替罗非班治疗的疗效和安全性分析[J].山东医药,2009,49(37)：63-64
[219]张孝忠,张军,王红,等.国产替罗非班在急性冠脉综合症介入治疗中应用的安全性及长期疗效观察[J].中国全科医学,2010,13(2B)：535-536
[220]姜玉蓉,曾秋棠,杨俊,等.替罗非班在急性ST段抬高型心肌梗死非介入 治疗中的应用[J].临床心血管病杂志,2010,26(5)：356-359
[221]张红雨,王佩显,曹艳君,等.替罗非班在急性心肌梗死经皮冠状动脉介入治疗中的应用[J].临床荟萃,2010,25(1)：70-72
[222]陈雪斌,马利平,王秋芬.小剂量替罗非班治疗老年急性冠脉综合症的临床研究[J].中国心血管病研究,2009,7(9)：672-674
[223]崔晓琼,李彤,王怀祯,等.盐酸替罗非班在急性心肌梗死患者急诊冠状动脉介入治疗中的有效性和安全性评价[J].临床心血管病杂志,2010,26(5)：332-335