Christoph Olivier, MD, Cardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106 Freiburg, Germany, Tel.: + 49 761 270 34410, E-mail:
Thromb Haemost. 2014 Feb;111(2):266-72. doi: 10.1160/TH13-06-0508. Epub 2013 Oct 31.
The current standard of antiplatelet therapy of patients after myocardial infarction includes the P2Y12 receptor antagonists clopidogrel, prasugrel or ticagrelor. This study aimed to compare the antiplatelet effect of clopidogrel, prasugrel and ticagrelor in patients after myocardial infarction. In a single-centre registry the antiplatelet effect of clopidogrel, prasugrel and ticagrelor was investigated by aggregometry in patients after myocardial infarction. To assess the overall capacity of platelet aggregation whole blood was induced with thrombin receptor activating peptide (TRAP; 32 µM). To specifically quantify the effect of P2Y12 antagonists, whole blood was stimulated with 6.4 µM adenosine diphophosphate (ADP). Relative ADP induced aggregation (r-ADP-agg) was defined as the ADP-TRAP ratio to reflect an individual degree of P2Y12-dependent platelet inhibition.Platelet function of 238 patients was analysed [clopidogrel (n=58), prasugrel (n=65), ticagrelor (n=115)]. The r-ADP-agg was 35 ± 14% for patients receiving clopidogrel, 28 ± 10% for patients receiving prasugrel and 26 ± 11% for patients receiving ticagrelor. The r-ADP-agg was significantly lower in patients treated with prasugrel (p=0.0024) or ticagrelor (p<0.0001) compared to clopidogrel. There was no significant difference between patients receiving prasugrel or ticagrelor (p=0.2559). In conclusion, prasugrel and ticagrelor provide a stronger platelet inhibition compared to clopidogrel in patients after myocardial infarction. No significant difference in platelet inhibition was detected between prasugrel and ticagrelor. (registry for patients after Myocardial Infarction Treated with AntiPlatelet agents; DRKS00003146).
目前，心肌梗死后患者的抗血小板治疗标准包括 P2Y12 受体拮抗剂氯吡格雷、普拉格雷或替格瑞洛。本研究旨在比较氯吡格雷、普拉格雷和替格瑞洛在心肌梗死后患者中的抗血小板作用。在一项单中心注册研究中，通过血小板聚集仪检测心肌梗死后患者中氯吡格雷、普拉格雷和替格瑞洛的抗血小板作用。为了评估血小板聚集的整体能力，用血栓素受体激活肽（TRAP；32μM）诱导全血。为了特异性地量化 P2Y12 拮抗剂的作用，用 6.4μM 二磷酸腺苷（ADP）刺激全血。相对 ADP 诱导的聚集（r-ADP-agg）定义为 ADP-TRAP 比值，以反映个体的 P2Y12 依赖性血小板抑制程度。对 238 例患者的血小板功能进行了分析[氯吡格雷（n=58）、普拉格雷（n=65）、替格瑞洛（n=115）]。接受氯吡格雷治疗的患者 r-ADP-agg 为 35±14%，接受普拉格雷治疗的患者 r-ADP-agg 为 28±10%，接受替格瑞洛治疗的患者 r-ADP-agg 为 26±11%。与氯吡格雷相比，接受普拉格雷（p=0.0024）或替格瑞洛（p<0.0001）治疗的患者 r-ADP-agg 显著降低。接受普拉格雷和替格瑞洛的患者之间 r-ADP-agg 无显著差异（p=0.2559）。总之，与氯吡格雷相比，普拉格雷和替格瑞洛在心肌梗死后患者中提供了更强的血小板抑制作用。替格瑞洛与普拉格雷之间的血小板抑制作用无显著差异。（心肌梗死后接受抗血小板药物治疗的患者登记；DRKS00003146）。
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