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普拉格雷治疗氯吡格雷治疗高反应性血小板和冠状动脉支架置入史患者的抗血小板疗效。

Antiplatelet efficacy of prasugrel in patients with high on-clopidogrel treatment platelet reactivity and a history of coronary stenting.

机构信息

Deutsches Herzzentrum, Medizinische Klinik Rechts der Isar, Technische Universität München, Munich, Germany.

出版信息

Thromb Haemost. 2013 Mar;109(3):517-24. doi: 10.1160/TH12-08-0552. Epub 2013 Jan 17.

DOI:10.1160/TH12-08-0552
PMID:23328965
Abstract

Little is known about the antiplatelet action of the 3 rd generation thienopyridine prasugrel in patients showing high platelet reactivity (PR) levels on clopidogrel. Thus, we aimed to determine the antiplatelet efficacy of prasugrel loading (LD) and maintenance dose (MD) treatment in a registry of patients with high PR levels on clopidogrel and a consecutive switch over to prasugrel in a setting of routine platelet function testing. In our registry of patients treated by percutaneous coronary intervention (n=73) with high levels of PR on clopidogrel, the ADP-induced platelet aggregation (PA, in AU x min) was assessed on a Multiplate analyser 1) after clopidogrel LD, 2) after prasugrel LD and 3) on prasugrel MD (5 vs. 10 mg/day). In patients with high PR levels on clopidogrel, prasugrel LD resulted in significantly lower PA values (574 [462-698] vs. 156 [89-234] AU x min; p<0.0001). Only 2.7% of patients showed high PR (HPR, ≥468 AU x min) following prasugrel LD. On prasugrel MD, PA was significantly higher as compared to prasugrel LD (248 [145-406] vs. 156 [89-234] AU x min; p<0.0001) with more patients showing HPR on MD vs. LD (16.4% vs. 2.7%; p=0.009). For prasugrel MD, HPR rates were higher in 5 vs. 10 mg/day treated patients (46.2% vs. 10.0%; p=0.006). In conclusion, for patients with high PR levels on clopidogrel, prasugrel LD abolished this status in the majority of patients. However, prasugrel response variability was detected, being more pronounced on prasugrel MD vs. LD treatment. The clinical impact of these findings warrants further investigation.

摘要

关于在氯吡格雷显示高血小板反应性 (PR) 水平的患者中第三代噻吩吡啶普拉格雷的抗血小板作用知之甚少。因此,我们旨在确定在常规血小板功能检测背景下,氯吡格雷高 PR 水平患者中普拉格雷负荷(LD)和维持剂量(MD)治疗的抗血小板疗效。在我们的经皮冠状动脉介入治疗(n=73)患者登记处中,氯吡格雷的 PR 水平较高,在 1)氯吡格雷 LD 后,2)普拉格雷 LD 后和 3)普拉格雷 MD 后(5 与 10mg/天),使用 Multiplate 分析仪评估 ADP 诱导的血小板聚集(PA,以 AU x min 表示)。在氯吡格雷 PR 水平较高的患者中,普拉格雷 LD 导致 PA 值显著降低(574[462-698]与 156[89-234]AU x min;p<0.0001)。只有 2.7%的患者在接受普拉格雷 LD 后显示高 PR(HPR,≥468 AU x min)。与普拉格雷 LD 相比,普拉格雷 MD 时 PA 明显更高(248[145-406]与 156[89-234]AU x min;p<0.0001),MD 时与 LD 时相比,更多患者显示 HPR(16.4%比 2.7%;p=0.009)。普拉格雷 MD 时,5mg/天与 10mg/天治疗患者的 HPR 率更高(46.2%比 10.0%;p=0.006)。总之,对于氯吡格雷 PR 水平较高的患者,普拉格雷 LD 使大多数患者消除了这种状态。然而,检测到普拉格雷反应的变异性,与 LD 治疗相比,MD 时更为明显。这些发现的临床意义需要进一步研究。

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