University of Oklahoma Health Sciences Center, 920 Stanton L Young Blvd, WP 3010, Oklahoma City, OK 73104, USA.
Thromb Haemost. 2013 Feb;109(2):347-55. doi: 10.1160/TH12-06-0378. Epub 2012 Dec 6.
The prevalence of high platelet reactivity (HPR) in patients who have switched from clopidogrel to prasugrel during maintenance phase after an acute coronary syndrome (ACS) event is unknown. Therefore, the effect of switching from clopidogrel to prasugrel on the prevalence of HPR was evaluated. This analysis from the previously reported SWAP (SWitching Anti Platelet) study assessed HPR at baseline, 2 and 24 hours, and seven days after switching from clopidogrel to prasugrel maintenance dose (MD), with or without a prasugrel loading dose (LD) using four definitions: maximum platelet aggregation (MPA) >65% (primary endpoint), MPA >50%, P2Y12 reaction units (PRU) >235, and platelet reactivity index (PRI) ≥ 50%. A total of 95 patients were available for analysis; 56 patients provided DNA for genetic assessments of cytochrome P450 (CYP) 2C19. There were 26 (27.4%) patients with HPR at the end of the clopidogrel run-in (defined as MPA >65%). The HPR prevalence varied by each definition and ranged from 19% (PRU >235) to 68% (PRI ≥ 50 %). A significantly higher HPR prevalence was observed during clopidogrel versus the combined prasugrel therapy groups at seven days as measured by MPA >65% (21.2% vs. 4.5%, p<0.05), PRU >235 (18.8% vs. 0%, p=0.001), and PRI ≥ 50 % (66.7% vs. 7.9%, p<0.0001). There was a significantly higher percentage of subjects carrying at least one reduced function allele with HPR measured by MPA >65% (p=0.02) or PRU >235 (p=0.05) than non-carriers with HPR. Switching ACS patients during maintenance clopidogrel therapy to prasugrel with or without an LD is associated with a reduced HPR prevalence and may provide an alternative strategy to treat patients with HPR, independent of CYP2C19 genotype.
在急性冠脉综合征（ACS）事件后维持治疗期间从氯吡格雷转换为普拉格雷的患者中，高血小板反应性（HPR）的发生率尚不清楚。因此，评估了从氯吡格雷转换为普拉格雷对 HPR 发生率的影响。这项来自先前报道的 SWAP（SWitching Anti Platelet）研究的分析评估了从氯吡格雷转换为普拉格雷维持剂量（MD）后 2 小时和 24 小时以及 7 天时的 HPR，有无普拉格雷负荷剂量（LD），使用了四种定义：最大血小板聚集（MPA）＞65%（主要终点）、MPA＞50%、血小板二磷酸腺苷受体（P2Y12）反应单位（PRU）＞235 和血小板反应指数（PRI）≥50%。共有 95 名患者可进行分析；56 名患者提供了细胞色素 P450（CYP）2C19 的基因评估 DNA。在氯吡格雷洗脱期结束时，有 26 名（27.4%）患者存在 HPR（定义为 MPA＞65%）。HPR 的发生率因每种定义而异，范围为 19%（PRU＞235）至 68%（PRI≥50%）。在氯吡格雷洗脱期结束时，与联合普拉格雷治疗组相比，在第 7 天时，通过 MPA＞65%（21.2%比 4.5%，p＜0.05）、PRU＞235（18.8%比 0%，p=0.001）和 PRI≥50%（66.7%比 7.9%，p＜0.0001），HPR 的发生率显著更高。与非 HPR 携带者相比，用 MPA＞65%（p=0.02）或 PRU＞235（p=0.05）测量存在至少一个功能降低等位基因的患者中 HPR 的百分比显著更高。在维持氯吡格雷治疗期间将 ACS 患者从氯吡格雷转换为普拉格雷，无论 CYP2C19 基因型如何，与 HPR 发生率降低相关，可能为治疗 HPR 患者提供了另一种策略。
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