在日本稳定性冠状动脉疾病患者中，从维持性使用氯吡格雷转换为使用普拉格雷后血小板抑制作用增强。
Increased platelet inhibition after switching from maintenance clopidogrel to prasugrel in Japanese patients with stable coronary artery disease.
作者信息
Nishi Takeshi, Ariyoshi Noritaka, Nakayama Takashi, Fujimoto Yoshihide, Sugimoto Kazumasa, Takahara Masayuki, Wakabayashi Shinichi, Koshizaka Masaya, Hanaoka Hideki, Kobayashi Yoshio
机构信息
Department of Cardiovascular Medicine, Chiba University Graduate School of Medicine.
出版信息
Circ J. 2015;79(11):2439-44. doi: 10.1253/circj.CJ-15-0546. Epub 2015 Aug 27.
BACKGROUND
The pharmacodynamic effects of changing from standard-dose clopidogrel to low-dose (3.75 mg) prasugrel in Japanese patients are largely unknown.
METHODS AND RESULTS
A total of 53 consecutive Japanese patients with stable coronary artery disease (CAD) who received aspirin and clopidogrel were enrolled. Clopidogrel was switched to 3.75 mg prasugrel. At day 14, prasugrel was switched to 75 mg clopidogrel. Platelet reactivity was measured using the VerifyNow assay at baseline, day 14, and day 28. VerifyNow P2Y12 reaction units (PRU) >208 was defined as high on-treatment platelet reactivity (HPR). The prevalence of HPR (18.9% vs. 41.5% vs. 44.2%, P<0.001) and the PRU level (154.3±54.2 vs. 196.2±55.5 vs. 194.6±55.8, P<0.001) were significantly lower on prasugrel maintenance therapy compared with the clopidogrel therapy before and after switching. The CYP2C19 genotypes that account for the 3 phenotypes (ie, extensive metabolizer, intermediate metabolizer, and poor metabolizer) had a significant impact on platelet reactivity with clopidogrel (174.9±54.0 vs. 193.1±56.5 vs. 240.6±25.4 PRU, P<0.001) but not prasugrel (147.0±51.9 vs. 147.5±58.3 vs. 184.4±38.3 PRU, P=0.15).
CONCLUSIONS
Low-dose prasugrel achieves stronger platelet inhibition than clopidogrel in Japanese patients with stable CAD.
背景
在日本患者中，从标准剂量氯吡格雷转换为低剂量（3.75毫克）普拉格雷的药效学作用在很大程度上尚不明确。
方法与结果
连续纳入53例接受阿司匹林和氯吡格雷治疗的日本稳定性冠心病（CAD）患者。将氯吡格雷换用为3.75毫克普拉格雷。在第14天，将普拉格雷换用为75毫克氯吡格雷。在基线、第14天和第28天使用VerifyNow检测法测量血小板反应性。VerifyNow P2Y12反应单位（PRU）>208被定义为治疗中高血小板反应性（HPR）。与转换前后的氯吡格雷治疗相比，普拉格雷维持治疗时HPR的发生率（18.9%对41.5%对44.2%，P<0.001）和PRU水平（154.3±54.2对196.2±55.5对194.6±55.8，P<0.001）显著更低。解释3种表型（即广泛代谢者、中间代谢者和慢代谢者）的CYP2C19基因型对氯吡格雷的血小板反应性有显著影响（PRU分别为174.9±54.0对193.1±56.5对240.6±25.4，P<0.001），但对普拉格雷无显著影响（PRU分别为147.0±51.9对147.5±58.3对184.4±38.3，P=0.15）。
结论
在日本稳定性CAD患者中，低剂量普拉格雷比氯吡格雷能实现更强的血小板抑制作用。
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