TY - JOUR
T1 - Increased platelet inhibition after switching from maintenance clopidogrel to prasugrel in japanese patients with stable coronary artery disease
AU - Nishi, Takeshi
AU - Ariyoshi, Noritaka
AU - Nakayama, Takashi
AU - Fujimoto, Yoshihide
AU - Sugimoto, Kazumasa
AU - Takahara, Masayuki
AU - Wakabayashi, Shinichi
AU - Koshizaka, Masaya
AU - Hanaoka, Hideki
AU - Kobayashi, Yoshio
N1 - Publisher Copyright:
© 2015, Japanese Circulation Society. All rights reserved.
PY - 2015/10/23
Y1 - 2015/10/23
N2 - 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.
AB - 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.
KW - Clopidogrel
KW - Percutaneous coronary intervention
KW - Platelet resistance
KW - Prasugrel
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U2 - 10.1253/circj.CJ-15-0546
DO - 10.1253/circj.CJ-15-0546
M3 - Article
C2 - 26310876
AN - SCOPUS:84944750840
VL - 79
SP - 2439
EP - 2444
JO - Circulation Journal
JF - Circulation Journal
SN - 1346-9843
IS - 11
ER -