TY - JOUR
T1 - Platelet inhibition after loading dose of prasugrel in patients with ST-elevation and non-ST-elevation acute coronary syndrome
AU - Wakabayashi, Shinichi
AU - Kitahara, Hideki
AU - Nishi, Takeshi
AU - Sugimoto, Kazumasa
AU - Nakayama, Takashi
AU - Fujimoto, Yoshihide
AU - Ariyoshi, Noritaka
AU - Kobayashi, Yoshio
N1 - Funding Information:
Conflict of interest Dr. Kobayashi received research grant from Daiichi Sankyo (Tokyo, Japan). The other authors have no conflicts of interest to disclose.
Publisher Copyright:
© 2017, Japanese Association of Cardiovascular Intervention and Therapeutics.
PY - 2018/7/1
Y1 - 2018/7/1
N2 - The PRASFIT-ACS study showed the antiplatelet effect 2–4 h after prasugrel loading. However, there is little information about the antiplatelet effect <2 h after prasugrel loading dose, especially in patients with acute coronary syndrome (ACS). There had not been any comparison between ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation ACS (NSTE-ACS). Fifty patients with ACS (15 with STEMI and 35 with NSTE-ACS) were enrolled. They received a 20-mg prasugrel loading dose followed by a maintenance dose of 3.75 mg. Platelet reactivity [P2Y12 reaction units (PRU)] was evaluated by the VerifyNow assay at baseline, 30 min, 1, 2, 4, and 6 h, 1 week under prasugrel, and at 1 month after switching to clopidogrel. The primary end point was the change of PRU compared to the baseline. Furthermore, PRU after prasugrel loading between STEMI and NSTE-ACS was compared. A significant reduction in PRU from baseline was observed at ≥2 h after administration of prasugrel. In STEMI patients, a significant reduction in PRU was observed at 4 h after prasugrel loading. STEMI patients had higher PRU compared to NSTE-ACS patients at 2, 4, and 6 h after prasugrel loading. Utilizing >208 PRU as a cutoff value, STEMI patients had a higher prevalence of high on-treatment platelet reactivity at 2–6 h and 1 week after loading. Rapid antiplatelet effect is not achieved by low-dose prasugrel loading in STEMI patients. Platelet inhibition occurs earlier in NSTE-ACS patients, although it takes ≥2 h after loading in the majority of patients.
AB - The PRASFIT-ACS study showed the antiplatelet effect 2–4 h after prasugrel loading. However, there is little information about the antiplatelet effect <2 h after prasugrel loading dose, especially in patients with acute coronary syndrome (ACS). There had not been any comparison between ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation ACS (NSTE-ACS). Fifty patients with ACS (15 with STEMI and 35 with NSTE-ACS) were enrolled. They received a 20-mg prasugrel loading dose followed by a maintenance dose of 3.75 mg. Platelet reactivity [P2Y12 reaction units (PRU)] was evaluated by the VerifyNow assay at baseline, 30 min, 1, 2, 4, and 6 h, 1 week under prasugrel, and at 1 month after switching to clopidogrel. The primary end point was the change of PRU compared to the baseline. Furthermore, PRU after prasugrel loading between STEMI and NSTE-ACS was compared. A significant reduction in PRU from baseline was observed at ≥2 h after administration of prasugrel. In STEMI patients, a significant reduction in PRU was observed at 4 h after prasugrel loading. STEMI patients had higher PRU compared to NSTE-ACS patients at 2, 4, and 6 h after prasugrel loading. Utilizing >208 PRU as a cutoff value, STEMI patients had a higher prevalence of high on-treatment platelet reactivity at 2–6 h and 1 week after loading. Rapid antiplatelet effect is not achieved by low-dose prasugrel loading in STEMI patients. Platelet inhibition occurs earlier in NSTE-ACS patients, although it takes ≥2 h after loading in the majority of patients.
KW - Percutaneous coronary intervention
KW - Platelet resistance
KW - Prasugrel
KW - VerifyNow
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U2 - 10.1007/s12928-017-0475-8
DO - 10.1007/s12928-017-0475-8
M3 - Article
C2 - 28608310
AN - SCOPUS:85048812465
SN - 1868-4300
VL - 33
SP - 239
EP - 246
JO - Cardiovascular Intervention and Therapeutics
JF - Cardiovascular Intervention and Therapeutics
IS - 3
ER -