Optimal cutoff value of P2Y12 reaction units to prevent major adverse cardiovascular events in the acute periprocedural period: Post-hoc analysis of the randomized PRASFIT-ACS study

Masato Nakamura, Takaaki Isshiki, Takeshi Kimura, Hisao Ogawa, Hiroyoshi Yokoi, Shinsuke Nanto, Morimasa Takayama, Kazuo Kitagawa, Yasuo Ikeda, Shigeru Saito
2015 International Journal of Cardiology  
Few studies have examined the effects of on-treatment platelet reactivity on the risk of major adverse cardiovascular events (MACE). We aimed to determine the optimal cutoff value of P2Y 12 reaction units (PRUs) to prevent MACE occurring within 3 days after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). Methods: We performed post-hoc analyses of 1363 patients enrolled in PRASFIT-ACS, which compared the effects of a prasugrel regimen adjusted for Japanese patients
more » ... apanese patients (loading dose/maintenance dose: 20 mg/3.75 mg) with those of clopidogrel (300 mg/75 mg) on MACE and bleeding events for 24-48 weeks after PCI in ACS patients. PRU was serially measured using the VerifyNow® P2Y 12 assay and we assessed the relationship between PRU and MACE. Results: Receiver operating characteristic curve analysis showed that PRU ≤262 at 5-12 h after ADP receptor antagonist loading was the optimal cutoff value for preventing MACE at up to 3 days after PCI. The incidences of MACE were 5.2% and 10.8% in patients with PRU ≤262 or N 262, respectively (odds ratio 0.50, 95% confidence interval 0.25-0.99, p b 0.01). Significantly more prasugrel-treated patients had lower on-treatment platelet reactivity (defined as PRU ≤ 262) compared with clopidogrel-treated patients (79.9% vs. 30.4%, p b 0.0001). Similar differences were observed between the prasugrel and clopidogrel groups for patients with normal or reducedfunction CYP2C19 alleles. Conclusions: The optimal PRU cutoff value for preventing MACE was 262 in Japanese ACS patients. Prasugrel rapidly reduced PRU with a large proportion of patients having low on-treatment platelet reactivity.
doi:10.1016/j.ijcard.2015.01.026 pmid:25679803 fatcat:gveswbz5uvahhjmxzqlg2el4c4