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Clopidogrel resistance is more important in acute myocardial infarction (AMI). We investigated high on-treatment platelet reactivity (HTPR) in acute coronary syndrome (ACS).
Forty-six ACS patients undergoing percutaneous coronary intervention (PCI) were screened with CYP 2C19 *2, *3 loss-of-function (LOF) polymorphism and VerifyNow P2y12 assay at least 24 hours after clopidogrel 600mg loading, defining high on-treatment platelet reactivity (HTPR) as platelet reaction unit (PRU)>230. According to genotyping and VerifyNow, we decided on anti-platelet agents. Those with homozygous LOF allele and HTPR, we switched clopidogrel over to prasugrel (10mg/day) (Group 1). And, those with normal genotyping (*1*1) and normal platelet function (PRU<230), we maintained clopidogrel (75mg/day) (Group 4). Those with heterozygous LOF allele and HTPR, homozygous LOF allele and normal platelet function, and normal genotyping and HTPR were randomized to prasugrel (10mg/day) (Group 2) or clopidogrel (75mg/day) (Group 3). We checked VerifyNow again 1 month later. Among clopidogrel group (Group 3 and 4), we compared PRU between AMI (N=16) and unstable angina (UA) (N=9).
After 1 month, among clopidogrel group, PRU value decreased less in AMI than UA. (PRU 191±90 to 176±70 vs. 204±55 to 141±83; p (of Δ) = 0.034). And, there were decreases of HTPR patients in both groups (5/16 to 4/16 vs. 3/9 to 1/9).
Our study showed that there was unmet needs of clopidogrel in AMI compared with UA about HTPR. And, there was additional decrease of PRU after 1 month clopidogrel administration compared with baseline loading status in ACS.