Platelet Inhibition by Adjunctive Cilostazol Versus High Maintenance-Dose Clopidogrel in Patients With Acute Myocardial Infarction According to Cytochrome P450 2C19 Genotype

Abstract

Compared with high-MD clopidogrel, adjunctive cilostazol significantly enhances platelet inhibition and reduces the rate of HPR, especially in AMI patients with CYP2C19 loss-of-function variants. (Adjunctive Cilostazol Versus High Maintenance-Dose Clopidogrel in Acute Myocardial Infarction (AMI) Patients According to CYP2C19 Polymorphism [ACCELAMI2C19]; NCT00915733).

Optimizing Platelet Inhibition in Clopidogrel Poor Metabolizers

“…1). In this issue of JACC: Cardiovascular Interventions, the results of 3 independent investigations assessing these strategies among patients more prone to poorly metabolize clopidogrel based on the presence of CYP2C19 LOF alleles are reported and provide important insights on this ever-rising clinical quandary (5)(6)(7).…”

Tailored Adjunctive Cilostazol Therapy Based on CYP2C19 Genotyping in Patients With Acute Myocardial Infarction ― The CALDERA-GENE Study ―

“…23 Recent studies showed that the addition of cilostazol to DAPT (i.e., triple antiplatelet therapy) resulted in greater ADP-induced platelet inhibition compared with DAPT. 24- 27 The present finding suggested that adjunctive cilostazol therapy could be an alternative regimen for achieving enhanced platelet inhibition in carriers of CYP2C19 reduced-function alleles.…”

Cilostazol to Overcome High On-Treatment Platelet Reactivity in Korean Patients Treated With Clopidogrel and Calcium-Channel Blocker

“…14- 16 Compared with double-dose clopidogrel therapy (150 mg/day), TAPT was associated with a greater decrease in adenosine diphosphate (ADP)-induced platelet aggregation. 14, 15 The latter observation has been consistently observed in various high-risk clinical settings (ACS, diabetes, and complex PCI), including the carriage of the CYP2C19 loss-of-function allele. 15, 16 In addition, Yang et al 17 reported that platelets expressed the adenosine A2b receptor, which was upregulated under stress in vivo.…”