title: The relationship between on-clopidogrel platelet reactivity, genotype, and post-percutaneous coronary intervention outcomes in Chinese patients.
abstract: BACKGROUND
  High on-clopidogrel platelet reactivity reflects a poor response to clopidogrel and is associated with ischemic events, which has been attributed to several factors such as demographic, clinical characteristics and a polymorphism of CYP2C19. Some new platelet assays monitoring on-clopidogrel platelet reactivity are currently available in China, but their relevance to the CYP2C19 genotype and post-percutaneous coronary intervention outcomes remain to be elucidated.
  
  
  METHODS
  Patients were prospectively included if they had a successful percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) and received clopidogrel and aspirin. CYP2C19 loss-of function genotype, adenosine diphosphate (ADP)-induced maximum platelet aggregation rate (MPA ADP) measured by light transmittance aggregometry, ADP-induced platelet-fibrin clot strength (MA ADP) measured by thrombelastography, platelet reactivity index (PRI) measured by vasodilator-stimulated phosphoprotein phosphorylation (VASP), and the occurrence of 6-month major adverse cardiovascular events (MACE) were assessed in 178 patients.
  
  
  RESULTS
  High on-treatment platelet reactivity prevalence defined by MPA ADP > 46.0%, MA ADP > 47 mm and PRI > 50.0% was 27.0%, 24.2%, and 61.2%, respectively. ADP-specific assays (VASP PRI) differed according to CYP2C19 genotype, with a significant gene-dose effect (PMs > IMs > EMs, p < 0.05). Multivariate analysis showed MPA ADP > 46.0% and MA ADP > 47 mm to be independent predictors of MACE at 6 months.
  
  
  CONCLUSIONS
  CYP2C19 loss-of function genotypes with the *2 and/or *3 allele are highly prevalent in the Chinese population and are associated with higher residual platelet reactivity. High on-treatment platelet reactivity defined by MPA ADP or MA ADP predicts an increased risk of MACE for ACS patients undergoing PCI.
authors.affiliation: Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, Hubei 430030 , China.
authors.forename: Ning
authors.initials: N
authors.lastname: Tang
authors.forename: Shiyu
authors.initials: S
authors.lastname: Yin
authors.forename: Ziyong
authors.initials: Z
authors.lastname: Sun
authors.forename: Xiangdong
authors.initials: X
authors.lastname: Xu
authors.forename: Jin
authors.initials: J
authors.lastname: Qin
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000188:drug therapy* / Q000235:genetics / Q000628:therapy; D000368:Aged; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D002681:China; D000077144:Clopidogrel; D003131:Combined Modality Therapy; D065731:Cytochrome P-450 CYP2C19 / Q000235:genetics; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D013988:Ticlopidine
keywords: Acute coronary syndrome; CYP2C19; clopidogrel; platelet function assay