The relation between CYP2C19 genotype and phenotype in stented patients on maintenance dual antiplatelet therapy.

Journal Article (Journal Article)

Both high platelet reactivity (HPR) and CYP2C19 genotyping have been proposed to stratify cardiovascular event risk and to personalize maintenance dual antiplatelet therapy (DAPT) in stented patients. However, how well CYP2C19 genotype correlates with HPR in patients on maintenance DAPT is less clear. We determined the association of CYP2C19 loss-of-function (*2) and gain-of-function (*17) allele status with platelet reactivity in 118 stented patients on DAPT ≥2 weeks and in 143 patients with stable coronary artery disease on aspirin therapy alone. Thirty-three percent and 39% carried at least 1 copy of *2 and *17 alleles, respectively. Neither allele was associated with platelet reactivity in patients on aspirin therapy alone. On DAPT, platelet aggregation was higher in those with *2 allele than noncarriers (P ≤ .01) but did not differ between those with the *17 allele and noncarriers. The prevalence of HPR using the 20 μM adenosine diphosphate-induced aggregation cutpoint was 34% in the total population: 26% in *1/*1 homozygotes, 49% in those with the *2 allele, and 20% in those with the *17 allele (P = .006). Determination of diplotype status enhanced identification of HPR. However, platelet function on DAPT is highly variable within diplotype groups. Therefore, CYP2C19 genotype and HPR are imperfect correlates of each other. Because both predict cardiovascular events with similar risk ratios, CYP2C19 genotyping and HPR may provide complementary information to stratify risk and personalized DAPT in stented patients than either alone.

Full Text

Duke Authors

Cited Authors

  • Gurbel, PA; Shuldiner, AR; Bliden, KP; Ryan, K; Pakyz, RE; Tantry, US

Published Date

  • March 2011

Published In

Volume / Issue

  • 161 / 3

Start / End Page

  • 598 - 604

PubMed ID

  • 21392617

Pubmed Central ID

  • PMC3061841

Electronic International Standard Serial Number (EISSN)

  • 1097-6744

Digital Object Identifier (DOI)

  • 10.1016/j.ahj.2010.12.011


  • eng

Conference Location

  • United States