title: Impact of anemia on platelet response to clopidogrel in patients undergoing percutaneous coronary stenting.
abstract: High residual platelet reactivity (HRPR) on clopidogrel is a predictor of recurrent ischemic events in patients undergoing percutaneous coronary interventions (PCI). Significant intraindividual variability in platelet aggregation on repeat testing has been reported. To understand factors contributing to the variability in platelet aggregation testing, we examined clinical and laboratory elements linked to HRPR in 255 consecutive patients tested ≥12 hours after PCI using light transmission aggregometry (LTA) in response to adenosine diphosphate 5 μmol/L and VerifyNow P2Y12 assay (VNP2Y12; Accumetrics). HRPR was defined as >46% residual aggregation for LTA and >236 P2Y12 response units (PRUs) for VNP2Y12. On multivariate analysis the only variable independently associated with HRPR with both LTA and VNP2Y12 was laboratory-defined anemia. Prevalences of HRPR by LTA were 34.3% in anemic patients, 15.6% in patients with normal hemoglobin levels, and 59.8% versus 25.9% by VNP2Y12 (p <0.005 for the 2 comparisons). In a subgroup of 50 patients, testing was done before and after the clopidogrel loading dose. At baseline there were no differences in platelet aggregation with either assay; however, absolute decrease in reactivity after the clopidogrel load was significantly less in anemic patients compared to patients with normal hemoglobin (change in residual aggregation by LTA 15.8 ± 5.8% vs 28.8 ± 3.2%, p <0.05; change in PRU by VNP2Y12 56.5 ± 35.5 vs 145.0 ± 14.2 PRUs, p <0.05, respectively). In conclusion, anemia is an important contributor to apparent HRPR on clopidogrel and may explain some of the intraindividual variability of platelet aggregation testing.
authors.affiliation: Heart and Vascular Institute, University of Pittsburgh Medical Center, Pennsylvania, USA. tomac@upmc.edu
authors.forename: Catalin
authors.initials: C
authors.lastname: Toma
authors.forename: Firas
authors.initials: F
authors.lastname: Zahr
authors.forename: Diego
authors.initials: D
authors.lastname: Moguilanski
authors.forename: Sheree
authors.initials: S
authors.lastname: Grate
authors.forename: Roy W
authors.initials: RW
authors.lastname: Semaan
authors.forename: Nicole
authors.initials: N
authors.lastname: Lemieux
authors.forename: Joon S
authors.initials: JS
authors.lastname: Lee
authors.forename: Andrea
authors.initials: A
authors.lastname: Cortese-Hassett
authors.forename: Suresh
authors.initials: S
authors.lastname: Mulukutla
authors.forename: Sunil V
authors.initials: SV
authors.lastname: Rao
authors.forename: Oscar C
authors.initials: OC
authors.lastname: Marroquin
mesh_terms: D000244:Adenosine Diphosphate; D000368:Aged; D000740:Anemia / Q000097:blood*; D015906:Angioplasty, Balloon, Coronary; D000077144:Clopidogrel; D005260:Female; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests / Q000379:methods; D011446:Prospective Studies; D012042:Registries; D015607:Stents; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D006454:Hemoglobins; D010975:Platelet Aggregation Inhibitors; D000244:Adenosine Diphosphate; D000077144:Clopidogrel; D013988:Ticlopidine