Lund University is celebrating 350 years. Read more on lunduniversity.lu.se

Menu

Javascript is not activated in your browser. This website needs javascript activated to work properly.
You are here

Assessment of P2Y(12) inhibition with the point-of-care device VerifyNow P2Y12 in patients treated with prasugrel or clopidogrel coadministered with aspirin

Author:
  • Christoph Varenhorst
  • Stefan James
  • David Erlinge
  • Oscar Braun
  • John T. Brandt
  • Kenneth J. Winters
  • Joseph A. Jakubowski
  • Sylvia Olofsson
  • Lars Wallentin
  • Agneta Slegbahn
Publishing year: 2009
Language: English
Publication/Series: American Heart Journal
Volume: 157
Issue: 3
Document type: Journal article
Publisher: Mosby

Abstract english

Background Variability in response to thienopyridines has led to the development of point-of-care devices to assess adenosine diphosphate (ADP)-induced platelet aggregation. These tests need to be evaluated in comparison to reference measurements of P2Y(12) function during different thienopyridine treatments. Methods After a run-in on 75 mg aspirin, I 10 subjects were randomized to double-blind treatment with clopidogrel 600 mg loading dose (LD)/75 mg maintenance dose (MD) or prasugrel 60 mg LD/10 mg MD. Antiplatelet effects were evaluated by VerifyNow P2Y12 (VN-P2Y12) device (Accumetrics, San Diego, CA), vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay, and light transmission aggregometry (LTA). Prasugrel's and clopidogrel's active metabolite concentration were also determined. Results Dose- and time-dependent inhibition of P2Y(12) was evident with VN-P2Y12. There was strong correlation with VN-P2Y12 and VASP or LTA for all treatments through a wide range of P2Y(12) function. At high levels of P2Y(12) inhibition, platelet function measured by VN-P2Y12 was maximally inhibited and could not reflect further changes seen with VASP or LTA methods. Correlation was also observed between exposure to clopidogrel's active metabolite and VN-F`2Y12 during MD and LD, whereas it was observed only with prasugrel MD. Conclusion The VN-P2Y12 correlated strongly with inhibition of P2Y(12) function, as measured with either VASP or LTA. VN-P2Y12 also correlated to exposure to the active metabolite of prasugrel and clopidogrel up to levels associated with assumed saturation of the P2Y(12) receptor. (Am Heart J 2009; 1 57:562.e1-562.e9.)

Keywords

  • Cardiac and Cardiovascular Systems

Other

Published
  • ISSN: 1097-6744
E-mail: oscar [dot] braun [at] med [dot] lu [dot] se

Physician

Cardiology

+46 46 17 36 90

32

Project manager

Heart Failure and Mechanical Support

+46 46 17 36 90

32

Research project participant

Molecular Epidemiology and Cardiology

32

Lund University Diabetes Centre, CRC, SUS Malmö, Entrance 72, House 91:12. SE-205 02 Malmö. Telephone: +46 40 39 10 00