Thromb Haemost 2014; 111(02): 266-272
DOI: 10.1160/TH13-06-0508
Platelets and Blood Cells
Schattauer GmbH

Third generation P2Y12 antagonists inhibit platelet aggregation more effectively than clopidogrel in a myocardial infarction registry

Authors

  • Christoph B. Olivier

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany
  • Philipp Diehl

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany
  • Katharina Schnabel

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany
  • Patrick Weik

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany
  • Qian Zhou

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany
  • Christoph Bode

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany
  • Martin Moser

    1   Heart Center Freiburg University, Cardiology and Angiology I, Freiburg, Germany

Financial support: This work was supported by a grant from the Deutsche Forschungsgemeinschaft (OL 371/1–1 to Christoph B. Olivier).
Further Information

Publication History

Received: 23 June 2013

Accepted after major revision: 20 September 2013

Publication Date:
27 November 2017 (online)

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Summary

The current standard of antiplatelet therapy of patients after myocardial infarction includes the P2Y12 receptor antagonists clopidogrel, prasugrel or ticagrelor. This study aimed to compare the antiplatelet effect of clopidogrel, prasugrel and ticagrelor in patients after myocardial infarction. In a single-centre registry the antiplatelet effect of clopidogrel, prasugrel and ticagrelor was investigated by aggregometry in patients after myocardial infarction. To assess the overall capacity of platelet aggregation whole blood was induced with thrombin receptor activating peptide (TRAP; 32 μM). To specifically quantify the effect of P2Y12 antagonists, whole blood was stimulated with 6.4 μM adenosine diphophosphate (ADP). Relative ADP induced aggregation (r-ADP-agg) was defined as the ADP-TRAP ratio to reflect an individual degree of P2Y12-dependent platelet inhibition. Platelet function of 238 patients was analysed [clopidogrel (n=58), prasugrel (n=65), ticagrelor (n=115)]. The r-ADP-agg was 35 ± 14% for patients receiving clopidogrel, 28 ± 10% for patients receiving prasugrel and 26 ± 11% for patients receiving ticagrelor. The r-ADP-agg was significantly lower in patients treated with prasugrel (p=0.0024) or ticagrelor (p<0.0001) compared to clopidogrel. There was no significant difference between patients receiving prasugrel or ticagrelor (p=0.2559). In conclusion, prasugrel and ticagrelor provide a stronger platelet inhibition compared to clopidogrel in patients after myocardial infarction. No significant difference in platelet inhibition was detected between prasugrel and ticagrelor. (registry for patients after Myocardial Infarction Treated with AntiPlatelet agents; DRKS00003146).