Thromb Haemost 2013; 109(02): 177-178
DOI: 10.1160/TH12-12-0910
Invited Editorial Focus
Schattauer GmbH

High on-treatment platelet reactivity (HPR): What does it mean, and does it matter?

Shinya Goto
1   Department of Medicine (Cardiology), Tokai University School of Medicine, Isehara, Kanagawa, Japan
,
Aiko Tomiya
2   Department of Metabolic Systems Medicine, the Medical Institute of Medicine, Japan
› Author Affiliations
Further Information

Publication History

Received: 08 December 2012

Accepted: 07 January 2013

Publication Date:
29 November 2017 (online)

 

 
  • References

  • 1 Saucedo J, Angiolillo DJ, Deraad R. et al. for the SWAP Investigators.. Decrease in high on-treatment platelet reactivity (HPR) prevalence on switching from clopidogrel to prasugrel: insights from the switching anti-platelet (SWAP) study. Thromb Haemost 2013; 109: 347-355.
  • 2 CAPRIE Steering Committee.. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996; 348: 1329-1339.
  • 3 Hollopeter G, Jantzen HM, Vincent D. et al. Identification of the platelet ADP receptor targeted by antithrombotic drugs. Nature 2001; 409: 202-207.
  • 4 Bal Dit Sollier C, Berge N, Boval B. et al. Functional variability of platelet response to clopidogrel correlates with P2Y(12) receptor occupancy. Thromb Haemost 2009; 101: 116-122.
  • 5 Cattaneo M. Bleeding manifestations of congenital and drug-induced defects of the platelet p2y12 receptor for adenosine diphosphate. Thromb Haemost 2011; 105 (Suppl. 01) S67-74.
  • 6 Pereillo JM, Maftouh M, Andrieu A. et al. Structure and stereochemistry of the active metabolite of clopidogrel. Drug Metab Dispos 2002; 30: 1288-1295.
  • 7 Savi P, Pereillo JM, Uzabiaga MF. et al. Identification and biological activity of the active metabolite of clopidogrel. Thromb Haemost 2000; 84: 891-896.
  • 8 Goto S, Tamura N, Eto K. et al. Functional significance of adenosine 5‘-diphosphate receptor (p2y(12)) in platelet activation initiated by binding of von willebrand factor to platelet gp ibalpha induced by conditions of high shear rate. Circulation 2002; 105: 2531-2536.
  • 9 Goto S, Ikeda Y, Murata M. et al. Epinephrine augments von willebrand factor-dependent shear-induced platelet aggregation. Circulation 1992; 86: 1859-1863.
  • 10 Goto S, Sakai H, Goto M. et al. Enhanced shear-induced platelet aggregation in acute myocardial infarction. Circulation 1999; 99: 608-613.
  • 11 Serebruany VL. Viewpoint: paradoxical excess mortality in the PLATO trial should be independently verified. Thromb Haemost 2011; 105: 752-759.
  • 12 Wallentin L, Becker RC, James SK. et al. The PLATO trial reveals further opportunities to improve outcomes in patients with acute coronary syndrome. Thromb Haemost 2011; 105: 760-762.
  • 13 Ohman EM, Roe MT. Explaining the unexpected: insights from the PLATelet inhibition and clinical Outcomes (PLATO) trial comparing ticagrelor and clopidogrel. Thromb Haemost 2011; 105: 763-765.
  • 14 Serebruany VL, Atar D. Viewpoint: Central adjudication of myocardial infarction in outcome-driven clinical trials--common patterns in TRITON, RECORD, and PLATO?. Thromb Haemost 2012; 108: 412-414.
  • 15 Verheugt FW. Outcomes of positive randomised controlled clinical trials: double-blind or double vision?. Thromb Haemost 2012; 108: 410-411.
  • 16 Serebruany VL. Viewpoint: Reversible nature of platelet binding causing transfusion-related acute lung injury (TRALI) syndrome may explain dyspnea after ticagrelor and elinogrel. Thromb Haemost 2012; 108: 1024-1027.
  • 17 Schrör K. ‘Reversible nature of platelet binding causing transfusion-related acute lung injury (TRALI) syndrome may explain dyspnea after ticagrelor and elinogrel’ - a hypothesis that remains unproven. Thromb Haemost 2012; 108: 1028-1030.
  • 18 Gurbel PA, Roe MT, Jakubowski JA. et al. Translational platelet research in patients with coronary artery disease: what are the major knowledge gaps?. Thromb Haemost 2012; 108: 12-20.