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Emergence of the concept of platelet reactivity monitoring of response to thienopyridines
  1. L Bonello1,2,3,
  2. A De Labriolle1,
  3. M Scheinowitz1,
  4. G Lemesle4,
  5. P Roy1,
  6. D H Steinberg1,
  7. T L Pinto Slottow1,
  8. R Pakala1,
  9. A D Pichard1,
  10. P Barragan5,
  11. L Camoin-Jau3,
  12. F Dignat-George3,
  13. F Paganelli2,
  14. R Waksman1
  1. 1
    Department of Internal Medicine, Division of Cardiology, Washington Hospital Center, Washington DC, USA
  2. 2
    Département de Cardiologie, Hopital Universitaire Nord de Marseille, Marseille, France
  3. 3
    Laboratoire d’Hématologie, Unite Inserm UMRS 608, UFR de Pharmacie, Hopital de la Conception, Marseille, France
  4. 4
    Service de Cardiologie B et Centre Hémodynamique, Hopital Cardiologique, Centre Hospitalier Regional et Universitaire de Lille, Lille, France
  5. 5
    Département de Cardiologie, Clinique les fleurs, Ollioules, France
  1. Dr R Waksman, Washington Hospital Center, 110 Irving Street, NW, Suite 4B-1, Washington, DC 20010, USA; ron.waksman{at}medstar.net

Abstract

Clinical trials have demonstrated the beneficial impact of clopidogrel in preventing major adverse cardiovascular events (MACE), particularly in patients undergoing percutaneous coronary intervention (PCI). The concept of biological clopidogrel resistance emerged with the finding of persistent platelet activation despite clopidogrel therapy in some patients. Further, a link between biological clopidogrel resistance and thrombotic recurrence after PCI was observed and a threshold of platelet reactivity (PR) for thrombotic events was suggested. Consistently, in recent trials, enhanced PR inhibition translated into a reduction in the rate of MACE after PCI. This review aims to present the emergence of the concept of PR monitoring in patients undergoing PCI following recent advances in this field.

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Footnotes

  • Competing interests: None.

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