Using Platelet Function Testing to Guide Antiplatelet Therapy

Authors

  • Matthew D. Linden

    Corresponding author
    1. The Centre for Microscopy, Characterisation and Analysis, The University of Western Australia, Nedlands, WA, Australia
    • Correspondence to: Matthew D. Linden, M510, The Centre for Microscopy, Characterisation and Analysis, The University of Western Australia, 35 Stirling Highway, Nedlands 6009, Western Australia, Australia.

      E-mail: matthew.linden@uwa.edu.au

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ABSTRACT

Clinical Development Phases I-III Regulatory, Quality, Manufacturing

Platelets are subcellular fragments in blood whose activation is central to atherothrombosis and cardiovascular events. Platelet activation is complex, with multiple pathways of initiation and amplification involved. Antiplatelet drugs may target any of these pathways to diminish the propensity of platelets to become activated. The most well-established antiplatelet drugs, aspirin and thienopyridines, target the thromboxane and adenosine diphosphate auto-amplification pathways of platelet activation, respectively. These are very effective medicines, but response varies and residual on-treatment platelet function is associated with poorer clinical outcomes. Alternative antiplatelet therapies are available and more are in development. Therefore, tailoring antiplatelet therapy to on-treatment platelet activation is an appealing strategy and the subject of investigation. There are many different approaches to measuring platelet activation and response to stimulation with antiplatelet therapy, but there is very little agreement between them regardless of the cutoffs used. Therefore, selection of the appropriate platelet function test is important in assessing on-treatment platelet activation for guided therapy. Recent research has shown that tailoring antiplatelet therapy can improve these laboratory measures of platelet activation, but clinical studies that assess cardiovascular benefit against potential for increased bleeding are required.

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