Longitudinal assessment of von Willebrand factor antigen and von Willebrand factor propeptide in response to alteration of antiplatelet therapy after TIA or ischaemic stroke
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The impact of commencing or changing antiplatelet therapy on von Willebrand factor antigen (VWF:Ag) and von Willebrand factor propeptide (VWF:Ag II) levels has not been comprehensively assessed following TIA or ischaemic stroke. In this pilot, longitudinal, observational analytical study, VWF:Ag and VWF:Ag II levels were simultaneously quantified in platelet poor plasma by ELISA in patients within 4 weeks of TIA or ischaemic stroke (baseline), and then 14 days (14d) and >90 days (90d) after altering antiplatelet therapy. Ninety-one patients were recruited. Eighteen were initially assessed on no antiplatelet therapy, and then after 14d (N = 17) and 90d (N = 8) on aspirin monotherapy; 21 patients were assessed on aspirin and after 14d and 90d on clopidogrel; 52 were assessed on aspirin monotherapy, and after 14d and 90d on aspirin and dipyridamole combination therapy. VWF:Ag, VWF:Ag II levels and VWF:Ag/VWF:Ag II ratio were unchanged at 14d and 90d in the overall study population (p ≥ 0.1). VWF:Ag and VWF:Ag II levels remained stable at 14d and 90d after commencing aspirin (p ≥ 0.054), and after changing from aspirin to clopidogrel (p ≥ 0.2). Following the addition of dipyridamole MR to aspirin, there was a significant reduction in VWF:Ag levels at 14d (p = 0.03) and 90d (p = 0.005), but not in VWF:Ag II levels (p ≥ 0.3). The addition of dipyridamole to aspirin led to a persistent reduction in VWF:Ag but not in VWF:Ag II levels, suggesting that dipyridamole may inhibit release of platelet-derived VWF:Ag following TIA or ischaemic stroke.
Keywordsvon Willebrand factor von Willebrand factor propeptide TIA Stroke Aspirin Dipyridamole Clopidogrel High on treatment platelet reactivity
Dr. Tobin’s research was funded by the IICN-Serono Fellowship, Meath Foundation, Lundbeck Neurosciences Bursary programme, and by unrestricted educational grant funding from Merck Serono Ireland, Brennan and Company, Ireland, and Biogen Idec Ireland Limited. Dr. Kinsella’s research was funded by the Stanley Thomas Johnson Foundation, and by unrestricted educational grant funding from Bayer Schering Ireland, Pfizer Ireland and Elitech UK. Dr. Kavanagh’s research was funded by the Health Research Board Ireland. Dr. McCabe’s research programme was part-funded by grant support from the Programme for Research in Third Level Institutions in Ireland (Cycle 4), co-funded by the European Regional Development Fund.
Conflicts of interest
None of the authors report any conflicts of interest or other disclosures. None of the above charities or funding bodies had any influence on study design or conduct, data analysis or interpretation, or had any influence on the decision to submit the final manuscript for publication.
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