Copyright © 2002 by the European Society of Cardiology.
A study of platelet activation in atrial fibrillation and the effects of antithrombotic therapy
a Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK
b INSERM U.311, Etablissement Francais du Sang, Strasbourg, France
revised March 11, 2002; accepted March 13, 2002
Abstract
Background Platelet function may be abnormal in patients with atrial fibrillation (AF) and could be related to abnormal thrombogenesis. The aim of this cross-sectional study was to investigate new aspects of platelet biology in AF, predominantly focusing on platelet activation and the effects of concomitant antiplatelet and anticoagulant therapy.
Patients and Methods The study group of 238 patients were (i) 93 patients on no antithrombotic therapy, (ii) 60 patients taking 75–325mg aspirin/day, and (iii) 85 patients on dose-adjusted warfarin (International Normalised Ratio [INR] range 2·0–3·0). Results were compared with those from 50 age- and sex-matched normal subjects. Platelet markers (plasma ß-thromboglobulin, soluble glycoprotein V [both ELISA]), coagulation markers (fibrin D-dimer [ELISA] and fibrinogen [Clauss]), and platelet aggregation in response to standard platelet agonists were studied.
Results ß-thromboglobulin (P=0·01), soluble glycoprotein V (P<0·001) and fibrin D-dimer (P=0·002) were higher in untreated AF patients compared to healthy controls. AF patients on warfarin had lower fibrin D-dimer (P<0·001) when compared to AF patients on no therapy. Plasma fibrinogen and platelet aggregation was no different between patients with AF and healthy controls. Aspirin use was associated with reduced platelet aggregation response to epinephrine (P=0·01), whilst patients established on warfarin had significantly lower plasma fibrin D-dimer levels.
Conclusion AF patients exhibit changes in plasma markers of platelet function but no significant abnormalities of platelet aggregation. However, treatment with warfarin or aspirin failed to demonstrate any significant benefit on platelet activation, although warfarin use was associated with reduced thrombogenesis (fibrin D-dimer). We suggest that platelet activation may not play an important role in the pathogenesis of thromboembolism in AF. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.
Key Words: Atrial fibrillation, platelets, beta-thromboglobulin, soluble glycoprotein V, platelet aggregation, fibrin D-dimer.
f1 Correspondence: Professor G. Y. H. Lip, Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, B18 7QH, UK.
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