title: Platelet adhesion in atrial fibrillation.
abstract: BACKGROUND
  Increased platelet activation has been reported in nonvalvular atrial fibrillation (AF) but it remains unclear whether or not this is due to the underlying cardiovascular diseases, clinical subtype of AF and the influence of anti-thrombotic therapy.
  
  
  METHODS
  Platelet adhesion in AF patients was assessed using a 'platelet adhesion assay', and compared to both 'healthy controls' and 'disease controls' (patients with hypertension, coronary artery disease, diabetes or stroke but in sinus rhythm).
  
  
  RESULTS
  AF patients on no anti-thrombotic treatment (N=20) had increased platelet adhesion compared to 'healthy controls' (N=57) (p=0.044). Initiating treatment with both aspirin and warfarin resulted in significant reduction in platelet adhesion in AF patients (p=0.014 and 0.019 respectively). AF patients on optimal anti-thrombotic therapy (N=98) had no significant difference in platelet adhesion compared to 'healthy controls' and 'disease controls' (p=0.312). Platelet adhesion failed to distinguish between 'high-risk' (i.e. CHADS score > or = 2) and 'low-risk' (i.e. CHADS score < 2) AF patients (p=0.352). Amongst the clinical parameters that contribute to increased stroke risk in AF, platelet adhesion was only correlated with age (r=0.215, p=0.034), and not with other stroke risk factors. There was no significant difference in platelet adhesion between paroxysmal and permanent AF (p=0.618).
  
  
  CONCLUSIONS
  There is a significant, albeit weak, excess of platelet adhesion in AF patients on no anti-thrombotic therapy compared to 'healthy controls'. In optimally treated AF patients, platelet adhesion is not different to both 'healthy' and 'disease controls'. It is possible that abnormal platelet adhesion does not significantly contribute to the increased risk of stroke and thromboembolism that persists despite anti-thrombotic treatment in AF or in identifying 'high-risk' AF patients.
authors.affiliation: Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK.
authors.forename: Anirban
authors.initials: A
authors.lastname: Choudhury
authors.forename: Irene
authors.initials: I
authors.lastname: Chung
authors.forename: Andrew
authors.initials: A
authors.lastname: Blann
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000367:Age Factors; D000368:Aged; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000097:blood*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010973:Platelet Adhesiveness / Q000187:drug effects / Q000502:physiology*; D012307:Risk Factors; D014859:Warfarin / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D014859:Warfarin; D001241:Aspirin