title: Do atrial differences in endothelial damage, leukocyte and platelet activation, or tissue factor activity contribute to chamber-specific thrombogenic status in patients with atrial fibrillation?
abstract: BACKGROUND
  Thrombi form mainly in the left rather than the right atria of patients with atrial fibrillation (AF), the reason of this predilection being unknown.
  
  
  OBJECTIVE
  The purpose of this study was to investigate whether atrial-specific differences in endothelial damage, leukocyte activation, platelet stimulation, and tissue factor activity occur in patients with AF.
  
  
  METHODS
  Twenty-two patients (16 men, 6 women; age 56 ± 8 years; 16 paroxysmal AF, 6 persistent AF) with AF undergoing pulmonary vein isolation were investigated. Blood samples from the left and the right atrium were obtained at the start of the procedure. Microparticles (MPs) released by apoptotic/stimulated cells were measured by capture assays. Their procoagulant abilities were quantified by functional prothrombinase and tissue factor assays and their cellular origin were determined (endothelium, platelet, leukocyte). Platelet reactivity was evaluated by whole blood flow cytometry for expression of platelet P-selectin (CD62P), active glycoprotein IIb/IIIa receptor (PAC-1). Platelet aggregation was evaluated using ADP, TRAP and collagen-induced whole blood aggregometry.
  
  
  RESULTS
  There were no atrial-specific differences in the levels of total procoagulant MPs, leukocyte-derived-MPs or platelet-derived MPs. Conversely, endothelial-derived MPs and tissue factor activity and collagen-induced platelet aggregation were slightly elevated in the right atrium (P < 0.05).
  
  
  CONCLUSIONS
  Our data show no evidence for increased thrombogenic status in the left atrium that would account for its greater propensity for thrombus formation in patients with AF.
authors.affiliation: University of Strasbourg, EA7293 Stress vasculaire et tissulaire, Strasbourg, France.
authors.forename: Laurence
authors.initials: L
authors.lastname: Jesel
authors.forename: Thomas
authors.initials: T
authors.lastname: Arentz
authors.forename: Claudia
authors.initials: C
authors.lastname: Herrera-Siklody
authors.forename: Dietmar
authors.initials: D
authors.lastname: Trenk
authors.forename: Fatiha
authors.initials: F
authors.lastname: Zobairi
authors.forename: Malak
authors.initials: M
authors.lastname: Abbas
authors.forename: Reinhold
authors.initials: R
authors.lastname: Weber
authors.forename: Jan
authors.initials: J
authors.lastname: Minners
authors.forename: Florence
authors.initials: F
authors.lastname: Toti
authors.forename: Olivier
authors.initials: O
authors.lastname: Morel
mesh_terms: D001281:Atrial Fibrillation / Q000097:blood / Q000175:diagnosis*; D055252:Cell-Derived Microparticles / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000502:physiology*; D013925:Thromboplastin / Q000378:metabolism; D013927:Thrombosis / Q000097:blood / Q000175:diagnosis*
chemical_list: D013925:Thromboplastin
keywords: apoptosis; arrhythmia; microparticles; stroke; thrombosis; tissue factor