title: Effect of physical exercise on platelet activity and the von-Willebrand-factor in patients with persistent lone atrial fibrillation.
abstract: BACKGROUND
  The risk of stroke is of great clinical importance in patients with atrial fibrillation (AF). It is not known whether physical exercise influences plasma coagulation and platelet aggregability during AF. The purpose of this study was to assess the effect of physical exercise on platelet activity, thrombin generation, and levels of von-Willebrand-factor in patients with persistent AF.
  
  
  METHODS
  Thirteen patients with lone AF (>or=1 year) were compared with 13 matched patients in sinus rhythm. Patients with AF were anticoagulated effectively with coumarin. All patients underwent bicycle ergometry using a respiratory gas exchange technique for 20 min at one-third of the age-adjusted maximal workload. Thereafter, workload was increased until maximal exercise capacity was reached. Platelet factor-4 (PF-4), beta-thromboglobulin (beta-TG; marker for platelet activation), von-Willebrand-factor (vWF; marker for endothelial dysfunction), prothrombin fragment F1 + 2 (F1 + 2; marker for thrombin generation) and fibrinogen levels were determined throughout the study in all patients.
  
  
  RESULTS
  Gas exchange variables, hemodynamic parameters and norepinephrine levels were comparable in the groups during moderate (45 +/- 5 W) and heavy exercise (198 +/- 38 W). In contrast to moderate exercise, PF-4 and beta-TG levels increased to 212 +/- 56% ( p < 0.05) and to 145 +/- 24% ( p < 0.05), respectively, in patients with AF during heavy exercise. In contrast, physical exercise had no significant effect on platelet activity in patients with sinus rhythm. Levels of vWF increased by delta24% ( p < 0.05) in all patients during maximal exercise, whereas F1 + 2 levels increased only in patients with sinus rhythm.
  
  
  CONCLUSIONS
  Heavy physical activity increases platelet activity and vWF levels during AF, whereas moderate exercise has no procoagulatory effect. Coumarin therapy prevents exercise-induced thrombin generation only. Future studies are needed to prove the hypothesis that heavy physical exercise is a risk factor for thromboembolic events in patients with AF.
authors.affiliation: Department of Internal Medicine, University Hospital Magdeburg, Magdeburg, Germany. andreas.goette@medizin.uni-magdeburg.de
authors.forename: Andreas
authors.initials: A
authors.lastname: Goette
authors.forename: Mathias
authors.initials: M
authors.lastname: Weber
authors.forename: Uwe
authors.initials: U
authors.lastname: Lendeckel
authors.forename: Tobias
authors.initials: T
authors.lastname: Welte
authors.forename: Gerd
authors.initials: G
authors.lastname: Lutze
authors.forename: Helmut U
authors.initials: HU
authors.lastname: Klein
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000534:rehabilitation*; D016022:Case-Control Studies; D002908:Chronic Disease; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation; D011336:Probability; D011659:Pulmonary Gas Exchange; D012016:Reference Values; D018570:Risk Assessment; D012494:Sampling Studies; D012720:Severity of Illness Index; D020521:Stroke / Q000517:prevention & control*; D014841:von Willebrand Factor / Q000032:analysis*
chemical_list: D014841:von Willebrand Factor