title: Activation of the hemostatic mechanism after pharmacological cardioversion of acute nonvalvular atrial fibrillation.
abstract: BACKGROUND
  Given that the restoration of sinus rhythm after chronic atrial fibrillation is associated with embolic events, anticoagulation is prescribed before and after pharmacological and electrical cardioversion. However, the need for anticoagulation in patients with acute atrial fibrillation (lasting <48 hours) who undergo cardioversion is less clear. In addition, it is not known whether cardioversion to sinus rhythm determines a hypercoagulable state in these patients.
  
  
  RESULTS
  In 21 patients with acute nonvalvular atrial fibrillation, plasma median concentrations of thrombin-antithrombin complex, a marker of thrombin generation, significantly increased from 2.8 ng/mL (interquartile range, 2.1 to 4.0 ng/mL) on hospital admission to 3.5 ng/mL (interquartile range, 2.9 to 6.0 ng/mL) after cardioversion to sinus rhythm obtained by means of infusion of antiarrhythmic drugs and decreased to 2.5 ng/mL (interquartile range, 2.0 to 3.5 ng/mL) at the 1-month follow-up visit (P=.04). Similarly, the levels of fibrinopeptide A, a marker of thrombin activity, increased from 1.1 nmol/L (interquartile range, 0.7 to 1.5 nmol/L) at baseline to 1.8 nmol/L (interquartile range, 1.1 to 3.0 nmol/L) after cardioversion and returned to 0.8 nmol/L (interquartile range, 0.6 to 1.1 nmol/L) at the 1-month follow-up visit (P=.02).
  
  
  CONCLUSIONS
  A significant increase in plasma levels of the markers of thrombin generation and activity was observed in patients with acute atrial fibrillation early after pharmacological cardioversion to sinus rhythm. This is the first biochemical evidence that cardioversion of recent-onset atrial fibrillation determines a hypercoagulable state.
authors.affiliation: 2nd Division of Cardiology, Niguarda Hospital, Milano, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Oltrona
authors.forename: M
authors.initials: M
authors.lastname: Broccolino
authors.forename: P A
authors.initials: PA
authors.lastname: Merlini
authors.forename: A
authors.initials: A
authors.lastname: Spinola
authors.forename: A
authors.initials: A
authors.lastname: Pezzano
authors.forename: P M
authors.initials: PM
authors.lastname: Mannucci
mesh_terms: D000208:Acute Disease; D000638:Amiodarone / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D000990:Antithrombin III / Q000032:analysis; D001281:Atrial Fibrillation / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology*; D015415:Biomarkers; D004198:Disease Susceptibility; D005260:Female; D005344:Fibrinopeptide A / Q000032:analysis; D005424:Flecainide / Q000627:therapeutic use; D006487:Hemostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D011405:Propafenone / Q000627:therapeutic use; D013917:Thrombin / Q000096:biosynthesis; D013923:Thromboembolism / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*
chemical_list: D000889:Anti-Arrhythmia Agents; D015415:Biomarkers; C046193:antithrombin III-protease complex; D005344:Fibrinopeptide A; D011405:Propafenone; D000990:Antithrombin III; D010447:Peptide Hydrolases; D013917:Thrombin; D005424:Flecainide; D000638:Amiodarone