title: Electrophysiologic procedures and activation of the hemostatic system.
abstract: BACKGROUND
  Thromboembolism occurs in 0.4% to 2% of the subjects undergoing radiofrequency ablation (RFA), but its mechanisms remain unclear. Our aim was to evaluate several parameters of the hemostatic system in relation to the electrophysiologic procedure.
  
  
  METHODS
  Thirty consecutive patients were enrolled in the study. Fifteen underwent electrophysiologic study and 15 underwent radiofrequency ablation. Before the ablation procedure, all subjects were given an intravenous heparin bolus (2500 IU). Blood samples were drawn immediately before, at the end of, and 24 hours after the procedures. Spontaneous platelet aggregation in whole blood and in platelet-rich plasma, markers of clotting activation (prothrombin fragment 1+2 and the thrombin-antithrombin complex) and the fibrinolytic system (plasminogen activator inhibitor and D-dimer) levels were evaluated.
  
  
  RESULTS
  At the end of the procedure, spontaneous platelet aggregation in whole blood, prothrombin fragment 1+2, thrombin-antithrombin complex, and D-dimer levels increased significantly in all patients. The hemostatic changes were more marked after RFA than after electrophysiology. Spontaneous aggregation in whole blood, prothrombin fragment 1+2, and thrombin-antithrombin complex levels at 24 hours after the procedure were similar to those observed before the procedure in both groups; D -dimer levels were still elevated with respect to preprocedure levels, with a trend toward higher levels in patients undergoing RFA rather than electrophysiology. A significantly more marked activation of coagulation (prothrombin fragment 1+2, P <.005) was found in patients in whom the mean duration of energy application was higher than 23.5 seconds.
  
  
  CONCLUSIONS
  Our data suggest that antithrombotic prevention with a prolonged administration of heparin and/or the association of antiplatelet agents should be considered in patients undergoing RFA.
authors.affiliation: Istituto di Clinica Medica Generale e Cardiologia, Università di Firenze, Florence, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Michelucci
authors.forename: E
authors.initials: E
authors.lastname: Antonucci
authors.forename: A A
authors.initials: AA
authors.lastname: Conti
authors.forename: A
authors.initials: A
authors.lastname: Alessandrello Liotta
authors.forename: S
authors.initials: S
authors.lastname: Fedi
authors.forename: L
authors.initials: L
authors.lastname: Padeletti
authors.forename: M C
authors.initials: MC
authors.lastname: Porciani
authors.forename: D
authors.initials: D
authors.lastname: Prisco
authors.forename: R
authors.initials: R
authors.lastname: Abbate
authors.forename: G F
authors.initials: GF
authors.lastname: Gensini
mesh_terms: D000328:Adult; D000368:Aged; D001777:Blood Coagulation / Q000187:drug effects*; D004564:Electrocoagulation / Q000009:adverse effects*; D004594:Electrophysiology; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006493:Heparin / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D013927:Thrombosis / Q000097:blood / Q000209:etiology* / Q000517:prevention & control*
chemical_list: D005343:Fibrinolytic Agents; D006493:Heparin