Endothelial damage and activation of the hemostatic system during radiofrequency catheter isolation of pulmonary veins

To determine the systemic thrombogenic effect of radiofrequency catheter isolation of the pulmonary veins (PVI) in the treatment of atrial fibrillation. We studied endothelial damage marker (von Willebrand factor [vWf]), fibrinolysis markers (tissue plasminogen activator [t-PA], plasminogen activator inhibitor-1 [PAI-1]) and coagulation activation markers (D-dimer [DD]) in 30 patients (pts) undergoing PVI. Heparin was administered continuously after double transseptal puncture in all pts. Concentrations of vWf and t-PA were significantly increased after accomplishing PVI compared to the baseline values, and elevated levels persisted 24 hours later ( p < 0.01). PAI-1 levels decreased following PVI compared to the baseline levels ( p = 0.02). PAI-1 levels normalized 24 hours after the procedure. DD increased continuously during the procedure with the peak following PVI ( p < 0.01). Higher DD concentrations persisted 24 hours later ( p = 0.02). In a multivariate analysis, total procedure time correlated significantly with the peak vWf and DD concentrations, while total RF energy dose correlated only with peak vWf ( r = 0.82). Time to heparin administration correlated with DD levels prior to the first RF pulse ( r = 0.83, p < 0.01) as well as after PVI ( r = 0.75, p < 0.01). A group of patients heparinized within the first hour of the PVI procedure had normal preablation DD levels and significantly mitigated DD levels following PVI compared to the group of patients heparinized later ( p < 0.01). Pulmonary vein ablations cause an increased systemic procoagulant state as reflected by fibrin turnover, fibrinolysis activation and endothelial perturbation. The activation of the coagulation cascade could be decreased by early heparin administration.