LAUSR

Ablation of atrial fibrillation is based on the isolation of the pulmonary veins (PVI) from the left atrium. Cerebral thromboembolism is a rare but serious complication of PVI, which highlights the importance of peri-procedural anticoagulation. Studying the coagulation and endothelium activation during PVI in case of using different anticoagulation protocols. 52 patients undergoing PVI with cryoballoon technique were involved and were grouped according to three different pre-procedural anticoagulation strategies: in the first group patients received no anticoagulation before the procedure (non anticoag., 24 patients)-, in the second group patients received uninterrupted vitamin K antagonist therapy, and their INR value was in therapeutic range on the day of the procedure (VKA group, 11 patients) and in the third group patients were on uninterrupted dabigatran therapy (dabigatran group, 17 patients). Two blood samples were taken during PVI from the left atrium, the first one before ablation or iv. heparin administration, the second one directly after the last application at the end of the procedure. The samples were used to measure D-dimer, plasmin antiplasmin (PAP) complex, a2 plasmin inhibitor (a2PI), plasminogen, FVIII activity, von Willebrand factor (VWF) antigen levels. D-dimer levels increased in all three groups after ablation, but in the samples of patients on dabigatran therapy we detected significantly lower D-dimer levels in the pre- and post-procedural samples compared to patients on other therapeutic strategies (median values before or after PVI: non anticoag.: 0.48 and 1.09 mgFEU/L; VKA: 0.33 and 0.72 mgFEU/L, dabigatran: 0.12 and 0.30 mgFEU/L, p<0.001 non anticoag. vs. dabigatran, p<0.01 VKA vs. dabigatran). PAP complex values were increasing parallel with D-dimer levels and only in the dabigatran group did not increase significantly. VWF antigen and FVIII activity increased significantly in all three groups after ablation, but there was no significant difference between the groups. the safest anticoagulation strategy for patients undergoing PVI was uninterrupted dabigatran therapy. The extend of endothelial damage was not affected by anticoagulation.