LAUSR

Abstract Funding Acknowledgements Type of funding sources: None. Background Previous studies showed a release of neuronal injury markers during catheter ablation of atrial fibrillation using thermal energies such as radiofrequency or cryothermy. Pulsed field ablation (PFA), that is characterized by its tissue specificity, serves as an innovative technique for pulmonary vein isolation (PVI). Purpose To investigate the amount of neuronal injury marker release in patients undergoing first PVI using different ablation modalities. Methods We included 65 consecutive patients (age 69 ± 11 years, 52% females) that underwent PVI for the first time with either radiofrequency using standard ablation settings (RF; n = 11), radiofrequency with high-power short-duration (HPSD; n = 32) or PFA (PFA; n = 17) for atrial fibrillation. Protein S100B levels and Neuron-specific enolase (NSE) in coronary sinus blood were detected before and after PVI. The release of neuronal injury markers was assessed according to the ablation technique used. Results The change in high-sensitivity troponin (hsTnT) levels was similar in all groups (RF: Δ175.6±181.9 ng/l; HPSD: Δ153.1±233.5 ng/l; PFA: Δ181.1±257.6 ng/l; p=0.632). NSE was significantly released only in patients treated with PFA-PVI (25.2±13.4 to 45.2±24.9 ng/ml; p<0.001), but not in patients treated with RF-PVI or HPSD-PVI (both p>0.05). S100B was released in patients treated with RF-PVI (79.7±32.2 to 118.6±46.4 pg/ml; p=0.006) and PVI-PFA (80.6±38.1 to 138.1±82.7 pg/ml; p=0.002) after the procedure, while there was only a numerically increase in patients treated with PVI-HPSD (88.6±38.7 to 109.1±54.2 pg/ml; p=0.172). We detected no correlation between the release of neuronal biomarkers (Δ NSE and Δ S100B) and cardiac damage (Δ hsTnT) (all p>0.05). The ΔNSE/ΔhsTnT ratio (p<0.001), and the ΔS100B/ΔhsTnT ratio (p=0.002) was higher in patients undergoing PFA-PVI (ΔNSE/ΔhsTnT 0.19±0.20; ΔS100B/ΔhsTnT 0.75±1.35), than in patients undergoing RF-PVI (ΔNSE/ΔhsTnT 0.0±0.06; ΔS100B/ΔhsTnT 0.35±0.32) and HPSD-PVI (ΔNSE/ΔhsTnT 0.04±0.11; ΔS100B/ΔhsTnT 0.13±1.55). Conclusion The release of neuronal injury markers differs according to the technique used for PVI. Patients treated with PFA showed a higher release of neuronal injury markers compared to radiofrequency ablation, that was not explained by more myocardial damage. Future research needs to investigate the prognostic relevance in terms of atrial fibrillation recurrence of the neural injury induced by PFA compared to radiofrequency PVI.