Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w

Pulmonary Vein Isolation with Pulsed Field Ablation Leads to a Release of Neuronal Injury Markers
M. Spieker1, S. Angendohr1, A. G. Bejinariu1, D. Glöckner1, C. Brinkmeyer1, J. Schmidt1, M. Kelm1, O. R. Rana1
1Klinik für Kardiologie, Pneumologie und Angiologie, Universitätsklinikum Düsseldorf, Düsseldorf;

Background:

Catheter ablation of atrial fibrillation using thermal energies such as radiofrequency or cryothermy is associated with indiscriminate tissue destruction. Pulsed field ablation (PFA) serves as a novel modality for pulmonary vein isolation (PVI), which is characterized by its tissue specificity.

Aims: 

We aimed to investigate whether the PFA technique used for PVI also impacts the release of neuronal injury markers in patients undergoing first PVI.

Methods: 

The study population consisted of 65 consecutive patients (age 69 ± 11 years, 52% females) undergoing 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 AF. Neuron-specific enolase (NSE) and protein S100B levels in coronary sinus blood were measured immediately 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)(Fig. 1A). 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)(Fig. 1C). 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)(Fig. 1B). There was no correlation between cardiac damage (Δ hsTnT) and the release of neuronal biomarkers (Δ NSE and Δ S100B) (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: 

Pulmonary vein isolation with PFA was associated with the release of neuronal injury markers. The release of neuronal injury markers was higher in patients treated with PFA compared to radiofrequency ablation, and not explained by more myocardial damage. Future studies need to focus on the prognostic impact in terms of AF recurrence of the neural injury induced by PFA compared to radiofrequency PVI.

Figure 1. (A) Change in hsTnT prior and immediately after the procedure according to technique used. (B) Comparison of S100B release after RF-PVI, HPSD-PVI and PFA-PVI. (C) Comparison of NSE release after RF-PVI, HPSD-PVI and PFA-PVI. Abbreviations: hsTNT=high-sensitive troponin T; RF=radiofrequency; HPSD=high-power short-duration; PFA=pulsed field ablation; PVI=pulmonary vein isolation.


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