Impact of the ablation technique on release of the neuronal injury marker S100B during pulmonary vein isolation

Author:

Scherschel Katharina123ORCID,Hedenus Katja34,Jungen Christiane235,Münkler Paula23,Willems Stephan34,Anwar Omar4,Klatt Niklas23,Eickholt Christian34,Meyer Christian1236ORCID

Affiliation:

1. Division of Cardiology, cardiac Neuro- and Electrophysiology Research Consortium (cNEP), EVK Düsseldorf, Kirchfeldstrasse 40, 40217 Düsseldorf, Germany

2. Clinic for Cardiology, University Heart & Vascular Centre, University Hospital Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany

3. DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Hamburg Germany

4. Department of Cardiology, Asklepios Klinik St. Georg, Lohmühlenstr. 5, 20099 Hamburg, Germany

5. Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands

6. Institute of Neural and Sensory Physiology, Medical Faculty, Heinrich Heine University Düsseldorf, Universitätsstrasse 1, 40225 Düsseldorf, Germany

Abstract

Abstract Aims S100B, a well-known damage-associated molecular pattern protein is released acutely by central and peripheral nerves and upon concomitant denervation in pulmonary vein isolation (PVI). We aimed to investigate whether the ablation technique used for PVI impacts S100B release in patients with paroxysmal atrial fibrillation (AF). Methods and results The study population consisted of 73 consecutive patients (age: 62.7 ± 10.9 years, 54.8% males) undergoing first-time PVI with either radiofrequency (RF; n = 30) or cryoballoon (CB; n = 43) for paroxysmal AF. S100B determined from venous plasma samples taken immediately before and after PVI increased from 33.5 ± 1.8 to 91.1 ± 5.3 pg/mL (P < 0.0001). S100B release in patients undergoing CB-PVI was 3.9 times higher compared to patients with RF-PVI (ΔS100B: 21.1 ± 2.7 vs. 83.1 ± 5.2  pg/mL, P < 0.0001). During a mean follow-up of 314 ± 186 days, AF recurrences were observed in 18/71 (25.4%) patients (RF-PVI: n = 9/28, CB-PVI: n = 9/43). Univariate Cox regression analysis indicated that an increase in S100B was associated with higher freedom from AF in follow-up (hazard ratio per 10  pg/mL release of S100B: 0.83; 95% confidence interval: 0.72–0.95; P = 0.007). Conclusion The ablation technique used for PVI has an impact on the release of S100B, a well-established biomarker for neural damage.

Funder

German Centre for Cardiovascular Research

Publisher

Oxford University Press (OUP)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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