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Sci Transl Med. 2019 May 22;11(493). pii: eaav7770. doi: 10.1126/scitranslmed.aav7770.

Cardiac glial cells release neurotrophic S100B upon catheter-based treatment of atrial fibrillation.

Author information

1
Department of Cardiology-Electrophysiology, cNEP (cardiac Neuro- and Electrophysiology research group), University Heart Centre, University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany.
2
DZHK (German Centre for Cardiovascular Research), partner site Hamburg/Kiel/Lübeck, 13347 Berlin, Germany.
3
Institute of Experimental Pharmacology and Toxicology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
4
Department of General and Interventional Cardiology, University Heart Center Hamburg, University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany.
5
Department of Clinical and Experimental Cardiology, Heart Center, Academic Medical Center, 1105 AZ, Amsterdam, Netherlands.
6
Institute of Neural and Sensory Physiology, Medical Faculty, University of Düsseldorf, 40225 Düsseldorf, Germany.
7
Cardiac Arrhythmia Center and Neurocardiology Research Center of Excellence, Molecular, Cellular and Integrative Physiology Interdepartmental Program, UCLA, Los Angeles, CA 90095, USA.
8
Department of Cardiology-Electrophysiology, cNEP (cardiac Neuro- and Electrophysiology research group), University Heart Centre, University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany. c.mey@web.de.

Abstract

Atrial fibrillation (AF), the most common sustained heart rhythm disorder worldwide, is linked to dysfunction of the intrinsic cardiac autonomic nervous system (ICNS). The role of ICNS damage occurring during catheter-based treatment of AF, which is the therapy of choice for many patients, remains controversial. We show here that the neuronal injury marker S100B is expressed in cardiac glia throughout the ICNS and is released specifically upon catheter ablation of AF. Patients with higher S100B release were more likely to be AF free during follow-up. Subsequent in vitro studies revealed that murine intracardiac neurons react to S100B with diminished action potential firing and increased neurite growth. This suggests that release of S100B from cardiac glia upon catheter-based treatment of AF is a hallmark of acute neural damage that contributes to nerve sprouting and can be used to assess ICNS damage.

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