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

Catheter ablation for atrial fibrillation induces intracardiac neural damage characterized by glial S100B release, which promotes nerve sprouting. Treating the nervous ticker Catheter ablation induces tissue damage in specific regions of the heart in patients with atrial fibrillation (rapid irregular heartbeat) to correct abnormal electrical signals. Although effective, the underlying mechanism remains incompletely understood. Scherschel et al. demonstrated that cryothermal ablation induced release of S100B, a marker of neuronal injury, from glial cells within mouse hearts. S100B stimulated nerve growth and reduced neuronal electrical activity. In patients receiving ablations, higher serum concentration of S100B after the procedure was associated with lower recurrence of atrial fibrillation. Further study is warranted to understand how ablation-induced injury to the intrinsic cardiac autonomic nervous system contributes to patient outcomes. 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.