Catheter ablation of atrial fibrillation induced the release of S100B from cardiac glia, and patients with higher S100B release were more likely to be AF-free during follow-up.
Observational
Does S100B release upon catheter ablation of atrial fibrillation correlate with AF freedom and induce neurotrophic effects?
S100B release during AF ablation serves as a biomarker for acute neural damage, contributes to nerve sprouting, and is associated with improved clinical freedom from AF.
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.
Scherschel et al. (Wed,) conducted a observational in Atrial fibrillation. Catheter ablation was evaluated on S100B release and AF freedom. Catheter ablation of atrial fibrillation induced the release of S100B from cardiac glia, and patients with higher S100B release were more likely to be AF-free during follow-up.