No abstract

The parasympathetic nervous system plays an important role in the pathophysiology of atrial fibrillation. Catheter ablation, a minimally invasive procedure deactivating abnormal firing cardiac tissue, is increasingly becoming the therapy of choice for atrial fibrillation. This is inevitably associated with the obliteration of cardiac cholinergic neurons. However, the impact on ventricular electrophysiology is unclear. Here we show that cardiac cholinergic neurons modulate ventricular electrophysiology. Mechanical disruption or pharmacological blockade of parasympathetic innervation shortens ventricular refractory periods, increases the incidence of ventricular arrhythmia and decreases ventricular cAMP levels in murine hearts. Immunohistochemistry confirmed ventricular cholinergic innervation, revealing parasympathetic fibres running from the atria to the ventricles parallel to sympathetic fibres. In humans, catheter ablation of atrial fibrillation, which is accompanied by accidental parasympathetic and concomitant sympathetic denervation, raises the burden of premature ventricular complexes. In summary, our results demonstrate an influence of cardiac cholinergic neurons on the regulation of ventricular function and arrhythmogenesis.

Purpose of Review: Atrial fibrillation (AF), the most common sustained arrhythmia, is associated with high rates of morbidity and mortality. Maintenance of stable sinus rhythm (SR) is the intended treatment target in symptomatic patients, and catheter ablation aimed at isolating the pulmonary veins provides the most effective treatment option, supported by encouraging clinical outcome data. A variety of energy sources and devices have been developed and evaluated. In this review, we summarize the current state of the art of catheter ablation of AF and describe future perspectives. Recent Findings: Catheter ablation is a wellestablished treatment option for patients with Enhanced Digital Features To view enhanced digital features for this article go to https://doi.org/10.6084/ m9.figshare.11357912.