One of the multiple factors believed to contribute to the initiation and maintenance of atrial fibrillation (AF) is altered activity of the autonomic nervous system. Debate continues about the role of the vagus nerve (CNX) in AF since its effect depends on the level of its activation as well as on simultaneous sympathetic activation. Surplus either vagal or sympathetic activity may rarely induce the development of AF; however, typically loss of balance between the both systems mediates the induction and maintenance of AF. Vagal stimulation has been proposed as a novel treatment approach for AF because the anti-arrhythmic effects of low-level vagus nerve stimulation have been shown both in patients and animal models. We hypothesize that in typical cases of AF without any clear trigger by either autonomic nervous system, significant changes in vagus somatosensory evoked potentials and a smaller cross-sectional area of CNX could be detected, representing functional and structural changes in CNX, respectively.
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