Marshaling the Autonomic Nervous System for Treatment of Atrial Fibrillation

A number of mechanisms have been proposed to explain the pathogenesis of atrial fibrillation (AF), and some are intricately linked to the autonomic nervous system (ANS) (1). A potential neural influence in AF was suggested by Coumel et al. (2) in 1978 and has since been extensively investigated. Experimentally, stimulation of autonomic nerves during the atrial refractory period has been shown to produce rapid ectopic beats from the pulmonary veins (PVs) and superior vena cava, which in turn can initiate AF (3,4). It is now well recognized that the ANS has an important contribution to the pathogenesis of AF (5,6). However, AF remains poorly understood, and the specific mechanisms underlying the relationship between the ANS and AF have yet to be fully elucidated. Despite this limited knowledge base, both cardiac and extra-cardiac autonomic structures (such as the renal arteries) have been targets of AF therapy (7).