Role of the autonomic nervous system in atrial fibrillation: pathophysiology and therapy.
Autonomic nervous system activation can induce significant and heterogeneous changes of atrial electrophysiology and induce atrial tachyarrhythmias, including atrial tachycardia and atrial fibrillation (AF). The importance of the autonomic nervous system in atrial arrhythmogenesis is also supported by circadian variation in the incidence of symptomatic AF in humans. Methods that reduce autonomic innervation or outflow have been shown to reduce the incidence of spontaneous or induced atrial arrhythmias, suggesting that neuromodulation may be helpful in controlling AF. In this review, we focus on the relationship between the autonomic nervous system and the pathophysiology of AF and the potential benefit and limitations of neuromodulation in the management of this arrhythmia. We conclude that autonomic nerve activity plays an important role in the initiation and maintenance of AF, and modulating autonomic nerve function may contribute to AF control. Potential therapeutic applications include ganglionated plexus ablation, renal sympathetic denervation, cervical vagal nerve stimulation, baroreflex stimulation, cutaneous stimulation, novel drug approaches, and biological therapies. Although the role of the autonomic nervous system has long been recognized, new science and new technologies promise exciting prospects for the future.
From the Department of Medicine, Division of Cardiology, The Krannert Institute of Cardiology (P.-S.C., S.-F.L.) and Department of Neurology (L.S.C.), Indiana University School of Medicine, Indianapolis; Department of Pathology and Laboratory Medicine, University of California, Los Angeles (M.C.F.); Institute of Biomedical Engineering, National Chiao Tung University, Hsinchu, Taiwan (S.-F.L.); and Department of Medicine, Montreal Heart Institute and Université de Montréal, Montreal, Quebec, Canada (S.N.).
Peng-Sheng
PS
Chen
Lan S
LS
Chen
Michael C
MC
Fishbein
Shien-Fong
SF
Lin
Stanley
S
Nattel
D000200:Action Potentials; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy*; D016275:Atrial Function / Q000187:drug effects*; D017763:Autonomic Denervation / Q000379:methods; D001341:Autonomic Nervous System / Q000187:drug effects* / Q000503:physiopathology / Q000601:surgery*; D017115:Catheter Ablation; D006325:Heart Atria / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D012307:Risk Factors; D016896:Treatment Outcome
D000889:Anti-Arrhythmia Agents
heart failure; myocardial infarction