Abstract
The past 5 years have seen great advances in the knowledge of neural mechanisms of atrial arrhythmogenesis. Direct autonomic nerve recordings demonstrate that simultaneous sympathovagal discharges and intrinsic cardiac nerve activities are common triggers of paroxysmal atrial tachycardia and atrial fibrillation. While activity of the autonomous nervous system (ANS) is crucial in triggering paroxysmal atrial fibrillation, a high incidence of sympathovagal co-activation at baseline is associated with a high vulnerability to pacing-induced sustained atrial fibrillation, suggesting that ANS has a role in the development of persistent atrial fibrillation. Modulation of ANS activity may constitute an important therapeutic strategy for the management of atrial tachyarrhythmias. Specifically, continuous, low-level stimulation of the left cervical vagus nerve effectively suppresses atrial tachyarrhythmias by reducing the nerve activity of the stellate ganglion. Clinically, compared with pulmonary vein isolation alone, the addition of ablation of intrinsic cardiac ganglia may confer better outcomes for patients with paroxysmal atrial fibrillation. These findings suggest that further investigation of the neural mechanisms of atrial arrhythmias might lead to better management of patients with atrial arrhythmias. In this article, we review the role of the ANS in the induction and maintenance of atrial arrhythmias and the role of neural modulation as a treatment strategy for atrial arrhythmias.
Highlights
Atrial fibrillation (AF) is the most common arrhythmia in developed countries and affects approximately 2.3 million people in the USA alone.[1]
Enhanced activity of these intrinsic cardiac nerves has been implicated in triggering focal AF that arises from pulmonary veins (PVs).[6,7]
We review the role of the autonomous nervous system (ANS) in the induction and maintenance of atrial arrhythmias, and discuss neural modulation as a treatment strategy for patients with atrial arrhythmias
Summary
Direct autonomic nerve recordings demonstrate that simultaneous sympathovagal discharges and intrinsic cardiac nerve activities are common triggers of paroxysmal atrial tachycardia and atrial fibrillation. Compared with pulmonary vein isolation alone, the addition of ablation of intrinsic cardiac ganglia may confer better outcomes for patients with paroxysmal atrial fibrillation. These findings suggest that further investigations in the neural mechanisms of atrial arrhythmias might lead to better management of patients with atrial arrhythmias. Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, 1801 North Capitol Avenue, E475, Indianapolis, IN 46202, USA Novel strategies, including neural ablation and neural stimulation, can reduce arrhythmogenic nerve activities but warrant further studies before they can be widely applied in clinical settings
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