Abstract
The autonomic nervous system (ANS) has a significant influence on the structural integrity and electrical conductivity of the atria. Aberrant activation of the sympathetic nervous system can induce heterogeneous changes with arrhythmogenic potential which can result in atrial tachycardia, atrial tachyarrhythmias and atrial fibrillation (AF). Methods to modulate autonomic activity primarily through reduction of sympathetic outflow reduce the incidence of spontaneous or induced atrial arrhythmias in animal models and humans, suggestive of the potential application of such strategies in the management of AF. In this review we focus on the relationship between the ANS, sympathetic overdrive and the pathophysiology of AF, and the potential of sympathetic neuromodulation in the management of AF. We conclude that sympathetic activity plays an important role in the initiation and maintenance of AF, and modulating ANS function is an important therapeutic approach to improve the management of AF in selected categories of patients. Potential therapeutic applications include pharmacological inhibition with central and peripheral sympatholytic agents and various device based approaches. While the role of the sympathetic nervous system has long been recognized, new developments in science and technology in this field promise exciting prospects for the future.
Highlights
Frontiers in NeuroscienceSympathetic Nervous System Activation and Its Modulation: Role in Atrial Fibrillation
The autonomic nervous system (ANS) has a significant influence on the structural integrity and electrical conductivity of the atria
In this review we focus on the relationship between the ANS, sympathetic overdrive and the pathophysiology of atrial fibrillation (AF), and the potential of sympathetic neuromodulation in the management of AF
Summary
Sympathetic Nervous System Activation and Its Modulation: Role in Atrial Fibrillation. Methods to modulate autonomic activity primarily through reduction of sympathetic outflow reduce the incidence of spontaneous or induced atrial arrhythmias in animal models and humans, suggestive of the potential application of such strategies in the management of AF. The heart is extensively innervated and effectively regulated by the autonomic nervous system (ANS) through its sympathetic and parasympathetic branches (Kimura et al, 2012). GP are clusters of ganglia from different subplexi and function as an intersection point of parasympathetic and sympathetic nerves and interconnect the intrinsic ANS (Armour et al, 1997; Hou et al, 2007; MalcolmeLawes et al, 2013). The instability theory of Ca2+-handling has been recently challenged (Christ et al, 2014; Greiser et al, 2014), raising the hypothesis that Ca2+-induced calcium release may mediate AF in structurally remodeled atria, demonstrating how a modified autonomic tone can cause AF (Nguyen et al, 2009)
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