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Review
. 2016 Jan;120(1-3):199-209.
doi: 10.1016/j.pbiomolbio.2015.12.015. Epub 2016 Jan 11.

The nervous heart

Crystal M Ripplinger  1 , Sami F Noujaim  2 , Dominik Linz  3
Affiliations
Review

The nervous heart

Crystal M Ripplinger et al. Prog Biophys Mol Biol. 2016 Jan.

Abstract

Many cardiac electrophysiological abnormalities are accompanied by autonomic nervous system dysfunction. Here, we review mechanisms by which the cardiac nervous system controls normal and abnormal excitability and may contribute to atrial and ventricular tachyarrhythmias. Moreover, we explore the potential antiarrhythmic and/or arrhythmogenic effects of modulating the autonomic nervous system by several strategies, including ganglionated plexi ablation, vagal and spinal cord stimulations, and renal sympathetic denervation as therapies for atrial and ventricular arrhythmias.

Keywords: Atrial fibrillation; Autonomic control; Cardiac nerves; Ventricular tachycardia/fibrillation.

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Figures

Figure 1
Figure 1
Mouse pulmonary vein ganglion stained with tyrosine hydroxylase (green, sympathetic), and choline acetyltransferase (red, parasympathetic). The ganglion is composed of sympathetic and parasympathetic somas. Staining was done as described earlier (Zarzoso et al., 2013). Scale bar: 50 μm.
Figure 2
Figure 2
Myocyte electrophysiological responses to sympathetic stimulation. NE binding to β-ARs activates PKA, which phosphorylates several intracellular targets, including IKs, ICaL, RyR, and PLB. Phosphorylation of IKs leads to APD shortening that may increase the dispersion of repolarization due to non-uniform innervation and resulting spatially non-uniform β-AR activation. Phosphorylation of ICaL, RyR, and PLB lead to increased intracellular [Ca2+], increased SR Ca2+ leak, and increased SR Ca2+ load. Collectively, these conditions are favorable for EAD and DAD formation. EADs may contribute to increased dispersion of repolarization and both EADs and DADs contribute to ectopic activity and focal arrhythmia.
Figure 3
Figure 3
Impact of ventricular injury on scar generation and subsequent development of a structural substrate for macroreentries and ventricular arrhythmias as well as on cardiac afferents resulting in sympathetic dysregulation and parasympathetic withdrawal. Different regulatory centers of cardiac efferent sympathetic (brain, stellate ganglion, renal sympathetic nerves) and parasympathetic (vagus nerve, spinal cord) activation are shown on the left. Interventional strategies to reduce sympathetic activation (e.g. by cardiac sympathetic denervation or renal denervation) or to increase the cardiac parasympathetic tone (e.g. by vagal stimulation and baroreceptor stimulation) are provided.
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