The role of the autonomic nervous system in cardiac arrhythmias: The neuro-cardiac axis, more foe than friend?

The autonomic nervous system (ANS) with its two limbs, the sympathetic (SNS) and parasympathetic nervous system (PSNS), plays a critical role in the modulation of cardiac arrhythmogenesis. It can be both pro- and/or anti-arrhythmic at both the atrial and ventricular level of the myocardium. Intricate mechanisms, different for specific cardiac arrhythmias, are involved in this modulatory process. More data are available for the arrhythmogenic effects of the SNS, which, when overactive, can trigger atrial and/or ventricular “adrenergic” arrhythmias in susceptible individuals (e.g. in patients with paroxysmal atrial fibrillation-PAF, ventricular pre-excitation, specific channelopathies, ischemic heart disease or cardiomyopathies), while it can also negate the protective anti-arrhythmic drug effects. However, there is also evidence that PSNS overactivity may be responsible for triggering “vagotonic” arrhythmias (e.g. PAF, Brugada syndrome, idiopathic ventricular fibrillation). Thus, a fine balance is necessary to attain in these two limbs of the ANS in order to maintain eurhythmia, which is a difficult task to accomplish. Over the years, in addition to classical drug therapies, where beta-blockers prevail, several ANS-modulating interventions have been developed aiming at prevention and management of arrhythmias. Among them, techniques of cardiac sympathetic denervation, renal denervation, vagal stimulation, ganglionated plexi ablation and the newer experimental method of optogenetics have been employed. However, in many arrhythmogenic diseases, ANS modulation is still an investigative tool. Initial data are encouraging; however, further studies are needed to explore the efficacy of such interventions. These issues are herein reviewed and old and recent literature data are discussed, tabulated and pictorially illustrated.