Several ANS-modulating interventions have been developed aiming at prevention and management of arrhythmias.
First-pass extracted concept
autonomic modulation of cardiac arrhythmias
Evidence Snippets
Supporting Sources
Linked Claims
In many arrhythmogenic diseases, autonomic nervous system modulation remains investigational, with encouraging initial data but a need for further efficacy studies.
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.
Parasympathetic overactivity may trigger vagotonic arrhythmias including paroxysmal atrial fibrillation, Brugada syndrome, and idiopathic ventricular fibrillation.
However, there is also evidence that PSNS overactivity may be responsible for triggering "vagotonic" arrhythmias (e.g. PAF, Brugada syndrome, idiopathic ventricular fibrillation).
Sympathetic overactivity can trigger adrenergic atrial or ventricular arrhythmias in susceptible individuals and can negate protective anti-arrhythmic drug effects.
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 ... while it can also negate the protective anti-arrhythmic drug effects.
The autonomic nervous system plays a critical role in modulating cardiac arrhythmogenesis and can exert both pro-arrhythmic and anti-arrhythmic effects at atrial and ventricular levels.
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.