Neuro-cardiac interaction in malignant ventricular arrhythmia and sudden cardiac death

Abstract

Sudden cardiac death as a result of lethal ventricular arrhythmias is a major cause of death in cardiac diseases such as heart failure and prior myocardial infarct. Activity of the autonomic nervous system is often abnormal where sympathetic activity is upregulated and vagal activity reduced in these conditions. The abnormal autonomic state has been shown to be a strong prognostic marker of increased mortality and propensity to lethal arrhythmias, for which there is no effective prevention. Research effort over the years has established good evidence for a causal link between autonomic disturbance and ventricular arrhythmias. However, the detailed electrophysiological mechanisms by which ventricular fibrillation occurs are still not clear and molecular processes which are modulated by autonomic nerve influences that either predispose the heart to or protect it from these arrhythmias are not fully understood. This review presents data from studies investigating the link between activity of the autonomic nervous system and ventricular arrhythmias, from seminal findings in classical studies to ongoing investigations, in the quest for a better understanding of the arrhythmogenic mechanisms underlying neurocardiac interactions with a view to the development of effective preventative and therapeutic strategies which are very much needed.

Region-specific parasympathetic nerve remodeling in the left atrium contributes to creation of a vulnerable substrate for atrial fibrillation

“…Influence of sympatho-vagal interactions on formation of arrhythmogenic substrate and creation of disorganized AF EGMs. The role of sympatho-vagal interactions in the genesis of ventricular arrhythmias has been well described, with vagal stimulation shown to attenuate sympathetic augmentation of arrhythmogenic substrate in the ventricle (30,31). More recently, sympatho-vagal interactions have been invoked in the creation of a vulnerable substrate for AF.…”

Polymorphic ventricular tachycardia associated with an episode of reflex syncope: Is this the needle in the haystack?

“…10 This is in keeping with the many studies demonstrating the antifibrillatory effect of vagal stimulation, which tends to accompany reflex syncope. 11 However, this may be an oversimplification. For example, episodes of arrhythmia in patients with Brugada syndrome most often occur during times of increased vagal tone, such as sleep and rest.…”

Supraventricular tachycardia, pregnancy, and water: A new insight in lifesaving treatment of rhythm disorders

“…A reduction in body fluid load may activate baroreceptors in the carotid sinus, thus promoting sympathetic activation. Sympathetic nervous system mediators seem to shorten the ventricular refractory period and action potential duration and promote a nonuniform cardiac anisotropy which can induce the dispersion of muscle cell refractoriness (which increases susceptibility to arrhythmias) (Ng, ). Narayan, Drinan, Lackey, and Edman () observed that the acute volume overload in dogs with structurally normal hearts was able to elevate T‐wave alternans, thus influencing the occurrence of arrhythmias.…”