Autonomic Modulation

Abstract

A variety of experimental and clinical reports have engendered a different approach to cardiac arrhythmias as well as other cardiovascular conditions. The focus of a new paradigm is the autonomic nervous system and its important role in various pathological states. From an overall standpoint, this new paradigm can be encompassed by the term “autonomic modulation,” which would include autonomic nerve stimulation or autonomic denervation to modulate the autonomic activity in physiological or pathophysiological functions of the heart as well as other visceral organ systems. Article see p 279 Vaso-vagal syncope is the most common form of neurally mediated syncope.1 The pathophysiology of vaso-vagal syncope is still controversial, but it is thought to be related to prolonged orthostatic stress, which causes increased peripheral venous pooling with a subsequent fall in venous return to the heart. This in turn causes a hypercontractile state, which leads to activation of ventricular mechanoreceptors and a sudden increase in the afferent neural traffic to the brain. The result is sympathetic withdrawal and parasympathetic enhancement that manifests as hypotension (vasodepressor type), bradycardia (cardioinhibitory type), and syncope.1 In other words, vaso-vagal syncope is a disorder caused by an abnormally amplified autonomic reflex involving both sympathetic and parasympathetic components. Over the past 2 decades, β-blockers, α-agonists, mineralocorticoids, selective serotonin reuptake inhibitors, and dual-chamber pacemaker implantation all produced initial promising but later disappointing results.1–3 Vaso-vagal syncope continues to be a vexing clinical arrhythmia. In this issue of Circulation Arrhythmia and Electrophysiology , Yao et al4 reported 10 patients who had drug-refractory, frequent, and highly symptomatic vaso-vagal syncope. Based on the hypothesis that …