Introduction
Vasovagal syncope (VVS) is the most common cause of syncope clinically characterized by bradycardia and/or hypotension, mediated by parasympathetic overactivity and/or sympathetic withdrawal, respectively (1). Similarly, some cases of atrioventricular block (AVB) may be related to vagal hyperactivity in which paroxysmal AVB is accompanied by a significant slowing of sinus rate; also referred to as functional AVB because there is no intrinsic abnormality in the atrioventricular conduction system (2). Functional AVB is typically associated with well-identifiable triggers and characteristic prodromal symptoms like VVS.
Although the reflex is benign and occurs in otherwise healthy persons, frequent episodes or events without prodrome are debilitating, can lead to injuries and affect long-term quality of life (QOL). There are limited non-pharmacological and medical therapies proven effective in randomized clinical trials (3, 4). Pacing is indicated in a select population of patients > 40 years with refractory VVS and documented asystole (5). However, the role of cardiac pacing for the prevention of syncope recurrences remains controversial due to difficulties to exclude potential role of the hypotensive/vasodepressor component during the episode. No studies have specifically investigated the effect of cardiac pacing in patients with functional AVB.
Small open-label cohort studies have shown that catheter ablation of ganglionated plexi (GPs) or cardioneuroablation (CNA) can have salutary effects in some patients with VVS and functional AVB. In this article, we aim to provide a detailed description of CNA, including a brief review of the anatomy of intrinsic cardiac autonomic nervous system (ANS), indications, pre- and post-procedure management, necessary equipment, and potential pitfalls.