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.