Introduction
High-grade atrioventricular block is defined by two or more consecutively non-conducted P waves, resulting in multiple P waves without QRS complexes. In adult patients, current European Society of Cardiology guidelines recommend pacemaker implantation in the absence of a reversible cause irrespective of symptoms. 1 However, this recommendation is not directly applicable to paediatric patients, in whom the aetiology, natural history, and adaptive capacity differ substantially. In children and adolescents, pacing decisions are commonly individualised based on symptoms, ventricular dysfunction, or risk of syncope or sudden cardiac arrest rather than the presence of atrioventricular block alone. Reference Baruteau, Pass and Thambo2
Cardioneuroablation is an emerging therapeutic approach that consists of endocardial ablation of cardiac parasympathetic ganglionated plexi located within paracardiac epicardial fat pads. Reference Pachón-M, Pachón-Mateos and Higuti3 By modulating cardiac autonomic function, this technique has shown benefits in conditions associated with or exacerbated by increased vagal tone—such as vasovagal syncope, functional atrioventricular block, and sinus node dysfunction. Reference Rakesh, Pachon and Pachon4–Reference Aksu, Gupta, Reddy and Morillo6 Evidence for cardioneuroablation in high-grade atrioventricular block is growing, although it remains a novel area in electrophysiology.
Case report
We report the case of a 15-year-old competitive basketball player, with a medical history of sickle cell trait, who presented at the emergency department with pleuritic chest pain subsequent to a chest trauma sustained during a basketball game. Initial evaluation included an electrocardiogram that revealed a second-degree Mobitz I atrioventricular block at rest. Physical examination and laboratory investigation results were within the normal limits. Subsequent comprehensive cardiac evaluation included Holter monitoring which recorded an average daytime heart rate of 77 bpm, night-time HR of 58 bpm, minimum of 43 bpm, and maximum of 151 bpm. Episodes included second-degree Mobitz I atrioventricular block, 2:1 atrioventricular block, and high-grade atrioventricular block with daytime pauses up to 5020 milliseconds. Analysis of the Holter monitoring tracing demonstrated progressive prolongation of the P–P interval during the blocked episode (≈1130 ms pre-block, increasing to ≈1780 ms and ≈1960 ms during atrioventricular block), indicating concomitant sinus slowing (Figure 1). The patient was asymptomatic with no prior syncope. Exercise stress test showed a normal chronotropic response. Transthoracic echocardiogram documented origin of the right coronary artery from the left coronary sinus and was otherwise normal. Patient anti-Sjögren’s-syndrome-related antigen A (anti-Ro/SSA) antibodies were tested and resulted negative. Adenosine testing was not performed.
Restored 24-hour Holter electrocardiogram tracing showing daytime complete atrioventricular block with a ventricular pause of 5020 milliseconds. The PP interval shows progressive prolongation from approximately 1130 ms before the onset of block to ∼1780 ms and then ∼1960 ms during the blocked episode, indicating concomitant sinus slowing consistent with global vagal activation.

The patient was unwilling to implant a pacemaker and due to his age and participation in competitive sports, cardioneuroablation was proposed and accepted as an alternative by patient and parents.
Electrophysiological study and cardioneuroablation were performed under general anaesthesia. Continuous 12-lead electrocardiogram and intracardiac electrograms were recorded on a multichannel system. Vascular access was obtained via the right femoral vein, and three catheters were positioned in the coronary sinus, His bundle, and left atrium via transseptal puncture. Heparin was administered to maintain an activated clotting time between 300 and 350 s.
Baseline assessment demonstrated a heart rate of 45 bpm (RR 1333 ms), atrio-His interval 200 ms, His-ventricular interval 50 ms, Wenckebach cycle length 1000 ms, and a corrected Sinus Node Recovery Time of 446 ms.
Pre-ablation vagal nerve stimulation at the jugular foramen provoked atrioventricular block with a 15-second pause, confirming a functional (vagally mediated) component. Electroanatomic mapping of both atria was performed using the CARTO 3 system and a multipolar PentaRay catheter to identify fractionated atrial potentials consistent with presumed ganglionated plexi. Electroanatomic maps and the sites of radiofrequency applications are shown in Figure 2.
Electroanatomic maps obtained during cardioneuroablation illustrating radiofrequency application sites (pink dots) in regions consistent with atrial ganglionated plexi. Multiple projections and transparency settings are shown to highlight relevant ablation targets. Pannels A to D: Right atrial-focused views demonstrating radiofrequency applications along the septal superior vena cava region (anterior and posterior aspects) and around the coronary sinus ostium. Pannels E to H: Left atrial-focused views demonstrating radiofrequency applications in regions adjacent to the pulmonary veins, including anterior to the right superior pulmonary vein, posterosuperior to the left superior pulmonary vein, posterior to the left inferior pulmonary vein, and superior to the right inferior pulmonary vein.

Radiofrequency ablation was delivered at these sites with an irrigated 3.5-mm tip catheter (20–30 W, 50°C; contact force 10–30 g). Post-ablation vagal stimulation did not reproduce atrioventricular block or pauses, confirming successful parasympathetic denervation.
A resting electrocardiogram and one-month Holter after cardioneuroablation showed no recurrence of Mobitz I atrioventricular block, supporting successful autonomic modulation. Nonetheless, an underlying intrinsic component cannot be fully excluded, given the mildly prolonged baseline AH (200 ms) and low resting HR (45 bpm) at baseline Electrophysiological Study. The follow-up Holter recorded daytime HR 59 bpm, night-time HR 49 bpm, minimum 39 bpm, and maximum 94 bpm, with no high-degree atrioventricular block.
Discussion
High-grade atrioventricular block may be associated with a potential risk of injury during syncope in young athletes. Although the risk of bradycardia-induced arrhythmia in structurally normal hearts is considered very low, the presence of prolonged daytime pauses warrants careful evaluation and individualised management. Reference Güler and Aksu7 Pacemaker implantation remains the traditional strategy, Reference Brignole, Moya and de Lange8 but it carries life-long trade-offs (generator replacements, lead issues, non-physiological pacing, atrial enlargement, and ventricular dysfunction) and may compromise competitive sports participation.
In our asymptomatic adolescent athlete, daytime pauses > 5 s were judged clinically relevant and, within a shared decision-making framework, supported intervention. Cardioneuroablation was selected as a pacemaker-sparing strategy.
Detailed analysis of the Holter recording demonstrated progressive prolongation of the P–P interval during the blocked episode (≈1130 ms before the onset of atrioventricular block to around 1780 ms and subsequently 1960 ms), indicating concomitant sinus slowing. This pattern is consistent with global vagal activation affecting both sinus node automaticity and atrioventricular nodal conduction. Despite this generalised autonomic effect, the dominant clinical manifestation was severe impairment of atrioventricular conduction, resulting in prolonged ventricular pauses. Such a dissociation between the degree of sinus slowing and the severity of atrioventricular block has been described in the context of regional heterogeneity of cardiac parasympathetic innervation, where vagal input may exert a disproportionate functional effect on the atrioventricular node.
In this adolescent athlete, the absence of structural heart disease, the normalisation of atrioventricular conduction with exercise, and the abolition of atrioventricular block during extracardiac vagal stimulation following cardioneuroablation strongly support a functional, vagally mediated component contributing to the high-grade atrioventricular block. Within a shared decision-making framework, and given the patient’s age and competitive sports participation, cardioneuroablation was therefore selected as a pacemaker-sparing strategy.
While the short-term outcome was favourable, important knowledge gaps remain regarding optimal patient selection, ganglionated plexi targeting strategies, and long-term durability of cardioneuroablation, particularly in paediatric and athletic populations.
Learning points
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• Functional high-grade atrioventricular block in young athletes may be associated with a potential risk of injury during syncope; the risk of bradycardia-induced arrhythmia in structurally normal hearts is very low.
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• Cardioneuroablation is a practical alternative in vagally mediated bradyarrhythmias (including functional atrioventricular block), potentially avoiding pacemaker implantation in selected patients.
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• Avoiding pacemaker implantation is especially relevant in the young and in athletes avoiding the life-long complications associated with pacemaker implantation and possible compromise of high-level competitive sports practice.
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• Although cardioneuroablation has shown promising results some aspects of the technique such as ganglionated plexi selection for ablation and identification of ganglionated plexi location and long-term outcomes are still missing.
Acknowledgements
None.
Financial support
This research received no specific grant from any funding agency, commercial, or not-for-profit sectors.
Competing interests
None.
