ArticleJournal of the American Heart Association2016
Atrioventricular Node Slow-Pathway Ablation Reduces Atrial Fibrillation Inducibility: A Neuronal Mechanism.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Delayed CAVB After SP Ablation for AVNRT: Mechanistic Insights Into FP Injury and Pacing Decision-Making.Pacing and clinical electrophysiology : PACE · 2026Article
- Unraveling the complexities of AVNRT ablation and its impact on electrophysiological features: A comprehensive review in children?ARYA atherosclerosis · 2025Article
- Late reversible complete atrioventricular block and PR interval normalization after antegrade slow pathway ablation for atrioventricular nodal re-entrant tachycardia with pre-existing PR prolongation.Journal of cardiology cases · 2022Article
- Antegrade slow pathway mapping of typical atrioventricular nodal reentrant tachycardia based on direct slow pathway capture.Journal of arrhythmia · 2021Article
- Targeting an electrotonic effect with ablation: Management of a symptomatic long PR interval.HeartRhythm case reports · 2020Article
- Electrophysiological changes in the conducting properties of fast pathway following modification of the slow pathway of the atrio ventricular node for atrio ventricular nodal re-entrant tachycardia.Pakistan journal of medical sciencesArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRadiofrequency ablation (RFA) for atrioventricular nodal reentrant tachycardia appears to reduce atrial tachycardia, which might relate to parasympathetic denervation at cardiac ganglionated plexuses. METHODS AND
resultsCompared to 7 control canines without RFA, in 14 canines, RFA at the bottom of Koch's triangle attenuated vagal stimulation-induced effective refractory periods prolongation in atrioventricular nodal and discontinuous atrioventricular conduction curves but had no effect on the sinoatrial node. RFA attenuated vagal stimulation-induced atrial effective refractory periods shortening and vulnerability window of atrial fibrillation widening in the inferior right atrium and proximal coronary sinus but not in the high right atrium and distal coronary sinus. Moreover, RFA anatomically impaired the epicardial ganglionated plexuses at the inferior vena cava‒inferior left atrial junction. This method was also investigated in 42 patients who had undergone ablation of atrioventricular nodal reentrant tachycardia, or 12 with an accessory pathway (AP) at the posterior septum (AP-PS), and 34 patients who had an AP at the free wall as control. In patients with atrioventricular nodal reentrant tachycardia and AP-PS, RFA at the bottom of Koch's triangle prolonged atrial effective refractory periods and reduced vulnerability windows of atrial fibrillation widening at the inferior right atrium, distal coronary sinus and proximal coronary sinus but not the high right atrium. In patients with AP-free wall, RFA had no significant atrial effects.
conclusionsRFA at the bottom of Koch's triangle attenuated local autonomic innervation in the atrioventricular node and atria, decreased vagal stimulation-induced discontinuous atrioventricular nodal conduction, and reduced atrial fibrillation inducibility due to impaired ganglionated plexuses. In patients with atrioventricular nodal reentrant tachycardia or AP-PS, RFA prolonged atrial effective refractory periods, and narrowed vulnerability windows of atrial fibrillation.
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