Experimental Model of Focal Atrial Tachycardia: Clinical Correlates

Liu, Yü; Scherlag, Benjamin J.; Fan, Yujiang; Mao, Jun; Hepler, Eric; Varma, Vandana; Male, Shailesh; Xia, Wenfang; Huang, He; Po, Sunny S.

doi:10.1111/jce.12160

Cited by 3 publications

(2 citation statements)

References 35 publications

(36 reference statements)

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“…The observed automaticity (7) and anisotropy ( 8) at the crista terminalis may partly explain the propensity for atrial arrhythmias to originate from this location. In keeping with this hypothesis, an experimental model of AT using inhibition of the atrial ganglionated plexi induced AT at sites similar to those reported clinically (9).…”

Section: Discussionsupporting

confidence: 72%

Atrial Tachycardia Arising From the Crista Terminalis, Detailed Electrophysiological Features and Long-Term Ablation Outcomes

Morris

Segan

Wong

et al. 2019

JACC: Clinical Electrophysiology

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Section: Discussionsupporting

confidence: 72%

Atrial Tachycardia Arising From the Crista Terminalis, Detailed Electrophysiological Features and Long-Term Ablation Outcomes

Morris

Segan

Wong

et al. 2019

JACC: Clinical Electrophysiology

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“…The other possibility of the Epi‐AT mechanism was that GP activity directly provoked the Epi‐ATs via their axons, which are distributed in the myocardium at the EASs. Previous canine experimental models 19 showed that focal AT was induced by GP stimulation. Another study 1 in silico for simulating the human heart demonstrated that GP stimulation, both sympathetic and parasympathetic, induced a spontaneous phase 3 early after‐depolarization like the action potentials and PV tachycardias adjacent to the stimulated GPs.…”

Section: Discussionmentioning

confidence: 97%

The characteristics and efficacy of catheter ablation of focal atrial tachycardia arising from an epicardial site

Yamamoto

Iwasaki

Fujimoto

et al. 2021

Clinical Cardiology

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Background Although epicardial structures around the atrium such as adipose tissue possess arrhythmogenicity, little is known about atrial tachycardias (ATs) originating from epicardial sites (Epi‐ATs). This study aimed to elucidate the prevalence, characteristics, and outcome after radiofrequency catheter ablation (RFCA) of Epi‐ATs and to reveal the association between Epi‐ATs and the epicardial structures. Methods The electrocardiographic, electrophysiologic, and anatomical properties and results of RFCA were analyzed in 42 patients with a total of 49 ectopic ATs. Results Six Epi‐ATs (12%) were observed in six patients (14%). Four of six were respiratory cycle‐dependent ATs and one was a swallowing‐induced AT. The Epi‐AT origins were adjacent to a pulmonary vein (five cases) and vein of Marshall (one case). A Valsalva maneuver or atropine infusion to define the arrhythmia mechanism affected the appearance of the Epi‐ATs. The congruity rate between epicardial adipose tissue and the AT origin was significantly higher (100% vs. 44%, p = .045), and the epicardial adipose tissue volume of the atrium was significantly larger (104.1 vs. 64.6 ml, p = .04) in the Epi‐AT group. Endocardial RFCA targeting the AT foci resulted in acute success in five of five cases. However, electrical isolation including of the AT foci resulted in acute failures (two of three cases) or a recurrence (one of one case). Conclusions Six Epi‐ATs were associated with thoracic veins and epicardial arrhythmogenic structures. The main cause provoking the Epi‐ATs was associated with autonomic nerve activity.

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Increase of Autonomic Nerve Factors in Epicardial Ganglionated Plexi During Rapid Atrial Pacing Induced Acute Atrial Fibrillation

Zhou

et al. 2017

Med Sci Monit

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BackgroundThe cardiac autonomic nervous system plays an essential role in epicardial ganglionated plexi (GP) regulation of atrial fibrillation onset and progression. To date, the activity of GP and the function of the cardiac autonomic nervous system are not well understood. The aim of this study was to determine alterations in epicardial GP cholinergic nerve, adrenergic nerve, and nerve growth factor expression using rapid atrial pacing to induce atrial fibrillation in canines.Material/MethodsNine healthy adult beagles were divided into two groups: the pacing experimental group (n=6) and the sham-operation control group (n=3). For the pacing group, high frequency pacing of the left atrial appendage was performed for eight hours. In the control group, electrodes were implanted without rapid atrial pacing. Immunocytochemistry was used to identify neurons positively expressing tyrosine hydroxylase, choline acetyl transferase, nerve growth factor and neurturin.ResultsAfter successfully establishing a rapid atrial pacing of the left atrial appendage induced atrial fibrillation model, we found that expression of choline acetyl transferase, tyrosine hydroxylase, nerve growth factor, and neurturin was significantly higher in the rapid atrial pacing group than the control group (p<0.05).ConclusionsIn our model, incremental excitability of both the adrenergic and cholinergic nerves led to frequent incidents of atrial fibrillation, which were possibly due to an imbalance of autonomic nerve factors in the epicardial GP during acute atrial fibrillation.

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Experimental Model of Focal Atrial Tachycardia: Clinical Correlates

Cited by 3 publications

References 35 publications

Atrial Tachycardia Arising From the Crista Terminalis, Detailed Electrophysiological Features and Long-Term Ablation Outcomes

Atrial Tachycardia Arising From the Crista Terminalis, Detailed Electrophysiological Features and Long-Term Ablation Outcomes

The characteristics and efficacy of catheter ablation of focal atrial tachycardia arising from an epicardial site

Increase of Autonomic Nerve Factors in Epicardial Ganglionated Plexi During Rapid Atrial Pacing Induced Acute Atrial Fibrillation

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