Experimental model for paroxysmal atrial fibrillation arising at the pulmonary vein-atrial junctions

Po, Sunny S.; Scherlag, Benjamin J.; Yamanashi, William S.; Edwards, Jeff T.; Jun, Zhou; Wu, Richard C.; Geng, Ning; Lazzara, Ralph; Jackman, Warren M.

doi:10.1016/j.hrthm.2005.11.008

Cited by 201 publications

(165 citation statements)

References 26 publications

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“…110,111 Stimulation of GP by pacing at the base of the PV can also provide a substrate of AF initiation from PV firing. 112,113 Studies have shown that the intrinsic ANS has a potential impact on acute atrial electrical remodeling induced by rapid atrial pacing.…”

Section: Section 2: Definitions Mechanisms and Rationale For Af Ablmentioning

confidence: 99%

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

Calkins,

Kuck,

Cappato

et al. 2012

Heart Rhythm

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Section: Section 2: Definitions Mechanisms and Rationale For Af Ablmentioning

confidence: 99%

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

Calkins,

Kuck,

Cappato

et al. 2012

Heart Rhythm

1,762

1,468

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“…Prior studies demonstrated that the cardiac ANS plays a critical role in the dynamics of AF initiation and maintenance. [2][3][4] Hyperactivity of the intrinsic cardiac ANS causes the release of excessive amount of acetylcholine and catecholamines and may lead to rapid firing from pulmonary veins (PVs) or non-PV sites. 4 Clinically, alterations of autonomic tone, involving the sympathetic and parasympathetic nervous systems, are implicated in initiating paroxysmal AF.…”

Section: Autonomic Nervous System In Afmentioning

confidence: 99%

Neural mechanisms of atrial fibrillation

Chen

2006

Heart Rhythm

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Purpose of review-The autonomic nerve system is a potentially potent modulator of the initiation and perpetuation of atrial fibrillation (AF). This review will briefly summarize the neural mechanisms of AF.Recent findings-Complex interactions exist between the sympathetic and parasympathetic nervous system on the atrial electrophysiologic properties. Direct autonomic recordings in canine models demonstrated simultaneous sympathovagal discharges are the most common triggers of paroxysmal atrial tachycardia and paroxysmal AF. Also, intrinsic cardiac autonomic nerve can serve as a sole triggering factor for the initiation of AF. Modulation of autonomic nervous system (ANS) by electrical stimulation has been tried as a treatment strategy clinically and experimentally. Recent studies showed that autonomic nervous system modulation can suppress the stellate ganglion nerve activity and reduce the incidence of paroxysmal atrial tachyarrhythmias in ambulatory dogs.Summary-The autonomic nerve system influences the initiation and perpetuation of AF. Scientific advances toward a better understanding of the complex interrelationships of the various components of the ANS will hopefully lead to improvement of treatments for this common arrhythmia.

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“…RAP can shorten ERP and increase ERP dispersion and ΣWOV, which were all reversed after GP ablation. Implementing GP ablation or autonomic blockers (atropine or propranolol) followed by RAP can prevent induced spontaneous AF and atrial electrical remodeling 26, 27. In our study, administrating A‐803467 can effectively attenuate ERP shortening and suppress increased ERP dispersion and ΣWOV, indicating a pharmacological denervation effect by this selective Na v 1.8 blocker.…”

Section: Discussionmentioning

confidence: 55%

Neuronal Na _v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

Chen

Shu

et al. 2016

JAHA

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BackgroundGanglionated plexus have been developed as additional ablation targets to improve the outcome of atrial fibrillation (AF) besides pulmonary vein isolation. Recent studies implicated an intimate relationship between neuronal sodium channel Nav1.8 (encoded by SCN10A) and AF. The underlying mechanism between Nav1.8 and AF remains unclear. This study aimed to determine the role of Nav1.8 in cardiac electrophysiology in an acute AF model and explore possible therapeutic targets.Methods and ResultsImmunohistochemical study was used on canine cardiac ganglionated plexus. Both Nav1.5 and Nav1.8 were expressed in ganglionated plexus with canonical neuronal markers. Sixteen canines were randomly administered either saline or the Nav1.8 blocker A‐803467. Electrophysiological study was compared between the 2 groups before and after 6‐hour rapid atrial pacing. Compared with the control group, administration of A‐803467 decreased the incidence of AF (87.5% versus 25.0%, P<0.05), shortened AF duration, and prolonged AF cycle length. A‐803467 also significantly suppressed the decrease in the effective refractory period and the increase in effective refractory period dispersion and cumulative window of vulnerability caused by rapid atrial pacing in all recording sites. Patch clamp study was performed under 100 nmol/L A‐803467 in TSA201 cells cotransfected with SCN10A‐WT,SCN5A‐WT, and SCN3B‐WT. IN a,P was reduced by 45.34% at −35 mV, and IN a,L by 68.57% at −20 mV. Evident fast inactivation, slow recovery, and use‐dependent block were also discovered after applying the drug.ConclusionsOur study demonstrates that Nav1.8 could exert its effect on electrophysiological characteristics through cardiac ganglionated plexus. It indicates that Nav1.8 is a novel target in understanding cardiac electrophysiology and SCN10A‐related arrhythmias.

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Experimental model for paroxysmal atrial fibrillation arising at the pulmonary vein-atrial junctions

Cited by 201 publications

References 26 publications

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

Neural mechanisms of atrial fibrillation

Neuronal Na _v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

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Experimental model for paroxysmal atrial fibrillation arising at the pulmonary vein-atrial junctions

Cited by 201 publications

References 26 publications

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

Neural mechanisms of atrial fibrillation

Neuronal Na v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

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Product

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Neuronal Na _v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention