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Acute Vagal Modulation of Electrophysiology of the Atrial and Pulmonary Veins Increases Vulnerability to Atrial Fibrillation

2011-02Journal article Open access
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dc.contributor.authorOliveira, MM
dc.contributor.authorNogueira da Silva, M
dc.contributor.authorGeraldes, V
dc.contributor.authorXavier, R
dc.contributor.authorLaranjo, S
dc.contributor.authorSilva, V
dc.contributor.authorPostolache, G
dc.contributor.authorCruz Ferreira, R
dc.contributor.authorRocha, I
dc.date.accessioned2019-11-12T16:30:29Z
dc.date.available2019-11-12T16:30:29Z
dc.date.issued2011-02
dc.description.abstractVagal activity is thought to influence atrial electrophysiological properties and play a role in the initiation and maintenance of atrial fibrillation (AF). We evaluated the effects of acute vagal stimulation on atrial conduction, refractoriness of atrial and pulmonary veins (PVs) and inducibility of AF. An open-chest epicardial approach was performed in New Zealand White rabbits with preserved autonomic innervation. Atrial electrograms were obtained with four unipolar electrodes placed epicardially along the atria (n = 22) and an electrode adapted to the proximal left PV (n = 10). The cervical vagus nerve was stimulated with bipolar platinum electrodes (20 Hz). Epicardial activation was recorded in sinus rhythm, and effective refractory periods (ERPs), dispersion of refractoriness and conduction times from high-lateral right atrium (RA) to high-lateral left atrium (LA) and PVs assessed at baseline and during vagal stimulation. Burst pacing (50 Hz, 10 s), alone or combined with vagal stimulation, was applied to the right (RAA) and left atrial appendage (LAA) and PVs to induce AF. At baseline, ERPs were lower in PVs than in LA and LAA, but did not differ significantly from RA and RAA, and there was a significant delay in the conduction time from RA to PVs compared with the activation time from RA to LA (P < 0.01). During vagal stimulation, ERP decreased significantly at all sites, without significant differences in the dispersion of refractoriness, and the atrial conduction times changed from 39 ± 19 to 49 ± 9 ms (RA to PVs; n.s.) and from 14 ± 7 to 28 ± 12 ms (RA to LA; P = 0.01). Induction of AF was reproducible in 50% of cases with 50 Hz and in 82% with 50 Hz combined with vagal stimulation (P < 0.05). During vagal stimulation, AF cycle length decreased at all sites, and AF duration changed from 1.0 ± 0.9 to 14.0 ± 10.0 s (P < 0.01), with documentation of PV tachycardia in three cases. In 70% of the animals, AF ceased immediately after interruption of vagal stimulation. We conclude that in the intact rabbit heart, vagal activity prolongs interatrial conduction and shortens atrial and PV ERP, contributing to the vulnerability to the induction and maintenance of AF. This model may be useful in the assessment of the autonomic influence in the mechanisms underlying AF.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationExp Physiol. 2011 Feb;96(2):125-33.pt_PT
dc.identifier.doi10.1113/expphysiol.2010.053280pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.17/3359
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWileypt_PT
dc.subjectAnimalspt_PT
dc.subjectAtrial Fibrillationpt_PT
dc.subjectCoronary Vesselspt_PT
dc.subjectFemalept_PT
dc.subjectHeart Atriapt_PT
dc.subjectHeart Conduction Systempt_PT
dc.subjectMalept_PT
dc.subjectPulmonary Veinspt_PT
dc.subjectRabbitspt_PT
dc.subjectVagus Nervept_PT
dc.subjectVagus Nerve Stimulationpt_PT
dc.subjectHSM CARpt_PT
dc.titleAcute Vagal Modulation of Electrophysiology of the Atrial and Pulmonary Veins Increases Vulnerability to Atrial Fibrillationpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage133pt_PT
oaire.citation.issue2pt_PT
oaire.citation.startPage125pt_PT
oaire.citation.titleExperimental Physiologypt_PT
oaire.citation.volume96pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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