Spatial Distribution and Frequency Dependence of Arrhythmogenic Vagal Effects in Canine Atria

Sharifov, Oleg F.; Zaitsev, Alexey V.; Rosenshtraukh, Leonid V.; Kaliadin, Y B S Alexandr; Beloshapko, G. G.; Yushmanova, A. V.; Schuessler, Richard B.; Boineau, John P.

doi:10.1111/j.1540-8167.2000.tb00176.x

Cited by 58 publications

(44 citation statements)

References 25 publications

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“…26 The present study complements our previous report that electric stimuli applied to the right-sided ventral mediastinal nerves coursing along the superior vena cava elicit atrial tachyarrhythmias that were consistently associated with repolarization changes within the upper portion of the RA subsidiary pacemaker complex in proximity to the superior vena cava ostium 16 ; the tachyarrhythmias thus induced were preceded by bradycardia in all cases. 19 This is in contrast with the present findings that the tachyarrhythmia sites of origin were identified from several LA locations and that only a minority of the tachyarrhythmias induced by left-sided dorsal mediastinal nerve stimulation were preceded by sinus cycle length prolongation.…”

Section: Sites Of Origin Of Atrial Premature Depolarizations and Initsupporting

confidence: 72%

Atrial Tachyarrhythmias and Repolarization Changes Induced by Discrete Activation of Dorsal Mediastinal Cardiac Nerves in Canines

Cardinal

Armour

Bouchard

et al. 2010

Circ: Arrhythmia and Electrophysiology

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Background-Chronotropic "vagal responses" elicited by high-frequency stimulation have been used to identify atrial targets for ablative treatment of atrial tachyarrhythmias (AT), whereas an anatomic approach consisting of extensive ablation of the ganglionated plexus areas has been proposed as an alternative. Therefore, there is a need for precise delineation of juxtacardiac nerves involved in AT initiation and clarification of their regional influences throughout the atria in relation to AT sites of origin, beyond chronotropic effects related to sinus node modulation. Methods and Results-Unipolar electrograms were recorded from 191 biatrial epicardial sites in 13 anesthetized canines, with concomitant left atrial endocardial recording from 63 sites in 5 of 13 animals. When electric stimuli were delivered to dorsal mediastinal nerves during the atrial refractory period, atrial premature depolarizations initiating AT were elicited in all animals, most frequently without prior sinus cycle length modification. Among 63 episodes, the sites of origin of early AT beats were localized to (1) the posterolateral left atrial wall in the pulmonary vein region (33%), (2) superior left atrial loci along the Bachmann bundle (55%), and (3) the region of Bachmann bundle insertion into the superior right atrial wall (11%). Moreover, the AT sites of origin were spatially concordant with regional waveform changes during the repolarization phase of unipolar recordings. AT induction and repolarization changes were abolished after atropine administration. Conclusions-Activation of individual dorsal mediastinal nerves induces AT arising from distinct sites of origin which are spatially concordant with regional atrial repolarization changes. (Circ Arrhythm Electrophysiol. 2010;3:511-520.)

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Section: Sites Of Origin Of Atrial Premature Depolarizations and Initsupporting

confidence: 72%

Atrial Tachyarrhythmias and Repolarization Changes Induced by Discrete Activation of Dorsal Mediastinal Cardiac Nerves in Canines

Cardinal

Armour

Bouchard

et al. 2010

Circ: Arrhythmia and Electrophysiology

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“…15,16 Vagal nerve stimulation appears to contribute to AF substrate by non-uniform shortening of atrial effective refractory periods, creating conditions conducive to reentry. 17,18 Vagal nerve stimulation can also create conditions for the emergence of focal triggers in the atrium, as suggested by studies conducted by Sharifov et al 19 More recently, both limbs of the autonomic nervous system have been shown to play a role in AF in at least some patients. Amar et al showed that onset of AF was preceded by a primary increase in sympathetic drive followed by marked modulation toward vagal predominance 20 Sharifov et al showed that although acetylcholine alone could induced AF in all the dogs that were studied, acetylcholine-induced AF was facilitated by isoproterenol, which decreased the concentration of acetylcholine required for AF induction and maintenance.…”

Section: 12mentioning

confidence: 83%

Role of the Autonomic Nervous System in the Creation of Substrate for Atrial Fibrillation

Arora¹,

Kadish²

2008

J.A.F.I.B

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“…In control, activation maps revealed typical excitation patterns for both atrial substrates (Fig. 3A) with the LPS situated consistently in the intercaval region and activation spreading smoothly over the RA in 70 -80 ms (34). In a simulation subset, immediately after ACh application, bradycardic impulses arose in the inferior central SAN but activation was monofocal.…”

Section: Discussionmentioning

confidence: 99%

Onset of atrial arrhythmias elicited by autonomic modulation of rabbit sinoatrial node activity: a modeling study

Munoz

Kaur

Vigmond

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Muñoz MA, Kaur J, Vigmond EJ. Onset of atrial arrhythmias elicited by autonomic modulation of rabbit sinoatrial node activity: a modeling study. Am J Physiol Heart Circ Physiol 301: H1974-H1983, 2011. First published August 19, 2011 doi:10.1152/ajpheart.00059.2011.-Neuronal modulation of the sinoatrial node (SAN) plays a crucial role in the initiation and maintenance of atrial arrhythmias (AF), although the exact mechanisms remain unclear. We used a computer model of a rabbit right atrium (RA) with a heterogeneous SAN and detailed ionic current descriptions for atrial and SAN myocytes to explore reentry initiation associated with autonomic activity. Heterogeneous acetylcholine (ACh)-dependent ionic responses along with L-type Ca current (ICa,L) upregulation were incorporated in the SAN only. During control, activation was typical with the leading pacemaker site located close to the superior vena cava or the intercaval region. With cholinergic stimulation, activation patterns frequently included caudal shifts of the leading pacemaker site and occasional double breakouts. The model became increasingly arrhythmogenic for the ACh concentration Ͼ20 nM and for large ICa,L conductance. Reentries obtained included counterclockwise rotors in the free wall, clockwise reentry circulating between the SAN and free wall, and typical flutter. The SAN was the cause of reentry with a common leading sequence of events: a bradycardic beat with shifting in the caudal direction, followed by a premature beat or unidirectional block within the SAN. Electrotonic loading, and not just overdrive pacing, squelches competing pacemaker sites in the SAN. Cholinergic stimulation concomitant with I Ca,L upregulation shifts leading pacemaker site and can lead to reentry. A heterogeneous response to autonomic innervation, a large myocardial load, and an extensive SAN in the intercaval region are required for neurally induced SAN-triggered reentry. electrophysiology; reentry; autonomic innervation ATRIAL FIBRILLATION (AF) is the most common and diverse cardiac arrhythmia (21). Experimental observations have illustrated the crucial role that neuronal mechanisms have in its initiation and maintenance (33). Atrial arrhythmias can be induced in dogs by localized electrical stimuli applied to nerve branches of the thoracic vagosympathetic complex (31) or mediastinal nerves (2, 31). Experiments show that acetylcholine (ACh) can trigger reentry and AF in the right atrium (RA) and that adrenergic stimulation facilitates both AF initiation and maintenance (33). Atropine completely abolishes bradycardia and subsequent tachyarrhythmias, indicating that cholinergic efferents play a predominant role in induction (33).Different studies describe a similar sequence of events for arrhythmias originating in the RA that were induced by neural stimulation: cycle length (CL) prolongation, often with leading pacemaker site (LPS) shifting, followed by an atrial premature beat (APB), and subsequent tachyarrhythmia (1, 2, 31, 33). The escape beat initiating the tachyarr...

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Spatial Distribution and Frequency Dependence of Arrhythmogenic Vagal Effects in Canine Atria

Cited by 58 publications

References 25 publications

Atrial Tachyarrhythmias and Repolarization Changes Induced by Discrete Activation of Dorsal Mediastinal Cardiac Nerves in Canines

Atrial Tachyarrhythmias and Repolarization Changes Induced by Discrete Activation of Dorsal Mediastinal Cardiac Nerves in Canines

Role of the Autonomic Nervous System in the Creation of Substrate for Atrial Fibrillation

Onset of atrial arrhythmias elicited by autonomic modulation of rabbit sinoatrial node activity: a modeling study

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