Origin and pharmacological response of atrial tachyarrhythmias induced by activation of mediastinal nerves in canines

Armour, J. Andrew; Richer, Louis-Philippe; Pagé, Pierre; Vinet, Alain; Kús, Teresa; Vermeulen, Michel; Nadeau, Réginald; Cardinal, René

doi:10.1016/j.autneu.2005.01.006

Cited by 39 publications

(80 citation statements)

References 24 publications

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“…As in experiments (2,16,31,33), cholinergic concomitant with adrenergic stimulation promoted reentry. We identified the pacemaker complex itself as a possible source of reentry.…”

Section: Discussionmentioning

confidence: 76%

“…The escape beat initiating the tachyarrhythmia is primarily located in either the intercaval region or an area underlying a major ganglionated plexus (2). However, the electrophysiologic conditions necessary that give rise to the preceding observations and reentry remain unelucidated.…”

mentioning

confidence: 99%

“…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 tachyarrhythmia is primarily located in either the intercaval region or an area underlying a major ganglionated plexus (2).…”

mentioning

confidence: 99%

“…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).…”

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confidence: 99%

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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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“…As in experiments (2,16,31,33), cholinergic concomitant with adrenergic stimulation promoted reentry. We identified the pacemaker complex itself as a possible source of reentry.…”

Section: Discussionmentioning

confidence: 76%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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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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“…In addition, temporary increases in autonomic neural conduction in the atrium change pacemaker activity. As a result, distance increases between new evolved areas from the AV node (12) . These pacemaker shifts cause temporary changes in P waves on ECG.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Severity of Obstructive Sleep Apnea and PR Interval

Karamanli¹,

Aygün²,

Akgedik³

2016

Kosuyolu Heart Journal

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Introduction: Relationship between obstructive sleep apnea (OSA) and electrocardiogram and OSA severity index relationship that may affect the PR interval were studied. Patients and Methods:This study included 85 people who had OSA diagnosed at our clinic between January 2013 and August 2013. Their polysomnography (PSG) reports were evaluated by physicians who are expert in their fi elds. Individuals with severe OSA diseases were categorized as group 1, and individuals with mild to moderate OSA were categorized as group 2.Results: Age distribution of individuals who participated to the study ranged from 20 years to 85 years (mean ± standard deviation, 45.5 ± 13.2 years). Fifty-one (60%) of those individuals were men, and 34 (40%) of them were women. The PR interval for the group who had severe OSA on PSG (group 1) was 163.1 ± 35.2 ms, and it was 147.8 ± 29.3 in group 2. Conclusion:It was observed that individuals having severe OSA had higher PR intervals than individuals who had mild to moderate OSA. It was determined that results were statistically signifi cant (p< 0.05, p= 0.032). We believe that apnea-hypopnea index, oxygen desaturation index, and arousal values, which are indications of OSA severity and parameters of hypoxia-reoxygenation, contribute to PR prolongation. Sonuç: Şiddetli OSA tanısı alan bireylerin, hafi f ve orta şiddette OSA tanısı alan bireylere göre PR sürelerinin yüksek olduğu görüldü. Sonucun istatiksel olarak anlamlı olduğu tespit edildi (p< 0.05, p= 0). OSA şiddeti göstergesi ve hipoksi-reoksijenizasyon parametreleri olan AHI (apne-hipopne indeksi), ODI (oksijen desaturasyon indeksi); arousal değerleri PR uzamasında katkı sağladığına inanmaktayız.

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