Roles of adrenergic and cholinergic stimulation in spontaneous atrial fibrillation in dogs

Sharifov, Oleg F.; Fedorov, Vadim V.; Beloshapko, G. G.; Glukhov, Alexey V.; Yushmanova, A. V.; Rosenshtraukh, Leonid V.

doi:10.1016/j.jacc.2003.09.030

Cited by 264 publications

(172 citation statements)

References 19 publications

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“…Consistently, Sharifov et al 25 showed that acetylcholine-mediated AF was facilitated by isoproterenol, which decreased the threshold of acetylcholine concentration for AF induction and increased AF duration. Patterson et al 26 showed that the synergistic action of both the sympathetic and the parasympathetic neurotransmitters is required to initiate rapid ectopic discharges in superfused pulmonary vein preparations.…”

Section: Discussionmentioning

confidence: 69%

Renal Sympathetic Denervation Suppresses Postapneic Blood Pressure Rises and Atrial Fibrillation in a Model for Sleep Apnea

Linz

Mahfoud²,

Schotten³

et al. 2012

Hypertension

203

126

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Abstract-The aim of this study was to identify the relative impact of adrenergic and cholinergic activity on atrial fibrillation (AF) inducibility and blood pressure (BP) in a model for obstructive sleep apnea. Obstructive sleep apnea is associated with sympathovagal disbalance, AF, and postapneic BP rises. Renal denervation (RDN) reduces renal efferent and possibly also afferent sympathetic activity and BP in resistant hypertension. The effects of RDN compared with ␤-blockade by atenolol on atrial electrophysiological changes, AF inducibility, and BP during obstructive events and on shortening of atrial effective refractory period 5 Severe bradycardia and atrioventricular conduction disturbances together with postapneic blood pressure (BP) rises during the arousal are frequently seen in OSA and suggest sympathovagal activation. 6,7 Although enhanced vagal tone is known to induce shortening of the atrial effective refractory period (AERP), increased sympathetic tone may increase spontaneous triggered activity, both of which, when simultaneously occurring, could induce and maintain AF. 8 In addition, repetitive postapneic BP surges may lead to atrial structural changes and, thus, an arrhythmogenic substrate for AF. Previously, we showed that negative tracheal pressure (NTP) during obstructive respiratory events leads to pronounced shortening of the AERP, thereby perpetuating AF.9 These electrophysiological changes were mainly mediated by increased vagal tone because they were completely inhibited by atropine or bilateral vagotomy. However, less is known about the relative impact of adrenergic and cholinergic activity on AF inducibility and maintenance in OSA. We hypothesized that modulation of the sympathetic nervous system might reduce AF susceptibility and postapneic BP rises in OSA. Renal denervation is a new therapeutic approach to reduce sympathetic activity, BP, and apnea-hypopnea index (OSA severity) in resistant hypertension. [10][11][12][13] However, the effect of RDN on AF inducibility and BP during and after obstructive events is unknown. We tested the effect of denervation of the afferent and efferent renal sympathetic nerves shown previously to reduce renal and whole body sympathetic activity 10-12 and compared it with ␤-receptor blockade by atenolol on atrial electrophysiological changes and postapneic BP rises in a pig model for OSA. To check whether RDN displays its

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Section: Discussionmentioning

confidence: 69%

Renal Sympathetic Denervation Suppresses Postapneic Blood Pressure Rises and Atrial Fibrillation in a Model for Sleep Apnea

Linz

Mahfoud²,

Schotten³

et al. 2012

Hypertension

203

126

View full text Add to dashboard Cite

show abstract

“…Changes in sympathetic or parasympathetic tone alter the atrial action potential, as well as the refractory period, provoking depolarizations and triggered activity [69][70][71] . One in three patients with paroxysmal AF, and up to 70% of younger patients, present with well-defined adrenergic or vagal triggers 72,73 .…”

Section: Autonomic Dysfunctionmentioning

confidence: 99%

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

et al. 2015

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Despite the important advances that have enabled better stroke prevention in atrial fibrillation (AF) and more effective maintenance of sinus rhythm over the past decades, a large unmet need to improve the prevention and treatment of AF remains. Mortality for AF remains at 3.5% per year, and death is often experienced as sudden death or as a result of heart failure 1,2 . Each year, approximately 20% of patients with AF need to be hospitalized 3,4 , and stroke occurs in 1.5% of patients with AF who are receiving anticoagulant drugs 5 . Furthermore, more than half of the patients with AF are symptomatic despite adequate anticoagulation and rate control 4,6 . In view of the projected increase in the incidence and prevalence of AF 7-9 , as well as the substantial burden of death and dis ability that is still associated with this condition 10 , the status quo is unacceptable.Current management of patients with AF comprises treatment of the accompanying cardiovascular conditions, oral anticoagulation, rate control -with medications that slow atrioventricular nodal recovery or, rarely, with atrioventricular nodal ablation -and rhythm-control therapy with antiarrhythmic drugs, electrical cardioversion, catheter ablation or, at times, AF surgery 11,12 . Unfortunately, most of these current approaches are disconnected from our understanding of the major mechanisms that cause AF 1,13,14 1,2,7,19,20 Abstract | Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.230 | APRIL 2016 | VOLUME 13 www.nature.com/nrcardio CONSENSUS STATEMENT © 2 0 1 6 M a c m i l l a n P u b l i s h e r s L i m i t e d . A l l r i g h t s r e s e r v e d .

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“…57 Some patients have a predominantly sympathetic or vagal overactivity leading to AF, however, a combined sympathovagal activation is most commonly responsible for AF triggering. 58,59 Modulation of the autonomic system and its sympathetic limb, in particular, is of therapeutic interest in AF. Moxonidine is a centrally acting sympathoinhibitory agent.…”

Section: Moxonidinementioning

confidence: 99%

Status of Antiarrhythmic Drug Development for Atrial Fibrillation

Hanley

Robinson

Kowey

2016

Circ: Arrhythmia and Electrophysiology

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Roles of adrenergic and cholinergic stimulation in spontaneous atrial fibrillation in dogs

Abstract: These data indicate that although both autonomic systems play a role in AF, cholinergic stimulation is likely the main factor for spontaneous AF initiation in this animal model. Adrenergic tone modulates the initiation and maintenance of cholinergically mediated AF.

Cited by 264 publications

References 19 publications

Renal Sympathetic Denervation Suppresses Postapneic Blood Pressure Rises and Atrial Fibrillation in a Model for Sleep Apnea

Renal Sympathetic Denervation Suppresses Postapneic Blood Pressure Rises and Atrial Fibrillation in a Model for Sleep Apnea

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

Status of Antiarrhythmic Drug Development for Atrial Fibrillation

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