Autonomic trigger patterns and anti-arrhythmic treatment of paroxysmal atrial fibrillation: data from the Euro Heart Survey

Vos, Cees B. de; Nieuwlaat, Robby; Crijns, Harry J.G.M.; Camm, A. John; LeHeuzey, Jean-Yves; Kirchhof, C; Capucci, Alessandro; Breithardt, Günter; Vardas, Panos; Pisters, Ron; Tieleman, Robert G

doi:10.1093/eurheartj/ehn025

Cited by 100 publications

(64 citation statements)

References 19 publications

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“…8,18,19 Interestingly, studies in lone AF patients and in animal models of both intermittent rapid atrial pacing and congestive heart failure have indicated that AF onset is associated with simultaneous sympathovagal activation rather than with an increase in vagal or sympathetic drive alone. [20][21][22][23] Previously we have shown increased AF susceptibility and AF duration caused by pronounced AERP shortening in a pig model for OSA.…”

Section: Discussionmentioning

confidence: 91%

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

Linz

Mahfoud²,

Schotten³

et al. 2012

Hypertension

204

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: 91%

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

Linz

Mahfoud²,

Schotten³

et al. 2012

Hypertension

204

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 . Low-level vagal stimulation prevents AF by decreasing sympathetic and parasympathetic cardiac responsiveness in animal models susceptible to AF 74 .…”

Section: Autonomic Dysfunctionmentioning

confidence: 99%

“…Low-level vagal stimulation prevents AF by decreasing sympathetic and parasympathetic cardiac responsiveness in animal models susceptible to AF 74 . High-intensity endurance training is an evolving risk factor underlying AF in middle-aged Europeans without overt structural heart disease 75,76 , which can be mediated by an elevated parasympathetic tone, structural changes, or by changes in ion-channel expression 14,73,77 . Similarly, AF in patients with obstructive sleep apnoea can be provoked by autonomic imbalance 14,78 .…”

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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“…There is evidence suggesting that the autonomic nervous system plays an important role in both the initiation and the maintenance of AF in humans. [30][31][32][33] Consistently, β-receptor blockade by metoprolol has been shown to maintain sinus rhythm after conversion from persistent AF in humans. 34 RDN may display comparable effects.…”

Section: Ecg-intervals (Ms)mentioning

confidence: 99%

Renal Sympathetic Denervation Provides Ventricular Rate Control But Does Not Prevent Atrial Electrical Remodeling During Atrial Fibrillation

et al. 2013

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A trial fibrillation (AF) is a frequent complication of longstanding hypertension and represents the most common cardiac arrhythmia causing significant morbidity and mortality.1-3 During AF, normal atrioventricular (AV) node conduction leads to a rapid and irregular ventricular rate, resulting in an impairment of left ventricular function and exercise capacity. 4 Rate control can be achieved by drugs modulating the autonomic nervous system, for example, by β-blockers. Genetic inhibition of inhibitory Gα protein in the AV node reduced heart rate (HR) and prevented AF-associated reduction of cardiac function in a porcine model for persistent AF. 5In addition, AF causes atrial electrical remodeling mainly characterized by a pronounced atrial effective refractory period (AERP) shortening perpetuating AF.6 Alterations in the autonomic nervous system may influence AF-induced atrial electrical remodeling and atrial arrhythmogenesis.7-9 Catheterbased renal denervation (RDN) is a new therapeutic approach to reduce sympathetic activity and blood pressure (BP) and to improve obstructive sleep apnea severity and glucose metabolism in resistant hypertension. [10][11][12][13][14][15] However, the effect of RDN on ventricular HR response during AF (rate control) and AF-induced electrical remodeling is unknown.Herein, we report on the effect of catheter-based RDN, shown previously to reduce renal and whole body sympathetic activity, 12-14 on rate control in a patient with permanent AF and resistant hypertension. Subsequently, we investigated the effect of denervation of the afferent and efferent renal sympathetic nerves in a pig model with short-term AF maintained by rapid atrial pacing. Methods Catheter-Based RDN in a Patient With AFThe patient gave written informed consent. Catheter-based RDN was performed as described previously.11-15 Renal angiogram was performed via femoral access to exclude renal artery stenosis. The treatment catheter (Symplicity Catheter System, Ardian/Medtronic USA) Abstract-Renal denervation (RDN) reduces renal efferent and afferent sympathetic activity thereby lowering blood pressure in resistant hypertension. The effect of modulation of the autonomic nervous system by RDN on atrial electrophysiology and ventricular rate control during atrial fibrillation (AF) is unknown. Here we report a reduction of ventricular heart rate in a patient with permanent AF undergoing RDN. Subsequently, we investigated the effect of RDN on AF-induced shortening of atrial effective refractory period, AF inducibility, and ventricular rate control during AF maintained by rapid atrial pacing in 12 pigs undergoing RDN (n=7) or sham procedure (n=5

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Autonomic trigger patterns and anti-arrhythmic treatment of paroxysmal atrial fibrillation: data from the Euro Heart Survey

Cited by 100 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

Renal Sympathetic Denervation Provides Ventricular Rate Control But Does Not Prevent Atrial Electrical Remodeling During Atrial Fibrillation

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