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The Role of Renal Sympathetic Denervation in Atrial Fibrillation.

ABSTRACT: Endocardial catheter ablation is a widely used alternative for the treatment of atrial fibrillation (AF). Despite technical improvements, and increased understanding of mechanism, and acquired technical experience over many years, the results are not yet optimal. This results in an ongoing search for new therapeutic approaches. Because cardiac sympathetic drive is potentially responsible for triggering and sustaining AF, modulation of sympathetic tone has been proposed as a viable treatment objective. The early attempts to test this concept were limited by nature=highly intrusive techniques but new approaches and targets have been recently introduced. Specifically, renal nerve ablation has been introduced and the first attempts to employ this technique for treatment of cardiac arrhythmias give as a promise of new therapeutic avenues in near future. This review focuses on the possible role of renal denervation in treatment of atrial fibrillation, the contemporary evidence supporting this approach, and the ongoing trials to establish its therapeutic role.

SUBMITTER: Kosiuk Md J

PROVIDER: S-EPMC4956128 | biostudies-literature | 2014 Feb-Mar

REPOSITORIES: biostudies-literature

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The Role of Renal Sympathetic Denervation in Atrial Fibrillation.

Kosiuk Md Jedrzej J Pokushalov Md Phd Evgeny E Hilbert Md Sebastian S Hindricks Md Gerhard G Bollmann Md PhD Andreas A S Steinberg Md Jonathan J

Journal of atrial fibrillation 20140228 5

Endocardial catheter ablation is a widely used alternative for the treatment of atrial fibrillation (AF). Despite technical improvements, and increased understanding of mechanism, and acquired technical experience over many years, the results are not yet optimal. This results in an ongoing search for new therapeutic approaches. Because cardiac sympathetic drive is potentially responsible for triggering and sustaining AF, modulation of sympathetic tone has been proposed as a viable treatment obje ...[more]

PMID: 27957040

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Project description:Background The autonomic nervous system response to apnea and its mechanistic connection to atrial fibrillation (AF) are unclear. We hypothesize that sensory neurons within the ganglionated plexi (GP) play a role. We aimed to delineate the autonomic response to apnea and to test the effects of ablation of cardiac sensory neurons with resiniferatoxin (RTX), a neurotoxic TRPV1 (transient receptor potential vanilloid 1) agonist. Methods Sixteen dogs were anesthetized and ventilated. Apnea was induced by stopping ventilation until oxygen saturations decreased to 80%. Nerve recordings from bilateral vagal nerves, left stellate ganglion, and anterior right GP were obtained before and during apnea, before and after RTX injection in the anterior right GP (protocol 1, n=7). Atrial effective refractory period and AF inducibility on single extrastimulation were assessed before and during apnea, and before and after intrapericardial RTX administration (protocol 2, n=9). GPs underwent immunohistochemical staining for TRPV1. Results Apnea increased anterior right GP activity, followed by clustered crescendo vagal bursts synchronized with heart rate and blood pressure oscillations. On further oxygen desaturation, a tonic increase in stellate ganglion activity and blood pressure ensued. Apnea-induced effective refractory period shortening from 110.20±31.3 ms to 90.6±29.1 ms ( P<0.001), and AF induction in 9/9 dogs versus 0/9 at baseline. After RTX administration, increases in GP and stellate ganglion activity and blood pressure during apnea were abolished, effective refractory period increased to 126.7±26.9 ms ( P=0.0001), and AF was not induced. Vagal bursts remained unchanged. GP cells showed cytoplasmic microvacuolization and apoptosis. Conclusions Apnea increases GP activity, followed by vagal bursts and tonic stellate ganglion firing. RTX decreases sympathetic and GP nerve activity, abolishes apnea's electrophysiological response, and AF inducibility. Sensory neurons play a role in apnea-induced AF.

Project description:Renal denervation (RD) was reported to reduce the susceptibility of atrial fibrillation (AF), but the underlying mechanism has not been well understood. This study was performed to investigate the effect of RD on the inducibility of AF in a rabbit model for atrial fibrosis and to explore the potential mechanisms. Thirty-five rabbits were randomly assigned into sham-operated group (n = 12), abdominal aortic constriction (AAC) group (n = 12) and AAC with RD (AAC-RD) group (n = 11). The incidence of AF induced by burst pacing in atriums was determined. Blood was collected to measure the levels of rennin, angiotensin II and aldosterone. Atrial samples were preserved to evaluate protein and gene expression of collagen, connective tissue growth factor (CTGF) and transforming growth factor-β1 (TGF-β1). Our data suggested cardiac structure remodeling and atrial fibrosis were successfully induced by AAC. Compared with the AAC group, the AAC-RD rabbits had smaller ascending aortic diameter and left ventricular end-systolic diameter. For burst pacing at the left atrium (LA), AF was induced in two of the 12 rabbits in the sham-operated group, 10 of the 12 rabbits in the AAC group, and 2 of the 11 rabbits in the AAC-RD group, with great difference among the three groups (P = 0.001). The percentage of LA burst stimulations with induced AF achieved 47.2% in the AAC group, which was higher than those in both the AAC-RD (12.1%) and the Sham-operated (5.6%) groups. Significantly increasing intercellular space in the AAC group (P<0.001) compared with the sham-operated rabbits. RD clearly decreased the volume fraction of collagen in LA and right atrium compared with that of the AAC group (P< 0.01). AAC-induced elevation of collagen I, CTGF and TGF-β1 was suppressed by RD. In conclusion, RD suppressed the inducibility of AF in a rabbit model for pressure associated atrial fibrosis, potentially by modulating renin-angiotensin-aldosterone system and decreasing pro-fibrotic factors.

Dataset Information

The Role of Renal Sympathetic Denervation in Atrial Fibrillation.

Publications

The Role of Renal Sympathetic Denervation in Atrial Fibrillation.

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