Abstract
BackgroundSympathetic activity involves the pathogenesis of atrial fibrillation (AF). Renal sympathetic denervation (RSD) decreases sympathetic renal afferent nerve activity, leading to decreased central sympathetic drive. The aim of this study was to identify the effects of RSD on AF inducibility induced by hyper-sympathetic activity in a canine model.MethodsTo establish a hyper-sympathetic tone canine model of AF, sixteen dogs were subjected to stimulation of left stellate ganglion (LSG) and rapid atrial pacing (RAP) for 3 hours. Then animals in the RSD group (n = 8) underwent radiofrequency ablation of the renal sympathetic nerve. The control group (n = 8) underwent the same procedure except for ablation. AF inducibility, effective refractory period (ERP), ERP dispersion, heart rate variability and plasma norepinephrine levels were measured at baseline, after stimulation and after ablation.ResultsLSG stimulation combined RAP significantly induced higher AF induction rate, shorter ERP, larger ERP dispersion at all sites examined and higher plasma norepinephrine levels (P<0.05 in all values), compared to baseline. The increased AF induction rate, shortened ERP, increased ERP dispersion and elevated plasma norepinephrine levels can be almost reversed by RSD, compared to the control group (P<0.05). LSG stimulation combined RAP markedly shortened RR-interval and standard deviation of all RR-intervals (SDNN), Low-frequency (LF), high-frequency (HF) and LF/HF ratio (P<0.05). These changes can be reversed by RSD, compared to the control group (P<0.05).ConclusionsRSD significantly reduced AF inducibility and reversed the atrial electrophysiological changes induced by hyper-sympathetic activity.
Highlights
Atrial fibrillation (AF) is a complex arrhythmia with multiple mechanisms
Zhao et al [13] showed that renal sympathetic denervation (RSD) could decrease episodes of atrial fibrillation (AF) during short-time rapid atrial pacing, which might correlate with decreased activity of both renin–angiotensin–aldosterone system (RAAS) and renal sympathetic nerve
We developed an animal model by delivering rapid atrial pacing in the presence of a hypersympathetic tone induced by stimulation of left stellate ganglion (LSG) to evaluate the effects of RSD on AF inducibility, atrial electrophysiological changes and cardiac autonomic activity
Summary
Atrial fibrillation (AF) is a complex arrhythmia with multiple mechanisms. Electrical, structural and neural remodelling contribute to the AF substrate. Linz et al [11] reported that RSD reduced blood pressure, atrial effective refractory period (ERP) shortening and inducibility of vagally mediated atrial fibrillation in a model of obstructive sleep apnea. They showed that electrical baroreflex stimulation significantly shortened atrial refractoriness, thereby causing increased AF inducibility. Zhao et al [13] showed that RSD could decrease episodes of AF during short-time rapid atrial pacing, which might correlate with decreased activity of both renin–angiotensin–aldosterone system (RAAS) and renal sympathetic nerve. The aim of this study was to identify the effects of RSD on AF inducibility induced by hyper-sympathetic activity in a canine model
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