Abstract
Correction: Catheter-Based Renal Sympathetic Denervation Significantly Inhibits Atrial Fibrillation Induced by Electrical Stimulation of the Left Stellate Ganglion and Rapid Atrial Pacing
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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