What is the clinical evidence from this study?

Study design: Other. Population: Atrial Fibrillation (n=16). Intervention: Catheter-based renal sympathetic denervation vs. Sham ablation. Primary outcome: Atrial fibrillation induction rate (p=<0.05).

November 6, 2013Open Access

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

Q: What are the key findings of this study?

Catheter-based renal sympathetic denervation significantly reduced atrial fibrillation inducibility and reversed atrial electrophysiological changes induced by hyper-sympathetic activity.

Key Result

Catheter-based renal sympathetic denervation significantly reduced atrial fibrillation inducibility and reversed atrial electrophysiological changes induced by hyper-sympathetic activity.

Structured PICO

Does catheter-based renal sympathetic denervation reduce AF inducibility in a canine model of acute AF mediated by hyper-sympathetic activity?

Population

16 adult mongrel dogs subjected to left stellate ganglion stimulation and rapid atrial pacing to evaluate the effects of renal sympathetic denervation on atrial fibrillation inducibility.

Intervention

Catheter-based radiofrequency ablation of the renal sympathetic nerve (4 ablations per artery, 6-8 watts for 60 seconds each).

Comparator

Sham ablation (catheter introduced into the renal artery on both sides, no further procedures performed for 30 minutes).

Outcome

Atrial fibrillation (AF) induction rate.surrogate

Catheter-based renal sympathetic denervation significantly reduced AF inducibility and reversed atrial electrophysiological changes in a canine model of hyper-sympathetic activity.

Main Result

p-value: p=<0.05

Limitations

Direct neural firing from the stellate ganglion or renal sympathetic nerve was not recorded.
The spectral index LF, obtained from systolic arterial pressure variability, was not tested.
Renal arteriography was not performed before and after ablation to check for renal artery stenosis.
Anaesthesia is known to interfere with cardiovascular autonomic control.
Long-term changes of AF induction, electrophysiological data, and norepinephrine concentrations were not investigated.

Abstract

BACKGROUND: Sympathetic 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. METHODS: To 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. RESULTS: LSG 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). CONCLUSIONS: RSD significantly reduced AF inducibility and reversed the atrial electrophysiological changes induced by hyper-sympathetic activity.

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