Key result
Renal denervation completely prevented the 1.5-fold increase in atrial fibrillation inducibility and 1.86-fold prolongation of atrial fibrillation duration induced by renal impairment in beagles.
Why the study?
Does renal denervation reduce atrial fibrillation inducibility in a beagle model of renal impairment?
Does renal denervation reduce atrial fibrillation inducibility in a beagle model of renal impairment?
In a beagle model of renal impairment, renal denervation suppressed atrial fibrillation inducibility by reducing sympathetic drive, RAAS activity, inflammation, and atrial fibrosis.
BACKGROUND: A close association exists between renal impairment (RI) and atrial fibrillation (AF) occurrence. Increased activity of the sympathetic nervous system (SNS) may contribute to the development of AF associated with RI. Renal denervation (RDN) decreases central sympathetic activity. OBJECTIVE: The main objective of the study was to explore the effects of RDN on AF occurrence and its possible mechanisms in beagles with RI. METHODS: Unilateral RI was induced in beagles by embolization of small branches of the renal artery in the right kidney using gelatin sponge granules in Model (n = 6) and RDN group (n = 6). The Sham group (n = 6) underwent the same procedure, except for embolization. Then animals in RDN group underwent radiofrequency ablation of the renal sympathetic nerve. Cardiac electrophysiological parameters, blood pressure, left ventricular end-diastolic pressure, and AF inducibility were investigated. The activity of the SNS, renin-angiotensin-aldosterone system (RAAS), inflammation and atrial interstitial fibrosis were measured. RESULTS: Embolization of small branches of the renal artery in the right kidney led to ischemic RI. Heart rate, P wave duration and BP were increased by RI, which were prevented or attenuated by RDN. Atrial effective refractory period was shortened and AF inducibility was increased by RI, which were prevented by RDN. Antegrade Wenckebach point was shortened, atrial and ventricular rates during AF were increased by RI, which were attenuated or prevented by RDN. Levels of norepinephrine, renin and aldosterone in plasma, norepinephrine, angiotensin II, aldosterone, interleukin-6 and high sensitivity C-reactive protein in atrial tissue were elevated, and atrial interstitial fibrosis was enhanced by RI, which were attenuated by RDN. CONCLUSIONS: RDN significantly reduced AF inducibility, prevented the atrial electrophysiological changes in a model of RI by combined reduction of sympathetic drive and RAAS activity, and inhibition of inflammation activity and fibrotic pathway in atrial tissue.
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Liang et al. (2015) studied Renal impairment and atrial fibrillation (n=18). Renal denervation vs. Sham procedure and renal impairment without denervation was evaluated on Atrial fibrillation inducibility (p=<0.05). Renal denervation completely prevented the 1.5-fold increase in atrial fibrillation inducibility and 1.86-fold prolongation of atrial fibrillation duration induced by renal impairment in beagles.
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