Abstract
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.
Highlights
Atrial fibrillation (AF) is one of the most common arrhythmia and associated with high morbidity and mortality, but its pathogenesis is insufficiently understood
We had four major findings, including 1) renal denervation (RD) reduced the susceptibility to AF in a rabbit model of atrial fibrosis induced by abdominal aortic constriction (AAC), 2) RD was verified to reduce atrial fibrosis and decrease Renin-Angiotensin-Aldosterone System (RAAS) activation induced by AAC, 3) RD decreased protein expression of pro-fibrotic factors as transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) in atrial tissues, and 4) The relationship among RD, RAAS, atrial fibrosis and the susceptibility to AF was preliminary established
It remains controversial on the effect of catheter-based renal sympathetic denervation on resistant hypertension [11,12,13,14,15], RD might provide a new therapeutic strategy for diseases which are closely associated with hyper-sympathetic activity
Summary
Atrial fibrillation (AF) is one of the most common arrhythmia and associated with high morbidity and mortality, but its pathogenesis is insufficiently understood. Micro-reentrant circuits and atrial remodeling are regarded as the key pathophysiological basis. It’s indicated autonomic nervous system plays an important role in the occurrence and maintenance of AF [1,2,3]. Pokushalov E, et al demonstrated renal denervation (RD) reduced AF recurrences when combined with pulmonary vein isolation (PVI) [4]. Animal experiments showed episodes of AF were decreased by renal sympathetic denervation during both 7-hour and prolonged rapid atrial pacing [5,6]. The potential mechanisms for RD to reduce the susceptibility of AF have not been clearly understood so far
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