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BS-512-02 AUTONOMIC NEUROMODULATION FROM RENAL SYMPATHETIC DENERVATION PREVENTS ATRIAL FIBRILLATION VULNERABILITY CAUSED BY CHRONIC OBSTRUCTIVE SLEEP APENA IN A RABBIT MODEL

      Background

      Obstructive sleep apnea (OSA) has been reproducibly identified as an important risk factor for AF. Chronic OSA (COSA) induces a sympathetic overactivity and plays a critical role in the initiation and maintenance of AF.

      Objective

      The aim of this study was to evaluate the autonomic modulation effect of renal artery denervation (RDN) in the treatment of AF in COSA.

      Methods

      Eighteen rabbits, randomized to sham control, COSA and COSA receiving RDN groups. All rabbits were injected at the tongue base under endoscopic guidance with normal saline (sham control) or liquid silicone (COSA and COSA-RDN) 1 month prior to the experiment. Combined surgical and chemical RDNs were approached through bilateral retroperitoneal flank incisions in COSA-RDN two months prior to the experiment. The atrial effective refractory period (ARP) and window of vulnerability (WOV, the difference between the longest and shortest coupling interval of the premature stimulus that induced AF) during sleeping were measured. Immunoblots and immunohistochemistry were evaluated after experiment.

      Results

      During sleep, the arterial PCO2 was higher in COSA (69.3±3.4 mmHg), when compared to sham control (50.5±8.0 mmHg, p=0.006) and COSA-RDN (47.6±2.9 mmHg, p=0.004) respectively. There were no differences of ARPs of biatria among 3 groups (Fig A). Spontaneous initiation of AF (Fig B) was found in 2 of 6 rabbits in COSA, but not in other rabbits during sleep. The AF WOV was elevated in COSA (33.8±8.8 ms), when compared to sham control (5.7±3.0 ms, p=0.01) and COSA-RDN (9.3±4.1 ms, p=0.04), respectively. There was an increase of tyrosine hydroxylase nerve innervation in left atrium in COSA, compared to sham control and COSA-RDN, whereas renal catecholamine was decreased in COSA-RDN, compared to sham control and COSA groups (Table). There were no ionic channel protein expression differences among groups (Fig C).