PO-01-191 CARDIAC NERVE ACTIVITY DURING APNEA IN ATRIAL FIBRILLATION PATIENTS

Abstract

The cardiac autonomic system (CAS) is involved in the pathogenesis of atrial fibrillation (AF), particularly in AF’s association with sleep apnea. The human CAS response to apnea has not been characterized. The feasibility of CAS nerve recordings in humans has not been established. To record apnea-induced CAS nerve activity in humans before and after AF ablation. Six patients (age 70.8 ± 12.2 years; 66.7% men) undergoing paroxysmal (2/6) or persistent (4/6) AF ablation were enrolled in this study under an IRB-approved protocol. Under ultrasound and fluoroscopy guidance, multipolar catheters (EPR800, Millar, Houston, or EP star, Baylis, Toronto, CA) were placed in the stellate ganglion (SG) bilaterally and in the vein of Marshall (VOM). Nerve signals were recorded using a head stage digitizer via customized adapters and sampled at 30 kHz with a Grapevine recording system (Ripple, Salt Lake City, UT). Under general anesthesia, monitoring of arterial blood pressure, peripheral O2 (pO2) saturation and end-tidal CO2, apnea was induced by stopping ventilation until pO2 reached 90%, after which ventilation resumed. Four apneas were preformed– 2 before and 2 after ablation. Spike2 software (Cambridge Electronic Design, Cambridge, UK) was used to resolve nerve spike morphology, automatically discern spike morphologies, and quantify nerve activity. In all 6 patients, we observed increased VOM local nerve activation triggered by apnea, which were abolished by VOM ethanol infusion and AF ablation. We observed SG activation triggered by apnea in 2 out of 6 patients. In both cases SG activation were exaggerated after VOM ethanol infusion and AF ablation (Figure). In 4/6 SG activations were not recordable. CAS recording in humans undergoing AF ablation is feasible albeit inconsistent in the SG. Apnea produces activations of the CAS. VOM ethanol eliminates local nerve responses to apnea.