P084 Does OSA endotype impact the incidence of atrial fibrillation and the severity of atrial remodelling? A retrospective cohort study.

Abstract Background Multiple studies have suggested that the prevalent sleep disorder obstructive sleep apnoea (OSA) plays a key role in initiating and progressing atrial fibrillation (AF) as well as impacting the response to arrhythmia pharmaco- and ablative therapy. The mechanisms underlying how OSA mediates this relationship however are poorly understood. It is now recognised that OSA is caused by four key pathophysiological factors (i.e., endotypic traits). These include a compromised upper airway anatomy, reduced pharyngeal dilator muscle effectiveness, low arousal threshold and a hypersensitive ventilatory control system (high loop gain). However, there have been no studies to date that have examined the relationship between the OSA endotypic traits in those individuals with OSA + AF as well as comparing them to OSA patients without AF (OSA-AF). Methods A cohort of 53 patients with moderate–severe OSA planned for AF ablation underwent a home or laboratory polysomnogram (PSG) as part of the previous SLEEP-AF project. We will extract measures of the four OSA traits from these PSGs using a validated methodology and compare the association with the severity of atrial remodelling. We will then also compare differences in the OSA traits against a cohort of matched patients without AF. Progress to date Thus far the data has been collated and is being exported into Matlab in order to extract the OSA traits. Intended outcome and impact We hypothesise that the presence of certain OSA endotypes may increase the rate and severity of atrial fibrillation. Knowledge of these underlying mechanisms may help guide targeted treatment interventions.