Fatigue and Cognitive Impairment in Adults With Primary Sclerosing Cholangitis: Results From Concept Elicitation Interviews.

Obstructive sleep apnea (OSA) is highly prevalent among patients with atrial fibrillation (AF) [, ] and significantly compromises the efficacy of rhythm control interventions []. Current patient assessment involves a thorough clinical evaluation, the use of validated sleep questionnaires, and comprehensive sleep studies to confirm the diagnosis of sleep-disordered breathing (SDB) []. However, the optimal screening modality for SDB in AF patients has yet to be established. While in-laboratory manually scored polysomnography (PSG) sleep recordings are the gold standard for the diagnosis of SDB, through the monitoring of brain activity (electroencephalography, EEG), eye movements (electrooculography, EOG), muscle activity (electromyography, EMG), heart rhythm (electrocardiography, ECG), respiratory airflow and effort, pulse oximetry, body position, and snoring [], the associated costs and logistical challenges limit its scalability for routine AF diagnosis and management. Consequently, home sleep apnea testing (HSAT) has emerged as a more feasible alternative. However, standard HSAT primarily monitors respiratory parameters and oxygen saturation levels but does not measure neurophysiological channels (EEG, EOG, and EMG), necessary to identify sleep stages and arousals []. These limitations diminish the effectiveness of diagnosing SDB beyond OSA. Crucially, it may lead to the underdiagnosis of OSA in patients with limited sleep duration or those exhibiting a high proportion of hypopneas associated with arousals rather than significant oxygen desaturation []. Furthermore, HSAT cannot adequately diagnose other sleep disorders common in AF patients, such as insomnia []. The diagnostic challenge arises from the overlapping nonspecific symptoms between AF and OSA []. Symptoms such as nocturnal dyspnea, fatigue, exercise intolerance, and cognitive alterations are frequently attributed solely to underlying cardiac disease and AF, leading to underdiagnosis of OSA [–]. Conversely, symptoms primarily driven by AF—such as nocturnal palpitations and sleep disruption—may be misattributed to OSA, potentially delaying appropriate cardiac evaluation. On the other hand, unrecognized OSA perpetuates and exacerbates AF through several well-characterized pathophysiological mechanisms, including intermittent hypoxemia, increased sympathetic activation, and cardiac structural remodeling [, ]. Given the substantial impact that OSA diagnosis has on AF outcomes, including increased recurrence rates after cardioversion, reduced efficacy of antiarrhythmic medications [], and higher cardiovascular mortality [], an accurate diagnosis of these patients becomes imperative.