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Journal Article
Obstructive sleep apnoea and atrial fibrillation: are we on time?
2024
Overview
Specifically, recurring apnoea–hypopnoea episodes, cortical arousals from sleep, and sleep fragmentation result in sympathetic overactivity and increased serum catecholamine levels, stimulating both heart rate and blood pressure. Additionally, 1) intermittent hypoxia promotes local and systemic inflammation, 2) oxidative stress and endothelial dysfunction induce atherosclerosis and 3) intrathoracic pressure fluctuation induces mechanical damage in vascular and cardiac structure and 4) negative intrathoracic pressure impairs LV filling and reduce stroke volume by means of increased venous return.4 All these conditions contribute to structural cardiac remodelling, including LV hypertrophy and left atrial enlargement and, over time, can lead to diastolic heart failure.5 Moreover, a final pathway leading to AF could be found in the modification of electrical proprieties of the atria. All these speculations suggest the need for more dedicated understanding of comorbid AF in patients with OSA and patients with OSA in AF. [...]the recent evolution in OSA therapy also opens the field for a personalised treatment approach.12 Ethics statements Patient consent for publication Not applicable.
Publisher
British Cardiovascular Society,BMJ Publishing Group LTD,BMJ Publishing Group
Subject
/ Atrial Fibrillation - complications
/ Atrial Fibrillation - diagnosis
/ Atrial Fibrillation - epidemiology
/ Atrial Fibrillation - etiology
/ Atrial Fibrillation - physiopathology
/ Continuous positive airway pressure
/ Heart
/ Humans
/ Hypoxia
/ Patients
/ Sleep Apnea, Obstructive - complications
/ Sleep Apnea, Obstructive - diagnosis
