The OSA and Afib Relationship: Guidance for Clinicians
Several pathophysiologic mechanisms linking OSA to the development of AF have been proposed. AF probably occurs as a complex interaction of several hemodynamic and sympathetic consequences of OSA. These include autonomic dysregulation, elevated sympathetic tone, oxidative stresses, endothelial dysfunction, and left atrial stretch.
OSA produces structural changes in the heart that can result in aberrant conduction and, subsequently, AF. Repetitive increases in upper airway resistance that occur with OSA produce alterations in the transpleural and intrathoracic pressure gradients. The resultant transmural force leads to atrial stretch, enlargement, and remodeling. This increase in left atrial volume is a well-established predisposing factor for AF.This altered pressure gradient also leads to autonomic dysregulation. In a study by Linz and colleagues, the increased negative tracheal pressure that occurs during obstructive events was shown to shorten the right atrial refractory period and increase susceptibility to AF through enhanced vagal activation.
Obstructive respiratory events produce intermittent desaturations, hypoxia, catecholamine release, and abrupt increases in arterial pressure. These phenomena result in endothelial dysfunction and sympathetic activation that could lead to AF. Whether the development of AF in patients with OSA is the result of a cumulative effect of these factors or a final etiologic factor in susceptible patients is not well established. AF is more common in patients with severe OSA than those with lower AHIs, which would suggest the former. Only a longitudinal study assessing derangements in left atrial size and function and the development of AF among patients with a wide range of OSA severity would be able to answer this clinical question.
Mechanism of AF in Patients With OSA
Several pathophysiologic mechanisms linking OSA to the development of AF have been proposed. AF probably occurs as a complex interaction of several hemodynamic and sympathetic consequences of OSA. These include autonomic dysregulation, elevated sympathetic tone, oxidative stresses, endothelial dysfunction, and left atrial stretch.
OSA produces structural changes in the heart that can result in aberrant conduction and, subsequently, AF. Repetitive increases in upper airway resistance that occur with OSA produce alterations in the transpleural and intrathoracic pressure gradients. The resultant transmural force leads to atrial stretch, enlargement, and remodeling. This increase in left atrial volume is a well-established predisposing factor for AF.This altered pressure gradient also leads to autonomic dysregulation. In a study by Linz and colleagues, the increased negative tracheal pressure that occurs during obstructive events was shown to shorten the right atrial refractory period and increase susceptibility to AF through enhanced vagal activation.
Obstructive respiratory events produce intermittent desaturations, hypoxia, catecholamine release, and abrupt increases in arterial pressure. These phenomena result in endothelial dysfunction and sympathetic activation that could lead to AF. Whether the development of AF in patients with OSA is the result of a cumulative effect of these factors or a final etiologic factor in susceptible patients is not well established. AF is more common in patients with severe OSA than those with lower AHIs, which would suggest the former. Only a longitudinal study assessing derangements in left atrial size and function and the development of AF among patients with a wide range of OSA severity would be able to answer this clinical question.
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