Mechanism and management of atrial fibrillation in the patients with obstructive sleep apnea

Abstract

Obstructive sleep apnea (OSA) is a highly prevalent disorder in patients with atrial fibrillation (AF). Although there has been an increase in the incidence of AF due to the aging population, it has been reported that OSA is still underdiagnosed because many patients remain asymptomatic or unaware of the symptoms associated with OSA, such as daytime sleepiness. Untreated OSA reduces the effectiveness of AF treatment, regardless of pharmacological or non-pharmacological modes of therapy, such as catheter ablation. Experimental and clinical studies have shown that OSA pathophysiology is multifactorial, comprising of hypoxemia, hypercapnia, autonomic dysfunction, negative intrathoracic pressure changes, and arousals of OSA, and lead to AF. Both the acute and long-term effects of obstructive apnea episodes are involved in the development of an arrhythmogenic substrate of AF. Undiagnosed OSA causes underutilized opportunities for more effective AF management. Therefore, it is important to screen for OSA in all patients being considered for rhythm control therapy. However, regardless of the growing evidence of the negative prognostic impact of OSA, there is a lack of awareness regarding this connection not only among patients but also among cardiologists and arrhythmia specialists. There is a barrier to performing a systemic screening for OSA in clinical practice. Therefore, it is important to establish a comprehensive OSA care team for the efficient diagnosis and treatment of OSA. This review provides the current understanding of OSA and its relationship to AF and the importance of the diagnosis and management of OSA in AF.

FIGURE 1

Suggested mechanisms linking OSA pathophysiology and arrhythmogenic substrate of AF. Multiple and complex OSA pathophysiologies develop both acute and long‐term arrhythmogenic substrates, leading to AF trigger and perpetuation. APD, action potential duration; Cx43, connexin‐43; ERP, effective refractory period; LA, left atrium; LV, left ventricle; OSA, obstructive sleep apnea; PV, pulmonary vein; RA, right atrium.

FIGURE 2

Association between intrathoracic pressure and LV transmural pressure. Patients with OSA presenting with a deep negative intrathoracic pressure of −50 mm Hg and normotension (systolic blood pressure = 120 mm Hg) had a ventricular transmural pressure of 170 mm Hg. This condition is similar to that in patients with hypertension (systolic pressure = 120 mm Hg) without normal negative intrathoracic pressure (−10 mm Hg). OSA: obstructive sleep apnea, LV, left ventricle.