Geovanini Glaucylara Reis, Lorenzi-Filho Geraldo
Sleep Laboratory, Pulmonary Division, Heart Institute (InCor), Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Genetics and Molecular Cardiology Laboratory, Heart Institute (InCor), Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
J Thorac Dis. 2018 Dec;10(Suppl 34):S4221-S4230. doi: 10.21037/jtd.2018.12.63.
Obstructive sleep apnea (OSA) is common among patients with cardiac rhythm disorders. OSA may contribute to arrhythmias due to acute mechanisms, such as generation of negative intrathoracic pressure during futile efforts to breath, intermittent hypoxia, and surges in sympathetic activity. In addition, OSA may lead to heart remodeling and increases arrhythmia susceptibility. Atrial distension and remodeling, that has been shown to be associated with OSA, is a well-known anatomical substrate for atrial fibrillation (AF). AF is the arrhythmia most commonly described in patients with OSA. Several observational studies have shown that the treatment of OSA with continuous positive airway pressure (CPAP) reduces recurrence of AF after electrical cardioversion and catheter ablation. There is also evidence that nocturnal hypoxemia, a hallmark of OSA, predicts sudden cardiac death (SCD) independently of well-established cardiovascular risk factors. Among patients with an implantable cardiac defibrillator, those with OSA have a higher risk of receiving treatment for life-threatening arrhythmias. Nocturnal hypoxemia may also increase vagal tone, which increases susceptibility to bradycardic and conduction rhythm disorders that have also been described in patients with OSA. In conclusion, there are several biological pathways linking OSA and increased cardiac arrhythmogenesis propensity. However, the independent association is derived from observational studies and the direction of the association still needs clarification due to the lack of large clinical trials. This review focuses on the current scientific evidence linking OSA to cardiac rhythm disorders and point out future directions.
阻塞性睡眠呼吸暂停(OSA)在心律紊乱患者中很常见。OSA可能由于急性机制导致心律失常,如在无效呼吸努力期间产生胸内负压、间歇性缺氧以及交感神经活动激增。此外,OSA可能导致心脏重塑并增加心律失常易感性。已证明与OSA相关的心房扩张和重塑是心房颤动(AF)的一个众所周知的解剖学基础。AF是OSA患者中最常描述的心律失常。多项观察性研究表明,持续气道正压通气(CPAP)治疗OSA可降低电复律和导管消融后AF的复发率。也有证据表明,夜间低氧血症作为OSA的一个标志,独立于已确立的心血管危险因素可预测心源性猝死(SCD)。在植入式心脏除颤器患者中,患有OSA的患者接受危及生命心律失常治疗的风险更高。夜间低氧血症也可能增加迷走神经张力,这增加了对缓慢性和传导性心律失常的易感性,这些心律失常在OSA患者中也有描述。总之,有几种生物学途径将OSA与心律失常发生倾向增加联系起来。然而,这种独立关联来自观察性研究,由于缺乏大型临床试验,关联方向仍需阐明。本综述重点关注将OSA与心律紊乱联系起来的当前科学证据,并指出未来方向。