Complications

Complication
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Whether CSA with a Cheyne-Stokes breathing pattern (CSA-CSB) is merely a reflection of a diseased myocardium or can itself contribute to increased morbidity and mortality has been debated. Several studies examined mortality and time to transplantation in patients with congestive heart failure (CHF), and a majority found that CSA-CSB was an independent risk factor for death or transplant. The activation of the sympathetic nervous system that occurs during apneic episodes is thought to be a major contributor.

Treatment with continuous positive airway pressure improves sleep quality, nocturnal oxygen levels, and left ventricular ejection fraction (LVEF), but does not appear to improve mortality.[22] In contrast, adaptive servoventilation has been associated with increased mortality rates in CHF patients with reduced ejection fraction and CSA.​[22]​​​​[46] Further longitudinal studies are needed to accurately identify the long-term impact of this and other forms of positive airway pressure in patients with CSA and CHF with varied LVEFs, as well as those with preserved ejection fraction.[46][56]​​​​

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Bilevel positive airway pressure has a trend toward worsening of the apnea-hypopnea index based on an increase in the number of central apneas in comparison to the same patients on continuous positive airway pressure treatment. This phenomenon could be explained by augmentation of ventilation during the hyperpneic phases of CSA breathing, thereby causing relative hypocapnia and increasing the risk of crossing the apneic threshold.[66]

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A bidirectional link between arrhythmias and sleep disordered breathing is suspected.[28]  CSA appears to be associated with a 2‐ to 3‐fold increased odds of developing atrial fibrillation (AF), with increased odds in older people.[28]​​[29][30] In patients with CSA with CSB, more ventricular ectopics were found during the hyperpneic phase, when chemostimulation, blood pressure, and heart rate reach their peak.​​​​[88] Furthermore, CSA was also found to be a predictor of sleep-specific lethal ventricular tachycardia in patients with heart failure.​[88] However, the majority of studies describing arrhythmias in sleep-related disorder cohorts suffer from a lack of clarity regarding the precise pathophysiological subtype, i.e., obstructive sleep apnea versus CSA, limiting the ability to assess causality.[28]​​

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