آپنه خواب مرکزی در نارسایی احتقانی قلب
Abstract
1- Background
2- Materials and methods
3- Results
4- Discussion
5- Conclusion
References
Abstract
Background
Adaptive servoventilation (ASV) effectively treats nocturnal respiratory events in patients with heart failure and reduced ejection fraction (HFrEF) and central sleep apnoea (CSA), but increased mortality has been reported. This study investigated changes in sleep architecture during ASV treatment in HFrEF patients.
Methods
A retrospective analysis of polysomnographic datasets for 30 ASV-treated patients with stable HFrEF and moderate-to-severe CSA was performed, including blinded analyses of total sleep time (TST), and percentage of REM and non-REM sleep (stages N1-N3).
Results
Follow-up was 109 ± 32 days; mean device usage was 6.0 ± 1.1 h/day. During ASV there was reduction of N1 (34 ± 20%/TST to 13 ± 5%/TST, p < 0.001) and N3 sleep (4 ± 6%/TST to 1 ± 4%/TST, p = 0.020), and increase of N2 (44 ± 14%/TST to 62 ± 7%/TST, p < 0.001) and REM-sleep (18 ± 8%/TST to 24 ± 6%/TST, p = 0.002).
Conclusions
Disturbances of sympatho-vagal balance during ASV might help explain increased mortality during ASV. Since sympathetic tone is highest in REM-sleep and vagal predominance occurs during N3 sleep, these findings generate new hypotheses for the increased mortality seen in SERVE-HF.
Background
Disturbed sleep architecture and reduced sleep duration is associated with cardiovascular mortality, reduced quality of life and impaired cognitive function (da Silva et al., 2016; Yang et al., 2015). Sleep-disordered breathing (SDB) is one of the most important factors disrupting sleep architecture, is highly prevalent in heart failure (HF) patients, and is the comorbidity most likely to impair sleep and quality of life due to sleep fragmentation caused by nocturnal disordered breathing events (Punjabi, 2008; Arzt et al., 2016). In principle, SDB is classified into two main types: obstructive sleep apnoea (OSA) and central sleep apnoea (CSA). With a prevalence of about 20%, OSA is the most frequent SDB subtype in the general population (Young et al., 2002). The main pathophysiological mechanism of OSA is futile respiratory efforts against collapsed upper airways. As cardiac function deteriorates, the prevalence of SDB increases markedly (Punjabi, 2008; Heinzer et al., 2015; Oldenburg et al., 2007). More than 50% of clinically stable HF patients with reduced left ventricular ejection fraction (HFrEF) present with moderate to severe SDB (Oldenburg et al., 2007). In particular, the proportion of central SDB increases as HF progresses, often manifesting as a periodic breathing pattern, classified as Hunter-Cheyne-Stokes respiration (CSR) (Oldenburg et al., 2007; Oldenburg, 2012). These breathing patterns can show long cyclic respiratory events (Oldenburg, 2012; Linz et al., 2011; Narkiewicz et al., 1999) resulting in phases of hypercapnia followed by arousals (Narkiewicz et al., 1999). The main mechanism is an increase in respiratory gain, leading to hyperventilation interrupted by repetitive sleep apnoeas (Türoff et al., 2017; Somers et al., 1989).