Original ArticleImpact of sleeping position on central sleep apnea/Cheyne–Stokes respiration in patients with heart failure
Introduction
Up to 50% of patients with heart failure (HF) have sleep-related breathing disorders; 40% exhibit central sleep apnea (CSA) or Cheyne–Stokes respiration, and 10% have obstructive sleep apnea (OSA) [1], [2].
The level of respiratory distress during sleep among patients with OSA varies according to position. For instance, patients have 40–50% lower apnea–hypopnea index (AHI) when sleeping on their side than in the supine position [3]. Cartwright defined “positional sleep apnea” as a 50% decrease in AHI in the lateral position compared with the supine position [4]. In fact, the severity of OSA in these patients is mostly related to the amount of time asleep in the supine position [5]. In contrast, patients in whom AHI in the lateral position does not decrease by ⩾50% relative to the supine position are defined as having “non-positional sleep apnea” [6]. Those with non-positional OSA have lower mean oxygen saturation, higher AHI and worse sleep quality than those with positional OSA [6].
Similarly to OSA, the effect of body position on Cheyne–Stokes respiration was first described in patients with stroke [7]. Several reports also indicate that CSA is improved in patients with various diseases when sleeping in the lateral position compared with the supine position [8], [9]. Interestingly, the AHI does not decrease in some patients when sleeping in the lateral position. Additionally, sleeping position could affect the severity of CSA in patients with HF, but the impact of sleeping position on CSA with Cheyne–Stokes respiration in patients with HF is not as well understood. Moreover, the prevalence and characteristics of positional and non-positional types of CSA have never been investigated thoroughly in such patients. Therefore, the present study examined the influence of sleeping position on CSA with Cheyne–Stokes respiration in patients with HF.
Section snippets
Patients
The study cohort comprised 71 consecutive patients with stable HF (51 men and 20 women) who underwent cardiopulmonary polygraphy and whose left ventricular ejection fraction was <0.45, determined by radionuclide or contrast ventriculography. The etiologies of HF were ischemic in 24 and non-ischemic in 47 patients. The amount of physical activity was measured using a specific activity scale in questionnaires regarding ordinary physical activities [10]. Patients with stroke, respiratory failure,
Results
The AHIs were <5.0, 5.0–14.9 and ⩾15.0/h in 15, 18 and 38 of the 71 patients, respectively. Five patients were excluded as they slept for <20 min in either the lateral or the supine position, while one patient was excluded because the body position sensor was lost during polygraphy. Of the 34 patients with AHI ⩾15.0/h, OSA dominated in 6 and CSA dominated in 28, and 25 with CAI ⩾10/h with less OAI (<5/h) (mean AHI, 28 ± 8/h and CAI, 21 ± 10/h) constituted the study group.
Discussion
Although positional sleep apnea in OSA is established, it has not been thoroughly investigated in patients with HF and CSA. The major findings of the present study are as follows: (1) hemodynamic features were more deteriorated in patients with non-positional CSA; (2) age, log10 BNP and LFCT were independent factors of the severity of positional CSA; (3) intensive treatment for HF changed non-positional to positional CSA in all eight patients tested; and (4) single night of positional therapy
Limitations
The present study has several limitations. First, our patients did not undergo polysomnography. A previous study [8] found greater central AHI during sleep stages 1 and 2 (43 and 37/h) and lower central AHI during slow-wave and rapid eye movement sleep (28 and 23/h). Moreover, the L/S ratio was also higher during sleep stages 1 and 2 (0.74 and 0.82) and lower during slow-wave and rapid eye movement sleep (0.25 and 0.52). Because sleep quality tended to be lower in patients with severe HF, we
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2017, Sleep MedicineCitation Excerpt :Thus, when CHF patients with CSA move from the supine to the left lateral position, cardiac haemodynamics slightly deteriorate (findings from this study) and are likely worse than in the right lateral position (inference from previous studies). Conversely, the severity of CSA markedly decreases from the supine to the lateral position ([2–5] and data from this study), with no significant difference between the right and left lateral positions [2,4]. It is, therefore, possible to conclude that the reduction in CSA severity from the supine to both lateral positions is not due to an improvement in cardiac haemodynamics.