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Updated: Feb 3, 2026

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
In patients with heart failure the burden of central sleep apnea increases in the late sleep hours
Shahrokh Javaheri1, Scott W McKane2, Nathan Cameron3
1Bethesda Montgomery Sleep Centre, Bethesda North Hospital, Cincinnati, OH.
Insights
Central sleep apnea (CSA) episodes increase in patients with heart failure during later sleep hours. This worsening burden of central sleep apnea suggests new therapeutic targets for heart failure management.
Area of Science:
- Cardiology
- Sleep Medicine
- Pulmonology
Background:
- Central sleep apnea (CSA) is prevalent in patients with left ventricular systolic dysfunction.
- Pathophysiological mechanisms suggest CSA may worsen during sleep.
Purpose of the Study:
- To investigate the hypothesis that CSA frequency increases during later non-rapid eye movement (NREM) sleep in patients with left ventricular dysfunction.
Main Methods:
- Polysomnography was performed on 41 patients with ejection fraction <40%.
- NREM sleep was divided into 8 segments to quantify central apnea index (CAI) and duration per segment.
- Data were analyzed for variations across sleep segments and halves of the night.
Main Results:
- CAI significantly increased from earlier to later sleep segments (segment 2: 21 events/hour vs. segment 8: 37 events/hour).
- Central apnea duration also increased in later sleep hours (segment 1: 22s vs. segment 8: 26s).
- A significant increase in CAI was observed in the second half of the night compared to the first.
Conclusions:
- Patients with left ventricular dysfunction and CSA experience an increased burden of central apneas later in the sleep cycle.
- These findings highlight the dynamic nature of CSA in heart failure and suggest potential therapeutic implications.
Study Objectives:
Periodic breathing with central sleep apnea (CSA) is common in patients with left ventricular systolic dysfunction. Based on the pathophysiological mechanisms underlying CSA, we hypothesized that the frequency of CSA episodes would increase in the late hours of non-rapid eye movement (NREM) of sleep.
Methods:
Forty-one patients with left ventricular ejection fraction <40% underwent full-night-attended polysomnography scored by a central core lab. Because central apneas occur primarily in NREM sleep, total NREM sleep time for each patient was divided into 8 equal duration segments. Segment event counts were normalized to an events/hour index based on sleep segment duration.
Results:
Central apnea index (CAI) varied among sleep segments (p = 0.001). As expected CAI was higher in segment 1 compared to segments 2 and 3, increasing during later segments. The minimum CAI occurred in segment 2 with mean ± SD of 21 ± 3 events/hour and maximum CAI was in segment 8 with 37 ± 4 events/hour. We also determined central apnea duration which varied among segments (p = 0.005), with longer durations later in the night (segment 1: 22 ± 1 seconds; segment 8: 26 ± 1 seconds, p < 0.001). Data were also analyzed including rapid eye movement (REM) sleep, with similar results. Further, comparison of CAI between the first and second half of the night showed a significant increase in the index. Circulation time did not change across the segments (p = 0.073).
Conclusions:
In patients with left ventricular dysfunction and CSA, central apnea burden (number and duration) increases during later hours of sleep. These findings have pathophysiological and therapeutic implications.
Clinical Trial Registration:
NCT01124370.
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