Effects of central apneas on sympathovagal balance and hemodynamics at night: impact of underlying systolic heart failure.
Central apnea
Heart failure
Sympathovagal balance
Journal
Sleep & breathing = Schlaf & Atmung
ISSN: 1522-1709
Titre abrégé: Sleep Breath
Pays: Germany
ID NLM: 9804161
Informations de publication
Date de publication:
06 2021
06 2021
Historique:
received:
03
01
2020
accepted:
09
07
2020
revised:
08
06
2020
pubmed:
24
7
2020
medline:
18
12
2021
entrez:
24
7
2020
Statut:
ppublish
Résumé
Increased sympathetic drive is the key determinant of systolic heart failure progression, being associated with worse functional status, arrhythmias, and increased mortality. Central sleep apnea is highly prevalent in systolic heart failure, and its effects on sympathovagal balance (SVB) and hemodynamics might depend on relative phase duration and background pathophysiology. This study compared the effects of central apneas in patients with and without systolic heart failure on SVB and hemodynamics during sleep. During polysomnography, measures of SVB (heart rate and diastolic blood pressure variability) were non-invasively recorded and analyzed along with baroreceptor reflex sensitivity and hemodynamic parameters (stroke volume index, cardiac index, total peripheral resistance index). Data analysis focused on stable non-rapid eye movement N2 sleep, comparing normal breathing with central sleep apnea in subjects with and without systolic heart failure. Ten patients were enrolled per group. In heart failure patients, central apneas had neutral effects on SVB (all p > 0.05 for the high, low, and very low frequency components of heart rate and diastolic blood pressure variability). Patients without heart failure showed an increase in very low and low frequency components of diastolic blood pressure variability in response to central apneas (63 ± 18 vs. 39 ± 9%; p = 0.001, 43 ± 12 vs. 31 ± 15%; p = 0.002). In all patients, central apneas had neutral hemodynamic effects when analyzed over a period of 10 min, but had significant acute hemodynamic effects. Effects of central apneas on SVB during sleep depend on underlying systolic heart failure, with neutral effects in heart failure and increased sympathetic drive in idiopathic central apneas.
Sections du résumé
BACKGROUND
Increased sympathetic drive is the key determinant of systolic heart failure progression, being associated with worse functional status, arrhythmias, and increased mortality. Central sleep apnea is highly prevalent in systolic heart failure, and its effects on sympathovagal balance (SVB) and hemodynamics might depend on relative phase duration and background pathophysiology.
OBJECTIVE
This study compared the effects of central apneas in patients with and without systolic heart failure on SVB and hemodynamics during sleep.
METHODS
During polysomnography, measures of SVB (heart rate and diastolic blood pressure variability) were non-invasively recorded and analyzed along with baroreceptor reflex sensitivity and hemodynamic parameters (stroke volume index, cardiac index, total peripheral resistance index). Data analysis focused on stable non-rapid eye movement N2 sleep, comparing normal breathing with central sleep apnea in subjects with and without systolic heart failure.
RESULTS
Ten patients were enrolled per group. In heart failure patients, central apneas had neutral effects on SVB (all p > 0.05 for the high, low, and very low frequency components of heart rate and diastolic blood pressure variability). Patients without heart failure showed an increase in very low and low frequency components of diastolic blood pressure variability in response to central apneas (63 ± 18 vs. 39 ± 9%; p = 0.001, 43 ± 12 vs. 31 ± 15%; p = 0.002). In all patients, central apneas had neutral hemodynamic effects when analyzed over a period of 10 min, but had significant acute hemodynamic effects.
CONCLUSION
Effects of central apneas on SVB during sleep depend on underlying systolic heart failure, with neutral effects in heart failure and increased sympathetic drive in idiopathic central apneas.
Identifiants
pubmed: 32700287
doi: 10.1007/s11325-020-02144-8
pii: 10.1007/s11325-020-02144-8
pmc: PMC8195752
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
965-977Subventions
Organisme : Else Kröner-Fresenius-Stiftung
ID : A 109
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