Abstract
Background
We previously showed in heart failure (HF) patients that obstructive respiratory events
during sleep and generation of negative intrathoracic pressure during Mueller manoeuvres,
mimicking obstructive apneas, acutely reduced stroke volume (SV). We also showed that
treating obstructive sleep apnea (OSA) with continuous positive airway pressure (CPAP)
increased left ventricular ejection fraction over a 1-month period. We therefore hypothesized
that, in HF patients, those with OSA would have greater overnight declines in SV and
cardiac output (CO) than in those without sleep apnea, and that therapy of OSA using
CPAP would prevent these declines.
Methods
We examined overnight percent change in SV and CO in 32 HF patients with and 28 without
OSA using digital photoplethysmography. Among patients with OSA, we also examined
changes in SV and CO during a CPAP titration study.
Results
During the baseline polysomnogram SV and CO decreased more overnight in those with
OSA than in those without sleep apnea (−12.6 ± 7.7% vs −3.2 ± 6.8%; P < 0.001 and −16.2 ± 9.9% vs −3.7 ± 8.3%; P < 0.001, respectively). Overnight changes in SV and CO correlated inversely with
total apnea-hypopnea index (r = −0.551; P < 0.001 and r = −0.522; P < 0.001, respectively). In 21 patients with OSA, CPAP reduced the total apnea-hypopnea
index from 37.7 ± 21.4 to 15.0 ± 16.0 (P < 0.001) in association with attenuation of the overnight reduction of SV (from −14.0
± 7.9% to −3.4 ± 9.8%; P = 0.002) and CO (from −17.2 ± 9.0% to −9.7 ± 10.7%; P = 0.042).
Conclusions
In patients with HF, coexisting OSA causes overnight declines in SV and CO that are
prevented through reversal of OSA by CPAP.
Résumé
Introduction
Nous avons précédemment montré chez les patients atteints d’insuffisance cardiaque
(IC) que les événements respiratoires obstructifs survenant durant le sommeil et que
la génération de pression intrathoracique négative durant la manœuvre de Mueller,
qui imite les apnées obstructives, réduisaient à court terme le volume d'éjection
(VE). Nous avons également montré que le traitement de l’apnée obstructive du sommeil
(AOS) à l’aide de la ventilation spontanée en pression positive expiratoire continue
(CPAP : continuous positive airway pressure) augmentait la fraction d’éjection ventriculaire gauche sur une période de 1 mois.
Par conséquent, nous avons posé l’hypothèse que les patients atteints d’IC qui ont
des AOS pourraient avoir des baisses plus importantes du VE et du débit cardiaque
(DC) au cours de la nuit que ceux n’ayant pas d’apnée du sommeil et que le traitement
de l’AOS par CPAP pourrait empêcher ces baisses.
Méthodes
Nous avons examiné la variation en pourcentage du VE et du DC au cours de la nuit
chez 32 patients souffrant d’IC et 28 patients n’ayant pas d’AOS à l’aide de la photopléthysmographie
numérique. Parmi les patients ayant des AOS, nous avons également examiné les changements
du VE et du DC au cours d’une étude de titrage de la CPAP.
Résultats
Le polysomnogramme initial a montré que le VE et le DC diminuaient plus durant la
nuit chez ceux ayant des AOS que chez ceux n’ayant pas d’apnée du sommeil (−12,6 ±
7,7 % vs −3,2 ± 6,8 %; P < 0,001 et −16,2 ± 9,9 % vs −3,7 ± 8,3 %; P < 0,001, respectivement). Les variations du VE et du DC au cours de la nuit ont corrélé
de manière inverse avec l’index d’apnées-hypopnées totales (r = −0,551; P < 0,001 et r = −0,522; P < 0,001, respectivement). Chez 21 patients ayant des AOS, la CPAP a réduit l’index
d’apnées-hypopnées totales de 37,7 ± 21,4 à 15,0 ± 16,0 (P < 0,001) tout en modérant la réduction du VE (de −14,0 ± 7,9 % à −3,4 ± 9,8 %; P = 0,002) et du DC (de −17,2 ± 9,0 % à −9,7 ± 10,7 %; P = 0,042) au cours de la nuit.
Conclusions
Chez les patients atteints d’IC, la coexistence d’AOS cause des baisses du VE et du
DC au cours de la nuit qui sont évitables en diminuant le nombre d’AOS à l’aide de
la CPAP.
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Article info
Publication history
Published online: January 14, 2015
Accepted:
January 4,
2015
Received:
November 27,
2014
Footnotes
See page 838 for disclosure information.
Identification
Copyright
© 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
