State-of-the-Art Paper
Obstructive Sleep Apnea and Heart Failure: Pathophysiologic and Therapeutic Implications

https://doi.org/10.1016/j.jacc.2010.08.627Get rights and content
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Obstructive sleep apnea (OSA) exposes the cardiovascular system to intermittent hypoxia, oxidative stress, systemic inflammation, exaggerated negative intrathoracic pressure, sympathetic overactivation, and elevated blood pressure (BP). These can impair myocardial contractility and cause development and progression of heart failure (HF). Epidemiological studies have shown significant independent associations between OSA and HF. On the other hand, recent prospective observational studies reported a significant association between the presence of moderate to severe OSA and increased risk of mortality in patients with HF. In randomized trials, treating OSA with continuous positive airway pressure suppressed sympathetic activity, lowered BP, and improved myocardial systolic function in patients with HF. These data suggest the potential for treatment of OSA to improve clinical outcomes for patients with HF. However, large-scale randomized trials with sufficient statistical power will be needed to ascertain whether treatment of OSA will prevent development of, or reduce morbidity and mortality from HF.

Key Words

heart failure
pathophysiology
prognosis
sleep apnea

Abbreviations and Acronyms

AF
atrial fibrillation
AHI
apnea-hypopnea index
BMI
body mass index
BP
blood pressure
CPAP
continuous positive airway pressure
CSA
central sleep apnea
HF
heart failure
HR
heart rate
LV
left ventricular
LVEF
left ventricular ejection fraction
OSA
obstructive sleep apnea
QOL
quality of life
RV
right ventricle/ventricular
SNA
sympathetic nervous system activity

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This study was supported by operating grants MOP-82731 and IS2-95225 from the Canadian Institutes of Health Research (CIHR), the latter in conjunction with an unrestricted research grant from Philips-Respironics Inc. in accordance with the policies of the CIHR's University-Industry program. Dr. Kasai was supported by an unrestricted research fellowship from Fuji-Respironics Inc. Dr. Bradley received grant support from Philips-Respironics Inc. in partnership with the CIHR.