Effects of sleep apnea on nocturnal free fatty acids in subjects with heart failure

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Sleep (Impact Factor: 5.06). 05/2011; 34(9):1207-13. DOI: 10.5665/SLEEP.1240
Source: PubMed

ABSTRACT Sleep apnea is common in patients with congestive heart failure, and may contribute to the progression of underlying heart disease. Cardiovascular and metabolic complications of sleep apnea have been attributed to intermittent hypoxia. Elevated free fatty acids (FFA) are also associated with the progression of metabolic, vascular, and cardiac dysfunction. The objective of this study was to determine the effect of intermittent hypoxia on FFA levels during sleep in patients with heart failure.
During sleep, frequent blood samples were examined for FFA in patients with stable heart failure (ejection fraction < 40%). In patients with severe sleep apnea (apnea-hypopnea index = 65.5 ± 9.1 events/h; average low SpO₂ = 88.9%), FFA levels were compared to controls with milder sleep apnea (apnea-hypopnea index = 15.4 ± 3.7 events/h; average low SpO₂ = 93.6%). In patients with severe sleep apnea, supplemental oxygen at 2-4 liters/min was administered on a subsequent night to eliminate hypoxemia.
Prior to sleep onset, controls and patients with severe apnea exhibited a similar FFA level. After sleep onset, patients with severe sleep apnea exhibited a marked and rapid increase in FFA relative to control subjects. This increase persisted throughout NREM and REM sleep exceeding serum FFA levels in control subjects by 0.134 mmol/L (P = 0.0038). Supplemental oxygen normalized the FFA profile without affecting sleep architecture or respiratory arousal frequency.
In patients with heart failure, severe sleep apnea causes surges in nocturnal FFA that may contribute to the accelerated progression of underlying heart disease. Supplemental oxygen prevents the FFA elevation.

Download full-text


Available from: Jonathan C Jun, Jan 02, 2014
  • [Show abstract] [Hide abstract]
    ABSTRACT: A European Respiratory Society research seminar on "Metabolic alterations in obstructive sleep apnoea (OSA)" was jointly organised in October 2009 together with two EU COST actions (Cardiovascular risk in the obstructive sleep apnoea syndrome, action B26, and Adipose tissue and the metabolic syndrome, action BM0602) in order to discuss the interactions between obesity and OSA. Such interactions can be particularly significant in the pathogenesis of metabolic abnormalities and in increased cardiovascular risk in OSA patients. However, studying the respective role of OSA and obesity is difficult in patients, making it necessary to refer to animal models or in vitro systems. Since most OSA patients are obese, their management requires a multidisciplinary approach. This review summarises some aspects of the pathophysiology and treatment of obesity, and the possible effects of sleep loss on metabolism. OSA-associated metabolic dysfunction (insulin resistance, liver dysfunction and atherogenic dyslipidaemia) is discussed from the perspective of both obesity and OSA in adults and children. Finally, the effects of treatment for obesity or OSA, or both, on cardio-metabolic variables are summarised. Further interdisciplinary research is needed in order to develop new comprehensive treatment approaches aimed at reducing sleep disordered breathing, obesity and cardiovascular risk.
    European Respiratory Journal 09/2011; 39(3):746-67. DOI:10.1183/09031936.00047010 · 7.13 Impact Factor
  • New England Journal of Medicine 03/2012; 366(10):963-4; author reply 965-6. DOI:10.1056/NEJMc1200497#SA1 · 54.42 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: INTRODUCTION: Obstructive sleep apnea (OSA) is a common medical disorder affecting at least 2 % of women and 4 % of men living in Western societies. Obesity, older age, male gender, alcohol and sedative use, smoking, craniofacial parameters, and volume overload are some of the risk factors for this disorder. DISCUSSION: OSA is a known risk factor complicating the course of arterial hypertension, heart failure, and chronic kidney disease. It is important to note that all of the aforementioned comorbid disorders are associated with volume overload. This explains why patients with OSA and comorbid disorders associated with fluid overload can benefit from treatment with diuretics and drugs modulating the renin-angiotensin-aldosterone system. Additionally, patients with heart failure and high sodium intake are at increased risk for OSA, further supporting the complex interrelationship. CONCLUSIONS: Hemodialysis and renal transplantation can markedly improve the severity of OSA in patients with concomitant kidney disease. Finally, there is a potential of a vicious cycle between OSA and fluid overload disorders, whereby OSA can contribute to the pathogenesis of arterial hypertension, heart failure, and chronic kidney disease, which in turn will significantly contribute to the course OSA.
    Sleep And Breathing 08/2012; DOI:10.1007/s11325-012-0755-6 · 2.87 Impact Factor