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: 4.59). 05/2011; 34(9):1207-13. DOI: 10.5665/SLEEP.1240
Source: PubMed


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.

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Available from: Jonathan C Jun, Jan 02, 2014
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    • "Barceló et al. showed that OSA patients have elevated levels of FFA, which can lead to increased cardiovascular and metabolic risk [32]. Moreover, an increased amount of nocturnal FFA was shown to be associated with accelerated cardiac disease progression in patient with OSA and concomitant heart failure [33]. "
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    • "Activation of the SNS during IH occurs through the hypoxic chemo-reflex in the carotid body and ablation of the carotid sinus nerve prevents IH-induced hypertension (Fletcher et al., 1992a,b; Fletcher, 2001; Prabhakar et al., 2007; Prabhakar and Kumar, 2010). We and others have recently shown that sleep apnea raises circulating FFA levels in proportion to the severity of hypoxia (Barcelo et al., 2011; Jun et al., 2011) suggesting that IH leads to exuberant lipolysis in adipose tissue. The FFA influx into the liver may induce insulin resistance and triglyceride biosynthesis leading to hepatic steatosis (Delarue and Magnan, 2007; Guilherme et al., 2008; Jocken and Blaak, 2008; Neuschwander-Tetri, 2010; Tilg and Moschen, 2010). "
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