© 2007 European Society of Cardiology
Obstructive sleep apnoea and adipocyte death
Faculty of Nutritional and Food Sciences, University of Porto 4200-465 Porto, Portugal
Department of Biochemistry (U38/FCT), Faculty of Medicine, University of Porto 4200-465 Porto, Portugal
* Corresponding author. E-mail address: isabelaz{at}med.up.pt
Key Words: Obstructive sleep apnoea • Adipocyte • Inflammation
Received June 28, 2006; Dear Editor
The recent review on heart failure and sleep apnoea by Ferreira et al. [1] correctly and clearly underlines the evidence-based association between those two conditions. However, as the authors clearly state, confounding factors such as obesity make the full meaning of that relationship uncertain. As it might be linked to adverse outcomes, it would be of utmost interest to clarify the nature of this association.
Inflammation with origin in adipose tissue leads to a number of important health complications, macrophage accumulation playing a central role in that physiopathology [2]. Cinti et al. [3] have provided sound evidence for macrophage aggregation around dead adipocytes, a phenomenon more frequent in adipose tissue with large size adipocytes.
In a recent publication [4] we show that adipocyte rupture, the more facile the bigger the adipocyte, is most probably at the origin of the inflammatory state accompanying obesity. Adipocyte rupture as the basis of inflammation with origin in adipose tissue is in good agreement with the fact that adipose tissue localization markedly influences its consequences on health, the most pathogenic obesity being the visceral one [5]. As a matter of fact, adipocytes in abdominal cavity are subject to suddenly varying pressures, as occurs for example during cough, abdominal crunch or diverse physical exercises [6].
Obstructive apnoeas during sleep elicit a series of mechanical responses. Futile inspiratory efforts against the occluded pharynx cause abrupt reductions in intrathoracic pressure, what has been shown to result in an increase in left ventricular transmural pressure [7]. Pressures as low as 65 mm Hg have been recorded during obstructive apnoeas in patients with heart failure [8]. This huge pressure variation may lead to intrathoracic adipocyte rupture. On the other hand, intrathoracic pressure variations will have direct repercussion on intra-abdominal pressure [6,9].
Shamsuzzaman et al. [10]) found that compared with control subjects matched for age, sex, and body mass index, patients with obstructive sleep apnoea had higher plasma C-reactive protein concentrations that were proportional to the frequency of apnoeas.
We suggest that intrathoracic and intra-abdominal pressure variations accompanying obstructive apnoeas will lead to adipocyte rupture, the subsequent inflammation impending on cardiovascular health. Measures to prevent adipocyte hypertrophy would most probably reduce the pathogenic burden of obstructive sleep apnoeas.
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- Ferreira S., Winck J., Bettencourt P., Rocha-Gonçalves F. Heart failure and sleep apnoea: to sleep perchance to dream. Eur J Heart Fail (2006) 8:227–236.
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- Cinti S., Mitchell G., Barbatelli G., et al. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lip Res (2005) 46:2347–2355.
[Abstract/Free Full Text] - Monteiro R., de Castro P.M., Calhau C., Azevedo I. Adipocyte size and liability to cell death. Obes Surg (2006) 16:804–806.[CrossRef][Web of Science][Medline]
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- Malone S., Liu P.P., Holloway R., Rutherford R., Xie A., Bradley T.D. Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure. Lancet (1991) 338:1480–1484.[CrossRef][Web of Science][Medline]
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- Shamsuzzaman A.S., Winnicki M., Lanfranchi P., et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation (2002) 105:2462–2464.
[Abstract/Free Full Text]
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