© 2007 European Society of Cardiology
Obstructive sleep apnoea and adipocyte death: Authors reply
São João Hospital, Porto, Faculty of Medicine, University of Porto Portugal
* Corresponding author. Alameda Hernâni Monteiro, 4200 Porto, Portugal. Tel.: +351 919875957. E-mail address: pbettfer{at}claranet.pt
Key Words: Obstructive sleep apnoea • Adipocyte • Inflammation • Pathophysiology
Received September 11, 2006; We thank Azevedo et al. for their interest in our review on heart failure and sleep apnoea [1].
We agree that obesity might be a confounding factor in the relationship between heart failure (HF) and obstructive sleep apnoea (OSA). The suggested hypothesis is attractive and pertinent and should lead to further investigation.
Sleep apnoea (SA) has been treated as a respiratory mechanical abnormality but evidence suggests that it is a systemic metabolic illness [2]. Inflammation is a potential mechanism for development and progression of HF in patients with SA [1]. Increased levels of C-reactive protein [3], interleukin-6 (Il-6) and tumor necrosis factor (TNF)-
[4] have been observed in OSA, both in plasma and in airways, and decrease with CPAP therapy [5].
Experimentally produced resistive breathing induces Il-6 and TNF- production [6]. Intermittent hypoxia and intrathoracic pressure variations might be pathophysiological links [7]. However, increasing body mass index correlates positively with both cytokine levels and SA severity [3,4]. Adipose tissue localization influences its pathogenicity [8]. Patients with OSA have a significantly greater amount of visceral fat without difference in total or subcutaneous body fat [2]. Visceral adipocytes in the abdominal cavity are more susceptible to rupture because they are bigger and more exposed to suddenly varying pressures [8]. This suggests that visceral obesity might play a central role in cardiovascular consequences of SA, through monocyte and inflammatory activation following adipocyte death triggered by pressure variations related to OSA, as hypothesized by Azevedo et al.
On the other hand, SA may accelerate cardiovascular and metabolic abnormalities, possibly through progressive elevations of stress hormones and cytokines [2]. TNF- correlates strongly with lipolysis and induces leptin secretion which has been associated with sympathetic systemic activation [9]. Elevated leptin levels were reported in OSA independently of obesity which might be related to higher levels of visceral fat [2]. Adiponectin levels are also increased, suggesting a stimulatory effect of OSA on the endocrine function of adipose tissue [10]. This leads to the hypothesis that SA may be responsible for cardiovascular consequences often attributed to obesity.
In summary, the pathophysiology of cardiovascular and metabolic complications of sleep apnoea is multifactorial and probably associated.
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