Épidémiologie du syndrome d’apnées-hypopnées obstructives du sommeil

Introduction Epidemiological cohorts based on population samples, established in the 1990s, have helped to clarify the prevalence of obstructive sleep apnoea syndrome (OSAS) and to identify key risk factors and co-morbidities. State of knowledge OSAS is a common disease whose prevalence increases with age. Its main risk factor is obesity, but familial and genetic predisposition may also promote the condition. The association of OSAS with increased cardiovascular mortality has been known for several years and has been confirmed by recent data from epidemiological cohorts showing increased mortality including an increased incidence of coronary events and stroke in particular in men aged below 70 years. Recent studies also show an independent association between OSAS and cancer mortality. Conclusions OSAS is a common disease whose prevalence continues to increase with the increase of obesity in the population. Large epidemiological studies have shown an independent relationship between OSAS and cardiovascular diseases, metabolic disorders and more recently cancer

Murine models of sleep apnea: functional implications of altered macrophage polarity and epigenetic modifications in adipose and vascular tissues

Obstructive sleep apnea (OSA) is a highly prevalent disease across the lifespan, is characterized by chronic intermittent hypoxia and sleep fragmentation, and has been independently associated with substantial cardiometabolic morbidity. However, the reversibility of end-organ morbidity with treatment is not always apparent, suggesting that both tissue remodeling and epigenetic mechanisms may be operationally involved. Here, we review the cumulative evidence focused around murine models of OSA to illustrate the temporal dependencies of cardiometabolic dysfunction and its reversibility, and more particularly to discuss the critical contributions of tissue macrophages to adipose tissue insulin resistance and vascular atherogenesis. In addition, we describe initial findings potentially implicating epigenetic alterations in both the emergence of the cardiometabolic morbidity of OSA, and in its reversibility with treatment. We anticipate that improved understanding of macrophage biology and epigenetics in the context of intermittent hypoxia and sleep fragmentation will lead to discovery of novel therapeutic targets and improved cardiovascular and metabolic outcomes in OSA

Microparticles and vascular dysfunction in obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is independently associated with various cardiovascular diseases, including myocardial infarction and stroke. OSA may promote atherosclerosis risk factors such as hypertension, diabetes and dyslipidaemia, and may have direct proatherogenic effects on the vascular wall. A growing number of studies have recently focused on the role of microparticles (MPs) in the atherogenic process. MPs are small plasma membrane vesicles that can be released by a variety of vascular or blood cells, and contain both membrane and cytosolic elements. Case–control studies have shown that platelet-, endothelium- and leukocyte-derived MP levels are increased in OSA. Experimental evidence has demonstrated that MPs from OSA patients induce endothelial dysfunction, inflammation and vascular hyperreactivity when injected into mice. In this review, we provide an overview of the main characteristics of MPs, their expression in OSA and their potential role in the atherogenic process associated with OSA

Fisher information and Shannon entropy for on-line detection of transient signal high-values in laser Doppler flowmetry signals of healthy subjects

Laser Doppler flowmetry (LDF) is an easy-to-use method for the assessment of microcirculatory blood flow in tissues. However, LDF recordings very often present TRAnsient Signal High-values (TRASH), generally of a few seconds. These TRASH can come from tissue motions, optical fibre movements, movements of the probe head relative to the tissue, etc. They often lead to difficulties in signal global interpretations. In order to test the possibility of detecting automatically these TRASH for their removal, we process noisy and noiseless LDF signals with two indices from information theory, namely Fisher information and Shannon entropy. For this purpose, LDF signals from 13 healthy subjects are recorded at rest, during vascular occlusion of 3 min, and during post-occlusive hyperaemia. Computation of Fisher information and Shannon entropy values shows that, when calibrated, these two indices can be complementary to detect TRASH and be insensitive to the rapid increases of blood flow induced by post-occlusive hyperaemia. Moreover, the real-time algorithm has the advantage of being easy to implement and does not require any frequency analysis. This study opens new fields of application for Fisher information and Shannon entropy: LDF \u27denoising\u27