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

Localization of transient signal high-values in laser Doppler flowmetry signals with an empirical mode decomposition

The laser Doppler flowmetry (LDF) technique provides the monitoring of microvascular blood flow perfusion. However, LDF monitors based on fiber-optic transducers have the serious drawback of generating TRAnsient Signal High-values (TRASH) in signals. These TRASH correspond to artifacts for clinicians as they prevent interpretations of the signal when they are numerous. Moreover, TRASH exclude the possibility of direct signal processing and analyses. Therefore, in clinical routines, a human visual inspection of LDF signals is necessary to detect TRASH and to process the signals accordingly. This may be very time consuming. An algorithm able to localize TRASH automatically for their removal is therefore of interest. However, the development of such an algorithm is not an easy task as TRASH amplitude can be lower, higher, or in the same amplitude range as responses to stimuli such as post-occlusive hyperemia. The recently introduced empirical mode decomposition (EMD) has the advantage of splitting any kind of signal into fast and slow oscillations. Relying on these properties, the authors evaluate the possibility for EMD to localize TRASH automatically. For this purpose, LDF signals from 28 men of different ages are recorded at rest, during a vascular occlusion of 3 min , followed by a post-occlusive hyperemia. For each signal containing TRASH, the first intrinsic mode function obtained with the EMD is processed with a running window-based analysis in which a thresholding of the local maxima is carried out for the localization of TRASH. From the data, the use of a window width of 25 s is suggested. The results show effective and potential usefulness of this algorithm for an automatic localization of TRASH. Moreover, the method proposed has the advantage of being insensitive to the rapid increases of blood flow induced by post-occlusive hyperemia, which is of interest for clinicians. Because it is both local and fully data adaptive, EMD appears as an appealing processing technique for overcoming some of the limitations of the LDF

Multifractality, sample entropy, and wavelet analyses for age-related changes in the peripheral cardiovascular system: Preliminary results

Using signal processing measures we evaluate the effect of aging on the peripheral cardiovascular system. Laser Doppler flowmetry (LDF) signals, reflecting the microvascular perfusion, are recorded on the forearm of 27 healthy subjects between 20–30, 40–50, or 60–70 years old. Wavelet-based representations, Hölder exponents, and sample entropy values are computed for each time series. The results indicate a possible modification of the peripheral cardiovascular system with aging. Thus, the endothelial-related metabolic activity decreases, but not significantly, with aging. Furthermore, LDF signals are more monofractal for elderly subjects than for young people for whom LDF signals are weakly multifractal: the average range of Hölder exponents computed with a parametric generalized quadratic variation based estimation method is 0.13 for subjects between 20 and 30 years old and 0.06 for subjects between 60 and 70 years old. Moreover, the average mean sample entropy value of LDF signals slightly decreases with age: it is 1.34 for subjects between 20 and 30 years old and 1.19 for subjects between 60 and 70 years old. Our results could assist in gaining knowledge on the relationship between microvascular system status and age and could also lead to a more accurate age-related nonlinear modeling

Microvascular endothelial function in obstructive sleep apnea: Impact of continuous positive airway pressure and mandibular advancement

ObjectivesEndothelial dysfunction has been proposed as a potential mechanism implicated in the pathogenesis of cardiovascular complications of obstructive sleep apnea syndrome (OSAS). This study aimed to evaluate the microvascular endothelial function (MVEV) in OSAS and the impact on MVEF of 2 months of treatment with continuous positive airway pressure (CPAP) and mandibular advancement device (MAD). Methods Microvascular reactivity was assessed using laser Doppler flowmetry combined with acetylcholine (Ach) and sodium nitroprusside (SNP) iontophoresis in 24 OSAS patients and 9 control patients. In 12 of the 24 OSAS patients, microvascular reactivity was reassessed after 2 months of CPAP and MAD using a randomized cross-over design. Results Ach-induced vasodilation was significantly lower in OSAS patients than in matched controls and correlated negatively with apnea hypopnea index (r = −0.49, p < 0.025) and nocturnal oxygen desaturations (r = −0.63, p < 0.002). Ach-induced vasodilation increased significantly with both CPAP and MAD. The increase in Ach-induced vasodilation under OSAS treatment correlated with the decrease in nocturnal oxygen desaturations (r = 0.48, p = 0.016). Conclusion Our study shows an impairment of MVEF in OSAS related to OSAS severity. Both CPAP and MAD treatments were associated with an improvement in MVEF that could contribute to improve cardiovascular outcome in OSAS patients

Titrated mandibular advancement versus positive airway pressure for sleep apnoea

The aim of this study was to compare mandibular advancement device (MAd) therapy and continuous positive airway pressure (CPAP) for obstructive sleep apnoea/hypopnoea syndrome (OSAHS) after one-night polysomnographic (PSG) titration of both treatments. 59 OSAHS patients (apnoea/hypopnoea index (AHI): 34±13 events·h−1; Epworth scale: 10.6±4.5) were included in a crossover trial of 8 weeks of MAd and 8 weeks of CPAP after effective titration. Outcome measurements included home sleep study, sleepiness, health-related quality of life (HRQoL), cognitive tests, side-effects, compliance and preference. The median (interquartile range) AHI was 2 (1–8) events·h−1 with CPAP and 6 (3–14) events·h−1 with MAd (p<0.001). Positive and negative predictive values of MAd titration PSG for treatment success were 85% and 45%, respectively. Both treatments significantly improved subjective and objective sleepiness, cognitive tests and HRQoL. The reported compliance was higher for MAd (p<0.001) with >70% of patients preferring this treatment. These results support titrated MAd as an effective therapy in moderately sleepy and overweight OSAHS patients. Although less effective than CPAP, successfully titrated MAd was very effective at reducing the AHI and was associated with a higher reported compliance. Both treatments improved functional outcomes to a similar degree. One-night titration of MAd had a low negative predictive value for treatment success

Atteinte pulmonaire sévère au cours de la neurofibromatose de type 1

Type 1 neurofibromatosis (NF1) is a hereditary disease inherited as an autosomal dominant. Respiratory involvement is rare. We report the case of a woman suffering from NF1 with mutation of the corresponding gene and with respiratory involvement combining diffuse parenchymatous lesions, severe precapillary pulmonary hypertension and an enlarging, spiculated pulmonary nodule, very suspicious of malignancy, though histological examination was not possible on account of the patient\u27s poor respiratory function. There was progressive deterioration of the patient\u27s respiratory condition, leading to death, despite the introduction of oral therapy combining a phosphodiesterase 5 inhibitor and an endothelin receptor antagonist. Our case illustrates the development of multiple severe respiratory pathologies in the setting of NF1. The specific contribution of the NF1 gene mutation in the pathophysiology of these different pulmonary manifestations needs to be examined in detail