Active clinical trials for "Sleep Apnea, Obstructive"

Obstructive sleep apnoea (OSA) is a highly prevalent sleep-related breathing disorder associated with adverse cardiovascular outcome. Underlying mechanisms are subject of debate. A causal relationship between OSA and systemic hypertension as well as peripheral endothelial dysfunction was shown, and there is accumulating evidence from physiologic and observational studies that cerebral autoregulation is insufficient to protect the brain from the nocturnal consequences of OSA. However, there are no data from randomised controlled trials proving a causal relationship between OSA and impaired cerebral vascular reactivity (CVR). The aim of this randomised controlled trial is to study the effects of a short-term CPAP withdrawal, and thus returning OSA, on daytime CVR and brain oxygenation to establish whether there is a causal relationship between OSA and cerebral vascular damage.

Acute consumption of dietary nitrate (as beetroot juice) has been shown to decrease systemic blood pressure in multiple populations as well as increase organ perfusion in areas of interest such as the pancreas and brain. Obstructive sleep apnoea syndrome (OSAS) is associated with high blood pressure, dysglycaemia and impaired vigilance. The effect of dietary nitrate in OSAS has not been reported.

Patients with obstructive sleep apnea (OSA) could have several anatomical causes of obstruction. A sleep endoscopy study is a technique to help determine the anatomical cause of OSA. This study will be using standard of care practice and infuse dexmedetomidine (DEX) to induce sleep. The goals of the study are to (1) confirm airway obstruction with endoscopic view and correlate that with Acoustic Respiratory Rate (RRa) signal at the moment of airway obstruction, and (2) characterize the EEG signals when subjects are under DEX sedation alone.

Sleep disordered breathing (SDB) is a common disease in both adults and children and is caused by the obstruction of the upper airway during sleep. Unlike adults, most cases of paediatric SDB are due to the presence of enlarged tonsils and adenoids, thus the main treatment option is adenotonsillectomy (AT). It is well known that obstructive sleep apnoea (OSA) in adults increases the risk for hypertension, coronary artery disease and stroke, and there is now mounting evidence that SDB also has a significant impact on the cardiovascular system in children with reports of elevated blood pressure, endothelial dysfunction and altered autonomic cardiovascular control. Oxidative stress seems to play a pivotal role in impairing flow-mediated dilation (FMD) and consequently enhancing cardiovascular risk in SDB patients but the underlying mechanism is still undefined. Previously, we demonstrated that endothelial dysfunction is directly related to NADPH oxidase activation. Furthermore, recently we assessed the association between OSA, endothelial dysfunction and oxidative stress in adults showing that increased NADPH oxidase-generated oxidative stress and arterial dysfunction are partially reversed by nasal continuous positive airway pressure treatment. There is evidence in literature that cardiovascular morbidities associated with SDB are potentially reversible in children; AT may have a significant role in reversing the cardiovascular sequelae of SDB (e.g. children with OSA). Nowadays, there aren't studies that analyzed the role of NADPH oxidase-generated oxidative stress in SDB children. The purpose of the current research project is to examine the role of NADPH oxidase activity, oxidative stress, inflammation and endothelial function in SDB children, understanding the mechanisms involved in this disease. Furthermore we will analyse the effect of a AT on inflammation, oxidative stress, NADPH oxidase activity and endothelial function in SDB children.

This is a randomized controlled study evaluating the impact of 2 months of oral appliance therapy on endothelial function in patients with severe obstructive sleep apnea syndrome intolerant to continuous positive airway pressure (CPAP) therapy.

The main objective is to evaluate an osteopathic compression of pterygopalatine node on sleep obstructive apnea syndrome (OSA).

Increased plasma triglyceride concentration is a common feature of the metabolic abnormalities associated with obesity and a major risk factor for cardiovascular disease. Obesity is a major risk factor for two conditions that appear to be increasing in prevalence in women: the polycystic ovary syndrome (PCOS) and sleep disordered breathing. PCOS affects 5-8% of women. Sleep disordered breathing affects up to 10% of women. Obstructive sleep apnea (OSA) is the most common cause for sleep disordered breathing and particularly prevalent in obese women with PCOS (~50%). Both PCOS and OSA augment the increase in plasma triglyceride (TG) concentration associated with obesity, and the effects of PCOS and OSA on plasma TG concentration appear to be additive. The mechanisms responsible for the adverse effects on plasma TG metabolism are not known. The primary goal of this project, therefore, is to determine the mechanisms responsible for the increase in plasma TG concentration in obese women with PCOS and OSA. It is our general hypothesis that alterations in the hormonal milieu that are characteristic of these two conditions are, at least in part, responsible for the increase in plasma TG concentration in obese women with the conditions. Furthermore, we hypothesize that the hormonal aberrations characteristic of the two conditions are particularly harmful to obese, compared with lean, women. The effects of PCOS on skeletal muscle protein metabolism are also not known. However, sex hormones are thought to be important regulators of muscle protein turnover suggesting that muscle protein metabolism is likely to be affected by PCOS. We will examine this by determining the effect of individual sex hormones on muscle protein metabolism and hypothesize that testosterone administration will stimulate muscle protein metabolism while estrogen and progesterone administration will inhibit muscle protein metabolism.

Continuous positive airway pressure (CPAP) continues to be the primary therapy prescribed for the treatment of obstructive sleep apnea (OSA). Although effective, adherence to CPAP is suboptimal in many patients, making alternative therapies desirable. Recently, a novel device (Provent™) has been developed for the treatment of snoring and OSA. The purpose of the current study is to examine how well the Provent™ device treats OSA with particular attention to the how the it may treat sleep apnea and who may most likely benefit from the use of this treatment.

To test whether baseline levels of slow wave activity (SWA) during sleep are lower in obese adults, and even lower in persons with sleep disordered breathing (SDB) compared to lean adults. To compare levels of SWA in individuals in relation to their sleep time, blood pressure, heart rate, and markers of glucose metabolism.

Overview of Protocol: Between Subject - Repeated Measures design will be used to assess the airway response of two groups of subjects under two different sedated conditions. Each group will be comprised of six subjects and will be categorized according to their baseline profile for risk for SDB (< 10 RDI or > 25 RDI). Some subjects will have been prescribed continuous positive airway pressure (CPAP) therapy by their treating physician as a result of their overnight sleep study. CPAP treatment is effective in splinting the airway open and thus decreasing the incident of airway collapse during sleep. Thus, CPAP utilization will also be tracked as an independent and continuous variable as regular CPAP use has been found to be associated with increased resistance to UAC (upper airway collapse). The experimental conditions will evaluate upper airway patency and instability in response to two forms of intravenous sedation: propofol and dexmedetomidine. Subjects will be continuously monitored during each experimental condition for respiratory effort and flow, and for EEG, EMG, and ECG. Respiratory instability will first be assessed while subjects are under sedation without any airway provocation. The degree of respiratory instability will be quantified in terms of the following measurements: a modified Respiratory Disturbance Index (RDIsedated), respiratory arousals, and minute ventilation. The apneic periods will be classified by their mixture of central and obstructive components.All outcome measurements are assessed over the period of sedation which last for approximately one hour. Upper airway patency will be quantified in terms of the critical pharyngeal pressure (Pcrit) (the pressure beyond which complete upper airway collapse occurs, see background).