Active clinical trials for "Sleep Apnea Syndromes"

Obstructive sleep apnea (OSA) is a frequently underdiagnosed condition that has emerged as an increasing medical problem with important social and financial implications worldwide. OSA is a well established risk factor for systemic hypertension myocardial infarction or stroke and it has been documented that blood pressure rises in a very consistent fashion during apneic episodes. The incidence of the episodes of apnea during sleep causes repeated subclinical acute kidney injuries (AKI) contributing to the development of CKD. One of the mechanisms responsible for AKI might be endothelial injury followed by an increase of central aortic pressure.

The purpose of this study is to demonstrate similar improvements in sleep-disordered breathing as determined by sleep study with microdebrider-assisted partial intracapsular tonsillectomy and adenoidectomy versus total Bovie electrocautery tonsillectomy and adenoidectomy.

Obstructive sleep apnea (OSA) is a serious sleep disorder in which a person repeatedly stops breathing, or experiences shallow breathing for short periods of time during sleep. Daytime sleepiness is a common symptom of OSA and may affect an individual's level of alertness throughout the day. The primary purpose of this study is to evaluate the relationship between the severity of sleep-disordered breathing and levels of daytime alertness at baseline (untreated state) in a group of subjects with and without sleep apnea. In addition the change in daytime sleepiness in subjects with sleep apnea being treated with a continuous positive airway pressure (CPAP) machine, a common treatment for OSA will also be assessed.

Obstructive Sleep Apnea (OSA) is the most common sleep disorder affecting up to 9-24 percent of middle aged adults, and is becoming increasingly implicated in the pathogenesis of hypertension, and other cardiovascular disorders. Up to half of patients with OSA have hypertension, and their risk of developing hypertension increases with the increasing severity of Sleep Apnea. Patients with OSA and no hypertension have endothelial dysfunction, which is believed to be the precursor for most cardiovascular disorders. The upper airway collapse and obstruction that occur in OSA result in a pattern of intermittent hypoxia, that has been shown to be the cause of the hypertension, and endothelial dysfunction found in patients with OSA. Intermittent hypoxia results in oxidative stress, which in turn is linked to the pathogenesis of hypertension and endothelial dysfunction. This protocol evaluates the role of the oxidative stress in endothelial function and blood pressure in patients with OSA. This is a pilot clinical study that will compare oxidative stress parameters, and endothelial function in patients with OSA before starting treatment with continuous positive airway pressure (CPAP) and 12 weeks post being on CPAP. These patients will be compared to control patients with no history of OSA. the study does not involve assignement to different treatments. All patients will receive the indicated treatment for OSA and measurements will be collected before and 12 weeks after adequate treatment.

OSA is associated with large negative swings in the intrathoracic pressure, significant increase in the sympathetic nerve activity and repetitive surges in blood pressure, along with episodic hypoxia and hypercapnea (8,9). These autonomic and respiratory changes may increase the cardiac muscle workload, cardiac dysrrhythmia, and exacerbate ischemia (10,11,12). Treatment with CPAP is the most successful therapeutic modality available for OSA. It is still not clear whether establishing the diagnosis of OSA and initiating treatment with CPAP while still in the hospital carries any benefit in the management of patients with acute heart failure. This study will evaluate the effect of work up and treatment of OSA on the outcome of patients hospitalized with acute CHF.

Obstructive Sleep Apnea (OSA) is a condition in which a person stops breathing for several seconds at a time due to relaxation of the throat muscles. This can occur many times during sleep. It is known to cause sleepiness and poor concentration during the day. Research indicates that OSA may be a modifiable risk factor for cardiovascular disease due to its association with hypertension, stroke, heart attack and sudden death. The standard therapy for symptomatic OSA is continuous positive airway pressure (CPAP). CPAP has been shown to effectively reduce snoring, obstructive episodes and daytime sleepiness and to modestly reduce blood pressure and other risk factors for cardiovascular disease. The overall aim of SAVE is to determine if CPAP can reduce the risk of heart attack, stroke or heart failure for people with OSA.

The hypothesis of this study is that either obstructive sleep apnea (OSA) or cigarette smoking (CS) exposure would produce oxidative stress and inflammation leading to endothelial injury, and the combined exposure would be additive or synergistic.

This study is designed to determine the effect of continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) on heart rate variability (HRV) in patients with obstructive sleep apnea (OSA).

Many studies have shown a high non-attendance rate in hospital outpatient clinics. The investigators have found a non-attendance rate of 25% in their asthma clinics and would like to investigate whether a reminder phone call will improve attendance rates. Patients will be randomised into two groups; one group will receive a reminder phone call one week prior to their hospital consultation and the other group will be managed in the standard manner (i.e. no reminder of any sort). The phone calls will be carried out on a Friday afternoon by a respiratory nurse specialist and a research officer for two asthma clinics based on a Wednesday morning and a Thursday afternoon.

Sleep Apnea is a prevalent condition that has been increasingly diagnosed in the adult population and is now considered an independent risk factor for the development of cardiovascular disease. A better understanding of the mechanisms associated with the development of cardiovascular disease in sleep apnea is needed. This research will investigate the function of the adenosine deaminase (ADA) in subjects with sleep disorders. This enzyme is responsible for metabolizing adenosine, a neuromodulator that is released during periods of sleep apnea and that has been found to promote vascular thrombosis. There are multiple types of ADA that are genetically determined and have different levels of function. Those different forms of this enzyme may determine groups that are more susceptible to the development of thrombosis. Given the known association between sleep apnea and thrombosis, this study will determine if polymorphisms of this enzyme are differentially found in subjects with sleep apnea as compared to other sleep disturbances. The overall objective of this experiment is to assess the presence of ADA polymorphisms in sleep apnea.