This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS) is arguably the most prevalent disease to be discovered in the twentieth century. Although its definition has been evolving in recent years, the syndrome involve a group of obese and non-obese patients in whom elevated airway resistance and/or apnea/hypopnea occur during sleep leading to cyclical hypoxemia with profound disruption of sleep architecture. Apnea in adults defined as absence of airflow at the nose or mouth for 10 seconds or more, whereas hypopnea is referred as reduction in airflow of 30% or more from the previous stable baseline lasting 10 seconds or more with or without desaturation (> 4% from baseline). Patients with OSAHS frequently complain of excessive daytime sleepiness, fragmented sleep, loud snoring, abnormal mentation, impotance, morning headaches, nocturia and insomnia. They may also suffer from severe physiologic consequences including hypertension, myocardial infarction, cerebrovascular accident, pulmonary arterial hypertension, polycythemia and heart failure (left and right). This syndrome has additional deleterious effects including risk for collateral damage to the general public a 8-fold increase in vehicle accident rates. Continues Positive Airway Pressure (CPAP) is the most commonly applied, cost-effective treatment for patients with OSAHS and, short of traceostomy, the only option with proven survival benefit. Other treatment modalities such as oral appliances, surgical reconstruction of upper airways or weight reduction can be tried in select patients but have not proven to reduce all cause mortality. Research has shown that OSAHS can impair left and right ventricular function in untreated patients. Therapy with CPAP has been shown to improve cardiopulmonary hemodynamics in these individuals. The main methods used to study cardiac dysfunction are echocardiography and heart catheterization. These are fairly accurate and provide useful information, but are expensive, time consuming, and in the case of catherterization are invasive putting the patient at risk of complications. Interest in determination of serum markers to study heart function has grown recently. B-type natriuretic peptide (BNP) is a marker of ventricular strain (right and left) and its levels rise during acute or chronic myocardial stress. BNP has recently been shown to be an important tool in the diagnosis of congestive heart failure and also have long-term prognostic value for patients with left-sided heart failure and pulmonary hypertension. To our knowledge, there has been no longitudinal study in the English literature showing correlation between serum BNP levels using it as a marker of ventricular strain and clinical response to CPAP treatment in patients with OSAHS. A single study revealed an increase in serum BNP levels in patients with OSAHS during an overnight polysomnographic study. However, utility of BNP in long-term follow-up of this group of patients has not been studied and unknown. Besides BNP, serum markers such as uric acid, leptin, C-reactive protein (CRP), endothelin-1, fibrinogen, IL-6 and nitric oxide have been studied in patients with OSAHS. Utility or clinical significance of these markers in patients with OSAHS are not well established to date.
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