The purpose of this study is to evaluate the relationships between prostanoids and various outcomes such as sleep disturbance, hypertension and arteriosclerosis in patients with sleep apnea syndrome(SAS). In the patients introduced to continuous positive airway pressure(CPAP) treatment, the effects of CPAP are also evaluated.
SAS is characterized by abnormality during sleep and hypoxemia from apnea and hypopnea, followed by systemic inflammation and organ dysfunction like cardiovascular diseases. Systemic inflammation causes the activation of arachidonic acid metabolism, producing prostaglandins (PGs) and leukotrienes (LTs). In addition, significant relationships between PGD2 and PGE2 and sleep, PGF2α and hypertension, PGI2 and thromboxane and platelet aggregation and so on are reported. Therefore, it is hypothesized that many prostanoids affect the pathophysiology of SAS. However, the relationships between prostanoids and clinical outcomes in patients with SAS are unknown. Although CPAP is the major treatment of SAS, the effects of CPAP on prostanoids are not known, either. Thus, the purpose of this study is to evaluate those relationships.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
46
CPAP treatment is to improve airway obstruct for obstructive sleep apnea, and after 3 months' treatment, we evaluate the effects.
Kyoto University, Graduate School of Medicine
Kyoto, Kyoto, Japan
metabolites of arachidonic acid in the urine and blood
Time frame: 3 months
Polysomnography measurements
Time frame: 3 months
Sleepiness and health-related quality of life
Time frame: 3 months
Blood pressure and pulse rate
Time frame: 3 months
Endothelial dysfunction
Time frame: 3 months
Platelet aggregation
Time frame: 3 months
Cardiac and neck echo cardiography
Time frame: 3 months
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