SLEEP APNEA AND C-REACTIVE PROTEIN OBSTRUCTIVE SLEEP APNEA SYNDROME (OSAS) IS A COMMON DISEASE THAT OCCURS IN ABOUT 2% TO 4% OF THE GENERAL POPULATION.1,2 PATIENTS WITH OSAS suffer from hypoxemia and hypercapnia during sleep

OBSTRUCTIVE SLEEP APNEA SYNDROME (OSAS) IS A COMMON DISEASE THAT OCCURS IN ABOUT 2% TO 4% OF THE GENERAL POPULATION.1,2 PATIENTS WITH OSAS suffer from hypoxemia and hypercapnia during sleep caused by repetitive nocturnal respiratory pauses. Moreover, nocturnal hypoxemia is considered to be associated with cardiovascular and cerebrovascular disease,3,4 although the association has not been fully explained. The relation between OSAS and vascular complications is supported by a high prevalence of OSAS in patients who have experienced a recent stroke or a transient ischemic attack5,6 and in those with coronary heart disease.7 Much attention has been paid to endothelial dysfunction, as opposed to the other various contributors to vascular diseases. Endothelial dysfunction, an early marker of atherosclerosis, develops as a result of arterial endothelial wall injury. Flowmediated dilatation (FMD) has been used as a noninvasive method to measure endothelial dysfunction. Ip et al showed that FMD is significantly correlated with the apnea-hypopnea index (AHI) in patients with OSAS.8 However, conflicting results have been presented by other studies. Kato et al failed to demonstrate a significant difference in FMD between OSAS patients and obese control subjects, although vasodilation was found to be blunted in response to acetylcholine in OSAS patients.9 In a large community sample of older adults, a significant linear association was found between the percentage of sleep time with an oxygen saturation below 90% and baseline arterial diameter rather than FMD.10 Thus, the relationship between FMD and OSAS still requires elucidation. C-reactive protein (CRP) is an important risk factor in atherosclerosis11 and in other cardiovascular diseases.12,13 Several studies have reported an increased CRP plasma level in OSAS. Repeated hypoxia in OSAS patients might induce proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α, which could elevate CRP. However, Guilleminault et al demonstrated no relationship between OSA and CRP in relatively less obese OSA patients14 and, rather, concluded that only body mass index (BMI) was significantly associated with a high CRP. Because both FMD and CRP are involved in the development of atherosclerosis, we reasoned that it would be interesting to measure FMD and CRP in OSAS patients to investigate the pathophysiology of cardiovascular complications. In the present study, we aimed (1) to study FMD and CRP in relation with OSAS severity and (2) to identify those variables that most importantly explain FMD and CRP changes in OSAS. Endothelial Dysfunction and C-Reactive Protein in Relation with the Severity of Obstructive Sleep Apnea Syndrome