Background/Aim. Previous population-based studies found association between duration of sleep and cardiovascular and metabolic comorbidities. Our aim was to investigate the association between the duration of sleep and cardiovascular and metabolic comorbidities in OSAS. Patients and Methods. The study enrolled 312 patients, who had polysomnography (PSG) during 2006-2007 and responded to a telephone-administered questionnaire providing information on characteristics of sleep on average 12 months after PSG. Results. Of the patients, 90 were female (28.8%), 173 (58.5) received the diagnosis of OSAS, 150 (45%) had no comorbidities, 122 had hypertension (HT), 44 had diabetes mellitus (DM), and 38 had coronary heart disease (CHD). Mean ± SD of age in years was , , , and for the no comorbidity, HT, DM, and CHD groups, respectively. Reported duration of sleep was not associated with any of the comorbidities in the overall group. In the analysis restricted to OSAS patients, sleep duration ≤6 hours was significantly associated with CHD after the adjustment for age, gender, and other associated factors (OR: 5.8, 95% CI: 1.0–32.6). Conclusions. Confirmation of the association between shorter duration of sleep and CHD will provide prognostic information and help for the management of OSAS. 1. Introduction Sleep loss is a common condition in modern society. Although the health effects of sleep deprivation have been obscure, recent epidemiological studies have revealed relationships between sleep deprivation and hypertension (HT), coronary heart disease (CHD), and diabetes mellitus (DM) [1]. Because sleep deprivation increases sympathetic nervous system activity, this increased activity serves as a common pathophysiology for HT, DM, and CHD. Previous studies showed that sleep duration less than 6 hours or more than 8 hours is associated with increased morbidity and mortality due to cardiovascular diseases in the general population [2, 3]. Obstructive sleep apnea syndrome (OSAS) is a common medical disorder that is growing in prevalence worldwide. It is characterized by recurrent cycles of intermittent hypoxia and there is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in OSAS patients through the activation of inflammatory pathways. Some excellent review articles have already summarized the effects of OSAS on HT, CHD, and DM [4–6]. The pathogenesis of cardiovascular disease in OSAS is not completely understood but is likely to be multifactorial, involving a diverse range of mechanisms including sympathetic nervous
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