Although obstructive sleep apnea and cardiovascular disease have common risk factors, epidemiologic studies show that sleep apnea increases risks for cardiovascular disease independently of individuals' demographic characteristics (i.e., age, sex, and race) or risk markers (i.e., smoking, alcohol, obesity, diabetes, dyslipidemia, atrial fibrillation, and hypertension). Individuals with severe sleep apnea are at increased risk for coronary artery disease, congestive heart failure, and stroke. The underlying mechanisms explaining associations between obstructive sleep apnea and cardiovascular disease are not entirely delineated. Several intermediary mechanisms might be involved including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress. Other abnormalities such as disorders in coagulation factors, endothelial damage, platelet activation, and increased inflammatory mediators might also play a role in the pathogenesis of cardiovascular disease. Linkage between obstructive sleep apnea and cardiovascular disease is corroborated by evidence that treatment of sleep apnea with continuous positive airway pressure reduces systolic blood pressure, improves left ventricular systolic function, and diminishes platelet activation. Several systematic studies are necessary to explicate complex associations between sleep apnea and cardiovascular disease, which may be compounded by the involvement of diseases comprising the metabolic syndrome (i.e., central obesity, hypertension, diabetes, and dyslipidemia). Largescale, population-based studies testing causal models linking among sleep apnea, cardiovascular morbidity, and metabolic syndrome are needed. keywords: Sleep apnea, cardiovascular disease, metabolic syndrome citation: Jean-Louis G; Zizi F; Clark LT; Brown CD; McFarlane SI. Obstructive sleep apnea and cardiovascular disease: role of the metabolic syndrome and its components.

Summary Sleep duration in America has gradually declined over the last four decades and appears to have reached a plateau for the last six years, with recent studies reporting that the population's current average sleep duration is approximately 6 hours. In this paper, we examine epidemiologic and community-based data on sleep complaints reported by American adults, specifically addressing the role of race/ethnicity in the subjective report of sleep problems. Subjective and objective findings indicate that black1 Americans have higher rates of long (≥ 9 h) and short (≤5 h) sleep than their white counterparts, and this may mediate a higher risk of cardiovascular disease (CVD), obesity and diabetes among blacks. In addition, studies show mixed results on sleep complaints among blacks compared to those among other ethnicities. This paper explores factors that may contribute to racial/ethnic differences in sleep including intra-ethnic variation, cultural biases, genetics and psychosocial factors.

Introduction Over the past half century, evidence has been accumulating on the emergence of obstructive sleep apnea (OSA), the most prevalent sleep-disordered breathing, as a major risk factor for cardiovascular disease. A significant body of research has been focused on elucidating the complex interplay between OSA and cardiovascular risk factors, including dyslipidemia, obesity, hypertension, and diabetes mellitus that portend increased morbidity and mortality in susceptible individuals. Conclusion Although a clear causal relationship of OSA and dyslipidemia is yet to be demonstrated, there is increasing evidence that chronic intermittent hypoxia, a major component of OSA, is independently associated and possibly the root cause of the dyslipidemia via the generation of stearoyl-coenzyme A desaturase-1 and reactive oxygen species, peroxidation of lipids, and sympathetic system dysfunction. The aim of this review is to highlight the relationship between OSA and dyslipidemia in the development of atherosclerosis and present the pathophysiologic mechanisms linking its association to clinical disease. Issues relating to epidemiology, confounding factors, significant gaps in research and future directions are also discussed.

BackgroundEpidemiologic studies show a curvilinear relationship between inadequate sleep (< 7 or > 8 hours) and obesity (Body Mass Index > 30 kg/m2), which have enormous public health impact.MethodsUsing data from the National Health Interview Survey, an ongoing nationally representative cross-sectional study of non-institutionalized US adults (≥18 years) (1977 through 2009), we examined the hypothesis that inadequate sleep is independently related to overweight/obesity, with adjustment for socio-demographic, health risk, and medical factors. Self- reported data on health risks, physician-diagnosed medical conditions, sleep duration, and body weight and height were used.ResultsPrevalence of overweight and obesity increased from 31.2% to 36.9% and 10.2% to 27.7%, respectively. Whereas prevalence of very short sleep (<5 hours) and short sleep (5–6 hours) has increased from 1.7% to 2.4% and from 19.7% to 26.7%, it decreased from 11.6% to 7.8% for long sleep. According to multivariate-adjusted multinomial regression analyses, odds of overweight and obesity associated with very short sleep and short sleep increased significantly from 1977 to 2009. Odds of overweight and obesity conferred by long sleep did not show consistent and significant increases over the years. Analyses based on aggregated data showed very short sleepers had 30% greater odds of being overweight or were twice as likely to be obese, relative to 7–8 hour sleepers. Likewise, short sleepers had 20% greater odds of being overweight or 57% greater odds of being obese. Long sleepers had 20% greater odds of being obese, but no greater odds of being overweight.ConclusionsOur findings support the hypothesis that prevalence of very short and short sleep has gradually increased over the last 32 years. Inadequate sleep was associated with overweight and obesity for each available year.