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Obstructive Sleep Apnea Therapy and Metabolic Outcomes

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Obstructive Sleep Apnea Therapy and Metabolic Outcomes Obstructive Sleep Apnea Therapy and Metabolic Outcomes Harneet K. Walia, MDa,b,*, Reena Mehra, MD, MSb,c,d KEYWORDS Obstructive sleep apnea Metabolic syndrome Obesity Hypertension Continuous positive airway pressure KEY POINTS There are both epidemiologic and experimental data implicating obstructive sleep apnea (OSA) as a key pathophysiologic factor in the evolution of metabolic dysfunction and as a culprit in increasing cardiovascular risk. The metabolic syndrome consists of a constellation of clinical risk factors encompassing truncal obesity, atherogenic dyslipidemia, elevated blood pressure, low glucose tolerance, and hyperinsu- linemia, which in aggregate set the stage for the development of diabetes mellitus and cardiovas- cular disease. Conceptual frameworks are emerging with respect to the mechanistic underpinnings of OSA including intermittent hypoxia, sleep fragmentation, systemic inflammation and oxidative stress that contribute to the various facets of metabolic dysfunction. Reversal of the adverse accompanying pathophysiologic effects of OSA can have an impact on metabolic outcomes. The data suggests that treatment of OSA may ameliorate some of the metabolic parameters of metabolic syndrome. INTRODUCTION with projections for a continued increase in fre- quency slated to reach levels in the epidemic Aligned with the obesity epidemic, metabolic realm.1 The metabolic syndrome consists of a dysfunction has evolved into a highly prevalent constellation of clinical risk factors encompassing condition with pervasive, far-reaching public health truncal obesity, atherogenic dyslipidemia (high implications. The metabolic syndrome, a term levels of triglyceride and low levels of high- characterized by a clustering of independent car- density lipoprotein [HDL] cholesterol), elevated diovascular risk factors, has a current estimated blood pressure (BP), low glucose tolerance, and prevalence of 30% in the United States population, hyperinsulinemia in the context of a prothrombotic Conflicts of Interest Declaration: R. Mehra serves on the Medical Advisory Board for Care Core National, has received funding from the National Institutes of Health for research, and her institution has received positive airway devices from Philips Respironics for research for which she is the Principal Investigator. H. Walia has no conflicts of interest to disclose. R. Mehra was partially supported through funding by the NIH NHLBI 1R01HL109493 and R21HL108226. a Center for Sleep Disorders, Neurologic Institute, Cleveland Clinic, 11203 Stokes Boulevard, 2nd Floor, Cleveland, Ohio 44104, USA; b Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA; c Sleep Disorders Research, Center of Sleep Medicine, Neuro- logic Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA; d Molecular Cardiology Department, Lerner Research Institute, Heart and Vascular Institute, Respiratory Institute, 9500 Euclid Avenue, Cleveland, Ohio, 44195, USA * Corresponding author. E-mail address: [email protected] Sleep Med Clin 8 (2013) 433–452 http://dx.doi.org/10.1016/j.jsmc.2013.07.009 1556-407X/13/$ – see front matter Ó 2013 Elsevier Inc. All rights reserved. sleep.theclinics.com 434 Walia & Mehra state and upregulation of systemic inflammation, mitigate cardiovascular risk, particularly in light which in aggregate set the stage for the devel- of data demonstrating synergism of OSA and opment of diabetes mellitus and cardiovascular metabolic syndrome in increasing cardiovascular disease.1,2 These risk factors result in serious risk.4 adverse health effects by interacting synergistically to increase cardiovascular morbidity and mortality 1,2 EPIDEMIOLOGY AND INTERRELATIONSHIPS by 2- to 3-fold. Diagnostic evaluation and tar- OF OBSTRUCTIVE SLEEP APNEA, METABOLIC geted intervention coupled with identification of SYNDROME, AND OBESITY critical contributors of metabolic syndrome are paramount in the paradigm of cardiovascular risk Identified relationships of OSA and metabolic syn- reduction. Reduction of cardiovascular risk is of drome are not unanticipated given the overlap of the utmost importance from the standpoint of pub- established associated factors including obesity, lic health imperatives as well as in targeting reduc- diabetes mellitus, and cardiovascular disease. tion of the high economic costs associated with The co-occurrence of metabolic risk factors for cardiovascular disease, namely, estimated direct both type 2 diabetes and cardiovascular disease and indirect costs of $500 billion in 2010 with (abdominal obesity, hyperglycemia, dyslipidemia, $150 billion resulting from loss of productivity and hypertension) suggested the existence of a related to disability and death.3 “metabolic syndrome,” also known as insulin resis- A wealth of both epidemiologic and experi- tance syndrome. According to criteria proposed by mental data have implicated obstructive sleep ap- the National Cholesterol Education Program nea (OSA) as a key pathophysiologic factor in the (NCEP) Adult Treatment Panel III, the metabolic evolution of metabolic dysfunction and as a culprit syndrome is defined by the presence of 3 or more in increasing cardiovascular risk. A singular chal- of the following: (1) abdominal obesity with waist lenge in investigating the interrelationships of circumference greater than 40 inches (102 cm) in obesity, metabolic syndrome, and OSA has been men and 35 inches (88 cm) in women, (2) serum tri- to effectively take into consideration and dissect glycerides of 150 mg/dL, (3) HDL cholesterol less the influence of OSA on metabolic syndrome inde- than 40 mg/dL in men and less than 50 mg/dL in pendent of the effect of obesity. OSA is a highly women, (4) BP greater than 130/85 mm Hg or prevalent disorder affecting approximately 15% drug treatment for hypertension, and (5) fasting of adults, characterized by reduction in upper glucose level greater than 110 mg/dL.5 The preva- airway muscle tone during sleep resulting in repet- lence of metabolic syndrome as defined by NCEP itive complete (resulting apnea) or partial (resulting criteria as per National Health and Nutrition Exam- in hypopnea) upper airway closure in the presence ination Survey (NHANES) data has undergone a of continued thoracoabdominal effort and, often, substantive increase from 22% in NHANES 1988 paradox. OSA results in accompanying physio- to 1994 to 34.5% in NHANES 1999 to 2002.6 Along logic perturbations including intermittent hypoxia, these lines, as expected, an age-dependent in- ventilatory overshoot hyperoxia, intrathoracic crease in the prevalence of metabolic syndrome pressure alterations, autonomic instability, and was also observed. Corroborating data from a sleep fragmentation. These effects then lead to large epidemiologic cohort, the Framingham Heart further adverse effects including increased sys- Study involving 3500 participants without diabetes temic inflammation and elevated oxidative stress. or cardiovascular disease at baseline, demon- The apnea-hypopnea index (AHI) is considered as strated an increase in prevalence of metabolic syn- the disease-defining metric for OSA, and is drome of 26.8% in men and 16.6% in women at defined by the number of apneas and hypopneas baseline, and an almost doubling of prevalence of per hour of sleep. Other measures used to ascer- the metabolic syndrome in both men and women tain the severity of OSA include the oxygen desa- after an 8-year follow-up period.7 A likely contrib- turation index and percentage of sleep time spent uting factor to the noted dramatic increase in prev- in hypoxia. Conceptual frameworks are emerging alence of metabolic syndrome is the concordant with respect to the mechanistic underpinnings of obesity epidemic, which has been observed across OSA that contribute to the various facets of meta- of range of ethnicities.8 bolic dysfunction, which are elaborated in this OSA is also a highly prevalent disorder with article. Furthermore, the effect of the reversal of prevalence estimates of 9% to 24%,9 with a the adverse accompanying pathophysiologic ef- distinct risk-factor profile characterized by fects of OSA on metabolic outcomes is reviewed increased risk in men; positive linear relationships herein. These areas of investigation are of para- with increasing age; and augmented risk related to mount importance in achieving the goal of ef- obesity, owing to mechanical effects on the upper fective treatment of metabolic parameters to airway predisposing to collapsibility, as well as Obstructive Sleep Apnea Therapy and Metabolic Outcomes 435 neurohumoral effects of adipokines and craniofa- metabolic syndrome was further substantiated cial structural alterations resulting in compromise by data from a British study showing a 9-fold of upper airway caliber and function.10 Adverse increased likelihood of metabolic syndrome in effects of OSA, including intermittent hypoxia men with OSA even after consideration of and autonomic nervous system fluctuations, obesity.13 Taken together, accumulating evidence contribute to the increased risk of intermediate points to a steadily increasing prevalence of meta- cardiovascular factors comprising metabolic syn- bolic syndrome and a high prevalence of OSA, drome, as well as a wealth of data supporting with risk-factor profiles derived from a “common relationships between OSA and increased cardio- soil,” and relationships that are strong in magni- vascular morbidity and mortality.11,12 Although tude seemingly
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