This Article Full Text Full Text (PDF) Online Supplement All Versions of this Article: 200602-270OCv1 175/2/190    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McArdle, N. Articles by Watts, G. Search for Related Content PubMed PubMed Citation Articles by McArdle, N. Articles by Watts, G.

Metabolic Risk Factors for Vascular Disease in Obstructive Sleep Apnea

A Matched Controlled Study

Royal Perth Hospital and School of Medicine and Pharmacology, University of Western Australia, Perth; and Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Perth, Australia

Correspondence and requests for reprints should be addressed to Nigel McArdle, M.D., Royal Perth Hospital, Respiratory Department Wellington St., 6000, Perth, Western Australia. E-mail: nmcardle{at}cyllene.uwa.edu.au

Rationale: Obstructive sleep apnea (OSA) is reported to have a metabolic profile predisposing to cardiovascular disease. However, previous case-control studies have not adequately controlled for confounders.

Objectives: To determine whether OSA is associated with increased insulin resistance and related metabolic risk factors.

Methods: We performed a matched case-control study (n = 42) examining putative metabolic risks among men with OSA attending a sleep clinic (apnea–hypopnea index [AHI] > 15] compared with no OSA (AHI < 5). Participants were matched for age ± 5 yr, body mass index ± 10%, and current smoking status. They were free of diabetes, clinically demonstrable cardiovascular disease, marked hypertension, and dyslipidemia.

Measurements and Main Results: Mean ± SD AHI was higher in patients with OSA (40 ± 27) than in control subjects (3 ± 1.3, p = 0.02), and median (interquartile range) nocturnal oxygen saturation was lower (OSA, 83 [76–88]; control, 91 [90–93]%; p < 0.001). Patients with OSA had a higher median (interquartile range) homeostasis model assessment score for insulin resistance (OSA, 1.7 [0.8–4.1]; control, 1.0 [0.7–1.8] mU·mmol/L²; p = 0.02), total cholesterol (OSA, 5.6 [4.8–6.2]; control, 4.8 [4.3–5.4] mmol/L; p = 0.049), and low-density-lipoprotein cholesterol (OSA, 3.8 [2.9–4.2]; control, 3.1 [2.6–3.6] mmol/L; p = 0.04). Patients with OSA had higher 24-h and nocturnal (12-h) urinary norepinephrine excretion and plasma leptin levels, and lower insulin-like growth factor (IGF)-1 levels (all, p 0.02). Multiple linear regression, adjusting for central obesity, age, and alcohol consumption, confirmed an independent association between OSA and metabolic risks (all, p < 0.05), with a trend for IGF-1 (p = 0.053).

Conclusions: In a sleep clinic population, men with OSA and no identifiable cardiovascular disease have increased insulin resistance and other metabolic changes that act to increase the risk of vascular disease, compared with age- and body mass index–matched attendees without OSA.

Key Words: sleep disorders • pathophysiology • vascular disease • insulin resistance

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Obstructive sleep apnea has been associated with increased vascular risk. There is increasing evidence of metabolic changes occurring in this condition that predispose to cardiovascular disease. What This Study Adds to the Field This study shows metabolic changes in a sleep clinic population of men with obstructive sleep apnea compared with control subjects matched for body mass index and age. Changes persisted when allowance was made for central obesity.

 

This article has been cited by other articles:

				P. Levy, M. R. Bonsignore, and J. Eckel Sleep, sleep-disordered breathing and metabolic consequences Eur. Respir. J., July 1, 2009; 34(1): 243 - 260. [Abstract] [Full Text] [PDF]

				L. Lavie and P. Lavie Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link Eur. Respir. J., June 1, 2009; 33(6): 1467 - 1484. [Abstract] [Full Text] [PDF]

				V. Savransky, J. Jun, J. Li, A. Nanayakkara, S. Fonti, A. B. Moser, K. E. Steele, M. A. Schweitzer, S. P. Patil, S. Bhanot, et al. Dyslipidemia and Atherosclerosis Induced by Chronic Intermittent Hypoxia Are Attenuated by Deficiency of Stearoyl Coenzyme A Desaturase Circ. Res., November 7, 2008; 103(10): 1173 - 1180. [Abstract] [Full Text] [PDF]

				A Barcelo, F Barbe, M de la Pena, P Martinez, J B Soriano, J Pierola, and A G N Agusti Insulin resistance and daytime sleepiness in patients with sleep apnoea Thorax, November 1, 2008; 63(11): 946 - 950. [Abstract] [Full Text] [PDF]

				R. L. Horner and T. D. Bradley Update in Sleep and Control of Ventilation 2007 Am. J. Respir. Crit. Care Med., May 1, 2008; 177(9): 947 - 951. [Full Text] [PDF]

				A. R. Schwartz, S. P. Patil, A. M. Laffan, V. Polotsky, H. Schneider, and P. L. Smith Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches Proceedings of the ATS, February 15, 2008; 5(2): 185 - 192. [Abstract] [Full Text] [PDF]

				E. Tasali and M. S. M. Ip Obstructive Sleep Apnea and Metabolic Syndrome: Alterations in Glucose Metabolism and Inflammation Proceedings of the ATS, February 15, 2008; 5(2): 207 - 217. [Abstract] [Full Text] [PDF]

				E. Tasali, B. Mokhlesi, and E. Van Cauter Obstructive Sleep Apnea and Type 2 Diabetes*: Interacting Epidemics Chest, February 1, 2008; 133(2): 496 - 506. [Abstract] [Full Text] [PDF]

				C. Selmi, N. Montano, R. Furlan, C. L. Keen, and M. E. Gershwin Inflammation and Oxidative Stress in Obstructive Sleep Apnea Syndrome Experimental Biology and Medicine, December 1, 2007; 232(11): 1409 - 1413. [Abstract] [Full Text] [PDF]

				J. Li, A. Nanayakkara, J. Jun, V. Savransky, and V. Y. Polotsky Effect of deficiency in SREBP cleavage-activating protein on lipid metabolism during intermittent hypoxia Physiol Genomics, October 19, 2007; 31(2): 273 - 280. [Abstract] [Full Text] [PDF]

				V. Savransky, A. Nanayakkara, J. Li, S. Bevans, P. L. Smith, A. Rodriguez, and V. Y. Polotsky Chronic Intermittent Hypoxia Induces Atherosclerosis Am. J. Respir. Crit. Care Med., June 15, 2007; 175(12): 1290 - 1297. [Abstract] [Full Text] [PDF]