Chest
Volume 134, Issue 4, October 2008, Pages 686-692
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Original Research
Sleep Medicine
Effects of Continuous Positive Airway Pressure on Cardiovascular Risk Profile in Patients With Severe Obstructive Sleep Apnea and Metabolic Syndrome

https://doi.org/10.1378/chest.08-0556Get rights and content

Background

The increased risk of atherosclerotic morbidity and mortality in patients with obstructive sleep apnea (OSA) has been linked to arterial hypertension, insulin resistance, systemic inflammation, and oxidative stress. We aimed to determine the effects of 8 weeks of therapy with continuous positive airway pressure (CPAP) on glucose and lipid profile, systemic inflammation, oxidative stress, and global cardiovascular disease (CVD) risk in patients with severe OSA and metabolic syndrome.

Methods

In 32 patients, serum cholesterol, triglycerides, high-density lipoprotein cholesterol, fibrinogen, apolipoprotein A-I, apolipoprotein B (ApoB), high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor (TNF)-α, leptin, malondialdehyde (MDA), and erythrocytic glutathione peroxidase (GPx) activity were measured at baseline and after 8 weeks of CPAP. The insulin resistance index (homeostasis model assessment [HOMA-IR]) was based on the homeostasis model assessment method, the CVD risk was calculated using the multivariable risk factor algorithm.

Results

In patients who used CPAP for ≥ 4 h/night (n = 16), CPAP therapy reduced systolic BP and diastolic BP (p = 0.001 and p = 0.006, respectively), total cholesterol (p = 0.002), ApoB (p = 0.009), HOMA-IR (p = 0.031), MDA (p = 0.004), and TNF-α (p = 0.037), and increased erythrocytic GPx activity (p = 0.015), in association with reductions in the global CVD risk (from 18.8 ± 9.8 to 13.9 ± 9.7%, p = 0.001). No significant changes were seen in patients who used CPAP for < 4 h/night. Mask leak was the strongest predictor of compliance with CPAP therapy.

Conclusions

In patients with severe OSA and metabolic syndrome, good compliance to CPAP may improve insulin sensitivity, reduce systemic inflammation and oxidative stress, and reduce the global CVD risk.

Trial registration

Clinicaltrials.gov Identifier: NCT00635674.

Section snippets

Subjects

Clinically stable subjects with severe OSA (≥ 30 obstructive apneas or hypopneas per hour of sleep and excessive daytime sleepiness) and metabolic syndrome20 were prospectively recruited in the sleep unit at the tertiary referral teaching hospital. Exclusion criteria were as follows: (1) endocrine or metabolic disorders other than metabolic syndrome; (2) history of myocardial infarction, angina, or stroke; (3) inflammatory or other chronic disease; (4) respiratory disorder other than OSA; (5)

Characteristics of the Subjects

Thirty-two of 66 subjects referred to our sleep unit between January 2007 and October 2007 met the inclusion criteria. Of the remaining patients, 9 had OSA but no metabolic syndrome, 3 had mild-to-moderate OSA, 6 had central sleep apnea, and 16 subjects did not have sleep-disordered breathing (Fig 1). No patient in the study cohort underwent surgery of the upper airway, changed hypolipidemic and/or antihypertensive medications, or changed weight (> 5%) during the follow-up. Baseline

Discussion

This observational study demonstrated that 8 week of CPAP therapy reduced the global CVD risk in patients with severe OSA and concurrent metabolic syndrome. Reductions in CVD risk were linked to reductions in BP and total cholesterol levels. In addition, patients effectively treated with CPAP had reductions in insulin resistance, TNF-α, and oxidative stress markers. Nevertheless, these beneficial effects of therapy were confined to the group of patients who used CPAP for ≥ 4 h/night.

Acknowledgment

The authors wish to express their gratitude to Mrs. Katarina Pollakova, the head nurse, and Mrs. Anna Schejbalova and Slavka Zemanova, the technicians in the sleep laboratory, Department of Respiratory Medicine, Faculty of Medicine and L. Pasteur Teaching Hospital, Kosice, Slovakia.

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    This work was supported by the Slovak Research and Development Agency under the contract No. APVV-0122-06, and Ministry of Health under the contract No. 2005/5-FNLPKE-01, Slovakia.

    This work was performed at the Department of Respiratory Medicine, Faculty of Medicine and L. Pasteur Teaching Hospital, Kosice.

    The authors have no conflicts of interest to disclose.

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).

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