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Volume 135, Issue 3, Pages 338-345 (10 July 2009)


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Continuous positive nasal airway pressure decreases levels of serum amyloid A and improves autonomic function in obstructive sleep apnea syndrome

Emi Kuramotoab, Saori Kinamia, Yoshihiro Ishidaa, Hideyuki Shiotanic, Yoshihiro NishimurabCorresponding Author Informationemail address

Received 1 June 2007; received in revised form 22 October 2007; accepted 30 March 2008. published online 01 July 2008.

Abstract 

Background

Obstructive sleep apnea syndrome (OSAS) is associated with the pathogenesis of cardiovascular disease, and inflammation and autonomic dysfunction. We investigated levels of serum amyloid A (SAA), a marker of inflammation, as well as autonomic nervous activity and pulse wave velocity (PWV) before and after nasal continuous positive airway pressure (nCPAP) therapy in patients with obstructive sleep apnea.

Methods and results

We separated 116 patients who were diagnosed with OSAS by polysomnography according to the apnea hypopnea index (AHI) into the following groups: Group 1 without or with mild OSAS (AHI<20, n=35), Group 2 with moderate OSAS (20=<AHI<40, n=35) and Group 3 with severe OSAS (AHI>=40, n=46). Serum level of SAA (p<0.05), brachial-ankle PWV (p<0.05) and BP (p<0.005) were significantly higher in Group 3 than in Group 1. Autonomic nervous activity assessed by autoregressive spectral analysis of heart rate variability showed that high frequency (HF) power, an indicator of vagal activity, was decreased in Groups 2 and 3 (p<0.05) and that low frequency/HF, an indicator of sympathetic activity, was increased in Group 3 (p<0.05). After 3 months of nCPAP therapy in Group 3 (n=38), SAA (p<0.05), PWV (p<0.001) and BP (p<0.05) were significantly decreased.

Conclusion

Markers of inflammation and autonomic dysfunction are increased in patients with OSAS, and nCPAP might help to reduce these risk factors for cardiovascular diseases.

a Department of Internal Medicine, Akashi Medical Center, Akashi, Japan

b Division of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan

c Faculty of Health Science, Kobe University Graduate School of Medicine, Kobe, Japan

Corresponding Author InformationCorresponding author. Division of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. Tel.: +81 78 382 5846; fax: +81 78 382 5859.

PII: S0167-5273(08)00552-4

doi:10.1016/j.ijcard.2008.03.078


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