Appropriate use of nasal continuous positive airway pressure decreases elevated C-reactive protein in patients with obstructive sleep apnea.
BACKGROUND
C-reactive protein (CRP) is an important risk factor for cardiovascular disease. Furthermore, it has been reported that levels of CRP are increased in patients with obstructive sleep apnea (OSA). The aim of this study was to examine the effects of long-term therapy with nasal continuous positive airway pressure (nCPAP) on CRP levels and to investigate whether compliance with nCPAP therapy more effectively attenuated markers of systemic inflammation in patients with OSA.


RESULTS
Fifty-five patients (mean [+/- SEM] age, 55 +/- 2 years; 44 male patients, 11 female patients) with newly diagnosed moderate-to-severe OSA (apnea-hypopnea index > 20 events/h) were studied before and after 6 months of nCPAP treatment. There was a significant reduction in CRP levels after nCPAP therapy (before nCPAP therapy, 0.23 +/- 0.03 mg/dL; after nCPAP therapy, 0.17 +/- 0.02 mg/dL; p < 0.01). Additionally, we divided these patients into two groups based on adherence to nCPAP therapy. A group of patients using nCPAP > 4 h/d and > 5 d/wk were designated as the good compliance group. The decrease in CRP concentration was significant (before nCPAP therapy, 0.23 +/- 0.04 mg/dL; after nCPAP therapy, 0.16 +/- 0.03 mg/dL; p < 0.05) in the good compliance group but not in the poor compliance group (before nCPAP therapy, 0.24 +/- 0.05 mg/dL; after nCPAP therapy, 0.20 +/- 0.05 mg/dL; p = 0.21). Furthermore, we divided those patients into a high CRP group (>/= 0.2 mg/dL) and a normal CRP group (< 0.2 mg/dL) before nCPAP therapy. The significant decrease in CRP levels in the good compliance group was evident only in those patients with an initially elevated CRP level (before nCPAP therapy, 0.48 +/- 0.08 mg/dL; after nCPAP therapy, 0.29 +/- 0.06 mg/dL; p < 0.05).


CONCLUSIONS
Appropriate use of nCPAP in patients with OSA may be required to decrease elevated CRP levels, with possible implications for cardiovascular morbidity and mortality.
Ishida
Katsunori
K
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Kato
Masahiko
M
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan. Electronic address: mkato@grape.med.tottori-u.ac.jp.
Kato
Yosuke
Y
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Yanagihara
Kiyotaka
K
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Kinugasa
Yoshiharu
Y
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Kotani
Kazuhiko
K
Department of Clinical Laboratory Medicine, Jichi Medical University, Tochigi, Japan.
Igawa
Osamu
O
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Hisatome
Ichiro
I
Department of Genetic Medicine and Regenerative Therapeutics, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Shigemasa
Chiaki
C
Department of Cardiovascular Medicine, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Somers
Virend K
VK
Division of Cardiovascular Disease, Mayo Clinic, Rochester, MN.
D001794:Blood Pressure; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism*; D045422:Continuous Positive Airway Pressure; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010349:Patient Compliance; D020181:Sleep Apnea, Obstructive / Q000097:blood* / Q000503:physiopathology / Q000628:therapy*; D013997:Time Factors; D016896:Treatment Outcome
D008055:Lipids; D002097:C-Reactive Protein