Volume 15, Issue 4 pp. 424-429

N-terminal pro-brain natriuretic peptide for detection of cardiovascular stress in patients with obstructive sleep apnea syndrome

EDMOND VARTANY

EDMOND VARTANY

Section of Pulmonary, Sleep and Critical Care Medicine

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MICHAEL IMEVBORE

MICHAEL IMEVBORE

Section of Pulmonary, Sleep and Critical Care Medicine

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MARY O'MALLEY

MARY O'MALLEY

Section of Pulmonary, Sleep and Critical Care Medicine

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CHRISTOPHER MANFREDI

CHRISTOPHER MANFREDI

Section of Pulmonary, Sleep and Critical Care Medicine

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CAROL PASQUARELLA

CAROL PASQUARELLA

Section of Pulmonary, Sleep and Critical Care Medicine

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LEONARD SCINTO

LEONARD SCINTO

Department of Pathology, Norwalk Hospital, Norwalk, CT, USA

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JONATHAN FINE

JONATHAN FINE

Section of Pulmonary, Sleep and Critical Care Medicine

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First published: 17 November 2006
Citations: 16
Jonathan Fine, Norwalk Hospital 34 Maple Street, Norwalk, CT 06856, USA. Tel.: +1 203 852 2484; fax: +1 203 852 2738; e-mail: [email protected]

No financial disclosure for any of the authors.

Summary

Patients with obstructive sleep apnea syndrome (OSAS) have an elevated incidence of cardiovascular events that may be related to an increased ventricular load and hypoxemia caused by apneas and hypopneas. N-terminal pro-brain natriuretic peptide (NTproBNP) appears to be an excellent marker of myocardial stretch and could serve as an indicator of subclinical cardiac stress, thereby identifying a patient population at risk for cardiac effects from OSAS. Adult patients presenting with suspected OSAS and scheduled for nocturnal polysomnography were recruited. Patients with heart or renal failure or severe lung disease were excluded. NTproBNP was measured the evening before and the morning after sleep. Blood pressure (BP) was monitored intermittently throughout the night. Fifteen male and 15 female subjects with a mean ± SD body mass index of 38.2 ± 9.8 were studied. Mean Apnea–Hypopnea Index (AHI) was 38.4 ± 26, with 17 subjects having severe OSAS (AHI > 30). No subject had a significant rise in BP. NTproBNP values overnight decreased in 19 patients and rose in 11 (mean change 3.8 ± 33 pg mL−1), but only one patient had an abnormal morning value. Three patients had an abnormal NTproBNP value prior to sleep, but their levels decreased with sleep. No correlations were detected between the evening baseline or postsleep NTproBNP levels and OSAS. Monitoring pre- and postsleep NTproBNP levels revealed no association with the occurrence or degree of OSAS, making it unlikely that NTproBNP could serve as a marker of cardiac stress in OSAS patients with stable BP and without overt heart failure.

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