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P101. BNP IN OBSTRUCTIVE SLEEP APNEA SYNDROME IS DECREASED BY NASAL
CONTINUOUS POSITIVE AIRWAY PRESSURE
AHMED DHIA EL-EUCH, SAMEH MSAAD, RAHMA GARGOURI, NAJLA BAHLOUL, AMINA
KOTTI, RIM MARAKCHI, WAJDI KETATA, SAMY KAMMOUN
SERVICE DE PNEUMOLOGIE-ALLERGOLOGIE, CHU HEDI CHAKER - SFAX
Background
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is associated with cardiovascular morbidity
and mortality, which can be improved by using continuous positive airway pressure (CPAP) therapy.
However, the pathophysiological links between the two kinds of disease and the mechanism of
the CPAP effect remain incompletely understood. We aimed to inquire into the myocardial
involvement in this relationship. We suggested that serum brain natriuretic peptide (BNP) is
sensitive enough to detect myocardial stress caused by OSAHS.
Design and methods
Sixty-four subjects without cardiovascular disease (21 controls, 24 normotensive OSAHS patients,
and 19 hypertensive OSAHS patients) were analyzed for serum BNP at baseline and serially over
6 months. CPAP was applied to 23 patients with severe OSAHS.
Results
At baseline, the serum BNP levels were significantly higher (p=0.0001) in the OSAHS group
(22.3±14.79 pg/ml) than in the control group (9.2±6.75 pg/ml). Increased serum BNP levels were
significantly associated with mean transcutaneous oxygen saturation (SpO2) (p0.0001), minimal
SpO2 (p=0.002), oxygen desaturation index (p=0.001), and total sleep time spent with SpO2 lower
than 90% (p=0.002). All patients with elevated BNP levels (≥37 pg/ml) had moderate or severe
OSAHS (11/43 OSAHS patients). The more severe the OSAHS, the higher the BNP levels were.
However, only the difference between severe and mild OSAHS was statistically significant
(p=0.029). Hypertensive OSAHS patients had the highest baseline BNP levels (27.7±16.74 pg/ml).
They were significantly higher (p=0.001) than in normotensive OSAHS patients (18±11.72 pg/ml)
(p=0.039) and the controls (9.2±6.75 pg/ml). As compared with baseline, treatment with CPAP
significantly decreased BNP levels in both hypertensive and normotensive OSAHS patients
(respectively, from 36±16.10 to 29.7±14.29 pg/ml, p0.001, and from 20±10.09 to 16±8.98 pg/ml,
p0.001). In contrast, the BNP levels slightly increased in the controls (from 9.2±6.75 to 9.5±7.02
pg/ml, p=0.029), but there was no statistically significant difference in comparison with the
baseline value. The effect of CPAP on BNP levels was more marked in patients with higher baseline
BNP levels and those with the most prolonged nocturnal desaturation (p=0.001, r=0.65). It was also
more marked in hypertensive OSHAS patients (p=0.015, r=0.72) in comparison with normotensive
OSAHS patients (p=0.03, r=0.62).
Conclusion
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