NT-pro-BNP in obstructive sleep apnea syndrome is decreased by nasal continuous positive airway pressure

Abstract

The aim of this study was to evaluate the impact of obstructive sleep apnea syndrome (OSAS) on B-type natriuretic peptide (BNP) and to determine the effect of nasal continuous positive airway pressure (nCPAP) treatment on BNP levels. Increased sympathetic activity, repetitive rises in blood pressure, and apnea-induced wall stress may contribute as a trigger to release BNP in OSAS. However, there is uncertainty about whether OSAS affects BNP and whether application of nasal continuous positive airway pressure (nCPAP) ventilation affects release of BNP. A prospective study in 69 consecutive patients with suspected sleep disordered breathing referred to our sleep laboratory was conducted. OSAS was confirmed in 26 normotensive and 34 hypertensive patients and ruled out in nine normotensive patients (controls) by polysomnography (PSG). Baseline N-terminal fragment of BNP prohormone (NT-pro-BNP) did not differ significantly between OSAS patients (hypertensive: mean +/-SEM 60.8+/-9.9 pg/ml, normotensive: 43.2+/-6.8 pg/ml) and controls (36.5+/-8.5 pg/ml). Application of CPAP resulted in a significant decrease of NT-pro-BNP in hypertensive (60.8+/-9.9 pg/ml to 47.6+/-7.4 pg/ml, p=0.023) and normotensive OSAS (43.2+/-6.8 pg/ml to 29.6+/-5.3 pg/ml, p=0.0002). In contrast, controls showed no significant differences in NT-pro-BNP after a second PSG (36.5+/-8.5 pg/ml to 40.7+/-12.3 pg/ml, p=0.597). Normotensive and hypertensive OSAS was not associated with a significant elevation of NT-pro-BNP. Application of nCPAP decreased NT-pro-BNP levels significantly in normotensive and, in particular, hypertensive OSAS. These findings may provide further evidence of the potential for nCPAP to improve cardiovascular comorbidity and co-mortality in OSAS and sleep disordered breathing, in general.