How does serum brain natriuretic peptide level change under nasal continuous positive airway pressure in obstructive sleep apnea-hypopnea syndrome?

Abstract

BackgroundObstructive 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 methodsSixty-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.ResultsAt 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) (p<0.0001), 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, p<0.001, and from 20±10.09 to 16±8.98 pg/ml, p<0.001). 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).ConclusionBNP seems to be sensitive enough to detect myocardial stress caused by OSAHS. As such, it is a potential marker for screening of preclinical cardiovascular damage in patients with untreated OSAHS. Application of CPAP decreases levels significantly in normotensive and particularly in hypertensive OSAHS. These findings are consistent with previous results suggesting the potential benefits of CPAP on cardiovascular outcome in OSAHS patients.

The effectiveness of hardware CPAP therapy in heart failure with preserved left ventricular ejection fraction and obstructive sleep apnea syndrome

“…Исходный уровень NT-proBNP мы ассоциировали с лучшим клиническим эффектом проводимой СРАР-терапии, что можно объяснить патогенетической ролью данной биомолекулы. Приведенное утверждение согласуется с результатами работ других авторов [18].…”

Impact of Snoring on the Cardiovascular System and its Treatment: Positive and Negative Effects of Continuous Positive Airway Pressure in Sleep Apnea

“…A study by Valo et al in the year 2015, showed a significant decrease in NT-proBNP with a single night CPAP treatment; however, hs trop-T remained unaltered [2]. Two studies conducted in 2016 by Strehmel et al and Msaad et al showed a marked reduction in BNP levels in both normotensive and hypertensive patients; however, no significant changes were observed in cTnT levels due to the CPAP treatment [11,3].…”

“…biomarkers [3]. According to The Sleep Heart Health Study, Wisconsin Sleep Cohort Study, and the Seventh Report of the Joint National Committee on the management of high blood pressure, OSA is one of the major identifiable causes of HTN [4].…”

“…Researchers are trying to prove the benefits of CPAP as first-line treatment in OSA in reducing daytime sleepiness and improving the quality of life [6]. There is sufficient data available to prove the decrease in the incidence of premature ventricular beats, brain natriuretic peptide (BNP) levels in CHF patients, new CV events in CAD, and HTN in coronary artery bypass graft patients [1,3,5]. Although the CPAP's usefulness on hemodynamic parameters like blood pressure, preload, afterload, and cardiomyocyte function is consistent according to some observers [5], others state that the association of OSA severity and the biomarkers, as well as the effects of CPAP on circulating levels of these biomarkers, is still to be established conclusively [7].…”

“…There is considerable evidence available that links an association between obstructive sleep apnea-hypopnea syndrome (OSAHS) and increased cardiovascular (CV) morbidity and mortality. However, the involved pathological mechanism is not clear, nor is the role of cardiac biomarkers [ 3 ]. According to The Sleep Heart Health Study, Wisconsin Sleep Cohort Study, and the Seventh Report of the Joint National Committee on the management of high blood pressure, OSA is one of the major identifiable causes of HTN [ 4 ].…”