Changes in Post-treatment Serum BNP Levels in Patients with Obstructive Sleep Apnea Syndrome

Research Article

Austin J Otolaryngol. 2014;1(1): 5.

Changes in Post-treatment Serum BNP Levels in Patients with Obstructive Sleep Apnea Syndrome

Fujioka T*, Iguchi H, Ohya M and Yamane H

Department of Otolaryngology and Head & Neck Surgery, Osaka City University Graduate School of Medicine, Japan

*Corresponding author: Takanori Fujioka, Department of Otolaryngology and Head & Neck Surgery, Osaka City University Graduate School of Medicine,1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan

Received: May 18, 2014; Accepted: July 21, 2014; Published: July 26, 2014


Objective: Severe sleep apnea syndrome (SAS) is known to cause heart failure. Various treatments are currently available for SAS, and it is important to assess the alleviation of physical burden on the patient as a result of these treatments. We investigated whether SAS treatment improves serum brain natriuretic peptides (BNP) levels.

Subjects and methods: The subject sample comprised 129 patients aged 14–84 years. Apnea hypopnea index (AHI) and serum BNP levels were measured in all patients. Each patient received suitable treatment; 3 months and 6 months after the start of the treatment, AHI and serum BNP level measurements were repeated, and the values for each patient were analyzed.

Results: The correlation coefficients for the associations of baseline AHI and serum BNP levels with those at 3 and 6 months after treatment initiation ranged from 0.6 to 0.8. Treatment-induced variations in AHI and serum BNP levels exhibited similar correlations.

Conclusion: SAS patients receiving treatment showed decreased serum BNP levels regardless of the type of treatment.

Keywords: Brain natriuretic peptides; Sleep apnea syndrome; Treatment; Apnea hypopnea index


SAS: Sleep Apnea Syndrome; EDS: Excessive Daytime Sleepiness; BNP: Brain Natriuretic Peptide; AHI: Apnea Hypopnea Index; nCPAP: Nasal Continuous Positive Airway Pressure; ANP: Atrial Natriuretic Peptide; NT-proBNP: N-terminal Pro-BNP; RAA: renin– angiotensin–aldosterone


Sleep apnea syndrome (SAS) is a combination of nighttime snoring, nocturnal awakening, frequent nocturnal urination, and decreased quality of sleep. SAS leads to excessive daytime sleepiness (EDS), decreased ability to concentrate, and mood changes, which may affect the social activities of patients. SAS is also associated with a high incidence of comorbidities, including cardiovascular diseases, such as hypertension and ischemic heart disease, as well as cerebrovascular disease and respiratory impairment with or without subjective symptoms; these comorbidities may cause sudden death [1].

The concept of SAS was proposed by Guilleminault in 1976 [2]. And it is currently considered a common condition. However, objective studies regarding whether the current treatments are actually suitable for SAS patients have not been conducted. The first and foremost aim of SAS treatment is to prevent complications, among which cardiovascular disease needs particular attention. Patients with SAS, even those without subjective symptoms or clinical problems, increase cardiac load over a prolonged period during sleep, which is believed to result in a condition similar to very mild heart failure. Because of this, among all SAS complications, we focused on heart failure, because it requires long-term treatment and follow-up. Therefore, we examined how the serum brain natriuretic peptide (BNP) levels, a commonly used biomarker in the diagnosis of heart failure in cardiovascular medicine, fluctuate in patients treated for SAS.

Patients and Methods

One hundred twenty nine outpatients aged 14-84 years old who presented with subjective symptoms, including daytime sleepiness, snoring, sleep apnea, nocturnal awakening, and headaches while awake, who were examined by our department for sleep apnea were included in our study. All subjects were strongly suspected of having SAS on the basis of medical history, visual examination of the nasopharynx and larynx, and fiberscopic findings of the larynx, and an apnea hypopnea index (AHI) obtained by sleep study. Sleep apnea was defined as having an AHI of ≥5 with EDS, which is the current generally accepted definition. At the time of the examination, the purpose of our study was explained to the patients, and verbal and written consent was obtained for all data items used. Furthermore, the absence of any pre-existing abnormality was confirmed by plain radiography of the chest and electrocardiography. And in this study, AHI is definited SAS in30 or more.

Serum BNP levels were measured using the chemiluminescent enzyme-linked immunosorbent assay (PATHFAST BNP™, Mitsubishi Chemical Yatron). All patients with serum BNP levels above the normal 18.4 pg/mL as recorded at the baseline examination and during follow-up were asked to consult the department of cardiovascular medicine, where normal cardiac function was confirmed. Moreover, because beta-blockers and diuretics are known to decrease serum BNP levels, we also checked that patients were not taking these medications.

AHI was measured using the apnea monitor (LS-100) manufactured by Fukuda Denshi. After an automated analysis of the results using the analysis software included in the device (Ver.01-03), we visually checked all data and made appropriate corrections. In the present study, all patients had AHI levels suggestive of severe SAS.

The general choice of treatment method is summarized in Figure 1. AHI was determined on the basis of visual examination of the oropharynx, soft X-ray findings, fiberscopic findings of the larynx, and the apnea monitor. Surgery is usually the treatment of choice when hypertrophy of the palatine tonsils or the adenoids is believed to be the principal cause of SAS. If the symptoms persist after surgery or in those without these findings, nasal continuous positive airway pressure (nCPAP) may be considered. In the present study, however, no patients had pharyngeal abnormalities. NCPAP, which is covered by health insurance in Japan, was chosen by patients with an AHI ≥40 as measured by an apnea monitor. Furthermore, nCPAP was performed using either the REMstar Auto with C-Flex™ or REMstar Auto M Series with C-Flex™. The data obtained from these devices were analyzed using the specialized software “Encore Pro ver.1.8.49.” If the narrowing of the nasal airway was considered the cause of SAS, surgery was performed on the paranasal sinuses, nasal septum, or inferior turbinate surgery was performed, and patients unsuitable for surgery were treated using antiallergic agents (Olopatadine hydrochloride and Cetirizine hydrochloride) or nasal drops (Fluticasone propionate). Furthermore, patients in whom retrognathia-induced pharyngeal narrowing was believed to have caused SAS were requested to wear a mouthpiece. In patients who underwent continuous treatment, AHI and serum BNP levels were measured every 3 months after treatment initiation. For patients using nCPAP, the device was equipped for AHI measurement; therefore, the values obtained from with the device were used.