Therapeutic Strategies for Sleep Apnea in Hypertension and Heart Failure

Akiko Noda,Yoshinari Yasuda,Seiko Miyata

doi:10.1155/2013/814169

Akiko Noda, Yoshinari Yasuda + Show 1 more

Open Access

https://doi.org/10.1155/2013/814169

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Journal: Pulmonary Medicine	Publication Date: Jan 1, 2013
Citations: 60	License type: CC BY 3.0

Affiliation: Nagoya University, Chubu University

Abstract

Sleep-disordered breathing (SDB) causes hypoxemia, negative intrathoracic pressure, and frequent arousal, contributing to increased cardiovascular disease mortality and morbidity. Obstructive sleep apnea syndrome (OSAS) is linked to hypertension, ischemic heart disease, and cardiac arrhythmias. Successful continuous positive airway pressure (CPAP) treatment has a beneficial effect on hypertension and improves the survival rate of patients with cardiovascular disease. Thus, long-term compliance with CPAP treatment may result in substantial blood pressure reduction in patients with resistant hypertension suffering from OSAS. Central sleep apnea and Cheyne-Stokes respiration occur in 30–50% of patients with heart failure (HF). Intermittent hypoxemia, nocturnal surges in sympathetic activity, and increased left ventricular preload and afterload due to negative intrathoracic pressure all lead to impaired cardiac function and poor life prognosis. SDB-related HF has been considered the potential therapeutic target. CPAP, nocturnal O2 therapy, and adaptive servoventilation minimize the effects of sleep apnea, thereby improving cardiac function, prognosis, and quality of life. Early diagnosis and treatment of SDB will yield better therapeutic outcomes for hypertension and HF.

Highlights

Obstructive sleep apnea syndrome (OSAS) is characterized by recurrent episodes of sleep apnea accompanied by hypoxia, fluctuations in heart rate and blood pressure (BP), frequent arousal, and consequent sleep fragmentation, resulting in an activation of the sympathetic nervous system [1,2,3,4,5,6,7]
We previously reported that repeated episodes of endapneic arousal or hypoxia and consequent sleep fragmentation were associated with an increase in nocturnal BP, possibly leading to sustained hypertension and left ventricular (LV) hypertrophy [4,5,6]
We reported that nocturnal oxygen desaturation, sleep fragmentation, and increased sympathetic activity impaired daytime baroreflex sensitivity and nitric oxide (NO) production in patients with moderate-to-severe OSAS [20, 21]

Summary

Introduction

Obstructive sleep apnea syndrome (OSAS) is characterized by recurrent episodes of sleep apnea accompanied by hypoxia, fluctuations in heart rate and blood pressure (BP), frequent arousal, and consequent sleep fragmentation, resulting in an activation of the sympathetic nervous system [1,2,3,4,5,6,7]. Treatment of sleep apnea with nocturnal continuous positive airway pressure (CPAP) in individuals with congestive HF treats sleep-disordered breathing (SDB), and results in improved LV function, alleviated HF symptoms, and reduced sympathetic activation due to decreased norepinephrine secretion [12]. Cross-sectional studies have demonstrated consistent results that moderateto-severe OSAS (AHI >15 events/h) increases the risk of developing hypertension [17].

Results

Conclusion