Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control

Abstract

Hypertensive patients with obstructive sleep apnea syndrome (OSAS) constitute a high-risk group for metabolic syndrome. OSAS directly induces negative intrathoracic pressure and decreases pulmonary stretch receptor stimulation, chemoreceptor stimulation, hypoxemia, hypercapnia and microarousal. These changes potentiate various risk factors, including the sympathetic nervous system, renin-angiotensin-aldosterone system and inflammation. Early detection and treatment of OSAS in asymptomatic hypertensive patients is essentially important to prevent hypertensive target organ damage and subsequent cardiovascular events. Continuous positive airway pressure (CPAP) therapy, a first-line treatment in hypertensive patients with moderate to severe OSAS, reduces ambulatory BP level, particularly during the sleep period, and midnight BP surge. However, individual differences in the BP-lowering effect of CPAP have been observed. OSAS hypertensive patients who do not tolerate CPAP remain at a high risk for cardiovascular disease because of negative intrathoracic pressure and need more aggressive antihypertensive treatment to achieve 24-h BP control with nocturnal BP o120/70 mm Hg.

Simplified Berlin Questionnaire for Screening of High Risk for Obstructive Sleep Apnea Among Thai Male Healthcare Workers

“…A previous study indicated that Thai male patients with OSA may not have tiredness or daytime sleepiness [7]. Hypertension is known to be associated with OSA [13]. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) guidelines indicates that OSA is a cause of hypertension [14].…”

Nocturnal blood pressure and cardiovascular disease: a review of recent advances

“…58 Associations between obstructive sleep apnea (OSA) and high BP have been confirmed, and nondipping was found in 48-84% of the patients with OSA. [59][60][61] The mechanisms contributing to nondipping or nocturnal hypertension in OSA are multifactorial, including hypoxia-and hypercapnea-induced sympathetic nerve activation, renin-angiotensin-aldosterone activation, endothelial dysfunction and increased vascular stiffness. [59][60][61][62] The effectiveness of OSA treatment with continuous positive airway pressure (CPAP) was modest and the results are conflicting.…”

“…[59][60][61] The mechanisms contributing to nondipping or nocturnal hypertension in OSA are multifactorial, including hypoxia-and hypercapnea-induced sympathetic nerve activation, renin-angiotensin-aldosterone activation, endothelial dysfunction and increased vascular stiffness. [59][60][61][62] The effectiveness of OSA treatment with continuous positive airway pressure (CPAP) was modest and the results are conflicting. 62 Haentjens et al 63 examined the effects of CPAP on 24-hour BP with a meta-analysis of 572 patients from 12 randomized controlled trials.…”

A Case of Dural Arteriovenous Fistulas at the Craniocervical Junction Presenting with Occipital/Neck Pain Associated with Sleep

“…A possible explanation for the presentation of the present patient is that the increased venous pressure caused by CHF and OSAS while sleeping in the supine position may have resulted in occipital/neck pain (10,11). Moreover, venous pressure in the neck, where the DAVFs were located in the present patient, is generally approximately 20-40 mm Hg lower than the aortic pressure in the upright position, which is caused by gravity; in contrast, venous pressure in the thoracolumbar region, where spinal DAVFs are usually located, is generally approximately 20-40 mm Hg higher than the aortic pressure in the upright position.…”