Sleep apnea and cardiovascular disease: an American Heart Association/American College of Cardiology Foundation Scientific Statement from the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing.

Journal of the American College of Cardiology (Impact Factor: 15.34). 09/2008; 52(8):686-717. DOI: 10.1016/j.jacc.2008.05.002
Source: PubMed
1 Follower
  • [Show abstract] [Hide abstract]
    ABSTRACT: The somnology occupies a firm place in medical care of the ENT physician. The S3 guideline "non-restorative sleep/sleep" defines the standards in diagnosis and therapy. Among the sleep-disordered breathing obstructive sleep apnea syndrome is the most common sleep breathing disorder among those aged 30-60 years. The diagnostics is based on a stepwise approach by ambulatory polygraphy and subsequent inpatient polysomnography. Depending on the focus degree of OSA and symptoms of the patient various treatment options surgical and conservative for the ENT specialist are available today. The superior form of therapy for all severities of OSA remains the non-invasive nocturnal airway pressure (CPAP). Detailed knowledge of sleep medicine is essential for differential diagnosis and the correct treatment decision. An interdisciplinary collaboration with a neurologist, pediatrician or pulmonologist should be included in more complex cases. © Georg Thieme Verlag KG Stuttgart · New York.
    Laryngo-Rhino-Otologie 01/2015; 94(1):42-54. DOI:10.1055/s-0034-1395533 · 0.99 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnoea, is associated with impaired vascular function despite unaltered response to nitric oxide donors. This study addressed whether arginase contributes to the endothelial dysfunction in CIH rats. Adult male Sprague-Dawley rats were exposed for 21 days to CIH (5% oxygen, 12 times/h, 8 h/day). The internal carotid arteries were isolated to study endothelial nitric oxide synthase (eNOS) and arginase-1 levels by western blot and immunohistochemistry, and their vasoactive responses using wire myography. Relaxation to sodium nitroprusside (SNP; nitric oxide donor) in the presence or absence of soluble guanylyl cyclase inhibitor, and acetylcholine with and without a NOS inhibitor [N-nitro-L-arginine (L-NA)] and the arginase inhibitor BEC were determined. Arteries from the CIH rats presented higher active contraction induced by KCl (3.5 ± 0.4 vs. 2.3 ± 0.2 N/m), augmented media-to-lumen ratio (∼40%), decreased relaxation to acetylcholine (12.8 ± 1.5 vs. 30.5 ± 4.6%) and increased sensitivity to SNP (pD2 7.3 ± 0.1 vs. 6.7 ± 0.1). Arginase inhibition reversed the impaired acetylcholine-induced relaxation in CIH arteries (49.5 ± 7.4%), an effect completely blocked by L-NA. In the carotid arteries, arginase-1 protein level was increased, whereas eNOS levels decreased in the CIH arteries. The current results suggest that endothelial dysfunction in CIH-induced hypertension may result from imbalanced arginase-1 to eNOS expression, vascular remodelling and increased contractile capacity, rather than decreased vascular response to nitric oxide.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Chronic intermittent hypoxia (CIH), the main characteristic of obstructive sleep apnoea, enhances carotid body (CB) chemosensory discharges during normoxia and hypoxia, and elicits hypertension. These alterations are attributed to oxidative stress, since antioxidants prevent the enhanced CB chemosensory discharges and the hypertension. In this report, we discuss new evidence supporting that oxidative stress-induced upregulation of pro-inflammatory cytokines (i.e. TNF-α and IL-1β) in the CB are involved in the chemosensory potentiation and the hypertension following CIH. Anti inflammatory treatment with ibuprofen prevents the increased TNF-α and IL-1β levels in the CB and the hypertension, but does not reduce the enhanced chemosensory hypoxic response and the local oxidative stress in the CB. In contrast, antioxidant treatment with ascorbic acid prevents the increased cytokines levels and CB oxidative stress, the chemosensory potentiation and the hypertension. Thus, the enhanced CB chemosensory responses to hypoxia depend critically on the oxidative stress, but not on the increased TNF-α and IL-1β in the CB. We discuss a possible role for pro-inflammatory cytokines in the development of the hypertension produced by CIH, acting on cardiorespiratory centres located in the central nervous system.This article is protected by copyright. All rights reserved
    Experimental physiology 12/2014; DOI:10.1113/expphysiol.2014.079525 · 2.87 Impact Factor