کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3069061 1188262 2006 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Le syndrome d'apnées obstructives du sommeil, une cause majeure et encore méconnue d'hypertension artérielle
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی مغز و اعصاب بالینی
پیش نمایش صفحه اول مقاله
Le syndrome d'apnées obstructives du sommeil, une cause majeure et encore méconnue d'hypertension artérielle
چکیده انگلیسی
Obstructive Sleep Apnea (OSA) is a major cause of cardiovascular morbidity and mortality. Obstructive events like apneas and hypopneas induce repeated hypoxia-reoxygenation sequences, opposite direction changes in CO2, intra-thoracic pressure changes and recurrent micro-arousals. These different stimuli activate the autonomic nervous system and specifically generate permanent sympathetic hyper activity. More - over, there is an increased endothelial responsiveness and a deficit in NO-mediated endothelial vasodilation during OSA. Lastly, reductions in baroreflex sensitivity and in sinusal variability also generate increased blood pressure. Both community and clinical studies found the close association between OSA and Hypertension. The relative risk of hypertension in the presence of OSA is ranging between 1.5 and 2.9 when controlling for all confounding factors. In clinical populations, hyper - tension is primarily diastolic particularly in middle age subjects and in case of severe OSA. In subjects unknown as being hypertensive, there is a high prevalence of clinical and ambulatory HT in OSA subjects without significant cardiovascular risk. More than two thirds of OSA subjects actually exhibit clinical or masked hypertension, a condition only revealed by blood pressure ambulatory measurement. These subjects already exhibit vascular changes such as increased intima media thickness and augmented arterial stiffness. Thus, OSA is now recognised as the first aetiology to explore in case of unexplained hypertension. CPAP treatment reduces mean 24-hour BP by 2 to 10 mm Hg. The larger BP reduction is obtained in the most severe OSA and those being hypertensive at baseline. There is also apparently a limited reduction in BP in non-sleepy OSA, themechanism being still unknown. The variable response to intermittent hypoxia and some possible common biological mechanisms might be involved and are currently being investigated in clinical and animal studies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Médecine du Sommeil - Volume 3, Issue 8, June 2006, Pages 19-24
نویسندگان
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