Résumé :
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Aim : To observe the interactions between OSA (obstructive sleep apneea) and cardiovascular pathology and diseases. Materials and methods : articles from medical literature with theme OSA and cardiovascular risk and diseases with interest for prospective cohort studies and randomized controlled trials looking for medical subjects like : OSA, increased sympathetic activation, vascular endothelial dysfunction, increased oxidative stress, inflammation, increased platelet aggregability, metabolic dysregulation, hypertension, ischemic heart disease, heart failure, arrhythmia, OSA treatment. Results : At adult population the mean prevalence of OSA is 5%, 2 times more frequent at male patients. The mild OSA was difined as apneea/hypopnea index between 5-15, moderate between 15-30 and severe with more than 30 apneea/hipopnea index. The apneea/hipopnea events result in desaturation, sleep fragmentation and arrousals. In consequence there are many important pathophysilogic cardiovascular events classified as : acute- increased sympathetic activation with pulmonary and systemic vasoconstriction, tachycardia, intrathoracic pressure changes with decreasing heart preload and increasing overload and chronic -permanent sympathetic activation also during daytime with vasoconstriction, heart rate variability decreasing and blood pressure variability increasing, vascular endothelial dysfunction with decreasing of NO production and endotelin increasing, oxidative stress increasing by cells activation and free radicals production, inflammation by cytokines production, increased platelet aggregability, metabolic dysregulation with leptin and insulin increasing and insulin resistance increasing with risk of diabetes development. All these acute and chronic events have their contribution on development and progression of cardiovascular diseases like : hypertension, ischemic heart disease with a mortality by myocardial infarction of 38% at patients with OSA comparative with 9% at patients without OSA, heart failure, half of patients with diastolic dysfunction having an index apneea/hypopnea > 10, cardiac arrhythmia like sinus bradycardia, atrial fibrillation and atrioventricular block and perhaps also cerebrovascular diseases and stroke. The most efficient treatment for OSA was CPAP (continuous positive airways pressure) therapy and also it was demonstrated his contribution on reduction of all mechanisms described above implicated in development and progression of cardiovascular diseases. Conclusions : The OSA implication in pathophysiology of cardiovascular diseases was recognized. OSA could be a risk factor in disease initiation and progression and also could coexist undiagnosed in patients with cardiovascular diseases aggravating them and making more resistant to treatment. The OSA treatment with CPAP has an important contribution on cardiovascular diseases improvement.
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