[Cardiovascular abnormalities in patients with obstructive sleep apnoea syndrome].

Katedry i Kliniki Chorób Wewnetrznych Akademii Medycznej w Lublinie.
Wiadomości lekarskie (Warsaw, Poland: 1960) 02/2005; 58(1-2):78-83.
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The activation of adrenergic and renin-angiotensin-aldosterone (RAA) systems observed in patients with obstructive sleep apnoea syndrome (OSA) strongly affects functional status of the cardiovascular system. In this paper we discuss the link between obstructive sleep apnoea syndrome and common cardiovascular diseases such as systemic and pulmonary hypertension, ischaemic heart disease, stroke, arrhythmia and ventricular hypertrophy. We also present the importance of early pharmacologic treatment in preventing cardiac hypertrophy and ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

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    ABSTRACT: Elevated superoxide formation in cardiac extracts of apolipoprotein E-knockout (apoE-KO) mice has been reported. In addition, we previously reported that hypoxia increased oxidative stress in the aortas of apoE-KO mice, although we did not examine the effect of hypoxia on the heart. The aim of this study was to investigate the effect of chronic hypoxia on the left ventricular (LV) remodeling in apoE-KO mice treated with or without an angiotensin II receptor blocker. Male apoE-KO mice (n=83) and wild-type mice (n=34) at 15 weeks of age were kept under hypoxic conditions (oxygen, 10.0+/-0.5%) and treated with olmesartan (3 mg/kg/day) or vehicle for 3 weeks. Although LV pressure was not changed, hypoxia caused hypertrophy of cardiomyocytes and increased interstitial fibrosis in the LV myocardium. Furthermore, nuclear factor-kappaB (NF-kappaB) and matrix metalloproteinase (MMP)-9 activities were increased in apoE-KO mice exposed to chronic hypoxia. Olmesartan effectively suppressed the 4-hydroxy-2-nonenal protein expression and NF-kappaB and MMP-9 activities, and preserved the fine structure of the LV myocardium without affecting the LV pressure. In conclusion, olmesartan reduced oxidative stress, and attenuated the hypoxia-induced LV remodeling, in part through the inhibition of NF-kappaB and MMP-9 activities, in apoE-KO mice.
    Full-text · Article · Jan 2008 · Hypertension Research