Study On The Pathogenesis In The Morbidity Of Cerebrovascular Disease In Aged SAS Patients

Objective:Sleep apnea syndrome is considered as an independent risk factor of stroke, but the mechanisms are not clear. In our study, the maleic dialdehyde (MDA) and superoxide dismutase (SOD) are used as index to oxidative stress, the endothelial nitric oxide synthase (eNOS) and flow-mediated dilation (FMD) are used as index to the endothelial function tumor necrosis factor-α(TNF-α) and high sensitive C-reactive protein (hs-CRP) are used as index to the inflammation and the crotid intima-media thickness (IMT) are used as index to the atherosclerosis. We analyze the level of oxidative stress, inflammation, endothelial function and the extent of atherosclerosis in the SAS patients with stroke, SAS patients without stroke and the stroke patients without SAS. And to explore the mechanisms SAS caused cerebral vascular disease and to explore the pathogenesis of oxidative stress, inflammation on endothelial function, thereby further result atherosclerosis and ultimately increase the incidence of stroke.Methods:Eighty-six patients were divided into 3 groups, SAS patients with stroke (n=32), SAS patients without stroke (n=28) and the stroke patients without SAS (n=26). All the groups undergo high-frequency doppler echocardiography to evaluate IMT of carotid artery. Body height, body weight, triglycerid (TG), total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), MDA, SOD, TNF-α, hs-CRP, eNOS are measured in all groups. FMD of brachial artery is examined using high-frequency echocardiography, which is indicated by diastolic inner diameter changing rate (D%) and calculate the body mess index (BMI). Analyze the association between those parameter and IMT of carotid artery in SAS patients with stroke and that of independent risk factor and the association between those parameter and RDI in SAS patients with stroke to study if the parameters is correlation with the extent of SAS.Results:(1) SBP, IMT, D%, hs-CRP, eNOS, MDA, SOD, TNF-α, BMI and PP are significantly differente in the three groups (P<0.05, P<0.01). The age, sex, the morbility of the hypertension, the coronary artery disease and diabetes mellitus, mean arterial blood pressure (MAP), diastolic blood pressure (DBP), TC, TG, HDL-C and LDL-C are not different in the three groups (P>0.05). (2) There is positive correlation between carotid-IMT and SBP,BMI,TC,PWV,hs-CRP,TNF-α,MDA,RDI (P<0.05, P<0.01). Inversely there is negative correlation between carotid-IMT and SOD, D%, MmSO2, eNOS in SAS patients with stroke (P<0.05,P <0.01). However, carotid-IMT doesn't correlate with DBP, MAP, PP, TG, HDL-C, LDL-C (P>0.05). Linier regression analysis shows that MDA, TC, RDI are independent risk factor for carotid-IMT. (3) There is positive correlation between RDI and BMI, hs-CRP, TNF-α, MDA (P<0.05, P<0.01). Inversely there is negative correlation between RDI and SOD, D%,eNOS in SAS patients with stroke (P<0.05, P<0.01). However, RDI doesn't correlate with SBP, DBP, MAP, PP, TC, TG, HDL-C, LDL-C (P>0.05). (4) There is negative correlation between FMD and hs-CRP, TNF-α, MDA (P<0.01). Inversely there is positive correlation between FMD and SOD in SAS patients with stroke (P<0.01). (5) There is negative correlation between eNOS and hs-CRP, TNF-α, MDA (P<0.01). Inversely there is positive correlation between eNOS and SOD in SAS patients with stroke (P<0.01).Conclusion:(1) There is a higher level of oxidative stress, inflammation and more severe endothelial dysfunction in the SAS patients with stroke than the others, the oxidative stress and inflammation maybe the mechanism of stroke in the SAS patients. (2) Oxidative stress, inflammation and the endothelial dysfunction can increase the degree of atherosclerosis. (3) The more severe intermittent hypoxia is, the more higher level of oxidative stress, inflammation and endothelial dysfunction are. (4) There is a higher level of oxidative stress and inflammation in SAS patients without stroke than the stroke patients without SAS, that maybe the result of chronic intermittent hypoxia.