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Objective: Coronary atherosclerotic heart disease refers to heart diseases caused by myocardial ischemia and hypoxia even necrosis due to atherosclerosis which leads to lumens stenosis or obstruction, or (and) fuctional changes in coronary arteries. These diseases are collectively called coronary heart disease (CHD). They are also known as ischemic heart disease. With regard to the mechanism of the disease, most scholars advocate the”endothelial injury hypothesis”, beliving that the end-results of each cause of the disease are the injury of intima, while the formation of atherosclerotic lesions is the result of arterial’s inflammatory and fibrous hyperplasia to intima injury, which directivly cause the dysfunction of Vascular Endothelial Cell(VEC). VEC has functions of secretion, synthesis, anticoagulation and plays a substantial role on internal environment stationary state.Lipid dysbolism is the major risk factor for Atherosclerosis, which is also the component of Metabolic Syndrome. Hypertriglyceridemia after meals, which is another major risk factor[1], has affinity to Atherosclerosis, independent of high density lipoproteins(HDL) and low density lipoproteins(LDL). Our body has experienced lipid meteblism after meals in most of times a day, so the level of fasting plasma lipid can hardly reflex this development objectively. Recent years, the level of plasma lipid after meals becomes a hot sopt to reseach. Atorvastatin is a commonly used Statins which has functions of remarkbly reducing the plasma lipid, as well as improving endothelial function, anti-inflammatory resopnce, anti-thrombopoiesis, antioxidation, stabablizeing atheromatous plaque and so on.Methods: 60 patients came to the 2nd affiliated hospital of Hebei Medical University with coronary artery disease were enrolled in this study since the Mar.2009 to Sep.2010 (36 male, 24 female). All the patients were mearured to the WHO’s diagnostic standard for CHD in 1979. Fasting Triglyceride(TG) <2.0mmol/L, Fasting Total Cholesterol<5.2mmol/L. Removing conditions are: acute myocardial infarction(AMI) within 4 weeks, rheumatic heart disease , heart failure, malignant arrhythmia, cardiogentic shock, secondary hypertension, diabetes mellitus and glucose tolerance abnormal, acute and chronic infetions, graveness wound and major operation, stoke, graveness liver and kidney insufficiency, metabolic disease and malignant tumor. After recording the informations in detail, the age, sex, BMI, blood pressure, blood glucose, fasting lipid level, showed no difference in all subjects. These qualified 60 subjects were dividied into 3 groups (each n=20) at randome: the high-fat diet group, the intervention group, the low-fat diet group. The high-fat diet group and intervention group were given fat meal lowding test in the morning. The low-fat diet group was given meals with low fat contained. Each group was taken 5ml blood at the moment of fasting, 2hour, 4hour after treatment, while the changes of flow-mediated dilatation rate (FDM, which represents endothelium-dependent vasodilation) and nitroglycerin-mediated dilatation rates(NDM, which represents endothelium-independent vasodilation) were detected at the same time with brachial artery ulrasound. The results were collected and analyzed with statistical software in the end.Results:1 TG of high-fat diet group and intervention group in both 2 and 4 hour were significantly higher than fasting level, which has statistical significance (P<0.05). TG was no statistical deference before and after treatment in low-fat diet group .2 TG of high-fat diet group and intervention group in 4 hour were significantly higher than low-fat diet group, which has statistical significance (P<0.05). TG of high-fat diet group was a little bit higher than intervention group, while TG was no signicantly difference between two group in 2hour (P<0.05).3 EDD function in high-fat diet group was signicantly damaged (P<0.05), with FDM decreasing from (3.38±2.34)% to (1.27±2.31)%; EDD function in intervention group was signicantly damaged(P<0.05), with FDM decreasing from (3.27±2.56)% to (2.11±1.07)%;EDD and EID function were no difference before and after treatment.4 EDD function in 4hour has signicantly difference among 3 groups (P<0.05), while damage of intervention group was less than high-fat diet group.Conclusions:1 This test has comfirmed that TG of CHD patients increase gradualy after having a high-fat diet. Given 80mg Atorvastatin, TG was lower than high-fat diet group in 4hour, indicating that Atorvastatin can prevent TG increasing excessively after taking a high-fat diet.2 The impairment of EDD in high-fat diet group was heavier than that of intervention group. Both EDD and EID were no different from fasting, indicating that Atorvastatin has protective effect on endothelial cells.
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