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Effect of simvastatin on C-reactive protein in patients with coronary heart disease of blood lipid and C

Author: SunZhiLiang From: www.yourpaper.net Posted: 2010-06-24 14:22:20 Read:
[Key words] coronary heart disease; simvastatin; blood lipid; C reactive protein
Coronary heart disease is coronary heart disease coronary artery atherosclerosis, means for or with spasm in myocardial ischemia is the main characteristic of heart disease.The clinical manifestations of various angina, myocardial infarction, arrhythmia and heart failure and other types of.With the change of people's lifestyle, the disease has become the leading cause of death in Chinese population.Statins have lipid-lowering effects, and anti-inflammatory effects, this study is to explore the effect of simvastatin on angina pectoris of lipids and C reactive protein.
1 materials and methods
1.1 the research object in this study a total of 64 cases were selected, are in line with WHO on ischemic heart disease diagnostic criteria.All of the cases were in 2003 May to 2009 June in our hospital department of internal medicine, course ranging from 3 months to 12 years.Male 39 cases, female 25 cases, age 43 ~ 78 years old.
1.2 research methods and treatment for 64 cases of patients were randomly divided into simvastatin group (n=32) and control group (n=32 cases), two groups were smoking prohibition; hypertension, blood pressure control.Simvastatin group at the age of 44 ~ 78 (65.1 7.5) years old, male 19 cases, female 13 cases, the duration of 4 months to 12 years of age; control group 43 ~ 77 (64.3 7.2) years old, male 20 cases, female 12 cases, the duration of 3 months to 11 years.The control group used isosorbide mononitrate (Xinkang, North China Pharmaceutical Group Corporation) 40mg intravenous drip, 100mg aspirin, metoprolol before bedtime: 12.5mg, 2 /d, perindopril 4mg, 1 times /d, a total of 4 weeks of treatment.The treatment group based on the oral simvastatin (Zocor, Hangzhou MSD Pharmaceutical Co. Ltd.) 20mg, before bedtime, taking 4 weeks.All of the subjects excluded diabetes, systemic infection, myocardial infarction, arrhythmia, heart failure, cancer and other diseases.
1.3 detection equipment and project (1) of all the patients were given routine ECG examination at admission and discharge, observed ST-T changes.(2) all blood samples were in the first day after admission and 4 weeks after the treatment, blood samples collected, in the early morning fasting state extraction, centrifugal separation of 5min in serum, medical refrigerator (Haier digital Prince) save -20 , batch determination.(3) and high sensitive C reactive protein (hs-CRP) concentration: hs-CRP was measured by immunoturbidimetry, use hs-CRP detection reagent (Backman), the sensitivity is 0.1mg, the instrument for BT-2000 automatic biochemical analyzer (Italy).
1.4 statistical methods all data were statistically analyzed by using statistical software SPSS10.0, the parameter values are used (x s) said, the measurement data between two groups were compared, using t test.
The results of 2
There was no significant difference in 2.1 patients in the two groups in general compared two groups of patients with age, sex, hypertension, serum cholesterol, triglyceride, low density lipoprotein, high sensitive C reactive protein, difference (P> 0.05) course.
2.2 simvastatin treatment group and control group before and after treatment in each parameter in table 1.Comparison between the treatment group and the control group simvastatin, triglyceride, total cholesterol and low density lipoprotein decreased significantly in treatment group, the high density lipoprotein increased significantly.The control group after treatment, triglyceride, total cholesterol, low density lipoprotein and high density lipoprotein cholesterol did not change significantly, the differences were significant compared with the treatment group.Two groups of patients in the control group serum hs-CRP decreased slightly, but simvastatin treatment group decreased more obviously, there was significant difference between the two groups.The two groups after treatment in patients with chest pain disappeared, ST-T returned to normal, no significant difference between the two groups.Table 1 before and after treatment in the two groups of lipid, hs-CRP note: TG: TC: total cholesterol; triglyceride; LDL-C: low density lipoprotein cholesterol; HDL-C: high density lipoprotein cholesterol; hs-CPR: high sensitivity C reactive protein; simvastatin treatment group before and after treatment, *P< < 3; 0.05 strong>

Modern medical research shows that, high blood lipids, hypertension, smoking, obesity, reduced physical activity and other risk factors, eventually intimal injury, caused by arterial intimal inflammation reaction, and the formation of atherosclerotic plaque is reacted to the results of arterial intimal injury, and eventually lead to stenosis of the artery lumen, cause angina pectoris in serious coronary heart artery stenosis led to myocardial ischemia.
C reactive protein is the inflammatory response is a sensitive but not specific markers, some people think that C reactive protein is the strongest risk index of cardiovascular disease, the possible mechanism of it on coronary heart disease: (1) the influence of high concentrations of serum C reactive protein can promote endothelial cell proliferation, leading to arterial intimal thickening, speed up the process of atherosclerosis.(2) C reactive protein damage to vascular endothelial cells, the endothelial cells to reduce NO and prostaglandin release, the vasorelaxant effects of [1].The increasing of the concentration of hs-CRP is often associated with higher cardiovascular events associated probability.In this experiment, hs-CRP generally increased in patients with angina pectoris, suggest angina pectoris patients showed severe inflammatory reaction, inhibit the inflammation of coronary artery can effectively protect the cardiovascular [2].
Statins besides lipid-lowering effects, there are anti-inflammatory effect, it can weaken the granulocyte -- endothelial cell adhesion, inhibit platelet activation factor and leukotriene [3].CRP as the inflammatory markers sensitive, significantly increase the expression of endothelial cell adhesion factors and cytokines.The experiment indicates that, after 1 months treatment with simvastatin 20mg, the treatment group before treatment, hs-CRP (3.35 1.77) mg/L, discharge reduced to (1.63 1.72) mg/L, and the control group before treatment hs-CRP (3.37 1.68) mg/L, (3.34 1.63 at discharge for) mg/L, show that simvastatin can significantly decreased the levels of hs-CRP, to play anti-inflammatory, stabilization of atherosclerotic plaque, the enhancing effect of [4] vascular endothelial function.Long-term application of simvastatin stable patients with coronary heart disease, to prevent further deterioration may.Simvastatin treatment group and control group by angina, anti-ischemic therapy, two patients with chest pain were disappeared, ECG showed ST-T returned to normal, but the control group before and after treatment of hs-CRP did not decrease, suggesting that vascular endothelial inflammation without control, patients will likely be repeated [5], and simvastatin treatment group after treatment hs-CRP fully returned to normal, suggesting the patient's condition is transformed to a good direction.
1 Bhagatk, Valanle P.Inflammatory cytokines impair Endothe lium-dependent dilatation in human veins in vivo.Circulation, 1997,96:3042-3047.

2 Xie Hongzhi, Zhu Wenling. Study on syndrome and high sensitivity C reactive protein of coronary artery disease and metabolism. Journal of Cardiology, 2007, 35:527-530.

3 Deng Huafei, Xiong Yan. Non lipid-lowering effect and cardiovascular protection statins. Journal of Chinese physician, 2004, 6:572-573.

4 Liu Yanhong, Zhang Mei, Zhang Lingmei, et al. Short-term simvastatin on myocardial ischemia reperfusion in rats after muscle effect of no-reflow and its potential mechanism. Journal of Cardiology, 2008, 36:729-734.

5 Chen Hong, Ren king-yee, Wu Bei, et al. Effect of withdrawal of simvastatin on vascular endothelial function in patients with coronary heart disease and coronary heart disease risk factors. Journal of Cardiology, 2007, 35:531-535.
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