依那普利对急性心肌梗死患者脂蛋白(a)和氧自由基的影响

背景许多研究已表明血管紧张素转换酶抑制剂具有独立于降压以外抗动脉粥样硬化的血管保护作用,但其机制未完全明确.目的研究血管紧张素转换酶抑制剂对急性心肌梗死患者脂蛋白(a)和氧自由基的影响,探讨血管紧张素转换酶抑制剂抗动脉粥样硬化的机制.设计以急性心肌梗死患者为研究对象的观察对比研究.单位解放军总医院南二科.对象选择2001-04/2002-08在天津港口医院心内科住院的急性心肌梗死患者35例,男19例,女16例,年龄42～75岁,平均(62±9)岁.随机分为两组,治疗组20例,对照组15例.纳入标准符合世界卫生组织的急性心肌梗死诊断标准者;排除标准肾功能不全、休克、低血压者及曾服血管紧张素转换酶抑制剂有过敏及明显咳嗽史者.所有患者于发病前2周未服用过血管紧张素转换酶抑制剂并且同意参加本研究.方法治疗组于心梗后第3天晨起予依那普利5mg口服1次,若无首剂低血压反应,于心梗后第4天开始口服依那普利5 mg/次,2次/d,连续2周,再予10mg/次,2次/d,连续2周.对照组不用依那普利.分别于服药前、服药后2周和4周时两组同时取血,检测血清中的脂蛋白(a)、氧自由基、三酰甘油、总胆固醇、高密度脂蛋白胆固醇和载脂蛋白(a).主要观察指标两组患者用药前后三酰甘油、总胆固醇、高密度脂蛋白胆固醇、载脂蛋白(a)及血清中的脂蛋白(a)、氧自由基水平的比较.结果依那普利能明显降低急性心肌梗死患者氧自由基水平,用药前、用药2周和用药4周的氧自由基水平分别为(1423.14±216.23),(1 076.62±287.12)和(566.57±138.02)U/mL(t=2.937,3.571,P＜0.01),但不影响脂蛋白(a)和血脂水平(P＞0.05).结论依那普利通过抗氧化作用来抑制急性心肌梗死患者动脉粥样硬化的进程,改善其预后,但不降低血脂水平,为依那普利抑制急性心肌梗死患者动脉粥样硬化的机制提供了理论参考.

Effect of Enalapril on lipoprotein(a) and oxygen-derived free radicals in patients with acute myocardial infarction

BACKGROUND: Many studies have suggested that angiotensin-converting enzyme inhibitors(ACEI) protect blood vessels through anti-atherosclerosis independent of lowering blood pressure, but its mechanism is still unclear.OBJECTIVE: To investigate the anti-atherosclerotic mechanism of ACEI by observing the effects of Enalapril on lipoprotein(a) and oxygen free radicals in patients with acute myocardial infarction (AMI) .DESIGN: A controlled study based on the observation of the patients with AMI.SETTING: Second Department of the South Building, General Hospital of Chinese PLAPARTICIPANTS: Thirty-five inpatients with AMI(19 males and 16 females, aged 42 -75 years old, and averaged (62 ± 9) years old and hospitalized at the Department of Cardiology of Tianjin Harbor Hospital from April 2001 to August 2002 were chosen. These patients were randomly divided into 2 groups: the therapeutic group(20 cases) and the control group(15cases). Inclusion criteria: the diagnosis of patients with AMI was confirmed by WHO criteria. Exclusion criteria: patients with renal dysfunction, shock,hypotension, a history of allergy to ACEI, and a history of severe cough induced by ACEI. All patients had not taken ACEI in the past 2 weeks and agreed to participate in this study.METHODS: On early morning of the third day after AMI, patients in the treatment group took 5 mg of Enalapril one time. If they had no first-dose reaction of hypotension, on the fourth day after AMI, the patients of the treatment group were given a dose of 5 mg twice per day for the following 2 weeks. Then, they were given the drug at a dose of 10 mg twice per day for 2 weeks. The patients in the control group were not given Enalapril. Blood samples were taken respectvely prior to the administration and 2 weeks and 4 weeks after the administration in the two groups. Serum content of lipoprotein(a), oxygen free radicals, triglyceride, total cholesterol, high density lipoprotein(HDL) cholesterol, Apo(a) were measured.MAIN OUTCOME MEASURES: We compared the level of serum of lipoprotein (a), oxygen free radicals (OFR), triglyceride, total cholesterol,HDL cholesterol, Apo(a) pre-treatment and post-treatment respectively in patients of the two groups.RESULTS: Serum levels of OFR were significantly lowered in the treatment group, which were(1 423.14±216.23), (1 076.62±287.12) and (566.57 ± 138.02) U/mL respectively 2 weeks and 4 weeks before and after the treatment(t =2. 937, 3. 571, P ＜0. 01), but there were no significant changes in serum concentrations of lipoprotein(a) and lipids( P ＞ 0.05) .CONCLUSION: Enalapril improved the prognosis of patients with AMI by antioxidation, but not by lowering the serum levels of lipoprotein(a) and lipids. The study can serve as a theoretical reference that the mechanism of Enalapril might inhibit atherosclerosis in patients with AMI.