不同他汀类药物对动脉粥样硬化疗效的比较研究

目的观察不同他汀类药物对动脉粥样硬化疗效的比较研究。方法 240例动脉粥样硬化患者随机分为A、B、C、D4组,每组60例,A组采用阿托伐他汀治疗,B组采用辛伐他汀治疗,C组采用氟伐他汀治疗,D组给予饮食控制。服药前和服药6个月末,比较TC、TG、HDL-C、LDL-C、血浆高敏C反应蛋白(hs-CRP)、颈动脉斑块面积及内膜中层厚度(IMT)的变化。结果治疗6个月后A、B、C 3组TC、TG、HDL-C、LDL-C、hs-CRP水平、颈动脉斑块面积及IMT与治疗前相比差异均有统计学意义(P<0.05),但D组与治疗前比较差异无统计学意义(P>0.05)。结论他汀类药物对动脉粥样硬化斑块具有较好的疗效,不同种类的他汀类药物疗效没有明显差异。     

高龄男性高脂血症合并冠心病患者使用氟伐他汀疗效及安全性研究

目的探讨氟伐他汀80mg/d与氟伐他汀40mg/d70岁以上男性高脂血症合并冠心病患者调脂治疗的疗效及安全性。方法采用随机对照研究,选择118例血脂未达标的高龄男性高脂血症合并冠心病患者,随机分为氟伐他汀80mg/d组与氟伐他汀40mg/d组,分别监测治疗前、治疗4周、治疗12周的TC、TG、HDL-C、LDL-C、ALT、CK水平。结果氟伐他汀80mg/d与氟伐他汀40mg/d均能显著降低TC、LDL-C的水平（P〈0.01）,并且80mg/d组作用优于40mg/d组（P〈0.05）。结论氟伐他汀80mg/d与氟伐他汀40mg/d均能显著改善TC、LDL-C的水平,氟伐他汀80mg/d组显著优于氟伐他汀40mg/d组,而2种剂量的安全性均良好。     

不同剂量氟伐他汀对冠心病患者瘦素、脂联素的影响

目的:探讨瘦素、脂联素在冠心病发病过程中的作用以及氟伐他汀用于治疗冠心病的理想剂量.方法:将住院确诊为冠心病的160例患者随机分成两组,每组80例,均在冠心病常规治疗的基础上服用氟伐他汀.第1组口服常规剂量40mg/d,第2组口服强化剂量80 mg/d.分别于治疗前和治疗2个月后测定两组患者血清瘦素、脂联素的浓度.同时设第3组为健康对照组.结果:与治疗前相比,服用氟伐他汀2个月后,两组患者总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇( LDL-c)、C反应蛋白(CRP)和血清瘦素水平均明显降低(均P＜0.05),高密度脂蛋白胆固醇(HDL-c)、血清脂联素水平均较治疗前明显升高(均P＜0.05);与常规降脂组相比,强化降脂组TC、LDL-c下降幅度和HDL-c升高幅度更明显(均P＜0.05),而TG、CRP、瘦素水平降低幅度,脂联素水平升高幅度,两组之间无较大差异(均P＞0.05).结论:血清瘦素、脂联素与冠心病密切相关.氟伐他汀可显著降低冠心病患者瘦素水平,升高脂联素水平,并且与常规降脂治疗相比,强化降脂治疗能够提供更好的保护作用.     

Long-term Cardiac Outcomes in Renal Transplant Recipients Receiving Fluvastatin: The ALERT Extension Study

Renal transplant recipients (RTR) have an increased risk of premature cardiovascular disease. The ALERT study is the first trial to evaluate the effect of statin therapy on cardiac outcomes following renal transplantation. Patients initially randomized to fluvastatin or placebo in the 5-6 year ALERT study were offered open-label fluvastatin XL 80 mg/day in a 2-year extension to the original study. The primary endpoint was time to first major adverse cardiac event (MACE). Of 1787 patients who completed ALERT, 1652 (92%) were followed in the extension. Mean total follow-up was 6.7 years. Mean LDL-cholesterol was 98 mg/dL (2.5 mmol/L) at last follow-up compared to a pre-study level of 159 mg/dL (4.1 mmol/L). Patients randomized to fluvastatin had a reduced risk of MACE (hazards ratio [HR] 0.79, 95% CI 0.63-0.99, p = 0.036), and a 29% reduction in cardiac death or definite non-fatal MI (HR 0.71, 95% CI 0.55-0.93, p = 0.014). Total mortality and graft loss did not differ significantly between groups. Fluvastatin produces a safe and effective reduction in LDL-cholesterol associated with reduced risk of MACE in RTR. The lipid-lowering and cardiovascular benefits of fluvastatin are comparable to those of statins in other patient groups, and support use of fluvastatin in RTR.     

降脂治疗对老年人原发性高血压血脂和胰岛素抵抗的影响

目的观察氟伐他汀对老年人原发性高血压、高血脂胰岛素抵抗的影响.方法78例老年轻中度高血压患者随机分成对照组、氟伐他汀组和二甲双呱组,三组均使用非洛地平作为降压药,治疗3个月.结果三组血压均明显下降,差异有显著性(P＜0.01);氟伐他汀组LDL-C、TC下降与治疗前相比,差异有显著性(P＜0.05、P＜0.01),与二甲双呱组、对照组相比,TC差异有显著性(P＜0.01).治疗后空腹和2 h胰岛素水平,氟伐他汀组与二甲双呱组均下降,差异有显著性(P＜0.05,P＜0.01),2h胰岛素水平二甲双呱组与对照组相比差异有显著性(P＜0.05);三组ISI与治疗前相比,均有显著改善,差异有显著性(P＜0.05).结论氟伐他汀可改善老年人高血压痛胰岛素抵抗,降低血脂和血胰岛素水平.     

氟伐他汀加用地尔硫卓对心脏X综合征患者的治疗效果

目的观察地尔硫卓治疗心脏X综合征患者的疗效。方法将47例心脏X综合征患者随机接受氟伐他汀（23例,氟伐他汀组）或氟伐他汀+地尔硫卓（24例,联合用药组）治疗,随访治疗3个月后的临床情况并复查平板运动试验及一氧化氮（NO）、血浆内皮素-1（ET-1）的含量。结果各组用药后平板运动试验到达终点时间均显著延长（氟伐他汀组P<0.05;联合用药组P<0.01）。两组临床胸痛发生率及平板运动试验阳性率均显著降低（均P<0.01）。NO、HDL-C水平明显升高,TC、TG、LDL-C、ET-1水平明显下降。与对照组相比联合用药组平板运动试验中到达运动终点时间显著延长（P<0.05）,临床胸痛发生率显著降低（P<0.05）。结论氟伐他汀能明显改善X综合征患者的内皮细胞功能,加用地尔硫卓更能提高患者的运动耐量及缓解临床症状。     

氟伐他汀对急性心肌梗死后左室重构的实验研究

目的观察氟伐他汀对急性心肌梗死兔早期左室重构和心功能的影响。评价C反应蛋白（CRP）对心肌梗死后左室重构的预测价值。方法将梗死后24h存活兔随机分成：AMI模型组（M组，n=11），AMI氟伐他汀组（F组，n=12），另设假手术组（S组，n=10）。给药2周后，测血流动力学参数，比较各组间左室重构各指标。结果与假手术组相比，AMI模型组左室舒张末压（LVEDP）、左室重量（LVW）、左室重量指数（LVWI）、血CRP均显著增加（P＜0．05），左室收缩压（LVSP）、左室内压最大上升和下降速率（±dp／dtmax）均显著降低（P＜0．05）。与AMI模型组相比，AMI氟伐他汀组LVEDP、LVW、LVWI、血CRP均显著降低（P＜0．05），LVSP、±dp／dtmax均显著增加（P＜0．05）。结论氟伐他汀减少心梗后CRP的作用可能是其减轻急性心肌梗死后早期左室重构的机制之一。高浓度血CRP是预测心肌梗死急性期发生心室重构的预测因素。     

不同剂量氟伐他汀对血脂正常的早期糖尿病肾病的影响

目的 观察不同剂量氟伐他汀治疗血脂正常的早期糖尿病肾病（DN）的疗效,探讨其对肾脏的保护作用.方法 60例血脂正常的早期DN患者随机分为A、B两组,各30例,均给予常规降糖治疗外,A组给予氟伐他汀40 mg·d^-1,B组给予氟伐他汀80 mg·d^-1,睡前一次口服,观察6个月.比较两组治疗3个月、6个月前后24小时尿蛋白排泄率（UAER）、糖化血红蛋白（HbA1C）、甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、丙氨酸氨基转移酶（ALT）、天门冬酸氨基转移酶（AST）、肌酸激酶（CK）的变化.结果 两组治疗前后TG、TC、LDL-C、HDL-C、HbA1C、ALT、AST、CK水平均无统计学差异（P＞0.05）.无论何种给药剂量治疗后UAER显著下降,且随治疗时间延长效果更显著（P＜0.05）;B组比A组改善更明显,差异有统计学意义（P＜0.05）.结论 氟伐他汀具有非依赖降脂的肾脏保护作用,且在一定程度上具有剂量和时间依赖性.     

The pharmacology of fluvastatin,a new HMG-CoA reductase inhibitor

As a therapeutic class, the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors are highly effective at lowering low-density lipoprotein cholesterol (LDL-C) levels. In addition, they are well tolerated and well suited to a broad range of patients with primary (type IIa or IIb) hypercholesterolemia. The most recently approved HMG-CoA reductase inhibitor, fluvastatin sodium (Lescol®, Sandoz Pharmaceuticals Corp.), is the only entirely synthetic agent in this class. This agent has a distinct biopharmaceutic profile that may be responsible for certain safety benefits. Fluvastatin exhibits a favorable drug-interaction profile when used in combination with cyclosporine, fibric acids, erythromycin, or niacin. To date, no case of drug-related myopathy or rhabdomyolysis has been documented in any patient receiving fluvastatin. The hepatotoxicity profile of fluvastatin is also favorable; liver-enzyme testing—required with all HMG-CoA reductase inhibitors—is recommended less frequently during the first year of therapy with this agent than with the other HMG-CoA reductase inhibitors. Both its favorable safety profile and its cost effectiveness render fluvastatin a highly attractive option when therapy calls for moderate reductions in cholesterol levels.     

A comparison of the effects of fluvastatin and bezafibrate on exercise metabolism: a placebo-controlled study in healthy normolipidaemic subjects

1 We have examined the interaction between aerobic exercise and lipid-lowering drugs in a crossover study of 16 healthy normolipidaemic volunteers who each received 21 days' treatment with bezafibrate (400  mg), fluvastatin (40  mg), and placebo, in random order.
2 Fluvastatin treatment reduced pre-exercise total cholesterol (TC) by 23% ( P <0.0001), low-density lipoprotein cholesterol (LDL-C) by 33% ( P <0.0001), and plasma triglycerides by 11%, compared with pre-treatment values. Bezafibrate reduced TC by 11% ( P <0.01); LDL-C by 9%; and plasma triglycerides by 40% ( P <0.01), compared with pre-treatment values.
3 During exercise, in comparison with placebo, and fluvastatin treatment, respectively, bezafibrate significantly reduced mean fat oxidation: 31% vs 39%, P =0.035, 31% vs 39%, P =0.002, plasma free fatty acid (FFA) availability, e.g. after 90  min of exercise: ( t 90) 520 vs 662  μmol  l⁻¹, P =0.054, 520 vs 725  μmol l⁻¹, P =0.016, and plasma levels of glycerol ( t 90): 59 vs 74  μmol l⁻¹, P =0.037, 59 vs 73  μmol l⁻¹, P =0.016. Fluvastatin had no impact on fat metabolism in comparison with placebo.
4 Reduced plasma FFA concentration and lower fat oxidation during prolonged exercise on bezafibrate treatment may be due to an inhibition of hepatic acetyl coenzyme A carboxylase, resulting in reduced FFA release from adipose tissue.
5 The possibility that impaired fat metabolism on fibrates could induce premature fatigue during exercise of moderate duration and intensity should be examined in hyperlipidaemic patients.