匹伐他汀钙片治疗高胆固醇血症的有效性和安全性研究

目的 评价匹伐他汀钙片治疗高胆固醇血症的有效性和安全性.方法 360例高胆固醇血症患者接1∶1∶1比例随机分为匹伐他汀钙片l mg组、2 rng组和阿托伐他汀钙片10 mg组,经4周筛选期后,符合入选标准的患者接受l mg/2 mg匹伐他汀钙片或10 mg阿托伐他汀钙片治疗(一日1次,口服),治疗8周,观察各组治疗前后血清低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)和甘油三酯(TG)变化情况.结果 治疗8周后各组LDL-C下降显著,分别为-30.06％、-35.04％和-34.34％,组间差异无统计学意义.匹伐他汀钙片2 mg组降低LDL-C的疗效非劣于阿托伐他汀钙片组,匹伐他汀钙片1 mg组降低LDL-C的疗效劣于阿托伐他汀钙片组.治疗4、8周后匹伐他汀钙降低TC、HDL-C和TG作用与阿托伐他汀钙比较差异无统计学意义.结论 匹伐他汀钙片治疗高胆固醇血症安全有效.     

阿托伐他汀与非诺贝特治疗高脂血症的比较

目的:比较阿托伐他汀与非诺贝特治疗高脂血症的疗效及安全性.方法:高脂血症86例,随机分为阿托伐他汀组43例,给阿托伐他汀10 mg,qd,共8周;非诺贝特组43例,给非诺贝特200 mg,qd,共8周.结果:两组治疗4周,胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-ch)均开始显著下降(P<0.01), 治疗8周高密度脂蛋白胆固醇(HDL-ch) 开始显著上升(P<0.05); 阿托伐他汀组治疗8周TC下降较非诺贝特组明显(P<0.05);不良反应发生率阿托伐他汀组9.3%,非诺贝特组4.7%,差异有极显著性(P<0.01).结论:两药均有明显的调脂作用,阿托伐他汀治疗8周TC下降明显优于非诺贝特,非诺贝特的不良反应发生率较低.     

阿托伐他汀治疗高脂血症33例

目的:观察阿托伐他汀治疗高脂血症的疗效及安全性.方法:对33例高脂血症患者给予口服阿托伐他汀10 mg`d 1,治疗4周.治疗前后分别测定胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL C)等.结果:治疗4周后TC、TG、LDL C水平与治疗前比较有明显降低,未见明显不良反应.结论:阿托伐他汀调脂疗效好,不良反应少.     

健脾化痰祛瘀方结合阿托伐他汀钙片治疗痰浊壅盛型高脂血症的临床观察

目的:观察健脾化痰祛瘀方结合阿托伐他汀钙片治疗痰浊壅盛型高脂血症的临床疗效。方法:采用前瞻性研究方法,将80例高脂血症(痰浊壅盛型)患者分为治疗组(中药+阿托伐他汀钙片)与对照组(阿托伐他汀钙片)各40例。2组患者均常规晚餐时服用阿托伐他汀钙片10mg,qd;治疗组加服健脾化痰祛瘀方。疗程均为8周。观察血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)的变化。结果:治疗组总有效率(92.5%)优于对照组(85.0%);2组TC、TG、LDL-C、HDL-C改善及头昏眩晕、身重困倦、胸闷心悸、腹胀纳呆等积分比较,治疗组症状改善均明显优于对照组(P<0.05);治疗过程中2组均未见明显不良反应。结论:中药联合阿托伐他汀钙片治疗痰浊壅盛型高脂血症优于单纯用阿托伐他汀钙片治疗,且2组安全性相当。     

阿托伐他汀治疗血脂谱异常症68例

目的观察阿托伐他汀治疗血脂谱异常症的临床疗效。方法患者每天口服阿托伐他汀钙片(又名立普妥)30 mg,第4周和8周后复查血脂,分析疗效。结果 4周后,血清胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)等均有下降,治疗8周后血清胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)有了显著下降(P<0.01),三酰甘油(TG)在8周后也有显著下降(P<0.05),高密度脂蛋白胆固醇(HDL-C)在8周后升高,差异具有显著性(P<0.05)。结论阿托伐他汀治疗血脂谱异常症疗效确切。     

阿托伐他汀钙片对冠心病合并高脂血症调脂疗效观察

目的 通过对阿托伐他汀钙片治疗冠心病合并高脂血症患者的疗效观察,探讨阿托伐他汀钙片的疗效性.方法 将符合入选标准的80例冠心病合并高脂血症的住院患者随机单盲分为治疗组和对照组,每组40例.治疗组给予阿托伐他汀钙片20 mg/d,口服,1次/d,对照组给予血脂康3片/d,口服,3次/d,2组分别在治疗前、治疗后4周、8周...     

阿托伐他汀钙片治疗高脂血症100例的临床疗效观察

目的 观察阿托伐他汀钙片治疗高脂血症的临床疗效及不良反应.方法 通过参阅相关文献资料,以及对我院2011-2012年100例服用阿托伐他汀钙片的高脂血症患者的临床疗效及不良反应进行归纳分析.结果 阿托伐他汀钙片可改善血脂水平,不良反应少.结论合理应用阿托伐他汀钙片及其他他汀类药物,对预防其不良反应有重要意义.     

阿托伐他汀钙片对冠心病合并高脂血症调脂疗效观察

目的：研究阿托伐他汀钙片对冠心病合并高脂血症的调脂疗效,探讨最佳用药剂量。方法120例冠心病合并高脂血症患者随机分为观察组与对照组,各60例,均在冠心病基础治疗基础上联用阿托伐他汀钙片,观察组40 mg/d,对照组20 mg/d。分别于用药前、用药6周、用药12周行血脂检查,以评定调脂疗效;统计用药期间肝肾功能损害及肌溶解等不良反应发生率。结果所有患者经治疗后总胆固醇(TC)、甘油三脂(TG)、低密度脂蛋白胆固醇(LDL-C)均呈显著下降趋势,而高密度脂蛋白胆固醇(HDL-C)呈显著上升趋势,同时观察组用药6周、用药12周与对照组对比,差异均有统计学意义(P<0.05)。两组不良反应发生率对比,差异无统计学意义(P>0.05)。结论对冠心病合并高血脂患者,可应用阿托伐他汀钙片降血脂,且宜选择高剂量用药方案。     

阿托伐他汀钙片治疗2型糖尿病合并高脂血症疗效观察

目的观察阿托伐他汀钙片治疗2型糖尿病合并高脂血症的疗效。方法 60例2型糖尿病合并高脂血症患者予阿托伐他汀钙片治疗8周,观察其临床疗效及治疗前后血脂和肝功能变化。结果治疗8周后,TC水平下降,总有效率为100%;LDL-C水平下降,总有效率为100%;TG水平下降,总有效率为95%。治疗后,TC、TG、LDL-C水平均低于治疗前,HDL-C水平高于治疗前,差异均有统计学意义(P<0.05)。结论阿托伐他汀钙片能迅速有效调节2型糖尿病伴高脂血症患者的血脂异常,降低心脑血管卒中的危险性,且不良反应轻微,值得推广应用。     

阿托伐他汀类药物治疗血脂紊乱的临床观察

目的观察阿托伐他汀治疗高血脂症的临床疗效。方法选择符合条件的高血脂症住院患者60例,给予口服阿托伐他汀10 mg,每日1次,患者在治疗期间进行标准的低胆固醇饮食维持合理的膳食。所有患者于治疗前及治疗后2周、4周,采用酶联免疫吸附法测定血浆总胆固醇(TC),低密度脂蛋白胆固醇(LDL-C)及甘油三脂(TG)的浓度,同时用药前后检测肝、肾功能、血浆肌酸激酶(CK)、血常规、心电图各一次。结果60例高脂血症患者中,36例患者在服用阿托伐他汀钙片2周后,TC、LDL-C及TG有不同程度的改善,有效率为60%。有24例患者降低效果未达标,治疗4周后,14例患者的TC、LDL-C及TG指标中有1~2项达到有效,总有效率为83.3%。有4例患者服用阿托伐他汀钙片TC、LDL-C及TG下降不明显。经统计学分析,治疗前后有显著差异(P<0.05)。结论阿托伐他汀类药物治疗高血脂症患者取得了较好的疗效。     

Impact of short‐term low‐dose atorvastatin on low‐density lipoprotein and high‐density lipoprotein subfraction phenotype

Statins can significantly reduce low‐density lipoprotein–cholesterol (LDL‐C) and modestly raise or not alter high‐density lipoprotein–cholesterol (HDL‐C). However, their impact on high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) subfractions has been less examined. The aim of the present study was to investigate the short‐term impact of low‐dose atorvastatin on HDL and LDL subfractions in humans. In this randomized study, data from 52 subjects were analysed. Thirty‐seven patients with atherosclerosis were randomized to treatment with atorvastatin 10 mg/day (n = 17) or 20 mg/day (n = 20) for 8 weeks, with 15 healthy subjects without therapy used as a control group. The lipid profile and lipoprotein subfractions were determined using the Lipoprint system at baseline and at 8 weeks. The data suggest that atorvastatin treatment (10 and 20 mg/day) for 8 weeks significantly decreases LDL‐C levels and reduces the cholesterol concentration of all LDL subfractions, which is accompanied by an increase of the mean LDL particle size. Although 10 mg/day atorvastatin treatment for 8 weeks had no impact on the HDL subfraction, 20 mg/day atorvastatin for 8 weeks significantly increased the cholesterol concentration of large HDL particles and decreased the cholesterol concentration of small HDL particles without changing serum HDL‐C levels in patients with atherosclerosis. Therefore, the results suggest that 20 mg/day atorvastatin treatment for 8 weeks may result in a favourable modification of the HDL subfraction phenotype in addition to its effects on the cholesterol concentration of all LDL subfractions and mean LDL particle size.     

Effect of short term treatment with simvastatin and atorvastatin on lipids and paraoxonase activity in patients with hyperlipoproteinaemia

OBJECTIVE: High-density lipoprotein (HDL)-associated paraoxonase (PON) activity may play an important role in the inhibition of low-density lipoprotein (LDL) oxidation. Previous studies have demonstrated that serum PON activity is decreased in patients with hyperlipoproteinaemia and coronary heart disease. The study presented here examined the effect of short-term treatment with simvastatin and atorvastatin on lipids and PON activity in patients with hyperlipoproteinaemia. RESEARCH DESIGN AND METHODS: A prospective, non-blinded, single-group, cross-over, comparative trial was performed. Following an 8-week dietary run-in period, 49 patients (23 men and 26 women, mean age: 59.8 +/- 7.9 years) with Fredrickson type IIa. and IIb. hyperlipoproteinaemias were randomized to receive either simvastatin 20 mg/day or atorvastatin 10 mg/day for 3 months. Following an 8-week washout period, patients were crossed-over to receive the other drug for a further 3 months. Serum lipids were measured and serum PON activity was determined spectrophotometrically using paraoxon as a substrate. RESULTS: Simvastatin treatment significantly reduced serum cholesterol, LDL-cholesterol (LDL-C) and apolipoprotein (apo) B levels (p < 0.001). Atorvastatin had a more pronounced cholesterol, LDL-C- and apo B-lowering effect (p < 0.001) compared with simvastatin. Both statins also significantly reduced serum triglyceride levels (p < 0.01). Simvastatin and atorvastatin caused no significant change in the levels of HDL-cholesterol (HDL-C) and apo A1. HDL-associated PON activity did not change significantly after simvastatin therapy, but significantly increased after atorvastatin treatment (p < 0.05). CONCLUSIONS: Short-term administration of simvastatin did not increase PON activity. Atorvastatin treatment had a favourable effect on lipid profile and increased the activity of HDL-associated PON.     

The DISCOVERY PENTA study: a DIrect Statin COmparison of LDL-C Value--an Evaluation of Rosuvastatin therapY compared with atorvastatin

BACKGROUND: International guidelines emphasize the need to achieve recommended low-density lipoprotein cholesterol (LDL-C) levels in order to reduce morbidity and mortality associated with coronary heart disease (CHD). However, many patients with hypercholesterolemia fail to achieve LDL-C goals on treatment. OBJECTIVE: The primary objective was to compare the efficacy of rosuvastatin and atorvastatin for enabling patients to achieve National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) LDL-C goals. Secondary objectives were European LDL-C goal achievement, changes in the lipid profile, and safety. RESEARCH DESIGN AND METHODS: This 12-week, multicenter, multinational, randomized, open-label trial compared the efficacy and safety of rosuvastatin 10 mg with atorvastatin 10 mg in statin-na?ve and switched patients with primary hypercholesterolemia from Brazil, Colombia, Mexico, Portugal, and Venezuela. RESULTS: A total of 1124 patients with similar baseline characteristics were randomized to the two treatment groups. After 12 weeks of treatment, a significantly greater percentage of patients receiving rosuvastatin 10 mg compared with atorvastatin 10 mg achieved NCEP ATP III LDL-C goals (71.2% vs 61.4%, p < 0.001), 1998 European LDL-C goals (73.5% vs 59.2%, p < 0.001) and 2003 European LDL-C goals (58.9% vs 44.6%, p < 0.001). Rosuvastatin treatment was associated with significant reductions in LDL-C and total cholesterol (TC) and, in statin-na?ve patients, a significant increase in high-density lipoprotein cholesterol (HDL-C) compared with atorvastatin treatment. Both treatments were well tolerated with a similar incidence of adverse events. Clinically significant elevations in creatinine, creatine kinase or hepatic transaminases were low and similar between treatment groups. CONCLUSIONS: Rosuvastatin 10 mg is significantly more effective at achieving NCEP ATP III and European LDL-C goals, lowering LDL-C and TC in both na?ve and switched patients and increasing HDL-C in na?ve patients than atorvastatin 10mg, with a similar safety and tolerability profile. This study also provides evidence regarding the comparative effects of rosuvastatin versus atorvastatin in Latin American and Portuguese populations.     

LDL-C/HDL-C ratio in subjects with cardiovascular disease and a low HDL-C: results of the RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) study

BACKGROUND: The ratio of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol (LDL-C/HDL-C) is a reliable predictor of cardiovascular risk. Low HDL-C levels in patients with coronary artery disease are associated with a high risk for cardiovascular events. OBJECTIVES: This study compared the effects of rosuvastatin and atorvastatin on the LDL-C/HDL-C. METHODS: Patients aged 40-80 years with established cardiovascular disease and HDL-C < 1.0 mmol/L (< 40 mg/dL) entered as a 6-week dietary run-in period, before randomisation to open-label treatment with rosuvastatin 10 mg (n = 230) or atorvastatin 20 mg (n = 231) for 6 weeks. Doses were increased after 6 weeks to rosuvastatin 20 mg or atorvastatin 40 mg, and after 12 weeks to rosuvastatin 40 mg or atorvastatin 80 mg. Serum lipid parameters were measured at baseline and 6, 12 and 18 weeks. RESULTS: After 6 weeks of treatment, mean percentage change from baseline in LDL-C/HDL-C ratio was -47.0% in the rosuvastatin group and -41.9% in the atorvastatin group (p < 0.05 for between-group comparison). After 12 and 18 weeks of treatment, change from baseline was -53.0% and -57.3%, respectively, for rosucastatin, compared with -47.9% and -49.6%, respectively, for atorvastatin (p < 0.01 and p < 0.001, respectively, for between-group comparison). Rosuvastatin also reduced LDL-C, total cholesterol/HDL-C significantly more than atorvastatin at all three time points, and significantly improved total cholesterol/HDL-C and apolipoprotein B/A-I ratios. CONCLUSIONS: Rosuvastatin 10, 20 and 40 mg is significantly more effective than atorvastatin 20, 40 and 80 mg, respectively, in improving the LDL-C/HDL-C ratio in patients with cardiovascular disease and low HDL-C. Further studies are required to clarify the benefits of rosuvastatin for reduction of cardiovascular risk.     

Efficacy of combination of atorvastatin and micronised fenofibrate in the treatment of severe mixed hyperlipidemia

OBJECTIVES: In patients with mixed lipid disorders, monotherapy may not effectively control all lipid abnormalities. We undertook this study to assess the efficacy of fenofibrate in combination with atorvastatin in patients with severe mixed dyslipidemia. METHODS: This was an 18-week, open-label study conducted in our lipid clinic. After a 6-week dietary baseline phase, patients received 200 mg/day micronised fenofibrate for 6 weeks. At the end of this period the subjects discontinued this treatment and received 40 mg/day atorvastatin for 6 weeks. Finally 200 mg/day of micronised fenofibrate was added to the statin therapy. RESULTS: Administration of micronised fenofibrate reduced serum triglycerides (P < 0.01) and total cholesterol and low-density lipoprotein (LDL) cholesterol (P < 0.05 for both parameters), while it evoked a significant increase in serum high-density lipoprotein (HDL) cholesterol levels (P < 0.05). Atorvastatin monotherapy induced a more pronounced decrease of total and LDL cholesterol. However, plasma triglycerides, although significantly lower than baseline values (P < 0.05), were higher than the values observed during treatment with fenofibrate. Moreover, serum HDL cholesterol concentrations were higher during fibrate therapy than during the statin one. During the combination therapy, the decrease in triglycerides was greater than that observed with fenofibrate alone, while the decrease in LDL cholesterol was more pronounced than that observed with atorvastatin alone. CONCLUSION: The combination of atorvastatin with micronised fenofibrate in patients with severe mixed dyslipidemia may have a favourable effect on some major coronary artery disease risk factors.     

Influence of atorvastatin on serum amyloid A-low density lipoprotein complex in hypercholesterolemic patients

The complex of serum amyloid A(SAA) and low-density lipoprotein (LDL), SAA-LDL, is considered a new and unique marker of oxidatively-modified LDL particles, which is associated with atherosclerotic conditions. This study investigated the influence of atorvastatin treatment on circulating SAA-LDL levels among asymptomatic hypercholesterolemic patients. A total of 26 patients (mean age 63 years) received 10 mg/daily atorvastatin during a 12-week treatment period. The levels of LDL cholesterol and SAA-LDL, but not high-sensitivity C-reactive protein and SAA, were significantly reduced after the treatment. Stepwise adjusted regression analyses revealed that changes of SAA-LDL were significantly and positively correlated with those of SAA, while absolute changes were small, which warrants further investigation. The results suggest that atorvastatin may beneficially reduce SAA-LDL, and SAA-LDL may be a sensitive measure for monitoring the efficacy and antioxidant functions of atorvastatin.     

A comparison of simvastatin and atorvastatin up to maximal recommended doses in a large multicenter randomized clinical trial

OBJECTIVE: At higher doses, simvastatin has been shown to produce significantly greater increases in high-density lipoprotein (HDL) cholesterol and apolipoprotein (apo) A-I than atorvastatin. To extend and confirm these findings, a 36-week, randomized, double-blind, dose-titration study was performed in 826 hypercholesterolemic patients to compare the effects of simvastatin and atorvastatin on HDL cholesterol, apo A-I, and clinical and laboratory safety. PRIMARY HYPOTHESIS: Simvastatin, across a range of doses, will be more effective than atorvastatin at raising HDL cholesterol and apo A-I levels. METHODS: A total of 826 hypercholesterolemic patients were enrolled in this double-blind, randomized, parallel, 36-week, dose-escalation study. Patients randomized to simvastatin received 40 mg/day for the first 6 weeks, 80 mg/day for the next 6 weeks, and remained on 80 mg/day for the final 24 weeks. Patients randomized to atorvastatin received 20 mg/day for the first 6 weeks, 40 mg/day for the next 6 weeks, and 80 mg/day for the remaining 24 weeks. RESULTS: During the first 12 weeks of the study, simvastatin increased HDL cholesterol and apo A-I more than the comparative doses of atorvastatin, while producing slightly lower reductions in low-density lipoprotein (LDL) cholesterol and triglycerides. At the maximal dose comparison, simvastatin 80 mg and atorvastatin 80 mg, the HDL cholesterol and apo A-I differences favoring simvastatin were larger than at the lower doses. In addition, at the maximal dose comparison, the incidence of drug-related clinical adverse experiences was approximately two-fold higher with atorvastatin 80 mg than with simvastatin 80 mg (23 versus 12%, p < 0.001), due predominantly to a greater incidence of gastrointestinal symptoms with atorvastatin (10 versus 3%, p < 0.001). The incidence of clinically significant alanine aminotransferase elevations was also higher with atorvastatin 80 mg than with simvastatin 80 mg (3.8 versus 0.5%, p < 0.010), especially in women (6.0 versus 0.6%). CONCLUSIONS: At the doses compared in this study, simvastatin led to greater increases in HDL cholesterol and apo A-I levels than atorvastatin. At the maximum dose comparison, there were fewer drug-related gastrointestinal symptoms and clinically significant aminotransferase elevations with simvastatin.     

Effect of Atorvastatin versus Simvastatin on Lipid Profile and Plasma Fibrinogen in Patients with Hypercholesterolaemia: A Pilot, Randomised, Double-Blind, Dose-Titrating Study

OBJECTIVE: To investigate the effect of atorvastatin vs simvastatin on lipid profile and plasma fibrinogen in patients with hypercholesterolaemia. PATIENTS: 30 outpatients (25 men), with a median age of 51 years were studied. Eight patients had established coronary artery disease (CAD) and four had diabetes mellitus at baseline. 11 patients presented a Frederickson's IIb phenotype and 19 a IIa phenotype at baseline. STUDY DESIGN: After a 6-week placebo period, patients were randomly assigned to simvastatin (10 mg/day, n = 15) or atorvastatin (10 mg/day, n = 15). Lipid profile, apolipoproteins B and A-I and plasma fibrinogen were measured for a 16-week period, at 4-week intervals. Thereafter, the dose of each drug was doubled only in patients with low density lipoprotein cholesterol (LDL-C) levels above 130 mg/dl for a further 16-week period. RESULTS: Ten of 15 patients on atorvastatin 10mg (66%) and four of 15 on simvastatin 10mg (27%) achieved the LDL-C <130 mg/dl goal. Apolipoprotein B was reduced by both drugs (-33%, p < 0.001 for atorvastatin and -18%, p < 0.05 for simvastatin), but plasma fibrinogen and triglyceride were reduced only by atorvastatin (-20%, p < 0.01; -36%, p < 0.001, respectively). During the second 16-week period seven of 11 patients receiving the simvastatin 20mg dose (64%) achieved the LDL-C <130 mg/dl goal. The comparison of atorvastatin 10mg with simvastatin 20mg showed that the drugs appear to be equipotent in terms of LDL-C lowering. CONCLUSIONS: Atorvastatin in equipotent doses to simvastatin appeared to be more effective than the latter in reducing triglyceride and plasma fibrinogen in patients with hypercholesterolaemia, mainly in those with Frederickson's phenotype Iib.     

(TTA)n Polymorphism in 3‐Hydroxy‐3‐Methylglutaryl‐Coenzyme A and Response to Atorvastatin in Coronary Artery Disease Patients

Abstract: 3‐Hydroxy‐3‐methylglutaryl‐coenzyme A reductase inhibitors have been used clinically for lowering total and low‐density lipoprotein cholesterol. Interindividual pharmacological differences observed with this treatment have been attributed to genetic differences. The aim of this study was to assess the association in the low‐density lipoprotein cholesterol reduction by atorvastatin and (TTA)n polymorphism in the 3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase gene in patients with coronary artery disease. Changes in total cholesterol levels, triglycerides, high‐sensitivity C‐reactive protein and free F₂‐isoprostanes were also evaluated. In an open study, patients received 40 mg atorvastatin daily for 8 weeks. Genotyping was done through polymerase chain reaction. The genotype distribution of the 3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase (TTA)n polymorphism was: >10/>10 in 22 out of 64 patients (34%), >10/10 in 14 out of 64 patients (22%) and 10/10 in 28 out of 64 patients (44%). The reduction of low‐density lipoprotein cholesterol levels by atorvastatin was not different between allelic variants (TTA)n repeat polymorphism. Reductions in high‐sensitivity C‐reactive protein were observed in atorvastatin‐treated patients with alleles >10/>10 and 10/10. Free F₂‐isoprostanes and total cholesterol were also significantly lower after treatment for all alleles, irrespective of type of polymorphism. In conclusion, the changes induced by atorvastatin treatment on low‐density lipoprotein cholesterol, total cholesterol, triglycerides, high‐sensitivity C‐reactive protein and free F₂‐isoprostane concentrations were not related to the presence of 3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase polymorphism (TTA)n.     

Pharmacoeconomic assessment of HMG-CoA reductase inhibitor therapy: an analysis based on the CURVES study

We conducted a post hoc pharmacoeconomic analysis of a multicenter, open-label, randomized, parallel-group, 8-week efficacy-safety comparison of five HMG-CoA reductase inhibitors-atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin. The 534 patients requiring cholesterol-lowering therapy took the drugs for 8 weeks with 15 different regimens. Low-density lipoprotein (LDL) was measured after 6 weeks of diet (baseline) and after 8 weeks of treatment with a study drug. At dosages of 10, 20, and 40 mg/day, atorvastatin was associated with significantly greater reductions in LDL than equivalent dosages of the other agents. Cost-effectiveness calculated as the annual acquisition cost/percentage LDL reduction was greatest with atorvastatin 10 mg ($17.96), fluvastatin 40 mg ($19.83), atorvastatin 20 mg ($22.85), and atorvastatin 40 mg ($24.96). All other dosages were above $25.00/year/percentage LDL reduction. Atorvastatin was the most cost-effective HMG-CoA reductase inhibitor. Fluvastatin 40 mg/day also had a favorable cost:effectiveness ratio but lowered LDL only by 23%.