Objective To systematically review the effectiveness and safety of Zhibitai vs. atorvastatin in the treatment of hyperlipidemia. Methods Randomized controlled trials (RCTs) about Zhibitai vs. atorvastatin for hyperlipidemia were electronically retrieved in databases of PubMed, CENTRAL (Issue 7, 2010), CBM,CNKI, VIP and WanFang Data from inception to July, 2012. Two reviewers independently screened literature, extracted data, and assessed methodological quality. Then, meta-analysis was conducted using RevMan 5.2 software. Results A total of 4 RCTs involving 519 cases were included. The results of meta-analysis showed, Zhibitai was superior to atorvastatin in reducing TG levels after 8-week treatment (MD= −0.12, 95%CI −0.23 to −0.01, P=0.03) and increasing HDL-C levels after 8-week treatment (MD= −0.16, 95%CI −0.22 to −0.11, P=0.000 01). But there was no significant difference in decreasing TC levels and LDL-C levels after 4-week treatment and 8-week treatment as well as decreasing TG levels after 4-week treatment between the two groups. No obvious adverse reaction occurred in the two groups, but atorvastatin may impair liver function. Conclusion Current evidence with weak strength shows that, Zhibitai is superior to atorvastatin in reducing TG levels, and increasing HDL-C levels after 8 weeks. However, they are alike in other blood-fat index and safety. Due to the limited quantity and quality of the included studies, more high quality RCTs are needed to verify the above conclusion.
Objective To assess the effectiveness and safety of nine lipid-lowing agents in the national essential drug list (2000) and provide evidence for the adjustment and selection of essential drugs. Methods Based on principles of health technology assessment (HTA) and evidence-based medicine, we searched for all published clinical studies about these drugs from the following databases: MEDLINE (1966-2002.8), The Cochrane Library, EMBASE (1974-2002), CBMdisk (1979-2002.8) and VIP (1989-2002.8), the database of National Center for Adverse Drug Reaction(ADR) Monitoring of China and the database of WHO Uppsala drug monitoring center. Included studies were appraised, analyzed and compared for the reduction of triglyceride (TC) or low density lipoprotein (LDL-C), the prevention for the coronary events and the incidence of ADR. Results The results from comparative trials for lipid-lowing agents showed that the equivalent dose of statins for 25% reduction of LDL-C was atorvastatin 10 mg/d, simvastatin 20 mg/d, pravastatin 40mg/d, lovastatin 40 mg/d, cerivastatin 0.3 mg/d and fluvastatin 80 mg/d. It was difficult to compare fenofibrate with gemfibrozil, acipimox with statins or fibrates based on available data. The study on the primary and secondary prevention of cardiovascular events showed that pravastatin and lovastatin were effective in primary prevention, and long-term use could reduce the incidence of cardiovascular disease.Gemfibrozil could reduce the mortality from coronary heart disease (CHD) but the overall mortality was not changed. Pravastatin, simvastatin, atorvastatin, fluvastatin, gemfibrozil and fenofibrate had a confirmed effect in secondary prevention. Data from large-scale clinical trials and the reports from ADR monitoring center of England, America, Canada and Australia suggested that the statins which had rare ADR were safe and tolerated. Rhabdomyolysis was rare but had a serious adverse reaction associated with statins. The rate of fatal rhabdomyolysis related to cerivastatin was the highest among 6 statins. The safety of simvastatin, lovastatin and atorvastatin was lower than cerivastatin but higher than simvastatin and atorvastatin. The number of ADR reports of fenofibrate was fewer than that of gemfibrozil. Conclusions At present, the best evidence focused on pravastatin, simvastatin and lovastatin are widely used and have a confirmed safety and efficacy. Atorvastatin, fluvastatin and fenofibrate still need more data to confirm their effects on coronary heart disease prevention. The drugs which were shown to be inferior or insufficient evidence are cerivastatin, gemfibrozil and acipimox.
Objective To observe the effects of different doses of atorvastatin on bleomycin-induced pulmonary fibrosis in rats. Methods Seventy-five healthy female SD rats were randomly divided into five groups ( 15 rats in each group) , ie. a normal group , a model group, a 10 mg/ kg atorvastatin-treated group, a 20 mg/ kg atorvastatin-treated group, and a 40 mg/ kg atorvastatin-treated group. The rats in the model group and treatment groups were instilled with bleomycin in trachea( 5 mg/kg) , and the normal group were instilled with equal volume of normal saline. The treatment groups were gastric gavaged with different doses of atorvastatin each day from2 nd day on after instillation, and the normal group and model group were gavaged with normal saline. Blood samples were obtained from abdominal aorta in five rats in each group and blood gas analysis was performed on1st week, 2nd week and 4th week respectively after BLM instillation. Then the animals were killed and lung tissue samples were harvested for histopathology study. HE and Masson staining were used to determine the extent of alveolus inflammation and pulmonary fibrosis respectively.Histoimmunochemical stain were used to determine the protein levels of transforming growth factor-β1 ( TGF-β1 ) and connective tissue growth factor( CTGF) in pulmonary tissues. Results The arterial partial pressure of oxygenate ( PaO2 ) in the treatment groups were increased gradually with the increasing of therapeutic dose at each time point and decreased with prolongation of time in the same group. The protein levels of TGF-β1 and CTGF in pulmonary tissues were decreased gradually with prolongation of time. TGF-β1 and CTGF expressed obviously less in the treatment groups than those in the model group at each time point .The higher therapeutic doses were, the less the expressions of TGF-β1 and CTGF were. Conclusion Atorvastatin has remarkable inhibitory effects on BLM-induced pulmonary fibrosis of rats in a dose- and timedependentmanner.
Objective To systematically assess the effectiveness and safety of atorvastatin in patients with dilated cardiomyopathy (DCM) complicating chronic heart failure (CHF). Methods Databases including PubMed, The Cochrane Library, EMbase, CNKI, CBM, and VIP were searched from inception to November 2011 to collect randomized controlled trials (RCTs) on atorvastatin for DCM accompanied with CHF. According to the inclusion criterion, relevant articles were screened. Then we extracted data, assessed quality, and performed meta-analysis using RevMan 5.0. Results A total of 11 RCTs involving 648 patients were included. The result of meta-analyses showed that compared with the control group at the sixth month after treatment, in the atorvastatin group, left ventricular ejection fraction (LVEF) obviously (MD=3.92, 95%CI 1.93 to 5.92, P=0.000 1) and 6-minute walk distance (MD=13.15, 95%CI 5.47 to 20.83, P=0.000 8) increased. Besides, serum level of CRP obviously decreased in the atorvastatin group (MD=1.91, 95%CI 3.03 to 0.79, P=0.000 9). Conclusion Current evidence indicates that atorvastatin, based on routine treatment, can improve cardiac function to some extent, increase LVEF, and reduce serum levels of inflammatory markers for patients with DCM complicating CHF. Therefore, atorvastatin is likely to be a safe and effective drug for non-ischemic cardiomyopathy due to DCM, which still has to be proved by more large-scale and high-quality clinical trials.
Objective To explore the effects of aggressive lipid lowering therapy and its influence on cardiovascular events using lipitor (20 mg daily) for Chinese people after percutaneous coronary intervention (PCI). Methods We did a double-blind and randomized controlled trial. From July 2005 to June 2006, 120 patients with PCI procedure who were discharged from the Shanghai Chest Hospital were randomly divided into aggressive lipid lowering group (atorvastatin 20 mg daily, n=60) and an ordinary lipid lowering group (atorvastatin 10 mg daily, n=60). The trial treatment was administered from the day of PCI to the third month after PCI. Atorvastatin at 10 mg daily was then used until one year after PCI. Blood biochemistry, cardiovascular events and drug adverse reactions were compared between the two groups. Results Among the 120 patients, 5 discontinued treatment and 4 more withdrew from the study. Therefore 115 and 111 were included in our main analyses [Comment from Mike: it is not ITT if the 5 who discontinued treatment are excluded] and a per-protocol (PP) analysis, respectively. Baseline clinical characteristics were comparable between the two groups. The reduction in TG and the increase in HDL-C were similar between the two groups (Pgt;0.05), but the reductions in LDL-C and TC were significantly different between the two groups (Plt;0.05). This was observed from the beginning of follow-up to the third month after PCI. In the PP analysis, the percentage of patients whose LDL-C met the predefined requirement at the third month in the 20 mg group was significantly higher than in the group receiving the lower dose (87.03% vs. 70.17%, P=0.031). A similar result was also obtained if the patients who withdrew were retained in the analysis (P=0.044). The change in C reaction protein (CRP) from baseline at the first and the third month was significantly different between the two groups (Plt;0.05), but become relatively stable at the sixth month (Pgt;0.05). The mean follow-up duration was 6.5±3.0 months in the higher dose group, with 1 case of recurring angina pectoris and 1 case of revascularization were identified. It was 7.2±3.6 months in the 10 mg daily group, with 3 cases of recurring angina pectoris, 1 case of nonfatal myocardial infarction, 2 cases of revascularization and 1 case of sudden cardiogenic death. The difference in the Kaplan-Meier event curves was of borderline statistical significance from the fourth month (P=0.048). Drug adverse reactions were mild and myopathy was not identified in any patients. Conclusions After PCI procedure, the use of atorvastatin 20 mg daily for aggressive lipid lowering was safe and effective.
ObjectiveTo observe and analyze the short-term efficacy of different statins on acute myocardial infarction in patients with premature coronary heart disease. MethodWe selected 70 patients with acute myocardial infarction admitted into our hospital for treatment of premature coronary artery disease between January 2012 and June 2013. The patients were randomly divided into experimental group (n=35) and control group (n=35). The experimental group were treated with rosuvastatin, and the control group of patients were given atorvastatin. We observed the rate of overall efficiency within 6 months after treatment, and total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), hepersensitive C-reactive protein (hs-CRP), left ventricular ejction fraction (LVEF), and flow-mediated dilation (FMD) were also observed before and after treatment. ResultsThe overall efficacy rate in the experimental group at 6 months was 94.3% and in the control group was 88.6% with no significant difference between each other (P>0.05). TG and FMD of patients in the experimental group at 6 months did not significantly change (P>0.05), while LVEF of the experimental group was significantly higher (P<0.05), and hs-CRP, TC, LDL-C, and HDL-C of the experimental group were significantly lower than the control group (P<0.05). ConclusionsShort-term comprehensive efficacy of rosuvastatin for treatment of premature coronary artery disease in patients with acute myocardial infarction is superior to atorvastatin.
ObjectiveTo investigate the effects and mechanism of atorvastatin in the experimental pulmonary fibrosis. MethodsFifty-four C57BL/6 mice were randomly divided into a control group,a bleomycin group and an atorvastatin group. The mice in the bleomycin group and the atorvastatin group received a single dose intratracheal injection of bleomycin (2.5 mg/kg),while the mice in the control group were injected with isodose physiological saline. The mice in the atorvastatin group were treated with atorvastatin 10 mg·kg-1·d-1 by intragastric administration the day after bleomycin instillation. All groups were sacrificed on the day 3,14 and 28,respectively. HE staining and Masson staining were used to detect the architecture of alveolar and the deposition of cellularity and collagen. RT-PCR and immunohistochemical technology were performed to detect the expression of Krüppel like factor 4 (KLF4). Zymography was used to investigate the activation of matrix metalloproteinase-2(MMP-2). ResultsAfter the treatment of bleomycin,the lung tissues showed acute inflammation on the day 3,the collagen deposition was more obvious and the architecture of alveolar was destroyed on the day 14. The alveolar structure,the inflammation and collagen deposition were attenuated on the day 28 compared with the day 14. Compared with the bleomycin group,the inflammation and the collagen deposition were significantly reduced in the atorvastatin group (P<0.05). Compared with bleomycin group,the expression of KLF4 significantly decreased in the atorvastatin group,although the expression of KLF4 mRNA increased on the day 3 compared with the bleomycin group (0.502±0.261 vs. 0.326±0.164,P<0.05). The expression of KLF4 protein on the day 3 was significantly decreased compared with the bleomycin group (0.048±0.015 vs. 0.130±0.017,P<0.05). After the intervention of bleomycin,the activation of MMP-2 on the day 3 and 14 significantly increased compared with the control group (3.136±1.321 and 3.449±0.356 vs. 0.983±0.147,P<0.05),and significantly decreased after the treatment of atorvastatin (2.191±0.800 and 2.506±0.761). ConclusionAtorvastatin may have anti-inflammation and anti-fibrosis activities in experimental pulmonary fibrosis through KLF4 pathway.
ObjectTo observe the clinical efficacy and safety of the combination therapy of atorvastatin and JiangZhi Decoction (ZJD) for primary hyperlipidemia (Tan Zhuo Zu E Zheng) and to analyze the interactions of drugs in hypolipidemic effect. MethodsA 2*2 factorial design, single-blind, stratified randomized controlled trial according to the level of lipid was conducted. Primary hyperlipidemia (Tan Zhuo Zu E Zheng) patients met the inclusion criteria were divided into 5 groups:ATV 10 mg group (group A), ATV 20 mg group (group B), ATV 10 mg+JZD group (group C), ATV 20 mg+JZD group (group D), JZD group (group E). After two weeks treatment, the efficacy and safety among the 5 groups were compared. ResultsA total of 92 patients were included, of which, 20 were in group A, 25 in group B, 21 in group C, 17 in group D, and 9 in group E. The results showed that:(1) There was no significant difference between group C and group B in the reduction of serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) (PTC=0.226, PLDL-C=0.818). (2) The results of 2*2 factorial analysis showed that, there was no significant interaction between TCM factor and western medicine factor (PTC=0.605, PLDL-C=0.843). (3) There were no significant differences in safety outcomes among 5 groups (all P values >0.05). ConclusionATV 10 mg+JZD and ATV 20 mg have a similar efficacy in reducing TC and LDL-C. There is no obvious interaction between JZD and ATV in hypolipidemic effect, and the combination therapy of ATV and JZD is safe.
ObjectiveTo investigate the effects of migration and expression from chemokine receptor 4 (chemokine receptor-4, CXCR4) of rat bone marrow mesenchymal stem cells (BMSCs) which were pretreated by atorvastatin (ATV) in vitro.MethodsIsolated, cultivated, identified the BMSCs, pretreated P4-P6 of BMSCs with different concentrations of ATV for 12 hours. The experimental group was divided into control group, 0.1 nM/L (group 0.1 nM), 1 nM/L (1 nM group), 10 nM/L (10 nM group), 100 nM/L (100 nM group), 1 000 nM/L (1 000 nM group). The mRNA and protein of CXCR4 were determined by real time-polymerase chain reaction and Western blot. Immunofluoreseence assay were used to detect the expression levels of CXCR4. The migration ability of BMSCs were measured by transwell chamber.ResultsImmunofluoreseence assay showed the protein level of CXCR4 of group 1 nM and 10 nM were significantly higher than the other group. RT-PCR and Western blot showed the protein and mRNA level of CXCR4 in 10 nM was higher than that in group 1 nM. The migration ability of group 10 nM was higher than 1 nM and control group.ConclusionsATV can be dose-dependent promote expression levels of CXCR4 of BMSCs cultivated in vitro.
ObjectivesTo systematically review the influence of nifedipine combined with atorvastatin on hypertension in patients with hypertension.MethodPubMed, EMbase, The Cochrane Library, CBM, CNKI, WanFang Data and VIP databases were electronically searched to collect randomized controlled trials (RCTs) of nifedipine combined with atorvastatin on hypertension in patients with hypertension from inception to November 20th, 2018. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using Stata 12.0 software.ResultsA total of 17 RCTs involving 1 838 patients were included. The results of meta-analysis indicated that nifedipine combined with atorvastatin was superior to nifedipine alone on SBP (MD=−8.937, 95%CI−11.913 to −5.962, P<0.001), DBP (MD=−3.702, 95%CI−6.626 to −0.778, P=0.013) and total effective rate (RR=1.24, 95%CI 1.07 to 1.44, P=0.003). There was no significant difference between two groups in the incidence of adverse reactions (P>0.05).ConclusionsCurrent evidence shows that nifedipine combined with atorvastatin can significantly improve total effective rate, decrease the level of SBP and DBP, and increasing of dose not increase the incidence of adverse reactions. Due to limited quality and quantity of the included studies, more high quality studies are required to verify above conclusions.