Effects of statins on circulating oxidized low-density lipoprotein in patients with hypercholesterolemia

Recently, it has been reported that circulating oxidized low-density lipoprotein (Ox-LDL) might be a pivotal indicator for coronary artery disease and the severity of acute coronary syndromes. The purpose of this study was to investigate the effects of statins on Ox-LDL in patients with hypercholesterolemia. Sixteen patients with hypercholesterolemia were randomly assigned to 2 groups, one received 10 mg of pravastatin (n = 8) and the other received 20 mg of fluvastatin (n = 8). The plasma level of Ox-LDL was measured using a newly developed sandwich enzyme-linked immunosorbent assay (ELISA) method. There were no differences between the two groups in Ox-LDL, total cholesterol (TC), or LDL cholesterol (LDL-C) at the baseline. The reduction in Ox-LDL in the fluvastatin group was significantly higher than that in the pravastatin group (47.5% versus 25.2%, P = 0.033). The reductions in TC and LDL-C did not differ between the two groups. CONCLUSION: The present study has shown for the first time that the level of circulating Ox-LDL was significantly decreased by treatment with statins. In addition, the lowering effect of statins on the circulating Ox-LDL was independent of their lipid-lowering effect. Fluvastatin was more effective than pravastatin with regard to decreasing the circulating Ox-LDL.     

Comparing the effects of five different statins on the HDL subpopulation profiles of coronary heart disease patients

We compared the effects of five different statins (atorvastatin, simvastatin, pravastatin, lovastatin, and fluvastatin) on the lipid, lipoprotein, and apolipoprotein (apo) A-I-containing high-density lipoprotein (HDL) subpopulation profiles of 86 coronary heart disease (CHD) patients. Patients with established CHD, and low density lipoprotein (LDL) cholesterol (C)>130 mg/dl, and triglyceride (TG)<400 mg/dl, were treated with atorvastatin 20, 40, and 80 mg/day and one of the other four statins at 20, 40, and when available 80 mg/day in increasing doses (4 weeks of each dose) in a randomized crossover fashion. There was an 8-week placebo controlled washout period between different drug treatments. All five statins on each dose resulted in significant reductions in total- and LDL-C compared to placebo treatment. There were also decreases in plasma TG and increases in HDL-C and apoA-I concentrations, but not all treatments changed these parameters significantly. Each statin except fluvastatin improved the HDL subpopulation profile by increasing the concentrations of the large, cholesterol-rich, LpA-I alpha-1 and prealpha-1 HDL subpopulations. CHD patients have significantly lower concentration of the large, LpA-I alpha-1 HDL particles compared to controls. Our data indicate that statins which are the most effective in lowering LDL-C and TG are also the most effective agents in modifying the HDL subpopulation profile in CHD patients towards the patterns found in healthy individuals. The order of efficacy of statins in increasing alpha-1 HDL subpopulation was: atorvastatin, simvastatin, pravastatin, lovastatin and fluvastatin.     

氟伐他汀对高脂血症患者的血脂及细胞粘附分子的影响

为研究氟伐他汀对高脂血症患者的降脂作用及对细胞粘附分子的影响。选择高脂血症患者 5 8例 (男性 35例 ,女性 2 3例 ) ,予氟伐他汀 4 0mg口服 ,每晚一次 ,一周后改为 2 0mg ,每晚一次 ,疗程 6～ 8周。分别观测治疗前后血脂及细胞粘附分子的情况。结果发现 ,治疗后患者总胆固醇、甘油三酯、低密度脂蛋白、血清可溶性细胞间粘附分子 1和血清可溶性血管细胞粘附分子 1明显降低 (P <0 .0 5 ) ,而高密度脂蛋白升高不明显。此结果提示 ,氟伐他汀不但能降低总胆固醇、甘油三酯及低密度脂蛋白水平 ,而且能降低血清可溶性细胞间粘附分子 1和血清可溶性血管细胞粘附分子 1浓度。     

Fibromuscular cap composition is important for the stability of established atherosclerotic plaques in mature WHHL rabbits treated with statins.

We examined the relationship between plaque vulnerability and fibromuscular cap composition using hydrophilic pravastatin and lipophilic fluvastatin. WHHL rabbits aged 10 months were given pravastatin (50 mg/kg) or fluvastatin (20 mg/kg) for 52 weeks. The atherosclerotic lesions were immunohistochemically or conventionally stained and the components were analyzed with a color image analyzer. Compared with the control group, the plasma cholesterol levels were decreased by about 25% in both statin groups. Pravastatin decreased the lipid components (macrophages+extracellular lipids) in whole aortic plaques by 34% and the fibrous caps of coronary plaques by 55%. Fluvastatin decreased the fibromuscular components (smooth muscle cells+collagen fibers) in whole aortic plaques and in the fibromuscular caps of the aortic and coronary plaques. In the pravastatin group, the vulnerability index, the ratio of (lipid components)/(fibromuscular components), was decreased in whole aortic plaques by 28% and in the fibromuscular caps of coronary lesions by 61%, while the indexes were increased in the fluvastatin group. The incidence of vulnerable plaques was decreased by 74% in the coronary plaques of the pravastatin group. Our results suggest that the stability of atheromatous plaques was improved due to a decrease of the lipid components and vulnerability index of the fibromuscular cap by pravastatin.     

Preliminary report: kinetic studies on the modulation of high-density lipoprotein, apolipoprotein, and subfraction metabolism by sex steroids in a postmenopausal woman

To investigate the effects of estrogens and androgens on the metabolism of high density lipoproteins (HDL) and low density lipoproteins (LDL), a normolipidemic postmenopausal woman was studied under the following conditions: (1) during supplementation with ethinyl estradiol (0.06 mg/d); (2) without sex steroid therapy; (3) during treatment with stanozolol, an androgenic, anabolic steroid (6 mg/d). During these manipulations HDL and LDL cholesterol levels fluctuated widely but reciprocally: during estrogen supplementation HDL increased while LDL decreased; during stanozolol HDL-C decreased while LDL-C increased. Simultaneous changes in post-heparin plasma hepatic triglyceride lipase activity paralleled those of LDL (and opposed those of HDL), decreasing with estrogen and increasing with stanozolol. During all three phases, autologous 125I-HDL turnover studies disclosed similarities between HDL2 and apolipoprotein A-I metabolism and between HDL3 and apolipoprotein A-II metabolism. In the untreated state the residence times of HDL2 and apo A-I were only half those of HDL3 and apo A-II. During estrogen treatment HDL2 and apo A-I, residence times were selectively prolonged, coming to resemble those of HDL3 and apo A-II, which remained unchanged. By contrast, during stanozolol treatment HDL3 and apo A-II residence times were selectively reduced, coming to resemble those of HDL2 and apo A-I, which remained unchanged. Apo A-I levels increased on estrogen and decreased on stanozolol, while apo A-II remained stable. Hence, estrogen increased HDL primarily by retarding the catabolism of the HDL2 subfraction rich in apo A-I, whereas stanozolol decreased HDL by accelerating the catabolism of HDL3, relatively rich in apo A-II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Time course of rapid C-reactive protein reduction by pravastatin in patients with stable angina

The evidence has indicated that rapid reduction of inflammatory marker, such as C-reactive protein (CRP) could be achieved by administration of a statin. However, limited information is available in evaluating the short-term time course of CRP reduction in patients with coronary artery disease by use of a statin. Forty-two patients with stable angina were randomly assigned to 20 mg/d or 40 mg/d group of pravastatin. Blood samples were drawn at days 0, 1, and 14 for measuring lipid profile, CRP levels, and hepatic enzymes in all patients. The results showed that both doses of pravastatin induced significant reductions in median CRP levels and in mean CRP levels, respectively, at day 1 (20% in the 20 mg/d group and 17.6% in the 40 mg/d group; 15% in the 20 mg/d group and 10% in the 40 mg/d group) as well as at day 14 (28.6% in the 20 mg/d group and 33.3% in the 40 mg/d group; 25% in the 20 mg/d group and 22.8% in the 40 mg/d group) compared with baseline data without a dose-dependent manner. In addition, no changes were found at day 1 regarding lipid profile; however, both doses of pravastatin induced significant reductions in total cholesterol (TC, 22% and 30%), and low-density lipoprotein (LDL) cholesterol (30% and 40%) compared with baseline at 14 days. The higher dose of pravastatin resulted in significantly greater reductions in TC and LDL cholesterol compared with the 20 mg/d dose (p = 0.05, p = 0.01, respectively). A less significant reduction was observed in triglycerides level (16% and 24%) compared with TC and LDL cholesterol. There was no significant difference in mean high-density lipoprotein (HDL) cholesterol levels compared with baseline in both groups. These data suggested that a common daily dose of pravastatin resulted in rapid reduction of CRP within 24 hours and of lipid profile within 2 weeks, and the benefit to the vascular endothelium might occur quickly by reduction of CRP levels, which may be clinically important for patients in a high-risk subgroup, such as acute coronary artery disease.     

小剂量普伐他汀与非诺贝特联合治疗混合型高血脂症临床疗效及安全性

目的探讨小剂量普伐他汀与非诺贝特联合应用治疗混合型高血脂症的临床疗效及安全性。方法混合型高血脂症患者189例,随机分为3组,即普伐他汀组(10mg/d,n=64)、非诺贝特组(200mg/d,n=63)、联合治疗组(普伐他汀10mg/d+非诺贝特200mg/d,n=62),治疗12周;12周时单药治疗血脂水平未全部达标者再随机分为3组,即联合治疗组、普伐他汀20mg治疗组及非诺贝特组,再治疗12周。观察治疗前后主要血脂水平的变化率、达标率及不良反应。结果(1)12周时联合治疗组血清总胆固醇(TC)、低密度脂蛋白胆固醇LDL-C、三酰甘油(TG)下降的幅度及血清高密度脂蛋白胆固醇(HDL-C)升高的幅度均高于单独用药组(P值均<0.01);TC、LDL-C、TG3项全部达标率也高于单独用药组(P均<0.01)。(2)单独用药血脂参数未全部达标者(n=35)改为联合治疗组治疗12周后TC及LDL-C下降的幅度与普伐他汀20mg组比较,差异无统计学意义,而降低TG及升高HDL-C幅度高于普伐他汀20mg组(P值均<0.01);联合治疗组与单用非诺贝特组比较,降低TC、LDL-C、TG及升高HDL-C的幅度高于非诺贝特组(P值<0.01或<0.05);联合用药组3项全部达标率为44%,而普伐他汀20mg组及非诺贝特组全部达标为21%、17%(P值均<0.01)。(3)联合治疗的不良反应与单独用药相比没有明显增加。结论小剂量普伐他汀(10mg/d)与非诺贝特(200mg/d)联合治疗混合型高血脂症,较单独用药更有效、更全面地改善各项血脂水平,具有良好的安全性和耐受性。     

Comparisons of effects of statins (atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin) on fasting and postprandial lipoproteins in patients with coronary heart disease versus control subjects

The effects of atorvastatin at 20, 40, and 80 mg/day on plasma lipoprotein subspecies were examined in a randomized, placebo-controlled fashion over 36 weeks in 97 patients with coronary heart disease (CHD) with low-density lipoprotein (LDL) cholesterol levels of >130 mg/dl and compared directly with the effects of fluvastatin (n = 28), pravastatin (n = 22), lovastatin (n = 24), and simvastatin (n = 25). The effects of placebo and 40 mg/day of each statin were also examined in subjects with CHD with subjects in the fasting state and in the fed state 4 hours after a meal rich in saturated fat and cholesterol and compared with results in age- and gender-matched control subjects. At all doses tested in the fasting and fed states, atorvastatin was significantly (p <0.01) more effective in lowering LDL cholesterol and non-high-density lipoprotein (HDL) cholesterol than all other statins, and significantly (p <0.05) more effective than all statins, except for simvastatin, in lowering triglyceride and remnant lipoprotein (RLP) cholesterol. At 40 mg/day in the fasting state, atorvastatin was significantly (p <0.01) more effective than all statins, except for lovastatin and simvastatin, in lowering cholesterol levels in small LDL, and was significantly (p <0.05) more effective than all statins, except for simvastatin, in increasing cholesterol in large HDL and in lowering LDL particle numbers. Our data indicate that atorvastatin was the most effective statin tested in lowering cholesterol in LDL, non-HDL, and RLP in the fasting and fed states, and getting patients with CHD to established goals, with fluvastatin, pravastatin, lovastatin, and simvastatin having about 33%, 50%, 60%, and 85% of the efficacy of atorvastatin, respectively, at the same dose in the same patients.     

Antioxidant supplements block the response of HDL to simvastatin-niacin therapy in patients with coronary artery disease and low HDL

One strategy for treating coronary artery disease (CAD) patients with low HDL cholesterol (HDL-C) is to maximally increase the HDL-C to LDL-C ratio by combining lifestyle changes with niacin (N) plus a statin. Because HDL can prevent LDL oxidation, the low-HDL state also may benefit clinically from supplemental antioxidants. Lipoprotein changes over 12 months were studied in 153 CAD subjects with low HDL-C randomized to take simvastatin and niacin (S-N), antioxidants (vitamins E and C, beta-carotene, and selenium), S-N plus antioxidants (S-N+A), or placebo. Mean baseline plasma cholesterol, triglyceride, LDL-C, and HDL-C levels of the 153 subjects were 196, 207, 127, and 32 mg/dL, respectively. Without S-N, lipid changes were minor. The S-N and S-N+A groups had comparably significant reductions (P相似文献   

Effect of levothyroxine on total lipid profiles as assessed by analytical capillary isotachophoresis in a patient with hypothyroidism

The patient was a 51-year-old Japanese female who had been diagnosed with hyperlipidemia. At the first medical examination, her serum levels of total cholesterol (TC) and triglyceride (TG) were 482 and 205 mg/dl, respectively. Since hyperlipidemia was not improved by pravastatin, atorvastatin or niceritrol, and since the levels of thyroid-stimulating hormone (TSH) and free T4 were 730 IU/ml and 0.3 ng/dl, respectively, the patient was diagnosed as secondary hyperlipidemia with hypothyroidism. A method for the charge isolation of lipoproteins using capillary isotachophoresis (cITP) is proposed as a clinical application because it allows us to quantitatively measure electronegative low-density lipoprotein cholesterol (LDL-C), a potent marker of coronary heart disease. After 5 months of treatment with levothyroxine, Serum TC and LDL-C levels drastically decreased without statin treatment and high-density lipoprotein cholesterol (HDL-C) increased. In the lipoprotein profiles as assessed by cITP after treatment with levothyroxin, all HDL-C subfractions were increased and fast-migrating LDL/electronegative LDL appeared to be greatly reduced after treatment, while the area under the non-modified LDL peak was increased. The cITP analysis was able to obtain more information about coronary risk factors and may be clinically useful for evaluating the effect of treatment with levothyroxine in patients with hypothyroidism and secondary hyperlipidemia.     

Anti-oxidative effect of fluvastatin in hyperlipidemic type 2 diabetic patients

An open-label prospective cross-over trial was performed to evaluate the antioxidative effect of fluvastatin in Japanese type 2 diabetics with hyperlipidemia. The study subjects were 10 patients who were on pravastatin (10 mg/day) or simvastatin (5 mg/day). After at least 12 weeks of continuous pravastatin or simvastatin therapy, the drugs were washed out for 12 weeks and replaced with fluvastatin (30 mg/day), then the treatment was continued for another 12 weeks. Total cholesterol and LDL cholesterol were efficiently and comparably reduced by all three statin agents. There were no differences in serum parameters of oxidative stress such as malondialdehyde-modified low-density lipoprotein, thiobarbituric acid-reactive substances, and 8-iso-prostaglandin F2alpha between pravastatin/simvastatin and fluvastatin. However, fluvastatin, but not pravastatin/simvastatin, significantly reduced 3,5,7-cholestatriene in erythrocyte membrane, representing the extent of membrane cholesterol peroxidation. Our data demonstrated that fluvastatin has a unique anti-oxidative effect in patients with type 2 diabetes and hyperlipidemia, compared with other statins.     

Effect of fluvastatin slow-release on low density lipoprotein (LDL) subfractions in patients with type 2 diabetes mellitus: baseline LDL profile determines specific mode of action

The objective of this study was to determine the effect of slow-release (XL) fluvastatin on low density lipoprotein (LDL) subfractions in type 2 diabetes. A multicenter, double-blind, randomized, parallel-group comparison of fluvastatin XL 80 mg (n = 42) and placebo (n = 47), each given once-daily for 8 wk, in 89 patients with type 2 diabetes (HbA1c: 7.2 +/- 1.0%, LDL cholesterol (LDL-C): 3.4 +/- 0.7 mmol/liter, high density lipoprotein cholesterol: 1.1 +/- 0.3 mmol/liter, and triglycerides (TG): 2.4 +/- 1.4 mmol/liter). At baseline and on treatment, plasma lipoproteins were isolated and quantified. Eight weeks of fluvastatin treatment decreased total cholesterol (-23.0%, P < 0.001), LDL-C (-29%, P < 0.001) and TG (-18%, P < 0.001), compared with placebo. At baseline, there was a preponderance of dense LDL (dLDL) (apolipoprotein B in LDL-5 plus LDL-6 > 25 mg/dl) in 79% of patients, among whom fluvastatin decreased all LDL subfractions, reductions in dLDL being greatest (-28%, P = 0.001; cholesterol in dLDL -29%). In patients with low baseline dLDL (apolipoprotein B in LDL-5 plus LDL-6 相似文献   

Lipid Lowering Therapy with Fluvastatin and Pravastatin in Patients with HIV Infection and Antiretroviral Therapy: Comparison of Efficacy and Interaction with Indinavir

Abstract. Background: Lipoprotein disorders in HIV-positive patients receiving highly active antiretroviral therapy (HAART) are becoming a major concern in HIV treatment, since there is growing evidence for an association between HAART-induced hyperlipidemia and increased cardiovascular risk. Yet relatively few data are available on the possible interactions of HAART and treatment with statins. Patients and Methods: In this prospective study, 25 HIV-positive, treatment-experienced patients (five female, 20 male, all Caucasian) were treated with either fluvastatin or pravastatin. Total cholesterol, low density lipoprotein (LDL) and high density lipoprotein (HDL) levels, and serum triglycerides were determined at regular intervals, as well as therapeutic drug monitoring to assess possible drug interactions. Results: In 13 pravastatin-treated patients, a decrease in total cholesterol levels (from 7.12 mmol/l to 6.29 mmol/l) after 12 weeks of therapy was seen. In 12 patients treated with fluvastatin, a permanent reduction of total cholesterol (from 6.46 mmol/l to 5.31 mmol/l) after 12 weeks was observed. The reduction of LDL levels was 30.2% in the fluvastatin group and 14.4% in the pravastatin group. In eight patients receiving an indinavir-containing HAART, indinavir plasma levels were not significantly influenced. No effect on triglycerides or HDL was observed. Conclusion: Fluvastatin and pravastatin are efficient in lowering total and LDL cholesterol levels in HIV-positive patients receiving HAART. Furthermore, no influence on indinavir plasma levels could be observed. Therefore, both compounds seem to be a viable treatment option in HAART-induced hypercholesterolemia.     

Serum lipid comparison in patients treated by statins or fibrates: existence of bad HDL-C responders to statins

INTRODUCTION: Major cardiac events are strongly associated with high levels of low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C). The HDL-C target level (40 mg/dl) is often not achieved with statins. The aim of this study was to compare the proportions of patients achieving the HDL-C target levels after one year of treatment with statins or fibrates. Furthermore, a subgroup with low HDL-C levels during statin treatment was investigated and suggestions are made for a better management of these patients. METHODS: A survey of lipid levels, cardiovascular disease and risk factors in 120 outpatients treated with a statin or a fibrate for hyperlipidaemia (total cholesterol (TC) > 250 mg/dl or triglycerides (TG) > 200 mg/dl after diet). After one year of treatment the proportions of patients achieving the target levels for TC, LDL-C, HDL-C,TG,TC/HDL-C and LDL-C/HDL-C are compared for statins and fibrates. RESULTS: The proportions of patients achieving the target lipid levels with statins or fibrates are comparable except for HDL-C. Compared to the baseline, the proportion of patients achieving the HDL-C target level of 40 mg/dl increases only by 8.3% for statins and by 42.9% for fibrates. In total, 38.5% of the statin group had low HDL-C-levels after one year of treatment. Among these patients, eight were treated with a fibrate before the statin and six were treated with a fibrate afterwards. In those 14 patients, mean HDL-C increased during fibrate treatment by 48.5% and TC/HDL-C and LDL-C/HDL-C decreased by 25.7 and 26.5%, respectively as compared with statins. CONCLUSIONS: Patients with low levels of HDL-C during statin treatment had far better levels of HDL-C, TC/HDL-C and LDL-C/HDL-C with fibrates. A randomised double-blind crossover trial with simvastatin and fenofibrate has been initiated to corroborate these findings.     

Association of apolipoprotein (Apo)E genotype with plasma apo E levels

The purpose of this study was to investigate the effects of apolipoprotein (apo) E genotype on plasma apo E levels as well as serum total, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride, and glucose values in 734 middle-aged and elderly, female and male subjects. Apo E allele frequencies were similar to those reported in other Caucasian populations. After adjustment for medications, alcohol use, smoking, age, and body mass index, apo E genotype was noted to have significant effects on apo E, total cholesterol, LDL cholesterol, and glucose levels in females, and on apo E, LDL cholesterol, and HDL cholesterol levels, as well as the total cholesterol (TC)/HDL cholesterol ratio in males. Female and male subjects with the apo E4 allele had significantly (P<0.05) lower plasma apo E (25 and 15%) and higher LDL cholesterol levels (5 and 2%), while those with the apo E2 allele had significantly (P<0.05) higher apo E (32 and 27%) and lower LDL cholesterol levels (10 and 10%) than the apo E3/3 group. Moreover, female apo E4 carriers had significantly (P<0.05) lower glucose values (11%) than the apo E3/3 group. These data are consistent with the concept that, in addition to the well known effects of apo E genotype on LDL-C values, this locus plays a very significant role in modulating plasma apo E levels.     

Lipid‐Altering Efficacy of Ezetimibe/Simvastatin 10/20 mg Compared to Rosuvastatin 10 mg in High‐Risk Patients with and without Type 2 Diabetes Mellitus Inadequately Controlled Despite Prior Statin Monotherapy

Aims: This post hoc analysis compared the effects of switching to ezetimibe/simvastatin 10/20 mg (EZE/SIMVA) or rosuvastatin 10 mg (ROSUVA) in uncontrolled high‐risk hypercholesterolemic patients with/without type 2 diabetes mellitus (T2DM) despite statin monotherapy. Methods: Patients (n = 618) at high risk for coronary vascular disease with elevated LDL‐C ≥100 and ≤190 mg/dL despite use of statins were randomized 1:1 to double‐blind EZE/SIMVA 10/20 mg or ROSUVA 10 mg for 6 weeks. Patients were classified as having T2DM based on ≥1 of the following: diagnosis of T2DM, antidiabetic medication, or FPG ≥126 mg/dL. This analysis evaluated percent changes from baseline in lipids among patients with (n = 182) and without T2DM (n = 434). Results: EZE/SIMVA was more effective than ROSUVA at lowering LDL‐C, TC, non‐HDL‐C, and apo B in the overall study population and within both subgroups. Numerically, greater between‐treatment reductions in LDL‐C, TC, non‐HDL‐C, and apo B were seen in patients with T2DM versus those without T2DM. A significant interaction (P= 0.015) was seen for LDL‐C indicating that patients with T2DM achieved larger between‐group reductions versus those without T2DM. Conclusions: Switching to EZE/SIMVA 10/20 mg versus ROSUVA 10 mg provided superior lipid reductions in patients with/without T2DM.     

Lipid-altering efficacy and safety profile of combination therapy with ezetimibe/statin vs. statin monotherapy in patients with and without diabetes: an analysis of pooled data from 27 clinical trials

Aim: This post hoc analysis compared the lipid‐altering efficacy and safety of ezetimibe 10 mg plus statin (EZE/statin) vs. statin monotherapy in hypercholesterolaemic patients with and without diabetes. Methods: A pooled analysis of 27 previously published, randomized, double‐blind, active‐ or placebo‐controlled clinical trials comprising 21 794 adult patients with (n = 6541) and without (n = 15253) diabetes receiving EZE/statin or statin alone for 4–24 weeks evaluated percentage change from baseline in lipids and other parameters. Consistency of the treatment effect across the subgroups was tested using treatment × subgroup interaction. No multiplicity adjustments were made. Results: Treatment effects within both subgroups were generally consistent with the overall population. EZE/statin was more effective than statin alone in improving low‐density lipoprotein cholesterol (LDL‐C), total cholesterol (TC), high‐density lipoprotein cholesterol (HDL‐C), triglycerides (TGs), non‐HDL‐C, apolipoprotein (apo) B and high‐sensitivity C‐reactive protein (hs‐CRP) in the overall population and both subgroups. Patients with diabetes achieved significantly larger reductions in LDL‐C, TC and non‐HDL‐C compared with non‐diabetic patients. Incidences of adverse events or creatine kinase elevations were similar between groups. A small but significantly higher incidence of alanine aminotransferase or aspartate aminotransferase elevations was seen in patients receiving EZE/statin (0.6%) vs. statin monotherapy (0.3%) in the overall population. Conclusions: Treatment with EZE/statin vs. statin monotherapy provided significantly larger reductions in LDL‐C, TC, TG, non‐HDL‐C, apo B and hs‐CRP and significantly greater increases in HDL‐C, with a similar safety profile in patients with and without diabetes. Reductions in LDL‐C, TC and non‐HDL‐C were larger in patients with diabetes than in patients without diabetes.     

普伐他汀对红细胞膜n-6、n-3脂肪酸成分影响的研究

目的　观察普伐他汀对原发性高脂血症患者红细胞膜 n3、n6脂肪酸成分的影响。方法　 32例原发性高脂血症患者应用普伐他汀 10 m g qd,采用自身对照的方法分别于治疗前、治疗后 6周及 12周时测定患者血浆脂质成分 ,并用气相色谱法测定红细胞膜脂肪酸成分。结果　本组患者经治疗后胆固醇 (TC)、三酰甘油 (TG)、低密度脂蛋白胆固醇 (L DL- C)、载脂蛋白 B10 0 (apo B10 0 )均明显降低 (P<0 .0 5～ 0 .0 0 1) ;高密度脂蛋白胆固醇 (HDL- C)均升高 (P<0 .0 5～ 0 .0 0 1) ,红细胞膜 n- 6脂肪酸 ,以花生四烯酸为代表 (AA )显著降低 (P<0 .0 1) ,n- 3脂肪酸 ,即廿碳五烯酸 (EPA)和廿二碳六烯酸 (DHA )均显著升高 (P<0 .0 1)。 n- 6 / n- 3比值有降低 ,TC、TG、L DL - C下降与红细胞膜 AA / EPA、AA/ DHA比值降低呈显著正相关 (P<0 .0 1)。结论　普伐他汀在有效调节血脂的同时能调节红细胞膜 n3、n6脂肪酸成分     

老年患者应用不同类型他汀类药物的疗效及安全性评价

目的观察不同剂量和类型他汀类药物在老年高脂血症患者中应用的疗效与安全性。方法回顾性分析456例老年高脂血症患者服用他汀类药物情况,根据服药情况分为:阿托伐他汀组(169例)、辛伐他汀组(110例)、普伐他汀组(137例)和氟伐他汀组(40例);又根据《中国成人血脂异常防治指南》将患者分为中危(41例)、高危(232例)和极高危(183例)。观察治疗8周后血脂水平及不良反应。结果与治疗前比较,阿托伐他汀组、辛伐他汀组、普伐他汀组和氟伐他汀组治疗8周后血清TC、LDL-C水平均明显降低(P0.05,P0.01)。4组治疗前后血清TG水平差异无统计学意义(P0.05)。阿托伐他汀组、辛伐他汀组治疗8周后血清TC、LDL-C变化率与普伐他汀组、氟伐他汀组比较差异有统计学意义(P0.05)。各组中高危患者服用标准剂量他汀类药物治疗后,LDL-C达标率均在80%以上,极高危患者达标率为44.1%～55.7%。结论多数老年高脂血症患者服用小剂量和(或)标准剂量他汀类药物血脂即可达标。且治疗安全性好,无严重不良反应发生。     

氟伐他汀对高脂血症患者血小板CD 6 2p的影响

目的探讨氟伐他汀对高脂血症患者血小板活化功能的影响。方法测定30例高胆固醇血症和混合性高脂血症患者(治疗组)降脂治疗前和治疗(氟伐他汀20mg／d)4周、8周后及30例健康者(对照组)的总胆固醇、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇及血小板表面激活标记物CD62p。结果治疗组患者CD62p较对照组明显增高(P<0．01),氟伐他汀治疗4周,8周后CD62p较治疗前明显下降(P<0．01)。结论氟伐他汀治疗高胆固醇血症患者,在降脂的同时,可抑制血小板活性。