A multicenter, randomized, double-blind clinical trial comparing the low-density lipoprotein cholesterol-lowering ability of lovastatin 10, 20, and 40 mg/d with fluvastatin 20 and 40 mg/d

BACKGROUND: The available statin drugs have similar pharmacodynamic properties but are not equal in low-density lipoprotein cholesterol (LDL-C)-lowering efficacy. OBJECTIVE: The aim of this study was to compare the effects of lovastatin and fluvastatin in lowering LDL-C. METHODS: This was a prospective, randomized, double-blind study of patients aged >20 years with primary hypercholesterolemia conducted at 44 clinical sites across the United States. After a 6-week National Cholesterol Education Program (NCEP) Step I diet lead-in period in patients taking lipid-lowering drugs at screening, patients were randomized to receive lovastatin 10, 20, or 40 mg/d or fluvastatin 20 or 40 mg/d (the doses available at the time the study was conducted) for 6 weeks. Patients not taking lipid-lowering drugs at screening and who had been following the Step I diet for at least 6 weeks proceeded to the treatment phase. All patients received instruction for a Step I diet, which they followed throughout the treatment phase. After the treatment period, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), LDL-C, and triglycerides were measured, and TC:HDL-C and LDL-C:HDL-C ratios were calculated. RESULTS: A total of 838 patients (476 men, 362 women; mean [SD] age, 59 [12] years) were included in the study. Lovastatin 20 and 40 mg/d significantly reduced mean LDL-C compared with the same dosages of fluvastatin. TC and the LDL-C:HDL-C ratio decreased more with lovastatin than with fluvastatin at a given dose level. Approximately 50% of patients treated with lovastatin 20 and 40 mg/d compared with approximately 25% treated with fluvastatin 20 and 40 mg/d reached NCEP Adult Treatment Panel II LDL-C goals. CONCLUSION: In this small study population of patients with primary hypercholesterolemia taking lipid-lowering drugs, short-term (6-week) treatment with lovastatin was more efficacious than fluvastatin in lowering cholesterol levels and reaching LDL-C treatment goals.     

Effect of APOE genotype on lipid levels in patients with coronary heart disease during a 3-week inpatient rehabilitation program

It has been suggested that the apolipoprotein E (APOE) genotype modifies the effect of dietary and pharmacological interventions for lowering lipid levels. We wanted to determine whether APOE genotyping information would be useful in making lipid-lowering treatment decisions in clinical practice. We included 981 patients with coronary heart disease (CHD) enrolled in an inpatient 3-week standardized rehabilitation program. Of these, 555 (57%) patients received continued statin therapy and 232 (24%) patients received newly initiated statin therapy. Dietary intervention was part of the program only for 194 (20%) patients. Total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC) levels decreased in all the groups of patients during rehabilitation. The decreases were less pronounced among the APOE E2 carriers. However, the observed variation among the groups with respect to reduction of lipid levels was accounted for mainly by the initial lipid levels (30-47%) and only marginally on the APOE genotype (1%) . We therefore found no evidence that APOE genotyping will be useful in guiding dietary or pharmacological lipid-lowering treatment decisions.     

Drug therapy for lipid disorders. Selecting appropriate lipid-lowering agents

Lipid abnormalities can be treated effectively with various lipid-lowering agents. However, it bears repeating that no patient with hyperlipidemia should be treated with drugs until an adequate trial of dietary intervention, which may take as long as six months, has been attempted. While knowledge of a patient's precise metabolic and genetic abnormality is often desirable, it generally is not necessary for the institution of lipid-lowering drug therapy. Judicious use of total cholesterol, high-density lipoprotein cholesterol, and total triglyceride measurements is sufficient for selection of the proper drug or drugs. A patient who does not respond should be referred to a specialized lipid center for more sophisticated evaluation and therapy.     

Twelve-week, multicenter, randomized, open-label comparison of the effects of rosuvastatin 10 mg/d and atorvastatin 10 mg/d in high-risk adults: a DISCOVERY study

BACKGROUND: Guidelines for the prevention of coronary heart disease (CHD) advocate reductions in low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) levels as the primary goals. However, approximately 50% to 60% of patients fail to reach recommended cholesterol goals. OBJECTIVES: The primary objective of this Direct Statin Comparison of LDL-C Values: An Evaluation of Rosuvastatin Therapy Compared with Atorvastatin (DISCOVERY) trial was to compare the efficacy of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors rosuvastatin calcium and atorvastatin calcium in achieving the 1998 Second Joint Task Force (JTF) of European and Other Societies on Coronary Prevention target for LDL-C. Secondary objectives included comparing the efficacy of rosuvastatin and atorvastatin in achieving the 1998 JTF-recommended goal for TC and modifying other lipid levels, and to compare the tolerability of the 2 statins. METHODS: This 12-week, randomized, open-label, 2-arm, parallel-group trial was conducted at 210 centers in Finland, Iceland, and Ireland. Patients aged > or =18 years with a high risk for CHD and primary hypercholesterolemia (LDL-C >3.5 mmol/L [>135 mg/dL]) were randomized (2:1) to receive rosuvastatin 10 mg or atorvastatin 10 mg PO OD for 12 weeks. Before randomization, statin-naive patients underwent 6 weeks of dietary counseling, whereas patients receiving treatment with a starting dose of another lipid-lowering therapy but with an LDL-C level >3.1 mmol/L (>120 mg/dL) were switched to study drug immediately after they were determined eligible for the study Patients were assessed for fasting lipid levels at weeks 0 and 12, and the proportions of patients attaining 1998 and 2003 JTF lipid goals (1998: LDL-C, <3.0 mmol/L [<116 mg/dL]; TC, <5.0 mmol/L [<193 mg/dL]; 2003: LDL-C, <2.5 mmol/L [<97 mg/dL]; TC, <4.5 mmol/L [<174 mg/dL]) were calculated. Tolerability was monitored for the 12-week study and for an additional 36-week optional extension period. RESULTS: One thousand twenty-four patients were randomized to treatment (568 men, 456 women; mean age, 60.7 years). Patient demographic characteristics were similar between the 2 treatment groups. The efficacy analysis consisted of 911 patients (504 men, 407 women; mean age, 60.7 years; mean body weight, 82.4 kg); 627 received rosuvastatin and 284 received atorvastatin. Compared with atorvastatin, rosuvastatin was associated with significantly greater reductions in LDL-C and TC (both, P < 0.05), and with a significantly greater increase in high-density lipoprotein cholesterol level (P < (105). A greater proportion of patients in the rosuvastatin group compared with the atorvastatin group reached the 1998 goals for LDL-C (83.4% vs 683%; P < 0.001) and TC (76.4% vs 59.5%; P < 0.001). Also, compared with the atorvastatin group, greater proportions of patients in the rosuvastatin group achieved the 2003 JTF goals for LDL-C and TC (both, P < 0.001). Both agents were well tolerated: serious drug-related events were observed in < or =3.0% of patients in each group, and no clinically significant differences were found between the 2 treatment groups. CONCLUSIONS: In this study of selected patients at high risk for CHD and with primary hypercholesterolemia, rosuvastatin 10 mg/d for 12 weeks was associated with significantly greater reductions in LDL-C and TC levels compared with atorvastatin 10 mg/d. Furthermore, significantly more patients receiving rosuvastatin achieved the 1998 and 2003 JTF-recommended lipid targets compared with those receiving atorvastatin. Both agents were well tolerated.     

Effect of Pravastatin in the Treatment of Patients with Type III Hyperlipoproteinemia

OBJECTIVE: To determine the efficacy and safety of pravastatin in the treatment of subjects with Type III hyperlipoproteinemia. DESIGN: Randomized, double-blind, placebo-controlled, crossover study. SETTING: Four lipid research clinics in the United States. PATIENTS: Twenty subjects between 18 and 70 years old with three diagnostic features of Type III hyperlipoproteinemia: very-low-density lipoprotein cholesterol (VLDL-C)/total plasma triglyceride ratio in excess of 0.30; beta-migrating VLDL pattern on agarose-gel electrophoresis; and the homozygous apolipoprotein E phenotype E(2)/E(2). After 4 weeks of dietary control, the subjects were eligible if their mean plasma total cholesterol level was at least 250 mg/dl and mean plasma trigylceraide level was at least 220 mg/dL. INTERVENTIONS: Subjects were randomly assigned to pravastatin 40 mg hs or placebo hs at the start of the first 6-week double-blind treatment period. After completing this phase, subjects entered a 4-week placebo/drug washout phase before crossing over to the opposite treatment for the second 6-week double-blind treatment period. MEASUREMENTS: Plasma VLDL-C and low density lipoprotein cholesterol (LDL-C) after ultracentrifugation and total triglyceride, cholesterol and high-density lipoprotein cholesterol (HDL-C) after 6 weeks of treatment; adverse clinical events and abnormal laboratory results. RESULTS: After 6 weeks of pravastatin theraphy, plasma levels of VLDL-C and LDL-C decreased 49% and 39%, respectively (p less-than-or-equal 0.01 vs. placebo). Total cholesterol and triglyceride concentrations decreased 36% and 22%, respectively (p less-than-or-equal 0.001 vs. placebo). Levels of HDL-C increased 8% (p less-than-or-equal 0.01 vs. placebo). Pravastatin was tolerated well. One marked laboratory abnormality, an asymptomatic elevation of creatine phosphokinase, resolved upon completing pravastatin treatment. CONCLUSIONS: Pravastatin lowers plasma VLDL-C, LDL-C, total cholesterol, and triglyceride and raises HDL-C in subjects with Type III hyperlipoproteinemia. The safety profile is excellent. Pravastatin reductase inhibitor therapy affords a useful approach to the management of Type III or remnant removal disease.     

Effects of high-intensity endurance and resistance exercise on HIV metabolic abnormalities: a pilot study

The purposes of this pilot study were to examine the effects of a 16-week supervised high-intensity combined endurance and resistance exercise training program on HIV-associated metabolic abnormalities (abdominal adiposity, dyslipidemia, and insulin resistance) and to explore methodological issues related to the design and implementation of the research protocol in preparation for a randomized controlled trial. A one-group pretest-posttest design was used, with outcomes measured at baseline and within 1 week after the conclusion of the training program. The exercise program consisted of 16 weeks (preceded by a 2-week phase-in period) of three endurance sessions (20 min at 70%-80% of VO (2max)) and two resistance sessions per week (one set of 8-10 repetitions at 80% of one-repetition maximum on seven exercises). Outcome measures included lipid levels (total, high-density lipoprotein, and low-density lipoprotein cholesterol and triglycerides), visceral and subcutaneous adipose area measured by electron beam tomography, fat and lean mass of trunk and limbs measured by dual-energy X-ray absorptiometry, and insulin sensitivity measured by the homeostatic model assessment. Nine participants were recruited, 5 of whom completed the intervention and had pretest and posttest data available for analyses. Aerobic capacity and strength improved over the course of the intervention. Statistically significant decreases were found for total and trunk fat mass (1,324.9 g [+/-733.6] and 992.8 g [+/-733.6], respectively). Triglycerides decreased by 59 mg/dL (+/-69.88), and insulin sensitivity decreased by 15.7% (+/-41.7%), neither of which was a statistically significant change. Results suggest that further testing of the combined exercise intervention in a randomized controlled design is warranted.     

Dietary management of hyperlipidemia

The atherogenic effects of low-density lipoprotein cholesterol (LDL-C) and the relationship between high levels of LDL-C and coronary heart disease are well established. The article briefly reviews significant research that has provided the rationale for dietary intervention in hyperlipidemia. The focus is the principles of dietary treatment and their clinical application. Methods of counseling and instruction aimed at lowering fat, cholesterol, and calorie consumption and strategies to improve patient compliance are discussed.     

Comparison of the efficacy and tolerability of pitavastatin and atorvastatin: an 8-week, multicenter, randomized, open-label, dose-titration study in Korean patients with hypercholesterolemia

BACKGROUND: Although previous studies have examined the efficacy of pitavastatin, its tolerability and effects on lipid concentrations have not been compared with those of atorvastatin in a multicenter, randomized study. OBJECTIVE: This trial compared the efficacy and tolerability of pitavastatin and atorvastatin in hypercholesterolemic Korean adults. METHODS: This 8-week, multicenter, randomized, open-label, dose-titration study was conducted at 18 clinical centers in Korea between May 2005 and February 2006. After a 4-week dietary lead-in period, patients with hypercholesterolemia were randomized to receive either pitavastatin 2 mg/d or atorvastatin 10 mg/d. Patients who had not reached the low-density lipoprotein cholesterol (LDL-C) goal by week 4 received a double dose of the assigned medication for an additional 4 weeks. Efficacy was evaluated in terms of achievement of the National Cholesterol Education Program Adult Treatment Panel III LDL-C goals and changes from baseline in other lipids and high-sensitivity C-reactive protein (hs-CRP). The tolerability profile was assessed by physical and electro-cardiographic examinations, laboratory tests, and recording adverse reactions at all visits. RESULTS: A total of 268 patients were randomized to treatment, and 222 (82.8%) completed the study (149 women, 73 men; mean age, 59 years; mean weight, 63.5 kg). At the end of the study, there was no significant difference between the pitavastatin and atorvastatin groups in the proportion of patients achieving the LDL-C goal (92.7% [102/110] vs 92.0% [103/112], respectively). In addition, there were no significant differences between groups in terms of the percent changes from baseline in LDL-C, total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), or hs-CRP. Twenty-six of 136 patients (19.1%) taking pitavastatin reported 35 treatment-emergent adverse reactions; 33 of 132 patients (25.0%) taking atorvastatin reported 39 treatment-emergent adverse reactions. Elevations in creatine kinase were observed in 6 patients (4.4%) in the pitavastatin group and 7 patients (5.3%) in the atorvastatin group. There were no serious adverse drug reactions in either group. CONCLUSIONS: In these adult Korean patients with hypercholesterolemia, pitavastatin and atorvastatin did not differ significantly in terms of the proportions of patients achieving the LDL-C goal; reductions in LDL-C, total cholesterol, and triglycerides; or increases in HDL-C. Both drugs were well tolerated.     

The risk groups for coronary heart disease in Koreans. Assessment by distribution of serum lipid concentrations.

Coronary heart disease is the most severe form of disease caused by atherosclerosis; and there is a strong relationship between serum lipid concentrations and atherosclerosis. By decade of life, means, standard deviations and selected percentiles were calculated according to sex for serum concentrations of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglyceride in 69,563 Koreans. The prevalence of dyslipoproteinemias which were related to high risk of coronary heart disease were assessed. The mean concentrations of serum total cholesterol and LDL-C in the Korean population were 5.02 mmol/l and 3.00 mmol/l. The 75th and 90th percentile concentrations of total cholesterol were 5.59 mmol/l and 6.24 mmol/l. The mean concentrations of serum triglyceride and HDL-C were 1.58 mmol/l and 1.30 mmol/l. The hyperlipoproteinemia type IV (4.8%) was the most frequent, followed by Type IIa (4.6%), hypoalphalipoproteinemia (3.3%), and type IIb (0.2%). According to the National Cholesterol Education Program Adult Treatment Panel II, 4.1% of Korean adults needed the initial drug therapy and 10.8% the initial dietary therapy for hypercholesterolemia. The age and sex-specific treatment guidelines for hypercholesterolemia would make it possible that early intervention could be applied to atherosclerosis in Korean adults.     

Comparative effects of simvastatin and lovastatin in patients with hypercholesterolemia. The Simvastatin and Lovastatin Multicenter Study Participants.

The efficacy, safety profile, and tolerability of the HMG-CoA reductase inhibitors simvastatin and lovastatin were compared in a multicenter, randomized, double-blind study in patients with moderate hypercholesterolemia. Commonly prescribed doses of these two drugs were used by 544 men and women, who followed an American Heart Association phase I diet during a 6-week baseline period and for the 24 weeks of active treatment. Simvastatin 10 mg and lovastatin 20 mg produced statistically significant reductions in total and low-density lipoprotein cholesterol (LDL-C). Patients receiving simvastatin 10 mg once daily and lovastatin 20 mg once daily experienced similar reductions in LDL-C and total cholesterol; however, simvastatin 20 mg was statistically superior to lovastatin 40 mg in decreasing these lipid fractions. For all treatment groups, increases in high-density lipoprotein cholesterol were inversely related to baseline levels. Moderate decreases in triglycerides occurred with all doses. Lipoprotein(a) levels, measured in a subset of patients, were similar before and after treatment. Both drugs were well tolerated.     

Effectiveness and tolerability of ezetimibe in patients with primary hypercholesterolemia: pooled analysis of two phase II studies

BACKGROUND: Ezetimibe (SCH 58235) is a novel cholesterol absorption inhibitor that selectively and potently blocks intestinal absorption of dietary and biliary cholesterol. OBJECTIVE: Data from 2 multicenter, placebo-controlled, double-blind, randomized, parallel-group, 12-week studies of ezetimibe were pooled to evaluate the drug's effect on lipid parameters in patients with primary hypercholesterolemia. METHODS: After dietary stabilization (National Cholesterol Education Program Step I diet or a stricter diet), washout of lipid-altering drugs, and a 6-week placebo lead-in period, patients with baseline plasma low-density lipoprotein cholesterol (LDL-C) levels > or = 130 and < or = 250 mg/dL and plasma triglyceride (TG) levels < or = 300 mg/dL were randomized to receive either ezetimibe 0.25, 1, 5, or 10 mg, or placebo administered once daily before the morning meal in study A (dose-response study) or ezetimibe 5 or 10 mg or placebo administered once daily before the morning meal or at bedtime in study B (dose-regimen study). RESULTS: A total of 432 patients were included in this pooled analysis, 243 in study A and 189 in study B. The 5- and 10-mg doses of ezetimibe significantly reduced LDL-C levels by 15.7% and 18.5%, respectively (P < 0.01 vs placebo) and significantly increased high-density lipoprotein cholesterol (hDL-C) levels by 2.9% and 3.5%, respectively (P < 0.05 vs placebo). A reduction in plasma TG levels was observed (P = NS). With the 10-mg dose of ezetimibe, 67.8% of patients achieved > or = 15% reduction in plasma LDL-C levels, and 22.0% achieved > or = 25% reduction. With the 5-mg dose, 54.0% of patients achieved > or = 15% reduction in plasma LDL-C levels, and 15.3% achieved > or = 25% reduction. The decrease in plasma LDL-C levels was significantly greater with ezetimibe 10 mg compared with ezetimibe 5 mg (P < 0.05). Ezetimibe was well tolerated, with an adverse event profile similar to that of placebo. Conclusions: In these two 12-week studies, ezetimibe significantly decreased plasma LDL-C levels and increased plasma HDL-C levels, with a tolerability profile similar to that of placebo.     

Effects of glyburide treatment on serum lipoprotein and apolipoprotein concentrations and ratios in non-insulin-dependent diabetes mellitus

Lipoproteins and apolipoproteins were studied in 28 patients with newly detected non-insulin-dependent diabetes mellitus (NIDDM) before and after combined dietary and glyburide treatment. The patients, aged 33 to 67 years and without coronary or other atherosclerotic diseases, displayed fasting blood sugar levels of over 140 mg/dl after four weeks of dietary treatment. Overnight fasting blood samples were collected before the beginning of the trial, after four weeks of dietary treatment, and after four and eight weeks of combined dietary and glyburide treatment. The pretrial levels of total serum cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1 and A2, and apolipoprotein B were similar to or even lower than those of nondiabetics; however, high-density lipoprotein cholesterol (HDL-C) levels and HDL-C% (the percentage of TC bound to HDL) were significantly lower in the diabetic patients. After combined dietary and glyburide treatment and normalization of blood sugar, apolipoprotein A1 and A2, HDL-C levels, and HDL-C% increased significantly. TC, TG, and LDL-C levels, although not exceeding the normal range, decreased significantly. HDL-C2 and HDL-C3 levels also increased, but the differences did not reach significance. Among the lipid, lipoprotein, and apolipoprotein ratios in the patients, only the ratios HDL-C:LDL-C, apolipoprotein A1:apolipoprotein B, and HDL-C: apolipoprotein B increased significantly as a result of the opposing responses of the protective lipoprotein HDL-C and apolipoprotein A1 and the atherogenic lipoprotein LDL-C and apolipoprotein B. The results demonstrate the favorable effects of combined dietary and sulphonylurea drug treatment on lipoproteins and apolipoproteins in NIDDM patients, thereby reducing coronary and atherosclerotic risks.     

Management of dyslipidaemia in HIV-infected patients receiving antiretroviral therapy

Dyslipidaemia associated with the treatment of HIV infection, particularly with the use of protease inhibitors (PIs), can raise cholesterol and triglyceride (TG) levels to the thresholds indicated for intervention. Recent evidence from epidemiological studies has shown that there are correlations between antiretroviral drug use and increased risks for, and incidences of, cardiovascular disease, including myocardial infarction and coronary heart disease. The primary goals of dyslipidaemia therapy for HIV patients are reductions of both low-density lipoprotein cholesterol (LDL-C) and markedly elevated TG levels. Dietary strategies and exercise programs may be tried, although these have shown inconsistent results. The two options for drug therapy are switching antiretroviral agents and using lipid-lowering drugs. Each approach is associated with advantages and limitations, and the need to maintain viral suppression must be balanced with the need to treat abnormal lipid levels. Most drug switches replace the PI component with drugs from another antiretroviral class. Selection of drug therapy for lipid lowering depends on the type of dyslipidaemia predominating and the potential for drug interactions. The use of the statins pravastatin and atorvastatin is recommended for the treatment of patients with elevated LDL-C levels and gemfibrozil or fenofibrate for patients with elevated TG concentrations. Development of new PIs with more favourable effects on the lipid profile should be of benefit.     

SCREENING AND TREATMENT FOR HYPERUPIDAEMIA IN NON-INSULIN-DEPENDENT DIABETES: A PROSPECTIVE ASSESSMENT OF 350 PATIENTS

SUMMARY This report presents experiences in screening 350 non-insulin-dependent diabetics for hypercholesterolemia and results of 1 year's treatment. Mean serum total cholesterol was 6.4 mmol/l at screening; 46 patients whose initial total serum cholesterol was above 7.0 mmol/l attended for detailed assessment and treatment. Mean total cholesterol concentrations fell between screening and review (7.8 vs 7.1 mmol/l, P<0.01). Levels fell below 7.0 mmol/l in 13 patients with diet alone. After excluding patients with secondary dyslipidaemia (including poor diabetic control), 10 patients received lipid-lowering drug treatment. Total cholesterol and triglyceride concentrations fell significantly and the HDL/non- HDL cholesterol ratio improved on treatment. Screening diabetic patients identifies a small group of hyperlipidaemic patients, whose lipoprotein profiles improve with drug treatment. Many of those screened, however, do not ultimately require drug treatment using a cut-off of 7.0 mmol/l.     

Relationship of apolipoprotein B levels to the number of risk factors for metabolic syndrome.

Low-density lipoprotein cholesterol (LDL-C) is the primary target of lipid-lowering therapy. However, all lipoproteins containing apolipoprotein B (apo B) appear to be atherogenic. Preferred targets of therapy therefore may include either the cholesterol in all apo B-containing lipoproteins (non-high-density lipoprotein cholesterol [non-HDL-C]) or total apo B itself. Apo B can be measured by three methods: chemically, by nuclear magnetic resonance (NMR), and by immunoassay. This study compares the first two methods as a function of the number of metabolic risk factors in patients with metabolic syndrome. Plasma lipid, lipoprotein cholesterol, and apo B levels were measured in 274 adults with varying numbers of metabolic syndrome components. Low-density lipoprotein (LDL) particle sizes were measured by gel electrophoresis and by NMR. Total apo B was estimated chemically and by conversion of NMR lipoprotein particle number, assuming one apo B molecule per lipoprotein particle. As the number of metabolic syndrome components increased, apo B rose by both chemical and NMR methods, but by chemical methods, increases were in the triglyceride-rich fraction, whereas by NMR, they were in LDL. The correlation between total apo B measured by the two methods was only moderate (r = .73). Further, non-HDL-C was more highly correlated with total apo B measured chemically than either LDL-C or total apo B by NMR. Non-HDL-C correlates highly with total apo B in patients with metabolic syndrome and had advantages as a target of therapy over LDL-C or NMR apo B.     

Dyslipidemia prevalence in a laboratory initiated screening program.

OBJECTIVE: Evaluate utilization and diagnosis rates in a self-pay, self-referred screening program for dyslipidemia. DESIGN: 301 patients self-referred to the clinical laboratory for lipid testing in a two-year period. The patient population that participated was characterized in terms of insurance status, gender, age, and known cardiovascular risk factors. Lipid profiles were characterized as measured by total cholesterol, triglycerides (TGs), low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL), and total cholesterol to HDL risk factor. SETTING: Clinical laboratory in an academic medical center. PATIENTS: Data from all patients that self-selected for screening were included. INTERVENTIONS: Immediate laboratory results with both verbal and written interpretations and recommendations were provided to the patients. MAIN OUTCOME MEASURES: Age, gender, insurance status, number of known risk factors, and lipid profiles in the subject group. RESULTS: The mean age of participants was 57 years. Men (197) outnumbered women (104) by almost 2:1; most (94%) had health insurance. At presentation, 44% of the patients had more than one risk factor for coronary heart disease (CHD). 151 individuals (50%) had lipid findings that would require at least dietary intervention by NCEP guidelines. CONCLUSION: A self-pay, self-referred screening program for lipid disorders is an effective means of improving screening and diagnosis rates. Patients with insurance were willing to pay for the convenience offered and men in particular were more likely to self-refer than women, independent of previous knowledge of risk factors or lipid disorders.     

短期运动和营养对肥胖少年部分代谢指标的影响

目的探讨不同干预手段对肥胖少年体质和部分代谢指标的影响。方法对94名超重和肥胖城区中学生分别实施为期10周的单纯营养、单纯运动以及运动结合营养的干预,比较受试者体质指标和部分代谢指标。结果运动、营养和运动结合营养干预均可降低体重指数、脂肪重量、体脂百分比,高密度脂蛋白胆固醇（HDL-C）水平下降。单纯运动组总胆固醇（TC）降低,空腹血清胰岛素（FINS）、胰岛素抵抗指数（HOMA-IR）、胰岛β细胞功能(HOMA-β)升高;单纯营养组TC、低密度脂蛋白胆固醇（LDL-C）降低;运动结合营养组TC、LDL-C降低,FINS、HOMA-β升高。结论10周运动结合营养改善血脂代谢的效果较好;运动、运动结合营养干预可有效改善超重/肥胖少年的胰岛素β细胞的分泌功能;但是3种干预方案对改善HDL-C及胰岛素抵抗的作用均不明显。     

Efficacy of atorvastatin for achieving cholesterol targets after LDL-cholesterol based dose selection in patients with type 2 diabetes

We analyzed the feasibility of an intensive lipid-lowering strategy based on a starting dose of atorvastatin according to baseline and target low-density lipoprotein cholesterol (LDL-C) level (<2.6 mmol/L) in 202 statin-na?ve patients with type 2 diabetes within 24 weeks. They were assigned to receive a daily dosage of atorvastatin based on their initial LDL-C levels. The primary endpoint was the proportion of patients achieving the LDL-C goal after 24 weeks of treatment. No changes were made in prescribed atorvastatin dosage. At the study end, 66.5% of the 188 patients completing the trial reached the LDL-C target (75%, 67%, 58% and 59% with 10, 20, 40 and 80 mg per day of atorvastatin, respectively) reached LDL-C target. Atorvastatin reduced the levels of total cholesterol, LDL-C, high density lipoprotein cholesterol (HDL-C) and triglycerides by 29%, 35%, 3% and 22%, respectively, and all statin doses were well tolerated. Thus, individualizing the starting dose of atorvastatin according to baseline and target LDL-C levels, allowed a high proportion of type 2 diabetic patients to achieve the target within 24 weeks.     

An evaluation of pharmaceutical treatment of dyslipidaemia among patients without diagnosed atherosclerotic disease in Belgium

The aim of this study was to assess the lipoprotein levels in patients without diagnosed atherosclerotic disease but treated with lipid-lowering drugs. During February and March 2002 all demands for continuation of reimbursement of lipid-lowering drugs were recorded at two regional offices of health insurance associations. A total of 1973 patients without diagnosed atherosclerotic disease were included (mean age 66 years). Mean total cholesterol (TC) was 5.39 mmol/l, high-density lipoprotein cholesterol (HDL-C) 1.50 mmol/l, low-density lipoprotein cholesterol (LDL-C) 3.16 mmol/l and triglycerides (TG) 1.59 mmol/l. Thirty-four per cent of the treated patients reached the TC target of 5.0 mmol/l or less. The LDL-C target level of 3.0 mmol/l or less was reached by 45% of the patients. Of the patients receiving a statin, 61% were not treated with the optimal doses. The treatment was adjusted in 15% of the patients who did not reach the combined endpoint.     

Efficacy of atorvastatin therapy in ischaemic heart disease - effects on oxidized low-density lipoprotein and adiponectin

The lipid-lowering and anti-atherosclerotic effects of atorvastatin (10 mg/day) were investigated by measuring changes in the levels of oxidized low-density lipoprotein (LDL), serum lipids (total cholesterol [TC], LDL-cholesterol [LDL-C] and triglycerides [TG]), and in the protein adiponectin. This was undertaken in 22 patients with ischaemic heart disease and serum LDL-C levels > 100 mg/dl. After 3 months of therapy, atorvastatin significantly decreased serum lipids, oxidized LDL was reduced from 457.0 +/- 148.6 to 286.9 +/- 88.5 nmol/l, and adiponectin increased from 9.7 +/- 7.4 to 13.9 +/- 9.98 microg/ml. No significant correlation was observed between adiponectin and LDL-C, TG and high-density lipoprotein cholesterol. Atorvastatin therapy was not associated with side-effects, such as myalgia and gastrointestinal disorders, and did not give abnormal laboratory test results. It is concluded that atorvastatin decreases serum lipid and oxidized LDL levels, and increases adiponectin levels in patients with ischaemic heart disease.