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Evan A Stein

Publications and source records attributed to Evan A Stein.

At least 19 recordsLinked to original sources
PubMed2006

Achieving LDL cholesterol, non-HDL cholesterol, and apolipoprotein B target levels in high-risk patients: Measuring Effective Reductions in Cholesterol Using Rosuvastatin therapY (MERCURY) II.

BACKGROUND: National Cholesterol Education Program Adult Treatment Panel III guidelines for patients at a high risk of coronary heart disease set a low-density lipoprotein cholesterol (LDL-C) target of < 100 mg/dL. This target can be difficult to attain with diet and current therapy. METHODS: In a 16-week multinational trial, 1993 high-risk patients were randomized to rosuvastatin 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg for 8 weeks. Patients either remained on starting treatment or switched to lower or milligram-equivalent doses of rosuvastatin for 8 more weeks. RESULTS: At 16 weeks, more patients achieved their LDL-C target by switching to rosuvastatin 10 mg than staying on atorvastatin 10 mg (66% vs 42%, P < .001) or simvastatin 20 mg (73% vs 32%, P < .001). Changing to rosuvastatin 20 mg brought more patients to their LDL-C target than staying on atorvastatin 20 mg (79% vs 64%, P < .001) or simvastatin 40 mg (84% vs 56%, P < .001). More very high risk patients achieved an LDL-C target of < 70 mg/dL when changed to rosuvastatin from atorvastatin or simvastatin (within-arm comparisons P < .01). More hypertriglyceridemic patients (triglycerides > or = 200 mg/dL) met LDL-C, non-high-density lipoprotein cholesterol (non-HDL-C), and apolipoprotein B targets by changing to rosuvastatin. Switching to rosuvastatin produced greater reductions in LDL-C, total cholesterol, non-HDL-C, apolipoprotein B, and lipid ratios. All treatments were well tolerated, with no differences among treatment groups in skeletal muscle, hepatic, or renal toxicity. CONCLUSION: Rosuvastatin 10 or 20 mg is an effective and safe therapeutic option for high-risk patients to achieve their lipid and apolipoprotein targets.

Aged↗
PubMed2005

Assessment of reaching goal in patients with combined hyperlipidemia: low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, or apolipoprotein B.

It is well established that patients with combined hyperlipidemia, defined as elevated triglyceride levels between 200 and 500 mg/dL and elevated low-density lipoprotein cholesterol >130 mg/dL, are at increased risk for coronary artery disease. The optimal assessment of reaching lipid goals in patients with combined hyperlipidemia is still far from settled and has been an area of revision and modification in recent guidelines. Although controversy remains as to the best single measurement to be used in treatment goals, current focus is on the use of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B. This article reviews the use of these 3 biomarkers in assessing cardiovascular risk, and the strategies for managing combined hyperlipidemia.

Apolipoproteins B↗
PubMed2004

Safety of rosuvastatin.

The safety and tolerability of rosuvastatin were assessed (as of August 2003) using data from 12,400 patients who received 5 to 40 mg of rosuvastatin in a multinational phase II/III program, which represented 12,212 patient-years of continuous exposure to rosuvastatin. An integrated database was used to examine adverse events and laboratory data. In placebo-controlled trials, adverse events, irrespective of causality assessment, occurred in 57.4% of patients who received 5 to 40 mg of rosuvastatin (n = 744) and 56.8% of patients who received placebo (n = 382). In fixed-dose trials with comparator statins, 5 to 40 mg of rosuvastatin showed an adverse event profile similar to those for 10 to 80 mg of atorvastatin, 10 to 80 mg of simvastatin, and 10 to 40 mg of pravastatin. Clinically significant elevations in alanine aminotransferase (>3 times the upper limit of normal) and creatine kinase (>10 times the upper limit of normal) were uncommon ( 10 times the upper limit of normal with muscle symptoms) that was possibly related to treatment occurred in <or=0.03% of patients who took rosuvastatin at doses <or=40 mg. A positive finding of proteinuria with dipstick testing at rosuvastatin doses <or=40 mg was comparable to that seen with other statins, and the development of proteinuria was not predictive of acute or progressive renal disease. No deaths in the program were attributed to rosuvastatin, and no rhabdomyolysis occurred in patients who received 5 to 40 mg of rosuvastatin. Rosuvastatin was well tolerated by a broad range of patients who had dyslipidemia, and its safety profile was similar to those of the comparator statins investigated in this extensive clinical program.

Adolescent↗
PubMed2004

Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial.

BACKGROUND: Non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein (apo) B, and lipid and apolipoprotein ratios that include both atherogenic and antiatherogenic lipid components have been found to be strong predictors of coronary heart disease risk. OBJECTIVE: The goal of this study was to examine prospectively the effects of rosuvastatin, atorvastatin, simvastatin, and pravastatin across dose ranges on non-HDL-C, apo B, apo A-I, and total cholesterol (TC):HDL-C, low-density lipoprotein cholesterol (LDL-C):HDL-C, non-HDL-C:HDL-C, and apo B:apo A-I ratios in patients with hypercholesterolemia (LDL-C > or =160 mg/dL and <250 mg/dL and triglycerides <400 mg/dL) in the Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin (STELLAR) trial. METHODS: In this randomized, Multicenter, parallel-group, open-label trial (4522IL/0065), patients > or =18 years of age received rosuvastatin 10, 20, 40, or 80 mg; atorvastatin 10, 20, 40, or 80 mg; simvastatin 10, 20, 40, or 80 mg; or pravastatin 10, 20, or 40 mg for 6 weeks. Pairwise comparisons were prospectively planned and performed between rosuvastatin 10, 20, and 40 mg and milligram-equivalent or higher doses of comparators. RESULTS: A total of 2268 patients were randomized to the rosuvastatin 10- to 40-mg, atorvastatin, simvastatin, and pravastatin groups. Fifty-one percent of patients were women, the mean (SD) age was 57 (12) years, and 19% had a documented history of atherosclerotic disease. Over 6 weeks, rosuvastatin significantly reduced non-HDL-C, apo B, and all lipid and apolipoprotein ratios assessed, compared with milligram-equivalent doses of atorvastatin and milligram-equivalent or higher doses of simvastatin and pravastatin (all, P < 0.002). Rosuvastatin reduced non-HDL-C by 42.0% to 50.9% compared with 34.4% to 48.1% with atorvastatin, 26.0% to 41.8% with simvastatin, and 18.6% to 27.4% with pravastatin. Rosuvastatin reduced apo B by 36.7% to 45.3% compared with 29.4% to 42.9% with atorvastatin, 22.2% to 34.7% with simvastatin, and 14.7% to 23.0% with pravastatin. The highest increase in apo A-I (8.8%) was observed in the rosuvastatin 20-mg group, and this increase was significantly greater than in the atorvastatin 40-mg and 80-mg groups (both, P < 0.002). CONCLUSION: Rosuvastatin 10 to 40 mg was more efficacious in improving the lipid profile of patients with hypercholesterolemia than milligram-equivalent doses of atorvastatin and milligram-equivalent or higher doses of simvastatin and pravastatin.

Aged↗
PubMed2004

Rosuvastatin improves the atherogenic and atheroprotective lipid profiles in patients with hypertriglyceridemia.

BACKGROUND: We examined the effects of rosuvastatin treatment on triglyceride levels and lipid measures in a parallel-group multicenter trial (4522IL/0035) in patients with hypertriglyceridemia (Fredrickson Type IIb or IV). METHODS: After a 6-week dietary lead-in period while on a National Cholesterol Education Program step I diet, 156 patients with fasting triglyceride levels >/= 300 and < 800 mg/dl were randomized to 6 weeks of double-blinded treatment: once-daily rosuvastatin of 5, 10, 20, 40 or 80 mg or placebo. The primary end point was mean percentage change from baseline in total serum triglyceride levels at week 6 as determined by analysis of variance. RESULTS: Rosuvastatin at all doses produced significant mean reductions in triglycerides compared with placebo (-18 to -40 compared with +2.9%, P </= 0.001); median reductions in triglycerides with rosuvastatin at 5-80 mg ranged from -21 to -46%. All doses of rosuvastatin significantly reduced levels of atherogenic lipoprotein and apolipoproteins over placebo, including low-density lipoprotein cholesterol, total cholesterol, non-high-density lipoprotein cholesterol, very-low-density lipoprotein cholesterol, apolipoprotein B and apolipoprotein C-III. Statistically significant increases in high-density lipoprotein cholesterol were observed with rosuvastatin doses > 5 mg. The occurrence of adverse events was generally low and not dose related, although some adverse events occurred more frequently in the rosuvastatin 80 mg group. CONCLUSIONS: Rosuvastatin reduced triglyceride levels and improved the overall atherogenic and atheroprotective lipid profiles in hypertriglyceridemic patients.

Analysis of Variance↗
PubMed2004

Lipid-modifying effects of rosuvastatin in postmenopausal women with hypercholesterolemia who are receiving hormone replacement therapy.

OBJECTIVE: To evaluate the efficacy and safety of rosuvastatin in postmenopausal women with hypercholesterolemia who are receiving hormone replacement therapy (HRT) in a randomized, double-blind, placebo-controlled trial. METHODS: After a 6-week dietary lead-in period, 135 postmenopausal women who had been taking a stable HRT regimen for at least 3 months were randomized to receive rosuvastatin 5 mg, 10 mg or placebo for 12 weeks. Fasting levels of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), and triglycerides (TG) were assessed at weeks 0, 2, 6, 10, and 12; apolipoprotein (Apo) B and Apo A-I were measured at weeks 0 and 12. RESULTS: Rosuvastatin 5 mg and 10 mg significantly reduced LDL-C by 38% (SE = 2.1) and 49% (SE = 2.1), respectively, compared with placebo (1% [SE = 2.1]; p < 0.001). TC, TG, Apo B, and all lipid ratios examined (LDL-C/HDL-C, TC/HDL-C, non-HDL-C/HDL-C, and Apo B/Apo A-I) were also reduced significantly by both rosuvastatin doses (p < 0.001). HDL-C levels increased significantly in the rosuvastatin groups (11% and 8% for 5 mg and 10 mg, respectively, vs. -0.5% for placebo; p < 0.001), as did Apo A-I levels (p < 0.05). The combination of rosuvastatin plus HRT was well tolerated with no apparent differences among treatments in the numbers or types of adverse events reported. CONCLUSIONS: Rosuvastatin 5 mg or 10 mg once daily is a well-tolerated and highly efficacious lipid-lowering therapy in postmenopausal women receiving HRT.

Administration, Oral↗
PubMed2003

Comparison of rosuvastatin versus atorvastatin in patients with heterozygous familial hypercholesterolemia.

Heterozygous familial hypercholesterolemia (HFH) is a common genetic disorder that confers a significantly increased risk of early coronary artery disease. This study compared atorvastatin and rosuvastatin in reducing low-density lipoprotein (LDL) cholesterol in HFH in a global, 18-week, weighted-randomization, double-blind, parallel-group, forced-titration study. Following a 6-week diet lead-in, 623 patients were randomized to 20 mg/day of atorvastatin (n = 187) or rosuvastatin (n = 436) with forced titration at 6-week intervals to 80 mg/day. The primary end point was percentage change in LDL cholesterol from baseline to week 18. At week 18, rosuvastatin therapy produced a significantly greater reduction in LDL cholesterol than atorvastatin (-57.9% vs -50.4%; p <0.001) and a significantly greater increase in high-density lipoprotein (HDL) cholesterol (12.4% vs 2.9%; p <0.001). Rosuvastatin also produced significantly greater reductions in apolipoprotein-B and all 4 major lipid ratios, as well as a significantly greater increases in apolipoprotein A-I (all p <0.001). More patients with HFH with coronary artery disease achieved the National Cholesterol Education Program Adult Treatment Panel III goal of LDL cholesterol <100 mg/dl (<2.6 mmol/L) on rosuvastatin 40 and 80 mg than atorvastatin 80 mg (17%, 24%, and 4.5%, respectively). High-sensitivity C-reactive protein median values were reduced by 33% to 34% in both the 80-mg rosuvastatin- and atorvastatin-treated groups. Both treatments were well tolerated. Thus, in HFH, rosuvastatin force titrated from 20 to 80 mg/day produced significantly greater reductions than atorvastatin 20 to 80 mg/day in LDL cholesterol and improvements in HDL cholesterol and other lipid parameters, and enabled more patients to achieve LDL cholesterol goals.

Adult↗
PubMed2003

Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).

The primary objective of this 6-week, parallel-group, open-label, randomized, multicenter trial was to compare rosuvastatin with atorvastatin, pravastatin, and simvastatin across dose ranges for reduction of low-density lipoprotein (LDL) cholesterol. Secondary objectives included comparing rosuvastatin with comparators for other lipid modifications and achievement of National Cholesterol Education Program Adult Treatment Panel III and Joint European Task Force LDL cholesterol goals. After a dietary lead-in period, 2,431 adults with hypercholesterolemia (LDL cholesterol > or =160 and <250 mg/dl; triglycerides <400 mg/dl) were randomized to treatment with rosuvastatin 10, 20, 40, or 80 mg; atorvastatin 10, 20, 40, or 80 mg; simvastatin 10, 20, 40, or 80 mg; or pravastatin 10, 20, or 40 mg. At 6 weeks, across-dose analyses showed that rosuvastatin 10 to 80 mg reduced LDL cholesterol by a mean of 8.2% more than atorvastatin 10 to 80 mg, 26% more than pravastatin 10 to 40 mg, and 12% to 18% more than simvastatin 10 to 80 mg (all p <0.001). Mean percent changes in high-density lipoprotein cholesterol in the rosuvastatin groups were +7.7% to +9.6% compared with +2.1% to +6.8% in all other groups. Across dose ranges, rosuvastatin reduced total cholesterol significantly more (p <0.001) than all comparators and triglycerides significantly more (p <0.001) than simvastatin and pravastatin. Adult Treatment Panel III LDL cholesterol goals were achieved by 82% to 89% of patients treated with rosuvastatin 10 to 40 mg compared with 69% to 85% of patients treated with atorvastatin 10 to 80 mg; the European LDL cholesterol goal of <3.0 mmol/L was achieved by 79% to 92% in rosuvastatin groups compared with 52% to 81% in atorvastatin groups. Drug tolerability was similar across treatments.

Adult↗
PubMed2003

Risk for myopathy with statin therapy in high-risk patients.

Emerging data suggest that the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) offer important benefits for the large population of individuals at high risk for coronary heart disease. This population encompasses a sizable portion of individuals who are also at high risk for drug-drug interactions due to their need for multiple medications. In general, statins are associated with a very small risk for myopathy (which may progress to fatal or nonfatal rhabdomyolysis); however, the potential for drug-drug interactions is known to increase this risk in specific high-risk groups. The incidence of myopathy associated with statin therapy is dose related and is increased when statins are used in combination with agents that share common metabolic pathways. Of particular concern is the potential for interactions with other lipid-lowering agents such as fibrates and niacin (nicotinic acid), which may be used in patients with mixed lipidemia, and with immunosuppressive agents, such as cyclosporine, which are commonly used in patients after transplantation. Clinicians should be alert to the potential for drug-drug interactions to minimize the risk of myopathy during long-term statin therapy in patients at high risk for coronary heart disease.

Calcium Channel Blockers↗
PubMed2003

Efficacy of rosuvastatin compared with other statins at selected starting doses in hypercholesterolemic patients and in special population groups.

A total of 5 randomized, double-blind trials in patients with hypercholesterolemia were prospectively designed to allow pooling of plasma lipid data after 12 weeks of treatment. The purpose was (1) to compare rosuvastatin 5 and 10 mg with atorvastatin 10 mg (data from 3 of the 5 trials); (2) to compare rosuvastatin 5 and 10 mg with simvastatin 20 mg and pravastatin 20 mg (data from 2 of the 5 trials); and (3) to summarize overall efficacy and subset analyses of rosuvastatin data from all 5 trials. Rosuvastatin 5 mg (n = 390) and 10 mg (n = 389) reduced low-density lipoprotein (LDL) cholesterol significantly more than did atorvastatin 10 mg (n = 393) (41.9% and 46.7% vs 36.4%, both p <0.001). Treatment with rosuvastatin 5 mg (n = 240) and 10 mg (n = 226) also resulted in significantly greater reductions in LDL cholesterol compared with both simvastatin 20 mg (n = 249) and pravastatin 20 mg (n = 252) (40.6% and 48.1% vs 27.1% and 35.7%, all p <0.001). Significant differences favoring rosuvastatin 10 mg were also observed for total cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, apolipoprotein (apo) B, and apo A-I versus atorvastatin 10 mg, and for total cholesterol, HDL cholesterol, triglycerides, non-HDL cholesterol, and apo B versus simvastatin 20 mg and pravastatin 20 mg. Analyses of all the rosuvastatin 10 mg data (n = 615) from the 5 trials in subgroups defined by age > or =65 years, female sex, postmenopausal status, hypertension, atherosclerosis, type 2 diabetes, and obesity showed that rosuvastatin had consistent efficacy across patient subgroups.

Adult↗
PubMed2003

Efficacy of rosuvastatin 10 mg in patients with the metabolic syndrome.

The constellation of risk factors known as the metabolic syndrome increases the risk of coronary artery disease at any low-density lipoprotein (LDL) cholesterol level. We performed an exploratory analysis of data from 5 trials to study the effects of rosuvastatin 10 mg on lipid levels and ratios in hypercholesterolemic patients (LDL cholesterol > or =160 mg/dL and <250 mg/dL) who met a modified National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) definition of the metabolic syndrome. Of 580 patients completing 12 weeks of treatment with rosuvastatin 10 mg, 194 (33%) met the definition of the metabolic syndrome by exhibiting > or =3 of the following: body mass index >30; triglycerides > or =150 mg/dL; high-density lipoprotein (HDL) cholesterol <40 mg/dL in men and <50 mg/dL in women; blood pressure > or =130/> or =85 mm Hg or receiving current medication for hypertension; and fasting blood glucose > or =110 mg/dL. Patients with the metabolic syndrome had higher triglyceride, non-HDL cholesterol, apolipoprotein B, and lipid ratios, and lower HDL cholesterol and apolipoprotein A-I levels, at baseline compared with patients without the metabolic syndrome. In patients with the metabolic syndrome, rosuvastatin 10 mg improved LDL cholesterol (-47%), non-HDL cholesterol (-43%), non-HDL cholesterol/HDL cholesterol ratio (-47%), apolipoprotein B (-37%), apolipoprotein B/apolipoprotein A-I ratio (-40%), triglycerides (-23%), apolipoprotein A-I (+7%), and HDL cholesterol (+10%)-in a manner similar to that in hypercholesterolemic patients who did not meet these criteria. Among patients who met the metabolic syndrome criteria and who had triglycerides > or =200 mg/dL, 64% met their ATP III non-HDL goals.

Adult↗
PubMed2003

The power of statins: aggressive lipid lowering.

A large body of evidence has demonstrated that reductions in low-density lipoprotein cholesterol (LDL-C) decrease the risk of coronary heart disease (CHD) and related adverse events. The greatest reductions in morbidity and mortality are attained in higher-risk patients, suggesting that targeting this group can maximize the cost-effectiveness of statins, since fewer patients need to be treated to prevent one event. High-risk individuals (those with preexisting CHD or CHD risk equivalents) require aggressive lipid lowering to achieve the stringent LDL-C goal levels established by the third report of the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP III). The hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, have assumed the central role in this setting because of their superior ability to reduce LDL-C across the spectrum of CHD risk. Rosuvastatin, a new agent in this class, reduces LDL-C to a significantly greater degree than atorvastatin, pravastatin, or simvastatin. The more aggressive goals put forward since ATP I (1987) have heightened interest in more efficacious statins. As a result, simvastatin, atorvastatin, and now rosuvastatin have been developed, adding sequentially greater LDL-C-reducing capacity for the physician. Substantially more patients, particularly high-risk patients, are thereby able to achieve NCEP ATP III target LDL-C levels with rosuvastatin. Other cholesterol-lowering drugs (bile acid sequestrants, niacin, plant stanols, and fibrates) are much less effective at lowering LDL-C and are much less well tolerated but may be useful when combined with statins. A novel class of agents, cholesterol transport inhibitors, have recently become available. These and other new agents hold promise to help achieve ATP III goals when used in combination regimens initiated with a statin.

Cholesterol, LDL↗
PubMed2003

Pharmacotherapy for dyslipidaemia--current therapies and future agents.

Current lipid-altering agents that lower low density lipoprotein cholesterol (LDL-C) primarily through increased hepatic LDL receptor activity include statins, bile acid sequestrants/resins and cholesterol absorption inhibitors such as ezetimibe, plant stanols/sterols, polyphenols, as well as nutraceuticals such as oat bran, psyllium and soy proteins; those currently in development include newer statins, phytostanol analogues, squalene synthase inhibitors, bile acid transport inhibitors and SREBP cleavage-activating protein (SCAP) activating ligands. Other current agents that affect lipid metabolism include nicotinic acid (niacin), acipimox, high-dose fish oils, antioxidants and policosanol, whilst those in development include microsomal triglyceride transfer protein (MTP) inhibitors, acylcoenzyme A: cholesterol acyltransferase (ACAT) inhibitors, gemcabene, lifibrol, pantothenic acid analogues, nicotinic acid-receptor agonists, anti-inflammatory agents (such as Lp-PLA(2) antagonists and AGI1067) and functional oils. Current agents that affect nuclear receptors include PPAR-alpha and -gamma agonists, while in development are newer PPAR-alpha, -gamma and -delta agonists, as well as dual PPAR-alpha/gamma and 'pan' PPAR-alpha/gamma/delta agonists. Liver X receptor (LXR), farnesoid X receptor (FXR) and sterol-regulatory element binding protein (SREBP) are also nuclear receptor targets of investigational agents. Agents in development also may affect high density lipoprotein cholesterol (HDL-C) blood levels or flux and include cholesteryl ester transfer protein (CETP) inhibitors (such as torcetrapib), CETP vaccines, various HDL 'therapies' and upregulators of ATP-binding cassette transporter (ABC) A1, lecithin cholesterol acyltransferase (LCAT) and scavenger receptor class B Type 1 (SRB1), as well as synthetic apolipoprotein (Apo)E-related peptides. Fixed-dose combination lipid-altering drugs are currently available such as extended-release niacin/lovastatin, whilst atorvastatin/amlodipine, ezetimibe/simvastatin, atorvastatin/CETP inhibitor, statin/PPAR agonist, extended-release niacin/simvastatin and pravastatin/aspirin are under development. Finally, current and future lipid-altering drugs may include anti-obesity agents which could favourably affect lipid levels.

Animals↗
PubMed2002

Effects of simvastatin on C-reactive protein in mixed hyperlipidemic and hypertriglyceridemic patients.

This study examined the effects of simvastatin on C-reactive protein (CRP) and other inflammatory markers in study subjects with significant elevations in triglyceride (TG) blood levels. CRP, vascular cellular adhesion molecule (VCAM), serum amyloid A (SAA), and interleukin 6 (IL-6) were measured in archived plasma samples from 2 multicenter, randomized, double-blind, placebo-controlled studies designed to examine the lipid-altering efficacy of simvastatin in study subjects with elevated TGs. In the first study, 130 study subjects with mixed hyperlipidemia (low-density lipoprotein [LDL] cholesterol > or =130 mg/dl; TGs 300 to 700 mg/dl) received placebo or simvastatin 40 or 80 mg once daily for three 6-week periods in a complete-block crossover design. In the second study, 195 study subjects with hypertriglyceridemia (TGs 300 to 900 mg/dl) received daily doses of placebo or simvastatin 20, 40, or 80 mg for 6 weeks. Significant but weak correlations were observed between baseline CRP values and baseline levels of LDL cholesterol and high-density lipoprotein (HDL) cholesterol, but not with TGs. CRP was also correlated with body mass index and fasting levels of glucose and insulin. Treatment with simvastatin 20, 40, and 80 mg led to significant reductions in CRP plasma levels versus placebo (p <0.05). Although CRP change was weakly correlated with changes in LDL cholesterol, TGs, and HDL cholesterol, results of regression analyses showed that only baseline CRP and treatment allocation were significant predictors of CRP response after 6 weeks of study drug administration. Simvastatin had no effect on VCAM, SAA, or IL-6. In summary, simvastatin significantly reduced CRP in patients with mixed hyperlipidemia and hypertriglyceridemia.

Anticholesteremic Agents↗