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Icosapent Ethyl (Eicosapentaenoic Acid Ethyl Ester): Effects Upon High-Sensitivity C-Reactive Protein and Lipid Parameters in Patients With Metabolic Syndrome.
Bays, HE, Ballantyne, CM, Braeckman, RA, Stirtan, WG, Doyle, RT, Philip, S, Soni, PN, Juliano, RA
Metabolic syndrome and related disorders. 2015;(6):239-47
Abstract
BACKGROUND The aim of this analysis was to examine the effects of icosapent ethyl (eicosapentaenoic acid ethyl ester, IPE) on high-sensitivity C-reactive protein (hsCRP) and lipid parameters in patients with metabolic syndrome, with and without stable statin therapy. METHODS This post hoc exploratory analysis evaluated patients with metabolic syndrome treated with IPE 4 grams/day, IPE 2 grams/day, or placebo in phase 3, randomized, placebo-controlled studies entitled: MARINE [triglyceride (TG) levels ≥500 and ≤2000 mg/dL] and ANCHOR [TG levels ≥200 and <500 mg/dL, despite low-density lipoprotein cholesterol (LDL-C) control with stable statin therapy]. RESULTS Compared with placebo in patients with metabolic syndrome in MARINE (n=204) and ANCHOR (n=645), at the approved dose of 4 grams/day, IPE significantly lowered hsCRP levels 40.0% (P=0.0007) in MARINE and 23.0% (P=0.0003) in ANCHOR. Compared with placebo in MARINE, which included patients with and without statin therapy, IPE 4 grams/day significantly reduced hsCRP levels 78.0% in statin-treated patients (P=0.0035, n=16). Compared with placebo in MARINE, IPE 4 grams/day significantly reduced TG levels (35.0%; P<0.0001), non-high-density lipoprotein cholesterol (non-HDL-C; 19.9%; P<0.0001), and apolipoprotein B levels (ApoB) (9.1%; P=0.0015) without raising LDL-C levels. Compared with placebo in ANCHOR, IPE 4 grams/day significantly reduced TG (21.7%; P<0.0001), non-HDL-C (13.5%; P<0.0001), ApoB (8.8%; P<0.0001), LDL-C (5.2%; P=0.0236), and HDL-C levels (4.0%; P=0.0053). CONCLUSIONS Compared with placebo, IPE 4 grams/day significantly lowered hsCRP levels and improved lipids without raising LDL-C levels in patients with metabolic syndrome and high (≥200 and <500 mg/dL) or very high (≥500 and ≤2000 mg/dL) TG levels, with or without stable statin therapy.
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Impact of pitavastatin on high-sensitivity C-reactive protein and adiponectin in hypercholesterolemic patients with the metabolic syndrome: the PREMIUM Study.
Matsubara, T, Naruse, K, Arakawa, T, Nakao, M, Yokoi, K, Oguri, M, Marui, N, Amano, T, Ichimiya, S, Ohashi, T, et al
Journal of cardiology. 2012;(5):389-94
Abstract
BACKGROUND Inflammatory reactions and oxidative stress, which are important in progression of atherosclerosis, are reported to be increased in individuals with metabolic syndrome (MetS). On the other hand, adiponectin levels are lowered. Since effects of pitavastatin on these parameters have not been reported in hypercholesterolemic patients with MetS, the present study was conducted. PURPOSE To evaluate the effects of pitavastatin on inflammatory reaction, oxidative stress, and plasma adiponectin levels in hypercholesterolemic MetS patients in a multicenter trial. METHODS This open-label, single group study was performed at 7 hospitals in Japan. Pitavastatin (2mg/day) was administered to 103 consecutive patients with hypercholesterolemia, subdivided into MetS and non-MetS for 12 weeks. Blood samples were collected after overnight fasting at the start of treatment (baseline) and after 12 weeks. RESULTS In the patients with MetS (n=69), mean values of plasma high-sensitivity C-reactive protein (hs-CRP) were significantly higher and mean values of plasma high-molecular-weight (HMW)-adiponectin significantly lower than in their counterparts without MetS (n=34). The baseline HMW-adiponectin and high-density lipoprotein cholesterol (HDL-C) values significantly correlated only in the MetS patients (r=0.318; p=0.01). In an effectiveness analysis including 94 patients (62 with MetS, 32 without MetS), the level of hs-CRP was significantly decreased in patients with MetS during the drug treatment, whereas HMW-adiponectin did not change. When patients with MetS were divided into two subgroups according to the percent changes in HDL-C, significantly greater increase in HMW-adiponectin by pitavastatin treatment was observed in the HDL-C ≥10% increase subgroup than in the HDL-C <10% increase subgroup (p=0.009). CONCLUSION Twelve weeks administration of pitavastatin, in addition to the antihyperlipidemic effects, may be beneficial as an anti-atherosclerotic therapy in hypercholesterolemic patients with MetS, taking changes in hs-CRP and HMW-adiponectin into consideration. ClinicalTrials.gov identifier: NCT00444717.
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The effect of rosuvastatin on incident pneumonia: results from the JUPITER trial.
Novack, V, MacFadyen, J, Malhotra, A, Almog, Y, Glynn, RJ, Ridker, PM
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2012;(7):E367-72
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Abstract
BACKGROUND Evidence from observational studies have raised the possibility that statin treatment reduces the incidence of certain bacterial infections, particularly pneumonia. We analyzed data from a randomized controlled trial of rosuvastatin to examine this hypothesis. METHODS We analyzed data from the randomized, double-blind, placebo-controlled JUPITER trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin). In this trial, 17,802 healthy participants (men 50 years and older and women 60 and older) with a low-density lipoprotein (LDL) cholesterol level below 130 mg/dL (3.4 mmol/L) and a high-sensitivity C-reactive protein level of 2.0 mg/L or greater were randomly assigned to receive either rosuvastatin or placebo. We evaluated the incidence of pneumonia on an intention-to-treat basis by reviewing reports of adverse events from the study investigators, who were unaware of the treatment assignments. RESULTS Among 17,802 trial participants followed for a median of 1.9 years, incident pneumonia was reported as an adverse event in 214 participants in the rosuvastatin group and 257 in the placebo group (hazard ratio [HR] 0.83, 95% confidence interval [CI] 0.69-1.00). In analyses restricted to events occurring before a cardiovascular event, pneumonia occurred in 203 participants given rosuvastatin and 250 given placebo (HR 0.81, 95% CI 0.67-0.97). Inclusion of recurrent pneumonia events did not modify this effect (HR 0.81, 95% CI 0.67-0.98), nor did adjustment for age, sex, smoking, metabolic syndrome, lipid levels and C-reactive protein level. INTERPRETATION Data from this randomized controlled trial support the hypothesis that statin treatment may modestly reduce the incidence of pneumonia. (ClinicalTrials.gov trial register no. NCT0023968.).
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Effect of atorvastatin on circulating hsCRP concentrations: a sub-study of the achieve cholesterol targets fast with atorvastatin stratified titration (ACTFAST) study.
Gensini, GF, Gori, AM, Dilaghi, B, Rostagno, C, Gaw, A, Blanco-Colio, LM, de Teresa, E, Egido, J, Farsang, C, Leiter, LA, et al
International journal of cardiology. 2010;(3):257-64
Abstract
BACKGROUND Elevated C-reactive protein (CRP) concentration is a risk factor for cardiovascular events that may add prognostic information. Statin treatment is associated with significant reductions in CRP concentrations, which appear to be unrelated to the magnitude of LDL-cholesterol reduction. We investigated the effect of atorvastatin, across its dose range, on high sensitivity (hs)CRP in subjects at high cardiovascular risk. METHODS ACTFAST was a 12 week, prospective, multicenter, open-label trial in which high-risk subjects were assigned a starting dose of atorvastatin (10, 20, 40 or 80 mg/d) based on LDL-C and status of statin use at screening (1345 statin-free [SF] and 772 previously statin-treated [ST]). RESULTS At baseline, ST subjects had significantly lower hsCRP levels than SF subjects (ST group 2.31, 95% CI 2.15, 2.48 mg/L vs. SF group 3.16, 95% CI 2.98, 3.34 mg/L, p<0.05). In the SF group, atorvastatin 10 to 80 mg significantly (p<0.01) reduced hsCRP levels in a dose dependent-manner. In ST group, additional hsCRP reductions were observed over the statin used at baseline, which were not dose-dependent. Atorvastatin significantly decreased hsCRP concentrations in subjects with or without diabetes or the metabolic syndrome. CONCLUSIONS Atorvastatin treatment at different doses, particularly 80 mg, significantly reduced hsCRP serum concentrations. This reduction was observed in both SF and ST groups and was independent of the presence of metabolic syndrome and/or diabetes. The beneficial effect of atorvastatin was evident at 6 weeks, supporting the practice of early introduction of higher doses of atorvastatin in high-risk patients.
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Effects of dietary fat modification on oxidative stress and inflammatory markers in the LIPGENE study.
Petersson, H, Risérus, U, McMonagle, J, Gulseth, HL, Tierney, AC, Morange, S, Helal, O, Shaw, DI, Ruano, JA, López-Miranda, J, et al
The British journal of nutrition. 2010;(9):1357-62
Abstract
Subjects with the metabolic syndrome (MetS) have enhanced oxidative stress and inflammation. Dietary fat quality has been proposed to be implicated in these conditions. We investigated the impact of four diets distinct in fat quantity and quality on 8-iso-PGF2α (a major F2-isoprostane and oxidative stress indicator), 15-keto-13,14-dihydro-PGF2α (15-keto-dihydro-PGF2α, a major PGF2α metabolite and marker of cyclooxygenase-mediated inflammation) and C-reactive protein (CRP). In a 12-week parallel multicentre dietary intervention study (LIPGENE), 417 volunteers with the MetS were randomly assigned to one of the four diets: two high-fat diets (38 % energy (%E)) rich in SFA or MUFA and two low-fat high-complex carbohydrate diets (28 %E) with (LFHCC n-3) or without (LFHCC) 1·24 g/d of very long chain n-3 fatty acid supplementation. Urinary levels of 8-iso-PGF2α and 15-keto-dihydro-PGF2α were determined by RIA and adjusted for urinary creatinine levels. Serum concentration of CRP was measured by ELISA. Neither concentrations of 8-iso-PGF2α and 15-keto-dihydro-PGF2α nor those of CRP differed between diet groups at baseline (P>0·07) or at the end of the study (P>0·44). Also, no differences in changes of the markers were observed between the diet groups (8-iso-PGF2α, P = 0·83; 15-keto-dihydro-PGF2α, P = 0·45; and CRP, P = 0·97). In conclusion, a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study.