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To assess the relationship between efficacy of treatment with rosuvastatin versus placebo and baseline CIMT, we analyzed the effects on the primary CIMT endpoint in participants stratified by baseline quartiles of CIMT (Q1-Q4) using all individuals with a baseline reading and at least one post-baseline CIMT reading. Statistical analysis was carried out using a multilevel repeated-measures linear mixed effects model.
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Old mice with cardiac-specific overexpression of constitutively active V12Rac1 (RacET) were compared with wild-type (WT) and WT undergoing transaortic constriction (TAC). In addition, samples of human left atrial appendages were analyzed in patients with sinus rhythm (SR) compared with patients with permanent AF matched for atrial diameter.
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Monthly LDL apheresis and atorvastatin 120 mg daily reduced LDL cholesterol preapheresis level to 4.8 mmol L(-1). When ezetimibe was given 10 mg day(-1) in combination with rosuvastatin 80 mg day(-1), LDL cholesterol was further lowered to 1.6 mmol L(-1), which made apheresis unnecessary. Cutaneous and tendon xanthomas disappeared completely and the intima-media thickness of the common carotid arteries decreased. At age 23 he developed a small myocardial infarction.
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We aimed to assess the effects of rosuvastatin treatment on lipid levels, a biomarker of oxidative stress, albuminuria, and kidney function in patients with diabetic nephropathy.
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Based on the results of this case, a possible pharmacologic interaction between rosuvastatin and acenocoumarol should be considered. Rosuvastatin might enhance the anticoagulant effect of acenocoumarol, and a rebound effect in cases of simultaneous discontinuation of both drugs might occur. Rosuvastatin should be administered with extreme caution in patients receiving long-term acenocoumarol therapy.
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Statins are the standard-of-care therapy for reducing low-density lipoprotein cholesterol (LDL-C) levels; however, combination with other lipid-modifying agents may be necessary to normalize lipid profiles in patients with mixed dyslipidemia who, in addition to high LDL-C, also have high triglycerides (TG) and low levels of high-density lipoprotein cholesterol (HDL-C).
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Rosuvastatin increased VEGF by +43% (p=0.004 vs. placebo) and decreased oxLDL by -27% (p=0.04 vs. placebo). This was associated with an elevation in CPC count by +224% (p=0.04 vs. placebo) and an augmentation of CPC integrative capacity by +91% (p=0.03 vs. placebo). Capillary density increased by +14% (p<0.001 vs. placebo), which was associated with an enhanced homing of CD34(+) stem cells. Rosuvastatin improved FMD by +163% (p<0.001 vs. placebo) and enhanced ejection fraction by +27% (p<0.001 vs. placebo).
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The subjects were 24 patients with noncardiogenic cerebral infarction complicated by dyslipidemia (low-density lipoprotein cholesterol [LDL-C] ≥ 140 mg/dL). Serum lipids and highly sensitive C-reactive protein (hs-CRP) were measured at the start of the study and at 3 and 12 months after the initiation of oral rosuvastatin (5 mg/day). Cardio-ankle vascular index (CAVI), intima-media thickness (IMT), and plaque score (PS) were also determined at the start of the study and at 12 months.