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In the Secondary Prevention of Acute Coronary Events-Reduction Of Cholesterol to Key European Targets (SPACE ROCKET) trial, we measured serum lipids of individuals on day 1 and between days 2 and 4 after acute myocardial infarction (AMI). Second, we performed a thorough literature review and compared all studies reporting data on absolute changes in lipids immediately after AMI, using weighted means.
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Serial intravascular ultrasound (IVUS) was used to compare the effects of moderate doses of rosuvastatin and atorvastatin on plaque regression in patients with intermediate coronary stenosis.
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This study shows that gene expression analysis together with bioinformatics pathway analysis has the potential to help predict and identify drug combination-specific complementary and side effects.
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A potential interaction between rosuvastatin and amiodarone resulted in asymptomatic elevation of serum transaminase levels in a 73-year-old woman.
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In Hungary the life expectancy have increased by 4.14 years between 1993 and 2006 and the improvement of cardiovascular mortality contributed to this with 1.85 years. Lipid lowering therapy and achievement of target lipid levels have become recently a crucial point of cardiovascular prevention. Despite the improving tendency the rate of achieving LDL-cholesterol goal is not higher than 1/3 and its main cause seems to be the fact that greater part of the physicians (56% of them in year 2007) - seeing the results with not convenient lipid levels - yield to it, do not modify the current treatment. However, there is growing evidence that the lower LDL-cholesterol level improves not only the clinical outcome but it is cost-effective as well. The most important trial performed recently using statin was the JUPITER study, in which patients with normal lipid levels and high hs-CRP level without known atherosclerotic disease were treated with 20 mg rosuvastatin or placebo. The primary endpoint (cardiovascular mortality, stroke, non fatal myocardial infarction, unstable angina and revascularization) decreased significantly by 44% and total mortality decreased by 20%. For the prevention of one primary event 23 patients for 5 years were necessary to be treated. The results raise the need for reconsidering principles and target levels of the primary prevention and warn that in the lipid lowering therapy a greater emphasis should be placed on the hs-CRP level.
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The incidence of periprocedural myocardial injury was higher in control group than loading dose group (CKMB: 10.17% vs. 25.86%, P = 0.027; Troponin I: 11.86% vs. 29.31%, P = 0.019). MACE occurred in 1.69% of patients in loading dose group and 12.07% of those in control group 3 months after procedure (P = 0.026), 3.39% vs. 17.24% at 6 months (P = 0.014). The levels of hs-CRP, IL-1, IL-6, and TNF-a in serum were not significantly different between the two groups before PCI, but after PCI they were significantly higher in control group.
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Hypertensive patients with left ventricular hypertrophy (LVH) are the most common high-risk group to develop heart failure with preserved ejection fraction. Recent reports have noted the favorable effect of statins on LVH. We evaluated the effect of rosuvastatin on cardiac remodeling, function, and progression to heart failure in a hypertensive rat model with established LVH. Dahl salt-sensitive rats were fed a high-salt diet until 13 weeks of age. After LVH was confirmed by echocardiography, rats were randomly assigned to control and statin treatment (n=18 each group). The statin-treated group was treated with rosuvastatin until 21 weeks of ages. Serial echocardiography, blood pressure monitoring, and miniaturized conductance catheter hemodynamic monitoring were performed at 21 weeks. Echocardiographic parameters were not significantly different between the groups. On hemodynamic monitoring, systolic performance parameters were similar between the groups, whereas end diastolic pressure-volume relationships were lower in the statin-treated group (0.014+/-0.008 versus 0.008+/-0.004 mm Hg/muL, P<0.05), suggesting improvement in myocardial stiffness. Pathological analysis showed attenuation of perivascular and interstitial fibrosis in the statin-treated group (P<0.02). Rosuvastatin therapy did not alleviate LVH in hypertensive rats with established LVH, but it attenuated myocardial fibrosis and LV stiffness. It seems that rosuvastatin has limited therapeutic value when used to prevent progression from LVH to heart failure in hypertensive hearts.
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A 7 × 3(2) full factorial design was adopted for optimization of oil ratio, Surfactant: Co-surfactant (S:CoS) ratio and oil:S/CoS ratio. Ternary phase diagrams were constructed for optimizing the system with drug loading (10 and 20%). The optimized SNEDD systems were evaluated according to their physical evaluation and drug release. Furthermore, the anti-hyperlipidemia efficacy was compared with commercially marketed product on rates followed by clinical study.
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Administration of 10 mg/day of rosuvastatin decreased total cholesterol by 41.7%, LDL cholesterol by 63.0%, and triglycerides by 10.7%, and increased HDL cholesterol by 6.3%. Pharmacological treatment with either rosuvastatin or metformin lead to reductions in IL-6, TNFalpha, GSH and GPx levels and an increase in the SOD level, and there were significant interactions between the two treatment groups for these variables.
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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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Statin interference has been suggested among the mechanisms of reduction of the antiplatelet effect of clopidogrel. We thus sought to assess the influence of rosuvastatin on clopidogrel antiplatelet action in high-risk (HR) cardiovascular patients. To set the level of platelet inhibition by combined antithrombotic treatments we retrospectively studied two populations of HR patients, one under aspirin alone, the other under aspirin plus rosuvastatin, before and after addition of clopidogrel. The effects of rosuvastatin compared with atorvastatin were then prospectively investigated in patients who underwent percutaneous coronary intervention (PCI), under clopidogrel and aspirin treatment. Light transmission platelet aggregation (LTA) was studied in response to adenosine diphosphate (ADP) (5 microM) or arachidonic acid (0.5 mM). The inhibitory effect of clopidogrel in reducing ADP-induced LTA was similar in the two HR groups of patients. No difference in ADP-induced platelet aggregation was observed in the two PCI groups of patients with either atorvastatin or rosuvastatin. In conclusion, rosuvastatin does not interfere with the antiplatelet effect of clopidogrel in patients with cardiovascular disease.
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This study demonstrated both statins failed to suppress AngII-induced AAA. In contrast, atorvastatin reduced AngII-induced atherosclerosis associated with no change in serum inflammatory markers but a shift to upregulation of anti-inflammatory status in lesions.
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A randomized, open-label, repeated-dose, two-way crossover drug interaction study of two treatments - 4 g P-OM3 plus 40 mg rosuvastatin or 40 mg rosuvastatin alone administered daily for 14 days each under fasting conditions--was conducted in 48 non-smoking healthy adults.
To examine in vivo the effect of ketoconazole on the pharmacokinetics of rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor.