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Crestor (Rosuvastatin)

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Crestor is a high-quality medication which is taken for the treatment of high level of cholesterol. This remedy is acting by slowing the production of cholesterol in the body. It is HMG-CoA reductase inhibitor (statin).

Other names for this medication:

Similar Products:
Altocor, Altoprev, Lescol, Mevacor, Pravachol, Crestor, Lipitor, Livalo, Zocor, Baycol, Lescol XL


Also known as:  Rosuvastatin.


Crestor is indicated to treat high level of cholesterol.

This remedy is acting by slowing the production of cholesterol in the body.

Crestor is also known as Rosuvastatin calcium, Rosuvas, Rozavel.

Crestor is HMG-CoA reductase inhibitor (statins).


Take Crestor tablets orally with or without food.

Do not crush or chew it.

Take Crestor once a day at the same time every day with water.

If you want to achieve most effective results do not stop taking Crestor suddenly.


If you overdose Crestor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Crestor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Crestor if you are allergic to Crestor components.

Do not take Crestor if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Crestor if you suffer from or have a history of liver, thyroid or kidney disease.

Be careful with Crestor if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Crestor if you have allergies to medicines, foods, or other substances.

Do not eat fattening food that is high in cholesterol.

Use Crestor with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Do not stop taking Crestor suddenly.

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Thirty healthy Chinese male volunteers were enrolled. The serum lipids, high-sensitivity C-reactive protein, and plasma fibrinogen were determined before and 72 hours after administration of 20 mg of rosuvastatin. The differentially expressed genes of peripheral leukocytes after administration of rosuvastatin were screened using human oligonucleotide microarray gene expression chips. Then four of the differentially expressed genes including ATM, CASP8, IL8RB and S100B were verified by real-time polymerase chain reaction (PCR).

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The primary end point was the occurrence of a first cardiovascular event (myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes).

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This historical cohort included patients with no prior CCD, aged 40-79 years, who initiated statin therapy with rosuvastatin 5 mg or simvastatin 20 mg in 2008-2009 in general practice. Follow-up started after a 1-year period used to select patients who regularly received the initial treatment. In an intention-to-treat analysis, patients were followed up to December 2011. In a per-protocol analysis, they were censored prematurely when they discontinued their initial treatment. Adjustment for baseline covariates (age, deprivation index, comedications, comorbidities, prior hospital admissions) was carried out by a Cox proportional hazards model. In the per-protocol analysis, estimation was done by "inverse probability of censoring weighting" using additional time-dependent covariates. Analyses were gender-specific.

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The COSMOS study will be the first multicenter cardiovascular study in a Japanese population and may provide new evidence on the effects of rosuvastatin on the progression of coronary atherosclerotic lesions.

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The effects on changes of LPL and EL mass differed depending on the lipid-lowering therapy, which may impact the prevention of atherosclerosis differently.

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Rosuvastatin is a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) that reduces low-density lipoprotein cholesterol levels to the greatest extent of all currently marketed statins. Prospective, randomized studies demonstrate the ability of rosuvastatin to reduce the risk of cardiovascular events and stabilize atherosclerosis. However, the efficacy of rosuvastatin in patient subpopulations (eg, patients with chronic kidney disease, women, ethnic subgroups) is not well described in the literature. To provide an updated, comprehensive review of the efficacy and safety of rosuvastatin, a literature search of PubMed was conducted using statins as a major topic, MESH topic, or a word in the title (including rosuvastatin, fluvastatin, atorvastatin, pitavastatin, lovastatin, pravastatin, and simvastatin). Publications selected for inclusion in this review were published from January 1, 2010 to December 31, 2013, and provide new information pertaining to the efficacy and safety of rosuvastatin.

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In conclusion, rosuvastatin 5 mg + fenofibric acid 135 mg resulted in comprehensive improvements in the lipid profile of patients with mixed dyslipidemia without unanticipated adverse events.

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Ninety-seven consecutive acute cerebral embolism patients were retrospectively surveyed. All had transesophageal echocardiography (TEE) to assess the presence or absence of CAP, defined as aortic wall thickness ≥4 mm or plaque ulceration. Patients received conventional antithrombotic therapy as clinically indicated. All patients with CAP were recommended to receive 5 mg rosuvastatin/day, administered by their attending physicians; not all physicians followed this recommendation. Six-month follow-up TEEs were performed in patients with CAP who received rosuvastatin. Major adverse cerebrovascular events (MACEs) comprised recurrent IS and death.

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Significant PI and mSBI reductions were observed in all three groups. PRF placement significantly enhanced improvements in periodontal parameters compared with OFD alone. Addition of 1.2% RSV gel to PRF resulted in significantly greater CAL gain and PD and IBD depth reductions over 9 months compared with other groups.

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Rosuvastatin, a strong statin, and colestimide, a new anion exchange resin, are both clinically beneficial drugs for treatment of hypercholesterolemia. The main purpose of the study was to compare the effects of rosuvastatin and colestimide on metabolic parameters, adipokines, and markers of oxidative stress and diabetic nephropathy in patients with type 2 diabetes complicated by hyperlipidemia.

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950 participants from the Multi-Ethnic Study of Atheroslcerosis (MESA) met all criteria for JUPITER entry. We compared coronary heart disease and cardiovascular disease event rates and multivariable-adjusted hazard ratios after stratifying by burden of CAC (scores of 0, 1-100, or >100). We calculated 5-year number needed to treat (NNT) by applying the benefit recorded in JUPITER to the event rates within each CAC strata.

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Lopinavir/ritonavir-containing antiretroviral therapy can cause hyperlipidaemia. However, most statins are contraindicated due to drug-drug interactions. Rosuvastatin undergoes minimal metabolism by CYP450, so no CYP450-based interaction with lopinavir/ritonavir is expected. This study explored the lipid-lowering effect of rosuvastatin and assessed the effect of lopinavir/ritonavir on the pharmacokinetics of rosuvastatin and vice versa.

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At baseline, median (interquartile range) PCSK9 concentrations were higher in women [73 (62-90)] ng/mL than in men [69 (57-81) ng/mL] (P<0.005). During 1 year, there was no change in PCSK9 concentrations in the placebo arm, suggesting stability in time. In contrast, the rosuvastatin increased PCSK9 by 35% in women [101 (82-117) ng/mL] and 28% in men [89 (71-109) ng/mL] (P<0.0001). Among those allocated to rosuvastatin, greater reductions in LDL-C were associated with greater increases in PCSK9 on both absolute and relative scales (r=-0.15, P<0.0005). Furthermore PCSK9 (rs11591147) did not alter the magnitude of LDL-C reduction associated with rosuvastatin use.

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Among participants in the rosuvastatin group, the mean (SD) baseline LDL cholesterol level of 155 (24.1) mg/dL declined to 78 (27.5) mg/dL, a mean reduction of 49% (P<.001 vs placebo group). The change in maximum CIMT for the 12 carotid sites was -0.0014 (95% CI, -0.0041 to 0.0014) mm/y for the rosuvastatin group vs 0.0131 (95% CI, 0.0087-0.0174) mm/y for the placebo group (P<.001). The change in maximum CIMT for the rosuvastatin group was -0.0038 (95% CI, -0.0064 to -0.0013) mm/y for the common carotid artery sites (P<.001), -0.0040 (95% CI, -0.0090 to 0.0010) mm/y for the carotid bulb sites (P<.001), and 0.0039 (95% CI, -0.0009 to 0.0088) mm/y for the internal carotid artery sites (P = .02). The change in mean CIMT for the rosuvastatin group for the common carotid artery sites was 0.0004 (95% CI, -0.0011 to 0.0019) mm/y (P<.001). All P values are vs placebo group. Overall, rosuvastatin was well tolerated with infrequent serious adverse cardiovascular events (6 participants [0.86%] had 8 events [1.1%] over 2 years).

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The human organic anion transporting polypeptide 2B1 (OATP2B1, SLCO2B1) is ubiquitously expressed and may play an important role in the disposition of xenobiotics. The present study aimed to examine the role of OATP2B1 in the intestinal absorption and tissue uptake of 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase inhibitors (statins). We first investigated the functional affinity of statins to the transporter as a function of extracellular pH, using OATP2B1-transfeced HEK293 cells. The results indicate that OATP2B1-mediated transport is significant for rosuvastatin, fluvastatin and atorvastatin, at neutral pH. However, OATP2B1 showed broader substrate specificity as well as enhanced transporter activity at acidic pH. Furthermore, uptake at acidic pH was diminished in the presence of proton ionophore, suggesting proton gradient as the driving force for OATP2B1 activity. Notably, passive transport rates are predominant or comparable to active transport rates for statins, except for rosuvastatin and fluvastatin. Second, we studied the effect of OATP modulators on statin uptake. At pH 6.0, OATP2B1-mediated transport of atorvastatin and cerivastatin was not inhibitable, while rosuvastatin transport was inhibited by E-3-S, rifamycin SV and cyclosporine with IC(50) values of 19.7 ± 3.3 μM, 0.53 ± 0.2 μM and 2.2 ± 0.4 μM, respectively. Rifamycin SV inhibited OATP2B1-mediated transport of E-3-S and rosuvastatin with similar IC(50) values at pH 6.0 and 7.4, suggesting that the inhibitor affinity is not pH-dependent. Finally, we noted that OATP2B1-mediated transport of E-3-S, but not rosuvastatin, is pH sensitive in intestinal epithelial (Caco-2) cells. However, uptake of E-3-S and rosuvastatin by Caco-2 cells was diminished in the presence of proton ionophore. The present results indicate that OATP2B1 may be involved in the tissue uptake of rosuvastatin and fluvastatin, while OATP2B1 may play a significant role in the intestinal absorption of several statins due to their transporter affinity at acidic pH.

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Randomized controlled and uncontrolled before-and-after trials evaluating the dose response of different fixed doses of rosuvastatin on blood lipids over a duration of three to 12 weeks.

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Our study subjects were treated with rosuvastatin (10 mg/day) over a period of 12 weeks. Blood was collected from these patients periodically and EPC levels were measured along with other biochemical parameters.

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An in vitro drugdrug interaction (DDI) study was performed to assess the potential for pradigastat to inhibit breast cancer resistance protein (BCRP), organic anion-transporting polypeptide (OATP), and organic anion transporter 3 (OAT3) transport activities. To understand the relevance of these in vitro findings, a clinical pharmacokinetic DDI study using rosuvastatin as a BCRP, OATP, and OAT3 probe substrate was conducted.

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To achieve enhanced estimates of rosuvastatin safety relative to other statins, by performing a meta-analysis of four rosuvastatin safety studies.

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An integrated database, consisting of 33 trials whose databases were locked up to and including September 16, 2005, was used to examine adverse events and laboratory data.

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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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This work supports the beneficial effects of rosuvastatin on venous thrombosis in mice with hyperlipidemia, due to its non-lipid lowering effects.

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Controversy persists regarding the extent of shared pathways between arterial and venous thrombosis and whether treatments of known efficacy for one disease process have consistent benefits for the other. Observational studies have yielded variable estimates of the effect of statin therapy on the risk of venous thromboembolism, and evidence from randomized trials is lacking.

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crestor drug classification 2017-09-30

Interventions to attenuate abnormal glycemia posttransplantation are required. In addition, surrogate markers of declining glycemic control are valuable. Statins may buy crestor have pleiotropic properties that attenuate abnormal glucose metabolism. We hypothesized statins would improve glucose metabolism and HbA1c would be advantageous as a surrogate for worsening glycemia. We conducted a prospective, randomized, placebo controlled, crossover study in 20 nondiabetic renal transplant recipients at low risk for NODAT and compared effects of rosuvastatin on insulin secretion/sensitivity. Mathematical model analysis of an intravenous glucose tolerance test determined first-phase insulin secretion, insulin sensitivity and disposition index. Second-phase insulin secretion was determined with a meal tolerance test. Biochemical/clinical parameters were also assessed. Rosuvastatin significantly improved total cholesterol (-30%, p < 0.001), LDL cholesterol (-44%, p < 0.001) and triglycerides (-19%, p = 0.013). C-reactive protein decreased but failed to achieve statistical significance (-31%, p = 0.097). Rosuvastatin failed to influence any glycemic physiological parameter, although an inadequate timeframe to allow pleiotropic mechanisms to clinically manifest raises the possibility of a type II statistical error. On multivariate analysis, glycated hemoglobin (HbA1c) correlated with disposition index (R(2)= 0.201, p = 0.006), first-phase insulin secretion (R(2)= 0.106, p = 0.049) and insulin sensitivity (R(2)= 0.136, p = 0.029). Rosuvastatin fails to modify glucose metabolism in low-risk patients posttransplantation but HbA1c is a useful surrogate for declining glycemic control.

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Maximal doses of atorvastatin and rosuvastatin are highly effective in lowering low-density lipoprotein (LDL) cholesterol and triglyceride levels; however, rosuvastatin has been shown to be significantly more effective than atorvastatin in lowering LDL cholesterol and in increasing high-density lipoprotein (HDL) and its subclasses. Our purpose in this post hoc subanalysis of an open-label study was to compare the effects of daily oral doses of rosuvastatin 40 mg with atorvastatin 80 mg over a 6-week period on direct LDL cholesterol and small dense LDL (sdLDL) cholesterol in 271 hyperlipidemic men and women versus baseline values. Rosuvastatin was significantly (p<0.01) more effective than atorvastatin in decreasing sdLDL cholesterol (-53% vs -46%), direct LDL cholesterol (-52% vs -50%), total cholesterol/HDL cholesterol ratio (-46% vs -39%), and non-HDL cholesterol (-51% vs -48%), The magnitude of these differences was modest, and the 2 statins caused similar decreases in triglyceride levels (-24% and buy crestor -26%). In conclusion, our data indicate that the 2 statins, given at their maximal doses, significantly and beneficially alter the entire spectrum of lipoprotein particles, but that rosuvastatin is significantly more effective than atorvastatin in lowering direct LDL cholesterol and sdLDL cholesterol.

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This was an observational analysis of prospectively collected data from primary care patients classified as new users of rosuvastatin or any other statin. New users (naïve or switched initiators) of rosuvastatin buy crestor were compared with initiators of other statins, as identified from automated healthcare databases in the first 1 to 2 years of rosuvastatin availability. Demographics, statin doses, previous statin use and other lipid-lowering therapies, and relevant comorbidities were recorded. The main outcome measure was proportion of naïve and non-naïve statin users in patients prescribed rosuvastatin or 'other statins'.

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There has been a steady increase in the epidemiology buy crestor of obesity over the last 30 years with developed countries leading the way. Oxidative stress was believed to be the principle contributor to the development of cardiovascular disorders that linked with obesity.

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There is evidence indicating that statins (3-hydroxy-methylglutaryl coenzyme A reductase inhibitors) may produce several cholesterol-independent antithrombotic effects. In this review, we provide an update on the current understanding of the interactions between statins and blood coagulation and their potential relevance to the prevention of venous thromboembolism (VTE). Anticoagulant properties of statins reported in experimental and clinical studies involve decreased tissue factor expression resulting in reduced thrombin generation and attenuation of pro-coagulant reactions catalysed by thrombin, such as fibrinogen cleavage, factor V and factor XIII activation, as well as enhanced endothelial thrombomodulin expression, resulting in increased protein C activation and factor Va inactivation. Observational studies and one randomized trial have shown buy crestor reduced VTE risk in subjects receiving statins, although their findings still generate much controversy and suggest that the most potent statin rosuvastatin exerts the largest effect.

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There is an unmet need of studies evaluating CVD prevention in IJD patients. We have buy crestor shown for the first time that long-term intensive lipid lowering with rosuvastatin improved arterial stiffness and induced a clinically significant BP reduction in patients with IJD. These improvements were linearly correlated and may represent novel insight into the pleiotropic effects by statins.

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This meta-analysis buy crestor provides evidence for improved efficacy in treating patients with hypercholesterolaemia with each sequential titration of rosuvastatin and a generally consistent tolerability profile across the dose range.

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BP and HR were recorded in unrestrained, nonanesthetized mice with implanted telemetry devices with or without rosuvastatin. Cardiac and aortic expression of endothelial NOS and caveolin-1 were measured by immunoblotting. Both systolic BP and HR were elevated in apoE-/- mice, with abolition of their circadian cycles. Spectral analysis showed an increase in their systolic BPV in the very-low-frequency (+17%) band and a decrease in HRV in the high-frequency (-57%) band, reflecting neurohumoral and autonomic dysfunction. Decreased sensitivity to acute injection of atropine or an NOS inhibitor indicated basal alterations in both parasympathetic and NOS buy crestor regulatory systems in apoE-/- mice. Aortic caveolin-1 protein, an inhibitor of endothelial NOS, was also increased in these mice by 2.0-fold and correlated positively with systolic BPV in the very-low-frequency band. Rosuvastatin treatment corrected the hemodynamic and caveolin-1 expression changes despite persisting elevated plasma cholesterol levels.

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Plasma CCL21 was measured at randomization in 1456 patients enrolled in the Controlled Rosuvastatin Multinational Trial in HF (CORONA) and in 1145 from the GISSI-HF trial. Association between CCL21 levels [given below as hazard ratio (HR) with 95% confidence interval (CI) for 1 SD increase] with all-cause (n = 741) or cardiovascular (CV) mortality (n = 576) was evaluated with multivariable Cox proportional hazard models, adjusting for clinical risk factors, C-reactive protein, and NT-proBNP. In multivariable Cox models, CCL21 was associated with higher risk of all-cause mortality (HR 1.16, 95% CI 1.02-1.32; P = 0.020) and CV mortality (HR 1.20, 95% CI 1.08-1.33; P < 0.001). When buy crestor the two trials were analysed separately, CCL21 had a similar influence on risk prediction. Finally, CCL21 had a modest but significant impact on the discriminatory properties of the model (all-cause mortality, change in Harrell's C-statistic 0.004, P = 0.001; CV mortality, change in C-statistic 0.002, P = 0.002).

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Forty-five patients with hypercholesterolemia and asymptomatic carotid atherosclerosis on baseline carotid ultrasound investigation (CUI) were examined with repeat CUI after 1 year of treatment (rosuvastatin 10 mg/day). Demographic and lifestyle data were collected. A physical examination was performed, and fasting venous blood samples were obtained. Total buy crestor cholesterol, low-density lipoprotein cholesterol and triglycerides decreased significantly (p < 0.001), while high-density lipoprotein cholesterol increased significantly (p < 0.001) during the intervention. The mean decreases in the IMT of the right and left common carotid arteries (CCAs) were 0.29 and 0.26 mm, respectively (p < 0.05 for each). Age and lipid profile parameters were significant predictors of change in CIMT in linear regression analyses after adjustment for established atherosclerosis risk factors.

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Of the buy crestor two new biomarkers studied in prognostic models in heart failure, NT-proBNP, but not hsCRP, added substantial and independent predictive information, for a range of clinical outcomes, to that provided by simple demographic, clinical, and biochemical measures. ApoA-1 was more predictive than LDL or HDL.

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This article provides information and a commentary on trials relevant to the pathophysiology, prevention and treatment of heart failure, presented at the American College of Cardiology 55th Annual Scientific Session held in March 2006. All reports should be considered as preliminary data, as analyses may change in the final publication. Darbepoetin alfa increased haemoglobin levels in heart failure patients and improved some aspects of quality of life compared to placebo. In the ASTEROID study rosuvastatin significantly reduced LDL-cholesterol levels and induced regression of atherosclerosis in patients with CAD. Rosuvastatin also produced a significant reduction in LDL-cholesterol levels in heart failure patients in the UNIVERSE study, but had no effect on left ventricular remodelling compared to placebo. The paediatric carvedilol study failed to show a benefit of carvedilol in children with heart failure. Ultrafiltration produced a greater weight and fluid loss than intravenous diuretics in heart failure patients with volume overload in the UNLOAD study but did not exert a greater improvement in breathlessness; however, ultrafiltration did reduce readmission rates. The ICELAND MI study showed that CMR imaging was more sensitive buy crestor than ECG or clinical criteria for detecting myocardial infarction.

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Bevezetés: A dyslipidaemia ismert cardiovascularis kockázati tényező. A lipidterápiában a célértékek elérésének fontos tényezője a megfelelő betegadherencia. Célkitűzés: A MULTI GAP (MULTI Goal Attainment Problem) 2013-as vizsgálatban atheroscleroticus betegségben szenvedő betegek esetében a statinterápia adherenciájának és perzisztenciájának felmérése, amely részben a vizsgálatban részt vevő orvosok becslésén, illetve 319, a megelőző évben elvégzett MULTI GAP vizsgálatban részt vett beteg esetében az Országos Egészségbiztosítási Pénztár vénykiváltási adatbázisán alapult. Módszer: A MULTI GAP 2013 vizsgálatban standard, strukturált kérdőívek segítségével 1519 beteg adatai kerültek feldolgozásra. Az elemzésben kiértékelésre kerültek az egyes ellátási szinteken elért lipidértékek, a kezelőorvos által vélt betegadherencia, a 319 beteg Országos Egészségbiztosítási Pénztár vénykiváltási adataira támaszkodó valós adherencia, a kezelőorvosok elégedettsége a statinterápia eredményeivel, illetve az adherencia és a lipideredmények összevetése. Eredmények: Az elmúlt 7 év felméréseinek adatait is figyelembe véve előtérbe kerültek a hatékonyabb statinok; az atorvastatin és rozuvastatin alkalmazásának összesített aránya 49%-ról 83%-ra, azaz mintegy 70%-kal nőtt. A betegadherencia vonatkozásában kimutatták, hogy a 2,5 mmol/l alatti LDL-koleszterin-értékeket elért betegeknél az 1 év alatt kiváltott receptek száma mintegy nyolc gyógyszertári beváltást jelentett. Ehhez képest a 2,5 mmol/l feletti LDL-koleszterin-értékű csoportban a gyógyszerkiváltás lényegesen alacsonyabb volt (5,3 és 6,3 közötti). Éves szinten a 10–12 és a 7–9 gyógyszerkiváltás szignifikánsan alacsonyabb LDL-koleszterin-szintet jelentett a semennyit (0), illetve az 1–3 receptet éves szinten kiváltók csoportjaihoz képest. A kezelőorvosok által 100%-os perzisztenciájúnak értékelt betegek valódi perzisztenciája 74%-os volt az Országos Egészségbiztosítási Pénztár adatbázisa szerint, amely mintegy 25%-kal alacsonyabb, mint a valóság. A kezelőorvosok a lipidcsökkentő terápia adherenciáját a betegek mintegy felében ítélték 100%-nak, ezzel szemben az Országos Egészségbiztosítási Pénztár adatai 36%-ot mutattak. A jobb adherenciájú betegek (90–100%) nagyobb arányban (59,5%) értek el 2,5 mmol/l alatti LDL-koleszterin-értékeket, mint az alacsonyabb adherenciájúnak tartott betegek. A kezelőorvosok elégedettsége a lipidértékekkel a 4,5–6 mmol/l közötti összkoleszterin-értékű csoportban 69–80%-ig terjedt, azonban igen magas, 53–54%-os elégedettséget mutattak a 7 feletti összkoleszterin-szintű betegek csoportjában. Következtetések: A vizsgálat eredményei szerint buy crestor a vélt adherencia lényegesen magasabb az Országos Egészségbiztosítási Pénztár adatain alapuló elemzéshez viszonyítva. Ugyanakkor a magas lipidértékű betegekkel szemben a kezelőorvosok megelégedettsége is igen magasnak bizonyult. Mindezek arra utalnak, hogy nemcsak a betegek, hanem az orvosok adherenciáját is javítani kell a lipidcsökkentő irányelvekhez. Orv. Hetil., 2014, 155(17), 669–675.

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CRP levels are still associated with the MetS in patients treated with intensive lipid lowering therapy. buy crestor

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In this randomised, parallel-group study, asymptomatic subjects at low risk of cardiovascular disease, but with evidence of atherosclerosis (defined as carotid IMT >or=1.2 mm and <3.5 mm), will receive rosuvastatin (40 mg/day) or placebo for 104 weeks. The study will enrol 840 European and US subjects randomised 5 Celexa Reviews Ocd :2 between rosuvastatin and placebo. The primary end point will be the change in carotid IMT from baseline to study end, measured using B-mode ultrasonography. Other efficacy end points include changes in the serum lipid profile and C-reactive protein. Safety parameters will also be assessed.

crestor medication 2017-02-27

clinicaltrials. Reglan 800 Mg gov Identifier: NCT01763866.

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Administered at maximal dosages, the most common statins--atorvastatin, simvastatin and rosuvastatin--lower Avapro 75mg Generic low-density lipoprotein cholesterol (LDLC) by an average of 37-57% in patients with primary hypercholesterolemia. We hypothesized novel genetic underpinnings for variation in LDLC levels in the context of statin therapy.

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In conclusion, both treatments, rosuvastatin and B-group vitamin supplementation, improved endothelial function in high-risk cardiovascular patients. The combination of both therapies had an additive effect on endothelial function suggesting Naprosyn 440 Mg different mechanisms of action.

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Familial hypercholesterolemia is a common inherited disorder causing markedly elevated low-density lipoprotein cholesterol (LDL-C) levels from birth and resulting in premature atherosclerosis. In children, statins have been shown to be effective in reducing LDL-C, restoring flow-mediated dilation, and slowing carotid intima-media thickening. However, few children in these Bactroban Buy Online trials achieved current LDL-C goals.

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The neuromuscular blocking potency of rocuronium is increased Propecia Dosage 5mg and recovery is delayed in rats that pre-treated with rosuvastatin.

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Although statins have been shown to prevent contrast-induced acute kidney injury in patients with acute coronary syndromes, the benefit of statins is not known for patients at high risk for nephropathy who undergo elective coronary angiography. Two hundred twenty consecutive statin-naive patients with chronic kidney disease (estimated glomerular filtration rate <60 ml/min/1.73 m(2)) who underwent elective coronary or peripheral angiography were randomly assigned to receive rosuvastatin (40 mg on admission, followed by 20 mg/day; n = 110) or no statin treatment (control group, n = 110). Contrast-induced acute kidney injury was defined by an absolute increase in serum creatinine of ≥0.5 mg/dl or a relative increase of ≥25% measured 48 or 72 hours after the procedure. Contrast-induced acute kidney injury occurred in 15 patients (7.2%), 9 (8.5%) in the control group and 6 (5.8%) in the rosuvastatin group (p = 0.44). The incidences of adverse cardiovascular and renal events (death, dialysis, myocardial infarction, stroke, or persistent renal damage) were similar between the two groups at follow-up. In conclusion, rosuvastatin did not reduce the risk for contrast-induced acute kidney injury Valtrex 30 Mg or other clinically relevant outcomes in at-risk patients who underwent coronary and peripheral vascular angiography.

crestor generic rosuvastatin 2015-08-12

This study indicated that the number of outcome events is less than 1 per 3000 person years. This study in more than 45,000 Dutch statin users suggests that rosuvastatin does not lead to an increased incidence of rhabdomyolysis, myopathy, acute renal failure or hepatic impairment compared to other statins.

crestor 10mg medication 2016-01-27

The in vitro sensitivity of Plasmodium falciparum to atorvastatin and rosuvastatin was assessed using chloroquine-sensitive and chloroquine-resistant strains. Although atorvastatin was more potent, it had weak activity (mean 50% inhibitory concentration of > or = 17 microM) and an indifferent interaction with chloroquine and dihydroartemisinin. Bioassay of plasma from an atorvastatin-treated subject showed similar results.

crestor generic alternative 2015-04-24

Activation of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase by angiotensin II is integral to the formation of oxidative stress in the vasculature and the kidney. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibition is associated with reductions of oxidative stress in the vasculature and kidney and associated decreases in albuminuria. Effects of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibition on oxidative stress in the kidney and filtration barrier integrity are poorly understood. To investigate, we used transgenic TG(mRen2)27 (Ren2) rats, which harbor the mouse renin transgene and renin-angiotensin system activation, and an immortalized murine podocyte cell line. We treated young, male Ren2 and Sprague-Dawley rats with rosuvastatin (20 mg/kg IP) or placebo for 21 days. Compared with controls, we observed increases in systolic blood pressure, albuminuria, renal NADPH oxidase activity, and 3-nitrotryosine staining, with reductions in the rosuvastatin-treated Ren2. Structural changes on light and transmission electron microscopy, consistent with periarteriolar fibrosis and podocyte foot-process effacement, were attenuated with statin treatment. Nephrin expression was diminished in the Ren2 kidney and trended to normalize with statin treatment. Angiotensin II-dependent increases in podocyte NADPH oxidase activity and subunit expression (NOX2, NOX4, Rac, and p22(phox)) and reactive oxygen species generation were decreased after in vitro statin treatment. These data support a role for increased NADPH oxidase activity and subunit expression with resultant reactive oxygen species formation in the kidney and podocyte. Furthermore, statin attenuation of NADPH oxidase activation and reactive oxygen species formation in the kidney/podocyte seems to play roles in the abrogation of oxidative stress-induced filtration barrier injury and consequent albuminuria.

crestor generic brand 2017-01-21

To investigate the effect of intensive rosuvastatin therapy on adhesion molecules in patients with peripheral atherosclerosis and explore the possible upstream mechanism.

crestor 80 mg 2015-01-03

Despite the favorable effects of reduction of low-density lipoprotein-cholesterol (LDL-C) levels in decreasing the risk of coronary heart disease, many patients treated with lipid-lowering HMG-CoA reductase inhibitors (statins) do not achieve goal LDL-C levels. This may be due to high doses of statins prescribed that could potentially induce adverse effects and compromise patient safety and compliance with considerable expense in the long-term. We compared the actions of rosuvastatin and atorvastatin, administered at the low dosages of 10 and 20 mg/day, respectively, in reducing plasma LDL-C levels and their effects on other components of the atherogenic lipid profile in patients with primary hypercholesterolemia.

crestor dosage amounts 2017-10-02

To estimate the cost-effectiveness of 10 mg rosuvastatin daily for older patients with systolic heart failure in the Controlled Rosuvastatin Multinational Study in Heart Failure (CORONA) trial.

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In the JUPITER trial, participants without prior cardiovascular disease or diabetes who had low-density lipoprotein cholesterol <130 mg/dL and C-reactive protein ≥2 mg/L were randomly allocated to rosuvastatin 20 mg or placebo and followed for the first cardiovascular disease events and adverse effects. We evaluated the effect of rs4363657 and rs4149056 in SLCO1B1, which encodes organic anion-transporting polypeptide OATP1B1, a regulator of hepatic statin uptake, on clinically reported myalgia.

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The percentage change of LDL-C ranged from -45% to -56% (mean, -51%) in the monotherapy groups and from -58% to -63% (mean, -60%) in the combination therapy groups. The percentage change was greater in the pooled combination therapy group than in the counterpart (P < 0.001 for the pooled groups); this difference was more obvious for regimens with a lower statin dose. The percentage reductions of total cholesterol and triglycerides were greater in the combination groups than in the monotherapy groups. The LDL-C target achievement rates were 64% to 87% (mean, 73%) in the monotherapy groups and 87% to 95% (mean, 91%) in the combination groups (P = 0.01 for the pooled groups). The rates were significantly greater in patients receiving the combination therapy than in the monotherapy at lower doses of rosuvastatin. The proportions of patients with various adverse events were not significantly different between the groups.

crestor 60 mg 2015-04-23

Among the recently reported cholesterol-lowering drug trials, the JUPITER (Justification for the Use of Statins in Primary Prevention) trial is unique: it reports a substantial decrease in the risk of cardiovascular diseases among patients without coronary heart disease and with normal or low cholesterol levels.