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The healthy endothelium plays a key roll in vascular regulation. This function can be examined non-invasively by use of B-mode ultrasound on the brachial artery. The aim of this study was to measure the effect of low-dose and high-dose lipid-lowering treatment with rosuvastatin on the endothelial function evaluated with endothelium-dependent and endothelium-independent flow-mediated dilatation (FMD).
Twelve and 24-hour post-PCI Creatine Kinase Muscle and Brain (CK-MB) elevation >3× occurred more frequently in the CG than in the RG and in the AG (at 24-h: 25.0 vs 7.1; p=0.003 and 25.0 vs 6.1; p=0.001). At 30-day, 6-and 12-month follow-up the incidence of cumulative MACCE was higher in CG than in the RG or AG (at 12-month: 41.0% vs 11.4% vs 12.0%; p=0.001). There was no difference between the RG and AG in terms of myocardial post-procedural necrosis and MACCE occurrence at follow-up.
The study enrolled 12 healthy Chinese volunteers (6 men: mean [SD] age, 22.3 [1.5] years; mean [SD] weight, 61.8 [2.4] kg [range, 59-64 kg]; 6 women: mean [SD] age, 21.6 [1.4] years; mean [SD] weight, 56.4 [6.4] kg [range, 50-64 kg]). Geometric mean (SD) C(max) values of 10.22 (8.05), 25.86 (18.77), and 44.99 (17.99) ng/mL were achieved at a median T(max) of 2.5 hours after administration of single doses of 5, 10, and 20 mg of rosuvastatin, respectively; the corresponding geometric mean (SD) values of AUC(0-t) were 73.67 (48.78), 210.21 (178.70), and 303.81 (193.29) ng/mL . h(-1), and the mean (SD) apparent elimination t(1/2) values were 13.01 (8.68), 13.33 (5.21), and 15.40 (5.43) hours after administration. The Student-Newman-Keuls test results found that C(max) and AUC(0-t) were both linearly related to dose. In men, the mean (SD) C(max) values were 7.57 (6.49), 20.43 (14.10), and 36.80 (15.64) ng/mL, and the mean (SD) AUC(0-t) values were 51.74 (33.92), 136.35 (97.18), and 232.25 (101.66) ng/mL x h(-1), with the 5-, 10-, and 20-mg doses of rosuvastatin, respectively. In women, the corresponding C(max) values were 13.40 (9.27), 32.44 (23.10), and 54.82 (16.78) ng/mL, and AUC(0-t) values were 99.99 (54.07), 298.85 (223.66), and 430.21 (194.61) ng/mL x h-1. Results of the t tests of (lg)C(max) and (lg)AUC(0-t) found no significant differences between the male and female groups. However, C(max) and AUC(0-t) values of 0.82 ng/mL and 6.87 ng/mL x h-1, respectively, after oral administration of 10 mg of rosuvastatin in the fed state were significantly different from the corresponding values under fasting conditions (both, P < 0.05). Two adverse events (pharyngitis and nausea) were reported in 3 subjects (2 women, 1 man) at the 20-mg fasting state. Two cases of elevated laboratory values (bilirubin, from 16.1 micromol/L at baseline to 31.4 micromol/L; phosphocreatine, from 141 U/L at baseline to 307 U/L) were found at the poststudy follow-up immediately after study completion in 2 volunteers (1 man, 1 woman) at the 10-mg fed state; both values had returned to normal 5 days later.
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Two-year change in GSM did not significantly differ between rosuvastatin and placebo in the total population, with a mean difference in the rate of change in GSM of 1.13 (95% confidence interval, -1.00 to 3.25). The effect of rosuvastatin differed across quintiles of baseline GSM values (P for interaction = .01). In the lowest quintile (n = 175) (i.e., in those with the most echolucent intima-media), the difference in the rate of change in GSM between rosuvastatin and placebo was 4.18 (95% confidence interval, -0.23 to 8.58). Increases in GSM were significantly related to decreasing low-density lipoprotein cholesterol levels in the lowest quintile (β = 0.76; 95% confidence interval, 0.26 to 1.25).
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Platelet-vessel wall interaction and thrombosis take place under dynamic conditions involving the interaction of the exposed damaged vascular wall with the circulating blood cells and proteins. Blood was perfused over type I collagen at different wall shear rates, and platelet deposition was measured by confocal microscopy. Perfused effluent blood was collected, platelets were sequentially extracted based on differential protein solubility, and proteins were separated by 2D gel electrophoresis. Blockade of 3-hydroxy-3-methylglutaryl-coenzyme A reductase significantly reduced platelet deposition and modulated the expression pattern of 18 proteins in the platelet subproteome. Among them, an increase in platelet surface 78-kDa glucose-regulated protein (GRP78), a stress-inducible multifunctional endoplasmic reticulum protein, was clearly apparent. Immunoprecipitation of platelet GRP78 revealed its interaction with tissue factor. Moreover, blockade of surface GRP78 resulted in a substantial increase in platelet deposition and tissue factor procoagulant activity and in a decrease in clotting time.
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Carotid artery stenting (CAS) is a worldwide diffuse intervention, but may be associated with distal plaque component embolization, and sometimes major and minor stroke. Statin use has been demonstrated to reduce atherosclerotic plaque burden, but its effect in reducing distal embolization during carotid stenting has not yet been well validated.
Pubmed, EMBASE, Cochrane Central Register of Controlled Trials and ISI Web of Science databases were systematically searched for randomized controlled trials (RCTs) up to June 2015. We assessed the incidence of MACE and PMI in all enrolled patients for subgroups stratified by clinical presentation and previous statin therapy during the follow-up period.
ODYSSEY Outcomes will determine whether the addition of the PCSK9 antibody alirocumab to intensive statin therapy reduces cardiovascular morbidity and mortality after ACS.
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Ezetimibe has been reported to provide significant incremental reduction in low-density-lipoprotein cholesterol (LDL-C) when added to a statin; however, its effect on coronary atherosclerosis has not yet been evaluated in detail. The aim of this study was to investigate the add-on effect of ezetimibe to a statin on coronary atherosclerosis evaluated by intravascular ultrasound (IVUS).In this prospective randomized open-label study, a total of 51 patients with stable coronary artery disease (CAD) requiring percutaneous coronary intervention (PCI) were enrolled, and assigned to a combination group (n = 26, rosuvastatin 5 mg/day + ezetimibe 10 mg/day) or a monotherapy group (n = 25, rosuvastatin 5 mg/day). Volumetric IVUS analyses were performed at baseline and 6 months after the treatment for a non-PCI site. LDL-C level was significantly reduced in the combination group (-55.8%) versus that in the monotherapy group (-36.8%; P = 0.004). The percent change in plaque volume (PV), the primary endpoint, appeared to decrease more effectively in the combination group compared with the monotherapy group (-13.2% versus -3.1%, respectively, P = 0.050). Moreover, there was a significant group × time interaction in the effects of the two treatments on PV (P = 0.021), indicating the regressive effect of the combination therapy on PV was greater than that of monotherapy for subtly different values of baseline PV in the two treatment groups. Moreover, percent change in PV showed positive correlations with percent change of LDL-C (r = 0.384, P = 0.015).Intensive lipid-lowering therapy with ezetimibe added to usual-dose statin may provide significant incremental reduction in coronary plaques compared with usual-dose statin monotherapy.
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Treatment with yellow wine increased NO production, eNOS activity, and eNOS protein expression, which decreases iNOS and ICAM-1 protein expression. We conclude that yellow wine may have similar beneficial effects as rosuvastatin on the cardiovascular system. These effects may be attributed to their anti-atherosclerotic actions.
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Expression of the organic anion transporting polypeptide 1B1 (OATP1B1) is regulated by transcription factor hepatic nuclear factor (HNF) 1alpha. The aim of this study was to investigate the effect of ursodeoxycholic acid (UDCA), an inhibitor of transcription factor HNF1alpha, on rosuvastatin and bilirubin kinetics in human healthy volunteers. Both substances are substrates of OATP1B1. Twelve subjects with OATP1B1(*)1b/(*)1b genotype predicting high transport activity were recruited for this randomized, crossover study. Each subject received a single p.o. dose of 20 mg of rosuvastatin after 14 days of p.o. intake of either 500 mg of UDCA or placebo. Plasma concentrations of rosuvastatin were determined on days 15 to 18 of each study period. Subjects were randomly assigned to UDCA or placebo group. Intake of UDCA led to a significant increase in rosuvastatin area under the curve (AUC)(0-72) from 128.5 ng/ml.h to 182.1 ng/ml.h(P = 0.008) compared with the control group. The oral clearance decreased from 155.2 l/h with placebo to 109.8 l/h with UDCA. In addition, the mean values of total bilirubin, conjugated bilirubin, and unconjugated bilirubin significantly increased to 139 +/- 39% (P = 0.003), 127 +/- 29% (P = 0.005), and 151 +/- 52% (P = 0.004), respectively, after UDCA treatment. These results in healthy volunteers confirm the findings from in vitro studies that UDCA inhibits OATP1B1 activity by inhibition of the transcription factor HNF1alpha. They highlight a novel mechanism of OATP1B1-based interaction that is mediated by transcription factor HNF1alpha.
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The mean systolic blood pressure (SBP) initially reached 164.26 mm Hg. During the whole follow-up, the reduction in mean SBP generally accounted for 22.6% (p = 0.000). At the study inclusion, the mean diastolic blood pressure (DBP) reached 99.38 mm Hg. The total decline in mean DBP was 19.3% (p = 0.000). The mean level of total cholesterol (TC) decreased significantly by 32.1% (p = 0.000); that of triglycerides (TG) also fell significantly by 31.8% (p = 0.04); that of high-density lipoproteins increased insignificantly by 11.1% (p = 0.599); that of low-density lipoproteins (LDL) dropped significantly by 47.5% (p = 0.000).
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Rosuvastatin ameliorates insulin sensitivity induced by HFD in rats. This effect is mediated by several mechanisms including reduction of leptin and enhancement of SIRT-1, PPAR-γ and GLUT-4 expression in white adipose tissue. SIRT1 could be considered a major mediator of the beneficial effects of rosuvastatin on insulin sensitivity in overweight rats induced by diet.
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The National Cholesterol Education Program Adult Treatment Panel III guidelines and the results of the Heart Protection Study have provided a stronger rationale to more aggressively treat high-risk patients to a low-density (LDL) cholesterol goal of less than 100 mL/dL. Two new therapies, ezetimibe and rosuvastatin, have recently been added to the lipid-lowering armamentarium to improve guideline adherence. Ezetimibe, a novel cholesterol absorption inhibitor, lowers LDL by 18% to 20% and can be used safely in combination with statins. Adding ezetimibe to a statin is comparable with the LDL-lowering efficacy of tripling the dose of the statin. Rosuvastatin is a highly efficacious statin providing 8% greater LDL reduction than equivalent doses of atorvastatin, and the starting dose of 10 mg/d provides nearly a 50% reduction in LDL cholesterol. There are several investigational drugs in development for the prevention and treatment of atherosclerosis. Of these investigational drugs, the most promising are the cholesterol ester transfer protein inhibitors, which have the potential to significantly raise high-density lipoprotein cholesterol and acetyl-coenzyme A: cholesterol acyltransferase inhibitors, which may directly inhibit the progression of atherosclerosis.
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Data were used from a trial on the effects of Rosuvastatin on rate of change in carotid intima-media thickness (CIMT). The reference treatment effect was derived from a complete data set. Scenarios and proportions of missing values in CIMT measurements were applied and LME analyses were used before and after MI. The added value of MI, in terms of bias and precision, was assessed using the mean-squared error (MSE) of the treatment effects and coverage of the 95% confidence interval.
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Thirty-six patients were randomly assigned to 10 mg/day of rosuvastatin (n = 18) or 20 mg/day of atorvastatin (n = 18) for 12 weeks. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-HDL-C, triglycerides (TG), fasting plasma glucose, insulin, homeostasis model assessment-insulin resistance (HOMA-IR), quantitative IS check index (QUICKI), adiponectin, leptin and high-sensitivity C-reactive protein (hsCRP) were measured at baseline and after 4 and 12 weeks.
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Fibrates activate peroxisome proliferator activated receptor α and exert beneficial effects on triglycerides, high-density lipoprotein cholesterol, and low density lipoprotein subspecies. Fenofibric acid (FA) has been studied in a large number of patients with mixed dyslipidemia, combined with a low- or moderate-dose statin. The combination of FA with simvastatin, atorvastatin and rosuvastatin resulted in greater improvement of the overall lipid profile compared with the corresponding statin dose. The long-term efficacy of FA combined with low- or moderate- dose statin has been demonstrated in a wide range of patients, including patients with type 2 diabetes mellitus, metabolic syndrome, or elderly subjects. The FA and statin combination seems to be a reasonable option to further reduce cardiovascular risk in high-risk populations, although trials examining cardiovascular disease events are missing.
Rosuvastatin (RSV) is a synthetic statin with favourable pharmacologic properties, but its local effect in bone has yet to be investigated. The aim of this study was to evaluate the potential of absorbable collagen sponge (ACS) as a carrier for RSV to enhance bone formation in critical-size cortical bone defects adjacent to titanium implants. ACS, treated with different concentrations of RSV (R1 = 8.7 + or - 1.8 microg; R2 = 52.0 + or - 4.4 microg; R3 = 259.1 + or - 8.8 microg) or phosphate-buffered saline alone, were placed into the bone marrow through a defect made in the proximal tibial cortical bone of New Zealand White rabbits. One empty defect (SHAM) served as an internal control in each animal. After a healing time of 4 weeks, a concentration-dependent increase of alkaline phosphatase activity in ACS treated with RSV was detected in the bone fluid after removing the implants. In addition, a significant concentration-dependent increase in BMP-2 mRNA levels was found in the cortical bone tissue adjacent to the RSV-treated ACS. The cortical architecture of bone defects analysed by micro-computed tomography showed a trend towards higher bone volume in the ACS+R1 group compared with SHAM, which was accompanied by an increase in the bone mineral density. Evaluation of histological sections showed new bone formation in ACS treated with RSV but not in untreated ACS. These results indicate that RSV, when administered locally in bone, may have a potential effect in stimulating bone formation.
With the growing clinical usage of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), the number of reports concerning serious drug-drug interaction has been increasing. Because recent studies have shown that conversion between acid and lactone forms occurs in the body, drug-drug interaction should be considered on both acid and lactone forms. Thus, we investigated the inhibitory effects of acid and lactone forms of eight statins, including one recently withdrawn, cerivastatin, and two recently developed, pitavastatin and rosuvastatin, on cytochrome P450 (CYP) 2C8, CYP2C9, and CYP3A4/5 metabolic activities and multidrug resistance protein 1 (MDR1) transporting activity.
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The results presented open the possibility that in humans, rosuvastatin may affect the metabolism of many drugs by influencing expression and activity of CYP2C6 (counterpart of human CYP2C9). Further studies are needed to elucidate the effects of this statin on CYP2C9 in humans.
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AMI and UA patients had higher NLRP3, cathepsin-B, interleukin-18 (IL-18), pro-IL-18, IL-1β, and pro-IL-1β expressions as compared with the control group (P<0.05). This corresponded with higher levels of serum total cholesterol, serum low-density lipoprotein cholesterol, and oxidized low-density lipoprotein in UA and AMI patients (P<0.05). Rosuvastatin at a concentration of 20 mg led to a significant decrease (P<0.05) in the expressions of NLRP3, cathepsin-B, and their downstream cytokines as compared with 5 mg rosuvastatin (P>0.05) from baseline to 4 weeks. This study also showed a positive correlation between NLRP3, cathepsin-B, and downstream inflammatory mediators.
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Rosuvastatin lowered free fatty acids (FFA), triglycerides, and increased insulin sensitivity, without affecting cholesterol. Rosuvastatin lowered the plaque volume, inhibited macrophage, lipid and oxLDL accumulation, and decreased the oxLDL-to-LDL ratio of plaques in the aortic arch. It increased superoxide dismutase 1 (SOD1), CD36, LXR-alpha, ABCA-1 and PPAR-gamma RNA expression in aortic extracts. SOD1 was the strongest inverse correlate of oxLDL. In THP-1 macrophages and foam cells, expression of SOD1 was lower than in THP-1 monocytes. Rosuvastatin restored expression of SOD1 in THP-1 macrophages and foam cells.
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Coronary Heart Disease (CHD) is the most important complication and the leading cause of death in patients with type 2 diabetes mellitus (T2DM). Hypercholesterolemia is an important modifiable risk factor for CHD. Statins are the first line drugs for the treatment of hypercholesterolemia in DM. Comparative studies between different statins are available but different doses of the same statin have not been compared in our population. The objective of this study is to compare mean reduction in serum LDL-C level after using 5mg and 10mg of rosuvastatin among T2DM patients with hypercholesterolemia. This study will help finding lowest effective dose of rosuvastatin to achieve internationally set low density lipoprotein cholesterol (LDL-C) goals.