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Exposure (as based on area under the curve) to simvastatin and 6β-hydroxyacid simvastatin increased (90 % confidence interval) 4.63-fold (3.90, 5.50) and 3.71-fold (3.19, 4.32), respectively, when comparing day 9 and day 1. On day 9, exposure to atorvastatin was similar but Cmax decreased, while both variables decreased for ortho-hydroxy atorvastatin when compared to day 1. On day 31, after prolonged administration of ACT-178882, exposure to atorvastatin, ortho-hydroxy atorvastatin, simvastatin, and 6β-hydroxyacid simvastatin decreased by 14, 19, 21, and 27 %, respectively, when compared to day 9. However, on this day, exposure to simvastatin and its metabolite was still markedly higher when compared to day 1. Effects of ACT-178882 had largely dissipated on day 41.
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Exogenous CO constricted, rather than dilated, arterioles from both age groups. This constriction was reduced by endothelial removal or NOS inhibition in juvenile, but not weanling, arterioles. In contrast, this constriction was abolished by K(+) channel inhibition in weanling, but not juvenile, arterioles. The heme precursor delta-aminolevulinic acid constricted juvenile arterioles but did not affect weanling arterioles. The heme oxygenase inhibitor chromium (III) mesoporphyrin IX abolished the endothelium-dependent dilation of juvenile arterioles to simvastatin, and reduced ACh- and simvastatin-induced dilations of weanling arterioles.
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We analysed 25,075 patient exposures from high-risk patients. Paired comparisons were made between each rosuvastatin dose and an equal or higher dose of either atorvastatin or simvastatin, with a series of meta-analyses that included only randomised studies that directly compared rosuvastatin and its comparator treatments.
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We describe two patients treated with a combination of cyclosporin and simvastatin who had to be hospitalized due to rhabdomyolysis. As suggested by reduced cyclosporin clearance, both patients had impaired activity of the hepatic cytochrome P450 enzyme system, which may have contributed to the development of rhabdomyolysis. After cessation of treatment with simvastatin and intensive hydration, both patients recovered within one week. While rhabdomyolysis has been described in several patients receiving the combination lovastatin/cyclosporin, so far only one case has been reported in patients treated with simvastatin/cyclosporin. Our cases therefore suggest that this complication may be more frequent than previously suspected. In patients treated with cyclosporin, HMG-CoA reductase inhibitors should be used cautiously, and concomitant administration of drugs inhibiting the hepatic cytochrome P450 enzyme system should be avoided.
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It was an experimental study. Forty adult male Wistar rats were randomly divided into normal control group (10 rats) and diabetes mellitus group (30 rats). Four months later, according to whether treated with simvastatin or not, the diabetes mellitus group randomly divided into simvastatin intervention group (20 rats) and diabetic positive control group (10 rats). Simvastatin was injected into the vitreous in the simvastatin intervention group, but not in the diabetic positive control group. Seven days later, after the examination of electroretinogram (ERG), all rats were sacrificed, and their eyeballs were enucleated. Enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry method were performed to determine the expression of CTGF in the vitreous and retina. Terminal DNA transferase-mediated dUTP nick end labeling (TUNEL) method was used to detect apoptosis of retina cells. Concentration of CTGF in the vitreous, retinal expression of CTGF, retinal cellular apoptosis index, ERG-b wave and oscillatory potentials (OPs) of rats in each group were compared using analysis of variance LSD test methods.
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In asymptomatic AS patients without known atherosclerotic disease or diabetes mellitus, ELI provides independent and additional prognostic information to that derived from conventional measures of AS severity, suggesting that ELI should be measured in such patients.
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Recent clinical studies have demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are effective in the prevention of cardiovascular events and regression of atherosclerotic lesions evaluated by angiography. In this study, the authors investigated how lipid-lowering therapy effects on the progression of aortic atherosclerosis by using plain and enhanced computed tomography (CT) of the lower abdominal aorta. Twenty-nine hyperlipidemic patients (mean age 61.4 +/- 7.2 yr) were enrolled in a prospective open-labeled study. All patients underwent baseline CT scanning of abdominal aorta, screening for serum lipid profile and coagulation-fibrinolysis measurement, then treatment with simvastatin was begun. After 2 years, a follow-up CT scan was done and atherosclerotic lesions were compared between baseline and on-treatment scan. In spite of significant improvement of lipid and fibrinolytic profiles by simvastatin administration, mean aortic wall thickening volume (AWV) was increased during observation period. When patients were divided into subgroups by the levels of on-treatment LDL cholesterol (LDL-C), development rate of AWV was more potently suppressed in patients whose on-treatment LDL-C were below 125 mg/dL (median LDL-C). We could not find any associations of coagulation-fibrinolysis measurements with atherosclerotic lesions. In regard to aortic calcification volume (ACV), low levels of total and HDL cholesterol and higher age were associated with aortic calcification at baseline. These results suggest that aggressive treatment with LDL-C below 125 mg/dL may suppress the progression of wall thickening and factors that promote arterial calcifications and those for wall thickening may be different.
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For the doses assessed, EZE/SIMVA was more effective compared with ATORVA in lowering the lipoprotein and apolipoprotein ratios that might be considered secondary measures of CHD risk.
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Aralia mandshrica is a well-known traditional Chinese medicine from Northeast China commonly used to treat digestive, circulatory and immune system disorders. Calenduloside E is one of its bioactive components currently under evaluation as a pure drug. In this study, a highly sensitive and rapid method based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) for the simultaneous quantitation of calenduloside E and its active metabolite oleanolic acid in beagle dog plasma has been developed and validated. Samples containing the ammonium salt of simvastatin acid as internal standard (IS) were purified by solid phase extraction and separated on a SUPELCO Ascentis-C18 column (50mm×4.6mm i.d., 5μm) using gradient elution with 0.35% formic acid and acetonitrile. Analytes and IS were detected in a cycle time of 5min after ionization in the negative ion mode by multiple reaction monitoring of the precursor-to-product ion transitions at m/z 631.4→455.4 and m/z 435.4→319.0 for calenduloside E and IS respectively and by single ion monitoring of the ion at m/z 455.4 for oleanolic acid. The method was linear over the concentration range 0.4-100ng/mL for both analytes using 0.5mL plasma. Inter- and intra-day precisions were both <6.96% with accuracies <6.40%. In the pharmacokinetic (PK) study, beagle dogs were given oral doses of calenduloside E (1.05, 2.10 and 4.20mg/kg) and an intravenous injection of 2.10mg/kg. The absolute bioavailability of calenduloside E was only 0.58%. Area under the plasma concentration time curve (AUC(0-t)) for the oral doses of calenduloside E was approximately dose proportional while other PK parameters (t1/2, Tmax and MRT) showed no significant differences among the three doses (P>0.05). The PK data provide a useful platform on which to base future clinical studies of calenduloside E.
To investigate the effects of simvastatin on atherosclerosis and central aortic pressure in ApoE-knockout (ApoE-/-) mice.
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For high-risk patients who do not achieve guideline-recommended LDL-C levels, more intensive treatment including statin-uptitration to higher doses or potency, as well as combination therapy may be considered. A better understanding of statin treatment patterns in real-world clinical practice may contribute to improved lipid-lowering management in these patients.
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Guidelines published in 2011 by the European Atherosclerosis Society and the European Society of Cardiology recommend a goal of either low-density lipoprotein cholesterol (LDL-C) <70 mg/dl (~1.8 mmol/l) or ≥ 50% reduction in LDL-C for patients at very high cardiovascular risk. The aim of this study was to determine the percentage of high-risk patients from the VOYAGER individual patient data meta-analysis treated with rosuvastatin 10-40 mg, atorvastatin 10-80 mg or simvastatin 10-80 mg who achieved this goal.
Lipid-modifying therapy in Norway is dominated by statin monotherapy. In this analysis of primary-care patients, maximal reductions in cholesterol levels were seen within the first 3-4 months after therapy initiation. After 12 months of treatment, 67% of patients remained above recommended cholesterol levels. More effective and well tolerated treatment strategies are needed to improve the probability of patients achieving cholesterol treatment goals.
The restenosis rates after coronary angioplasty persist as an important problem even though multiple drug therapies and different devices have been tried. The reduction of the cholesterol and low density lipoproteins levels (and their oxidation) have proved to have a beneficial effect on atherosclerosis evolution. Both the lipid lowering and antioxidant agents have caused a reduction in the neointimal formation generated with the angioplasty balloon in animals, and their combination to improve endothelial dysfunction in humans. The aim of the present study is to prove whether the whole administration of two potent agents such as simvastatin and probucol, which reduce the lipid levels and their oxidation, are able to lessen the restenosis related process.
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Drugs acting on the renin angiotensin system (RAS), such as angiotensin converting enzyme (ACE) inhibitors and sartans, have been used for hypertension treatment in the HIV-negative population. These drugs reduce hypertension related cardiovascular diseases such as renal impairment in the general population. Limited data show similar findings also in the HIV-positive population. A new drug called aliskiren has recently become available on the market: it is able to block the RAS by a different mechanism acting as direct renin inhibitor. No data are available about the use of aliskiren in HIV-positive patients.
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A nested case-control study was conducted by using data from the National Health Insurance Research Database of Taiwan. Among 24,975 patients with MI, 2686 case patients with pneumonia requiring hospitalization were age- and sex-matched with 10,726 control patients using the incidence density sampling approach. Duration and dosage of statin use were obtained from pharmaceutical claims. Conditional logistic regression analyses were used to estimate the risk of hospitalization for pneumonia associated with statin use adjusted for patient's demographics, medical conditions and prescribed medications.
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To investigate whether the water extractives of regulating qi and blood prescription (WQBP) had effects on early atherosclerosis of apolipoprotein E-deficient mice (ApoE-mice) at the age of 19 weeks or not, and to explore the possible mechanisms.
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To examine whether statins are capable of modulating collagen gene expression in cultured systemic sclerosis dermal fibroblasts.
A number of mechanisms have been proposed to explain the pleiotropic effect of statin therapy to reduce sympathetic outflow in cardiovascular disease. We tested the hypothesis that statin treatment could improve baroreflex gain-sensitivity triggered by morphological adaptations in the mechanoreceptor site, thus reducing sympathetic activity, regardless of arterial pressure (AP) level reduction. Male spontaneously hypertensive rats (SHR) were divided into control (SHR, n = 8) and SHR-simvastatin (5 mg/kg/day, for 7 days) (SHR-S, n = 8). After treatment, AP, baroreflex sensitivity (BRS) in response to AP-induced changes, aortic depressor nerve activity, and spectral analyses of pulse interval (PI) and AP variabilities were performed. Internal and external carotids were prepared for morphoquantitative evaluation. Although AP was similar between groups, sympathetic modulation, represented by the low frequency band of PI (SHR: 6.84 ± 3.19 vs.
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Patients who should be treated with both warfarin and a statin are frequently seen in vascular clinics. The risk for bleeding and potential drug interactions should be considered when prescribing both medications together. This study aimed to compare the risk for gastrointestinal bleeding among different statin exposures with concomitant administration of warfarin.
From the PHARMO Database Network a cross-sectional cohort was constructed. The descriptive study included patients on lipid modifying therapy (LMT) in 2009, classified as high cardiovascular risk based on a history of T2DM or CVE, with 2010 LDL-C levels above 1.8 mmol/L (2011 European Society of Cardiology [ESC] target). Sub-cohorts were created: T2DM + CVE from the T2DM cohort and multiple CVE from the CVE only cohort.
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Treatment with simvastatin (10 mg/kg), the extract (400 and 600 mg/kg) significantly (P =0.033) lowered the total cholesterol, triglycerides, low density lipoproteins (LDL) levels and significantly (P =0.05) increased the level of high density lipoproteins (HDL) in comparison with the negative control group. There was no significant difference between the cholesterol lowering effect of the extract and that of simvastatin (P =0.991). The haemoglobin concentration, packed cell volume, red and white blood cell counts of treated animals did not produce any significant change (P =0.705). The LD(50) showed that the extract has a wide margin of safety.