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Lower statin doses than those currently advised reduced the risk of coronary heart disease to a greater extent than anticipated in patients with familial hypercholesterolaemia. With statin treatment, such patients no longer have a risk of myocardial infarction significantly different from that of the general population.
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47 adult male Sprague-Dawley rats were divided into 6 groups: sham-operated, SAH treated with vehicle, SAH treated with low dose simvastatin (1 mg/kg), high dose simvastatin (20 mg/kg), SAH treated with simvastatin plus the PI3K inhibitor (wortmannin), and sham-operated plus wortmannin. Simvastatin was administered intraperitoneally 30 minutes after SAH created by the standard endovascular perforation model. Histological parameters of the ipsilateral internal carotid artery (ICA-diameter, perimeter, and wall thickness) and neurological score were assessed at 24 hours.
Of the 25 420 patients who met the eligibility criteria for study inclusion, the mean (SD) age was 66.1 (5.8) years, and 14 112 (55.5%) were female. Additionally, 19 232 patients (84.1%) were white, 1252 (5.5%) were black, and 1558 (6.8%) were Latino. After accounting for baseline low-density lipoprotein levels, persons who filled prescriptions for statins continuously for 2 years had a 21% reduced risk of glaucoma compared with nonusers (adjusted HR, 0.79; 95% CI, 0.66-0.96; P = .02). There was no additional protective effect associated with taking the highest dosage of statins (80 mg) compared with a lower dosage (40 mg) (HR, 1.03; 95% CI, 0.59-1.80; P = .91). The protective effect of the following statins on OAG risk did not differ compared with atorvastatin, an inexpensive generic statin: lovastatin (HR, 1.09; 95% CI, 0.71-1.68; P = .69), cerivastatin (HR, 0.61; 95% CI, 0.09-4.41; P = .63), rosuvastatin (HR, 0.83; 95% CI, 0.48-1.44; P = .51), fluvastatin (HR, 0.89; 95% CI, 0.39-2.02; P = .78), pravastatin (HR, 1.29; 95% CI, 0.93-1.79; P = .13), and simvastatin (HR, 1.03; 95% CI, 0.83-1.29; P = .78).
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To investigate, in hypercholesterolemic patients, whether a combination of pravastatin with the antioxidant, vitamin E, has greater effects on the activity of CETP and of LCAT than does pravastatin alone.
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External beam radiotherapy and beta-radioimmunotherapy (RIT) are effective treatments for lymphoid malignancies. The development of RIT with alpha-emitters is attractive, owing to the high (LET) nature and short path length of alpha particles allowing for higher tumor cell kill and lower toxicity to healthy tissues.
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The objective was to assess the consistency of effect of switching to ezetimibe/simvastatin 10/20 mg versus doubling the baseline statin dose (to simvastatin 40 mg or atorvastatin 20 mg) or switching to rosuvastatin 10 mg across subgroups of subjects with (n = 617) and without (n = 191) metabolic syndrome (MetS).
Astrocytes play a fundamental role in glutamate metabolism by regulating the extracellular levels of glutamate and intracellular levels of glutamine. They also participate in antioxidant defenses, due to the synthesis of glutathione, coupled to glutamate metabolism. Although the cause of Alzheimer's disease (AD) remains elusive, some changes in neurochemical parameters, such as glutamate uptake, glutamine synthetase activity and glutathione have been investigated in this disease. A possible neuroprotective effect of two statins, simvastatin and pravastatin (administered p.o.), was evaluated using a model of dementia, based on the intracerebroventricular (ICV) administration of streptozotocin (STZ), and astrocyte parameters were determined. We confirmed a cognitive deficit in rats submitted to ICV-STZ, and a prevention of this deficit by statin administration. Moreover, both statins were able to prevent the decrease in glutathione content and glutamine synthetase activity in this model of AD. Interestingly, simvastatin increased per se glutamate uptake activity, while both statins increased glutamine synthetase activity per se. These results support the idea that these drugs could be effective for the prevention of alterations observed in the STZ dementia model and may contribute to reduce the cognitive impairment and brain damage observed in AD patients.
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We present a case demonstrating clinical, electrophysiological, serological, and radiological evidence of a myopathy induced by ranolazine, in a patient otherwise asymptomatic on chronic statin therapy. The patient developed proximal weakness, serum creatine kinase levels of 1875 U/L, electromyography with muscle membrane instability and small short-duration motor unit potentials, and magnetic resonance imaging evidence of muscle edema. The manifestations began within one week of initiation of ranolazine and improved within days after discontinuation. Ranolazine is a weak inhibitor of CYP3A4 known to increase the serum level of simvastatin and its active metabolite 2-fold. We postulate that the addition of ranolazine to a medical regimen that included atorvastatin induced a myoncecrotic myopathy.
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Grapefruit juice increases the bioavailability of several drugs known to be metabolized by CYP3A4. We wanted to investigate a possible interaction of grapefruit juice with lovastatin, a cholesterol-lowering agent that is partially metabolized by CY P3A4.
Rats were randomly assigned to controls, Bleomycin, Bleomycin plus Simvastatin from day 1 to 28 and Bleomycin plus Simvastatin from day 13 to 28. 28 days after Bleomycin instillation, right ventricular systolic pressure (RVSP), right ventricular mass (RV/(LV+S)), right ventricular and circulating brain natriuretic peptide (BNP) levels were determined to assess pulmonary hypertension. Pulmonary hydroxyproline content (HPC), pulmonary connective tissue growth factor (CTGF) transcription and lung compliance (LC) were analysed to characterize pulmonary fibrosis. Exercise capacity was determined by treadmill tests.
Fenofibric acid activates peroxisome proliferator-activated receptor alpha to modify fatty acid and lipid metabolism. Fenofibric acid is the first member of the fibric acid derivatives (fibrates) class approved for use as combination therapy with HMG-CoA reductase inhibitors (statins). In three randomized, double-blind, multicenter, phase III trials in adult patients with mixed dyslipidemia, up to 12 weeks' treatment with once-daily fenofibric acid 135 mg plus a low- or moderate-dose statin (atorvastatin 20 or 40 mg, rosuvastatin 10 or 20 mg, or simvastatin 20 or 40 mg) improved high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels to a significantly greater extent than statin monotherapy, and improved low-density lipoprotein cholesterol (LDL-C) levels to a significantly greater extent than fenofibric acid monotherapy. In a 52-week, open-label, multicenter, extension study, HDL-C, TG, and LDL-C levels continued to improve, or were maintained, during combination therapy with once-daily fenofibric acid 135 mg plus a moderate-dose statin (atorvastatin 40 mg, rosuvastatin 20 mg, or simvastatin 40 mg). Once-daily fenofibric acid 135 mg plus a statin was generally as well tolerated as monotherapy with fenofibric acid 135 mg/day or the corresponding statin dosage in the three phase III trials in patients with mixed dyslipidemia. The incidence of adverse events was similar between the combination therapy group and both monotherapy groups. In the extension trial, once-daily fenofibric acid 135 mg plus a moderate-dose statin (atorvastatin 40 mg, rosuvastatin 20 mg, or simvastatin 40 mg) for up to 52 weeks was generally well tolerated.
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There is evidence to suppose that cholesterol-lowering medicine might confer protection against dementia, probably via modulation of cholesterol synthesis in the brain. The aim of the present study was to investigate the potential influence of statins and cholesterol diet on selected parameters relevant to Alzheimer's disease pathophysiology.
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A growing body of evidence indicates that statins decrease perioperative cardiovascular risk and that these drugs may be particularly efficacious in diabetes. Diabetes and hyperglycemia abolish the cardioprotective effects of ischemic preconditioning (IPC). The authors tested the hypothesis that simvastatin restores the beneficial effects of IPC during hyperglycemia through a nitric oxide-mediated mechanism.
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Previously recognized pharmacogenomic associations with drug efficacy have been further validated (e.g. with clopidogrel and warfarin) and shown to influence clinically important outcomes. The clinical significance of variants modulating toxicity (e.g. SLCO1B1 with simvastatin) has also been confirmed. The genetic contribution to variable efficacy and toxicity of other important classes of cardiovascular drugs, such as beta-blockers, is becoming increasingly recognized. Prospective trials testing whether the use of genomic information improves clinical care are underway. Guidance based on the most well-established pharmacogenomic findings has appeared in prescribing labeling and is in the early stages of being implemented into routine clinical care.
Energy loss index decreased (0.85 cm(2)/m(2) vs. 0.77 and 0.75 cm(2)/m(2)) and the prevalence of low stress-corrected midwall shortening increased (10% vs. 26% and 63%) with increasing LV global load (all p < 0.001). The EF was low in only 2% of patients. Patients with low-flow AS had higher LV global load and more often low midwall shortening than those with normal-flow AS (9.66 +/- 2.23 mm Hg/ml.m(2.04) and 77%, vs. 6.38 +/- 2.04 mm Hg/ml.m(2.04) and 30%, respectively, p < 0.001). In logistic regression analysis, LV global load was a main predictor of low stress-corrected midwall shortening independent of male sex, concentric LV geometry, LV hypertrophy (all p < 0.001), concomitant hypertension, and aortic regurgitation.
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Objectif : Trouver des rapports de cas portant sur la rhabdomyolyse provoquée par les statines et résumer les facteurs prédisposants communs, les symptômes, les résultats diagnostiques, les résultats fonctionnels, les caractéristiques, le traitement et la réadaptation. Méthodes : On a cherché dans les bases de données MEDLINE, CINAHL, SCOPUS et PEDro (1990–2013) des rapports de cas pertinents en utilisant les termes de recherche Statins, Rhabdomyolysis, Myalgia, Muscle damage, Muscle injury et Myopathy. Un chercheur en a évalué la pertinence (en fonction du titre et du résumé) et deux autres ont revu indépendamment les articles pertinents pour déterminer s'il fallait les inclure dans la recherche. Résultats : Au total, 112 cas répondaient aux critères d'inclusion. La majorité des cas portaient sur des hommes (70 %) et les plus de 45 ans (âge moyen de 64 [ET 14] ans). La simvastatine a été la statine incriminée le plus souvent dans les rapports (n=55), la majorité des cas signalant l'utilisation simultanée de médicaments comme des fibrates (n=25). La faiblesse (n=65) et les douleurs musculaires (n=64) étaient les symptômes les plus courants. Dans 19 cas, le patient a été aiguillé vers la réadaptation, mais les rapports ne décrivent pas le traitement. Conclusion : On a signalé une rhabdomyolyse causée par les statines plus souvent lorsqu'elles étaient conjuguées à d'autres médicaments, ce qui en a accentué l'effet. Des recherches s'imposent pour déterminer le rôle de l'exercice et de la réadaptation à la suite d'une rhabdomyoloyse causée par les statines puisque les dommages musculaires peuvent être graves et qu'elles peuvent avoir des effets à long terme sur la fonction musculaire.
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Patients under statin treatment developing MODS might have a better outcome than patients without statin therapy, probably by reduction of inflammatory responses and increase of vagal activity in MODS.
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Individuals with newly recorded pneumonia, diagnosed between 1996 and 2006 and aged 45 years and older, were matched with up to five controls by age, sex, general practice, and calendaryear Odds ratios for pneumonia associated with statin use were adjusted for smoking status, deprivation, comorbidities, use of acid-lowering drugs, influenza, and pneumococcal vaccines.
We examined the antioxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin), on superoxide anion formation activated by angiotensin II (Ang II) in vitro. The effects of fluvastatin were also compared to simvastatin and a water-soluble analog of alpha-tocopherol, trolox. Treatment of human aortic smooth muscle cells (hASMC) with Ang II for 24 hours resulted in a 3.2 +/- 0.5-fold increase in intracellular superoxide anion formation as detected by lucigenin assay. hASMC treated with clinical concentrations of fluvastatin (0-100 nM) showed a dose-dependent decrease in Ang II-activated superoxide anion formation. The addition of similar concentrations of trolox to hASMC inhibited Ang II-activated superoxide anion formation in a dose-dependent manner. However, simvastatin at similar doses failed to inhibit Ang II-activated superoxide anion formation by hASMC. Our results indicate that in addition to its hypocholesterolemic effect, fluvastatin may have direct antioxidative effects, suggesting its possible protective effect on atherosclerotic process.
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The expression of ccn2 (ctgf) mRNA was transiently upregulated by fetal calf serum. Very rapid onset but short lasting ccn2 (ctgf) mRNA expression was observed after stimulation with lysophosphatidic acid, a bioactive lipid, which activates G protein coupled receptors. Induction of ccn2 (ctgf) mRNA expression by transforming growth factor beta (TGF-beta) was more prolonged and lasted for more than one day. The small GTPases of the Rho family were essential for basal as well as induced ccn2 (ctgf) expression: preincubation of the cells with toxin B from Clostridium difficile abrogated ccn2 (ctgf) mRNA expression. HMG CoA reductase inhibitors, which are therapeutically used as lipid lowering drugs, interfere with the isoprenylation and thus activation of Rho proteins. Simvastatin, an HMG CoA reductase inhibitor, inhibited ccn2 (ctgf) mRNA expression in a concentration dependent manner (IC(50): 1-2 microM).