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Time being sedentary increased and physical activity levels decreased in the total sample over 6 months of drug treatment, independent of group assignment. Our results suggest that statins do not influence physical activity levels any differently from placebo, and the lack of inclusion of a placebo condition may provide insight into inconsistencies in the literature.
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The ASCOT-LLA and ALLHAT-LLT trials provide conflicting evidence of the efficacy of statins in decreasing cardiovascular (CV) morbidity and mortality in hypertensive patients. We performed a meta-analysis to compare the overall efficacy of statins in hypertensive and nonhypertensive patients enrolled in major randomized clinical trials. We systematically reviewed PubMed publications from 1985 onward for placebo-controlled randomized trials that examined the effect of statins on cardiac morbidity and mortality. Only trials that followed >or=1,000 patients for >or=2 years were included in the meta-analysis. Outcomes included cardiac or CV death, major coronary events, or major CV events. Pooled estimates of relative risk (RR) were calculated separately for hypertensive and nonhypertensive patients. The moderating effect of the percentage of hypertensive patients at baseline was tested using meta-regression. Besides the ASCOT-LLA and ALLHAT-LLT, 12 trials enrolling 69,984 patients met inclusion criteria. Overall, in these 12 trials, statin therapy decreased cardiac death by 24% (RR 0.76, 95% confidence interval [CI] 0.71 to 0.82). There was no evidence of difference in RR estimates for hypertensive (RR 0.78, 95% CI 0.72 to 0.84) and nonhypertensive (RR 0.76, 95% CI 0.72 to 0.80) patients. Similarly, meta-regression showed that the efficacy of statins was not moderated by the percentage of hypertensive patients at baseline (Q estimate 1.51, p=0.22). In conclusion, statin therapy effectively decreases CV morbidity and mortality to the same extent in hypertensive and nonhypertensive patients.
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Although torcetrapib substantially raised HDL cholesterol and lowered LDL cholesterol, it also increased systolic blood pressure, and did not affect the yearly rate of change in the maximum intima-media thickness of 12 carotid segments. Torcetrapib showed no clinical benefit in this or other studies, and will not be developed further.
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The aim of the present study was to develop a chromatographic method for the analysis of atorvastatin, o- and p-hydroxyatorvastatin (acid and lactone forms) in human plasma after administration of atorvastatin at the lowest registered dose (10 mg) in clinical studies. Sample preparation was performed by solid-phase extraction and was followed by separation of the analytes on an HPLC system with a linear gradient and a mobile phase consisting of acetonitrile, water and formic acid. Detection was achieved by tandem mass spectrometry operated in the electrospray positive ion mode. Validation of the method for the compounds for which reference compounds were available (acid forms of atorvastatin, o- and p-hydroxyatorvastatin) showed linearity within the concentration range (0.2-30 ng/ml for atorvastatin acid and p-hydroxyatorvastatin acid, and 0.5-30 ng/ml for o-hydroxyatorvastatin acid) (r2 > or = 0.99, n = 5 for all analytes). Accuracy and precision (evaluated at 0.5, 3 and 30 ng/ml for atorvastatin, p-hydroxyatorvastatin and 1, 3 and 30 ng/ml for o-hydroxyatorvastatin) were both satisfactory. The detection limit was 0.06 ng/ml for atorvastatin and p-hydroxyatorvastatin, and 0.15 ng/ml for o-hydroxyatorvastatin. The method has been successfully applied in a clinical study where atorvastatin, o- and p-hydroxyatorvastatin (both acid and lactone forms) could be detected in a 24-h sampling interval after administration of the lowest registered dose of atorvastatin (10 mg) for one week.
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To investigate the effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor on the tissue damage and fibrosis of obstructed ureters, 80 rats were studied.
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This report investigated the relationship between anthropometric measurements of body fat distribution and lipid response to statins in hypercholesterolemic hypertensive patients.
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The present study reveals that HDL cholesterol reduction after high-dose atorvastatin is an early and transient event in HFH patients which magnitude depends on the presence of a residual LDL-R activity.
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Atorvstatin does not affect insulin sensitivity and the adiponectin or leptin levels in hyperlipidemic Type 2 diabetes.
To study whether high-dose versus usual-dose statin treatment reduces the incidence of peripheral artery disease (PAD) and what is the effect of high-dose statin treatment on cardiovascular disease (CVD) outcome in patients with PAD.
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Sexually selected traits like complex vocalizations or vibrant colors communicate reliable information about mate quality when they are costly to display. Although several general condition-dependent mechanisms underlying the acquisition of mating advertisements have been identified, we rarely know the precise physiological and molecular challenges that animals must meet to develop their sexual ornaments. The flashy pigment-based colors commonly displayed by birds are ideal candidates for investigating the pathways and demands of sexual-signal expression, because we know the biochemical currency with which the trait is produced. Carotenoid colors in birds, for example, are derived from pigments that are acquired from the diet and assimilated into feathers and bare parts. In previous work, we showed that variation in the sexually attractive red carotenoid-colored beak of male zebra finches (Taeniopygia guttata) was predicted not by the amount of food or pigments ingested, but by the levels of carotenoids that birds circulated in blood. Here we elucidate a novel physiological mechanism by which birds are able to accumulate high levels of carotenoids in the body and develop a colorful bill. Carotenoids are transported through the bloodstream bound to lipoproteins. We assayed a critical component of lipoprotein particles-cholesterol-and found that males with higher cholesterol levels circulated more carotenoids and displayed redder beaks. Experimental supplementation of dietary cholesterol elevated carotenoid levels in the blood and beak hue. Experimental reductions in blood cholesterol, using the human lipid-lowering agent atorvastatin, diminished blood carotenoids and faded the beak; carotenoid and cholesterol levels were restored, however, by subsequent addition of dietary cholesterol. These results suggest that the production of circulating lipoproteins critically regulates the development of a colorful sexually selected trait in zebra finches.
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We included all randomized controlled trials (RCTs) comparing statins (any type and dosage) versus placebo or no treatment, administered within two weeks of the onset of acute ischemic stroke or TIA.
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In the primary prevention of the cardiovascular disease in type 2 diabetic patients, the use of Atorvastatin 10 mg is cost-effective, with a cost per LYG and per QALY below that of other alternatives widely used in the Spanish National Health System, and also below a value considered as a reasonable threshold for our country, which might unofficialy be around 30,000 euro/ QALY.
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In the atorvastatin group, myocardial cells were lined up more orderly and myocardial fibrosis level was decreased compared to the model group. The expressions of GRP78, caspase-12 and CHOP in myocardial cells were decreased in atorvastatin group. Moreover, in the atorvastatin-treated group the cell apoptosis rate was reduced and the endoplasmic reticulum (ER) stress was activated in response to heart failure and angiotensin II (Ang II) stimulation.
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First-degree relatives of patients with premature CAD have an increased risk for cardiovascular disease (CVD), whereas events are poorly predicted in these individuals. Surrogate markers, such as CCS, might refine risk scoring. Nevertheless, the outcome of the St. Francis Heart trial, which investigated the effect of atorvastatin 20 mg/day in asymptomatic individuals with CCS above the 80th percentile, did not reach statistical significance.
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For the period of twelve months 46 patients with primary HLP (group S) (LDL-C > 4.1 mmol/l a TG < 3.5 mmol/l), were treated with atorvastatine 20 mg or simvastatine 40 mg. Patients with LDL-C > 4.1 mmol/l along with TG > 3.5 mmol/l were randomly divided into two groups. The SF group was treated with a combination of statin + 200 mg micronized fenofibrate each day, and group SR received together with statin a compound containing n-3 polyene fatty acids (PUFA n-3) in the daily dose of 3.6 g. After one year lasting therapy we found beside the positively influenced concentration of atherogenic lipids and lipoproteins in the group S and SF a significantly reduced concentration of conjugated dienes (CD) in LDL ( -21, resp. 16%, both P < 0.05); the test of KD kinetics in LDL in the group S has marginal increase of the lag phase (P = 0.06) and in the groups S and SR also a significant improvement of ED (increase by the flow of mediated vasodilation, FMD) by 20%, resp. by 18% (both P < 0.05) and in the SR group a significant decrease of microalbuminuria. We did not proved significant concentrations of insulin, C-peptide or indexes showing the degree of IR (HOMA and QUICKI) CONCLUSIONS: Long-lasting hypolipidemic treatment positively affected in our study the oxidative stress and ED, however, it did not resulted in changes of IR.
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Because of well established outcome measures, the lipid-lowering drugs Pravastatin and Atorvastatin (serum low-density lipoprotein cholesterol, LDL-C) and the anti-glaucoma drugs Timolol and Latanoprost (intraocular pressure, IOP) were chosen for this investigation. Studies were identified by a standardized MEDLINE search. RCTs investigating the above identified medications administered as monotherapy, and in defined dosages, were included. Publication year, baseline (= pre-treatment value in the treatment group of interest) and post intervention means, number of patients and the assignment to experimental or control group were extracted for each study.
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Atorvastatin 10 mg/day did not produce decrements to cognitive performance. In addition, biochemical and demographic measures and the receipt of atorvastatin versus placebo did not individually or in combination predict cognitive performance on measures of attention and concentration.
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Matrix metalloproteinases (MMPs) have been implicated in the pathophysiology of acute pulmonary embolism (APE)-induced pulmonary hypertension. Here, we evaluate the effects of atorvastatin pretreatment on APE-induced pulmonary hypertension, 24-hr mortality rate, and changes in plasma and lung MMP-2 and MMP-9 activities.
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A 44-year-old male patient with a single vessel ischaemic heart disease was referred to the lipid clinic for management of hypercholesterolaemia after an episode of admission with thrombocytopenic purpura secondary to atorvastatin. Atorvastatin was discontinued and his platelet counts improved gradually with steroids. He is now established on a different statin with no further episodes of thrombocytopenia. Though a drug challenge was never done, an idiosyncratic reaction to the initial statin seems to be the most likely cause.
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The aim of the study was to evaluate the effects of lifestyle changes followed by treatment with atorvastatin in dyslipidemic HD patients.
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ASCOT compared the effect of atenolol combined with a thiazide versus amlodipine with perindopril in hypertensive patients. It also studied the effect of atorvastatin in those with normal cholesterol. ASCOT concluded that reductions in cardiovascular events with atorvastatin were significant, and that amlodipine-based treatment prevented more cardiovascular events. The latter seemed to be due to better control of central blood pressure. Both statin and amlodipine-based treatments were cost-effective. According to the ASCOT study, it does matter how blood pressure is lowered.
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Endothelial progenitor cells (EPCs) play an important role in vascular repair and maintenance of vascular homeostasis through re-endothelialization and neovascularization. Cardiovascular risk factors that contribute to coronary artery disease (CAD) have been shown to negatively impact EPCs, although the mechanisms are poorly understood. MicroRNAs (miRNAs) which negatively regulate gene expression at the post-transcriptional level have been shown to impact endothelial cell (EC) angiogenic actions, but little is known about their role in modulating EPC function. In this study we first investigated if EPCs expressed EC specific, angiogenesis-related miRNAs; then determined whether the expression of these miRNAs was altered in EPCs from CAD patients as compared with healthy controls. Furthermore, we examined if atorvastatin, known to increase circulating EPC numbers, had any effect on EPC miRNA expression. We found EPCs produced miR-126, miR-130a, miR-221, miR-222 and miR-92a which have thus far been identified as the most important angiogenic miRNAs. Dysregulation of these miRNAs was detected in EPCs from CAD patients and atorvastatin treatment selectively impacted miRNA expression in EPCs. Our data provide evidence that angiogenic miRNAs might play an important role in the control of EPC function, and that their dysregulation might contribute to EPC dysfunction in patients suffering from coronary artery disease. These findings might lead to the development of novel therapeutic modalities for the prevention and treatment of CAD.
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Statins have been reported to affect blood vessel formation. Thrombospondin-1 (TSP-1) is a multifunctional protein that affects vasculature systems such as platelet activation, angiogenesis, and wound healing. This study was designed to investigate the effect of atorvastatin on TSP-1 synthesis in thrombin-stimulated human umbilical vein endothelial cells (HUVECs), and its regulation by mevalonate or its derivatives. The results showed that atorvastatin down-regulated TSP-1 expression in HUVECs. This effect was fully reversed by mevalonate, farnesylpyrophosphate (FPP), and gerarylgeranylpyrophosphate (GGPP). Furthermore, farnesyltransferase and geranylgeranyltransferase inhibitors decreased TSP-1expression. It was also found that thrombin increased TSP-1 expression in HUVECs. Atorvastatin (0.1, 1, and 10 muM) decreased TSP-1 in thrombin-stimulated cells (45%, 66%, and 80%). Mevalonate partially reversed this inhibitory effect of atorvastatin on TSP-1, whereas the presence of FPP and GGPP did not alter TSP-1. Rho-kinase inhibitor neutralized the up-regulation of TSP-1 induced by thrombin. In conclusion, atorvastatin inhibits TSP-1 expression in endothelial cells via the mevalonate pathway. Rho protein activation is necessary for up-regulation of TSP-1 synthesis induced by thrombin. Because FPP and GGPP are essential for the activity of Rho proteins, inhibition of these proteins may constitute the mechanism by which atorvastatin inhibits thrombin up-regulated TSP-1 expression.
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CD40 is a marker of immunological activation and is expressed in the atherosclerotic lesions. We studied whether CD40 and cholesterol synthesis pathways are associated with each other.
In subjects with low HDL cholesterol levels, CETP inhibition with torcetrapib markedly increased HDL cholesterol levels and also decreased LDL cholesterol levels, both when administered as monotherapy and when administered in combination with a statin.
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CFR was measured using an intracoronary Doppler wire in 102 patients with AMI at baseline and at 8 months. Changes in the absolute number of circulating angiogenic cells were measured at baseline, 1 day, 5 days and at 8 months. Stented patients were randomly assigned to either low-dose atorvastatin 10 mg (ATOR10, n=52) or moderate-dose atorvastatin 40 mg (ATOR40, n=50). Setting University Hospital.
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Atorvastatin is a new member of the class of drugs which inhibit the enzyme Hydroxy-Methylglutaryl Co-A reductase, the rate limiting step in cholesterol biosynthesis.
Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO). Experiment 1 was used to evaluate time course expressions of 12/15-LOX, mitogen-activated protein kinase (MAPK), phosphorylated-p38MAPK (phospho-p38MAPK) and cytosolic phospholipase A2 (cPLA2) after cerebral ischemia, seven time points were included. Experiment 2 was used to detect atorvastatin's neuroprotection in the acute phase of ischemic stroke; atorvastatin was administered immediately after MCAO. Neurological deficit, brain water content and infarct size were measured at 24h after stoke. Immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to analyze the expression of 12/15-LOX, p38MAPK, phospho-p38MAPK and cPLA2. Experiment 3 was used to detect atorvastatin's influence on blood-brain barrier (BBB).
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Underdosing of simvastatin in 2011 with average prescribed dose of 23.7 mg; however, not for atorvastatin (20.91 mg) or rosuvastatin (15.02 mg). High utilization of generics versus originators at 93-99% for atorvastatin and simvastatin, with limited utilization of single-sourced statins (22% of total statins - defined daily dose basis), mirroring Netherlands, Sweden and UK. Generics priced 33-51% below originator prices.
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The right carotid artery of 24 New Zealand rabbits was injured with an angioplasty balloon. Animals were perfused intravenously with saline (100 mL) during the experiment and divided into three groups: group-A, control; group-B, exposed to NPs (2 mL) obtained from calcified aortic valves; and group-C, exposed to NPs (2 mL) and treated postoperatively with atorvastatin (2.5 mg/kg/24 h). At 30 days, both carotid arteries were removed and examined histologically. Blood measurements were monitored during the study.