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There is extensive but controversial evidence on the diverse effects of statins on the level of high-density lipoprotein cholesterol (HDL-C). Some of these effects may limit the benefits of statins in terms of cardiovascular risk reduction. To identify the conditions for beneficial effects, this study investigated the response to atorvastatin and simvastatin treatment in type 2 diabetic patients with elevated low-density lipoprotein cholesterol (LDL-C).
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Chronic subdural haematoma (CSDH) is a common neurosurgical condition. Burr-hole for drainage is an effective treatment. However, recurrence can be up to 8-33% and is associated with morbidities and mortalities. The underlying pathogenesis was postulated to be localised inflammation and pathological aberrant vessels formation. Atorvastatin, an HMG-CoA reductase inhibitor, is a type of lipid-lowering medication. In animal studies and a preliminary clinical trial, Atorvastatin was shown to be effective in the treatment of CSDH. It was found to inhibit inflammation and promote vascular maturation at the neomembrane of CSDH. Our study aimed to investigate the efficacy of Atorvastatin in CSDH. During the study period from January to December 2014, Atorvastatin was used in 12 CSDH patients with Glasgow Coma Scale (GCS) 13-15 or Markwalder's Grading Scale (MGS) Grade 0-2. They were retrospectively compared with GCS- and MGS-matched controls who had not used statin. Improvement with haematoma resolution at 3 months was 75% (9/12) for the Atorvastatin group, versus 42% (5/12) for the Control group (p = 0.0977). The risk of deterioration requiring burr-hole drainage was 16.7% (2/12) in the Atorvastatin group, versus 58.3% (7/12) in the Control group (p = 0.0447). The Odds Ratio (OR) of deterioration requiring burr-hole drainage with Atorvastatin was 0.143 (95%CI: 0.021-0.958), which favours the use of Atorvastatin in CSDH (p = 0.0451). The Number needed to treat (NNT) was 2.4 (p = 0.0447; 95%CI: 1.31-14.93). In conclusion, this retrospective cohort comparison study has shown that CSDH with Atorvastatin had a lower rate of deterioration and burr-hole drainage.
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This study assessed atorvastatin safety among Asian patients enrolled in 58 randomized clinical trials.
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A progressive reduction in the benefit of intensive LLT with atorvastatin 80 mg over pravastatin 40 mg occurred in statin-naïve ACS patients as baseline LDL-C declined. (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 [PROVE IT-TIMI 22]; NCT00382460).
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Statins are used for treatment of hypercholestremia. Common adverse reports associated with use of statins are generalized bodyache, rhabdomyolysis, muscles weakness and gastrointestinal disorders. The current work is an attempt to explain how smooth muscles of gastrointestinal tissues are affected by the current statins (Simvastatin, atorvastatin, fluvastatin and rosuvastatin).
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The addition of low-dose sirolimus to enalapril and statin is safe, stabilizes renal function and reduces glomerular proliferative lesions in patients with poor prognosis IgA nephropathy.
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NCB-02 had a favourable effect, comparable to that of atorvastatin, on endothelial dysfunction in association with reductions in inflammatory cytokines and markers of oxidative stress. Further studies are needed to evaluate the potential long-term effects of NCB-02 and its combination with other herbal antioxidants.
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The ATP-binding-cassette transporter A1 (ABCA1) plays an essential role in cellular cholesterol efflux and helps prevent macrophages from becoming foam cells. The statins are widely used as cholesterol-lowering agents and have other anti-atherogenic actions. We tested the effects of four different statins (fluvastatin, atorvastatin, simvastatin, and lovastatin) on ABCA1 expression in macrophages in vitro. The statins suppressed ABCA1 mRNA expression in RAW246.7 and THP-1 macrophage cell lines and in mouse peritoneal macrophages. The effect was time- and dose-dependent and was abolished by the addition of the post-reductase product, mevalonate. These findings imply that there is a possible modulation of the well-known beneficial effects of the statins on the reverse cholesterol transport pathway.
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Cardiovascular event risk and mortality risk were used as outcomes. Statin efficacy at LDL-c and cardiovascular events levels lowering data was obtained from a systematic review of literature. A decision analytic model was developed to perform a cost-effectiveness analysis comparing atorvastatin 10mg/day and simvastatin 40 mg/day to placebo treatment in patients with dyslipidemia in Brazil. The target population of this study was a hypothetic cohort of men and women with a mean age of 50 years old and high risk of cardiovascular disease. The model includes only direct costs obtained from Ambulatory and Hospital Information System and Price Database of Brazilian Ministry of Health. The comparative cost-effectiveness analysis itself was done through Excel spreadsheets covering a 5 -years time horizon.
The expected 5-yr decline in renal function was not observed. Estimated GFR improved in both treatment groups but was significantly greater with 80 mg than with 10 mg, suggesting this benefit may be dosage related.
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Three large secondary prevention studies have shown that, in patients with a history of cardiovascular disease, statin treatment reduces the risk of further events and lowers overall mortality. In these studies, total mortality was reduced by as much as 30% in high-risk groups and 22% in average-risk groups. However, these studies did not include patients immediately after the coronary event. There are many benefits to early intervention with statin therapy in patients with acute coronary syndromes, including reduction of the risk of a subsequent event, which is highest immediately after the index event. Early treatment may reduce this likelihood in the first months after a coronary event by stabilizing atherosclerotic plaques and improving endothelial function in addition to lowering low-density lipoprotein cholesterol levels. This article reviews the case for early statin therapy in patients with a history of coronary heart disease. Results of clinical studies have now shown early statin therapy to be safe and cost-effective in reducing in-hospital and 6-month mortality.
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The focus of lipid-lowering therapy with drugs is prevention of complications of atherosclerosis. Landmark clinical trials have demonstrated that lowering low density lipoprotein cholesterol (LDL-C) may not only reduce coronary artery disease (CAD) risk but also may slow the progression and even induce regression of atherosclerosis in the coronary arteries. In addition, much attention has been given in recent years to the importance of triglyceride-rich lipoprotein (TRL) as a CAD risk factor, and the benefit of reducing plasma triglyceride levels and raising high density lipoprotein cholesterol (HDL-C) levels to prevent the recurrence of coronary events. Lipid-lowering drugs should be used within the framework of a systematic approach to treatment. Consideration must be given to the lipoprotein abnormality, the severity of disease, the role of combination therapy, and the spectrum of action of the drug and its pleiotropic effects (ie, effects beyond the expected action on lipoproteins). Five major agents have been used for the treatment of dyslipidemias. Three (resins, probucol and statins) target LDL-C, and two (fibrates and niacin) target primarily TRL and HDL-C. Fibrates and statins are the drugs of choice. Fibrates correct many abnormalities of lipoprotein metabolism in addition to having beneficial pleiotropic effects such as reducing fibrinogen and plasma viscosity. They inhibit the transcription of apolipoprotein (apo) CIII and enhance that of apoAI and lipoprotein lipase. Statins are safe and potent drugs for reducing LDL-C levels, and their efficacy in primary and secondary prevention of CAD has been amply demonstrated. They share a modes effect of raising HDL-C levels. Their pleiotropic effects, which include improvement of endothelial dysfunction, are numerous and may contribute to their spectacular beneficial effect of reducing CAD risk. They have effects that are complementary to those of fibrates, but the two drugs should be combined with caution because of the danger of myopathy. Atorvastatin is a major addition to this class of drugs because of its high efficacy and large spectrum of action. It lowers LDL-C levels effectively, not only in patients with severe forms of hypercholesterolemia but also in those with homozygous familial hypercholesterolemia. The effect of atorvastatin on LDL-C may be further enhanced by combining it with a resin. The ability of atorvastatin to lower triglyceride levels as well as LDL-C levels indicates that combined hyperlipidemia, a condition that, in the past, was best controlled with combination therapy, can now be treated with a single drug. It is also effective in patients with isolated hypertriglyceridemia and, although less potent than fenofibrate at reducing TRL and increasing HDL-C, it has a greater impact on the atherogenic risk ratios such as LDL-C:HDL-C. The profile of its pleiotropic effects is promising.
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Statins, HMG-CoA reductase inhibitors, are used widely in the treatment of hypercholesterolemia. Apart from lowering lipid levels, statins have been shown to have anti-inflammatory effects. Previously we showed that atorvastatin inhibits NF-kappaB activation, dose and time dependently, in LPS-TLR4 signaling pathway. In this study, we investigated the anti-inflammatory mechanism of atorvastatin via Toll-like receptor 4 (TLR4) in murine pro-B cell lines transfected with TLR4. Co-treatment of LPS-stimulated cells with both atorvastatin and mevalonate rescued NF-kappaB activation and TLR4 blockade demonstrated that atorvastatin does not exert its inhibitory effect via TLR4 receptor-ligand binding mechanism. Further investigation into the anti-inflammatory mechanism has shown that atorvastatin causes an impairment of TLR4 recruitment into the lipid raft thereby affecting anti-inflammatory responses. In contrast, mevalonate repaired lipid raft function leading to TLR4 clustering in the lipid raft. Together, these data suggest that atorvastatin exerts its anti-inflammatory effect via lipid raft modification. This novel finding offers another insight into the pleiotropic effects of atorvastatin and may be applicable to other pattern recognition receptors that utilize membrane lipid raft as a platform for signal transduction.
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In these 2 large, randomized clinical trials, carriers of the KIF6 719Arg allele were not at increased cardiovascular risk and did not obtain consistent cardiovascular benefit from high-dose statin therapy compared with noncarriers.
Hematologic parameters such as mean platelet volume (MPV), red cell distribution width (RDW), and neutrophil to lymphocyte (N/L) ratio are associated with increased cardiovascular risk. We investigated the effect of atorvastatin on hematologic parameters in patients with hypercholesterolemia. A total of 79 patients with hypercholesterolemia and 47 normocholesterolemic healthy participants were included. Patients with hypercholesterolemia received 10 to 80 mg/d atorvastatin during a 24-week period. Hematologic parameters were measured at baseline and after 6 months. Atorvastatin treatment produced a significant decrease in MPV levels (9.3 ± 1.3 vs 9.1 ± 1.2 fL, P = .008) and platelet count (259 ± 61 vs 248 ± 51 10(9)/L, P = .005). The N/L ratio decreased significantly after atorvastatin treatment from 2.9 ± 1.2 to 2.6 ± 1.1, (P = .014). The RDW and platelet distribution width levels were not different among the study groups, before and after treatment. Atorvastatin may beneficially reduce MPV levels and N/L ratio. This antiplatelet and anti-inflammatory effect of atorvastatin treatment could play a role in reducing cardiovascular risk.
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This was a post hoc analysis of a randomized, double-blind, 6-week study of adults 18-79 years with cardiovascular disease and diabetes mellitus with low-density lipoprotein cholesterol (LDL-C) ≥70 and ≤160 mg/dl. The percent change in LDL-C and other lipids was estimated within each subgroup separately. Safety and tolerability were assessed.
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The aim of this study was to compare the effect of atorvastatin treatment on high-grade yellow coronary plaques (grade ≥ 2, group H) vs. low-grade yellow plaques (grade ≤ 1, group L).
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Twenty three patients (mean age 61.4 ± 7.4 years, 87.0% men) were included in the study, of which 12 received high-dose atorvastatin prior to PCI. The mean number of EPC-CFUs before PCI was higher in patients treated with high-dose atorvastatin vs. low-dose statins (165.8 ± 58.8 vs. 111.7 ± 38.2 CFUs/plate, respectively, p < 0.001). However, 24 h after the PCI, the number of EPC-CFUs was similar (188.0 ± 85.3 vs. 192.9 ± 66.5 CFUs/plate in patients treated with high-dose atorvastatin vs. low- dose statins, respectively, p = 0.15). There were no statistical significant differences in FACS analyses between the 2 groups.
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Currently the apolipoprotein B:AI ratio integrates information about the potential for cardiovascular disease (CVD) risk reduction better than any other lipid or lipoprotein index. Certainly it could, with benefit, replace serum cholesterol and HDL cholesterol in the estimation of CVD risk. Defining the therapeutic target of statin therapy in terms of serum apolipoprotein B (apo B) rather than LDL cholesterol could also help to optimize statin treatment. Deciding whether a therapeutic response is adequate also requires knowledge of whether there is persisting hypertriglyceridaemia, because this gives an indication of whether small dense LDL is likely to have been satisfactorily reduced. Raising low levels of HDL, probably best measured as apo AI, may also prove to be an important aim of treatment. This is, however, a more complex issue and also depends on the mechanism by which a particular therapy alters HDL levels and on whether the capacity of HDL to perform its anti-inflammatory and antioxidative functions is restored. A meta-analysis of randomized clinical trials of statins in which apo B and apo AI have been reported could provide valuable information.
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Relative to non-2/2 haplotype (n = 23), subjects with the 2/2 haplotype (n = 14) had significantly increased plasma concentrations of total, LDL-cholesterol, and total apoB (P < 0.05). The fractional catabolic rate (FCR) of LDL-apoB was significantly lower in 2/2 subjects compared with non-2/2 subjects (P < 0.05), with an associated increase in LDL-apoB pool size in the former group. Sixteen subjects were then treated with 40 mg atorvastatin (6 weeks): 2/2 subjects (n = 8) had a significantly greater reduction in plasma concentrations of cholesterol and total apoB and in LDL-apoB pool size, as well as a greater increase in LDL-apoB FCR compared with non-2/2 subjects. There were no significant treatment-related between-haplotype differences in VLDL-apoB kinetics or in plasma concentrations of lathosterol and campesterol.
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Statins inhibit endogenous cholesterol synthesis, up-regulate low-density lipoprotein (LDL) receptor expression in mammalian liver cells, and thus decrease circulating LDL-cholesterol concentrations. As cholesterol seems to play a role in the development of neurodegenerative diseases, it is of interest to evaluate the effect of high dosages of statins (eg, atorvastatin or simvastatin) on brain cholesterol metabolism. Plasma samples from 44 participants (aged 30-69 years, 16 men and 18 women) of an earlier randomized, placebo-controlled, double-blind trial, who took 40 mg atorvastatin or 80 mg simvastatin daily for 2 months, were used to analyze total cholesterol, its precursor lathosterol, and its metabolites 24(S)-hydroxycholesterol and 27-hydroxycholesterol. Despite a significant decrease in absolute plasma concentrations of oxysterols, total cholesterol, and its endogenous synthesis rate, indicated by a decreased ratio of lathosterol to cholesterol, the plasma 24(S)-hydroxycholesterol to cholesterol ratio, a surrogate marker of brain cholesterol homeostasis, remained unchanged. Short-term high-dose atorvastatin and simvastatin treatment does not seem to influence brain cholesterol metabolism in patients with moderately elevated plasma cholesterol levels.
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Results from the PROVE IT trial suggest that patients with acute coronary syndrome (ACS) treated with atorvastatin 80 mg/day (A80) have significantly lower rates of cardiovascular events compared with patients treated with pravastatin 40 mg/day (P40). In a genetic post hoc substudy of the PROVE IT trial, the rate of event reduction was greater in carriers of the Trp719Arg variant in kinesin family member 6 protein (KIF6) than in noncarriers. We assessed the cost effectiveness of testing for the KIF6 variant followed by targeted statin therapy (KIF6 Testing) versus not testing patients (No Test) and treating them with P40 or A80 in the USA from a payer perspective.
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Between April 1991 and December 2003, we retrospectively evaluated 336 heart transplant patients (including 55 women) with regard to the occurrence of possible adverse effects of statins (rhabdomyolysis, myalgia, hepatotoxicity, high CK without muscle symptoms, and others). Resolution on reduction of dosage or discontinuance and/or change of statin were deemed to constitute confirmation of cause. Relations were sought between adverse effects and age, sex, immunosuppressive therapy, kidney failure, body mass index (BMI), arterial hypertension, and diabetes mellitus.
Among the 16 860 patients, the mean age was 63 years and 74% were male. Overall, 78% of the patients had documented CHD, 40% had CVD, 5% had PAD and 21% reported more than one condition. The median time from initial diagnosis of vascular disease to screening was 18 months. At screening, the proportions who took various treatments were 83% for antiplatelet agents, 49% for beta-blockers, 47% for statins and 28% for angiotensin-converting enzyme inhibitors. The proportion treated with statin was much higher in CHD than in CVD or PAD patients (61% vs. 10% vs. 22% respectively) and decreased significantly with time from initial diagnosis. Simvastatin (mainly 20 mg) and atorvastatin (mainly 10 mg) each accounted for about 40% of total statin use.
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To examine how pharmacy bargaining activities affect reimbursement rates in Medicare Part D prescription drug plan (PDP) contracts, controlling for pharmacy quality attributes, market structures, and area socioeconomic status.
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The recently identified lipid-regulated group of ATP-binding cassette (ABC) transporters acts in various cells and tissues that are important for total body lipid homeostasis. ABCA1 and ABCG1 are key regulators of high-density lipoprotein (HDL) metabolism, acting as protective factors against the development of atherosclerosis. Recent data regarding how these ABC transporters control cholesterol and phospholipid homeostasis have provided valuable insights into the mechanisms of mRNA and protein expression, intracellular trafficking, surface membrane localization and interaction with binding partners and lipoproteins. These studies have identified several potential new targets, including nuclear receptors, ABCA1-interactive proteins and apolipoprotein A-I mimetics, which could be promising tools for raising HDL levels and improving the pharmacological treatment of cardiovascular disease.
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Exposure to ticagrelor and its active metabolite, AR-C124910XX, was generally unchanged by a single dose of either statin, except for a minor increase in ticagrelor C(max) in the presence of simvastatin. Effects of ticagrelor on atorvastatin pharmacokinetics were modest and unlikely clinically relevant, while with simvastatin, changes were slightly larger, and simvastatin doses >40 mg with ticagrelor should be avoided.