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Zocor (Simvastatin)

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Zocor is an HMG-CoA reductase inhibitor. Zocor is used to reduce the risk of heart attack, stroke, and death due to coronary heart disease. It also reduces the risk of heart attack, stroke, blood vessel blockage, or chest pain caused by angina, it lows high cholesterol and triglycerides and increases high-density lipoprotein (HDL, "good") cholesterol levels. Zocor works by reducing the production of certain fatty substances in the body, including cholesterol.

Other names for this medication:

Similar Products:
Crestor, Zetia, Tricor, Pravachol, Mevacor, Lipitor


Also known as:  Simvastatin.


Zocor is an HMG-CoA reductase inhibitor.

Zocor is used to: reduce the risk of heart attack, stroke, and death due to coronary heart disease; reduce the risk of heart attack, stroke, blood vessel blockage, or chest pain caused by angina; low high cholesterol and triglycerides; increase high-density lipoprotein (HDL, "good") cholesterol levels.

Zocor is also known as Imvastatin, Simlup, Simcardis, Ranzolont, Simvador.

Zocor works by reducing the production of certain fatty substances in the body, including cholesterol.

Generic name of Zocor is Simvastatin.

Brand name of Zocor is Zocor.


Take Zocor orally.

Take Zocor with or without food.

Do not use grapefruit or grapefruit juice while taking Zocor. Eating grapefruit or drinking grapefruit juice may increase the amount of Zocor in blood, what may increase the serious side effects.

If you want to achieve most effective results do not stop taking Zocor suddenly.


If you overdose Zocor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Zocor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Zocor if you are allergic to Zocor components.

Be careful with Zocor if you're pregnant or you plan to have a baby. Do not use it if you are a nursing mother.

Be careful with Zocor if you suffer from low blood pressure, kidney problems, diabetes, serious infection, metabolism problems, hormonal problems.

Do not use potassium supplements or salt substitutes.

Avoid eating grapefruit or drinking grapefruit juice while taking Zocor.

While taking Zocor, you can make laboratory tests (blood cholesterol levels, liver function tests, creatine phosphokinase blood levels) to monitor the condition of your health.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Be very careful when you are driving machine.

Do not stop taking Zocor suddenly.

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Chronic obstructive pulmonary disease (COPD) is characterised by mucus hyper-production. This pathology, together with other inflammatory contributions, leads to airway obstruction and breathing complications. Newer therapeutic approaches are of increased interest, including the use of HMG-CoA reductase inhibitors. Retrospective studies have shown that statins are effective in reducing patient mortality and blood cytokines levels. These findings suggest statins may also provide a new therapeutic approach in COPD treatment.

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Patients under lipid lowering therapy and managed by general practitioners were included. LDL-cholesterol therapeutic objective was defined according to the number of cardiovascular risk factors associated with dyslipidemia (AFSSAPS-2005 guidelines).

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Simvastatin (SIM), a widely used anti-lipidemic drug, has been identified as a bone anabolic agent. Its poor water solubility and the lack of distribution to the skeleton, however, have limited its application in the treatment of bone metabolic diseases. In this study, an amphiphilic macromolecular prodrug of SIM was designed and synthesized to overcome these limitations. The polyethylene glycol (PEG)-based prodrug can spontaneously self-assemble to form micelles. The use of SIM trimer as the prodrug's hydrophobic segment allows easy encapsulation of additional free SIM. The in vitro studies showed that SIM/SIM-mPEG micelles were internalized by MC3T3 cells via lysosomal trafficking and consistently induced expression of both BMP2 and DKK1 mRNA, suggesting that the prodrug micelle retains the biological functions of SIM. After systemic administration, optical imaging suggests that the micelles would passively target to bone fracture sites associated with hematoma and inflammation. Furthermore, flow cytometry study revealed that SIM/SIM-mPEG micelles had preferred cellular uptake by inflammatory and resident cells within the fracture callus tissue. The treatment study using a mouse osteotomy model validated the micelles' therapeutic efficacy in promoting bone fracture healing as demonstrated by micro-CT and histological analyses. Collectively, these data suggest that the macromolecular prodrug-based micelle formulation of SIM may have great potential for clinical management of impaired fracture healing.

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Hepatic uptake carriers of the organic anion-transporting peptide (OATP) family of solute carriers are more and more recognized as being involved in hepatic elimination of many drugs and potentially associated drug-drug interactions. The gemfibrozil-statin interaction was studied at the level of active hepatic uptake as a model for such drug-drug interactions. Active, temperature-dependent uptake of fluvastatin into primary human hepatocytes was shown. Multiple transporters are involved in this uptake as Chinese hamster ovary or HEK293 cells expressing either OATP1B1 (K(m) = 1.4-3.5 microM), OATP2B1 (K(m) = 0.7-0.8 microM), or OATP1B3 showed significant fluvastatin uptake relative to control cells. For OATP1B1 the inhibition by gemfibrozil was substrate-dependent as the transport of fluvastatin (IC(50) of 63 microM), pravastatin, simvastatin, and taurocholate was inhibited by gemfibrozil, whereas the transport of estrone-3-sulfate and troglitazone sulfate (both used at 3 microM) was not affected. The OATP1B1- but not OATP2B1-mediated transport of estrone-3-sulfate displayed biphasic saturation kinetics, with two distinct affinity components for estrone-3-sulfate (0.23 and 45 microM). Only the high-affinity component was inhibited by gemfibrozil. Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). The results indicate that the in vitro engineered systems can not always predict the behavior in more complex systems such as freshly isolated primary hepatocytes. Therefore, selection of substrate, substrate concentration, and in vitro transport system are critical for the conduct of in vitro interaction studies involving individual liver OATP carriers.

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Compared with controls, patients with EH had increased IL-1beta [992+/-151 pg/ml, 912+/-102 pg/ml vs. 599+/-93 pg/ml; P<0.05] secretion by PBMCs after stimulated by angiotensin II. Simvastatin treatment had a significant effect of decreasing IL-1beta [668+/-98 vs. 923+/-67 pg/ml; P<0.05] secretion in PBMCs. The reductions were not correlated to changes in plasma lipids.

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A case of spontaneous biceps tendon rupture in a physician during therapy with the combination of simvastatin and ezetimibe (Vytorin) is reported. Rechallenge produced tendinopathy in the contralateral biceps tendon that abated with drug discontinuation. Tendon rupture generally occurs in injured tendons. Physiological repair of an injured tendon requires degradation and remodeling of the extracellular matrix through matrix metalloproteinases (MMPs). Statins are known to inhibit MMPs. It was hypothesized that statins may increase the risk of tendon rupture by altering MMP activity. In conclusion, statins may increase the risk of tendon rupture by altering MMP activity.

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After 8 weeks of treatment, LDL-C concentrations were reduced by 42.5% from baseline in patients receiving atorvastatin and 34.8% in those receiving simvastatin (p = 0.0006). Patients treated with atorvastatin also had a significantly greater reduction in very-low-density lipoprotein cholesterol (VLDL-C), TG, and total cholesterol (TC) after 8 weeks of treatment. The significantly greater reductions in LDL-C, VLDL-C, TG, and TC from baseline achieved with atorvastatin were still observed after an additional 8 weeks of treatment with 20 mg study medication. Both drugs increased high-density lipoprotein cholesterol (HDL-C) concentrations after 16 weeks of treatment, with no significant difference between the two treatments. After 16 weeks of treatment, 93% of atorvastatin and 85% of simvastatin patients had achieved their National Cholesterol Education Program LDL-C goals. No deaths occurred in the study population and the incidence of treatment-emergent adverse events was the same in the two groups (28%). Only one patient who was treated with simvastatin had a transaminase or creatine phosphokinase concentration that was more than three-fold the upper limit of normal.

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Patients who switched from atorvastatin to simvastatin between July 2006 and January 2008 were retrospectively identified from a US medical and pharmacy claims database, and matched with controls remaining on atorvastatin. Outcomes measured were the number of switched patients receiving a simvastatin milligram dose>or=2 times their previous atorvastatin dose, changes in LDL-C levels, and percentage of patients achieving recommended LDL-C targets. All study variables were analyzed descriptively.

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In this phase 2 study, 61 patients received treatment with irinotecan (65 mg/m(2) ) and cisplatin (30 mg/m(2) ) on Days 1 and 8 every 3 weeks until either death or disease progression occurred. Patients also received oral simvastatin (40 mg daily) during the course of chemotherapy. The primary endpoint was 1-year survival. Secondary endpoints included the response rate (RR), progression-free survival (PFS), and toxicity.

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The lipid-lowering drugs, statins, induce apoptosis in a variety of tumor cells. Here we investigated the apoptotic effect of the lipophilic statin, simvastatin, in C6 glioma cells and the underlying effects on intracellular signal transduction. Simvastatin inhibited cell proliferation totally after 20h of treatment as shown by the decrease in proliferating cell nuclear antigen expression in the nucleus. Subsequently, simvastatin caused apoptotic cell death by shrinkage of cytoplasm and condensation of chromatin, and DNA fragmentation. The features of apoptosis were visible only after 48 h of treatment, possibly reflecting a requirement for cell commitment to growth arrest. In immunocytochemical and immunoblotting experiments we have shown that simvastatin markedly increased the phosphorylation of ATF-2 and c-jun in the nucleus of the C6 glioma cells at early time points which was preserved even 24 h after treatment. In contrast, activities of protein kinases Erk1/2 and AKT in the cell survival pathway remained unchanged throughout the treatment. Selective inhibitor of JNK, but not p38 kinase, reduced simvastatin-induced cell death and ATF-2 and c-jun phosphorylation suggesting that JNK-dependent activation of ATF-2 and c-jun may play an important role in simvastatin-induced proliferation inhibition and apoptosis in C6 glioma cells. These observations suggest that statins may have clinical significance in the prevention of glial tumors beyond their cholesterol-lowering effect and JNK may be a rational target for sensitizing glioma cells to chemotherapeutic agents.

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A Simon two-stage, single-arm, phase II study was performed to test the efficacy and safety of the addition of simvastatin to cetuximab in patients with a KRAS mutation in their CRC tumour who were previously treated with fluoropyrimidine, oxaliplatin and irinotecan based regimens. The primary endpoint was to test the percentage of patients alive and free from progression 12.5 weeks after the first administration of cetuximab. Our hypothesis was that at least 40% was free from progression, comparable to, though slightly lower than in KRAS wild-type patients.

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Ubiquinone (Ub) is the only known endogenously synthesized lipid soluble antioxidant. It is synthesized from intermediates in the cholesterol metabolic pathway. Our goal was to identify the Ubs and determine the concentration and distribution of Ubs in the rat lens and the effect of treatment with simvastatin, a cholesterol synthesis inhibitor, on lens levels.

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This case demonstrates a possible association between acute pancreatitis and nilotinib use. Although a rare phenomenon, clinicians should be alert for signs and symptoms of pancreatitis, as treatment with nilotinib for CML is becoming more common.

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The study is a prospective, randomised, open label trial with blinded end point assessment and balanced randomisation (1:1) conducted in 10 outpatient clinics in Denmark. The primary end point after 5 years of follow-up is a composite of death from cardiovascular causes, non-fatal myocardial infarction, non-fatal stroke and cardiac revascularisation. Secondary outcomes are: the proportion of patients achieving low-density lipoprotein cholesterol <2.5 mmol/L, glycated haemoglobin <48 mmol/mol, blood pressure <140/90 mm  Hg for patients without diabetes and <130/80 mm Hg for patients with diabetes and normoalbuminuria (urinary albumin creatinine ratio <30 mg/g) after 1 year of follow-up and the proportion of patients in each treatment group achieving low RA disease activity after 1 year, defined as a disease activity score C-reactive protein (DAS28-CRP) <3.2 and a DAS28-CRP score <2.6 after 12, 24 and 60 months. Furthermore, all hospitalisations for acute and elective reasons will be adjudicated by the event committee after 12, 24 and 60 months. Three hundred treatment-naive patients with early RA will be randomly assigned (1:1) to receive either conventional treatment administered and monitored by their general practitioner according to national guidelines (control group) or a stepwise implementation administered and monitored in a quarterly rheumatological nurse-administered set-up of behaviour modification and pharmacological therapy targeting (1) hyperlipidaemia, (2) hypertension, (3) hyperglycaemia and (4) microalbuminuria (intervention group).

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A total of 20,536 people were assigned randomly to simvastatin 40 mg daily or placebo for an average of 5 years. Five baseline N-BNP groups were defined (<386; 386 to 1,171; 1,172 to 2,617; 2,618 to 5,758; and > or =5,759 pg/ml).

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The patients with CAD and obesity presented at baseline significantly increased hs-CRP level, insignificantly decreased FMD and lower PON1 activity compared to non-obese individuals. There was no association of obesity with 8-iso-PGF2α in the CAD and control group. The PON1 activity was significantly higher in 192R carriers in patients and controls, irrespective of obesity. Obesity was not associated with the effects of simvastatin on PON1 activity, urine 8-iso-PGF2α, and TNF-α, whereas it blunted its effect on the FMD improvement. The Q192R polymorphism was associated with simvastatin effectiveness on hs-CRP and FMD.

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Three review authors independently assessed trial quality and extracted data.

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Simvastatin interacts with the RA system, inducing the expression of the key protein regulating the uptake of retinol (STRA6) and the expression of apoptosis-promoting CRABP2. These effects may contribute to cooperative apoptosis-inducing effects of simvastatin and RA and support the examination of these compounds in the treatment of endometriosis.

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Male Sprague-Dawley rats were fed a diet containing cholesterol for 10 days to induce hypercholesterolemia. The NAD levels in the plasma and liver and hepatic ACMSD activity were determined. In vitro study, the expression of ACMSD and the transcriptional factors that regulate cholesterol metabolism were determined using rat primary hepatocytes treated with cholesterol and 25-hydroxycholesterol or simvastatin, a statin medication, by quantitative real-time PCR analysis and Western blotting analysis.

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Statins are widely prescribed medicines and are also available in fixed dose combinations with other drugs to treat several chronic ailments. Given the safety issues associated with statins it may be important to assess feasibility of a single time concentration strategy for prediction of exposure (area under the curve; AUC). The peak concentration (Cmax) was used to establish relationship with AUC separately for pravastatin and simvastatin using published pharmacokinetic data. The regression equations generated for statins were used to predict the AUC values from various literature references. The fold difference of the observed divided by predicted values along with correlation coefficient (r) were used to judge the feasibility of the single time point approach. Both pravastatin and simvastatin showed excellent correlation of Cmax vs. AUC values with r value ≥ 0.9638 (p<0.001). The fold difference was within 0.5-fold to 2-fold for 220 out of 227 AUC predictions and >81% of the predicted values were in a narrower range of >0.75-fold but <1.5-fold difference. Predicted vs. observed AUC values showed excellent correlation for pravastatin (r=0.9708, n=115; p<0.001) and simvastatin (r=0.9810; n=117; p<0.001) suggesting the utility of Cmax for AUC predictions. On the basis of the present work, it is feasible to develop a single concentration time point strategy that coincides with Cmax occurrence for both pravastatin and simvastatin from a therapeutic drug monitoring perspective.

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Of 239 respondents (62 from ANZ and 177 from UK) 58% worked in teaching hospitals; most (78.2%) practised in 'closed' units with a mixed medical and surgical case mix (71.0%). The most frequently prescribed statins were simvastatin (77.6%) in the UK and atorvastatin (66.1%) in ANZ. The main reasons cited to explain the choice of statin were preadmission prescription and pharmacy availability. Most respondents reported never starting statins to prevent (65.3%) or treat (89.1%) organ dysfunction. Only a minority (10%) disagreed with a statement that the risks of major side effects of statins when prescribed in critically ill patients were low. The majority (84.5%) of respondents strongly agreed that a clinical trial of statins for prevention is needed. More than half (56.5%) favoured rates of organ failure as the primary outcome for such a trial, while a minority (40.6%) favoured mortality.

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LDL-C goal achievement rates and reductions in LDL-C, total cholesterol and non-high-density lipoprotein cholesterol (HDL-C) were similar in patients with and without the MS within statin treatment groups; triglycerides were reduced more and HDL-C tended to be increased more in patients with the MS, as expected. Treatment with rosuvastatin 10 mg was more effective in allowing patients with and without the MS to reach European and ATP III LDL-C goals, compared to atorvastatin 10 mg, simvastatin 20 mg and pravastatin 40 mg (p < 0.0001 for all comparisons); consistently produced greater reductions in LDL-C, total cholesterol and non-HDL-C, compared to these treatments; and produced similar or greater reductions in triglycerides and increases in HDL-C, compared to the other treatments.

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Fewer cardiovascular events and deaths were predicted to occur in the group treated with higher-intensity statins, and the incremental cost-effectiveness ratio (ICER) was estimated at pound11 103/QALY. The ICER remained below the pound20 000 threshold for 20-39-year-olds and 40-59-year-olds, but rose above this threshold in individuals aged over 60 years. One-way sensitivity analysis showed that results were most sensitive to variation in treatment effect on mortality and the cost of high-intensity statins.

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Effects of pravastatin and simvastatin on the humoral immune response were studied using Cunningham's method of the IgM plaque-forming cell (PFC) assay system in mice. The vehicle (0.5% CMC), pravastatin (1 mg/body : about 50 mg/kg) or simvastatin (0.5 mg/body : about 25 mg/kg) were given orally for 14 days in experiment Exp-I and Exp-II. The vehicle, pravastatin (0.5 mg/body : about 25 mg/kg) or simvastatin (0.25 mg/body : about 12.5 mg/kg) were given orally 29 times for 32 days in Exp-III. There were no significant differences in the mean numbers of PFCs per 10(6) splenocytes between the pravastatin groups and the vehicle groups. In the simvastatin groups, however, there were significant reductions of the numbers of PFCs in Exp-I, Exp-II and Exp-III, as compared with the vehicle group. Based on these results, it was considered that suppressive effect on IgM antibody production was induced by simvastatin, whereas such a suppression was not observed with pravastatin.

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Large-scale randomized controlled trials (RCTs) have well demonstrated the beneficial effects of cholesterol-lowering treatment with statins in patients at high risk of vascular disease. However, large statin RCTs were usually restricted to the typical 5-6 years. Moreover, non-cardiovascular events, especially the risk of cancer, probably failed to emerge within a restricted period of 6 years. The aim of this study was to evaluate the long-term efficacy and safety of statin treatment by performing a meta-analysis of statin RCTs with extended follow-up beyond 6 years. Six RCTs with post-trial follow-up were eligible for inclusion, involving 47,296 patients with total follow-up ranging from 6.7 to 14.7 years. During the post-trial period, all the surviving participants were advised to take a statin and the cholesterol level were almost identical between the original statin group and the original placebo group. Over the entire 6.7-14.7 years of follow-up, a significant reduction in the rates of all-cause mortality (relative risk 0.90, 95% confidence interval 0.85-0.96; P=0.0009), cardiovascular mortality (0.87, 0.81-0.93; P<0.0001) and major coronary events (0.79, 0.72-0.86; P<0.00001) was observed in favour of the original statin group. During 2-year post-trial period, further reduction in all-cause mortality (0.83, 0.74-0.93; P=0.001), cardiovascular mortality (0.81, 0.69-0.95; P=0.01) and major coronary events (0.77, 0.63-0.95; P=0.01) was observed among initially statin-treated patients. Over the entire follow-up period, statin treatment did not increase the incidence of cancers (0.99, 0.95-1.04; P=0.79), deaths from cancers (1.00, 0.93-1.07; P=0.98) and non-cardiovascular mortality (0.95, 0.90-1.00; P=0.07). In conclusion, statin treatment beyond 6 years is effective and safe in patients at high risk of vascular events. Moreover, earlier treatment with statin may not only preserve the initial benefit but also have further survival benefit for additional 2 years. Further studies are called for to explore the underlying mechanisms.

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Sequential arterial injury augments the thrombotic response suggesting that the propensity for arterial thrombosis is at least partially acquired. This thrombotic augmentation can be acutely attenuated by intravenous lovastatin which may result from a pleiotropic impact on platelet function. These results appear to be a class effect of 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors.

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A structured framework was applied to demonstrate considerations when tackling challenging medication regimens.

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A total of 6,080 cases and 24,320 controls were examined. The mean age was 74 years, and the majority of patients were Caucasian (88%) and male (99%). Filled prescriptions of statins were recorded less frequently in cases (49%) than in controls (52%; OR: 0.88; 95% confidence interval (95% CI): 0.83-0.93). This inverse association remained significant after adjusting for inflammatory bowel disease, diabetes severity, cholecystectomy, liver disease, filled prescriptions for sulfonylurea, aspirin or NSAID use, or colorectal evaluation. Simvastatin comprised the majority (87%) of statin-filled prescriptions, and the association with risk of CRC with simvastatin was very similar to that of any statin. No significant associations were observed between the risk of CRC and nonstatin cholesterol (OR: 1.02; 95% CI 0.88-1.18) or triglyceride-lowering medications (OR: 0.96; 95% CI: 0.87-1.05). The significant inverse association was limited to Caucasians, patients without history of polyps, patients aged 65 years and older, and patients with colon cancer (excluding rectum).

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zocor 20 mg 2017-02-27

Switching from any statin to another non-equipotent lipid lowering treatment (LLT) may cause a low-density lipoprotein cholesterol increase buy zocor and has been associated with a higher probability of negative cardiovascular outcomes. The aim of the study was to assess the impact of switching from rosuvastatin to any other LLT on clinical outcomes in primary care.

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The estimated annual drug cost per 1000 patients treated with atorvastatin was pound 289000, with simvastatin pound 315000, with pravastatin pound 333000 and with fluvastatin pound 167000. The percentages of patients achieving target are 74.4%, 46.4%, 28.4% and 13.2% for atorvastatin, simvastatin, pravastatin and fluvastatin, respectively. Incremental drug cost per extra patient treated to LDL-C and TC targets compared with fluvastatin were pound 198 and pound 226 for atorvastatin, pound 443 and pound 567 for simvastatin and pound buy zocor 1089 and pound 2298 for pravastatin, using 2002 drug costs.

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Watanabe heritable hyperlipidemic rabbits aged three months (young group) or 10 buy zocor months (adult group) received 10 mg/kg of simvastatin daily for 24 weeks. Serum levels of total cholesterol, triglycerides, and beta-lipoproteins were reduced significantly in the treated animals but not in untreated controls. The decreases were greater in the young than in the adult animals. Levels of high-density lipoprotein cholesterol were not affected by treatment. At 24 weeks, the extent of atheromatous lesions on the thoracic-abdominal aorta was lower in the treated animals than in the controls, but the difference was significant only in the young animals. The results indicate that simvastatin would be effective in the treatment of atherosclerosis.

simvastatin zocor reviews 2016-02-08

Traumatic brain injury (TBI) is an environmental risk factor for Alzheimer's disease (AD). Increased brain concentrations of amyloid-β (Aβ) peptides and impaired cerebral blood flow (CBF) are shared pathologic features of TBI and AD and promising therapeutic targets. We used arterial spin-labeling magnetic resonance imaging to examine if CBF changes after TBI are influenced by human Aβ and amenable to simvastatin therapy. CBF was measured 3 days and 3 weeks after controlled cortical impact (CCI) injury in transgenic human Aβ-expressing APP(NLh/NLh) mice compared to murine Aβ-expressing C57Bl/6J wild types. Compared to uninjured littermates, CBF was reduced in the cortex of the injured hemisphere in both Aβ transgenics and wild types; deficits were more pronounced in the transgenic group, which exhibited injury-induced increased concentrations of human Aβ. In the hemisphere contralateral to CCI, CBF levels were stable in Aβ transgenic mice but increased in wild-type mice, both relative to uninjured littermates. Post-injury treatment of Aβ buy zocor transgenic mice with simvastatin lowered brain Aβ concentrations, attenuated deficits in CBF ipsilateral to injury, restored hyperemia contralateral to injury, and reduced brain tissue loss. Future studies examining long-term effects of simvastatin therapy on CBF and chronic neurodegenerative changes after TBI are warranted.

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This study aims to determine whether buy zocor aspirin or simvastatin have beneficial biologic or clinical effects in patients with PAH. The safety and side effects of these commonly prescribed cardiovascular drugs will also be assessed.

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With the increasing knowledge on the pathogenesis of atherosclerosis, it appears that the prevention of cardiovascular disease in the future will involve, besides risk factor correction, direct pharmacological control of processes occurring in the arterial wall. Among them, a pivotal role is played by smooth muscle cell migration and proliferation that, together with lipid deposition, buy zocor are prominent features of atherogenesis and restenosis after angioplasty. Mevalonate and other intermediates (isoprenoids) of cholesterol synthesis are essential for cell growth, hence drugs affecting this metabolic pathway are potential antiatherosclerotic agents. Recently we provided evidence that fluvastatin, simvastatin, lovastatin, but not pravastatin, dose-dependently decrease smooth muscle cell migration and proliferation, independently of their hypocholesterolemic properties. The in vitro inhibition of cell migration and proliferation induced by simvastatin and fluvastatin (70-90% decrease) was completely prevented by the addition of mevalonate and partially (80%) by farnesol and geranylgeraniol, confirming the specific role of isoprenoid metabolites--probably through prenylated proteins--in regulating these cellular events. The present results provide evidence that HMG-CoA reductase inhibitors interfere directly with processes involved in atherogenesis--beyond their effects on plasma lipids--partially through local inhibition of isoprenoid biosynthesis.

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The aim of our study was to assess whether statins have dose-dependent effects on risk of symptomatic intracerebral hemorrhage (sICH) and outcome buy zocor after intravenous thrombolysis for ischemic stroke.

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Dyslipidemia conveys a major increased risk of future cardiovascular events in older persons. Data from large randomized controlled trials buy zocor confirm that statin therapy is as beneficial in older adults as it is in younger persons in both primary and secondary prevention. National guidelines support the use of statin therapy to reduce low-density lipoprotein cholesterol in older adults, with the recommended goal of <100 mg/dL in high-risk patients and an optional goal of <70 mg/dL in very high-risk patients. In the majority of high-risk older patients, these levels of low-density lipoprotein cholesterol can be achieved with initial low doses of an efficacious statin, but in some clinical situations, combination therapy may be considered. Moreover, statins appear to be safe and well tolerated in older age groups. Because of heightened risks of drug-drug interactions, the likelihood of polypharmacy in seniors, and issues of tolerability and convenience, monotherapy with low doses of an efficacious statin may be preferable to combination therapy in elderly individuals.

simvastatin zocor generic 2017-10-25

Wounds and wound healing have always been one of the most important subjects that experimental researches were dedicated to. Simvastatin has been used for long as a common lipid lowering agent which was reported to have some buy zocor pleiotropic effects such as antioxidation, anti-inflammation and immunomodulation. In this study we aimed to determine the effect of simvastatin on wound healing process in laboratory rats by means of stereological and histopathological analyses. 36 male Sprague-Dawley rats (220 ± 20 g) with a 1 cm(2) circular full-thickness wound on their back were divided into three groups: SS group that received a gel with 2% concentration of simvastatin; UW group that received no treatment but daily irrigation with normal saline; Base group that was treated with the gel base. Duration of the study was 12 days and at the end, wound closure rate, grade of inflammation, granulation-tissue formation, ulceration, epithelization, fibroblast proliferation, collagen-bundles synthesis, and vascularization were determined. Outcome of this study revealed that Simvastatin improves the wound healing by its anti-inflammatory and epithelization induction effect as well as statistically significant induction of fibroblast proliferation and collagen bundle synthesis which were reported by our stereological and histopathological investigations. Results of the present study demonstrated that topical Simvastatin enhances the wound healing process through affecting different aspects of tissue regeneration; however, further researches are needed to find the exact mechanism, advantages and disadvantages of this chemical agent.

zocor 10mg medication 2017-12-31

At baseline, median Lp(a) concentrations were 327 mg/l and 531 mg/l in the atorvastatin and simvastatin arms, respectively (p = 0.03). In the atorvastatin arm, Lp(a) concentrations decreased to 243 mg/l after one year (p < 0.001) and to 263 mg/l after two years (p < 0.001). In the simvastatin arm, Lp(a) concentrations decreased to 437 mg/l after one year (p < 0.001) and to 417 mg/l after two years (p < 0.001). The difference in Lp(a) reduction between the two treatment arms was significant after one year (p = 0.004), but not after two years (p = 0.086). Lp(a) concentrations at baseline were not related to cardiovascular events at baseline. There was no correlation between baseline Lp(a) concentrations and low density lipoprotein cholesterol concentrations buy zocor or intima-media thickness at baseline. Change in Lp(a) concentrations was not correlated with change in intima-media thickness after one or two years.

zocor overdose 2015-04-01

The propose of the present study was to determine the potential protective effects of simvastatin (SIMV) on Cr (VI)- buy zocor induced nephrotoxicity in rat.

zocor pill 2015-02-16

To investigate buy zocor levels of serologic markers, which may be useful surrogates for activity of vascular disease after administration of statin.

zocor 10 mg 2016-04-23

To examine the mechanisms of action of resveratrol and its interaction with simvastatin buy zocor on growth and the mevalonate pathway in rat theca-interstitial cells.

zocor brand name 2015-08-29

The aim of this study was to demonstrate the cholesterol-lowering effect of electroacupuncture (EA) at the acupoint of Fenglong (ST40) in mice and to investigate its molecular mechanism by using genome-wide gene expression profile analysis. Mice with hypercholesterolemia induced by a high-cholesterol diet were randomly divided into EA at ST40 group (EG), EA at non-acupoint group (ENG), and simvastatin group (DG). A lipid profile of both the plasma and liver indicated that EA at ST40 had the same hypocholesterolemic effect as that of simvastatin, while EA at non-acupoint failed to produce the same effect. The global gene expression profile showed that EA at ST40 not only regulated the expression of genes which were directly involved in the cholesterol metabolism in the liver, but also significantly affected the expression of genes involved in signal transduction, transcription regulation, cell cycle, cell adhesion, immunity and stress. The buy zocor gene expression pattern was further verified by real-time RT-PCR. The mechanism by which EA at ST40 regulated liver cholesterol metabolism is discussed. We conclude that the hypocholesterolemic effect is specific to EA at ST40 and not due to general electrical stimulation of muscles. The comprehensive gene expression profile analysis appears particularly useful in the search for EA-induced changes in cholesterol regulation.

zocor 80mg tab 2016-08-20

Fourteen patients with familial hypercholesterolaemia were managed with dietary advice and simvastatin for 12 months. Either nicotinic acid or cholestyramine resin was added to the regimen if serum cholesterol was not less than 5.5 mmol/l within 18 weeks. After dietary advice but before commencing pharmacotherapy for hyperlipidaemia, arterial stiffness was measured in the common carotid and common femoral arteries. These studies were repeated after 12 Lasix 5 Mg months on pharmacotherapy. The primary objective of this study was to determine whether arterial stiffness could be altered with total cholesterol and low density lipoprotein (LDL) cholesterol lowering. Over the 12 month interval, serum total cholesterol, LDL cholesterol and triglycerides fell significantly, whereas high density lipoprotein (HDL) cholesterol and body mass index (BMI) rose significantly. Mean supine blood pressure did not change significantly. Arterial stiffness in the common carotid artery decreased from 1.04 +/- 0.21 x 10(5) N/m2 to 0.63 +/- 0.06 x 10(5) N/m2 (T = -2.67, P < 0.01) over the interval. Stiffness of the common femoral artery decreased from 2.10 +/- 0.57 x 10(5) N/m2 to 0.83 +/- 0.15 x 10(5) N/m2 (T = -2.73, P < 0.01). The change in arterial stiffness was not directly related to changes in circulating lipids or supine blood pressure. Increase in BMI, however, correlated with change in arterial stiffness in the common femoral artery (Rs = 0.53, P < 0.05) but not in the common carotid artery. An increase in BMI was associated with a smaller decrease in common femoral arterial stiffness. Aggressive hypolipidaemic therapy was therefore associated with a favourable effect on arterial wall stiffness.(ABSTRACT TRUNCATED AT 250 WORDS)

zocor drug category 2017-03-01

The Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) study was designed when Amoxil Online Uk considerable disagreement existed as to relative benefits and risks of cholesterol reduction. Between June 1990 and December 1992, 9,014 patients aged 31-75 years were randomized to receive either pravastatin 40 mg once daily or placebo. These patients had experienced either acute myocardial infarction or unstable angina within the preceding 3 months to 3 years and had total cholesterol levels of 155-271 mg/dl (4.0-7.0 mmol/liter). All patients received dietary advice. The LIPID study is projected for conclusion in 1997, after a follow-up period of at least 5 years. The primary study endpoint is mortality due to coronary artery disease (CAD). The Scandinavian Simvastatin Survival Study (4S) is the first secondary prevention trial to show a reduction in total mortality with lipid-lowering therapy. However, the LIPID study should continue for the following reasons: (1) important differences exist between the LIPID study and 4S cohorts. Overall, > 80% of the LIPID patients could not have been included in 4S on the basis of their cholesterol level, age, or history of CAD; (2) the LIPID study will also provide important information on noncoronary mortality and on other groups, such as women and diabetic patients, who have been underrepresented in previous trials; (3) the LIPID study design allows for clinical management, including lipid-lowering therapy, to be at the discretion of the physician managing a trial patient. The 4S results have been brought to the attention of all LIPID investigators, Institutional Ethics Committees, the physicians of the individual patients, and the patients themselves.(ABSTRACT TRUNCATED AT 250 WORDS)

zocor 40mg medication 2015-02-03

A total of 291 patients with primary hypercholesterolemia [total plasma cholesterol > or = 6.20 mmol/liter (> or = 240 mg/dl)] were enrolled in an open, randomized, parallel, comparative study of simvstatin and pravastatin. All patients started or continued a standard lipid-lowering diet for > or = 6 weeks before entry into the 4-week placebo baseline period. There were 145 patients who received simvastatin and 146 patients who received pravastatin, both at the commonly recommended starting dose of 10 mg once daily, for a treatment period of 6 weeks. Concentrations of total cholesterol in plasma were reduced by 23% with simvastatin Cymbalta Drug Info , and by 16% with pravastatin. Concentrations of low-density lipoprotein cholesterol in plasma were reduced by 32 and 22%, and high-density lipoprotein cholesterol concentrations were increased by 7 and 5% with simvastatin and pravastatin, respectively. Plasma triglyceride concentrations were reduced by 13% with simvastatin and by 6% with pravastatin. Adverse experiences were similar between treatment groups and both drugs were well tolerated. In each treatment group, 3 patients were withdrawn from the study for clinical adverse experiences; 1 patient in the pravastatin group required a reduction in dose to 5 mg/day because of insomnia. At the commonly recommended starting dose for each, simvastatin had a significantly greater lipid-lowering effect than pravastatin. Both drugs were well tolerated.

zocor pill identifier 2016-11-26

The aims of this study were to determine the Moduretic Dosage Bodybuilding views and experiences of Scottish GPs towards CVD risk assessment by community pharmacists and the supply and sale of simvastatin.

zocor low dose 2016-01-05

Statin therapy decreases low-density lipoprotein cholesterol levels and the risk of coronary heart disease but has a considerable short-term effect on health care budgets. The cost effectiveness of rosuvastatin (Crestor) has been compared with those of atorvastatin, pravastatin, and simvastatin in lowering low-density lipoprotein cholesterol levels and achieving National Cholesterol Education Program Adult Treatment Panel III low-density lipoprotein cholesterol goals. The analysis was conducted from the perspective of health care payers in the United States. Clinical data were obtained from Mobic 30 Mg the Statin Therapies for Elevated Lipid Levels Compared Across Doses to Rosuvastatin (STELLAR) trial. Drug costs were based on wholesale acquisition costs. Cost effectiveness was assessed with the net monetary benefit approach and a 1-year time horizon. Rosuvastatin at 10 mg, the recommended starting dose, was the most cost-effective statin over a large range of "willingness-to-pay" values for a unit of clinical effect (i.e., a 1% decrease in low-density lipoprotein cholesterol or a patient achieving the goal).

zocor user reviews 2016-06-13

The immunomodulatory effects of hydroxy methyl glutaryl-coenzyme A Astelin Dosage Information reductase inhibitors have been increasingly recognized. Previous studies have demonstrated an ameliorative influence of pravastatin on hemodynamically compromising rejection after heart transplantation. A recent observational trial suggested that simvastatin 20 mg/day was associated with trends to lower survival and more adverse effects than pravastatin 40 mg/day.