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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:
Actalipid, Docsimvasta, Doctiverine, Dosavastatin, Lipex, Lipinorm, Lodales, Normotherin, Simbastatin, Simcard, Simgal, Simvastatina, Simvastatinum, Simvofix, Simvor, Sinvacor, Sivastin, Statinal, Vasilip, Zeid, Zocord, Zorced, Zorstat, Zosta, Zostin, Zostine, Zovast, Zovastin, Zovatin, Zurocid

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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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The addition of the HMG-CoA reductase inhibitors lovastatin, pravastatin, or simvastatin to diet therapy in children > or =10 years of age may be effective when diet therapy alone has failed to obtain the recommended maximum LDL-C concentration of 130 mg/dL. The use of statins during childhood and adolescence is generally safe, but large, long-term studies should be performed before statins are routinely prescribed to children with elevated cholesterol or lipoprotein concentrations.

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To design a refill-based adherence algorithm suitable for short observation periods, and compare it to 2 reference measures.

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The simvastatin-treated groups had significantly higher ratios of PaO(2)/FiO(2) and lower values of respiratory index than the control group. We observed that simvastatin reduced CPB-induced toll-like receptor 4 and nuclear factor-kappaB expressions in CPB groups (p < 0.01, versus control group). The levels of interleukin-6, tumor necrosis factor-alpha, and monocyte chemotactic protein-1 in serum, bronchoalveolar lavage fluid, and lung tissues increased in CPB groups, whereas pretreatment with simvastatins reduced these inflammatory marks in a dose-dependent manner (p < 0.01, versus control group). Furthermore, pretreatment with simvastatin had a lower lung injury score (p < 0.05, versus control group).

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We studied the effects of the 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors simvastatin and pravastatin on the in vitro susceptibility of low-density lipoprotein (LDL) to oxidation. Twenty-three hypercholesterolaemic patients (mean serum cholesterol 9.7 mmol l-1) were treated with increasing doses of either simvastatin or pravastatin for 18 weeks. No significant differences in effect on lipid levels between the two drugs were found. Treatment resulted in lowering of total cholesterol and LDL-cholesterol by maximally 30% and 34%, respectively. Chemical composition analysis showed that LDL particles contained relatively more protein and less free cholesterol and cholesteryl-ester after treatment. The LDL cholesterol/protein ratio decreased from 1.24 +/- 0.21 to 0.97 +/- 0.23 (n = 20). By continuous monitoring of in vitro oxidation it appeared that LDL was less susceptible to oxidation after drug treatment. Maximal rate of diene production was significantly decreased from 19.7 +/- 3.1 to 18.5 +/- 3.3 nmol min-1 mg-1 LDL; total diene production decreased significantly from 420.3 +/- 67.6 to 380.5 +/- 49.1 nmol mg-1 LDL; the lag time was unchanged throughout the study. These studies show that HMG-CoA reductase inhibitors reduce the oxidizability of LDL by altering its composition.

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Simvastatin reduced enhanced sCD40L levels together with amelioration of endothelial dysfunction. Treatment with simvastatin might downregulate enhanced CD40L-CD40 interactions in CAPD patients.

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HA promoted actin stress fiber and lamellipodia formation and dose-dependently induced ASMC migration without effect on proliferation. Pull-down assay of Rho protein activity indicated that HA activated RhoA and Rac. HA-induced ASMC migration was not affected by the RhoA inhibitor Tat-C3 (10 microg/ml), the Rho kinase inhibitor Y-27632 (10 microM) and blocking anti-CD44 antibody ,but was reduced by the non-selective Rho protein inhibitor simvastatin (10 microM), the Rac inhibitor LT-toxin (1 mug/ml), small interfering RNA (siRNA) targeting Rac and the phosphatidyl inositol 3-kinase (PI3K) inhibitor LY294002 (25 microM), which also blocked HA-induced Rac activation. CD44 knockdown by siRNA inhibited HA-mediated RhoA activation without effect on ASMC migration. In contrast, siRNA targeting RHAMM inhibited both HA-induced migration and Rac activation.

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Simvastatin drives a mechanism for promoting chondrogenesis of IVD cells partially mediated by upregulated BMP-2 through the inhibition of mevalonate pathway.

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Recent large-scale trials have consistently documented the fact that a 25-35% reduction in low-density lipoprotein cholesterol (LDL-C) can delay the progression of atherosclerosis. This raises the question as to how much it is possible to reduce serum cholesterol using feasible therapies. The aim of this study was to investigate the cholesterol-lowering efficacy of a triple therapy combining bile acid malabsorption with the inhibition of cholesterol synthesis and absorption.

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Ezetimibe use has increased rapidly in Australia since receiving public subsidy. Although the indications for subsidy are very restricted, there appears to have been widespread use, not explained by differential geographical IHD death rates. Latest guidelines still question the value of ezetimibe, so further discussion about whether the public spending on this medication for any potential improvement in population health outcomes is justified.

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Lipoprotein-associated phospholipase A2 (Lp-PLA(2)) is a novel inflammatory biomarker that is associated with increased cardiovascular disease risk independent of and additive to traditional risk factors. Lp-PLA(2) activity is correlated with the degree of inflammation in the atherosclerotic plaque. In human blood, approximately 80% of Lp-PLA(2) is associated with low-density lipoproteins (LDL). Thus, it is hypothesized that changes in Lp-PLA(2) should imitate the changes in the LDL cholesterol Famvir Online .

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Sixty-eight patients were enrolled (36 in the AS arm and 32 in the A arm). The RR was 5.7% (95% confidence interval [CI], 0.7-19.2%) for AS and 9.4% (95% CI, 2.0-25.0%) for A (P = 0.440). In arms AS and A, the median progression-free survival (PFS) was 1.0 vs. 3.6 months (P = 0.240) and the overall survival was 10.0 vs. 7.0 months (P = 0.930), respectively. Skin rash, stomatitis, and diarrhea were the most common adverse events in both arms. More grade 3 or 4 diarrhea was observed in arm A (18.8% vs. 5.6% in arm AS). In all patients, the median PFS for treatment including afatinib was not correlated with the status of EGFR mutation (P=0.122), EGFR fluorescence in situ hybridization (P=0.944), or EGFR immunohistochemistry (P=0.976). However, skin rash severity was significantly related to the risk of progression for afatinib (hazard Cytoxan Generic Price ratio for skin rash grade ≥ 2 vs. grade < 2, 0.44; 95% CI, 0.25-0.78; P = 0.005).

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Statins are frequently given in conjunction with clopidogrel for prophylaxis and therapy of coronary heart disease. The antiplatelet effect of clopidogrel may be attenuated by lipophilic statins such as atorvastatin. It was the aim of Viagra Generic Online this study to measure the antiplatelet effect of clopidogrel and the incidence of cardiovascular events after stent implantation in patients with coronary artery stenting.

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Comparing with the negative contrast group: the quantity of liver microsome protein, the activity of CYP3A and the metabolism of Legal Online Cialis simvastatin in positive control group were all increased markly (P < 0.05). In high dose group, the quantity of liver microsome protein and the activity of CYP3A were both increased significantly (P < 0.05), and the metabolism of simvastatin also accelerate obviously (P < 0.05). But in the low dose group significant distinction of every index was not found.

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Market research surveys can be a source of up-to-date information about current clinical practices. Data from one such survey, Cholesterol Monitor (made available by Merck & Co., Inc., Whitehouse Station, N.J., USA) was examined to ascertain to what extent management of cholesterol in six European countries conforms with the advice of the joint Task Force of the European Society of Cardiology, European Atherosclerosis Society and European Society of Hypertension for prevention of coronary heart disease (CHD). Rates of cholesterol testing in patients with CHD varied from less than 50% in the UK to more than 80% in France and Italy. Across Europe, the average cholesterol levels in surveyed patients was 6 mmol/l, and the average intervention level was 7.5 mmol/l. In all countries, there was evidence of a substantial treatment Trileptal Generic gap, even among high-risk patients with established CHD. This gap took the form of non-treatment of a proportion of patients whose risk status merited intervention on the basis of expert recommendations and the results of the Scandinavian Simvastatin Survival Study (in which sustained lowering of total and low-density lipoprotein cholesterol reduced total and coronary mortality in patients with baseline total cholesterol as low as 5.5 mmol/l). The findings indicate that a concerted programme of physician education is required if the recommendations of the joint Task Force are to be put into effect, and if the present nontreatment/undertreatment of cholesterol in high-risk patients is to be corrected.

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Although statins are widely prescribed as cholesterol-lowering drugs, a number of studies suggest that these compounds may have anabolic effects on bone. Our aim was to assess whether simvastatin affects the rate of fracture healing in humans. A prospective, double-blind, randomized controlled trial was performed. Individuals who had sustained an undisplaced, extra-articular fracture of the distal radial metaphysis were recruited from a trauma clinic. Patients were randomized to receive simvastatin 20 mg once daily or a placebo. Regular clinical and radiological follow-up was undertaken for a 12 week period. Dual-energy X-ray absorptiometry assessment of bone mineral density was conducted at 2 and 12 weeks postinjury. Biochemical markers of bone turnover were assayed during the study period. Time to fracture union was defined as the time to cortical bridging in four cortices on plain radiographs. In addition, the rate of trabecular union was assessed. Eighty patients were recruited, of which 62 completed the study (31 in each group). Study cohorts were matched for age and gender. For patients receiving simvastatin therapy, the mean time to fracture union was 71.6 days (SD 22.2 days, SEM 3.8 days). This compared to 71.3 days (SD 21.3, SEM 4.1 days) for Zofran Generic Medication the control cohort (p = 0.6481). There was no significant difference between bone mineral density or bone biochemical markers between groups (p > 0.05). Despite promising results from in vivo and in vitro animal studies, simvastatin at a treatment dose of 20 mg once daily does not affect the rate of fracture healing in humans.

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There was a relatively Zantac Generic Price high risk of gastrointestinal bleeding with rosuvastatin when administered concomitantly with warfarin.

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Simvastatin displays significant Depakote 500mg Generic antimyeloma activity in vitro. Further research is warranted for elucidation of the modulated molecular pathways and clinical relevance.

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Homogeneous poly(ε-caprolactone) (PCL) and poloxamines (PLXs) porous blends were prepared using a supercritical carbon dioxide-assisted foaming/mixing (SFM) approach aiming to obtain cytocompatible implantable materials presenting tunable morphologies, bioerosion rates, bioactive molecules release and osteogenic features. Pure PCL, pure PLXs (T908 and T1107 varieties) and three distinct PCL:PLX 75:25, 50:50, 25:75% w/w blends, with and without the osteogenic and angiogenic bioactive molecule simvastatin were processed at constant pressure of 20 MPa and temperature of 40 °C or 43 °C, for T1107 and T908, respectively. Obtained porous blends were characterized applying a wide range of techniques and in vitro methods. Calorimetric analysis showed that hydrophilic T908 and T1107 PLXs are miscible with PCL for all tested compositions. Prepared PCL:PLX porous blends rapidly lost mass when immersed into phosphate buffer pH 7.4 due to PLXs dissolution and then went through slow and almost constant erosion rates for the subsequent weeks due to PCL slow hydrolytic degradation, which explains the rapid initial release of simvastatin and its subsequent sustained release for longer periods of time. PCL and PCL:PLX 75:25% w/w porous blends, containing or not simvastatin, showed a high cytocompatibility with Evista Prices Canada SAOS-2 cells. In addition, prepared biomaterials promoted mesenchymal stem cells proliferation and their differentiation into osteoblasts. Overall, obtained results showed novel possibilities of addressing local treatment of small bone defects/fractures using highly porous PCL:PLX homogeneous blends.

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For the initial admission, 153 patients were audited, with 84 patients contacted one year later. Demographic data, treatment status, and cholesterol levels were analysed both on admission and at follow up.

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Statins and fibrates are both effective in the treatment of hyperlipidaemias but are not recommended in combination because episodes of rhabdomyolysis have followed combined lovastatin-gemfibrozil therapy. We assessed treatment with dual bezafibrate-simvastatin therapy in routine clinical practice. In 22 patients, total cholesterol, LDL-cholesterol and triglycerides fell by 20.1% (P < 0.0001), 35.1% (P < 0.001) and 31% (P < 0.05) respectively, and HDL-cholesterol rose by 18.4% (P < 0.05) on combination therapy. The reduction in cholesterol followed the introduction of simvastatin, while the decrease in triglycerides followed treatment with bezafibrate. No patient developed myopathy. We conclude that dual simvastatin-bezafibrate therapy is well tolerated and may reduce triglyceride concentrations, but offers no advantage in cholesterol reduction over treatment with simvastatin alone.

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Statins have been suggested to improve cardiac function, but the evidence underlying beneficial effects of statins in heart failure (HF) is insufficient. We analyzed plasma N-terminal prohormone brain natriuretic peptide (NT-proBNP) levels and cardiac function in patients with HF of various etiologies, and who were treated with or without statins.