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Zocor (Simvastatin)
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Zocor

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.

Description

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.

Dosage

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.

Overdose

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

Storage

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.

Contraindications

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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Lens photographs were graded for the presence and severity of cortical, nuclear, and posterior subcapsular cataract.

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A total of 28 BSXSB male mice with LN (16 weeks) were randomly divided into observation group and the comparison group, observation group was given 6 mg•kg(-1)•d(-1) simvastatin in 0.1% PBS lavage for 4 weeks, the comparison group was not given any treatment. Blood urea nitrogen (BUN) level and urine trace albumin (Scr) level of two groups were determined. The expression of IL17, HMGB1 and TLR4 protein was detected using immune histochemical method, and the kidney histological damage was observed.

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Of the 310 patients enrolled into the year 2 study, 287 (93%) completed therapy. The mean cumulative exposure to combination therapy was 743 days across the studies. Adverse event rates were similar for all three combination therapy groups. No deaths or treatment-related serious adverse events occurred. The incidence of discontinuation due to adverse events was 2.9% overall. Rhabdomyolysis was not reported in any group. Overall, fenofibric acid + moderate-dose statin for > or =2 years resulted in sustained improvements in HDL-C (+17.4%), TG (-46.4%) and LDL-C (-40.4%).

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Our findings demonstrate that the effects of simvastatin on learning and memory are independent of amyloid beta protein levels. The mechanisms by which simvastatin exerts its beneficial effects may be related to modulation of signaling pathways in memory formation.

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In the context of an international multi-center clinical trial being undertaken in China, 5585 patients with atherosclerotic ischemic stroke were screened in 39 prestigious hospitals in 10 cities. The characteristics collected through electronic questionnaire were described and analyzed.

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Some statins (simvastatin, lovastatin, and atorvastatin) are metabolized by cytochrome P450s 3A4 (CYP3A4). Inhibitors of CYP3A4 including some calcium channel blockers (CCBs) might increase statin blood concentration, owing to drug-drug interactions. Risk of adverse events such as acute kidney injury might occur following the coprescription of CYP3A4-metabolized statins and CCBs that inhibit CYP3A4.This was a population-based cohort study. The study analyzed data of patients treated between 1997 and 2011, retrieved from Taiwan's National Health Insurance database. We enrolled 32,801 patients who received coprescription of statins and CCBs that inhibit CYP3A4 (amlodipine, diltiazem, felodipine nicardipine, nifedipine, and verapamil). These patients were divided into 2 groups, according to whether they had received CYP3A4-metabolized statins (lovastatin, simvastatin, and atorvastatin) or non-CYP3A4-metabolized statins (fluvastatin, rosuvastatin, and pitavastatin). These 2 groups were 1:1 matched by age, gender, and Carlson comorbidity index. All outcomes were assessed within 90 days following drug coprescription.In this study, 5857 patients received coprescription of CYP3A4-metabolized statins and CCBs that inhibit CYP3A4. There were no differences in comorbidity or use of antihypertensive drugs between patients who received CYP3A4-metabolized statins and those who received non-CYP3A4-metabolized statins. Patients who received CYP3A4-metabolized statins had significantly higher risk of acute kidney injury (adjusted odds ratio [OR] = 2.12; 95% CI = 1.35-3.35), hyperkalemia (adjusted OR = 2.94; 95% CI = 1.36-6.35), acute myocardial infarction (adjusted OR = 1.55; 95% CI = 1.16-2.07), and acute ischemic stroke (adjusted OR = 1.35; 95% CI = 1.08-1.68) than those who received non-CYP3A4-metabolized statins.This nationwide cohort study demonstrated the increased risk of adverse events following the coprescription of CYP3A4-metabolized statins and CCBs that inhibit CYP3A4. Therefore, it is important to take into account the potential adverse events while coprescribing CYP3A4-metabolized statins and CCBs that inhibit CYP3A4.

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Three-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitors (statins) are first-line treatments for hypercholesterolemia. Although exceedingly well tolerated, treatment with statins incurs a small risk of myopathy or potentially fatal rhabdomyolysis, particularly when coadministered with medications that increase their systemic exposure. Studies compared the multiple-dose pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with 4 inhibitors of cytochrome P450-3A4 isoenzymes in healthy subjects. Compared with pravastatin alone, coadministration of verapamil, mibefradil, or itraconazole with pravastatin was associated with no significant changes in pravastatin pharmacokinetics. However, concomitant verapamil increased the simvastatin area under the concentration:time curve (AUC) approximately fourfold, the maximum serum concentration (C(max)) fivefold, and the active metabolite simvastatin acid AUC and C(max) approximately four- and threefold, respectively (all comparisons p <0.001). Similar (greater than fourfold) important increases in these parameters and a >60% increase in the serum half-life (p = 0.03) of atorvastatin were observed when coadministered with mibefradil. The half-life of atorvastatin also increased by approximately 60% (p = 0.052) when coadministered with itraconazole, which elicited a 2.4-fold increase in the C(max) of atorvastatin and a 47% increase in the AUC (p <0.001 for C(max) and AUC). Clarithromycin significantly (p <0.001) increased the AUC (and C(max)) of all 3 statins, most markedly simvastatin ( approximately 10-fold increase in AUC) and simvastatin acid (12-fold), followed by atorvastatin (greater than fourfold) and then pravastatin (almost twofold). Pravastatin has a neutral drug interaction profile relative to cytochrome P450-3A4 inhibitors, but these substrates markedly increase systemic exposure to simvastatin and atorvastatin.

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To assess whether drug treatment in common practice can prevent disease, we analysed four preventive cardiovascular randomised clinical trials (RCTs), expressing efficacy by 1-year Number Needed to Treat (NNT) in RCT and common practice effectiveness by the Disease Impact Number (DIN) in all subjects at risk and by the Population impact Number (PIN) in the entire population, based on a Swedish population survey. Adjustments were made for non-adherence. Calculations were made of alternative 1-year drug costs and number of years an average general practitioner (GP) would need to work in order to prevent one event using the actual treatment. Secondary prevention of MI by simvastatin (NNT, DIN and adjusted PIN = 37, 93 and 2657; GP work time 2.7 years; drug costs Euro 1020 - 13505), and prevention of stroke by antihypertensive treatment in high-risk subjects (elderly with systolic blood pressure > 160 mm Hg; NNT, DIN and adjusted PIN = 167, 239 and 11950; GP work time 6 years; drug costs Euro 6095 - 51567) appeared medically and economically effective. Primary prevention of MI by pravastatin (NNT, DIN and adjusted PIN 208, 2080 and 24470; GP work time 12.2 years; drug costs Euro 5736 - 117676) or by antihypertensive drug treatment in low-risk subjects (diastolic blood pressure 90-99 mm Hg) (NNT, DIN and adjusted PIN 1667, 3334 and 116982; GP work time 58.5 years; drug costs Euro 60895 - 511718) seemed ineffective and expensive.

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During treatment mean LDL-cholesterol levels were 2.7 mmol/l in the simvastatin group and 2.1 mmol/l in the atorvastatin group. A major coronary event occurred in 463 (10.4%) simvastatin patients and in 411 (9.3%) atorvastatin patients (p = 0.07). Death from any cause occurred 374 (8.4%) in the simvastatin group and 366 (8.2%) in the atorvastatin group (p = 0.81). Nonfatal acute myocardial infarction occurred 321 (7.2%) and 267 (6.0%) in the two groups (p = 0.02). Patients in the atorvastatin group had higher rates of drug discontinuation due to non-serious adverse events; transaminase elevation resulted in 43 (1.0%) versus 5 (0.1%) withdrawals (p <0.001).

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Men and women (age > or = 18 years) with documented CHD and on a stable dose of simvastatin 10 mg or 20 mg for at least 6 weeks were recruited for this study. After a 4-week simvastatin 10 or 20 mg plus placebo and diet run-in period, patients were eligible for randomization if LDL-C > 2.60 and < or = 4.20 mmol/l and triglycerides (TG) < or = 4.00 mmol/l. Eligible patients were randomized to a double-blind comparative study with ezetimibe 10 mg co-administered with on-going simvastatin 10 mg or 20 mg (n=181) versus placebo to match ezetimibe co-administered with simvastatin 10 mg or 20 mg (n=191) for 6 weeks.

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Patients were followed up at 4-month intervals for 36 months for VF progression per Anderson's criteria. Clinical parameters were checked for association with progression in multivariate analysis.

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Statins are being widely used for the therapy and prevention of several types of tumors, including human chronic myelogenous leukemia, but the underlying molecular mechanisms still remain unknown. Therefore, inhibition of cell proliferation, apoptosis and involved molecules were investigated in K562 cells after incubation with simvastatin.The results showed that simvastatin diminished K562 cell proliferation and induced apoptosis. At the same time, the level of reactive oxygen species (ROS) and intracellular calcium concentration increased. Furthermore, nitric oxide (NO) content and inducible NO synthase (iNOS) mRNA expression were significantly higher in the simvastatin-treated group than in the corresponding control group. The elevated ROS level and intracellular calcium concentration, enhanced mRNA expression of iNOS and total NO content might be responsible for the apoptotic and anti-proliferative effects of simvastatin in K562 cells.

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Myocyte size and total collagen content of placebo and simvastatin groups did not show a statistically significant difference at any biopsy time point. Myocardium TNF-alpha content (% tissue area stained) at 1 week after transplantation was similar in the simvastatin and placebo groups. At the 24(th) week after transplantation, when compared with Week 1 values, we found a significant decrease in myocardium TNF-alpha content in the simvastatin group (15.0% +/- 2.3% vs 5.8% +/- 2.4%, p = 0.02) that was not observed in the placebo group (15.0% +/- 1.5% vs 12.0% +/- 2.6%, p = not significant).

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On the basis of this in vitro model of asthma, we suggest that the combination of a statin and a corticosteroid could augment the Treg/Th17 cell ratio and thus more effectively suppress airway inflammation in asthma patients. This may be particularly relevant in the treatment of severe asthma where Th17 cells are activated and linked to neutrophilic inflammation.

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Sterol 27-hydroxylase has been suggested to be involved in an alternative pathway for the elimination of cholesterol from macrophages and early atherosclerotic lesions. We have previously shown that human lung macrophages as well as monocyte-derived macrophages have a relatively high activity of sterol 27-hydroxylase (CYP27). This enzyme converts intracellular cholesterol into 27-hydroxycholesterol and cholestenoic acid that flux from cultured cells into the medium. It is shown here that human monocytes have very low CYP27 activity and CYP27 mRNA levels. During differentiation into macrophages, both CYP27 activity and CYP27 mRNA levels increase markedly after 4 days of culture in serum-free medium. Addition of macrophage-colony stimulating factor had no significant effect on the induction and addition of fetal calf serum had an inhibitory effect. Cholesterol synthesis was found to be a critical factor for the production of 27-oxygenated products by the macrophages cultured in serum-free medium. The increased capacity of the differentiated cells to eliminate intracellular cholesterol is of interest and supports the contention that CYP27 is an antiatherogenic factor.

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Endothelial dysfunction and C-reactive protein play a pivotal role in development of atherosclerosis and act as markers for future adverse cardiac events. Statins reduce C-reactive protein levels and improve endothelial function. However, little information is available on endothelial function and its determinants in veins. We investigated the association between saphenous vein endothelial function and C-reactive protein levels in patients treated with statins undergoing coronary artery bypass surgery.

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A randomised, double-blind study.

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The fixed combination therapy with ezetimibe/simvastatin showed a clinically significant additional lipid-lowering potential as compared with established statin monotherapies and enabled more patients at cardiovascular risk to reach the LDL-C target level of <100 mg/dl.

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Thirty-seven participants (exercise plus statins: n = 18; exercise only: n = 19) completed the study. Cardiorespiratory fitness increased by 10% (p < 0.05) in response to exercise training alone, but was blunted by the addition of simvastatin resulting in only a 1.5% increase (p < 0.005 for group by time interaction). Similarly, skeletal muscle citrate synthase activity increased by 13% in the exercise-only group (p < 0.05), but decreased by 4.5% in the simvastatin-plus-exercise group (p < 0.05 for group-by-time interaction).

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We examined the effects of four 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (pravastatin, simvastatin, fluvastatin, and cerivastatin) on the production and expression of inflammatory cytokines and on enzyme expression involving prostaglandin and superoxide production in cultured human umbilical vein endothelial cells (HUVEC). All HMG-CoA reductase inhibitors significantly reduced interleukin-1beta and -6 mRNA expression and their protein levels in the culture medium, and also inhibited cyclooxygenase-2 mRNA expression and their protein levels. And these drugs induced peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma mRNA expression and their protein levels in HUVEC and hepatocyte. Moreover, the mRNA levels of p22phox, a 22-kD subunit and the protein levels of p47phox, a 47-kD subunit of nicotine adenine dinucleotide phosphate (NADPH) oxidase, was decreased by treatment with either simvastatin, fluvastatin or cerivastatin, and this effect was reversed by mevalonate, geranylgeraniol, farnesol, and cholesterol. The changes induced by HMG-CoA reductase inhibitors might be due to regulation of cellular cholesterol content level, cellular cholesterol metabolic pathway, and cellular PPARalpha activity, which was related with inflammation. This unique anti-inflammatory effect in addition to its hypolipidemic action, may be beneficial in preventing the vascular complications that are induced by hyperlipidemia.

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CHD/CHD risk-equivalent patients in a large US managed-care database, who added ezetimibe onto simvastatin, atorvastatin, or rosuvastatin, had greater LDL-C reductions and goal attainment than those who uptitrated these statin therapies. Our study suggests that high-risk CHD patients in need of more intensive LDL-C lowering therapy may benefit by adding ezetimibe onto statin therapy.

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The relationship between lipoprotein(a) [Lp(a)] and metabolism of triglyceride-rich lipoproteins (TRL) was studied in 58 untreated patients with familial combined hyperlipidemia (FCH) from eight different kindreds, 17 spouse controls, and 17 unrelated controls. Lp(a) plasma concentrations were not significantly different between FCH subjects (343 +/- 61 mg/L, mean +/- SEM) and controls (249 +/- 52 mg/L). In FCH, log-transformed Lp(a) levels correlated positively with postheparin lipoprotein lipase ([LPL] r = .61, P = .0002) and hepatic lipase ([HL] r = .46, P = .008) activities and total plasma cholesterol level (r = .30, P = .03). In controls, Lp(a) correlated with LPL (r = .50, P = .04) and total plasma cholesterol level (r = .51, P = .003). In eight FCH patients, treatment with the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin resulted in significantly increased mean LPL activities and plasma Lp(a) concentrations. In three of these FCH patients, repeated measurements during 1 year demonstrated that changes in Lp(a) concentrations were paralleled by similar changes in LPL activity, but not HL activity. The observed correlation between postheparin plasma lipolytic activities and Lp(a) plasma concentrations suggests a connection between the metabolism of TRL and Lp(a).

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ISRCTN62019087.

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Hyperglycemia may potentiate the adverse renal effects of angiotensin II (AII). In the kidney, the major target of AII action is the glomerular mesangial cell, where its hemodynamic and proinflammatory action contributes to renal injury. AII action is mediated by several types of cell receptors. Among those, the AT1 receptor has been best studied using specific AII receptor blockers (ARBs). These agents have emerged as major new modalities in the prevention and amelioration of renal disease where the ARB renoprotective anti-inflammatory properties could be more important than previously appreciated. Like the ARBs, statins may also modulate inflammatory responses that are renoprotective and complement their cholesterol-lowering effects.

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A total of 3337 adult patients with diabetes were identified with new use of statin therapy during the identification period. A total of 9% (n = 301) started on rosuvastatin, 49.4% (n = 1,649) on atorvastatin, 20.7% (n = 690) on simvastatin, 7.0% (n = 234) on pravastatin, 11.7% (n = 391) on lovastatin and 2.2% (n = 72) on fluvastatin. After controlling for covariates, rosuvastatin patients experienced a significantly greater decrease in LDL-C from baseline (38.7%) than patients taking atorvastatin (34.2%) (p = 0.05), simvastatin (31.5%), pravastatin (24.2%), fluvastatin (26.3%) or lovastatin (24.9%) (p < 0.0001). Rosuvastatin users were significantly more likely to attain LDL-C goal than those taking the other statins (odds ratio: 0.44, 0.28, 0.14, 0.14, 0.19, respectively; p < 0.001). Predicted percent attaining goal was significantly greater for those taking rosuvastatin (87.3%) than for those taking atorvastatin (76.9%), simvastatin (68.7%), pravastatin (55.0%), lovastatin (55.3%) or fluvastatin (61.3%) (p < 0.001).

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To evaluate the nature, type and prevalence of potential drug-drug interactions (DDIs) in prescriptions dispensed in community pharmacies in Thessaloniki, Greece. Secondary objectives included the classification of DDIs as per pharmacotherapeutic class of the medications and the investigation of the relationship between medical specialties and the frequency of potential DDIs, as well as the relationship between DDIs and prescription size. Setting DDIs are a common cause of adverse drug reactions (ADRs) among patients using multiple drug therapy. In Greece a reliable computerized surveillance system for monitoring potential DDIs is not yet fully established. As a result, the prevalence of such DDIs in prescriptions dispensed by community pharmacies in Greece is unknown.

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medication zocor 2015-10-21

Discuss the contribution of low-density lipoprotein subclass buy zocor abnormalities to cardiovascular risk among individuals with low high-density lipoprotein cholesterol levels.

zocor 100 mg 2017-06-25

18,144 patients were enroled with either ST segment elevation MI (STEMI, n = 5,192) or UA/non-ST segment elevation MI (UA/NSTEMI, n = 12,952) from October 2005 to July 2010. Primary endpoint occured in 2 742 patients (34.7 %) treated with simvastatin in monotherapy and in 2 572 patients (32.7 %) (p = 0.016) treated with combination. Compared to patients with coronary heart disease given the drug simvastatin plus a placebo, those given both simvastatin and the non-statin drug, ezetimibe, had a 6.4 % lower combined risk of subsequent buy zocor heart attack, stroke, cardiovascular death, rehospitalization for unstable angina and procedures to restore blood flow to the heart. Heart attacks alone were reduced by 13 %, and non-fatal stroke by 20 %. Deaths from cardiovascular disease were statistically the same in both groups. Patients were followed an average of approximately six years, and some as long as 8.5 years. Approximately 2 patients out of every 100 patients treated for 7 years avoided a heart attack or stroke [Number Needed to Treat (NNT) = 50/7 years].

zocor simvastatin reviews 2015-06-04

Our population was predominantly female (75%) and of African ancestry (95%); average age 60 years. Patients with CKD required a 24% lower dose than the comparison group (mean [SD]=35.9 [10.7] vs. 47.0 [11.2] mg per week, P=0.003) and spent less time in therapeutic range required increased clinic management versus the comparison group, as indicated by a buy zocor significantly higher proportion of clinic visits at which dose changes occurred (22% vs. 12%, P<0.001) and a decreased time between scheduled visits (mean [SD] of 16.0 [3.2] days vs. 19.7 [3.4] days, respectively, P=0.001).

simvastatin zocor reviews 2016-12-09

Both treatments reduced plasma LDL-C levels to a similar extent while HDL-C levels remained statistically unchanged after both experimental phases. However, compared to atorvastatin, plasma apoA-I concentrations were significantly higher after treatment with simvastatin (1.33 +/- 0.07 g/L versus 1.23 +/- 0.07 g/L, P = 0.05). Treatment with simvastatin also induced a significant increase in apoA-I production rate compared to atorvastatin (15.2 +/- 3.0 mg/kg/d versus 13.2 +/- 2.6 mg/kg/d buy zocor , P = 0.05). There was no statistical difference in apoA-1 fractional catabolic rate between simvastatin and atorvastatin (0.26 +/- 0.05 pool/d versus 0.24 +/- 0.04 pool/d).

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Statins may promote vasodilation following subarachnoid hemorrhage (SAH) and improve buy zocor the response to blood pressure elevation. We sought to determine whether simvastatin increases cerebral blood flow (CBF) and alters the response to induced hypertension after SAH.

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The results confirmed the efficacy of the combination of fenofibrate and simvastatin. The combined therapeutic approach was shown to be safe for the treatment of primary mixed hyperlipidaemia, at least in patients with normal buy zocor hepatic and renal function.

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PASMC isolated from rats and cultured in vitro were randomly divided into four groups (n=6 each): control, platelet-derived growth factor buy zocor (PDGF) treatment, PDGF+simvastatin treatment, and PDGF+simvastatin+parthenolide (NF-κB inhibitor) treatment. MTT colorimetric assay and flow cytometry were performed to detect cell proliferation and cell cycle distribution. Immunohistochemistry was performed to detect the expression of NF-κB protein. Real-Time PCR was performed to detect NF-κB mRNA expression.

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Circulating CD34+KDR+ EPC levels were reduced by nearly 40% in obese men with the metabolic syndrome compared to non-obese healthy controls (331 +/- 193 vs. 543 +/- 164 EPC/mL, P = 0.006). In a randomized double-blind cross-over study comparing intensive lipid-lowering treatment using 80 mg simvastatin mono-treatment with combination treatment of 10 mg simvastatin and 10 mg ezetimibe, we found a similar treatment effect buy zocor on EPC levels. Secondary analyses of these data suggested that both treatment regimens had increased circulating EPCs to control levels (626 +/- 428 after combination treatment, P < 0.01; 524 +/- 372 EPC/mL after monotherapy, P < 0.05). Serum levels of EPC-mobilizing factor SCF-sR correlated with reduced EPC levels and normalized concurrently with treatment.

zocor 60 mg 2015-11-27

Chronic periodontal defects were created bilaterally in seven 1-year-old beagle dogs: 3-walled intrabony defects distal of the mandibular second premolar and mesial of the fourth premolar and Class II furcation defects at the buccal furcation of the mandibular first molars. The edentulous space distal to the mandibular canine was left undisturbed. After 16 weeks of buy zocor healing, defect sites were treated with scaling and root planing, and mandible sides were randomly selected to receive three weekly injections of 0.5 mg simvastatin in 30 microl methylcellulose gel and contralateral gel alone (n=3) or 2.0 mg simvastatin/methylcellulose gel and contralateral gel alone (n=4). Two months following drug application, block sections, including teeth and surrounding tissues, and submandibular lymph nodes were obtained for histomorphometric analysis.

zocor low dose 2017-07-27

The treatment of acute respiratory distress syndrome (ARDS), most commonly seen buy zocor during the organ dysfunction remains unsatisfied. Presently, the stem/progenitor cell-based endogenous repair has been aroused attention enormously. This report investigated the effects of retinoic acid (RA) plus simvastatin (SS) with respect to dynamics of lung repair cells as well as to elucidate the underlying mechanism.

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In segments of human varicose veins, endothelial function was assessed by measuring relaxation induced by acetylcholine in noradrenaline-precontracted preparations. In addition, concentration-response curves to acetylcholine were obtained before and after incubation with the arterial endothelium protectant agents captopril, losartan, troglitazone, pravastatin, or simvastatin. The antivaricose agent escin was also tested. Mean acetylcholine-induced relaxation of varicose venous rings was about 13%, approximately one third of that reported for control buy zocor saphenous veins. Concentration-response curves to acetylcholine were ''u'' shaped, the result of endothelium-mediated relaxation at low concentrations, superseded by subsequent smooth muscle contractile responses. Relaxation was enhanced by the endothelium-protecting agents and by escin, troglitazone being the least, and simvastatin the most effective. It was concluded that endothelial dysfunction is present in varicose veins, that this anomaly can be reverted by cardiovascular protecting agents, and that it can play a role in the pathogenesis and treatment of chronic venous insufficiency.

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Daily diary records of positive and negative affects and of events and biweekly measures of depressive symptoms. Affect ratings were obtained using the Lawton positive and negative affect scales; independent raters coded the buy zocor valences of events.

zocor 10 mg 2015-12-30

In clinical practice, persistence with statin therapy is poor. While little is known about relative persistence to specific statins, previous studies have observed greater persistence in patients who achieve greater degrees of lipid buy zocor lowering. Identification of statin therapies which improve patient persistence has the potential to improve the quality of patient care and clinical outcomes. Therefore, we assessed patient persistence with atorvastatin and simvastatin in primary and secondary prevention patients enrolled in managed care.

zocor 80mg tab 2017-01-17

Cerebral vasospasm and related delayed ischaemic deficits ( Deltasone 60 Mg DIDs) occur in about 17% to 40% of patients with aneurysmal subarachnoid haemorrhage (SAH) and lead to a poor outcome. Cholesterol-reducing agents might improve unfavourable outcomes.

drug zocor 2015-12-05

We monitored collagen- or ADP-induced platelet aggregation, CD36, PAC-1 and CD62 expression on platelet surface and thromboxane generation after Voltaren Gel Dosage incubation with pravastatin, simvastatin, atorvastatin and/or ASA.

zocor generic brand 2017-09-10

We aimed to investigate hypercholesterolaemia-induced early renal lesions which result in abnormal expression of endothelin A receptor (ET(A)R), induced nitric Allegra 20 Mg oxide synthase (iNOS) and matrix metalloproteinase 9 (MMP-9). We hypothesized that this is due to an upregulated endothelin (ET) pathway consequent to hypercholesterolaemia and that CPU0213, a dual ET antagonist, could mitigate these changes.

zocor generic equivalent 2016-02-04

The incidence of the structural features on the self-assembly of different poloxamines Luvox Drug Information (the conventional sequential Tetronic 304, 901, 904, 908, 1107, 1301, and 1307; a reverse-sequential counterpart Tetronic 150R1; and a chemically modified derivative, N-methylated Tetronic 1107) was thoroughly studied in 10 mM HCl by means of pi-A isotherm, surface tension, and pyrene fluorescence measurements. The size and size distribution of the aggregates were investigated by dynamic and static light scattering, and the morphology was probed by transmission electron microscopy. The abilities of the different derivatives to solubilize the drug simvastatin were also evaluated. Poloxamines with both higher PO/EO ratio and molecular weight (T1301 and T150R1) led to micelles with larger and more hydrophobic cores, particularly adequate for hosting hydrophobic molecules and protecting the labile lactone form of simvastatin from hydrolysis. On the other hand, the hydroxy acid form of simvastatin interacted with the central ethylenediamine group under alkaline pH (T304) or when a permanent positive charge due to methylation was present. Micelles of long poloxamine molecules containing large PPO blocks (with 23-29 units, namely, T1301, T1307, and T150R1), particularly the one that also has long PEO blocks, were the most physically stable toward dilution.

zocor dosage 2016-08-24

Lovastatin and simvastatin are very potent and effective inhibitors of P-gp transport with IC50's of 26 and 9 microM, respectively, for the human enzyme. Atorvastatin is also an effective P-gp inhibitor, but at higher concentrations. Uniquely, pravastatin, whose functional groups render it an inferior inhibitor of P-gp in the whole cell, had no effect in this assay. This Vantin Dose result is consistent with known clinical interactions. The effect of these statins on ATP consumption by P-gp was also assessed, and the Km results were congruent with the IC50 observations.

zocor blockbuster drug 2015-04-08

Both statins increased NO levels and NOS3 mRNA expression but no influence was observed for ezetimibe Valtrex Dosage Forms treatment. Atorvastatin, simvastatin and ezetimibe down-regulated the expression of miR-221, whereas miR-222 was reduced only after the atorvastatin treatment. The magnitude of the reduction of miR-221 and miR-222 after treatment with statins correlated with the increment in NOS3 mRNA levels. No influence was observed on the miR-1303 expression after treatments.

zocor pill identifier 2017-10-17

There was a statistically significant reduction in LDL-C levels in both the AG (-42.4%+/-15%) (P<.001) and the simvastatin group (-39.6%+/-20%) (P<.001). No significant differences were noted between groups. The AG also demonstrated significant reductions in triglycerides (-29% vs -9.3%; 95% confidence interval, -61 to -11.7; Combivir Scored Tablets P=.003) and weight (-5.5% vs -0.4%; 95% confidence interval, -5.5 to -3.4; P<.001) compared with the simvastatin group.

zocor with alcohol 2017-10-28

To review the cytochrome P450 system and associated metabolic differences between the HMG-CoA reductase Cozaar Medication inhibitors.

zocor dosage information 2015-12-13

The fusiform stroma cells in the tooth extraction socket began to express TGF-beta1, BMP-2 and VEGF mRNA in both experimental and control groups from one week after tooth extraction until the end of experiment. The expression of TGF-beta1 and BMP-2 mRNA in the experimental Duricef Acne Review group was significantly up-regulated after one, two and four weeks, and expression of VEGF mRNA was significantly increased after one and two weeks compared with that in the control group.

zocor brand name 2016-01-20

Our meta-analysis demonstrates that statin therapy has a beneficial effect on aortic arterial stiffness. Further studies should be conducted to assess the effects of this therapy on arterial stiffness at various Aricept Drug Class sites and conditions.

zocor dosage elderly 2016-12-08

Inclusion of several post hoc analyses from large RCTs and substantial heterogeneity in secondary Propecia 5 Mg outcome analyses.

zocor drug category 2015-06-22

Inflammation plays a key role in progression and destabilization of atherosclerotic plaque. 18F-fluorodeoxyglucose PET is a promising tool for visualizing inflammation of atherosclerotic plaque. Antiinflammatory action is one of the pleiotropic effects of statins.

zocor tablet 2016-02-03

The type and rate of statins dispensed to NSSPP beneficiaries changed from 1999 to 2013 in response to the availability of new agents and publication of the JUPITER trial. The overall proportion of NSSPP beneficiaries dispensed a statin increased approximately 4-fold during the study period. In 2013, rosuvastatin was the most commonly dispensed statin (44.1%) followed by atorvastatin (39.1%).

zocor overdose 2016-12-18

Statins, lipid-lowering agents for the prevention of atherosclerosis and fatal coronary heart diseases, have pleiotropic modalities on the function and physiology of vascular smooth muscle that include anti-contractile and pro-apoptotic effects. These effects were suggested to stem from the inhibition of small GTPase Rho A, but they are largely regarded as distinct and unrelated. Recently, we discovered that simvastatin causes both contractile dysfunction and apoptosis of vascular smooth muscle cells (VSMCs), reflecting that they may be closely related, yet their connecting link remains unexplained. Here, we elaborated the mechanism underlying simvastatin-induced apoptosis of normal VSMCs in connection with contractile dysfunction. Repeated oral administration of simvastatin to rats in vivo resulted in contractile dysfunction and apoptosis of vascular smooth muscle, of which pattern was well reproduced in rat VSMCs in vitro. Of note, contractile dysfunction and apoptosis occurred in concerted manners both in vivo and in vitro in the aspects of time course and dose of exposure. In rat VSMCs, simvastatin impaired the activation of small GTPases, RhoA along with Rac-1, which resulted in the disruption of actin integrity, a pivotal factor both for the generation of contractile force and survival of VSMCs. In line with the disruption of actin integrity, Bmf, a pro-apoptotic factor bound to intact actin, dissociated and translocated into mitochondria, which corresponded well with the dissipation of mitochondrial membrane potential, caspase-3 activation and ultimately apoptosis. These events were all rescued by an actin stabilisation agent, jasplakinolide as well as geranylgeraniol, indicating that damages of the actin integrity from disrupted activation of RhoA/Rac-1 lies at the center of simvastatin-induced contractile dysfunction and apoptosis in vascular smooth muscle.