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PubMed2001

[Simvastatin attenuates cardiovascular effects and oxidative stress induced by angiotensin II].

The effects of an HMG-CoA reductase inhibitor, simvastatin (statin, 60 mg/Kg/24 h by forced feeding), were studied on the development of hypertension, cardiac hypertrophy and oxidating stress induced by chronic perfusion of angiotensin II (ANG II, 200 ng/Kg/min s.c., for 10 days) in the rat. The statin was giver 24 hours before, and during the 10 days of ANG II. At the end of the study, mean blood pressure was measured and blood sampling performed under anaesthesia (sodium pentobarbital). The cardiac mass index was measured (cardiac mass/body weight, mg/Kg). TBARS (thiobarbituric acid reactive substances), representing the index of lipid peroxidation, was assessed by fluorimetry. The statin attenuated the development of hypertension (131 +/- 9 vs 164 +/- 4 mmHg) and the increase in cardiac mass (3.13 +/- 0.09 vs 3.46 +/- 0.09 mg/g) associated with ANG II. The overproduction of TBARS induced by ANG II was partially prevented by simvastatin (598 +/- 40 vs 794 +/- 79 pmol/mL). These results indicate that simvastatin attenuates the cardiovascular effects and lipid peroxidation induced by chronic administration of angiotensin II.

Angiotensin II↗
PubMed2002

Myopathy secondary to simvastatin in a type 2 diabetic patient.

The most important but rare adverse effect of simvastatin is myopathy. In megatrials with simvastatin, the overall incidence of myopathy is 0.025%. We present a case of myopathy presenting as proximal muscle weakness in both upper limbs secondary to simvastatin which reversed spontaneously after cessation of the drug.

Anticholesteremic Agents↗
PubMed2000

[Effects on simvastatin in continuous ambulatory peritoneal dialysis patients with hyperlipidemia].

The therapeutic effects of simvastatin on hyperlipidemia and its protective effects on residual renal function (RRF) in continuous ambulatory peritoneal dialysis (CAPD) patients with hyperlipidemia were observed. Forty-seven CAPD patients were randomly divided into two groups, the treatment group and control group. The treatments of two groups were the same except that the treatment group patients were additionally given simvastatin 20 mg.d-1. The results were that, after 12-week treatment, the total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), and apoprotein B100 (ApoB100) in the treatment group significantly decreased, but high density lipoprotein (HDL) and apoprotein A1 (ApoA1) significantly increased compared with the control group (all P < 0.05); one year later, RRF of patients of both groups all decreased but there was no significant difference between them. The results suggest that simvastatin can effectively normalize lipidemia, but has no protective effect on RRF in CAPD patients.

Adult↗
PubMed2003

[Efficacy and safety of simvastatin in patients with hypercholesterolemia (results of a Multicenter Clinical Study)].

AIM: To assess efficacy and safety of a generic preparation of simvastatin Vasilip (KRKA) in ischemic heart disease patients with hypercholesterolemia or combined hyperlipidemia. MATERIAL: Patients (n=167, age 36-73 years) with ischemic heart disease and moderate hypercholesterolemia or combined hyperlipidemia. METHODS: Duration of simvastatin administration was 12 weeks. All patients received 20 mg/day for 6 weeks. Then those patients who did not achieve target low density lipoprotein (LDL) cholesterol level (3.0 mmol/l) were given 40 mg/day for 6 more weeks. Other patients continued to take 20 mg/day. RESULTS: The use of Vasilip was associated with lowering of total, LDL cholesterol and triglycerides (by 28, 39 and 10%, respectively) and 18% elevation of high density lipoprotein cholesterol. Target LDL CH level was achieved in 107 patients (66.9%). In 47 patients (29.4%) LDL CH concentration remained higher than target level but decrease of LDL CH exceeded 10%. Six patients (3.8%) did not respond to therapy. Treatment was stopped because of adverse effects in 2.4% of patients. CONCLUSION: A generic preparation of simvastatin Vasilip in a 12-week open noncomparative study demonstrated substantial lipid lowering activity and did not induce serious adverse reactions.

Cholesterol↗
PubMed2003

The influence of apolipoprotein B and E gene polymorphisms on the response to simvastatin therapy in patients with hyperlipidemia.

OBJECTIVE: To investigate the effect of apolipoprotein B (apoB) and E (apoE) genetic variations on lipid profile at baseline (before treatment), and also on the subsequent response to simvastatin therapy. METHODS: Eighty-eight patients with hyperlipidemia were treated with simvastatin 5mg daily. The plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and apo B were measured pre-treatment and at the end of the 4th, 8th and 12th post-treatment week. Polymorphisms of apoB at XbaI locus and apoE were determined by restriction fragment length polymorphism (RFLP). RESULTS: In all patients, relative frequencies of X- allele and X+ allele were 0.943 and 0.057 for apoB gene respectively. For apoE gene the relative frequency of epsilon2 allele was determined as 0.182, epsilon3 as 0.580 and epsilon4 as 0.238. The reduction in TC level was more prominent in patients carrying X- allele than in those with X+ allele following treatment (-23. 9% vs. -13. 6%, P < 0. 05). Compared with patients carrying epsilon3 or epsilon4 allele, those with epsilon2 allele showed a significantly higher percentage in reduction of apoB level after treatment (P < 0.05). CONCLUSION: The relative frequency of apoB X+ allele is high in patients with hyperlipidemia, in whom the TC-lowering efficacy is decreased following treatment of simvastatin. The relative frequencies of epsilon2 and epsilon4 are also high in hyperlipidemic patients, and the epsilon2 allele is associated with reduction in apoB level during lipid-relating therapy.

Aged↗
PubMed2003

Statins: new data in secondary prevention and diabetes. Pravastatin and simvastatin are the best-assessed statins.

The efficacy of pravastatin and simvastatin was first shown several years ago in patients with coronary heart disease. Other trials have since been published. In the HPS trial, which studied patients with coronary heart disease, other cardiovascular conditions, or diabetes, simvastatin significantly reduced the risk of death, coronary events and stroke when compared with placebo. In the ALLHAT-LLT trial, in patients with treated hypertension, pravastatin did not reduce overall mortality. In the PROSPER trial, in patients aged over 70 with cardiovascular disease or cardiovascular risk factors, pravastatin reduced the incidence of coronary events relative to placebo, but did not reduce overall mortality. Pharmacovigilance studies suggest there is no difference between these four statins in terms of their potential to cause rhabdomyolysis. Taken together, these trials show that statin use can be extended to patients with levels of LDL-cholesterol over 2.4 mmol/l (0.9 g/l) if they have coronary heart disease (and no hypercholesterolaemia), a history of ischaemic stroke, or lower-limb arterial disease. Statins can also be prescribed for diabetic patients with no signs of cardiovascular disease but whose LDL-cholesterol exceeds 3.4 mmol/l (1.3 g/l). Clinical trial data support the use of pravastatin or simvastatin in these situations, at a dose of 20 or 40 mg daily. Plasma creatine phosphokinase assay should be done if muscle symptoms occur or if the patient has a particular risk of rhabdomyolysis.

Aged↗
PubMed2003

Simvastatin-induced rhabdomyolysis in a CsA-treated renal transplant recipient.

BACKGROUND: Cardiovascular disease is the most common cause of morbidity and mortality among long-term renal transplant recipients, and hyperlipidemia is an important risk factor for the development of cardiovascular and peripheral vascular disease. The prevalence of post-transplantation hyperlipidemia ranges from 16% to 78% of recipients. Lipid-lowering strategy with the use of statins has been shown shown to reduce the cardiovascular risks related to hyperlipidemia, but concomitant use of HMG-CoA reductase inhibitors and cyclosporine A may increase the risk of rhabdomyolysis or myoglobinuric acute graft failure due to drug-drug interactions with cyclosporine A. CASE REPORT: We describe the case of a 53-year-old woman, a renal transplant recipient, who developed rhabdomyolysis following simvastatin lipid-lowering therapy. Immunosuppressive treatment included cyclosporine A, azathioprine and prednisone. After 32 days of simvastatin treatment she was hospitalized for profound muscle pain and weakness with a rise in serum creatine kinase to 60.000 IU/l and serum creatinine to 147 Kmol/l. No further deterioration in renal graft function during hospitalization was observed. 10 days after simvastatin was stopped and the daily CyA dose was reduced the patient was asymptomatic, with serum creatine kinase 67 IU/l and serum creatinine level within normal range. CONCLUSIONS: Renal transplant recipients treated with cyclosporin A, and also receiving statins for postransplantational hyperlipidemia, as well as for the prophylaxis of chronic rejection, should be monitored carefully both for CyA blood levels and for possible muscle toxicity.

Adult↗
PubMed1992

Effect of simvastatin in CAPD patients with hypercholesterolemia.

The effect of simvastatin on serum total and HDL cholesterol and total triglyceride levels in 20 hypercholesterolemic patients on CAPD treatment was studied. The drug was given at the initial dose of 10 mg/day which was doubled up to 40 mg/day. Two non-compliant patients stopped the drug in the first week of treatment. One patient had vomiting and stopped simvastatin. One patients reduced the dose from 20 to 10 mg/day because of increase in CPK level. The study was completed in 16 patients. Serum cholesterol decreased from 318 +/- 39 to 208 +/- 34 mg/dl (p < 0.001), triglyceride from 317 +/- 129 to 278 +/- 160 mg/dl and HDL cholesterol from 43 +/- 13 to 35 +/- 11 mg/dl. The effective does was 10 mg/day in 4 cases, 20 mg/dl in 7 and 40 mg/dl in 5. In CAPD patients, simvastatin is safe and effective in lowering serum cholesterol. The clinical significance of the decrease in HDL cholesterol and its possible effect on clinical outcome are still unknown.

Anticholesteremic Agents↗
PubMedDate not supplied

[Severe polymyositis with simvastatin use].

INTRODUCTION: Myotoxicity is the most common adverse reaction of statins, being its frequency less than 0.5%. Mild myopathy reversible after statin withdrawal is the most common event. We present a case of severe polymyositis which was likely to be induced by simvastatin. CASE REPORT: 75 years old man with hypercholesterolemia treated with simvastatin 20 mg/day for 6 months started previous 2 months with proximal limb weakness, dysphagia and myalgias during exercise that did not release after simvastatin withdrawal. Laboratory findings showed increased creatinin kinase (6,010 UI/L), raised aldolase (51 UI/L) and lactic acid dehydrogenase (1,406 UI/L). Muscular biopsy showed abundant inflammatory cell infiltration in perivascular areas, muscle fibre necrosis with miofagocitosis and considerable variation in fibre size, some of them reaching 210 mm. Treatment with cortico esteroids was started and 4 months later clinical remission and nomalization of creatinin kinase was observed. DISCUSSION: Mechanisms of statins induced myotoxicity are not well known. Studies in rats suggest a muscle membrane defect (increased membrane fluidity) and abundant signs of damage (fiber necrosis, hipercontraction) but no cellular infiltrates were seen, pointing to a non inflammatory myopathy which was dose dependent. In our case, and Giordano s et al, the remission of the disease with cortico esteroid therapy and the finding of abundant inflammatory cell infiltration suggest the implication of immunological mechanism and not only a muscle membrane defect.

Aged↗
PubMed2004

The effect of simvastatin associated with ranitidine and alcohol upon serum lipids.

Statins are highly effective in lowering TC and LDL-C but the increasing of HDL-C is modest and the cost of long-term treatment is too high. On the other hand it is known that the association of H2 receptor blockers increases the plasmatic level of statins, and moderate alcohol consumption increases HDL-C. The purpose of the study was to compare the effect of statins alone and in association with either H2 receptor blockers or alcohol upon serum lipids in dyslipidemic patients. Three groups of dyslipidemic patients were studied, each of them consisting of 20 patients. The group A was treated with simvastatin 20 mg/day, the group B with simvastatin 20 mg/day + ranitidine 150 mg/day and the group C with simvastatin 20 mg/day + 30 g alcohol/day. Before and after two weeks treatment TC, LDL-C, HDL-C and TG were determined in each patient. For the group A patients the studied lipid fractions were modified into the limits described by the literature; for the group B patients, the decreasing of LDL-C was significantly, higher than for A group; for the group C patients, the incresing of HDL-C was significantly, higher than for A group, after two week alcohol consumption. In conclusions, the association of H2 receptor blockers increases the effect of statins upon dyslipidemia and the association of statins with moderate alcohol consumption increases the effect of statins upon HDL-C but the clinical implication has to be established.

Adult↗
PubMedDate not supplied

Effect of simvastatin and fluvastatin on plasma fibrinogen levels in patients with primary hypercholesterolemia.

The aim of the study was to compare the effect of treatment with two different statins on plasma fibrinogen levels in patients with primary isolated hypercholesterolemia. Sixty three patients enrolled into the study were randomly divided into two groups, treated with simvastatin (20 mg/d) or fluvastatin (40 mg/d), respectively. Plasma lipid profile and fibrinogen levels were measured after 4 and 12 weeks of the therapy. Both drugs decreased total and LDL cholesterol and apoprotein B levels. Simvastatin additionally reduced triglyceride levels. After 4 weeks of treatment both drugs tended to increase plasma fibrinogen levels, while after 12 weeks fibrinogen level was significantly increased in the simvastatin-treated patients. The effect on fibrinogen did not correlate with their lipid-lowering potential, gender and was similar in patients positive and negative for anti-Helicobacter pylori or anti-Chlamydia pneumoniae antibodies. Our results support the findings about a relatively weak effect of statin therapy on plasma fibrinogen level and partially explain contradictory results of previous studies.

Adult↗
PubMed2005

Rosuvastatin is cost-effective in treating patients to low-density lipoprotein-cholesterol goals compared with atorvastatin, pravastatin and simvastatin: analysis of the STELLAR trial.

BACKGROUND: Rosuvastatin calcium (CRESTOR) has demonstrated superior efficacy in reducing low-density lipoprotein cholesterol (LDL-C). However, healthcare providers and authorities require information on its cost-effectiveness in the treatment of dyslipidaemia. DESIGN: A retrospective pharmacoeconomic analysis was performed using data from the Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin (STELLAR) trial. The cost-effectiveness of rosuvastatin 10-40 mg was compared with atorvastatin 10-80 mg, pravastatin 10-40 mg and both branded and generic simvastatin 10-80 mg in achieving Third Joint European Task Force LDL-C goals in patients with hypercholesterolaemia. METHODS: The analysis was conducted from the perspective of the UK National Health Service, using clinical data from the STELLAR trial and drug acquisition costs. Cost-effectiveness was compared using incremental cost-effectiveness ratios (ICERs), with sensitivity analyses applied to both efficacy and cost parameters. RESULTS: In terms of patients achieving goal, rosuvastatin 10 mg dominated (was more effective at equal or lower cost) atorvastatin 10 and 20 mg, pravastatin 20 and 40 mg, branded simvastatin 10-80 mg and generic simvastatin 40 and 80 mg. Where rosuvastatin 10 mg did not dominate, ICERs ranged from 36 pounds sterling to 162 pounds sterling per extra patient to goal. Rosuvastatin 20 and 40 mg were cost-effective compared with milligram-equivalent and higher doses of other branded statins. Sensitivity analyses showed that the results were robust to variations in both statin efficacy and price. CONCLUSION: In patients with hypercholesterolaemia, rosuvastatin is a cost-effective statin option in treating to LDL-C goals.

Atorvastatin↗
PubMed2005

Clinical study on the effect of simvastatin on butyrylcholinesterase activity.

Although the physiological function of serum butyrylcholinesterase (BuChE) has not yet been clarified, there is evidence that this enzyme is involved in serum lipoprotein metabolism. It has been suggested that serum BuChE is positively correlated with LDL (low-density lipoprotein) and negatively with HDL (high-density lipoprotein) levels. The objective of this study was to determine whether the activity of BuChE changes during treatment with simvastatin (CAS 79902-63-9). The effects of simvastatin therapy on serum lipoproteins and plasma BuChE activity were studied in 15 patients with type IIa and 17 patients with type IIb hyperlipoproteinemia. Beside the expected influence on serum lipid concentration, a statistically significant decrease in BuChE activity in patients with hyperlipoproteinemia type IIa and IIb during treatment with simvastatin was not observed.

Adult↗
PubMed2005

[Effects of simvastatin on the left ventricular hypertrophy in spontaneously hypertensive rats and its relationship with the expression of protein kinase B].

OBJECTIVE: To investigate the effects of simvastatin on left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) and its possible mechanism. METHODS: Sixteen male SHRs were randomly divided into 2 equal groups: treatment group and SHR control to be given simvastatin or glucose-normal saline by oral gavage for 10 weeks. Eight Wistar-Kyoto (WKY) rats were given normal saline as normal controls. Blood pressure was measured before the experiment and then once every week after the beginning of experiment. By the end of the experiment the rats were killed and their hearts were taken out to measure the left ventricle weight/body weight. RT-PCR was used to detect the mRNA expression of atrial natriuretic peptide (ANP) and of protein kinase B (PKB) in myocardium. Western blotting was used to examine the protein expression of PKB. RESULTS: (1) The systolic blood pressure of the SHR normal control and treatment groups were 221 mm Hg +/- 10 mm Hg and 217 mm Hg +/- 8 mm Hg respectively (P > 0.05) and the systolic pressure of the normal control group was 126 +/- 6 mm Hg, significantly lower than those of the 2 SHR groups (both P < 0.01). (2) The LVW/BW values of the SHR control group were 3.04 mg/g +/- 0.12 mg/g, 3.73 mg/g +/- 0.08 mg/g, and 4.10 mg/g +/- 0.13 mg/g in the normal control group, SHR treatment group and SHR control group respectively with significant difference between any 2 groups (all P < 0.01). (3) The mRNA expression levels of ANP were 0.44 +/- 0.33, 0.27 +/- 0.03, and 0.17 +/- 0.33 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). (4) The mRNA expression levels of PKB were 0.45 +/- 0.05, 0.32 +/- 0.03, and 0.19 +/- 0.02 in the SHR control group, SHR treatment group, and normal control group respectively (P < 0.01 or P < 0.05). CONCLUSION: Simvastatin reverses LVH and myocyte phenocyte transformation in the SHRs with the possible mechanism of decreasing the expression level of PKB.

Animals↗
PubMed2005

[A case of drug-induced pneumonia possibly associated with simvastatin].

A 59-year-old woman was admitted because of general fatigue, cough and progressive dyspnea about 5 months after treatment with simvastatin for hyperlipidemia. A chest radiograph and computed tomography scans revealed ground glass and reticular opacities in the right middle and lower lung fields. The percentage of peripheral blood eosinophils was elevated. After simvastatin was discontinued and administration of prednisolone was started, eosinophilia and reticular shadows improved. Drug lymphocyte stimulation test (DLST) for simvastatin was positive, so we diagnosed drug induced eosinophilic pneumonia. Now hyperlipidemia is treated frequently with HMG-CoA reductase inhibitor, but there are few reports demonstrating lung injury by this drug. We should be aware of lung side effects of HMG-CoA reductase inhibitor.

Female↗
PubMed2005

[Effects of simvastatin on TGF-beta system of diabetic rat kidneys].

OBJECTIVE: To investigate the effects and mechanism of renal benefit of simvastatin on diabetic rat kidneys. METHODS: Twenty STZ-induced SD rats and 10 normal rats were assigned to diabetic rat (DM) group, simvastatin [ 4 mg/( kg x d) ] treatment (S) group and normal control (C) group. Immunohistochemistry, RT-PCR and western-blot were employed to examine the changes of the mRNA and protein expression of TGF-beta1 and Tbeta II R in the kidneys of the rats. RESULTS: Compared with the normal control group, both the mRNA and protein expression of TGF-beta1 and Tbeta II R in the diabetic rat group and treatment group were significantly increased (P < 0.05). Compared with the diabetic rat group, simvastatin could markedly decrease the mRNA and protein expression of TGF-beta1 and Tbeta II R (P < 0.05). CONCLUSION: Simvastatim may play a protective role in the diabetic kidneys by down-regulating TGF-beta1 and Tbeta II R and inhibiting the TGF-beta signal pathway.

Animals↗
PubMed2006

[The IDEAL study comparing simvastatin 20-40 mg versus atorvastatin 80 mg for secondary prevention after myocardial infarction: between two ideas of the ideal].

The IDEAL ("Incremental Decrease in End Points Through Aggressive Lipid Lowering") study compared the effects of two strategies of lipid lowering on the risk of cardiovascular disease among patients with a previous myocardial infarction. In this prospective, randomized, open-label, blinded end-point evaluation trial, patients were randomly assigned to receive a high dose of atorvastatin (80 mg/day; n = 4439), or an usual dose of simvastatin (20 mg/day, titrated up to 40 mg/day if necessary; n = 4449). During treatment, mean LDL cholesterol levels were 104 mg/dl in the simvastatin group and 81 mg/dl in the atorvastatin group (p < 0.001). After a median follow-up of 4.8 years, no significant difference was observed in the primary outcome of major coronary events (defined as coronary death, confirmed nonfatal acute myocardial infarction, or cardiac arrest with resuscitation), but the risk of other composite secondary end points (i.e., major cardiovascular events, all cardiovascular events, all coronary events) was statistically reduced in the atorvastatin group compared to the simvastatin group. There were no differences in cardiovascular or all-cause mortality between the two groups. In conclusion, patients with myocardial infarction may benefit from intensive lowering of LDL cholesterol without an increase in noncardiovascular mortality or other serious adverse reactions.

Anticholesteremic Agents↗
PubMed2006

Dose-finding study of high-dose simvastatin combined with standard chemotherapy in patients with relapsed or refractory myeloma or lymphoma.

In vitro statins induce apoptosis in myeloma and lymphoma cells in a dose-and time-dependent way. In combination with dexamethasone and doxorubicin, statins have a chemo-sensitizing effect. Twenty-eight patients with relapsed myeloma or lymphoma were treated with a dose-escalating regimen of simvastatin for 7 days followed by VAD in myeloma patients and CHOP in lymphoma patients. The maximum tolerated dose was 15 mg/kg/day simvastatin. The most frequently reported side-effects were fatigue, gastrointestinal CTC grade 1-2 and neutropenic fever. The dose-limiting toxicity was neutropenic sepsis and grade 3 gastrointestinal side effects. High-dose simvastatin given immediately prior to chemotherapy is safe and tolerable up to a dose of 15 mg/kg/day.

Aged↗