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PubMed2006

[Short term simvastatin use in patients with heart failure of ischemic origin. Changes of blood lipids, markers of inflammation and left ventricular function].

AIM: To study changes of left ventricular function and some markers of inflammation during use of simvastatin in patients with ischemic systolic heart failure. METHODS: Statin naive patients (n=70) with coronary heart disease (CHD), NYHA class II-IV HF and LV ejection fraction (EF) 35% or less after 1 month of stabilization were randomized to simvastatin 40 mg/day (n=36) or no statin (n=34). Lipids, tumor necrosis factor alpha (TNF), and C-reactive protein (CRP) were measured and echocardiography carried out at baseline and in 4 months. In patients with sinus rhythm (n=48) left ventricular diastolic function was assessed by Doppler echo. Seven patients were not restudied and analysis included data from 32 (statin) and 31 (control) patients. RESULTS: Groups were similar except baseline CRP which was significantly higher in controls. In statin treated patients reduction of low density lipoprotein (LDL) cholesterol (CH) was 42%, triglyceride levels also significantly decreased. High density lipoprotein CH rose by 14.4 and 12.9% in statin and control groups, respectively. Despite lower initial level decrease of CRP was significant only in statin group. No significant changes of TNF occurred in either group. Left ventricular EF rose equally in statin treated (+5.7+/-4.7%) and untreated (+4.1+/-4.6%) patients (p=ns). Significant increase of peak atrial filling velocity (A) and decrease of E/A in statin group were difficult to interpret in the presence of systolic dysfunction. CONCLUSION: Short term simvastatin use in patients with systolic heart failure due to CHD caused lowering of LDLCH and CRP however this was not associated with changes of left ventricular EF different from those in control group.

Aged↗
PubMedDate not supplied

Simvastatin did not prevent nor restore ovariectomy-induced bone loss in adult rats.

Current published results on whether statins have beneficial effects on bone metabolism have been conflicting so far. In order to further investigate if statins were promising candidates for the treatment for osteoporosis, we conducted a study in which rats were ovariectomized (OVX) at 6 months of age, allowed to lose bone for 60 days and followed by oral administration of simvastatin at the dose levels of 0.3-10 mg/kg/d for 60 days. PGE2 (6 mg/kg) was used as a positive control. Study endpoints included bone histomorphometry on the proximal tibial metaphysis (PTM) and the tibial diaphysis (TX), dual-energy X-ray absorptiometry on the right femur and micro computed tomography (ICT) on the 5th lumbar vertebra (LV). After 120 days of OVX, cancellous bone lost by 80% in the PTM and 18% in the LV accompanied by increased bone formation and resorption. Simvastatin at all dose levels did not affect bone volume, bone formation rate and bone erosion surface when compared to 120 day ovariectomized animals at all bone sites studied. By contrast, PGE2 restored cancellous and cortical bone area to sham control levels. In conclusion, this study demonstrated that unlike PGE2, oral administration of simvastatin did not have effects on cancellous or cortical bone formation and resorption; and consequently was not able to prevent further bone loss or restore bone mass in the osteopenic, OVX rats.

Absorptiometry, Photon↗
PubMed1991

Comparative and simultaneous effects of simvastatin and ciprofibrate on plasma lipid parameters and upon hepatic drug metabolizing and peroxisome proliferation marker enzymes in the male Wistar rat.

The effects of an associated treatment with Ciprofibrate and Simvastatin upon plasma lipid parameters, liver Mixed Function Oxidases enzymes and peroxisomal markers have been studied in male Wistar rats. The association was efficient upon triglycerides, but not upon cholesterol. The inducive and proliferative effects commonly exerted by Ciprofibrate (5 mg/kg/day) were not significantly modified by the simultaneous treatment with Simvastatin (10 mg/kg/day). The increase of the seric alanine amino transferase activity was however much more pronounced after the associated treatment than after single administration of Ciprofibrate or Simvastatin.

Animals↗
PubMed1991

[Effects of simvastatin on atherogenic blood lipid pattern].

The effect of a 6-month treatment with simvastatin, an HMG CoA-reductase inhibitor, on serum lipoprotein pattern was investigated in patients affected by primary hypercholesterolemia. After 4-6 weeks of lipid lowering diet, 46 patients showing serum cholesterol greater than 250 mg/dl and triglycerides less than 200 mg/dl were included in the study and treated with simvastatin (10-30 mg/day) plus diet. Serum total cholesterol, LDL-cholesterol, apolipoprotein B and triglycerides levels significantly decreased at the end of the follow-up (-27%, -33%, -22%, -26% respectively). Apolipoprotein A1 showed a significant increase as well as HDL-cholesterol, HDL3-cholesterol and apolipoprotein A1/B ratio. This study provides further findings on the simvastatin efficacy to normalize the lipoprotein pattern in primary hypercholesterolemia.

Adult↗
PubMed1991

[Cost-effectiveness of lowering of blood cholesterol using simvastatin and cholestyramine].

With use of a model of the costs and effects of cholesterol lowering therapy in the primary prevention of coronary heart disease, the cost-effectiveness of simvastatin and cholestyramine in the Netherlands have been estimated. Costs per year of life saved by cholestyramine therapy are several times greater than those of simvastatin therapy and compared unfavorably with those of generally accepted health care programs in the Netherlands. Cholesterol-lowering with simvastatin in men can be cost-effective when therapy is initiated at an early age. At cholesterol levels between 6.5 and 8 mmol/l, however, therapy should be restricted to men with at least one, preferably two additional risk factors such as hypertension or diabetes mellitus. Among women, cholesterol lowering can only be cost-effective when therapy is limited to women with diabetes mellitus or severely elevated serum cholesterol levels.

Adult↗
PubMed1991

Lowering of plasma cholesterol levels in animals by lovastatin and simvastatin.

Lovastatin and simvastatin are potent competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Key inhibit the synthesis of cholesterol in cultured HepG23 cells, rat hepatocytes and in rats. The primary target organ of cholesterol synthesis inhibition by lovastatin and simvastatin is the liver. Lovastating and simvastatin lower levels of plasma cholesterol in rats, dogs and rabbits by inhibition the endogenous cholesterol synthesis and induction of LDL receptor in the liver.

Animals↗
PubMed1991

[Treatment of hypercholesterolemic patients of different age with simvastatin: 1-year study].

Nowadays there is no direct evidence that lowering cholesterol may reduce the CHD in the elderly; however, several evidences suggest the potential benefit of a dietetic and/or pharmacologic intervention in healthy young-old hypercholesterolemics. In this study we evaluated the efficacy and tolerability of simvastatin, alone or in combination with cholestyramine, in two groups of patients (group A: age 30-55 years and group B: age 60-75 years) with primary hypercholesterolemia, over a 48-week period. In both groups Simvastatin induced a significant reduction in total and LDL cholesterol (p less than 0.001 both), with a decrease of the total/HDL cholesterol ratio (p less than 0.001). A reduction of the apo-B100 levels was also observed (respectively p less than 0.01 and p less than 0.001) with a significant improvement of the apo-B100/apo-A1 ratio (p less than 0.01). Simvastatin was well tolerated and free of remarkable side effects in both groups.

Adult↗
PubMed1990

[Therapy of hypercholesterolemia and hypertriglyceridemia. Comparison of the lipid-lowering effect of simvastatin and tiadenol].

A comparative trial was carried out on the effect on lipid metabolism of two drugs which inhibit the enzyme systems involved in cholesterol synthesis: tiadenol and simvastatin. The trial was performed in 40 patients with non familial and non secondary hypercholesterolemia. Subjects were divided into two groups of 20 patients each, one to be treated with tiadenol, the other with simvastatin. During the study period all patients followed a dietary regime of about 1500 cal daily. Thirty days before the trial, patients were given a placebo daily, and this was followed by thirty days with the drugs studied. Prior to the placebo period and at the end of the experimental period, blood was drawn for the assessment of total cholesterol, esterified cholesterol, VLDL-, LDL- and HDL-cholesterol, apolipoprotein B, phospholipids, and triglycerides. Both drugs were found to induce significant reductions of total cholesterol, VLDL, and LDL, a relative increase of HDL, and reduction of apolipoprotein B. Triglyceride blood level was markedly reduced in tiadenol-treated subjects, and to a lesser extent also in simvastatin-treated ones. This difference is attributed to the different levels at which the drugs interfere with the early steps of cholesterol synthesis. The authors conclude by pointing out that the two drugs should be used selectively according to the type of metabolic disorder prevalent in the individual patient.

Aged↗
PubMed1990

[Simvastatin (MK-733), a new HMG-CoA reductase inhibitor, in the treatment of hypercholesterolemia in elderly patients with atherosclerosis].

PURPOSE: To evaluate the efficacy and tolerability of simvastatin, a new and potent HMG-CoA reductase inhibitor, in the treatment of hypercholesterolemia in elderly patients. PATIENTS AND METHODS: Twenty patients, 14 female and 6 male, aged 65 to 72 years (x = 69 +/- 3), with total cholesterol (TC) above 260 mg/dl and triglycerides below 350 mg/dl were studied. All patients presented clinical evidences of atherosclerotic disease and were followed up for 6 months. Monthly visits were required for clinical and laboratory evaluation. The initial dosage of simvastatin was 10 mg/day; dosage was titrated up to 10 mg/day or to a minimum of 5 mg/day in intervals of at least 4 weeks, in order to maintain LDL-cholesterol below 140 mg/dl. To evaluate the changes on plasma lipid levels, the mean value of determinations during the placebo baseline period was compared to the mean value of determinations during the active treatment period. RESULTS: There were significant reductions of total cholesterol (-26.4%), triglycerides (-16.0%), LDL-cholesterol (-35.2%), VLDL-cholesterol (-15.4%), TC/HDL-C (-30.7%), and LDL/HDL-C (-39.5%). There was significant elevation of HDL-cholesterol (+5.2%), although this response was not uniform. The drug was well tolerated: only five patients reported transient clinical adverse experiences that subsided spontaneously. Two patients had elevation of CPK and one of TGP. The drug did not have to be discontinued in any case. Ophthalmological examinations performed before treatment compared to examinations at the end of the study showed no signficant alterations. CONCLUSION: Simvastatin in elderly patients appeared to be a potent TC and LDL-C lowering drug and presented mild but significant effect on the elevation of HDL-C. There was good tolerability, with low incidence of adverse experiences. This fact is important when one considers drug therapy for hypercholesterolemia in this age group.

Aged↗
PubMed1990

Simvastatin therapy for hypercholesterolaemia in patients with coronary heart disease.

The efficacy of simvastatin therapy for hypercholesterolaemia was evaluated in 26 patients with coronary heart disease, 20 of whom had undergone coronary artery bypass grafting. Simvastatin reduced total- and low-density lipoprotein (LDL) cholesterol from 8.3 to 5.1 (38%) and 6.3 to 3.3 mmol/L (48%) respectively, p less than 0.001; high-density lipoprotein (HDL) cholesterol increased from 1.19 to 1.24 mmol/L, p = NS. The changes in apoproteins A1 and B paralleled those of HDL- and LDL-cholesterol. There were no clinically important adverse effects. We conclude that simvastatin is effective lipid lowering therapy and can be used safely, in the short term, in patients with coronary heart disease.

Anticholesteremic Agents↗
PubMed1990

[HMG-CoA reductase inhibitors in familial hypercholesterolemia. Therapy with simvastatin alone and in combination with cholestyramine in low dosage; a report of 2 years experiences].

We have studied the effect of simvastatin, an inhibitor of the rate-limiting enzyme in cholesterol biosynthesis, alone and in combination with cholestyramine in 48 patients. Simvastatin 40 mg decreased total serum cholesterol, LDL cholesterol and apolipoprotein B by 35%, 40% and 35%, respectively, while HDL cholesterol and apolipoprotein A-I increased by 10% (p less than 0.01) and 7% (p less than 0.05), respectively. The addition of 8 g cholestyramine caused a further decrease in total cholesterol and LDL cholesterol to a total of 42% and 49%, respectively. Eighteen of the 48 patients have now been under combined treatment for 2 years. The initial high decreases in total cholesterol and LDL cholesterol were stabilized for the whole period. Some patients developed gastrointestinal complaints, which made necessary a reduction of simvastatin in two cases. Biochemical side effects (e.g. increases in CK and transaminases) were not observed.

Adult↗
PubMed1990

Simvastatin in the effective reduction of plasma lipoprotein levels in familial dysbetalipoproteinemia (type III hyperlipoproteinemia).

PURPOSE: Familial dysbetalipoproteinemia (type III hyperlipoproteinemia) is characterized by an increase of serum lipids caused by an accumulation of remnant particles of triglyceride-rich lipoproteins. We studied the efficacy of simvastatin, an inhibitor of the biosynthesis of cholesterol, in this disorder. PATIENTS AND METHODS: Twelve patients participated in an open-label study. After a three-week placebo period, they were treated with increasing doses (10 mg twice a day, 20 mg twice a day, and 40 mg twice a day) of simvastatin in six-week periods. RESULTS: With the 80-mg dose, the mean serum cholesterol level decreased from 12.30 +/- 4.96 to 5.29 +/- 1.24 mmol/L (mean reduction, 54%) and the mean serum triglyceride level decreased from 8.77 +/- 7.16 to 3.61 +/- 1.33 mmol/L (-48%); this was due to a decrease in very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) lipids. There was a decrease in the ratio of VLDL cholesterol to serum triglycerides and in the apolipoproteins B and E, suggesting a reduction in the amount of circulating atherogenic remnant particles. Except for a slight increase in serum alanine aminotransferase levels in three patients, no side effects were observed. CONCLUSION: These data show that levels of serum lipids can be effectively reduced by simvastatin in familial dysbetalipoproteinemia.

Adult↗
PubMed1989

[Effect of a long-term treatment with simvastatin, an inhibitor of HMG-CoA reductase, in dyslipidemic patients at high risk].

The reduction of total and LDL cholesterol (TC and LDLc), apoprotein B (ApoB) and in some instances triglycerides (TG) and the increase of HDL cholesterol (HDLc) and apoprotein A (ApoA) seem to be associated to a reduced coronary risk. Aim of our work was to evaluate the effects of a chronic treatment with the HMG-CoA reductase inhibitor simvastatin (MK-733), in a group of 8 dyslipidemic patients, 5 women and 3 men, aged between 48 and 69 years (mean age 59 +/- 8 years) at high risk being already affected by clinical compliances of atherosclerosis and not previously controlled by diet and/or other antidyslipidemic drugs. At the beginning and at the end (6 months) of this open study it was performed a clinical, ECG and ophthalmological examination, as well as an evaluation of the routine laboratory parameters. The initial dosage of simvastatin was a tablet of 10 mg/day, increased after a month to 20 mg and then to 40 mg/die. The mean dosage was 26.25 mg at the 3rd month and 21.25 mg at the 6th. Long-term simvastatin treatment was well tolerated (lack of important side effects as well as of significant changes of other clinical and laboratory parameters) and effective, reducing significantly (p less than 0.01) TC (317.9 +/- 30.8 vs 238.5 +/- 37.9 mg/dl), LDLc (210.6 +/- 48 vs 147.9 +/- 52 mg/dl), ApoB (144.7 +/- 17.5 vs 104.5 +/- 18), and TG (272.9 +/- 184 vs 200.5 +/- 117.6 mg/dl) and increasing in contrast HDL and ApoA values.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Low-dose effect of simvastatin (MK-733) on serum lipids, lipoproteins, and apolipoproteins in patients with hypercholesterolemia.

The effects of simvastatin (MK-733), a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on serum lipids, lipoproteins, and apolipoproteins were investigated in 29 patients (12 men, 17 women, aged 37 to 73) with moderate to severe hypercholesterolemia. It was given in doses of 2.5 mg/day for four months and 5 mg/day for the succeeding four months. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein (apo) B decreased by 18% (263 +/- 7 mg/dl to 216 +/- 7 mg/dl, P less than 0.01), 24% (180 +/- 7 mg/dl to 136 +/- 7 mg/dl, P less than 0.01), and 21% (133 +/- 4 mg/dl to 104 +/- 3 mg/dl, P less than 0.01), respectively, four months after treatment. Similar reductions (17%, 24%, and 23%, respectively, P less than 0.01) were observed at eight months. A significant reduction in triglyceride (TG) was observed (173 +/- 15 mg/dl to 136 +/- 11 mg/dl at eight months, P less than 0.01), as was a significant increase in serum high-density lipoprotein cholesterol (HDL-C) (48 +/- 2 mg/dl to 52 +/- 2 mg/dl at eight months, P less than 0.01). However, apo AI and apo AII remained unchanged. Atherogenic indices of (TC--HDL-C)/ HDL-C, LDL-C/HDL-C, and apo B/Apo AI ratios were significantly (P less than 0.01) reduced after treatment. No significant changes were observed in lipoprotein lipase, hepatic TG lipase, and lecithin: cholesterol acyltransferase (LCAT) activities. Simvastatin was well tolerated and no critical side effects were noted in the eight-month study period. These data indicate that simvastatin, even at a low dose of 2.5 to 5 mg daily, causes consistent reductions in serum TC, LDL-C, apo B, and TG, and a rise in HDL-C and antiatherogenic lipoproteins.

Adult↗
PubMed1995

Simvastatin added to ursodeoxycholic acid does not enhance disappearance of gallstone fragments after shock wave therapy.

Inhibitors of the HMG-CoA reductase have been shown to further reduce the biliary cholesterol saturation in patients treated with oral bile acids for cholesterol gallbladder stones. It was the aim of our study to evaluate the efficacy of simvastatin in addition to ursodeoxycholic acid in the dissolution of gallstone fragments after shock wave lithotripsy and adjuvant bile acid dissolution therapy. Eighteen patients with a single radiolucent gallbladder stone and a serum cholesterol of more than 250 mg/dl were randomly assigned to receive either ursodeoxycholic acid alone (750 mg per day, group A, n = 9) or in combination with simvastatin (20 mg per day, group B, n = 9) for the dissolution of the gallstone fragments generated by extracorporeal shock wave lithotripsy. The two groups were well matched regarding their baseline characteristics. At the primary end point of the study 6 months after lithotripsy, there was no difference between the groups in the rate of gallstone disappearance with 4 of 9 patients being stone free in each group. As evaluated by life table analysis, even further follow-up showed no significant difference between the groups (P = 0.8). In group B, serum cholesterol levels decreased by 22% at 3 months (P = 0.01 vs. baseline) and by 24% at six months (P = 0.02) during treatment while no significant change was observed in group A. With both regiments, no adverse effects were observed. While simvastatin added to ursodeoxycholic acid resulted in a decrease of elevated serum cholesterol levels in gallstone patients, it did not enhance stone disappearance after shock wave lithotripsy and adjuvant bile acid dissolution therapy.

Anticholesteremic Agents↗
PubMed1995

Simvastatin treatment of hypercholesterolemia in patients with insulin dependent diabetes mellitus.

The effects of 16 weeks therapy with the HMG-CoA reductase inhibitor Simvastatin 10-20 mg (n = 12) was compared to placebo (n = 13) in 25 euthyreoid males with insulin dependent diabetes mellitus and fasting total serum cholesterol above 6 mmol/l. Insulin dependence was defined as a glucagon stimulated C-peptide level less than 0.6 mmol/l. The study was placebo-controlled, double-blind with a parallel group design. Body weight, blood pressure, glycemic control as well as liver enzymes were unchanged and simvastatin was well tolerated by all patients. Ophthalmological slitlamp examination before and at the end of the study period did not show development of new lenticular opacities. Simvastatin decreased serum total cholesterol from 6.7 +/- 1.0 mmol/l (mean +/- SD) to 4.9 +/- 0.4 (p < 0.001 vs. placebo) and LDL-cholesterol from 4.6 +/- 0.7 mmol/l to 2.8 +/- 0.3 (p < 0.001 vs. placebo). HDL-cholesterol and triglycerides remained unaltered. A positive influence on the atherosclerotic process in patients with insulin dependent diabetes mellitus remains, however, to be proven.

Adult↗
PubMed1994

Clinical investigation on the hypolipidemic effect of simvastatin versus probucol in hemodialysis patients.

In chronic renal failure hypertriglyceridemia is a well-known complication that persists during hemodialysis treatment: it may be one of the major risk factor for cardiovascular death in these patients. We studied the effects of two lipid lowering drugs; simvastatin (20 mg/day for six months) and probucol (500 mg/day for six months), on lipid profile in 12 hemodialysis patients. Simvastatin therapy reduced plasma total cholesterol by 26% (p > 0.002), LDL-cholesterol by 36% (p > 0.002) and triglycerides by 28% (p > 0.05): plasma HDL-cholesterol and apo-A were raised, but not significantly. Probucol therapy decreased plasma triglycerides by 38% (p > 0.05), total cholesterol by 15% and LDL-cholesterol by 19%: plasma HDL-cholesterol and apo-A were decreased but not significantly. No side effects occurred with either drug. These data suggest that in hemodialysis patients both simvastatin and probucol profoundly affect the lipid profile, as well as the triglyceride levels.

Aged↗
PubMed1993

[Psychiatric disorders with use of simvastatin].

Three patients are described with serious psychiatric complications related to use of simvastatin. The psychiatric symptoms concerned were mainly depression, anxiety and suicidal tendencies but also psychotic symptoms. The hypothesis is developed that in a particular population psychiatric (mood) disorders may be triggered by use of simvastatin or other cholesterol lowering compounds. A low or lowered cholesterol level may be related to disturbances in the cerebral serotonin metabolism. It may be necessary to be more alert for psychiatric (mood) disorders when a cholesterol lowering treatment (with simvastatin) is started and to stop it when psychiatric symptoms develop, or grow worse.

Adult↗