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PubMed2005

[The effect of hypolipemic therapy with diet and simvastatin on the course of angina pectoris and the results of exercise stress test in patients with coronary artery disease].

UNLABELLED: Statins are the multi-directorial acting drugs in atherosclerosis prevention, which decrease the overall and cardiovascular mortality. The aim of this study was to estimate the effect of six-month long hypolipemic therapy with diet and 20 mg of simvastatin on clinical intensity of angina pectoris and the course of exercise stress test. PATIENTS AND METHODS: We studied 44 patients with typical anginal chest pain. In all blood sampling and treadmill stress test were made, and next in all hypolipemic diet and simvastatin 20 mg were recommended. After four weeks and six months of treatment clinical assessment and exercise test were made. RESULTS: After four weeks and six month long observation period the decrease of total and LDL cholesterol, triglycerides and fibrinogen were found. Moreover, we have observed the improvement in frequency of anginal symptoms, their intensity in CCS classification and number of nitroglycerin tablets taken per week. The course of exercise test was also ameliorated: the percentage of patients, in whom stress test was finished because of chest pain was decreased, time of chest pain duration after exercise cessation was shorter, the percentage of patients with significant ST interval depression diminished, maximal ST interval depression as well as the time of significant ST interval depression duration also decreased. Although improvement in values of mentioned parameters, after six months long therapy with simvastatin the percentage of patients with Duke's treadmill score value showing intermediate cardiovascular risk (between -10 and +4) increased. In conclusion, therapy with hypolipemic diet and simvastatin already after four weeks decreased plasma lipids and fibrinogen levels and improved the course of angina pectoris and exercise stress test, what suggested its effectiveness not only as the treatment improving atherosclerosis risk factors, but also with prompt and clinical important effect ameliorating the handicapped coronary reserve.

Adult↗
PubMed1991

[Comparison about the efficacy and tolerability between simvastatin and bezafibrate in the treatment of hypercholesterolemia].

Simvastatin and bezafibrate actions on blood lipids and their side effects were compared in a double-blind trial involving 24 adults with severe type IIa or IIb primary hypercholesterolemia (mean plasma cholesterol = 4.35 g/l). During a 12-week period, the patients received either bezafibrate, 600 mg 3 times a day, or simvastatin, 10 or 20 mg once a day, with a doubling of the dosage at week 6 if the LDL-cholesterol level remained above 1.40 g/l. Simvastatin significantly reduced LDL-cholesterol by -39.5% (p less than 0.001), total cholesterol by 33.9% (p less than 0.005) and apoprotein B by -28% (p less than 0.001). Bezafibrate significantly reduced LDL-cholesterol (-19.8%, p less than 0.001) and total cholesterol (-17.5%, p less than 0.002), but not apoprotein B. Bezafibrate also reduced triglycerides by -26.6% and raised HDL-cholesterol by +27.6%. Simvastatin was more effective than bezafibrate in lowering LDL-cholesterol (p less than 0.002), total cholesterol (p less than 0.005) and apoprotein B (p less than 0.05). Tolerance of both drugs was considered excellent.

Adult↗
PubMed1991

A 6-month trial of simvastatin (HMG-CoA reductase inhibitor) in the treatment of hypercholesterolaemia.

The aim of this study was to evaluate the long-term efficacy and tolerability of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor simvastatin, over a 24-week period. Patients (108) with primary hypercholesterolaemia were clinically, haematologically and biochemically evaluated and established on a cholesterol-lowering diet. After a wash-out period free from other lipid-lowering drugs and a baseline period on placebo of 1 month each, 10 mg simvastatin was introduced at night. The dose was increased to 20 mg and 40 mg at 6 and 12 weeks' follow-up respectively if the total cholesterol (TC) level was still above 5.17 mmol/l. Follow-up took place every 6 weeks and included lipid, haematological, biochemical and clinical evaluation. A full ophthalmological evaluation was conducted at baseline and at 24 weeks' follow-up. Overall the TC level was reduced below the baseline level by 34.3% at week 18 of follow-up and 32.5% at week 24. Patients with higher initial TC levels showed greater TC lowering in response to simvastatin than did those with lower initial TC levels. A group of 45 patients was followed up for an additional 12 weeks after the end of the trial and maintained TC reductions similar to those at the end of the trial. Fourteen patients experienced adverse effects which were thought to be drug-related. One patient was withdrawn from the trial after developing conjunctivitis that proved to be related to the use of simvastatin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

[Evaluation of tolerance, efficacy and safety of 3-year simvastatin use in the treatment of primary hypercholesterolemia].

Simvastatin (synvinolin MK-733) is a potent inhibitor of 3-HMG-CoA-reductase, the key enzyme for cholesterol biosynthesis. To investigate the efficiency and safety of this new drug on a long term basis, simvastatin was administered for 3 years to ten patients with type II hyperlipoproteinemia. Daily dosages were 20 or 40 mg. The drug therapy produced a significant reduction in serum levels of total cholesterol (19-34%), LDL-cholesterol (26-44%) and Apo B (19-33%). Triglycerides decreased moderately (2-23%) while HDL-cholesterol and Apo A1 changed only slightly (-3 to 6% and 5-13% respectively). Simvastatin was well tolerated. No consistent adverse clinical or biochemical effects were observed during the three-year therapy. The results indicate that simvastatin is a promising new therapy for high risk hypocholesterolemic patients.

Aged↗
PubMedDate not supplied

Simvastatin in the treatment of hypercholesterolemia in elderly patients.

Twenty elderly (mean age, 69 years), hypercholesterolemic patients (low-density lipoprotein [LDL] levels greater than or equal to 160 mg/dl) were supplied a lipid-lowering diet for one month and then received 10 mg of simvastatin daily for 12 months. Total cholesterol levels fell significantly, from 304.6 mg/dl at baseline to 277.4 mg/dl after one month on the diet, to 245.9 mg/dl after one month of simvastatin, and to 216.1 mg/dl after two months of simvastatin; total cholesterol levels remained significantly lower (221.6 mg/dl at month 12). LDL levels decreased significantly, from 217.6 mg/dl at baseline to 130.4 mg/dl at month 12. High-density lipoprotein levels increased significantly only at months 2 and 3. Apolipoprotein (apo) A levels increased significantly, from 147.2 mg/dl at baseline to 217.9 mg/dl at month 12. There were no significant changes in triglyceride or apo B levels. No changes in blood pressure, heart rate, or body weight or in results of laboratory tests were noted. Few side effects were reported. It is concluded that simvastatin is safe and effective in the treatment of hypercholesterolemia in elderly patients.

Aged↗
PubMed1990

The effects of simvastatin on serum lipoproteins in severe hypercholesterolaemia.

The effects of simvastatin, an inhibitor of cholesterol synthesis, on serum lipids, lipoprotein composition and apolipoproteins were evaluated in a total of 50 patients with hypercholesterolaemia. In the first study, 24 patients (mean serum cholesterol 10.74 +/- 1.59 mmol/l) were treated with simvastatin 40 mg daily for 24 wk. Serum cholesterol and low density lipoprotein (LDL) cholesterol decreased to average values 29-36% and 35-42% below the basal value, respectively. Serum triglycerides decreased by 16-28%, and high density lipoprotein (HDL) cholesterol increased by 6-11%. Apolipoprotein A-I concentration increased 6-8% and that of apolipoprotein B decreased 29-33%. The composition of LDL remained unchanged whereas the very low density lipoproteins became enriched in triglycerides. Lipoprotein Lp(a) was not affected. In the second study 26 patients (mean serum cholesterol 12.35 +/- 2.05 mmol/l) were treated with simvastatin 40 mg daily as monotherapy or combined with a bile acid binding resin for 2 yr. Serum cholesterol levels decreased to values which remained stable throughout the entire study period; after 2 yr this decrease amounted to 43%. Compared to monotherapy, combination therapy yielded a further 12% decrease of cholesterol. In the entire group, triglycerides decreased by 16% and HDL cholesterol increased by 9%. Side effects were limited to slight increases in alanine aminotransferase and creatine phosphokinase in some patients. Simvastatin appears to be an important asset in the treatment of hypercholesterolaemia.

Adult↗
PubMed1990

Effects of simvastatin and cholestyramine in familial and nonfamilial hypercholesterolemia. Multicenter Group I.

Simvastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was compared with cholestyramine resin in a randomized open-label 12-week multicenter study of 251 high-risk patients with familial or nonfamilial hypercholesterolemia. Simvastatin, 20 mg and 40 mg daily, produced mean reductions in total cholesterol of 26% and 33%, respectively, and reductions in low-density lipoprotein cholesterol level of 32% and 40%. Cholestyramine resin, 4 to 12 g twice daily, reduced total cholesterol and low-density lipoprotein cholesterol levels 15% and 21%, respectively. High-density lipoprotein cholesterol levels were increased 8% to 10% by all treatments. Plasma triglyceride levels were moderately decreased by simvastatin treatment, while triglyceride levels increased with cholestyramine treatment. Simvastatin was better tolerated than cholestyramine, which had numerous gastrointestinal tract side effects. No patient had a serious drug-related adverse event.

Adult↗
PubMed1989

Simvastatin reduces platelet thromboxane formation and restores normal platelet sensitivity against prostacyclin in type IIa hypercholesterolemia.

The effect of lowering total serum cholesterol and low-density lipoprotein (LDL) cholesterol on platelet function, thromboxane formation and platelet sensitivity against PGI2 was studied in platelet-rich plasma ex vivo. Additionally, PGI2 receptors were determined in membrane preparations of these platelets. Twelve patients suffering from familial hyperlipoproteinemia type IIa (FH) were treated for 8 months with simvastatin (20-40 mg/day) and compared with 10 untreated FH patients and 10 untreated normocholesterolemic subjects. Compared with those of healthy controls, platelets of untreated FH patients were hyperreactive, as shown by an enhanced aggregation response and release of ATP and thromboxane after stimulation by collagen (0.3-5 micrograms/ml) and ADP (0.3-10 micrograms/ml). Simvastatin reduced the total and LDL serum cholesterol towards control levels while HDL cholesterol remained unchanged. This was accompanied by a significant decrease of platelet aggregation, thromboxane formation and ATP secretion being no more different from normocholesterolemic controls. In addition, the reduced platelet sensitivity against prostacyclin (aggregation, stimulation of cAMP formation) in untreated FH patients was improved to normal values by simvastatin. This was associated with a significant elevation of the reduced prostacyclin binding sites and might be explained by an improved access of prostacyclin to its receptors at platelet membranes. These data demonstrate that the reduction of total and LDL serum cholesterol by simvastatin results in a normalization of platelet function by (i) reduction of platelet hyperreactivity and (ii) improvement of the sensitivity against prostacyclin towards normal via enhanced PGI2-binding sites.

Adenosine Triphosphate↗
PubMed1989

[Effects of simvastatin on plasma levels of lipids, lipoproteins and apolipoproteins in primary hypercholesterolemia].

To evaluate the effectiveness, tolerance and safety of simvastatin (MK 733), a new HMG-CoA reductase inhibitor, a 28-week, single blind study with placebo was carried out on 10 patients suffering from primary hypercholesterolaemia. All patients followed the AHA Phase 1 or Phase 2 diet and underwent active treatment for 24 weeks with increasing doses of simvastatin from 10 to 40 mg in a single evening administration. A reduction in plasma levels of total cholesterol (-29%, p less than 0.001 and -41%, p less than 0.001), LDL cholesterol (-35%, p less than 0.001 and -49%, p less than 0.001), VLDL cholesterol (-9%, ns and -38%, ns), Apo-B (-27%, p less than 0.005 and -37%, p less than 0.001), Apo-A2 (-3%, ns and -3%, ns), and triglycerides (+2%, ns and -10%, ns), was obtained in the VIth and XXIVth week. There was also an increase in HDL cholesterol (+4%, ns and +17%, p less than 0.05), HDL2 subfractions (+9%, p less than 0.05 and +36%, p less than 0.05), HDL3 (+3%, ns and +11%, ns) and Apo-A1 (+7%, ns and +4%, ns). In all patients, simvastatin was generally tolerated and there were no clinical, laboratory or ophthalmological side-effects related to the drug. If long-term studies confirm its safety, simvastatin will offer excellent prospects for the prevention of ischaemic cardiopathy.

Anticholesteremic Agents↗
PubMed1989

[Efficacy and safety of simvastatin, a new cholesterol-lowering drug].

The effects of simvastatin, an inhibitor of cholesterol synthesis, was studied in 50 patients with hypercholesterolaemia. In the first study, 24 patients with serum cholesterol levels of 10.74 +/- 1.59 mmol/l were treated with simvastatin 40 mg daily for 6 months. Serum cholesterol levels decreased within 4 to 8 weeks to stable values 30 to 36% below the basal value. Serum triglycerides decreased by 16 to 28% and high density lipoprotein (HDL) cholesterol increased by 6 to 11% on average. In the second study, 26 patients with serum cholesterol levels of 12.35 +/- 2.05 mmol/l were treated with simvastatin 40 mg daily as monotherapy or combined with a bile acid binding resin for 2 years. Cholesterol levels decreased to values which remained stable throughout the entire study period; after 2 years the decrease amounted to 43%. Compared with monotherapy, combination with a bile acid binding resin yielded a further 12% decrease of cholesterol. In the entire group, triglycerides decreased by 16% and HDL cholesterol increased by 9% on the average. Side effects were limited to slight increases in alanine aminotransferase and creatine phosphokinase occurring in some patients. Simvastatin appears to be an important asset in the treatment of hypercholesterolaemia.

Anticholesteremic Agents↗
PubMed1988

[Effects of simvastatin on plasma lipids, lipoproteins and apoproteins (A1 and B). 24 cases of major primary hypercholesterolemia].

We studied the effects of simvastatin (MK 733), a new competitive inhibitor of HMG CoA reductase, alone and in combination with a bile acid sequestrant, cholestyramine, on serum levels of lipoproteins and apoproteins A1 and B, in 24 patients with familial hypercholesterolemia. After simvastatin treatment (40 mg/day) alone for 12 weeks, serum total and low density lipoprotein cholesterol decreased by 31 and 36 percent respectively. With the addition of cholestyramine, there was a 41 per cent total decrease in serum cholesterol from the control value and a 50 percent decrease in low density lipoprotein cholesterol. After cholestyramine treatment alone for 12 weeks, serum total and low density lipoprotein cholesterol decreased by 20 percent and 29 percent respectively. With the addition of simvastatin (20 mg per day), there was a 32 percent total decrease in serum cholesterol from the control value and a 43 percent decrease in low density lipoprotein cholesterol. High density lipoprotein cholesterol remained unchanged. No major adverse effect was observed. If long term safety can be confirmed, the simvastatin-cholestyramine regimen may prove useful in heterozygous familial hypercholesterolemia.

Adult↗
PubMed1995

Baseline serum cholesterol and treatment effect in the Scandinavian Simvastatin Survival Study (4S)

We examined the relation between the risk of major coronary events (coronary death and non-fatal myocardial infarction) and baseline cholesterol levels in patients with coronary heart disease, randomised to placebo or simvastatin therapy in the Scandinavian Simvastatin Survival Study (4S). The relative risk reduction in the simvastatin group was 35% (95% CI 15-50) in the lowest quartile of baseline low-density-lipoprotein cholesterol and 36% (19-49) in the highest. Simvastatin significantly reduced the risk of major coronary events in all quartiles of baseline total, high-density-lipoprotein, and low-density-lipoprotein cholesterol, by a similar amount in each quartile.

Adult↗
PubMed1994

[Monitoring plasma levels of vitamin D metabolites in simvastatin (Zocor) therapy in patients with familial hypercholesterolemia].

BACKGROUND: Simvastatin is a hypolipidaemic agent, a statin which inhibits cellular cholesterol synthesis by blocking 3HMG CoA reductase. The authors present a report on levels of plasma metabolites of vitamin D after treatment with 10 and 20 mg simvastatin daily in 13 patients, heterozygotes with hypercholesterolaemia during a five-week period. METHODS AND RESULTS: During simvastatin treatment in all patients plasma levels, of the sum of hydroxylated vitamin D metabolites and 1,25-dihydroxyvitamin D after five weeks of treatment with 10 and 20 mg hypolipidaemic drug were examined. For assessment of vitamin D metabolites radioassay was used which assesses the sum of hydroxylated vitamin D metabolites, and radioimmunoanalysis for assessing the 1,25-dihydroxyvitamin D plasma level. For statistical evaluation the non-parametric Friedman test and simultaneous testing was used. CONCLUSIONS: Simvastatin raises the plasma levels of the sum of hydroxylated vitamin D metabolites and 1,25-dihydroxyvitamin D in a dose-dependent ratio. The authors recommend to monitor the plasma levels of vitamin D metabolites over a longer time period.

Adult↗
PubMed1994

Selective inhibition of primary acute myeloid leukaemia cell growth by simvastatin.

Primary human acute myeloid leukaemic (AML) cells from bone marrow (BM) and peripheral (PB), the human myeloblastic leukaemia cell line (HL60) and normal human BM mononuclear cells were cultured in serum-free medium. The survival of progenitor cells from normal BM, HL60 and AML cell populations was reduced over a range of concentrations of simvastatin. This dose response relationship was more pronounced in HL60 and AML cell cultures, indicating greater sensitivity of AML progenitor cells compared with normal BM progenitors. Short-term exposure (18 h) to a range of concentrations of simvastatin showed the same differential response between leukaemic and normal BM cells in terms of clonogenicity. At a concentration of 10 micrograms/ml progenitor cell survival remained above 65% for normal BM while at this concentration leukaemia progenitor cell survival fell below 25% of the untreated values. The differential effect of simvastatin on normal and leukaemic progenitor cells may have value in the clinical management of AML. The possible use of simvastatin, or related drugs, as adjuvants to conventional chemotherapy including in vitro BM purging, merits consideration.

Acute Disease↗
PubMed1993

The effect of simvastatin treatment on the low-density lipoprotein subfraction profile and composition in familial hypercholesterolaemia.

The effect of simvastatin treatment on the low-density lipoprotein (LDL) subfraction profile was studied in 26 patients with familial hypercholesterolaemia. Before treatment LDL consisted of three LDL subfractions, using density-gradient ultracentrifugation (LDL1, LDL2 and LDL3) present in a relatively narrow density range (d = 1.030-1.045 g/ml). Simvastatin did not influence this profile with respect to the number and density range of the LDL subfractions. However, the composition of the isolated LDL subfractions changed after treatment, as evidenced by the reversal towards normal of the increased cholesterol/protein ratio (mean 1.51 before vs. 1.38 after therapy, p < 0.01; mean 1.36 in normolipidaemic subjects). When the subjects were stratified by their plasma triglyceride levels or the change in plasma triglycerides during simvastatin therapy, a strong dependence of the LDL subfraction profile and its composition on plasma triglyceride levels was observed; increasing plasma triglyceride levels were associated with a more dense LDL subfraction profile, characterized by a high relative contribution of dense LDL3 to total LDL and changes in LDL composition, reflected by a relatively low cholesterol/protein ratio. Our results indicate that in patients with familial hypercholesterolaemia: (1) plasma triglyceride levels have an important role in determining the properties of LDL and (2) simvastatin treatment results in changes in composition of LDL, which may affect the intrinsic metabolic characteristics and thus the atherogenic potential of LDL.

Adolescent↗
PubMed1993

[Clinical evaluation of simvastatin in the treatment of hyperlipidemia].

Fifty nine cases with hyperlipidemia were divided randomly into two groups. In group I, each patient took simvastatin 10-40mg/day (mean 17.9mg/day). In group 2, each patient took gemfibrozil 1200mg/day. After treatment with simvastatin, in comparing with baseline values, serum level of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) triglyceride (TG), apolipoprotein B (ApoB), and TC/HDL-C (high-density lipoprotein cholesterol) reduced by 34.6% (P < 0.001), 45.4% (P < 0.001), 22.1% (P < 0.01), 21.1% (P < 0.001), and 39.4% (P < 0.001) respectively, and HDL-C, apolipoprotein A-I(Apo A-I) and Apo A-I/Apo B elevated by 14.2%, 21.9% and 64.5% respectively. For lowering TC, LDL-C, Apo B and elevating Apo A-I/Apo B, Simvastatin was better than gemfibrozil (P < 0.01-0.001). However, for lowering TG, gemfibrozil was better than simvastatin (P < 0.001). As for increasing HDL-C and Apo A-I, no significant differences were found between the two groups. No significant side effects were found in all patients but one who developed hypersensitive eruption after gemfibrozil taken, and he was excluded from the trial.

Adult↗
PubMed1993

The effect of simvastatin on dyslipemia in continuous ambulatory peritoneal dialysis patients.

The efficacy of simvastatin, an inhibitor of HMG-CoA reductase, was evaluated in 14 nondiabetic hypercholesterolemic continuous ambulatory peritoneal dialysis (CAPD) patients with or without hypertriglyceridemia. Following a hypolipemic diet for 6 weeks, simvastatin was administered at a dose of 10 mg/day for 6 months. After 6 weeks on simvastatin, cholesterol was reduced by 22% (p < 0.001), triglycerides by 24% (p < 0.001), low-density lipoprotein (LDL) by 27% (p < 0.001), while high-density lipoprotein (HDL) increased by 18% (p < 0.005). These changes remained steady for 6 months. Apolipoprotein-B (Apo-B) was reduced by 17.8% (p < 0.0001), while Apo-A was stable. There were no liver function abnormalities observed. In 3 patients serum creatinine kinase (CK) was increased, and in 2 treatment was stopped. No new lens opacities or other side effects were detected. Simvastatin seems to be an effective and relatively well-tolerated drug for dyslipemias in CAPD.

Adult↗
PubMed1993

[Effectiveness and tolerability of simvastatin in subjects with primary hypercholesterolemia. Multicenter study].

The efficacy and safety of simvastatin were evaluated in an open multicenter study over a 24-week period. One hundred seventy-two patients (91 men, 81 women) with primary hypercholesterolemia (mostly polygenic) were enrolled in 14 Centers in Northern Italy. The mean age was 55.8 +/- 9.7 years and the mean baseline total cholesterol level was 305 +/- 59 mg/dL. After 4 weeks on an AHA step 1 diet, patients who met the inclusion criterion (total cholesterol > or = 250 mg/dL) were given simvastatin 10 or 20 mg in the evening. The dose could be titrated up to a maximum of 40 mg o.d. at week 6 and 12. No dose titration was allowed after week 12. One hundred forty-nine patients (86.6%) completed the study according to the protocol, 2 (1.2%) were withdrawn from the study because of adverse events not related to the drug, 21 (12.2%) were unavailable for follow-up. Simvastatin treatment was associated with a sustained dose-related reduction in total and LDL cholesterol (-28% and -39% respectively at the end of the study). Triglycerides showed a significant descending trend (-16% at week 24) and HDL-C increased by 9%. Apolipoproteins were measured in only 25 patients: apo B was reduced by 30% and apo A1 increased by 9%. Clinical side effects were not relevant. Mean levels of GOT, GPT and CPK significantly increased after 6 weeks on simvastatin, but remained stable and at any rate ioitlin the normal range thereafter. Eight patients (5.4%) experienced small transaminase level elevations (< 3ULN) and six (4%) small CPK elevations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗