cerivastatin and Coronary-Disease

Topics: Apolipoprotein E4; Apolipoproteins E; Cholesterol; Coronary Disease; Dose-Response Relationship, Drug; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypolipidemic Agents; Patient Compliance; Pyridines; Simvastatin; Time Factors; Treatment Outcome; United States

Five years ago, many critics questioned the value of lipid-lowering therapy. Today, the clinical benefits of statins are well documented, but the challenge remains to fully implement these benefits across the wide spectrum of the at-risk population, and continue to advance our understanding regarding the potential for the benefits of statins across an even broader range of select patient populations.

Topics: Atorvastatin; Clinical Trials as Topic; Coronary Disease; Drug Therapy, Combination; Fatty Acids, Monounsaturated; Fluvastatin; Heptanoic Acids; Humans; Hypolipidemic Agents; Indoles; Lovastatin; Pravastatin; Pyridines; Pyrroles; Simvastatin

Primary and secondary prevention trials have shown that use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (also known as statins) to lower an elevated low-density lipoprotein cholesterol level can substantially reduce coronary events and death from coronary heart disease. In 1987 and 1993, the National Cholesterol Education Program promulgated guidelines for cholesterol screening and treatment. Thus far, however, primary care physicians have inadequately adopted these guidelines in clinical practice. A 1991 study found that cholesterol screening was performed in only 23 percent of patients. Consequently, many patients with elevated low-density lipoprotein levels and a high risk of primary or recurrent ischemic events remain unidentified and untreated. A study published in 1998 found that fewer than 15 percent of patients with known coronary heart disease have low-density lipoprotein levels at the recommended level of below 100 mg per dL (2.60 mmol per L). By identifying patients with elevated low-density lipoprotein levels and instituting appropriate lipid-lowering therapy, family physicians could help prevent cardiovascular events and death in many of their patients.

Topics: Atorvastatin; Cholesterol, LDL; Coronary Disease; Fatty Acids, Monounsaturated; Fluvastatin; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Indoles; Lovastatin; Pravastatin; Pyridines; Pyrroles; Risk Factors; Simvastatin

In England, only 30% of patients with established coronary heart disease (CHD) and raised serum lipids, and fewer than 4% of individuals eligible for primary prevention, receive lipid-lowering therapy. Target total cholesterol concentrations are achieved in fewer than 50% of patients who do receive such treatment. Here, we review the use of statin therapy in the prevention of CHD events.

Topics: Anticholesteremic Agents; Atorvastatin; Coronary Disease; Drug Interactions; Fatty Acids, Monounsaturated; Fluvastatin; Heptanoic Acids; Humans; Hyperlipidemias; Indoles; Patient Selection; Pravastatin; Pyridines; Pyrroles; Risk Factors; Simvastatin; Treatment Outcome

Topics: Arteriosclerosis; Coronary Disease; Diabetes Complications; Diabetes Mellitus; Endothelium, Vascular; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Lipids; Pyridines; Randomized Controlled Trials as Topic

The triglyceride (TG) level is one of several lipid parameters that can aid prediction of coronary heart disease (CHD) risk. An elevated plasma TG level is strongly associated with an increased risk of CHD. Hypertriglyceridemia, the second most common dyslipidemic abnormality in hypertensive subjects after increased low-density lipoprotein cholesterol (LDL-C), is defined by the National Cholesterol Education Programme (NCEP) as a fasting TG level of > 2.26 mmol/l (> 200 mg/dl) and is recognised as a primary indicator for treatment in type IIb dyslipidemia. Raised TG levels can be present in individuals at risk for CHD when the total cholesterol is normal. However, not all individuals with raised TG levels have increased risk of CHD. Factors such as: diet, age, lifestyle, and a range of medical conditions, drug therapy and metabolic disorders, can all affect the TG level. In some of these circumstances, other factors protect against the risk of CHD, and can minimise or negate the effect of the risk factors present. Although TG reducing therapy has been shown to be associated with an improved clinical outcome, more research is needed to determine whether this is an independent effect of TG reduction or an effect of normalising the overall lipid profile in hypertriglyceridemic patients. Further trials are required to quantify the clinical benefits of lowering TG to 'target' levels and to confirm targets defined by NCEP-II (shown in Table 1). The role of TG in CHD pathogenesis is thought to involve several direct and indirect mechanisms, such as effects on the metabolism of other lipoproteins, transport proteins, enzymes, and on coagulation and endothelial dysfunction. More research is required to fully elucidate the role of TG, the ways in which it can influence other risk factors and the mechanism of its own more direct role in the atherogenic process. Patients with hypertriglyceridemia have been shown to respond well to dietary control and to the use of lipid lowering drugs such as 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG CoA) reductase inhibitors (known as statins), fibrates and nicotinic acids. However, recent retrospective real-life clinical studies show that only 38% of patients receiving some form of lipid-lowering therapy achieved NCEP-defined LDL-C target levels, demonstrating the need for the use of more aggressive treatment. In hypertriglyceridemic patients, the newer statins, cerivastatin and atorvastatin, have shown comparable efficacy in redu

Topics: Atorvastatin; Coronary Disease; Drug Therapy, Combination; Gemfibrozil; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertriglyceridemia; Hypolipidemic Agents; Niacin; Pyridines; Pyrroles; Risk Factors; Triglycerides

Hyperlipidemia is recognized as one of the major risk factors for the development of coronary artery disease and progression of atherosclerotic lesions. Dietary therapy together with hypolipidemic drugs are central to the management of hyperlipidemia, which aims to prevent atherosclerotic plaque progression, induce regression, and so decrease the risk of acute coronary events in patients with pre-existing coronary or peripheral vascular disease. In patients at high risk of coronary artery disease but without evidence of atherosclerosis, treatment is designed to prevent the premature development of coronary artery disease, whereas in those with hypertriglyceridemia, treatment aims to prevent the development of hepatomegaly, splenomegaly, and pancreatitis. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, are the most potent lipid-lowering agents currently available, and their use in the treatment of hyperlipidemia provides the focus for this review. Particular emphasis is given to cerivastatin, a new HMG-CoA reductase inhibitor that combines potent cholesterol-lowering properties with significant triglyceride-reducing effects. Recently completed primary and secondary intervention trials have shown that the significant reductions in low-density lipoprotein (LDL) cholesterol achieved with statins result in significant reductions in morbidity and mortality associated with coronary artery disease as well as reductions in the incidence of stroke and total mortality. Such benefits occur early in the course of statin therapy and have led to suggestions that these drugs may possess antiatherogenic effects over and above their capacity to lower atherogenic lipids and lipoproteins. Experimental studies have also shown statin-induced improvements in endothelial function, decreased platelet thrombus formation, improvements in fibrinolytic activity, and reductions in the frequency of transient myocardial ischemia.

Topics: Coronary Disease; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hyperlipidemias; Hypolipidemic Agents; Lovastatin; Pyridines; Safety; Simvastatin; Treatment Outcome

The effects of cerivastatin on antiatherogenic properties of high-density lipoproteins were studied in patients with coronary heart disease and hyperlipidemia. Apart from hypolipidemic effects, cerivastatin changed the phospholipid composition of high-density lipoproteins and improved their cholesterol-acceptor properties. This effect was most pronounced in the serum from patients with low content of high-density lipoprotein cholesterol. These data indicate that cerivastatin modulates antiatherogenic properties of high-density lipoproteins.

Topics: Adult; Aged; Arteriosclerosis; Cholesterol; Coronary Disease; Double-Blind Method; Humans; Hyperlipidemias; Lipoproteins, HDL; Male; Middle Aged; Phospholipids; Pyridines

The prevalence of coronary heart disease (CHD) is markedly increased in diabetic patients compared with non-diabetic individuals, and its prognosis is less good. Serum total and low-density lipoprotein (LDL) cholesterol concentrations have been shown to be powerful predictors of CHD morbidity and mortality in patients with type 2 diabetes. The available data suggest that the target cholesterol concentration in patients with diabetes should be similar to that in non-diabetic individuals with a previous myocardial infarction. This led us to investigate the efficacy, tolerability and safety of a new, highly potent statin, cerivastatin, in diabetic hyperlipidaemia.. This was a multinational, multicentre, double-blind, randomized study in type 2 diabetic patients with hypercholesterolaemia (LDL cholesterol >3.35 mmol/l; triglycerides <4.56 mmol/l). Eligible patients were randomly assigned to groups to receive cerivastatin 0.1 mg or 0.3 mg or placebo in a ratio of 2:2:1 for 12 weeks. They were monitored in the clinic every 4 weeks.. Of the 453 patients screened, 265 were allocated to the study groups. Fifty-one received placebo and 107 patients were assigned to each active treatment group (0.1 mg and 0.3 mg cerivastatin). At the close of the study, total cholesterol had decreased by 13.7% and 23.5%, LDL cholesterol decreased by 20.2% and 33.8%, and triglyceride concentrations decreased by 3.9% and 12.3% in the cerivastatin 0.1 mg and 0.3 mg groups, respectively. There was no significant difference between the groups in haemoglobin A1c, adverse events or increases in liver and muscle enzymes during the study period.. Hypercholesterolaemic patients with type 2 diabetes had a significant reduction in LDL cholesterol and total cholesterol concentrations after cerivastatin treatment once daily. The dose of 0.3 mg cerivastatin is effective in diabetic hypercholesterolaemia, with co-reduction of triglyceride concentrations. The effect of cerivastatin on coronary morbidity and mortality is currently being investigated in clinical trials.

Topics: Adult; Aged; Aged, 80 and over; Chi-Square Distribution; Coronary Disease; Diabetes Mellitus, Type 2; Double-Blind Method; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Hypertriglyceridemia; Male; Middle Aged; Pyridines; Risk Factors

It has been suggested that the apolipoprotein E (APOE) genotype modifies the effect of dietary and pharmacological interventions for lowering lipid levels. We wanted to determine whether APOE genotyping information would be useful in making lipid-lowering treatment decisions in clinical practice. We included 981 patients with coronary heart disease (CHD) enrolled in an inpatient 3-week standardized rehabilitation program. Of these, 555 (57%) patients received continued statin therapy and 232 (24%) patients received newly initiated statin therapy. Dietary intervention was part of the program only for 194 (20%) patients. Total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC) levels decreased in all the groups of patients during rehabilitation. The decreases were less pronounced among the APOE E2 carriers. However, the observed variation among the groups with respect to reduction of lipid levels was accounted for mainly by the initial lipid levels (30-47%) and only marginally on the APOE genotype (1%) . We therefore found no evidence that APOE genotyping will be useful in guiding dietary or pharmacological lipid-lowering treatment decisions.

Topics: Adult; Aged; Alleles; Apolipoprotein E2; Apolipoprotein E3; Apolipoprotein E4; Apolipoproteins E; Atorvastatin; Cholesterol, HDL; Cholesterol, LDL; Coronary Disease; Decision Making; Fatty Acids, Monounsaturated; Female; Fluvastatin; Genotype; Germany; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Indoles; Inpatients; Linear Models; Lovastatin; Male; Middle Aged; Multivariate Analysis; Pravastatin; Predictive Value of Tests; Pyridines; Pyrroles; Simvastatin; Triglycerides

Pulsatile forces regulate vascular remodeling and trigger vascular diseases such as saphenous vein graft disease. The saphenous vein is exposed to high pressure and pulsatility only after implantation. Statins have been proved to reduce the incidence of vein graft failure. Thus, we investigated the molecular mechanisms of pulsatile stretch-induced saphenous vein smooth muscle cell (SMC) proliferation and potential beneficial effects of statins.. Human saphenous vein SMCs were subjected to cyclic stretch (60 cycles/min) in Flex I plates. Cerivastatin and simvastatin significantly prevented stretch-induced increase in SMC proliferation. Stretch induced the membrane accumulation of Rho A and Rho kinase inhibitors (Y-27632 and hydroxyfasudil) and dominant negative Rho A mutant significantly prevented stretch-induced SMC proliferation. In addition, stretch increased the levels of both p44/42 mitogen-activated protein (MAP) kinase and Akt phosphorylation. MAP kinase kinase (MEK)1/2 inhibitor U0126, phosphatidylinositol (PI) 3-kinase inhibitors (wortmannin and LY294002), and dominant negative Akt mutant significantly prevented stretch-induced SMC proliferation. Cerivastatin significantly prevented stretch-induced membrane accumulation of Rho A. On the other hand, stretch-induced phosphorylation of p44/42 MAP kinase and Akt was not prevented by cerivastatin. Mevalonate restored the preventive effect of cerivasatain on stretch-induced Rho A membrane accumulation. Stretch induced hyperphosphorylation of retinoblastoma protein (pRb), which was prevented by cerivastatin and the Rho kinase inhibitors.. Statins prevent stretch-induced saphenous vein SMC proliferation via inhibition of the Rho/Rho-kinase pathway. This may explain the beneficial effects of this class of drug, especially for patients after coronary artery bypass grafting.

Topics: Blotting, Western; Cell Fractionation; Cell Membrane; Cell Proliferation; Cells, Cultured; Coronary Disease; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Intracellular Signaling Peptides and Proteins; Mitogen-Activated Protein Kinase 1; Muscle, Smooth, Vascular; Phosphorylation; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Pyridines; rho GTP-Binding Proteins; rho-Associated Kinases; Saphenous Vein; Signal Transduction; Stress, Mechanical

Therapeutic strategies to provide local inhibition of mitogen mediated proliferation and migration of human coronary artery smooth muscle cells (CASMC) by means of drug-eluting stents have been shown to enable effective limitation of neointimal hyperplasia. However, currently available drug-eluting stents utilize compounds that may also adversely affect endothelial regrowth, thus possibly precipitating subsequent cardiac events. Accordingly, identification of compounds that differentially inhibit smooth muscle and endothelial cell migration and proliferation could be of substantial clinical usefulness.. In addition to lipid lowering, statins are known to display auxiliary pleiotropic activities. The purpose of this study was to evaluate the effect of local administration of cerivastatin on proliferation, migration and cytotoxicity of CASMC as well as coronary artery endothelial cells (CAEC) and to evaluate the effect of cerivastatin-coated stents on the inhibition of neointima formation as well as endothelial regrowth within the stented vessel. Cerivastatin displayed a differential effect on CASMC as compared to CAEC with regard to proliferation and migration; both were more profoundly inhibited in CASMC. Appreciable cytotoxicity and pro-apoptotic effects were low in both cell lines at therapeutic concentrations. Cerivastatin-elution led to significant inhibition of neointima formation in the rat carotid stent model, endothelial coverage of in-stent vascular tissue was similar with control and cerivastatin-eluting stents.. As proof of principle, our study provides evidence that local application of a HMG-CoA reductase inhibitor on a drug-eluting stent platform can efficiently limit neointima formation. Consequently, these compounds warrant further clinical evaluation to confirm this finding. Our data further suggest that the anti-restenotic effect of local statin administration might be associated with a more protective interaction with the endothelium than that observed with compounds currently employed on drug-eluting stents.

Topics: Animals; Carotid Stenosis; Cell Movement; Cell Proliferation; Cells, Cultured; Coronary Disease; Coronary Vessels; Endothelial Cells; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Models, Animal; Muscle, Smooth, Vascular; Pyridines; Rats; Stents; Tunica Intima

Although statins are reported to have a cardioprotective effect, their immediate direct influence on ischemia-reperfusion injury and the underlying mechanisms remain obscure. We investigated these issues an in vivo canine model.. Dogs were subjected to coronary occlusion (90 minutes) and reperfusion (6 hours) immediately after injection of pravastatin (0.2, 2, or 10 mg/kg), pitavastatin (0.01, 0.1, or 0.5 mg/kg), or cerivastatin (0.5, 5, or 50 microg/kg). Then myocardial phosphatidylinositol 3-kinase (PI3-K) and 5'-nucleotidase activities were measured, as well as infarct size. After 15 minutes of reperfusion, pravastatin caused dose-dependent activation of Akt and ecto-5'-nucleotidase in the ischemic zone, and the effect was significant at higher doses. Pitavastatin also significantly increased these activities, and its optimal dose was within the clinical range, whereas cerivastatin caused activation at the lowest dose tested. In all cases, both Akt and ecto-5'-nucleotidase showed activation in parallel, and this activation was completely abolished by wortmannin, a PI3-K inhibitor. The magnitude of the infarct-limiting effect paralleled the increase in Akt and ecto-5'-nucleotidase activity and was blunted by administration of wortmannin, alpha,beta-methyleneadenosine-5'-diphosphate, or 8-sulfophenyltheophylline during reperfusion. Both collateral flow and the area at risk were comparable for all groups.. Activation of ecto-5'-nucleotidase after ischemia by PI3-K activation may be crucial for immediate infarct-size limitation by statins. There seems to be an optimal dose for each statin that is independent of its clinical cholesterol-lowering effect.

Topics: 5'-Nucleotidase; Adenosine Triphosphate; Androstadienes; Animals; Cardiotonic Agents; Chromones; Coronary Disease; Dogs; Dose-Response Relationship, Drug; Enzyme Activation; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Morpholines; Myocardial Infarction; Myocardial Reperfusion Injury; Phosphatidylinositol 3-Kinases; Phosphoinositide-3 Kinase Inhibitors; Pravastatin; Pyridines; Quinolines; Signal Transduction; Theophylline; Wortmannin

Topics: Aged; Aged, 80 and over; Anticholesteremic Agents; Contraindications; Coronary Disease; Creatine Kinase; Drug Interactions; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Monitoring, Physiologic; Muscular Diseases; Pyridines; Risk Factors

Topics: Aged; Aged, 80 and over; Anticholesteremic Agents; Contraindications; Coronary Disease; Creatine Kinase; Drug Interactions; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Monitoring, Physiologic; Muscular Diseases; Pyridines; Risk Factors

Topics: Aged; Aged, 80 and over; Anticholesteremic Agents; Contraindications; Coronary Disease; Creatine Kinase; Drug Interactions; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Monitoring, Physiologic; Muscular Diseases; Pyridines; Risk Factors

An economic model was developed to estimate the relative cost-effectiveness of alternative HMG-CoA reductase inhibitors (statins)--atorvastatin, cerivastatin, fluvastatin, pravastatin and simvastatin--to achieve target low-density lipoprotein cholesterol (LDL-C) levels in a population of secondary CHD prevention patients. By using a cholesterol target as the endpoint of interest and a dose titration approach, the model assumes that the statins demonstrate a class effect through cholesterol lowering. The model was used to estimate the proportion of patients achieving target LDL-C levels (< 3 mmol/l) under each scenario tested. Total costs and incremental cost-effectiveness relative to no treatment and to the lowest cost option were estimated for each scenario. Total costs were highest for pravastatin and lowest for cerivastatin. Compared with no treatment, the incremental cost per patient treated to target LDL-C varied between 383 Pounds (atorvastatin) and 1213 Pounds (pravastatin). Incremental cost-effectiveness ratios in comparison with the lowest cost treatment (cerivastatin) were 141 Pounds per additional patient achieving target LDL-C with atorvastatin, and 275 Pounds with simvastatin. Fluvastatin and pravastatin were both less effective and more expensive than the lowest cost therapy. Although cerivastatin was associated with lowest expected costs, therapy with atorvastatin achieved the lowest cost-effectiveness ratios. Hence atorvastatin would allow the largest number of patients to be treated to target LDL-C within a fixed drug budget. Choosing between drug therapies on the basis of price alone may be misleading if the effectiveness of therapies varies.

Topics: Atorvastatin; Cholesterol, LDL; Coronary Disease; Cost-Benefit Analysis; Fatty Acids, Monounsaturated; Fluvastatin; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Indoles; Models, Economic; Pravastatin; Pyridines; Pyrroles; Simvastatin

Endothelin-converting enzymes (ECEs) are the key enzymes in endothelin-1 (ET-1) generation. However, their pathophysiological role in patients with cardiovascular disease remains elusive.. Vascular reactivity to big endothelin-1 (bigET-1; 10(-9) to 10(-7) mol/L) and ET-1 (10(-9) to 10(-7) mol/L) were examined in the internal mammary artery (IMA, n=33) and saphenous vein (SV, n=27) of patients with coronary artery disease with identified cardiovascular risk factors. Vascular ECE activity was determined by conversion of exogenously added bigET-1 to ET-1. Tissue contents of bigET-1 and ET-1 were measured by radioimmunoassay. In addition, the effects of LDL and oxidized LDL on ECE-1 protein levels were determined by Western blot analysis in human IMA endothelial cells. In the IMA, vascular ECE activity showed an inverse correlation with serum LDL levels (r=-0.76; P<0.01) and systolic and diastolic blood pressure and a positive correlation with fibrinogen (r=0.58; P<0.05). In the SV, fibrinogen was the only parameter to be correlated with vascular ECE activity. Vascular tissue content of bigET-1 was attenuated in the IMA of patients with hyperfibrinogenemia but increased in patients with elevated systolic blood pressure and increased serum LDL levels (P<0.05). Most interestingly, LDL and oxidized LDL downregulated ECE-1 protein levels in human IMA endothelial cells (P<0.05).. These data demonstrate, for the first time, that vascular ECE activity is (1) inversely correlated with serum LDL levels and blood pressure and (2) positively associated with fibrinogen in human vascular tissue. Hence, ECE-1 activity may modulate cardiovascular risk in patients with coronary artery disease.

Topics: Aspartic Acid Endopeptidases; Coronary Artery Bypass; Coronary Disease; Down-Regulation; Endothelin-Converting Enzymes; Endothelium, Vascular; Female; Humans; Lipoproteins, LDL; Male; Metalloendopeptidases; Nitric Oxide; Oxidation-Reduction; Pyridines; Risk Factors; Stereoisomerism

The incidence of coronary heart disease (CHD) is greatly increased in overweight diabetic patients. Modification of dietary intake and weight loss improve hypercholesterolaemia. However, cholesterol goal levels are not achieved in several patients under this treatment. The aim of our study was to evaluate the effect of Cerivastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, in patients with type 2 diabetes mellitus. A population of 40 diabetic type 2 outpatients were analyzed in a prospective way. The mean+/-SD age was 60.7+/-11.6 years, with a diabetes duration of 8.5+/-6.6 years. All patients were treated with cerivastatin (0.2 mg once a day) for 6 months. Weight HbAlc fasting blood glucose, urine microalbuminuria, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were measured at the beginning of the study and again after 3 and 6 months of treatment with cerivastatin. An improvement in lipid levels was achieved, with a significant decrease in LDL-cholesterol (27.7%), total cholesterol (21.4%), triglycerides levels (10.4%) and a significant increase in HDL-cholesterol levels (8.3%) (P<0.05). Cardiovascular risk ratios such as; total cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol improved during treatment, decreasing 11.3% and 30%, respectively (P<0.05). Low incidence of side effects was demonstrated. In summary, cerivastatin improved lipid control in patients with type 2 diabetes, with a low incidence of side effects.

Topics: Aged; Cholesterol; Coronary Disease; Diabetes Mellitus, Type 2; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Incidence; Male; Middle Aged; Prospective Studies; Pyridines; Treatment Outcome

Topics: Coronary Disease; Humans; Hypercholesterolemia; Hyperlipidemias; Hypolipidemic Agents; Lipoproteins, HDL; Lipoproteins, LDL; Lovastatin; Pyridines; Risk Factors