title: Treating dyslipidemia with statins: the risk-benefit profile.
abstract: BACKGROUND
  Coronary heart disease (CHD), the result of coronary atherosclerosis, is the largest single killer of Americans. Central to the pathogenesis of atherosclerosis are the deposition and retention of cholesterol in the arterial walls. Lipid modification, therefore, is key to CHD prevention.
  
  
  METHODS
  Data from trials evaluating the safety and efficacy of several pharmacologic agents for dyslipidemia were thoroughly reviewed.
  
  
  RESULTS
  Agents such as bile acid sequestrants, fibric acids, and nicotinic acid have a role in treating dyslipidemia. However, statins are the safest and most effective of the lipid-modifying drugs, reducing the incidence of CHD by as much as 21% to 43%. Despite the overall safety and efficacy of these agents, many patients undergoing statin therapy fail to achieve the treatment goals specified in the National Cholesterol Education Program Adult Treatment Panel III guidelines, often because of suboptimal use, tolerability problems, or lack of compliance. Although adverse effects of statins are generally mild and transient, more serious adverse effects, including myotoxicity, liver toxicity, and rhabdomyolysis, are still possible with statin monotherapy and are more common in patients receiving concomitant therapy with other drugs metabolized by the cytochrome P-450 enzyme system.
  
  
  CONCLUSIONS
  Because of the overall safety and efficacy of the statins, more patients with or at risk for CHD should be receiving aggressive therapy to lower low-density lipoprotein cholesterol levels and reduce CHD risk.
authors.affiliation: Division of Cardiovascular Medicine, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA. ltclark@downstate.edu
authors.forename: Luther T
authors.initials: LT
authors.lastname: Clark
mesh_terms: D000069059:Atorvastatin; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D003327:Coronary Disease / Q000453:epidemiology / Q000401:mortality / Q000517:prevention & control*; D004347:Drug Interactions; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology; D000077340:Fluvastatin; D006538:Heptanoic Acids / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology; D007211:Indoles / Q000494:pharmacology; D008148:Lovastatin / Q000494:pharmacology / Q000627:therapeutic use; D017035:Pravastatin / Q000494:pharmacology / Q000627:therapeutic use; D011758:Pyrroles / Q000494:pharmacology / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D018570:Risk Assessment; D019821:Simvastatin / Q000494:pharmacology / Q000627:therapeutic use; D020521:Stroke / Q000453:epidemiology / Q000401:mortality / Q000517:prevention & control; D014280:Triglycerides / Q000097:blood; D014481:United States / Q000453:epidemiology
chemical_list: D008076:Cholesterol, HDL; D005229:Fatty Acids, Monounsaturated; D006538:Heptanoic Acids; D007211:Indoles; D011758:Pyrroles; D014280:Triglycerides; D000077340:Fluvastatin; D002784:Cholesterol; D008148:Lovastatin; D000069059:Atorvastatin; D019821:Simvastatin; D017035:Pravastatin