title: What is the most effective strategy for managing diabetic dyslipidaemia?
abstract: The dyslipidaemic profile of diabetes greatly contributes to the increased cardiovascular risk associated with the disorder, and evidence from many intervention trials using statins, fibrates, nicotinic acid or a nicotinic acid-statin combination, indicates the substantial cardiovascular risk reduction to be gained from lipid modification. Several large statin trials have demonstrated the efficacy of cholesterol-lowering in individuals with coronary heart disease and raised low-density lipoprotein-cholesterol (LDL-C) (>or=130 mg/dL; >or=3.4 mmol/L), but for the 40% of patients whose LDL-C is within recommended limits, many of whom have low high-density lipoprotein-cholesterol (HDL-C), an alternative strategy is necessary if excess risk is to be minimized. The veterans affairs high-density lipoprotein cholesterol intervention trial (VA-HIT) proved the efficacy of the fibric acid derivative, gemfibrozil, to elevate HDL-C and reduce triglycerides, with a resulting 22% relative risk reduction for cardiovascular death or non-fatal myocardial infarction, and even greater reductions in individuals with insulin resistance and diabetes. Increased HDL-C was independently predictive of reduction in coronary heart disease. In the Coronary Drug Project, individuals with diabetes or insulin resistance derived as much as 70% cardiovascular risk reduction from the HDL-C elevations achieved with nicotinic acid therapy. The effects of lowering LDL-C and raising HDL-C are additive and predictive of total cardiovascular event reduction, and by using statin-nicotinic acid combination therapy, cardiovascular risk reductions as great as 90% are possible. Such combination strategies offer patients the greatest opportunity for improved cardiovascular health and are likely to become the treatment strategy of the future.
authors.affiliation: University of Texas Health Science Center, Department of Medicine/Endocrinology, San Antonio, TX 78284-7877, USA. charles.reasner@uhs-sa.com
authors.forename: Charles A
authors.initials: CA
authors.lastname: Reasner
mesh_terms: D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy; D003920:Diabetes Mellitus / Q000097:blood* / Q000453:epidemiology; D003925:Diabetic Angiopathies / Q000097:blood / Q000188:drug therapy; D004359:Drug Therapy, Combination; D050171:Dyslipidemias / Q000453:epidemiology / Q000628:therapy*; D006331:Heart Diseases / Q000097:blood / Q000188:drug therapy; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007333:Insulin Resistance; D024821:Metabolic Syndrome / Q000097:blood / Q000503:physiopathology; D009525:Niacin / Q000627:therapeutic use; D009765:Obesity / Q000097:blood / Q000503:physiopathology; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D014280:Triglycerides; D009525:Niacin