What is the most effective strategy for managing diabetic dyslipidaemia?
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.
Reasner
Charles A
CA
University of Texas Health Science Center, Department of Medicine/Endocrinology, San Antonio, TX 78284-7877, USA. charles.reasner@uhs-sa.com
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
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D014280:Triglycerides; D009525:Niacin