Dovepress Atherogenic dyslipidemia and diabetes mellitus 36 48 27 22 11 16 23 43 55 13 25 19 21 Intervention CVD outcome RRR diabetes % Atorvastatin 10 mg Acute coronary events Simvastatin 40 mg Pravastatin 10 mg Atorvastatin 10 mg Simvastatin 10–40 mg Pravastatin 40 mg Pravastatin 40 mg CVA Major CHD event Any major CV Event Major CHD event Major CHD event Total CV events and procedures Total mortality Major CHD event Major CHD event Expanded endpoint Major CHD event Any CV event Study CARDS Primary prevention Primary and secondary prevention HPS ALLHAT ASCOT-LLA Secondary prevention 4S CARE LIPID Figure 1 effect of primary and secondary interventions for type 2 diabetics on CVD outcome. Notes: Copyright © 2006. American Diabetes Association. All rights reserved. Modified with permission from The American Diabetes Association from Solano MP, Goldberg RB. Lipid management from type 2 diabetes. Clin Diabetes. 2006;24(1):27–32. Abbreviations: 4S, Scandinavian Simvastatin Survival Study; ALLHAT, Antihypertensive and Lipid-Lowering Treatment to prevent Heart Attack Trial; ASCOT-LLA, Anglo- Scandinavian Cardiac Outcome Trial – Lipid Lowering Arm; RRR, relative risk reduction; CARDS, Collaborative Atorvastatin Diabetes Study; CARe, Cholesterol And Recurrent events; CHD, coronary heart disease; CV, cardiovascular; CVA, cerebrovascular accident; LiPiD, Long-Term intervention with Pravastatin in ischemic Disease. are LDL-C ,100 mg/dL for those without overt CVD, and LDL-C ,70 mg/dL for those with overt CVD.6,21 Non-HDL-C (calculated as total cholesterol – HDL cholesterol) is a secondary target for therapy in the NCEP-ATP III recommendations. The ADA and the American College of Cardiology recommend that non-HDL-C target goals for diabetics with overt CVD should be ,130 mg/dL and apolipoprotein-B ,80 mg/dL. Those diabetics without overt CVD are recommended to have non-HDL-C ,130 mg/dL and apolipoprotein-B ,90 mg/dL.22 This is due to the fact that LDL-C is not usually raised in diabetics, thus leaving the components that make up non-HDL-C, especially in the presence of hypertriglyceridemia, more representative and a more reliable measure of atherogenicity, such that there is discussion to advance non-HDL-C as a better predictor of CVD in diabetics.6,23,35 Reaching both these current LDL-C and non-HDL-C targets raises the issues of dosage requirements for Vascular Health and Risk Management 2010:6 lipid-lowering drugs, patient tolerability, and side effects either as single or combination treatment.24–26 Regardless, in the event that a single statin even at maximal dose is unable to achieve recommended goals, an alternative therapeutic goal is to lower LDL-C by approximately 30%–40% of the baseline value. Should that prove unattainable, consideration should be given to treatment with a combination of medica- tion classes (ie, statin + fibrate).6,21 As aforementioned, should the patient also be at high risk for developing vascular events, starting an HMG-CoA reductase inhibitor is beneficial, whilst considering the risks and side effects. Another avenue of diabetic lipid management involves the emerging science behind combining pharmacology and gene regulation. Newer findings Researchers studying adipose tissue as an endocrine organ have identified a number of lipid metabolism regulators. The peroxisome proliferator-activated receptor (PPAR) is a submit your manuscript | www.dovepress.com Dovepress 667