In type 2 diabetes in order to effectively prevent and treat cardiovascular disease, lipid-lowering therapy should be aggressively and comprehensively pursued. The American Diabetes Association (ADA) 2004 guidelines for the treatment of type 2 diabetes suggest that lowering LDL-C is the primary goal for reducing cardiovascular disease risk in type 2 diabetes, with a treatment goal of LDL-C <100 mg/dl (2.6 mmol/L), and for those older than 40 years of age, regardless of their baseline levels, the application of statins is encouraged to reduce LDL-C by 30 percent or more. Among them, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome C P450 3A4, while pravastatin, fluvastatin and risuvastatin are not, so the latter three have relatively few interactions with other drugs. Choosing the appropriate statin for a diabetic patient among the many statins available remains one of the numerous challenges facing clinicians. The 2004 Atorvastatin Collaborative Diabetes Study (CARDS) was the first prospective study designed to evaluate the primary prevention of major cardiovascular events in patients with type 2 diabetes alone. 80 mg treatment resulted in a 37% reduction in the primary endpoint event, a 32% reduction in all cardiovascular events, and a 27% reduction in all-cause mortality, suggesting that statin therapy is beneficial for the primary prevention of cardiovascular disease in patients with diabetes. CARDS further supports the need for earlier lipid-modifying therapy in patients with diabetes. In the Treat to New Target (TNT) trial, 10001 patients with stable coronary artery disease, serum LDL-C <2.59 mmol/L (100 mg/dl). Randomization to atorvastatin 10 mg/d or 80 mg/d treatment groups resulted in a 22% reduction in the relative risk of major cardiovascular events in the high-dose group (P<0.0001). The findings suggest that in patients with stable coronary artery disease, lowering LDL-C to 1.81 mmol/L (70 mg/dl) can further reduce the risk of cardiovascular events. The Incremental Decrease in Endpoints Through Aggressive Lipid lowering trial (IDEAL) also confirmed these findings. In the Atorvastatin versus Simvastatin Effects on Atherosclerosis Process Study (ASAP) and the Angiobiology of Cholesterol-Lowering Therapy Study (ARBITER), a reversal of atherosclerosis was found in high-risk patients taking atorvastatin 80 mg compared to patients taking other statins by measuring changes in carotid intima-media thickness (cIMT). In the Intensive Lipid Lowering Treatment Reversal of Atherosclerosis Study (REVERSAL), using intravascular ultrasound (IVUS) as a test, the results suggested that atorvastatin blocked plaque progression compared with pravastatin; also, there was a significant reduction in plaque volume in the most severely diseased segments in all patients in the atorvastatin group. The Nordic Simvastatin Survival Study (4S) showed a 55% reduction in coronary events in 202 diabetic patients treated with simvastatin (P=0.002). TC, LDL-C and TG decreased by a mean of 25%, 35% and 10%, respectively, and HDL-C increased by 8%. The heart protection study (HPS) enrolled 29% of the 5,963 diabetic patients (mainly type 2 diabetes) and reduced the risk of coronary events by 33% with simvastatin in the primary prevention study (P = 0.0003) and by 18% in the secondary prevention study (P = 0.002). mmol/L, between 2.6 and 3.4 mmol/L, or above 3.4 mmol/L, patients benefited from lipid-lowering therapy. The results of the SILHOUETTE study showed that HDL-C levels increased with increasing doses of simvastatin (from 40 mg to 80 mg), and in particular that it was effective in elevating HDL2, which has a better cardiovascular protective effect. Simvastatin was more effective than atorvastatin in elevating HDL-C: several clinical trials confirmed that 20 mg, 40 mg and 80 mg Simvastatin lowered LDL-C similarly to 10 mg, 20 mg and 40 mg atorvastatin, respectively. In contrast, the LDL-C equivalent doses of the two statins differed significantly in terms of raising HDL-C and ApoA1, with simvastatin significantly outperforming atorvastatin. In particular, high-dose atorvastatin had a much weaker effect on raising HDL-C and lowered ApoA1 rather than raising it. The STELLAR study, published in 2003 in the American Journal of Cardiology (Am J Cardiol), compared the efficacy of different doses of risuvastatin, simvastatin, atorvastatin, and pravastatin in lowering LDL-C. 2431 patients with hypercholesterolemia (LDL-C ≥160 mg/dl and <250 mg/dl; triglycerides <400 mg/dl) Adult patients were randomized to receive treatment with resulvastatin, atorvastatin, simvastatin (10, 20, 40, or 80 mg), and pravastatin (10, 20, 40 mg). After 6 weeks of treatment, the LDL-C-lowering effect of rosuvastatin 10 to 80 mg was shown to be significantly higher than that of other statins (P<0.001). This study showed that each dose of resulvastatin had a greater advantage in lowering LDL-C compared with atorvastatin, simvastatin, and pravastatin, resulting in a higher proportion of patients meeting the LDL-C control goals of the NCEP ATP III and European treatment guidelines. In addition, resulvastatin increased HDL-C in patients by an average of 7.7 to 9.6 percent, compared with an average increase of 2.1 to 6.8 percent in the other groups. This potent reduction in LDL-C and strong increase in HDL-C has led to a meaningful impact of resulvastatin in the treatment of atherosclerosis, as confirmed by the ASTEROID study published in ACC in 2006. In summary, it may be reasonable to prefer atorvastatin and resuvastatin in the presence of dyslipidemia and severe stenosis due to plaque in type 2 diabetic patients without low HDL-C, and to prefer simvastatin and resuvastatin in the presence of high LDL-C with low HDL-C in type 2 diabetic patients.