It has been demonstrate that atorvastatin 20 mg/d treatment for 8 weeks could result in a favorable modification of HDL subfraction phenotype. Treated with atorvastatin 20mg/d significantly increased the cholesterol concentration of large HDL particles and decreased the cholesterol concentration of small HDL particles although without changes of serum HDL-C level in patients with atherosclerosis. However, there are still lack of evidence on the effect of rosuvastatin treatment for HDL maturation(for the step of transformation of HDL3 to HDL2)and RCT process in CAD and Chinese patients. It has been demonstrated that Low HDL cholesterol is frequently associated with low HDL2b and high HDL cholesterol frequently associated with high HDL2b. As the investigators discussed above, compared to atorvastatin, rosuvastatin could significantly decrease LDL-C level and increase HDL-C level from baseline. So besides the basic effect of lowing LDL-C, it has a strong possibility that rosuvastatin therapy on CAD patients with hyperlipidemia could reverse the aberrant HDL maturation process via elevating lager HDL2 level, and then restore the RCT process to the normal to prevent atherosclerosis.