Plasma cholesterol levels are an important predictor of the risk of coronary heart disease, and elevated plasma cholesterol is associated with increased morbidity and mortality from coronary heart disease. Lowering cholesterol levels may reduce the incidence of coronary events. Over the past 50 years, several drugs representing different lipid-lowering therapeutic strategies have been developed; niacin became the first lipid-lowering drug in 1955; bile acid chelators were introduced in 1961; and fibrates were introduced in 1967. However, the clinical use of these drugs was not satisfactory because of their high side effects or low cost-effectiveness ratio. It was not until 1987 that statins, which represented a new development in the treatment of hyperlipidemia, were introduced and began to be widely used in clinical treatment. However, according to the results of the second study on the status of lipid treatment in China (25 tertiary hospitals nationwide from 2005 to 2007), among patients with coronary heart disease treated with statins, the proportions of high-risk patients with LDL-C <100 mg/dl and very high-risk patients with LDL-C <70 mg/dl who met the treatment target were 39% and 23%, respectively. As evidence-based medicine continues to accumulate, the NCEP ATP III guidelines for LDL-C treatment targets are moving in the direction of "lower is better". However, the majority of patients treated with statins fail to meet LDL-C treatment goals, so why? Statins mainly inhibit hepatic cholesterol synthesis, and their efficacy is dose-dependent, so to enhance LDL-C reduction, the dose of statin therapy needs to be increased. However, there is a "rule of six" for any statin, that is, doubling the dose of the drug only further reduces LDL-C by about 6%. In other words, the further therapeutic effect of doubling the dose of a statin after the initial dose is relatively small. Not only that, but the risk of adverse effects rises with increasing statin doses, with high-dose statin therapy causing liver enzyme levels to exceed the upper limit of normal by more than three times in a significant number of patients. For example, when the dose of atorvastatin was increased from 40 mg to 80 mg, the percentage of patients with elevated transaminase levels increased from 0.6% to 2.3%. Ezetimibe, a cholesterol absorption inhibitor class of lipid-lowering drugs, is distributed in the brush border of the small intestine, inhibits NPC1L1, and prevents cholesterol absorption from the intestinal lumen into the cells of the small intestine. Its mechanism of action is complementary to that of statins. The combination of ezetimibe and statins inhibits both sources of cholesterol absorption and synthesis, resulting in a potent cholesterol-lowering effect. Studies have shown that the combination further reduces LDL-C levels by 18% to 24% compared to statins alone. In patients with critical conditions such as coronary artery disease, ezetimibe in combination with statin therapy achieved LDL-C compliance rates of nearly 70%, compared to 17% in patients treated with statin alone. Indications for ezetimibe in combination with statin therapy: patients who cannot achieve the target with standard dose statin therapy, especially high-risk/very high-risk patients; patients who cannot tolerate or can only tolerate small dose statin therapy, such as the presence of ALT elevation, myositis, myopathy, etc.; patients with special populations, such as patients with familial hypercholesterolemia and patients with pure congenital glutathionemia.