Also, there is a need to consider how to disseminate and implement the guideline effectively using additional materials such as a quick reference guide, educational tools and patient leaflets. These factors are important but often ignored by guideline developers. Studies on the effectiveness of clinical guideline implementation strategies showed that successful guideline implementation strategies LY2157299 should be multifaceted, and actively engage clinicians throughout the process. Thus, future guidelines should pay more attention to the implementation process of guidelines. Myocardial infarction remains the leading cause of death and disability worldwide, accounting for up to 40% of all deaths. Due to high mortality and disability rates, MI is becoming a global epidemiological health concern. Rupturing of coronary atherosclerotic plaque with consequent platelet aggregation and thrombus formation is the major cause of MI. Many intrinsic and extrinsic risk factors for MI have been established, including dyslipidemia, hypertension, smoking, obesity, etc.. Atherogenic dyslipidemia is usually characterized by three lipid abnormalities: increases in plasma triglyceride, small low density cholesterol and very low density lipoprotein cholesterol levels, and decreased high-density lipoprotein cholesterol levels. Although the exact cellular and molecular mechanisms leading to the development of MI remain unclear, it is believed that functionally relevant mutations in the dyslipidemia-related genes may contribute to increased susceptibility to MI. Cholesteryl ester transfer protein is a plasma protein that mediates the exchange of neutral lipids, including cholesteryl esters and triglycerides between plasma lipoproteins. CETP plays a critical role in reverse cholesteryl transport of cholesteryl esters and triglycerides from HDL-C to LDL-C and VLDL-C. It is well established that HDL-C has a protective role against cardiovascular disease. Plasma HDL particles play an important role in removing cellular cholesterol and delivering it to the liver for re-utilization. Furthermore, it should be noted that levels of HDL-C is significantly negatively correlated with arterial stenosis whose occurrence is strongly associated with the phenomenon of plaque rupture. Thus higher levels of HDL-C tend to have fewer problems with cardiovascular diseases such as MI, while those with low HDL-C cholesterol levels may easily suffer from MI. Variation in CETP activity could influence HDL-C levels and thus contribute to increased susceptibility to cardiovascular disease such as MI. Genetic and epigenetic changes in the CETP gene may enhance plasma cholesteryl ester formation and lead to low HDL-C levels and thereby possibly explain the inter-individual differences in MI risk. CETP, a hydrophobic glycoprotein secreted mainly by the liver, catalyzes the transfer of cholesteryl esters from HDL to other lipoproteins and influences plasma HDL-C levels. Previous studies have demonstrated a protective effect of HDL-C against cardiovascular disease by inhibiting lipoprotein oxidation.