Editorial

Statins lower low density lipoprotein-cholesterol (LDL-C) level by inhibiting 3-hydroxy-methylglutaryl coenzyme A (HMG-CoA) reduc-tase. A meta-analysis of the primary and secondary prevention trials of statin therapy demonstrated the reduction of major coronary ev-ents, coronary revascularization, and stroke by 20 % per 1 mmol/L (39 mg/dL) reduction in LDL-C levels,1) and a linear relationship was sh-own between the cardiovascular event (coronary death or non-fatal myocardial infarction) rates and LDL-C level, during statin therapy in secondary prevention studies.2) It has been known for many years that atherosclerosis may be an inflammatory disease. The evolution of the atherosclerotic plaque is closely related to the inflammatory processes, such as the recruit-ment of inflammatory monocytes into the vascular wall, the trans-formation of monocytes into macrophages and foam cells, the re-lease of multiple cytokines and growth factors attracting vascular smooth muscle cells, weakening of a fibrous cap by matrix metal-loproteinase and the rupture of plaques with thrombus formation.3) Among the markers of systemic inflammation, C-reactive protein (CRP), which are synthesized by liver under the control of inflamma-tory cytokines including interleukin (IL)-6, has been shown to best predict future cardiovascular events. In a large, long-term prospec-tive study, the odds ratio for coronary heart disease was 1.45 in peo