Background: There are a lot of evidence that vascular wall inflammation plays a key role in the pathogenesis of vascular disease and the atherosclerotic process. The inflammatory reaction involves in all steps of atherogenesis from initial monocyte/macrophage recruitment to rupture of atheromatous plaque. Statin therapy has been known to regress atherosclerosis and to stabilize the unstable plaque by anti-inflammatory action. We observed the long-term changes in inflammatory reactants such as erythrocyte sedimentation rate, C-reactive protein, white blood cell count, fibrinogen, and lipoprotein(a)[Lp(a)] in both atherosclerotic patients and controls for 10 years. Methods: From 1993 to 2003, we investigated prospective analyses of 839(M:F=439:400) consecutive patients. The patients were divided into two groups. Diseased(group I, n=396) included patients with chronic stable angina, acute coronary syndrome, cerebral infarct, and peripheral vascular disease. Controls(group II, n=443) included patients not listed in group I. In each group, they were subdivided into statin subgroup(132 patients in group I, 114 patients in group II) and non-statin subgroup. Statin therapy was started according to guidelines of the National Cholesterol Education Program. Results: One year after statin therapy, a significant reduction in total cholesterol(p<0.05), LDL cholesterol(p<0.05), triglyceride(p<0.05) was found as expected; and hypercholesterolemia was lowered to the point where significant difference(p>0.05) was not noted between statin and non-statin subgroups in each group. Lp(a) remained constant throughout statin therapy just as other acute phase reactants, and no significant difference(p>0.05) in Lp(a) was noted within statin and non-statin subgroups[Figure]. Lp(a) was higher in statin group than in non-statin group. Conclusion: These results suggest that inflammatory reactants and Lp(a) do not correlate with the changes of serum cholesterol itself, and that both progress and regress of atherosclerosis may not be related to the degree of inflammation in terms of long-term aspects of atherosclerosis.