Aim To investigate the roles of inflammatory mediators in the pathogenesis of acute myocardial infarction (AMI). Methods Inflammatory mediators such as C reactive protein (CRP), tumor necrosis factor α (TNF α), and fibrinogen on the 1st, 4th, 7 th day and 2 months later of onset were measured in twenty nine cases with AMI. Results Concentrations of CRP did not show difference compared with the controls on the 1st day, but increased remarkably on the 4th day, and decreased on the 7th day. It normalized 2 months later. TNF α could only be detected in 6 samples among which 3 in control group and 3 in AMI group. Concentrations of fibrinogen increased on the 1st day, and continued increasing on the 4th and 7th day. It normalized 2 months later. Conclusions Changes of CRP was not the initiator of AMI but the reaction following AMI. The very low detectable rate of TNF α made it of little value as a risk factor of AMI. Fibrinogen might play roles in the pathogenesis of AMI.