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Objective Leukotriene B4 (LTB4) has been suggested as a modulator of atherosclerotic plaque instability.However, its role in EMMPRIN and MMP production in macrophages and its importance in the diagnosis of ACS is still unclear.Thus, this study investigated the role of LTB4 in up-regulating the expression of EMMPRIN and MMP-9 in macrophages, and the potential diagnostic implication for ACS using LTB4, EMMPRIN and MMP-9.Method The macrophage differentiated from THP-1 was stimulated with LTB4 in a different concentration, and then the expressions of EMMPRIN and MMP-9 were evaluated.The expression of EMMPRIN on peripheral blood mononuclear cells from 134 patients with coronary heart disease and29 patients non-coronary heart disease was determined by flow cytometry, while the LTB4 and MMP-9levels in serum were measured by ELISA.Blood lipid, CK, CK-MB, troponin-I, blood sedimentation and fibrinogen were detected as well.Result LTB4 up-regulated the expression of EMMPRIN in macrophages, as well as the expression and activation of MMP-9.The expression of EMMPRIN in UAP patients was significantly higher than that in CON and AMI groups (P<0.05).Subgroup analysis, which was classified by intermediate stage of the latest chest pain onset, indicated that the subgroups of UAP<1w and AMI>24h expressed EMMPRIN significantly higher.However, the levels of LTB4 and MMP-9 in AMI group were higher than the other three groups (P<0.01).LTB4 was significantly positively correlated with MMP-9(r=0.188, p<0.01),CK(r=0.486, P< 0.01), CK-MB(r=0.490,P< 0.01) and troponin-Ⅰ (r=0.414, P< 0.01), and negatively correlated with EMMPRIN(r =-0.337, P< 0.05).While EMMPRIN was significantly positively correlated with blood sedimentation (r=0.225, P< 0.05) and fibrinogen(r=0.210, P< 0.05).Conclusion LTB4 can stimulate the expression of EMMPRIN and MMP-9 in THP-1 derived macrophages, as well as the activation of MMP-9.LTB4 and MMP-9 were more expressed in AMI patients,positively correlated with the special markers ofAl I.EMMPRIN was expressed significantly on peripheral blood mononuclear cells of UAP patients in 24 hours to 1 week after chest pain onset, and was positively correlated with chronic inflammatory factors.LTB4, EMMPRIN and MMP-9, which might be served as potential risk factors for ACS, might be all involved in the development of unstable plaque process.