Abstract

Objective To investigate dynamic changes of plasma macrophage migration inhibitory factor(MIF)in patients with acute ST-segment elevated myocardial infarction(STEMI). Methods We continuously recruited 204 STEMI patients with primary percutaneous coronary intervention(PCI). Age and sex-matched patients with stable angina(n=30)and healthy subjects(n=65)were selected as control groups.Plasma MIF levels of admission, 24 h and 72 h after PCI were measured by enzyme linked immunosorbent assay(ELISA). STEMI patients were followed up for 36 months. Results Compared with control groups, plasma MIF levels of STEMI patients were significantly higher at admission and maintained at high levels until 24 h to 72 h[53.1(36.4, 81.9)ng/ml, 53.8(40.7, 67.7)ng/ml, 50.8(38.9, 66.0)ng/ml, respectively, P 0.05). Plasma MIF levels of admission was correlated positively with peak levels of creatine kinase-MB and troponin T(r=0.439 and 0.316, both P<0.001), negatively with left ventricular ejection fraction(LVEF)(r=-0.338, P<0.001). Plasma MIF levels at admission and 24 h post PCI were associated with high sensitive-C reactive protein(r=0.173 and 0.148, both P<0.05). MIF at 24 h post PCI correlated with dynamic monocyte counts within 72 h after STEMI(r=0.305, 0.195 and 0.237, all P<0.05). Also, MIF levels at 72 h post PCI were associated with monocyte counts at 24 h and 72 h post PCI(r=0.175 and 0.146, both P<0.05). Patients with higher MIF levels at admission(≥53.1 ng/ml)had 2.4-fold risk of major adverse cardiovascular and cerebral events(MACCE)during 36 months follow-up(95%CI: 1.12-5.20, P=0.025). Conclusions In patients with STEMI, the lasting elevated levels of plasma MIF during early phase after STEMI appear to be associated with enzymatic infarct size, acute cardiac function, inflammatory factor and circulatory monocyte counts.Admission MIF level was correlated with prognosis and can help predict long-term adverse outcomes. Key words: Macrophage migration-inhibitory factors; Coronary artery disease; Angioplasty, transluminal, percutaneous coronary; Inflammatory cells

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