Highlights • FKN involves in the inflammatory and remodeling processes after AMI. • FKN is negative correlated with myocardial salvage in STEMI patients underwent PCI. • Higher FKN level after primary PCI predicts worse MACE events in AMI patients. Abstract Background Recent studies demonstrated that fractalkine (FKN) is critically involved in the regulation of inflammation and cardiac function. Objective This study aimed to investigate the prognostic value of circulating FKN in patients with ST-elevated acute myocardial infarction (STEMI) after primary PCI. Methods We enrolled ninety consecutive STEMI patients and investigated the association of circulating FKN with myocardial salvage and the occurrence of major adverse cardiac events (MACE) after PCI. Results During a median follow-up of 387 days, total 15 MACE (16.67%) were registered in the study population. Patients with MACE were more likely to be occurred in elderly patients with 3-vessel disease. Correlation analysis demonstrated the level of FKN at day 1 after PCI (FKN@day-1) not only significantly correlated with the levels of hs-TnT at day 7 after PCI (R2 = 0.06; p = 0.02) but inversely correlated with the measurements of LVEF at 1-month observation (R2 = 0.10; p = 0.00). Kaplan-Meier survival analyses further revealed that patients with the level of FKN@day-1 above the median had a higher incidence of MACE compared with those whose FKN@day-1 levels below the median (log-rank test x2 = 13.29, p < 0.001). In addition, multivariate Cox regression analysis demonstrated that FKN@day-1 was an independent predictor of MACE (hazard ratio: 4.63; 95% confidence interval: 1.53–14.01; p = 0.00), together with WBC count and 3-vessel disease for STEMI patients. Conclusions Our study demonstrates that FKN@day-1 is negative correlated with myocardial salvage after acute myocardial infarction and might be a valuable prognostic marker of MACE in patients with STEMI undergone PCI. [ABSTRACT FROM AUTHOR]