Abstract
Objective — to assess the role of circulating markers of inflammation and macrophage migration inhibitory factor (MIF) in the development of left ventricular (LV) remodeling 6 months after acute ST‑segment elevation myocardial infarction (STEMI).
 Materials and methods. The study involved 120 patients after STEMI and successful primary percutaneous coronary intervention (PCI). Transthoracic echocardiography with Doppler was performed within 24 — 48 hours after PCI and after 6 months of follow‑up to assess LV remodeling. The levels of MIF and inflammatory markers were measured before and after PCI. All patients were divided into two groups according to the median MIF level < 2501 pg/ml (first group, n = 60) and > 2501 pg/ml (second group, n = 60).
 Results. Patients with the high levels of circulating MIF had a higher frequency of complications in the hospital and long‑term periods (p = 0.024), including newly diagnosed heart failure or decompensation with hospitalizations. High MIF levels in patients of the second group were accompanied by a significant enlargement of end‑diastolic and end‑systolic LV volumes (p = 0.028; p = 0.031, respectively), the development of secondary mitral regurgitation (p = 0.024) and decreased LV systolic function (p = 0.037). MIF threshold values for predicting remodeling > 2694 pg/ml (sensitivity 69.2 %, specificity 71.4 %, AUC = 0.714; 95 % CI 0.509 — 0.870; p = 0.0375) and LV dysfunction > 2484 pg/ml (sensitivity 90.0 %, specificity 58.0 %, AUC = 0.782; 95 % CI 0.675 — 0.867, p = 0.0003) were determined using ROC analysis. According to the results of univariate and multivariate analysis, levels of MIF (p = 0.028) and soluble suppressor of tumorigenesis‑2 (p = 0.042) were most significant predictors of LV remodeling. A correlation between the levels of MIF and white blood cells count (r = 0.33, p = 0.0001), C‑reactive protein (r = 0.19, p = 0.032), troponin (r = 0.44, p = 0.002) has been established.
 Conclusions. An early increase of MIF levels is associated with the development of adverse structural and functional changes in left ventricle of patients after acute ST‑segment elevation myocardial infarction.
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