Cardiovascular magnetic resonance tissue characterization of epicardial adipose tissue in acute STEMI: association with myocardial injury and systemic inflammation – exploratory pilot study

Background Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot with paracrine inflammatory properties implicated in coronary plaque instability. While cardiovascular magnetic resonance (CMR) enables detailed myocardial tissue characterization in ST-elevation myocardial infarction (STEMI), quantitative in vivo mapping of EAT has not been systematically explored. We aimed to assess EAT tissue characteristics using T1 and T2 mapping in acute STEMI and evaluate associations with myocardial injury and systemic inflammation. Methods We prospectively studied 12 patients with acute STEMI undergoing CMR in the acute phase and 9 patients with stable coronary artery disease as controls. The CMR protocol included LV volumes and ejection fraction (EF), late gadolinium enhancement (LGE), native myocardial T1 and T2 mapping, and extracellular volume (ECV). EAT thickness was measured in the 4-chamber view, and native T1 and T2 mapping were performed within EAT regions of interest. Serum IL-6 and NT-proBNP levels were obtained. Group comparisons were performed using Mann–Whitney U test and correlations using Spearman analysis. Results STEMI patients demonstrated higher myocardial T1/T2 and ECV compared with controls (p≤0.04). Within the STEMI cohort, EAT T1 mapping correlated inversely with EF (ρ=−0.62, p=0.031) and positively with LGE burden (ρ=0.64, p=0.023), infarct segment number (ρ=0.60, p=0.033), and ECV (ρ=0.57, p=0.048). EAT T2 mapping showed similar associations with EF (ρ=−0.60, p=0.038) and LGE (ρ=0.62, p=0.028). EAT thickness demonstrated weaker correlations compared with mapping parameters. IL-6 correlated with LGE (ρ=0.69, p=0.014), ECV (ρ=0.60, p=0.036), and EF (ρ=−0.65, p=0.023), and showed moderate positive associations with EAT mapping values, supporting a link between epicardial tissue remodeling and systemic inflammatory activation. Conclusions CMR-based quantitative characterization of epicardial adipose tissue is feasible in acute STEMI. Increased EAT T1 and T2 values are associated with myocardial injury severity and inflammatory activation, beyond simple volumetric assessment. These findings suggest that EAT mapping may provide incremental insight into myocardial–epicardial inflammatory interplay following STEMI. Larger studies are warranted to validate these exploratory observations.