INTRODUCTION

Left ventricular (LV) remodeling after ST-segment elevation myocardial infarction (STEMI) is explained only in part by the infarct size, and the inter-patient variability may be ascribed to different inflammatory response to myocardial injury. Epicardial adipose tissue (EAT) is a source of inflammatory mediators which directly modulates the myocardium. EAT increase is associated to several cardiovascular diseases; however, its response to myocardial injury is currently unknown. Among inflammatory mediators, IL-13 seems to play protective role in LV regeneration, but its variations after STEMI have not been described yet. Purpose: In the present study we analyzed the association between infarct-related changes of EAT and IL-13 in post-STEMI LV remodeling.

METHODS

We enrolled 100 patients with STEMI undergoing primary angioplasty. At the enrolment (T0) and after 3 months (T1), we measured EAT thickness by echocardiography and circulating levels of IL-13 by ELISA.

RESULTS

At T1, the 60% of patients displayed increased EAT thickness (ΔEAT > 0). ΔEAT was directly associated to LV end-diastolic volume ( = 0.42; = 0.014), LV end-systolic volume ( = 0.42; = 0.013) and worse LV ejection fraction (LVEF) at T1 ( = -0.44; = 0.0094), independently of the infarct size. In the overall population IL-13 levels significantly decreased at T1 ( = 0.0002). The ΔIL-13 was directly associated to ΔLVEF ( = 0.42; = 0.017) and inversely related to ΔEAT ( = -0.51; = 0.022), thus suggesting a protective role for IL-13.

CONCLUSION

The variability of STEMI-induced "inflammatory response" may be associated to the post-infarct LV remodeling. ΔEAT thickness and ΔIL-13 levels could be novel prognostic markers in STEMI patients.