AUTHOR=Parisi Valentina , Cabaro Serena , D’Esposito Vittoria , Petraglia Laura , Conte Maddalena , Campana Pasquale , Gerundo Gerardo , Abitabile Marianna , Tuccillo Andrea , Accadia Maria , Comentale Giuseppe , Pilato Emanuele , Sansone Mario , Leosco Dario , Formisano Pietro 

TITLE=Epicardial Adipose Tissue and IL-13 Response to Myocardial Injury Drives Left Ventricular Remodeling After ST Elevation Myocardial Infarction

JOURNAL=Frontiers in Physiology

VOLUME=11

YEAR=2020

URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2020.575181

DOI=10.3389/fphys.2020.575181

ISSN=1664-042X

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