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

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          Abstract

          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 ( r = 0.42; p = 0.014), LV end-systolic volume ( r = 0.42; p = 0.013) and worse LV ejection fraction (LVEF) at T1 ( r = −0.44; p = 0.0094), independently of the infarct size. In the overall population IL-13 levels significantly decreased at T1 ( p = 0.0002). The ΔIL-13 was directly associated to ΔLVEF ( r = 0.42; p = 0.017) and inversely related to ΔEAT ( r = −0.51; p = 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.

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          Most cited references31

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          2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation

          Héctor Bueno, Borja Ibanez, Stefan James … (2017)
          Article 0 comments Cited 2470 times – based on 0 reviews     Review now
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            Fourth Universal Definition of Myocardial Infarction (2018).

            Kristian Thygesen, Joseph Alpert, Allan S. Jaffe … (2018)
            Article 0 comments Cited 919 times – based on 0 reviews     Review now
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              Human epicardial adipose tissue is a source of inflammatory mediators.

              Tomasz Mazurek, LiFeng Zhang, Andrew Zalewski … (2003)
              Inflammatory mediators that originate in vascular and extravascular tissues promote coronary lesion formation. Adipose tissue may function as an endocrine organ that contributes to an inflammatory burden in patients at risk of cardiovascular complications. In this study, we sought to compare expression of inflammatory mediators in epicardial and subcutaneous adipose stores in patients with critical CAD. Paired samples of epicardial and subcutaneous adipose tissues were harvested at the outset of elective CABG surgery (n=42; age 65+/-10 years). Local expression of chemokine (monocyte chemotactic protein [MCP]-1) and inflammatory cytokines (interleukin [IL]-1beta, IL-6, and tumor necrosis factor [TNF]-alpha) was analyzed by TaqMan real-time reverse transcription-polymerase chain reaction (mRNA) and by ELISA (protein release over 3 hours). Significantly higher levels of IL-1beta, IL-6, MCP-1, and TNF-alpha mRNA and protein were observed in epicardial adipose stores. Proinflammatory properties of epicardial adipose tissue were noted irrespective of clinical variables (diabetes, body mass index, and chronic use of statins or ACE inhibitors/angiotensin II receptor blockers) or plasma concentrations of circulating biomarkers. In a subset of samples (n=11), global gene expression was explored by DNA microarray hybridization and confirmed the presence of a broad inflammatory reaction in epicardial adipose tissue in patients with coronary artery disease. The above findings were paralleled by the presence of inflammatory cell infiltrates in epicardial adipose stores. Epicardial adipose tissue is a source of several inflammatory mediators in high-risk cardiac patients. Plasma inflammatory biomarkers may not adequately reflect local tissue inflammation. Current therapies do not appear to eliminate local inflammatory signals in epicardial adipose tissue.
              Article 0 comments Cited 504 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Physiol
                Journal ID (iso-abbrev): Front Physiol
                Journal ID (publisher-id): Front. Physiol.
                Title: Frontiers in Physiology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-042X
                Publication date (Electronic): 15 October 2020
                Publication date Collection: 2020
                Volume: 11
                Electronic Location Identifier: 575181
                Affiliations
                [1] 1Department of Translational Medical Sciences, University of Naples Federico II , Naples, Italy
                [2] 2Casa di Cura San Michele , Maddaloni, Italy
                [3] 3URT “Genomics of Diabetes,” Institute of Experimental Endocrinology and Oncology, National Research Council , Naples, Italy
                [4] 4Department of Emergency Medicine, Ospedale del Mare , Naples, Italy
                [5] 5Department of Cardiology, Ospedale del Mare , Naples, Italy
                [6] 6Department of Advanced Biomedical Science, University of Naples Federico II , Naples, Italy
                [7] 7Department of Electrical Engineering and Information Technology, University of Naples Federico II , Naples, Italy
                Author notes

                Edited by: Rainer Schulz, University of Giessen, Germany

                Reviewed by: Susanne Rohrbach, Justus-Liebig-University Giessen, Germany; Marisol Ruiz-Meana, VHIR Vall d’Hebron Institut de Recerca, Spain

                *Correspondence: Valentina Parisi, valentina.parisi@ 123456unina.it

                †These authors have contributed equally to this work

                This article was submitted to Clinical and Translational Physiology, a section of the journal Frontiers in Physiology

                Article
                DOI: 10.3389/fphys.2020.575181
                PMC ID: 7593695
                PubMed ID: 33178043
                SO-VID: e4f69ad8-383b-451a-9130-52a2d2a04482
                Copyright © Copyright © 2020 Parisi, Cabaro, D’Esposito, Petraglia, Conte, Campana, Gerundo, Abitabile, Tuccillo, Accadia, Comentale, Pilato, Sansone, Leosco and Formisano.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 22 June 2020
                Date accepted : 22 September 2020
                Page count
                Figures: 3, Tables: 2, Equations: 0, References: 31, Pages: 8, Words: 0
                Categories
                Subject: Physiology
                Subject: Brief Research Report

                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: left ventricular remodeling,epicardial adipose tissue,inflammation,cytokines,biomarkers,echocardiography
                Data availability:
                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: left ventricular remodeling, epicardial adipose tissue, inflammation, cytokines, biomarkers, echocardiography

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