Epicardial Adipose Tissue Removal Potentiates Outward Remodeling and Arrests Coronary Atherogenesis.
Autor: | McKenney-Drake ML; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana., Rodenbeck SD; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana., Bruning RS; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; College of Pharmacy and Health Sciences, Butler University, Indianapolis, Indiana., Kole A; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Covance, Inc, Greenfield, Indiana., Yancey KW; Weldon School of Biomedical Engineering, Purdue University, Lafayette, Indiana., Alloosh M; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana., Sacks HS; Endocrinology and Diabetes Division, VA Greater Los Angeles Healthcare System, and David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California., Sturek M; Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Covance, Inc, Greenfield, Indiana. Electronic address: msturek@iu.edu. |
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Jazyk: | angličtina |
Zdroj: | The Annals of thoracic surgery [Ann Thorac Surg] 2017 May; Vol. 103 (5), pp. 1622-1630. Date of Electronic Publication: 2017 Feb 21. |
DOI: | 10.1016/j.athoracsur.2016.11.034 |
Abstrakt: | Background: Pericoronary epicardial adipose tissue (cEAT) serves as a metabolic and paracrine organ that contributes to inflammation and is associated with macrovascular coronary artery disease (CAD) development. Although there is a strong correlation in humans between cEAT volume and CAD severity, there remains a paucity of experimental data demonstrating a causal link of cEAT to CAD. The current study tested the hypothesis that surgical resection of cEAT attenuates inflammation and CAD progression. Methods: Female Ossabaw miniature swine (n = 12) were fed an atherogenic diet for 8 months and randomly allocated into sham (n = 5) or adipectomy (n = 7) groups. Both groups underwent a thoracotomy, opening of the pericardial sac, and placement of radioopaque clips to mark the proximal left anterior descending artery. Adipectomy swine underwent removal of 1 to 1.5 cm 2 of cEAT from the proximal artery. After sham or adipectomy, CAD severity was assessed with intravascular ultrasonography. Swine recovered for an additional 3 months on an atherogenic diet, and CAD was assessed immediately before euthanasia. Artery sections were processed for histologic and immunohistochemical analysis. Results: Severity of CAD as assessed by percent stenosis was reduced in the adipectomy cohort compared with shams; however, plaque size remained unaltered, whereas larger plaque sizes developed in sham-operated swine. Adipectomy resulted in an expanded arterial diameter, similar to the Glagov phenomenon of positive outward remodeling. No differences in inflammatory marker expression were observed. Conclusions: These data indicate that cEAT resection did not alter inflammatory marker expression, but arrested CAD progression through increased positive outward remodeling and arrest of atherogenesis. (Copyright © 2017 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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