title: Epicardial Adipose Tissue Removal Potentiates Outward Remodeling and Arrests Coronary Atherogenesis.
abstract: 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 cm2of 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.
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: Mikaela L
authors.initials: ML
authors.lastname: McKenney-Drake
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: Stacey D
authors.initials: SD
authors.lastname: Rodenbeck
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; College of Pharmacy and Health Sciences, Butler University, Indianapolis, Indiana.
authors.forename: Rebecca S
authors.initials: RS
authors.lastname: Bruning
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Covance, Inc, Greenfield, Indiana.
authors.forename: Ayeeshik
authors.initials: A
authors.lastname: Kole
authors.affiliation: Weldon School of Biomedical Engineering, Purdue University, Lafayette, Indiana.
authors.forename: Kyle W
authors.initials: KW
authors.lastname: Yancey
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana.
authors.forename: Mouhamad
authors.initials: M
authors.lastname: Alloosh
authors.affiliation: Endocrinology and Diabetes Division, VA Greater Los Angeles Healthcare System, and David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
authors.forename: Harold S
authors.initials: HS
authors.lastname: Sacks
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana; Covance, Inc, Greenfield, Indiana. Electronic address: msturek@iu.edu.
authors.forename: Michael
authors.initials: M
authors.lastname: Sturek
mesh_terms: D000273:Adipose Tissue / Q000601:surgery*; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000378:metabolism / Q000628:therapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology; D005260:Female; D007249:Inflammation / Q000378:metabolism / Q000628:therapy; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000473:pathology / Q000628:therapy; D011897:Random Allocation; D013552:Swine; D013556:Swine, Miniature; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers