title: Epicardial adipose excision slows the progression of porcine coronary atherosclerosis.
abstract: BACKGROUND
  In humans there is a positive association between epicardial adipose tissue (EAT) volume and coronary atherosclerosis (CAD) burden. We tested the hypothesis that EAT contributes locally to CAD in a pig model.
  
  
  METHODS
  Ossabaw miniature swine (n=9) were fed an atherogenic diet for 6 months to produce CAD. A 15 mm length by 3-5 mm width coronary EAT (cEAT) resection was performed over the middle segment of the left anterior descending artery (LAD) 15 mm distal to the left main bifurcation. Pigs recovered for 3 months on atherogenic diet. Intravascular ultrasound (IVUS) was performed in the LAD to quantify atheroma immediately after adipectomy and was repeated after recovery before sacrifice. Coronary wall biopsies were stained immunohistochemically for atherosclerosis markers and cytokines and cEAT was assayed for atherosclerosis-related genes by RT-PCR. Total EAT volume was measured by non-contrast CT before each IVUS.
  
  
  RESULTS
  Circumferential plaque length increased (p<0.05) in the proximal and distal LAD segments from baseline until sacrifice whereas plaque length in the middle LAD segment underneath the adipectomy site did not increase. T-cadherin, scavenger receptor A and adiponectin were reduced in the intramural middle LAD. Relative to control pigs without CAD, 11β-hydroxysteroid dehydrogenase (11βHSD-1), CCL19, CCL21, prostaglandin D2 synthase, gp91phox [NADPH oxidase], VEGF, VEGFGR1, and angiotensinogen mRNAs were up-regulated in cEAT. EAT volume increased over 3 months.
  
  
  CONCLUSIONS
  In pigs used as their own controls, resection of cEAT decreased the progression of CAD, suggesting that cEAT may exacerbate coronary atherosclerosis.
authors.forename: Mikaela L
authors.initials: ML
authors.lastname: McKenney
authors.forename: Kyle A
authors.initials: KA
authors.lastname: Schultz
authors.forename: Jack H
authors.initials: JH
authors.lastname: Boyd
authors.forename: James P
authors.initials: JP
authors.lastname: Byrd
authors.forename: Mouhamad
authors.initials: M
authors.lastname: Alloosh
authors.forename: Shawn D
authors.initials: SD
authors.lastname: Teague
authors.forename: Arturo A
authors.initials: AA
authors.lastname: Arce-Esquivel
authors.forename: John N
authors.initials: JN
authors.lastname: Fain
authors.forename: M Harold
authors.initials: MH
authors.lastname: Laughlin
authors.forename: Harold S
authors.initials: HS
authors.lastname: Sacks
authors.affiliation: Departments of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Drive, Room 385, Indianapolis, IN 46202-5120, USA. msturek@iu.edu.
authors.forename: Michael
authors.initials: M
authors.lastname: Sturek
mesh_terms: D000273:Adipose Tissue / Q000601:surgery*; D000818:Animals; D050197:Atherosclerosis / Q000175:diagnosis / Q000601:surgery*; D006348:Cardiac Surgical Procedures / Q000379:methods*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000601:surgery*; D004195:Disease Models, Animal; D018450:Disease Progression; D008297:Male; D010496:Pericardium / Q000601:surgery*; D013552:Swine; D013556:Swine, Miniature; D018084:Ultrasonography, Interventional