Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease.
BACKGROUND
Inflammation contributes to cardiovascular disease and is exacerbated with increased adiposity, particularly omental adiposity; however, the role of epicardial fat is poorly understood.


METHODS
For these studies the expression of inflammatory markers was assessed in epicardial fat biopsies from coronary artery bypass grafting (CABG) patients using quantitative RT-PCR. Further, the effects of chronic medications, including statins, as well as peri-operative glucose, insulin and potassium infusion, on gene expression were also assessed. Circulating resistin, CRP, adiponectin and leptin levels were determined to assess inflammation.


RESULTS
The expression of adiponectin, resistin and other adipocytokine mRNAs were comparable to that in omental fat. Epicardial CD45 expression was significantly higher than control depots (p < 0.01) indicating significant infiltration of macrophages. Statin treated patients showed significantly lower epicardial expression of IL-6 mRNA, in comparison with the control abdominal depots (p < 0.001). The serum profile of CABG patients showed significantly higher levels of both CRP (control: 1.28 +/- 1.57 microg/mL vs CABG: 9.11 +/- 15.7 microg/mL; p < 0.001) and resistin (control: 10.53 +/- 0.81 ng/mL vs CABG: 16.8 +/- 1.69 ng/mL; p < 0.01) and significantly lower levels of adiponectin (control: 29.1 +/- 14.8 microg/mL vs CABG: 11.9 +/- 6.0 microg/mL; p < 0.05) when compared to BMI matched controls.


CONCLUSIONS
Epicardial and omental fat exhibit a broadly comparable pathogenic mRNA profile, this may arise in part from macrophage infiltration into the epicardial fat. This study highlights that chronic inflammation occurs locally as well as systemically potentially contributing further to the pathogenesis of coronary artery disease.
Baker
Adam R
AR
Unit for Diabetes and Metabolism, Warwick Medical School, University of Warwick, Clinical Sciences Research Institute, UHCW Campus, Coventry, CV2 2DX, UK. a.r.baker@warwick.ac.uk
Silva
Nancy F da
NF
Quinn
David W
DW
Harte
Alison L
AL
Pagano
Domenico
D
Bonser
Robert S
RS
Kumar
Sudhesh
S
McTernan
Philip G
PG
D052242:Adiponectin / Q000032:analysis / Q000097:blood / Q000235:genetics; D000273:Adipose Tissue / Q000737:chemistry* / Q000473:pathology / Q000503:physiopathology; D002097:C-Reactive Protein / Q000032:analysis; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000032:analysis* / Q000235:genetics; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007328:Insulin / Q000008:administration & dosage; D015850:Interleukin-6 / Q000032:analysis / Q000235:genetics; D050152:Intra-Abdominal Fat / Q000503:physiopathology; D020738:Leptin / Q000097:blood / Q000235:genetics; D017493:Leukocyte Common Antigens / Q000032:analysis / Q000235:genetics; D008264:Macrophages / Q000737:chemistry / Q000473:pathology; D008875:Middle Aged; D010496:Pericardium / Q000737:chemistry* / Q000473:pathology / Q000503:physiopathology; D016133:Polymerase Chain Reaction; D011188:Potassium / Q000008:administration & dosage; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D052243:Resistin / Q000032:analysis / Q000097:blood / Q000235:genetics
D052242:Adiponectin; D016207:Cytokines; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007328:Insulin; D015850:Interleukin-6; D020738:Leptin; D012333:RNA, Messenger; D052243:Resistin; D002097:C-Reactive Protein; D017493:Leukocyte Common Antigens; D005947:Glucose; D011188:Potassium