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Surgical excision of coronary epicardial adipose tissue provides evidence for its role in coronary artery disease
Author(s) -
Schultz Kyle,
Boyd Jack,
Byrd James Patrick,
McKenney Mikaela,
Chawla Aarti,
Alloosh Mouhamad,
Teague Shawn,
Sacks Harold,
Sturek Michael
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.866.19
Subject(s) - medicine , coronary artery disease , cardiology , intravascular ultrasound , circumflex , coronary atherosclerosis , atheroma , coronary arteries , lumen (anatomy) , epicardial adipose tissue , artery , adipose tissue , pericardium
Coronary artery disease (CAD) is the accumulation of atherosclerotic plaque within the lumen of large epicardial conduit arteries. Past research has shown strong positive association between coronary epicardial adipose tissue (cEAT) and CAD. We tested a contributory role for cEAT in CAD by surgical excision of cEAT and longitudinal measures of CAD with intravascular ultrasound (IVUS). Ossabaw swine (N=8) were fed an atherogenic diet for 6 months to produce metabolic syndrome and CAD. IVUS was performed prior to an adipectomy of the cEAT on the proximal half of the left anterior descending (LAD) coronary artery, while the circumflex (CFX) was left as a sham control. Recovery of 3 months was allowed on the same diet, followed by IVUS measures of the LAD and CFX to determine atheroma changes. As predicted, there was an increase in CAD during recovery (p<0.05). The increase in the proximal LAD was only 10% of that in the CFX. Likewise an increase in the proximal and middle LAD combined was 38% of the same CFX region (p<0.05). Computed tomography (CT) showed increases in pericardial fat and association with CAD during recovery, but cEAT at the adipectomy site could not be quantified with CT. We conclude these data suggest cEAT removal decreased the progression of coronary atherosclerosis. (Support: NIH HL062552 , Cardiometabolic Disease Research Foundation, Memphis, TN)