Abstract 19182: Epicardial Adipose Tissue Volume Selectively Predicts Myocardial Redox State in Patients With Ischemic Heart Disease
Introduction: Myocardial redox state is a strong determinant of heart biology. Epicardial adipose tissue (EpAT) is in close contact with the human heart and it is likely that by secreting a wide range of adipokines it may affect the biology of the underlying myocardium.
Hypothesis: We hypothesised that EpAT volume may predict myocardial redox state and consequently myocardial function in ischaemic heart disease (IHD).
Methods: We recruited 38 patients undergoing coronary artery bypass grafting surgery. Patients underwent transthoracic echocardiography to assess cardiac function and cardiac computerised tomography to determine the volume of EpAT, pericardial (PerAT) and subcutaneous (ScAT) AT, by using a strictly pre-defined protocol. Samples of right atrium appendage were collected during surgery and myocardial NADPH oxidase activity was assessed by lucigenin-enhanced chemiluminescence (using its substrate -NAPDH 100uM +/- its specific inhibitor VAS2870 40uM).
Results: Increased EpAT volume index (EpAT volume/body surface area), but not PerAT or ScAT, was strongly associated with increased myocardial NADPH oxidase activity (Figure). EpAT volume index was not related with left ventricle (LV) mass index or LV systolic/diastolic function (p=NS for all). EpAT volume index was also unrelated to risk factors or body mass index (p=NS for all).
Conclusions: These findings introduce the concept of a local cross-talk between EpAT and the underlying myocardium in humans. EpAT volume can be used as a surrogate of myocardial redox state, and this may have direct implications in risk stratification of patients undergoing coronary bypass surgery.
Author Disclosures: A.S. Antonopoulos: None. N. Sabharwal: None. C. Shirodaria: None. A. Kelion: None. R. Uberoi: None. S. Anthony: None. R. Sayeed: None. S. Neubauer: None. K.M. Channon: None. C. Antoniades: None.
- © 2014 by American Heart Association, Inc.