Abstract 17579: Quantification of Femoral Adipose Tissue Provides Novel Mechanistic Insights Into the "Obesity Paradox": a Translational Approach
Introduction: Obesity has been paradoxically associated with a better outcome of CAD patients, while anthropometic measures of obesity provide limited information on adipose tissue (AT) biology. We hypothesised that quantification of femoral AT (FemAT) deposition using U/S can provide mechanistic insights into the obesity paradox.
Methods: FemAT biopsies from 185 pts undergoing coronary bypass surgery (CABG) were cultured ex vivo for secretome and gene expression studies. FemAT thickness was measured by U/S at both the anterior and exterior surface of the thigh, at the mid point of the distance between the iliac crest and the knee, and the average of both thighs was calculated. Malondialdehyde (MDA), a marker of oxidative stress, was measured in plasma and FemAT culture supernatants. Brachial artery (BA) flow mediated dilatation (FMD) and distensibility were assessed by U/S.
Results: FemAT thickness was only weakly correlated with BMI (r=0.235, p<0.001) and waist-to-hip ratio (WHR, r=-0.179, p<0.05), suggesting that it provides different information to classic anthropometrics in obesity. Patients with increased FemAT thickness had lower plasma MDA (A), better FMD (B) and greater BA distensibility (C), despite of being more obese. On the contrary BMI did not predict systemic oxidative stress or vascular function, while WHR was weakly correlated only with FMD (rho=-0.156, p<0.05). Increased FemAT thickness was associated with lower MDA release from FemAT culture supernatants (D), and lower IL6-receptor (E) / CD68 (F) expression in FemAT samples, suggesting lower endogenous oxidative stress, and less macrophages’ infiltration.
Conclusions: Femoral fat accumulation is associated with lower local AT inflammation and favourable systemic effects on vascular function in CAD. Combining imaging with AT biology could help to better understand the role of obesity-related vascular disease and provide an explanation to the “obesity paradox”.
Author Disclosures: A.S. Antonopoulos: None. M. Margaritis: None. L. Herdman: None. P. Coutinho: None. C. Psarros: None. J. Digby: None. G. Krasopoulos: None. M. Petrou: None. K.M. Channon: None. C. Antoniades: None.
- © 2014 by American Heart Association, Inc.