BACKGROUND AND AIM: Epicardial fat (EF), a true visceral adipose tissue (VAT) deposited around the heart, is considered as possible cardiovascular risk indicator, in view of its ability to produce and release several inflammatory adipo-cytokines. It is still not known whether increased cardiac adiposity is related to increased inflammatory adipo-cytokines in obesity. The aim of this study was to evaluate whether echocardiographic EF thickness, an indicator of cardiac adiposity, is related to circulating levels of inflammatory adipo-cytokines such as visfatin and plasminogen activator inhibitor-1 (PAI-1) in visceral obesity. METHODS AND RESULTS: EF thickness (measured by echocardiography), visfatin, PAI-1 antigen and some inflammatory markers were studied in 42 women, 27 of them severely obese (OB) (BMI 43.5+/-4.8 kg/m(2)) but with no apparent complications, and 15 normal-weight controls. Abdominal VAT in the OB was assessed by computed tomography. OB had thicker EF and higher visfatin and PAI-1 antigen concentrations than controls (P<0.0001). EF thickness, log-visfatin and log-PAI-1 antigen concentrations directly correlated with VAT (P<0.0001). Log-visfatin and log-PAI-1 antigen were correlated with EF thickness even after adjusting for indices of fat distribution (P<0.01 and P<0.001 respectively). Moreover, when dividing OB on the basis of median EF thickness, women with greater EF thickness had more VAT and higher adipo-cytokine concentrations and inflammatory markers. CONCLUSIONS: This study suggests that EF thickness, an indicator of cardiac adiposity, may be significantly related to inflammatory adipo-cytokines in visceral-obese patients. This suggests EF might be used as an easy and reliable marker of visceral adiposity and inflammation and as a cardiovascular risk indicator.
BACKGROUND AND AIM: Epicardial fat (EF), a true visceral adipose tissue (VAT) deposited around the heart, is considered as possible cardiovascular risk indicator, in view of its ability to produce and release several inflammatory adipo-cytokines. It is still not known whether increased cardiac adiposity is related to increased inflammatory adipo-cytokines in obesity. The aim of this study was to evaluate whether echocardiographic EF thickness, an indicator of cardiac adiposity, is related to circulating levels of inflammatory adipo-cytokines such as visfatin and plasminogen activator inhibitor-1 (PAI-1) in visceral obesity. METHODS AND RESULTS: EF thickness (measured by echocardiography), visfatin, PAI-1 antigen and some inflammatory markers were studied in 42 women, 27 of them severely obese (OB) (BMI 43.5+/-4.8 kg/m(2)) but with no apparent complications, and 15 normal-weight controls. Abdominal VAT in the OB was assessed by computed tomography. OB had thicker EF and higher visfatin and PAI-1 antigen concentrations than controls (P<0.0001). EF thickness, log-visfatin and log-PAI-1 antigen concentrations directly correlated with VAT (P<0.0001). Log-visfatin and log-PAI-1 antigen were correlated with EF thickness even after adjusting for indices of fat distribution (P<0.01 and P<0.001 respectively). Moreover, when dividing OB on the basis of median EF thickness, women with greater EF thickness had more VAT and higher adipo-cytokine concentrations and inflammatory markers. CONCLUSIONS: This study suggests that EF thickness, an indicator of cardiac adiposity, may be significantly related to inflammatory adipo-cytokines in visceral-obesepatients. This suggests EF might be used as an easy and reliable marker of visceral adiposity and inflammation and as a cardiovascular risk indicator.
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