TY - JOUR
TI - Visceral adipose tissue phenotype and hypoadiponectinemia are associated with aortic Fluorine-18 fluorodeoxyglucose uptake in patients with familial dyslipidemias
AU - Toutouzas, K.
AU - Antonopoulos, A.S.
AU - Koutagiar, I.
AU - Skoumas, I.
AU - Benetos, G.
AU - Kafouris, P.
AU - Miliou, A.
AU - Petrocheilou, A.
AU - Georgakopoulos, A.
AU - Oikonomou, G.
AU - Drakopoulou, M.
AU - Siores, I.
AU - Pitsavos, C.
AU - Antoniades, C.
AU - Anagnostopoulos, C.D.
AU - Tousoulis, D.
JO - Journal of Nuclear Cardiology
PY - 2021
VL - null
TODO - null
SP - null
PB - Springer-Verlag
SN - 1071-3581, 1532-6551
TODO - 10.1007/s12350-020-02472-y
TODO - null
TODO - Background: The role of adipose tissue (AT) in arterial inflammation in familial dyslipidaemias is poorly studied. We investigated the relationship between AT and arterial inflammation in patients with heterozygous familial hypercholesterolemia (heFH) and familial combined hyperlipidemia (FCH). Methods and Results: A total of 40 patients (20 heFH/20 FCH) and a subgroup of 20 of non-heFH/FCH patients were enrolled. Participants underwent blood sampling for serum adipokine measurements and Fluorine-18 fluorodeoxyglucose (18F-FDG) PET/CT imaging. Abdominal visceral (VAT) and subcutaneous (SAT) AT volumes and AT and abdominal aorta 18F-FDG uptake were quantified. FCH patients had increased VAT (pANOVA = 0.004) and SAT volumes (pANOVA = 0.003), lower VAT metabolic activity (pANOVA = 0.0047), and lower adiponectin levels (pANOVA = 0.007) compared to heFH or the control group. Log(Serum adiponectin) levels were correlated with aortic TBR (b = − 0.118, P = 0.038). In mediation analysis, VAT volume was the major determinant of circulating adiponectin, an effect partly mediated via VAT TBR. Clustering of the population of heFH/FCH by VAT volume/TBR and serum adiponectin identified two distinct patient clusters with significant differences in aortic TBR levels (2.11 ± 0.06 vs 1.89 ± 0.05, P= 0.012). Conclusions: VAT phenotype (increased VAT volume and/or high VAT TBR) and hypoadiponectinemia may account for the observed differences in arterial inflammation levels between heFH and FCH patients. © 2021, American Society of Nuclear Cardiology.
ER -