Epicardial adipose tissue in children with obesity: correlations with cardiometabolic parameters and treatment response
S Bidstrup Groth, M Loek, L A H Amstrup, T Hansen, N Vejlstrup, P L Madsen, T Jespersen, J C Holm, M A V LundAbstract
Background
Epicardial adipose tissue (EAT) is proposed as a unique cardiovascular risk marker in both adults and children, yet its role in early cardiovascular disease development remains poorly understood. Since childhood obesity significantly increases the risk of adult cardiovascular mortality, a deeper understanding of early markers like EAT could improve prevention strategies.
Purpose
We aimed to (1) quantify EAT in children with and without obesity, (2) assess correlations with cardiometabolic parameters and measures of adiposity, and (3) evaluate changes in EAT following initiation of obesity treatment.
Methods
In this longitudinal observational study, we included 100 children aged 10-14 years at initiation of obesity treatment and 50 population-based controls with normal weight. EAT was quantified at baseline and after 18 months by magnetic resonance imaging (MRI) on 4-chamber cines. Anthropometrics, blood samples, dual-energy x-ray absorptiometry (DXA), and MRI of the thorax and abdomen were obtained.
Results
At baseline, EAT was 40% higher in children with obesity (BMI-SDS 3.09±0.58) compared to normal-weight controls (BMI-SDS 0.10±0.94). EAT correlated positively with weight, waist circumference, body mass index (BMI), plasma triglycerides, visceral adipose tissue (VAT) and total body fat percentage, even when adjusting for sex, BMI standard deviation score (BMI-SDS) and height. Follow-up data was available for 93 children. When stratified by BMI-SDS reduction of 0.25, those with BMI-SDS reduction ≥0.25 had a 13% (p=0.002) reduction in EAT, while those with BMI-SDS reduction <0.25 had a 10% reduction in EAT (p=0.012) at follow-up. No significant difference in EAT reduction was observed between subgroups.
Conclusion
EAT is elevated in children with obesity and correlates with cardiometabolic risk markers. Notably, EAT decreased following initiation of obesity treatment regardless of the degree of BMI-SDS reduction, suggesting that factors beyond obesity reduction may contribute to EAT reduction.