Hemodynamic overload and intra-abdominal adiposity in obese children: Relationships with cardiovascular structure and function

Abstract

Background and aimsChildhood obesity promotes adverse changes in cardiovascular structure and function. This study evaluated whether these changes are related to intra-abdominal adiposity and associated cardiometabolic risk or to body-size induced hemodynamic overload. Methods and results55 obese children/adolescents and 35 healthy-weight controls underwent carotid, cardiac and abdominal ultrasound to assess carotid artery intima-media thickness (IMT), diameter, distension and stiffness, left ventricular (LV) dimension, mass and function and extent of intra-abdominal adiposity.As compared to controls with healthy BMI, obese children had higher systolic blood pressure (BP), stroke volume and lower total peripheral resistance (P < 0.001–0.0001), higher plasma triglycerides, glycated hemoglobin, insulin and HOMA-IR index (P = 0.01–<0.0001), higher carotid IMT, diameter and distension (P < 0.005–0.0005), higher LV diameter, wall thickness and mass (P < 0.001–0.0001), and impaired LV diastolic function assessed by myocardial longitudinal performance (P < 0.005). In entire population, independent determinants of carotid diameter, LV diameter, wall thickness and mass were fat-free mass (or stroke volume, respectively) and BP. Carotid distension was determined by carotid diameter and BP, and carotid IMT by carotid diameter, BP, HDL-cholesterol and glycated hemoglobin. LV diastolic performance was inversely related to preperitoneal fat thickness and plasma insulin levels. ConclusionsObese youths present signs of impaired lipid and glucose metabolism, hyperdynamic circulation and cardiovascular changes. Increase in LV dimensions and mass and in carotid diameter and distension seems to reflect adaptation to body-size induced increase in hemodynamic load, changes in LV diastolic performance a negative impact of intra-abdominal adiposity and associated metabolic risk, and increase in IMT both adaptive remodeling and metabolic risk.