Luc Bruyndonckx1, Vicky Y Hoymans2, Geert Frederix3, Ann De Guchtenaere4, Hilde Franckx4, Dirk K Vissers5, Christiaan J Vrints6, José Ramet7, Viviane M Conraads6. 1. Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, University Hospital Antwerp, Antwerp, Belgium; Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Antwerp, Belgium; Department of Pediatrics, University Hospital Antwerp, Antwerp, Belgium. Electronic address: luc.bruyndonckx@uantwerpen.be. 2. Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, University Hospital Antwerp, Antwerp, Belgium; Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Antwerp, Belgium. 3. Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, University Hospital Antwerp, Antwerp, Belgium. 4. Zeepreventorium, De Haan, Belgium. 5. Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium. 6. Laboratory of Cellular and Molecular Cardiology, Department of Cardiology, University Hospital Antwerp, Antwerp, Belgium; Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Antwerp, Belgium; Department of Cardiology, University Hospital Antwerp, Antwerp, Belgium. 7. Department of Pediatrics, University Hospital Antwerp, Antwerp, Belgium.
Abstract
OBJECTIVE: To examine the degree of microvascular endothelial dysfunction in relation to classical cardiovascular risk factors, arterial stiffness, and numbers of circulating endothelial progenitor cells (EPCs) and endothelial microparticles (EMPs), in obese and normal-weight children. STUDY DESIGN: Cross-sectional study with 57 obese (15.2±1.4 years) and 30 normal-weight children (15.4±1.5 years). The principal outcome was microvascular endothelial function measured with peripheral arterial tonometry. Fasting blood samples were taken for biochemical analysis and EMPs (CD31+/CD42b- particles) and EPCs (CD34+/KDR+/CD45dim/- cells) flow cytometry. Characteristics between groups were compared by use of the appropriate independent samples test; a stepwise multiple regression analysis was used to determine independent predictors of microvascular endothelial function. RESULTS: Microvascular endothelial function was significantly impaired in obese children and inversely correlated with body mass index Z scores (r=-0.249; P=.021) and systolic blood pressure (r=-0.307; P=.004). The number of EPCs was significantly lower in obese children and correlated with endothelial function (r=0.250; P=.022), and the number of EMPs was significantly greater in obese children and correlated inversely with endothelial function (r=-0.255; P=.021). Multivariate analysis revealed that systolic blood pressure and numbers of circulating EPCs and EMPs are important determinants of endothelial function. CONCLUSION: Obese children demonstrate impaired endothelial microvascular function, increased arterial stiffness, fewer EPCs, and more EMPs. Besides systolic blood pressure, EPC and EMP counts independently predict the presence of microvascular endothelial dysfunction.
OBJECTIVE: To examine the degree of microvascular endothelial dysfunction in relation to classical cardiovascular risk factors, arterial stiffness, and numbers of circulating endothelial progenitor cells (EPCs) and endothelial microparticles (EMPs), in obese and normal-weight children. STUDY DESIGN: Cross-sectional study with 57 obese (15.2±1.4 years) and 30 normal-weight children (15.4±1.5 years). The principal outcome was microvascular endothelial function measured with peripheral arterial tonometry. Fasting blood samples were taken for biochemical analysis and EMPs (CD31+/CD42b- particles) and EPCs (CD34+/KDR+/CD45dim/- cells) flow cytometry. Characteristics between groups were compared by use of the appropriate independent samples test; a stepwise multiple regression analysis was used to determine independent predictors of microvascular endothelial function. RESULTS: Microvascular endothelial function was significantly impaired in obesechildren and inversely correlated with body mass index Z scores (r=-0.249; P=.021) and systolic blood pressure (r=-0.307; P=.004). The number of EPCs was significantly lower in obesechildren and correlated with endothelial function (r=0.250; P=.022), and the number of EMPs was significantly greater in obesechildren and correlated inversely with endothelial function (r=-0.255; P=.021). Multivariate analysis revealed that systolic blood pressure and numbers of circulating EPCs and EMPs are important determinants of endothelial function. CONCLUSION:Obesechildren demonstrate impaired endothelial microvascular function, increased arterial stiffness, fewer EPCs, and more EMPs. Besides systolic blood pressure, EPC and EMP counts independently predict the presence of microvascular endothelial dysfunction.
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