Why the study?
Are retinal microvasculature characteristics associated with cardiovascular risk markers in children with overweight and obesity?
Are retinal microvasculature characteristics associated with cardiovascular risk markers in children with overweight and obesity?
In children, increasing BMI is associated with aberrant retinal arteriolar microvasculature, which correlates with cardiovascular risk markers like diastolic blood pressure and fasting plasma glucose.
Retinal arteriolar narrowing may flag early CV risk in obese children; hypothesis-generating for microvascular biomarkers, needs prospective validation.
To aim of this study was to evaluate characteristics of the retinal microvasculature, but particularly potential associations with classic and novel (endothelial function and low-grade inflammation)markers for cardiovascular risk, in a cohort of children with overweight and (morbid) obesity. Central retinal arteriolar equivalent(CRAE) and central retinal venular equivalent(CRVE) were assessed. CRAE was significantly lower and AVR significantly higher in children with morbid obesity than in children with overweight and normal weight(p < 0.01). CRVE did not differ significantly between the four weight categories. A multiple linear regression model with CRAE as dependent variable showed that only DBP z-score(β = -2.848,p = 0.029) and plasma glucose concentrations(β = 6.029,p = 0.019) contributed significantly to the variation in CRAE. Remarkably, despite a correlation between CRAE and circulating concentrations of the adhesion molecules VCAM-1 or ICAM-1, markers for inflammation and endothelial function did not contribute to the variation in CRAE. This is the first study showing in population of children with overweight and obesity that the retinal arteriolar microvasculature, but not venular diameter is aberrant, with increasing BMI z-score. CRAE was significantly associated with several cardiovascular risk markers, and multiple linear regression showed that a higher diastolic blood pressure z-score and lower fasting plasma glucose concentrations significantly contributed to the variance in CRAE.
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Rijks et al. (2018) studied this question.
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