Key result
Children with familial hypercholesterolemia displayed higher LDL aggregation and lower HAE/apoA-I ratio compared to healthy children, indicating increased atherogenicity of LDL and disrupted HDL function.
Why the study?
It was unknown whether children with familial hypercholesterolemia display alterations in LDL and HDL lipoprotein function.
Do children with familial hypercholesterolemia have disrupted lipoprotein function compared to healthy children?
Cross-Sectional (n=103)
Single-blind (analysts)
Do children with familial hypercholesterolemia have disrupted lipoprotein function compared to healthy children?
Children with familial hypercholesterolemia exhibit increased LDL aggregation and disrupted HDL function, which may contribute to early atherogenesis and increased cardiovascular risk.
Lipoprotein function in FH children remains incompletely characterized; hypothesis-generating for early atherosclerosis risk.
Background The functional status of lipoprotein particles contributes to atherogenesis. The tendency of plasma LDL particles to aggregate and the ability of HDL particles to induce and mediate reverse cholesterol transport associate with high and low risk for cardiovascular disease in adult patients, respectively. However, it is unknown whether children with familial hypercholesterolemia (FH) display lipoprotein function alterations. Hypothesis We hypothesized that FH children had disrupted lipoprotein function. Methods We analyzed LDL aggregation susceptibility and HDL-apoA-I exchange to apoA-I ratio (HAE/apoA-I ratio), and activity of four proteins that regulate lipoprotein metabolism (CETP, LCAT, PLTP and PON1) in plasma samples derived from children with FH (n = 47) and from healthy children (n = 56). Potential biological mechanisms behind any variation in lipoprotein functionalities were explored using an NMR-based metabolomics profiling approach. Results LDL aggregation was higher and HAE/apoA-I ratio was lower in FH children than in healthy children. LDL aggregation associated positively with LDL-C and negatively with triglycerides, and HAE/apoA-I ratio associated negatively with LDL-C. Generally, the metabolomic profile for LDL aggregation was a mirror image of that for HAE/apoA-I ratio. Conclusions FH children displayed increased atherogenicity of LDL and disrupted HDL function. These newly observed functional alterations in LDL and HDL may increase the risk for atherosclerotic cardiovascular disease in FH children.
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Christensen et al. (2020) conducted a cross-sectional in Familial hypercholesterolemia (n=103). Familial hypercholesterolemia vs. Healthy children was evaluated on LDL aggregation susceptibility and HDL-apoA-I exchange to apoA-I ratio (HAE/apoA-I ratio). Children with familial hypercholesterolemia displayed higher LDL aggregation and lower HAE/apoA-I ratio compared to healthy children, indicating increased atherogenicity of LDL and disrupted HDL function.
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