Assessment of Lp(a) role in all atherogenic lipoproteins possible with existing assays
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Utilizing commercially available assays, researchers demonstrated the feasibility of evaluating the contribution of lipoprotein(a) to all atherogenic lipoproteins at the National Lipid Association Scientific Sessions.
“Because clinical LDL cholesterol includes cholesterol from Lp(a), there has been interest in trying to deconstruct LDL cholesterol to understand the contribution that Lp(a) makes,” Michael Chilazi, MD, senior resident at Johns Hopkins Hospital affiliated with the Ciccarone Center for the Prevention of Cardiovascular Disease, said during a presentation.
According to the presentation, prior studies relied on mass estimations of cholesterol to calculate the contributions of Lp(a) to LDL, which were not accurate; however, Chilazi and colleagues hypothesized that particle-based measurement enables improved accuracy and can serve as a direct comparison of Lp(a) with other atherogenic particles.
“The objective of our study was to look at whether we could represent and illustrate how in a patient Lp(a) concentration contributes not only to just LDL but more broadly to all atherogenic particles, or as we call them, non-HDL particles,” Chilazi said.
To evaluate this, researchers utilized the Very Large Database of Lipids and included 158,260 patients with measured Lp(a) particle number and apolipoprotein B. According to the presentation, the concentration of non-HDL particles was calculated by converting ApoB from mass to molar concentration. In addition, the proportion of Lp(a) to non-HDL particles was measured across deciles of Lp(a) concentration and stratified based on demographic and lipid ranges.
According to the presentation, patients with the highest decile of Lp(a) concentration had upward of 15% of their total atherogenic particles composed of Lp(a).
When participants were evaluated based on sex, the researchers observed no between-group differences in proportion of Lp(a) concentration relative to all atherogenic particles.
The researchers also evaluated how the relationship between Lp(a) and non-HDL particles varied in relation to other atherogenic particles. According to the presentation, as triglyceride levels increased, the ratio of Lp(a) and non-HDL particles decreased.
This finding demonstrated the “larger contribution of VLDL to the atherogenic population,” Chilazi said during the presentation.
Similarly, as LDL increased, the fraction of Lp(a) particles to non-HDL particles decreased.
“This illustrates how, in patients with high LDL, their LDL contributions increasingly make up more of the atherogenic pie, so to speak, relative to Lp(a),” Chilazi said.
“We were able to demonstrate a novel method to quantify the contribution of Lp(a) to all atherogenic particles. Importantly, we used an approach that used commercially available assays that are used in clinical practice to both measure Lp(a) concentration and ApoB,” Chilazi said during the presentation. “This measurement is something we believe is feasible and easy to perform in real-world clinical settings. We believe that this method allows physicians and clinicians to qualitatively illustrate the degree of residual atherosclerotic CVD risk that might be mediated by Lp(a), something that is becoming increasingly relevant now with targeted therapies for Lp(a) and other lipoproteins beyond LDL.”
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Chilazi M, et al. 2021 Young Investigator Competition. Presented at: National Lipid Association Scientific Sessions; Sept. 24-26, 2021; Orlando, Fla. (hybrid meeting).
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