Abstract

BackgroundApolipoprotein B100 (ApoB100) determination is superior to low-density lipoprotein cholesterol (LDL-C) to establish cardiovascular (CV) risk, and does not require prior fasting. ApoB100 is rarely measured alongside standard lipids, which precludes comprehensive assessment of dyslipidemia.ObjectivesTo evaluate two simple algorithms for apoB100 as regards their performance, equivalence and discrimination with reference apoB100 laboratory measurement.MethodsTwo apoB100-predicting equations were compared in 87 type 2 diabetes mellitus (T2DM) patients using the Discriminant ratio (DR). Equation 1: apoB100 = 0.65*non-high-density lipoprotein cholesterol + 6.3; and Equation 2: apoB100 = −33.12 + 0.675*LDL-C + 11.95*ln[triglycerides]. The underlying between-subject standard deviation (SDU) was defined as SDU = √ (SD2B - SD2W/2); the within-subject variance (Vw) was calculated for m (2) repeat tests as (Vw) = Σ(xj -xi)2/(m-1)), the within-subject SD (SDw) being its square root; the DR being the ratio SDU/SDW.ResultsAll SDu, SDw and DR’s values were nearly similar, and the observed differences in discriminatory power between all three determinations, i.e. measured and calculated apoB100 levels, did not reach statistical significance. Measured Pearson’s product-moment correlation coefficients between all apoB100 determinations were very high, respectively at 0.94 (measured vs. equation 1); 0.92 (measured vs. equation 2); and 0.97 (equation 1 vs. equation 2), each measurement reaching unity after adjustment for attenuation.ConclusionBoth apoB100 algorithms showed biometrical equivalence, and were as effective in estimating apoB100 from routine lipids. Their use should contribute to better characterize residual cardiometabolic risk linked to the number of atherogenic particles, when direct apoB100 determination is not available.

Highlights

  • Low-density lipoproteins (LDL) and their very-low density lipoprotein (VLDL) precursors represent the major atherogenic particles

  • Both apolipoprotein B100 (apoB100) algorithms showed biometrical equivalence, and were as effective in estimating apoB100 from routine lipids. Their use should contribute to better characterize residual cardiometabolic risk linked to the number of atherogenic particles, when direct apoB100 determination is not available

  • Each contains a single apolipoprotein B100 molecule, which ensures the structural integrity of the lipoprotein, and binds to the hepatic receptor for catabolic removal of LDL

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Summary

Introduction

Low-density lipoproteins (LDL) and their very-low density lipoprotein (VLDL) precursors represent the major atherogenic particles. The relationships between LDL-C, non-HDL-C and apoB100 are often less convergent than expected, and less predictable in patients at high cardiometabolic risk, including those with high TG and/or the metabolic syndrome. In these patients, including those with type 2 diabetes mellitus (T2DM), non-HDL-C and apoB100 are less interchangeable than the reading of the general recommendations for the treatment of hypercholesterolemia would suggest. Apolipoprotein B100 (ApoB100) determination is superior to low-density lipoprotein cholesterol (LDL-C) to establish cardiovascular (CV) risk, and does not require prior fasting. ApoB100 is rarely measured alongside standard lipids, which precludes comprehensive assessment of dyslipidemia

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