# Lipoprotein(a) Concentration and Achieving Target Values of Low-Density Lipoprotein Cholesterol Calculated by Different Equations

## TL;DR

This study examines how different equations for calculating LDL cholesterol can be affected by elevated lipoprotein(a) levels, which may lead to misclassification of cardiovascular risk.

## Contribution

The study provides insights into how Lp(a) concentration affects LDL-C calculations and suggests thresholds for accurate LDL-C interpretation in patients with elevated Lp(a).

## Key findings

- Up to 90% of LDL-C calculated by certain equations may be due to Lp(a)-cholesterol in patients with elevated Lp(a).
- Using Martin–Hopkins and Sampson equations reclassified 10-13% of patients to a higher risk category compared to Friedewald.
- LDL-C corrected for Lp(a) reclassified 30-59% of patients to a lower risk category at clinically significant thresholds.

## Abstract

Background: Low-density lipoprotein cholesterol (LDL-C) is a major cardiovascular risk factor and an indicator of hypolipidemic therapy effectiveness. However, direct and calculated methods for determining “LDL-C” present the sum of the cholesterol in all apoB-containing lipoproteins, including lipoprotein(a) [Lp(a)]. There has been an ongoing debate about the correctness of LDL-C in patients with elevated Lp(a) concentrations up to now. The aim of this study was to evaluate the effect of Lp(a) concentration on the LDL-C calculated by different equations. Methods: The study included the results of fasting lipids and Lp(a) concentration of 566 measurements from 283 patients (before and after lipid-lowering therapy prescribing, after exclusion of 17 patients with incomplete data). LDL-C and LDL-C corrected for Lp(a)-cholesterol (LDL-Ccorr) were calculated by Friedewald, Martin–Hopkins, and Sampson equations. Results: We assessed 566 measurements of lipids and Lp(a). The number of values reclassified to a higher risk category was 10% and 13% with Martin–Hopkins and Sampson equations compared to the Friedewald formula. The percentage of Lp(a)-cholesterol (Lp(a)-C) in the LDL-C calculated by three formulas was up to 90% or more depending on the concentration of LDL-C and Lp(a). When stratified by clinically significant LDL-C thresholds, the proportion of values LDL-Ccorr reclassified to a lower risk category ranged from 30 to 59%. Conclusion: Comparison of LDL-C concentrations calculated by Friedewald, Martin–Hopkins, and Sampson equations showed high consistency in patients without elevated triglycerides. The LDLcorr is reasonable to use in patients with Lp(a) concentration ≥ 30 and ≥41 mg/dL when using the Martin–Hopkins and Sampson equations, respectively. These data may help clinicians interpret LDL-C goal attainment in patients with elevated Lp(a) and avoid misclassification driven by the Lp(a)-cholesterol component.