Comparison of Three Methods for LDLC Calculation for Cardiovascular Disease Risk Categorisation in Three Distinct Patient Populations.

Autor: Sun CJ; Division of Endocrinology and Metabolism, Department of Medicine, University of Ottawa, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada., McCudden C; Division of Biochemistry, Department of Pathology and Laboratory Medicine, The Ottawa Hospital, Ottawa, Ontario, Canada., Brisson D; Clinical Lipidology and Rare Lipid Disorders Unit, Department of Medicine, Université de Montréal Community Gene Medicine Center, Lipid Clinic Chicoutimi Hospital, and ECOGENE-21 Clinical and Translational Research Center, Chicoutimi, Québec, Canada., Shaw J; Division of Biochemistry, Department of Pathology and Laboratory Medicine, The Ottawa Hospital, Ottawa, Ontario, Canada., Gaudet D; Clinical Lipidology and Rare Lipid Disorders Unit, Department of Medicine, Université de Montréal Community Gene Medicine Center, Lipid Clinic Chicoutimi Hospital, and ECOGENE-21 Clinical and Translational Research Center, Chicoutimi, Québec, Canada., Ooi TC; Division of Endocrinology and Metabolism, Department of Medicine, University of Ottawa, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada. Electronic address: tcooi@toh.ca.
Jazyk: angličtina
Zdroj: The Canadian journal of cardiology [Can J Cardiol] 2023 May; Vol. 39 (5), pp. 668-677. Date of Electronic Publication: 2022 Dec 28.
DOI: 10.1016/j.cjca.2022.12.025
Abstrakt: Background: Limitations of the Friedewald equation for low-density-lipoprotein cholesterol (F-LDLC) calculation led to the Martin-Hopkins (M-LDLC) and Sampson-National Institutes of Health (S-LDLC) equations. We studied these newer calculations of LDLC for correlation and discordance for stratification into the Canadian Cardiovascular Society (CCS) 2021 Dyslipidemia Guidelines' cardiovascular disease (CVD) risk categories.
Methods: We performed analyses on lipid profiles from 3 populations: records of a hospital biochemistry laboratory (population 1), lipid clinic patients without select monogenic dyslipidemias (population 2A), and lipid clinic patients with familial hypercholesterolemia (FH; population 2B).
Results: There was very strong correlation among the 3 calculated LDLC. In populations 1 and 2A, M-LDLC and S-LDLC were progressively higher than F-LDLC as triglyceride (TG) levels increased from normal to ∼ 5 mmol/L. In population 2B, M-LDLC was higher than F-LDLC, but S-LDLC was progressively lower than F-LDLC. Using the CCS 2021 guidelines' 4 CVD risk categories, 7.0% (population 2A) to 7.2% (population 1) of cases for M-LDLC vs F-LDLC and 3.9% (population 2A) to 4.4% (population 1) of cases for S-LDLC vs F-LDLC were reclassified to an adjacent CVD risk category, mostly from a lower to a higher risk category.
Conclusions: Switching from F-LDLC to S-LDLC or M-LDLC can reclassify up to ∼ 4.4% or 7.2% of patients, respectively, to another CCS CVD risk category. The difference between F-LDLC and M-LDLC or S-LDLC is greater with higher TG, and with lower LDLC. We recommend that clinical laboratories switch to reporting results from either M-LDLC or S-LDLC, but S-LDLC should not be used in FH patients, pending further studies.
(Copyright © 2022 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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