Michel R Langlois1, M John Chapman2, Christa Cobbaert3, Samia Mora4, Alan T Remaley5, Emilio Ros6, Gerald F Watts7, Jan Borén8, Hannsjörg Baum9, Eric Bruckert10, Alberico Catapano11, Olivier S Descamps12, Arnold von Eckardstein13, Pia R Kamstrup14, Genovefa Kolovou15, Florian Kronenberg16, Anne Langsted14, Kari Pulkki17, Nader Rifai18, Grazyna Sypniewska19, Olov Wiklund8, Børge G Nordestgaard14. 1. Department of Laboratory Medicine, AZ St-Jan, Brugge, and University of Ghent, Belgium; michel.langlois@azsintjan.be. 2. National Institute for Health and Medical Research (INSERM), and Endocrinology-Metabolism Service, Pitié-Salpetriere University Hospital, Paris, France. 3. Department of Clinical Chemistry and Laboratory Medicine, Leiden University Medical Center, Leiden, the Netherlands. 4. Divisions of Preventive and Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. 5. Lipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD. 6. Lipid Clinic, Department of Endocrinology and Nutrition, Institut d'Investigacions Biomèdiques August Pi Sunyer, Hospital Clínic, Barcelona and Ciber Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Spain. 7. Lipid Disorders Clinic, Department of Cardiology, Royal Perth Hospital, University of Western Australia, Perth, Australia. 8. Sahlgrenska University Hospital, Gothenburg, Sweden. 9. Institute for Laboratory Medicine, Blutdepot und Krankenhaushygiene, Regionale Kliniken Holding RKH GmbH, Ludwigsburg, Germany. 10. Pitié-Salpetriere University Hospital, Paris, France. 11. Department of Pharmacological and Biomolecular Sciences, University of Milan, Italy. 12. Hopital de Jolimont, Haine-Saint-Paul, Belgium. 13. Institute for Clinical Chemistry, University Hospital Zurich, Zurich, Switzerland. 14. Herlev and Gentofte Hospital, Copenhagen University Hospital, University of Copenhagen, Copenhagen, Denmark. 15. Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece. 16. Department of Medical Genetics, Molecular and Clinical Pharmacology, Division of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria. 17. Department of Clinical Chemistry, University of Turku and Turku University Hospital, Turku, Finland. 18. Boston Children's Hospital, Harvard Medical School, Boston, MA. 19. Department of Laboratory Medicine, Collegium Medicum, NC University, Bydgoszcz, Poland.
Abstract
BACKGROUND: The European Atherosclerosis Society-European Federation of Clinical Chemistry and Laboratory Medicine Consensus Panel aims to provide recommendations to optimize atherogenic lipoprotein quantification for cardiovascular risk management. CONTENT: We critically examined LDL cholesterol, non-HDL cholesterol, apolipoprotein B (apoB), and LDL particle number assays based on key criteria for medical application of biomarkers. (a) Analytical performance: Discordant LDL cholesterol quantification occurs when LDL cholesterol is measured or calculated with different assays, especially in patients with hypertriglyceridemia >175 mg/dL (2 mmol/L) and low LDL cholesterol concentrations <70 mg/dL (1.8 mmol/L). Increased lipoprotein(a) should be excluded in patients not achieving LDL cholesterol goals with treatment. Non-HDL cholesterol includes the atherogenic risk component of remnant cholesterol and can be calculated in a standard nonfasting lipid panel without additional expense. ApoB more accurately reflects LDL particle number. (b) Clinical performance: LDL cholesterol, non-HDL cholesterol, and apoB are comparable predictors of cardiovascular events in prospective population studies and clinical trials; however, discordance analysis of the markers improves risk prediction by adding remnant cholesterol (included in non-HDL cholesterol) and LDL particle number (with apoB) risk components to LDL cholesterol testing. (c) Clinical and cost-effectiveness: There is no consistent evidence yet that non-HDL cholesterol-, apoB-, or LDL particle-targeted treatment reduces the number of cardiovascular events and healthcare-related costs than treatment targeted to LDL cholesterol. SUMMARY: Follow-up of pre- and on-treatment (measured or calculated) LDL cholesterol concentration in a patient should ideally be performed with the same documented test method. Non-HDL cholesterol (or apoB) should be the secondary treatment target in patients with mild to moderate hypertriglyceridemia, in whom LDL cholesterol measurement or calculation is less accurate and often less predictive of cardiovascular risk. Laboratories should report non-HDL cholesterol in all standard lipid panels.
BACKGROUND: The European Atherosclerosis Society-European Federation of Clinical Chemistry and Laboratory Medicine Consensus Panel aims to provide recommendations to optimize atherogenic lipoprotein quantification for cardiovascular risk management. CONTENT: We critically examined LDL cholesterol, non-HDL cholesterol, apolipoprotein B (apoB), and LDL particle number assays based on key criteria for medical application of biomarkers. (a) Analytical performance: Discordant LDL cholesterol quantification occurs when LDL cholesterol is measured or calculated with different assays, especially in patients with hypertriglyceridemia >175 mg/dL (2 mmol/L) and low LDL cholesterol concentrations <70 mg/dL (1.8 mmol/L). Increased lipoprotein(a) should be excluded in patients not achieving LDL cholesterol goals with treatment. Non-HDL cholesterol includes the atherogenic risk component of remnant cholesterol and can be calculated in a standard nonfasting lipid panel without additional expense. ApoB more accurately reflects LDL particle number. (b) Clinical performance: LDL cholesterol, non-HDL cholesterol, and apoB are comparable predictors of cardiovascular events in prospective population studies and clinical trials; however, discordance analysis of the markers improves risk prediction by adding remnant cholesterol (included in non-HDL cholesterol) and LDL particle number (with apoB) risk components to LDL cholesterol testing. (c) Clinical and cost-effectiveness: There is no consistent evidence yet that non-HDL cholesterol-, apoB-, or LDL particle-targeted treatment reduces the number of cardiovascular events and healthcare-related costs than treatment targeted to LDL cholesterol. SUMMARY: Follow-up of pre- and on-treatment (measured or calculated) LDL cholesterol concentration in a patient should ideally be performed with the same documented test method. Non-HDL cholesterol (or apoB) should be the secondary treatment target in patients with mild to moderate hypertriglyceridemia, in whom LDL cholesterol measurement or calculation is less accurate and often less predictive of cardiovascular risk. Laboratories should report non-HDL cholesterol in all standard lipid panels.
Authors: Safi U Khan; Muhammad U Khan; Shahul Valavoor; Muhammad Shahzeb Khan; Victor Okunrintemi; Mamas A Mamas; Thorsten M Leucker; Michael J Blaha; Erin D Michos Journal: Eur J Prev Cardiol Date: 2019-09-02 Impact factor: 7.804
Authors: M John Chapman; Alexina Orsoni; Ricardo Tan; Natalie A Mellett; Anh Nguyen; Paul Robillard; Philippe Giral; Patrice Thérond; Peter J Meikle Journal: J Lipid Res Date: 2020-04-15 Impact factor: 5.922
Authors: Gerald F Watts; Samuel S Gidding; Pedro Mata; Jing Pang; David R Sullivan; Shizuya Yamashita; Frederick J Raal; Raul D Santos; Kausik K Ray Journal: Nat Rev Cardiol Date: 2020-01-23 Impact factor: 32.419