Physiological Bases for the Superiority of Apolipoprotein B Over Low‐Density Lipoprotein Cholesterol and Non–High‐Density Lipoprotein Cholesterol as a Marker of Cardiovascular Risk

Journal of the American Heart Association - Tập 11 Số 20 - 2022
Tamara Glavinovic1, George Thanassoulis2, Jacqueline de Graaf3, Patrick Couture4, Robert A. Hegele5, Allan D. Sniderman6
1Division of Nephrology, Department of Medicine, McGill University Health Centre, Montreal, Quebec, Canada
2George Thanassoulis https://orcid.org/0000-0002-9930-7189 , Mike and Valeria Centre for Cardiovascular Prevention, Department of Medicine, , McGill University Health Centre, , Montreal, , Quebec, , Canada,
3Jacqueline de Graaf , University of Nijmegen Radboud University Medical Center, , Department of General Internal Medicine, , Nijmegen, , the Netherlands,
4Université Laval Centre Hospitalier Universitaire de Québec Quebec Canada
5Robert A. Hegele https://orcid.org/0000-0003-2861-5325 , Robarts Research Institute and Department of Medicine, Schulich School of Medicine and Dentistry, , Western University, , London, , Ontario, , Canada,
6Allan D. Sniderman https://orcid.org/0000-0002-3540-3956 , Mike and Valeria Centre for Cardiovascular Prevention, Department of Medicine, , McGill University Health Centre, , Montreal, , Quebec, , Canada,

Tóm tắt

In 2019, the European Society of Cardiology/European Atherosclerosis Society stated that apolipoprotein B (apoB) was a more accurate marker of cardiovascular risk than low‐density lipoprotein cholesterol (LDL‐C) and non–high‐density lipoprotein cholesterol. Since then, the evidence has continued to mount in favor of apoB. This review explicates the physiological mechanisms responsible for the superiority of apoB as a marker of the cardiovascular risk attributable to the atherogenic apoB lipoprotein particles chylomicron remnants, very low‐density lipoprotein, and low‐density lipoprotein particles. First, the nature and relative numbers of these different apoB particles will be outlined. This will make clear why low‐density lipoprotein particles are almost always the major determinants of cardiovascular risk and why the concentrations of triglycerides and LDL‐C may obscure this relation. Next, the mechanisms that govern the number of very low‐density lipoprotein and low‐density lipoprotein particles will be outlined because, except for dysbetalipoproteinemia, the total number of apoB particles determines cardiovascular risk, Then, the mechanisms that govern the cholesterol mass within very low‐density lipoprotein and low‐density lipoprotein particles will be reviewed because these are responsible for the discordance between the mass of cholesterol within apoB particles, measured either as LDL‐C or non–high‐density lipoprotein cholesterol, and the number of apoB particles measured as apoB, which creates the superior predictive power of apoB over LDL‐C and non–high‐density lipoprotein cholesterol. Finally, the major apoB dyslipoproteinemias will be briefly outlined. Our objective is to provide a physiological framework for health care givers to understand why apoB is a more accurate marker of cardiovascular risk than LDL‐C or non–high‐density lipoprotein cholesterol.

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Tài liệu tham khảo

10.1097/MOL.0000000000000330

10.1001/jamacardio.2019.3780

10.1093/eurheartj/ehz455

10.1001/jamacardio.2021.5080

10.1371/journal.pmed.1003062

10.1093/ije/dyaa216

10.1002/ana.25916

10.1161/CIRCULATIONAHA.121.053797

10.1016/S2666-7568(21)00086-6

10.1016/j.jacc.2021.01.027

10.1001/jamacardio.2021.5083

10.1515/cclm-2019-1253

10.1016/j.cca.2020.05.001

10.1016/0026-0495(83)90194-4

10.1016/S0022-2275(20)38178-5

10.1016/S0002-9149(03)00262-5

10.1007/978-90-368-0980-1

Kane JP, Havel RJ. In: Scriver C, ed The Metabolic Basis of Inherited Disease. 6th ed. McGraw‐Hill; 1139–1164.

10.1073/pnas.77.5.2465

10.1126/science.8511591

10.1161/JAHA.119.014711

10.1016/S0022-2275(20)38425-X

10.1016/S0022-2275(20)37199-6

Utermann G. The Metabolic and Molecular Bases of Inherited Disease. In: Scriver C, Beaudet AL, Sly WS, Valle D, eds. Lipoprotein(a). 8th ed. McGraw‐Hill; 2001:2753–2787.

10.1056/NEJMoa1109034

10.1016/j.clinbiochem.2020.09.007

10.1177/0004563220968473

10.1016/j.cjca.2021.02.017

10.1016/j.metabol.2016.02.008

10.1016/0009-8981(78)90038-4

10.1016/0021-9150(91)90050-D

10.1016/j.jacl.2018.09.006

10.1161/ATVBAHA.115.307044

10.1016/j.cca.2013.02.005

10.1194/jlr.R082271

10.1097/MOL.0000000000000192

10.1161/ATVBAHA.112.251116

10.1194/jlr.R800090-JLR200

10.1097/00041433-199908000-00008

10.1161/01.ATV.13.5.629

10.1161/01.ATV.18.2.147

10.1007/s00125-005-0125-z

10.1172/JCI112360

10.1016/j.metabol.2021.154887

10.1161/01.ATV.0000172689.53992.25

10.1016/0026-0495(86)90236-2

10.1016/0026-0495(81)90064-0

10.1007/BF01800473

10.1172/JCI107332

10.1055/s-2004-861490

Sniderman AD Castro Cabezas M Ribalta J Carmena R de Bruin TWA de Graaf J Erkelens DW Humphries SE Masana L Real JT et al. A proposal to redefine familial combined hyperlipidaemia ‐‐ third workshop on FCHL held in Barcelona from 3 to 5 May 2001 during the scientific sessions of the European Society for Clinical Investigation. 2002; 32:71–73.

10.1194/jlr.M400108-JLR200

10.1016/j.atherosclerosis.2021.05.007

10.3389/fendo.2020.00474

10.1172/JCI35206

10.1016/S0021-9150(99)00282-8

10.1016/S0021-9258(17)44822-8

10.1016/0026-0495(78)90151-8

10.1074/jbc.M413877200

10.1161/ATVBAHA.120.315204

10.1016/S0021-9150(01)00709-2

10.1161/ATVBAHA.108.179564

10.1016/j.jacc.2022.01.010

10.1016/S0022-2275(20)35728-X

10.1042/bst0110639

10.1161/01.CIR.74.4.805

10.1016/S0022-2275(20)33899-2

10.1172/JCI109490

10.1016/S0021-9258(18)34287-X

10.1016/S0021-9258(18)34288-1

10.1016/0002-8703(87)90617-X

10.1042/CS20090402

10.1161/01.ATV.0000155323.18856.a2

10.1194/jlr.M300448-JLR200

10.1194/jlr.R200004-JLR200

Nurmohamed NS, Ditmarsch M, Kastelein JJP. CETP‐inhibitors: from HDL‐C to LDL‐C lowering agents? Cardiovasc Res 2021 Epub ahead of print. PMID: 34849601.

10.1016/0021-9150(94)90129-5

10.1161/01.ATV.14.6.902

10.1056/NEJM196701052760107

10.1056/NEJM196701122760206

10.1056/NEJM196701192760305

10.1056/NEJM196701262760406

10.1056/NEJM196702022760507

Berberich AJ, Hegele RA. A modern approach to dyslipidemia. Endocr Rev 2021. Epub ahead of print. PMID: 34676866.

10.1038/nrendo.2010.50

10.1161/CIR.0000000000000625

10.1016/j.atherosclerosis.2018.06.859

10.1016/j.jacl.2020.01.003

10.1097/MOL.0000000000000796

10.1016/S0022-2275(20)38008-1

10.1111/j.1365-2362.1980.tb00004.x

10.1016/0026-0495(76)90089-5

10.1161/01.CIR.101.24.2777

10.1161/01.CIR.0000130646.93255.86

10.1161/01.ATV.0000077220.44620.9B

10.1136/bmjdrc-2019-001107

10.7326/0003-4819-135-6-200109180-00014

Sagris M, Antonopoulos AS, Theofilis P, Oikonomou E, Siasos G, Tsalamandris S, Antoniades C, Brilakis ES, Kaski JC, Tousoulis D. Risk factors profile of young and older patients with Myocardial Infarction. Cardiovasc Res 2021; Epub ahead of print. PMID: 34358302.

10.1093/eurheartj/ehp051

10.1016/j.jacl.2020.11.006

10.1016/S0021-9258(18)89180-3

10.1097/MED.0000000000000316

10.1016/j.jacl.2008.10.002

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Journal of the American Heart Association

Tập 11 Số 20

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