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Cited by 118Lipoproteins and Cardiovascular HealthAcute Myocardial Infarction ResearchDiabetes, Cardiovascular Risks, and Lipoproteins

Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

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Hagström, Emil, Steg, P. Gabriel, Szarek, Michael, Bhatt, Deepak L., Bittner, Vera A., Danchin, Nicolas, Diaz, Rafael, Goodman, Shaun G. +1727 more·2022·Circulation
DOI 10.1161/circulationaha.121.057807PMC PMC9422774
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Abstract

Background: Apolipoprotein B (apoB) provides an integrated measure of atherogenic risk. Whether apoB levels and apoB lowering hold incremental predictive information on residual risk after acute coronary syndrome beyond that provided by low-density lipoprotein cholesterol is uncertain. Methods: The ODYSSEY OUTCOMES trial (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) compared the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab with placebo in 18 924 patients with recent acute coronary syndrome and elevated atherogenic lipoproteins despite optimized statin therapy. Primary outcome was major adverse cardiovascular events (MACE; coronary heart disease death, nonfatal myocardial infarction, fatal/nonfatal ischemic stroke, hospitalization for unstable angina). Associations between baseline apoB or apoB at 4 months and MACE were assessed in adjusted Cox proportional hazards and propensity score–matched models. Results: Median follow-up was 2.8 years. In proportional hazards analysis in the placebo group, MACE incidence increased across increasing baseline apoB strata (3.2 [95% CI, 2.9–3.6], 4.0 [95% CI, 3.6–4.5], and 5.5 [95% CI, 5.0–6.1] events per 100 patient-years in strata <75, 75–<90, ≥90 mg/dL, respectively; P trend <0.0001) and after adjustment for low-density lipoprotein cholesterol ( P trend =0.035). Higher baseline apoB stratum was associated with greater relative ( P trend <0.0001) and absolute reduction in MACE with alirocumab versus placebo. In the alirocumab group, the incidence of MACE after month 4 decreased monotonically across decreasing achieved apoB strata (4.26 [95% CI, 3.78–4.79], 3.09 [95% CI, 2.69–3.54], and 2.41 [95% CI, 2.11–2.76] events per 100 patient-years in strata ≥50, >35–<50, and ≤35 mg/dL, respectively). Compared with propensity score–matched patients from the placebo group, treatment hazard ratios for alirocumab also decreased monotonically across achieved apoB strata. Achieved apoB was predictive of MACE after adjustment for achieved low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol but not vice versa. Conclusions: In patients with recent acute coronary syndrome and elevated atherogenic lipoproteins, MACE increased across baseline apoB strata. Alirocumab reduced MACE across all strata of baseline apoB, with larger absolute reductions in patients with higher baseline levels. Lower achieved apoB was associated with lower risk of MACE, even after accounting for achieved low-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol, indicating that apoB provides incremental information. Achievement of apoB levels as low as ≤35 mg/dL may reduce lipoprotein-attributable residual risk after acute coronary syndrome. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01663402.

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Crossref · 10.1161/circulationaha.121.057807

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  • The benefits of lipid-lowering therapy appear to correlate more closely with reductions in apoB than with triglyceride lowering alone.

    “At the same time, it is important to recognize that apoB remains the most informative single summary measure of atherogenic risk, as LDL apoB numerically dominates total apoB in most individuals; accordingly, the benefits of lipid-lowering therapy appear to correlate more closely with reductions in apoB (particle number) than with triglyceride lowering alone [2, 18, 19].”

    From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [19]

    The Results (page not provided) report greater alirocumab treatment benefit at lower achieved apoB levels, and the Discussion links lower achieved apoB with lower cardiovascular risk after acute coronary syndrome. The paper does not compare that association with triglyceride lowering alone, and its analysis concerns achieved apoB levels rather than directly comparing reductions in the two measures. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • ApoB remains the most informative single summary measure of atherogenic risk, as LDL apoB numerically dominates total apoB in most individuals.

    “At the same time, it is important to recognize that apoB remains the most informative single summary measure of atherogenic risk, as LDL apoB numerically dominates total apoB in most individuals; accordingly, the benefits of lipid-lowering therapy appear to correlate more closely with reductions in apoB (particle number) than with triglyceride lowering alone [2, 18, 19].”

    From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [19]

    The Clinical Implications section says apoB measures the total concentration of circulating atherogenic particles, and the Discussion reports that achieved apoB appeared more predictive of future cardiovascular events than achieved non–HDL cholesterol in this study. The paper does not establish that apoB is the most informative single measure across individuals or that LDL apoB numerically dominates total apoB in most people. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Hagström, E., Steg, P. G., Szarek, M., Bhatt, D. L., Bittner, V. A., Danchin, N., Diaz, R., Goodman, S. G., Harrington, R. A., Jukema, J. W., Liberopoulos, E., Marx, N., McGinniss, J., Manvelian, G., Pordy, R., Scemama, M., White, H. D., Zeiher, A. M., Schwartz, G. G., Schwartz, G. G., Bhatt, D. L., Bittner, V. A., Diaz, R., Goodman, S. G., Harrington, R. A., Jukema, J. W., Szarek, M., White, H. D., Zeiher, A. M., Tricoci, P., Roe, M. T., Mahaffey, K. W., Edelberg, J. M., Hanotin, C., Lecorps, G., Moryusef, A., Pordy, R., Sasiela, W. J., Tamby, J.-F., Diaz, R., Aylward, P. E., Drexel, H., Sinnaeve, P., Dilic, M., Lopes, R. D., Gotcheva, N. N., Goodman, S. G., Prieto, J.-C., Yong, H., López-Jaramillo, P., Pećin, I., Reiner, Z., Ostadal, P., Poulsen, S. H., Viigimaa, M., Nieminen, M. S., Danchin, N., Chumburidze, V., Marx, N., Liberopoulos, E., Carlos, P., Valdovinos, M., Tse, H.-F., Kiss, R. G., Xavier, D., Zahger, D., Valgimigli, M., Kimura, T., Kim, H. S., Kim, S.-H., Erglis, A., Laucevicius, A., Kedev, S., Yusoff, K., Ramos López, G. A., Alings, M., White, H. D., Halvorsen, S., Correa Flores, R. M., Sy, R. G., Budaj, A., Morais, J., Dorobantu, M., Karpov, Y., Ristic, A. D., Chua, T., Murin, J., Fras, Z., Dalby, A. J., Tuñón, J., de Silva, H. A., Hagström, E., Landmesser, U., Müller, C., Chiang, C.-E., Sritara, P., Guneri, S., Parkhomenko, A., Ray, K. K., Moriarty, P. M., Roe, M. T., Vogel, R., Chaitman, B., Kelsey, S. F., Olsson, A. G., Rouleau, J.-L., Simoons, M. L., Alexander, K., Meloni, C., Rosenson, R., Sijbrands, E. J. G., Tricoci, P., Alexander, J. H., Armaganijan, L., Bagai, A., Bahit, M. C., Brennan, J. M., Clifton, S., DeVore, A. D., Deloatch, S., Dickey, S., Dombrowski, K., Ducrocq, G., Eapen, Z., Endsley, P., Eppinger, A., Harrison, R. W., Hess, C. N., Hlatky, M. A., Jordan, J. D., Knowles, J. W., Kolls, B. J., Kong, D. F., Leonardi, S., Lillis, L., Lopes, R. D., Maron, D. J., Mahaffey, K. W., Marcus, J., Mathews, R., Mehta, R. H., Mentz, R. J., Moreira, H. G., Patel, C. B., Pereira, S. B., Perkins, L., Povsic, T. J., Puymirat, E., Roe, M. T., Jones, W. S., Shah, B. R., Sherwood, M. W., Stringfellow, K., Sujjavanich, D., Toma, M., Trotter, C., van Diepen, S. F. P., Wilson, M. D., Tze-Kay Yan, A., Schiavi, L. B., Garrido, M., Alvarisqueta, A. F., Sassone, S. A., Bordonava, A. P., Alves De Lima, A. E., Schmidberg, J. M., Duronto, E. A., Caruso, O. C., Novaretto, L. P., Hominal, M. A., Montaña, O. R., Caccavo, A., Gomez Vilamajo, O. A., Lorenzatti, A. J., Cartasegna, L. R., Paterlini, G. A., Mackinnon, I. J., Caime, G. D., Amuchastegui, M., Salomone, O., Codutti, O. R., Jure, H. O., Bono, J. O., Hrabar, A. D., Vallejos, J. A., Ahuad Guerrero, R. A., Novoa, F., Patocchi, C. A., Zaidman, C. J., Giuliano, M. E., Dran, R. D., Vico, M. L., Carnero, G. S., Guzman, P. N., Medrano Allende, J. C., Garcia Brasca, D. F., Bustamante Labarta, M. H., Nani, S., Blumberg, E. D., Colombo, H. R., Liberman, A., Fuentealba, V., Luciardi, H. L., Waisman, G. D., Berli, M. A., Garcia Duran, R. O., Cestari, H. G., Luquez, H. A., Giordano, J. A., Saavedra, S. S., Zapata, G., Costamagna, O., Llois, S., Waites, J. H., Collins, N., Soward, A., Aylward, P. E., Hii, C. L., Aylward, P. E., Shaw, J., Arstall, M. A., Horowitz, J., Ninio, D., Rogers, J. F., Colquhoun, D., Oqueli Flores, R. E., Roberts-Thomson, P., Raffel, O., Lehman, S. J., Aroney, C., Coverdale, S. G., Garrahy, P. J., Starmer, G., Sader, M., Carroll, P. A., Dick, R., Zweiker, R., Hoppe, U., Drexel, H., Huber, K., Berger, R., Delle-Karth, G., Frey, B., Weidinger, F., Faes, D., Hermans, K., Pirenne, B., Leone, A., Hoffer, E., Sinnaeve, P., Vrolix, M. C., Wolf, L. D., Wollaert, B., Castadot, M., Dujardin, K., Beauloye, C., Vervoort, G., Striekwold, H., Convens, C., Roosen, J., Barbato, E., Claeys, M., Cools, F., Terzic, I., Barakovic, F., Midzic, Z., Pojskic, B., Fazlibegovic, E., Dilic, M., Durak-Nalbantic, A., Kulić, M., Vulic, D., Muslibegovic, A., Goronja, B., Reis, G., Sousa, L., Nicolau, J. C., Giorgeto, F. E., Silva, R. P., Maia, L. N., Rech, R., Rossi, P. R., Cerqueira, M. J. A., Duda, N., Kalil, R., Kormann, A., Abrantes, J. A. M., Filho, P. P., Soggia, A. P., de Santos, M. O., Neuenschwander, F., Bodanese, L. C., Michalaros, Y. L., Eliaschewitz, F. G., Vidotti, M. H., Leaes, P. E., Botelho, R. V., Kaiser, S., Manenti, E. R. F. F., Precoma, D. B., Moura Jorge, J. C., Silva, P., Silveira, J. A., Saporito, W., Neto, J. A. M., Feitosa, G. S., Ritt, L. E. F., de Souza, J. A., Costa, F., Souza, W. K., Reis, H. J., Lopes, R. D., Machado, L., Aidar Ayoub, J. C., Todorov, G. V., Nikolov, F. P., Velcheva, E. S., Tzekova, M. L., Benov, H. 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Affiliations
  • Department of Cardiology, Université de Paris, Assistance Publique-Hôpitaux de Paris, Hôpital Bichat, FACT (French Alliance for Cardiovascular Trials), and INSERM U1148, France (P.G.S.).
  • Regeneron (United States) (US)
  • St. Michael's Hospital (CA)
  • University of Colorado Anschutz (US)
  • Instituto Cardiovascular de Rosario (AR)
  • Assistance Publique – Hôpitaux de Paris (FR)
  • SUNY Downstate Health Sciences University (US)
  • Leiden University Medical Center (NL)
  • National and Kapodistrian University of Athens (GR)
  • Universitätsklinikum Aachen (DE)
  • Goethe University Frankfurt (DE)
  • Inserm (FR)
  • Auckland City Hospital (NZ)
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2022-08-30
Volume
146
Issue
9
Pages
657-672
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/circulationaha.121.057807
PMC
PMC9422774
OpenAlex
W4283739701
Cited by
118
References
9
Citations by year
2026: 21 · 2025: 29 · 2024: 38 · 2023: 27 · 2022: 3
FWCI
23.42
Type
journal article
Language
en
Open access
Licence
Locations
  • Circulation (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Leiden Repository (Leiden University) (submittedVersion, cc-by-nc-nd)
  • Data Archiving and Networked Services (DANS) (submittedVersion, cc-by-nc-nd)
  • KTH Publication Database DiVA (KTH Royal Institute of Technology) (submittedVersion, other-oa)
  • HAL (submittedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
  • RWTH Publications (RWTH Aachen) (submittedVersion, other-oa)
  • Radboud Repository (Radboud University) (submittedVersion)
  • Radboud Repository (Radboud University) (submittedVersion, other-oa)
  • RWTH Publications (RWTH Aachen)
Funders
  • Amgen
  • Pfizer
  • Sanofi
  • Brigham and Women's Hospital
  • CSL Behring
  • Boston Scientific Corporation
  • Regeneron Pharmaceuticals
  • Belvoir Media Group
  • University of Alberta
  • Imperial College London
  • Institut National de la Santé et de la Recherche Médicale (U1148)
  • University of Toronto
  • Leids Universitair Medisch Centrum
  • National and Kapodistrian University of Athens
  • Université Paris Descartes
  • Uppsala Universitet
  • RWTH Aachen University
  • Assistance publique-Hôpitaux de Paris
  • Université de Paris
  • St. Jude Medical
  • Netherlands Heart Institute
  • Duke Clinical Research Institute
  • University of Colorado School of Medicine, Anschutz Medical Campus
  • Daiichi Sankyo Europe
Topics
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
apolipoprotein B, alirocumab, PCSK9 inhibitors, acute coronary syndrome, residual cardiovascular risk, major adverse cardiovascular events, LDL cholesterol, non-HDL cholesterol, atherogenic lipoproteins, statin therapy, lipid-lowering therapy, risk prediction, ODYSSEY OUTCOMES trial, propensity score matching
MeSH terms
Heart Disease Risk Factors, Anticholesteremic Agents, Apolipoproteins B, Cardiovascular Diseases, Cholesterol, Humans, Cholesterol, LDL, Risk Factors, Treatment Outcome, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Atherosclerosis, Acute Coronary Syndrome, Antibodies, Monoclonal, Humanized

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