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Lipoprotein(a), PCSK9 Inhibition, and Cardiovascular Risk: Insights From the FOURIER Trial
Open accessAbstract
Background: Lipoprotein(a) [Lp(a)] may play a causal role in atherosclerosis. PCSK9 (proprotein convertase subtilisin/kexin 9) inhibitors have been shown to significantly reduce plasma Lp(a) concentration. However, the relationship between Lp(a) levels, PCSK9 inhibition, and cardiovascular risk reduction remains undefined. Methods: Lp(a) was measured in 25 096 patients in the FOURIER trial (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk), a randomized trial of evolocumab versus placebo in patients with established atherosclerotic cardiovascular disease (median follow-up, 2.2 years). Cox models were used to assess the independent prognostic value of Lp(a) and the efficacy of evolocumab for coronary risk reduction by baseline Lp(a) concentration. Results: The median (interquartile range) baseline Lp(a) concentration was 37 (13–165) nmol/L. In the placebo arm, patients with baseline Lp(a) in the highest quartile had a higher risk of coronary heart disease death, myocardial infarction, or urgent revascularization (adjusted hazard ratio quartile 4: quartile 1, 1.22; 95% CI, 1.01–1.48) independent of low-density lipoprotein cholesterol. At 48 weeks, evolocumab significantly reduced Lp(a) by a median (interquartile range) of 26.9% (6.2%–46.7%). The percent change in Lp(a) and low-density lipoprotein cholesterol at 48 weeks in patients taking evolocumab was moderately positively correlated ( r =0.37; 95% CI, 0.36–0.39; P <0.001). Evolocumab reduced the risk of coronary heart disease death, myocardial infarction, or urgent revascularization by 23% (hazard ratio, 0.77; 95% CI, 0.67–0.88) in patients with a baseline Lp(a) >median, and by 7% (hazard ratio, 0.93; 95% CI, 0.80–1.08; P interaction=0.07) in those ≤median. Coupled with the higher baseline risk, the absolute risk reductions, and number needed to treat over 3 years were 2.49% and 40 versus 0.95% and 105, respectively. Conclusions: Higher levels of Lp(a) are associated with an increased risk of cardiovascular events in patients with established cardiovascular disease irrespective of low-density lipoprotein cholesterol. Evolocumab significantly reduced Lp(a) levels, and patients with higher baseline Lp(a) levels experienced greater absolute reductions in Lp(a) and tended to derive greater coronary benefit from PCSK9 inhibition. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT01764633.
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“In the FOURIER trial, greater MACE reductions were seen among patients whose highly elevated Lp(a) levels were reduced by evolocumab [193].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [193]
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“This finding has also been supported by randomised control trials which shown that PCSK9 inhibition with evolocumab provides modest (16%) reduction in Lp(a) levels in patients with high Lp(a) levels43.”
From Genetic insights into causal effects of lipids and lipid-modifying targets on calcific aortic valve stenosis: a Mendelian randomized study (2025) · cites this paper as [43]
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“The net effect is a muted class response, with Lp(a) typically lowering around 20 to 30%, well below the reductions seen with LDL C and ApoB [25].”
From Oral PCSK9 inhibitors for elevated LDL-C: A systematic review and meta-analysis of randomized trials (2026) · cites this paper as [25]
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“Although recent studies with PCSK9 inhibitors were not designed to target patients with high Lp(a) concentrations, they nevertheless revealed that patients with higher baseline Lp(a) concentration experienced greater absolute reductions in Lp(a) and tended to derive greater clinical benefit from PCSK9 inhibition [27,28].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [27]
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“evolocumab in the FOURIER trial reduced Lp(a) by a median of 26.9% at 48 weeks[2,25], and alirocumab in ODYSSEY OUTCOMES showed a median relative reduction of −23% by 4 months[3,26].”
From Oral PCSK9 inhibitors for elevated LDL-C: A systematic review and meta-analysis of randomized trials (2026) · cites this paper as [25]
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“In contrast, Mendelian randomization studies have consistently demonstrated that lifelong exposure to higher Lp(a) levels is strongly and causally associated with an increased risk of ASCVD [74,75].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [75]
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Citations
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TRIM31–LOX‐1 Axis: A Novel Therapeutic Frontier in Atherosclerosis
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Talkhan, A., Elkasaby, M. H., Osman, A. S. A., Elsharkawy, M. M., Shehata, M., khalefa, K. A., Seleim, A. M., Elezz, A. M. A., Fishman, W. H., & Aronow, W. S. (2026) · Cardiology in Review · doi:10.1097/crd.0000000000001473 · Cited by 1
Targeting Lipoprotein(a): A New Era in Cardiovascular Disease Prevention
Bene-Alhasan, Y. O., Nambi, V., Abushamat, L. A., & Ballantyne, C. M. (2026) · Methodist DeBakey Cardiovascular Journal · doi:10.14797/mdcvj.1836
“…of PCSK9 Inhibition in the Thrombolysis in Myocardial Infarction 57) and FOURIER (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk) trials, 75,76 the ODYSSEY Outcomes trial, 77 and the ORION trial—have each demonstrated sustained reductions in Lp(a).”
Lipoprotein(a) in the statin era: from risk marker to therapeutic target
Hong, R., 刘玉华, 李晓春, Liu, H., & 谢东阳 (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1938864
“In FOURIER, patients with higher baseline Lp(a) gained greater absolute risk reduction from evolocumab (O’Donoghue et al., 2019).”
Repeat measurement of lipoprotein(a): potential future clinical scenarios
Zeng, R., Zhang, M.-Z., & Li, J. (2026) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwag498
Emerging Prognostic Risk Factors in Acute Coronary Syndromes: Beyond Traditional Risk Assessment
Cangiano, L., Marenzi, G., Pontone, G., & Cosentino, N. (2026) · Journal of Clinical Medicine · doi:10.3390/jcm15187312
“Secondary analyses from both FOURIER and ODYSSEY OUTCOMES suggest that part of the cardiovascular benefit observed with PCSK9 inhibition may be attributable to reductions in Lp(a), particularly among patients with elevated baseline concentrations [16,17].”
Kafol, J., Fras, Z., Novakovic, M., Cevc, M., Krevel, B., Kafol, L., Kelenc, A., Kepic, K., Vrbinc, K. N., Švarc, M., et al. (2026) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2026.121912
Drug-Coated Balloons: A Potential Treatment Option for Stabilizing Vulnerable Plaque
Dijkstra, T. N., Rubio, P. M., Bosch, I. T., van Veelen, A., Nurmohamed, N. S., van de Vijver, W. R., Hennecken, J., Verpalen, V. A., Henriques, J. P. S., den Hartog, A. W., et al. (2026) · Journal of the Society for Cardiovascular Angiography & Interventions · doi:10.1016/j.jscai.2026.105575
Kim, H., Ahn, J., Kang, D.-Y., Wee, S.-B., An, S. Y., Park, H. S., Kim, J. H., Kim, A.-R., Park, D., Kim, Y., et al. (2026) · JACC Asia · doi:10.1016/j.jacasi.2026.08.016
Lipoprotein (a): from molecular structure features to diagnostic and treatment approaches
Skybchyk, V. А., Kysil, O. Y., Labinska, O., & Halkevych, M. (2026) · Acta Medica Leopoliensia · doi:10.25040/aml2026.1-2.030
Lipoprotein(a) Inhibition: Current Evidence, Therapeutic Landscape, and Future Directions
Sabouret, P. F., Giamundo, D. M., Popiołek-Kalisz, J., Spadafora, L., Bernardi, M., Asher, E., Mamas, M. A., Atar, D., & Andò, G. (2026) · Reviews in Cardiovascular Medicine · doi:10.31083/rcm55004
“Overall, PCSK9-directed therapies generally reduce Lp(a) by approximately 15–30%, an effect that is substantially smaller than that achieved with emerging Lp(a)-specific agents [7,8].”
Sechi, L. A., Bulfone, L., Vacca, A., Comand, J., Marcante, S., Brosolo, G., Pagano, C., & Catena, C. (2026) · Frontiers in Nephrology · doi:10.3389/fneph.2026.1950030
Farhan, M., Murtaza, M., Rasool, M. M., Khan, F. R., Amjad, H., Rai, K. D., Ali, S. M. E., Raza, A. A., Sohail, M. A., Samadi, A., et al. (2026) · Endocrinology Diabetes & Metabolism · doi:10.1002/edm2.70358
Mortada, I., Lee, A. W., Buckingham, D., Ebel, G., Long, N., Dileep, J., Sanjel, A., Al-Shammari, A., Blackwell, T. A., & Jneid, H. (2026) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2026.10.010
Enlicitide: The First Oral PCSK9i for Lowering Low-Density Lipoprotein Cholesterol
Klosko, R. C., Lussier, M. E., Nasuhidehnavi, A., & Clark, T. (2026) · Annals of Pharmacotherapy · doi:10.1177/10600280261494015
Gogan, A., Ardelean, S., Rus, D., Căruntu, F. R., Buz, B., Parvanescu, T., & Andor, M. (2026) · Biomedicines · doi:10.3390/biomedicines14102339
“Indirect evidence from PCSK9 inhibitor trials also suggests that higher baseline Lp(a) identifies greater residual cardiovascular risk [89,91,92].”
Parcha, V., & Bittner, V. (2026) · Current Atherosclerosis Reports · doi:10.1007/s11883-026-01474-4
Mikhael, F. G., Ayoub, C., Teperikidis, E., Biondi-Zoccai, G., Booz, G. W., Zouein, F. A., & Makarem, N. N. (2026) · Current Atherosclerosis Reports · doi:10.1007/s11883-026-01471-7
“This risk is independent of biomarkers such as LDL-C [4, 60].”
Association Between Lipoprotein A Levels and Vulnerable Atherosclerotic Plaques
Mahadevan, A., Jog, H., Dhananjaya, H., Patel, M., MARWAH, M. P. S., Gandhi, M., Vasudevan, S. S., Lekkala, S. P., Mehdi, H. K., & Desai, R. (2026) · The American Journal of the Medical Sciences · doi:10.1016/j.amjms.2026.10.004
Al-Malkawi, N., & Giret, A. (2026) · Corporate Social Responsibility and Environmental Management · doi:10.1002/csr.71025
Panagiotopoulos, E., Stefanou, M., Giannopapas, V., Bakola, E., Papagiannopoulou, G., Theodorou, A., Lambadiari, V., Romoli, M., Ikonomidis, I., Liberopoulos, E. N., et al. (2026) · Therapeutic Advances in Neurological Disorders · doi:10.1177/17562864261492827
Nezhad, S. A., Nouri, A. M. E., Moreines, L. T., Mangalesh, S., Rastgou, P., Maheshwari, M., Rossi, R., Damluji, A. A., & Nanna, M. G. (2026) · Diagnostics · doi:10.3390/diagnostics16213480
BindingDB Entry 50022006: Identification of benzothiazoles as novel PCSK9 inhibitors.
BindingDB (2025) · UC San Diego · doi:10.7270/q2hx1jb2
Qadeer, A., Khawar, M. M. H., Khawar, M., Malik, M. A., Forrester, A., Shah, S., Albayyaa, M., & Jneid, H. M. (2026) · Clinical Medicine Insights Cardiology · doi:10.1177/11795468261485547
Metadata
- Authors
- O’Donoghue, M. L., Fazio, S., Giugliano, R. P., Stroes, E. S. G., Kanevsky, E., Gouni-Berthold, I., Im, K., Lira Pineda, A., Wasserman, S. M., Češka, R., Ezhov, M. V., Jukema, J. W., Jensen, H. K., Tokgözoğlu, S. L., Mach, F., Huber, K., Sever, P. S., Keech, A. C., Pedersen, T. R., & Sabatine, M. S.
- Affiliations
- Brigham and Women's Hospital (US)
- Oregon Health & Science University (US)
- Amsterdam UMC Location University of Amsterdam (NL)
- Polyclinic for Endocrinology, Diabetes and Preventive Medicine, University of Cologne, Germany (I.G.-B.).
- Amgen, Thousand Oaks, CA (A.L.P., S.M.W.).
- Amgen (United States) (US)
- Charles University (CZ)
- National Cardiology Research Center, Moscow, Russia (M.V.E.).
- Leiden University Medical Center (NL)
- Aarhus University (DK)
- Cardiovascular Division, Hacettepe University, Ankara, Turkey (S.L.T.).
- University of Geneva (CH)
- Sigmund Freud Privatuniversität Wien (AT)
- Imperial College London (GB)
- The University of Sydney (AU)
- Oslo University Hospital (NO)
- ORCID
- Venue
- Circulation
- Published
- 2019-03-19
- Volume
- 139
- Issue
- 12
- Pages
- 1483-1492
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2940327706
- Cited by
- 984
- References
- 33
- Citations by year
- 2026: 133 · 2025: 153 · 2024: 157 · 2023: 134 · 2022: 120 · 2021: 100 · 2020: 122 · 2019: 64
- FWCI
- 97.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, cc-by)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Funders
- Abbott Laboratories
- Amgen
- Bristol-Myers Squibb
- Eli Lilly and Company
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- Sanofi
- Brigham and Women's Hospital
- Gilead Sciences
- Alnylam Pharmaceuticals
- Univerzita Karlova v Praze
- Aarhus Universitet
- Aarhus Universitetshospital
- Regeneron Pharmaceuticals
- Intarcia Therapeutics
- Amarin Corporation
- Medicines Company
- Mylan
- MyoKardia
- Imperial College London
- Universiteit Leiden
- Daiichi-Sankyo
- Eisai
- Novo Nordisk
- Leids Universitair Medisch Centrum
- Universitetet i Oslo
- Hacettepe Üniversitesi
- Université de Genève
- Universität zu Köln
- Novo Nordisk Fonden (NNF18OC0031258)
- Servier
- Esperion Therapeutics
- Medical Research Council
- National Health and Medical Research Council
- Sydney Medical School
- Janssen Research and Development
- Daiichi Sankyo Europe
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- lipoprotein(a), PCSK9 inhibitors, evolocumab, cardiovascular risk, atherosclerotic cardiovascular disease, coronary artery disease, myocardial infarction, urgent revascularization, LDL cholesterol, prognostic factors, FOURIER trial, LDL cholesterol lowering
- MeSH terms
- Proprotein Convertase 9, Adult, Aged, Aged, 80 and over, Anticholesteremic Agents, Double-Blind Method, Female, Humans, Cholesterol, LDL, Male, Middle Aged, Risk Factors, Placebo Effect, Proportional Hazards Models, Treatment Outcome, Lipoprotein(a), Atherosclerosis, Antibodies, Monoclonal, Humanized
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