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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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InfluentialLipoprotein(a) – treatments in development
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“…of CV events independent of LDL cholesterol levels and Lp(a) levels were reduced significantly by a median of 26.9% with evolocumab with absolute reductions being greater in patients with higher baseline Lp(a) levels and these patients tended to derive greater coronary benefit from evolocumab [30].”
InfluentialThe evolving therapeutic landscape of PCSK9 inhibition
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“FOURIER trial also demonstrated that patients with higher baseline Lp(a) levels experienced greater absolute Lp(a) reductions and tended to have greater benefit in reducing cardiovascular risk by evolocumab therapy [30].”
BackgroundLipoprotein (a) in familial hypercholesterolaemia
Durrington, P. N., Bashir, B., Bhatnagar, D., & Soran, H. (2022) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000839 · Cited by 6
“Secondly, in familial hypercholesterolaemia the presence of high Lp(a) militates in favour of adopting a therapeutic regime which will lower both LDL cholesterol and Lp(a), for example the introduction of PCSK9 inhibition earlier than might otherwise be the case [40] or in some cases LDL apheresis [41].”
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Is Lipoprotein(a) Clinically Actionable with Today’s Evidence? The Answer is Yes
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“Beyond the general recommendation for traditional risk factor control, the use of PCSK9 inhibitor (PCSK9i) monoclonal antibodies (mAbs) for managing elevated Lp(a) has been shown to reduce Lp(a) levels by up to 15–30% [41, 42].”
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“A FOURIER sub-study indicated a non-statistical decrease in CAS in the evolocumab group after only two years OR = 0.6 (CI = 0.40–1.09) [58], meaning that there could be potentially a reduction in CAS of 34%.”
MethodInfluentialStrategies for the Secondary Prevention of Atherosclerotic Cardiovascular Disease
Hurwitz, M., Agboola, O. J., Gami, A., Williams, M. S., Virani, S. S., Sharma, G. V., & Patel, J. (2025) · US Cardiology Review · doi:10.15420/usc.2024.33 · Cited by 10
“97,98”
Exosomal non-coding RNAs: key regulators of inflammation-related cardiovascular disorders
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“In contrast to statins, PCSK9 inhibitors offer the added advantage of reducing the presence of lipoprotein A, which is linked to enhancing the process of vascular calcification [63].”
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“Moreover, the bene fi cial e ff ects of PCKS9i may exceed the LDL-lowering e ff ect, as they lower lipoprotein(a) levels 14 and Although this study is not without limitations (eAppendix 2), we observed improved outcomes with greater LDL lowering by 30 days.”
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“…PCSK9 Inhibition in Subjects With Elevated Risk), the randomized control trial that compared evolocumab with placebo, patients with baseline Lp(a) in the highest quartile (> 165 nmol/L) had a higher risk for ASCVD events or urgent revascularization compared with those in the lowest quartile [35].”
Zulkapli, R., Muid, S. A., Wang, S. M., Yusof, M. Y. P. M., & Nawawi, H. M. (2025) · BMC Cardiovascular Disorders · doi:10.1186/s12872-025-04892-5 · Cited by 5
“To bridge this knowledge gap, our study utilized Lp(a) as an in vitro stimulant to investigate its impact on atherogenesis biomarkers, including PCSK9 expression, which has been implicated in Lp(a) metabolism through PCSK9 loss-of-function mutations [27, 28].”
Lepodisiran: Effects on Lipoprotein(a) and Cardiovascular Outcomes in Adults with Elevated Lp(a)
Kattamuri, L. P. V., Sharma, K., & Mukherjee, D. (2025) · Cardiovascular & Haematological Disorders - Drug Targets · doi:10.2174/011871529x390148250908045359 · Cited by 5
The discovery of PCSK9 as a pivotal point in the prevention of cardiovascular disease
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“In a post-hoc analysis of the FOURIER trial, participants with Lp(a) ≥ median (37 nmol/L) had a larger absolute risk reduction with evolocumab compared to those with Lp(a) median (2.5 % versus 1 %)[65].”
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“5,6 Accordingly, there is considerable interest in the development of novel therapeutic approaches to lowering Lp(a) levels.”
Aspirin and lipoprotein(a) in primary prevention
Bhatia, H. S. (2023) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000891 · Cited by 5
“Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) have been shown to modestly lower Lp(a) which may translate into an improvement in clinical outcomes based on secondary analyses of clinical trials [5,6]; however, PCSK9i are not specifically approved for this purpose.”
BackgroundCancro, F. P., Bellino, M., Silverio, A., Maio, M. D., Esposito, L., Palumbo, R., Manna, M., Formisano, C., Ferruzzi, G. J., Vecchione, C., et al. (2024) · Translational Medicine UniSa · doi:10.37825/2239-9747.1058 · Cited by 5
“…in patients with established CAD, respectively of evolocumab and alirocumab, showed not only a signi fi cant reduction in Lp(a) levels in these patients, but also a clinical bene fi t in terms of reduction of long-term cardiovascular events, independently from other serum lipoproteins [41,101].”
Renkens, M. P. L., Coerkamp, C. F., Witte, L. S., Sivanesan, S., Nurmohamed, N. S., Westerterp, M., Serruys, P. W. J. C., Onuma, Y., Grundeken, M. J., Kalkman, D. N., et al. (2024) · Expert Review of Cardiovascular Therapy · doi:10.1080/14779072.2024.2387678 · Cited by 5
“[48,49].”
Self-citationOral agents for lowering lipoprotein(a)
Nicholls, S. J., Nelson, A. J., & Michael, L. F. (2024) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000953 · Cited by 5
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Cequier, A. R., Arrarte, V., Campuzano, R., Castro, A., Cordero, A., Olmo, M. R. F., García–Moll, X., Gómez‐Doblas, J. J., de Sá, E. L., Núñez, J. E., et al. (2020) · REC CardioClinics · doi:10.1016/j.rccl.2020.10.017 · Cited by 5
The Suggestive Effect of Apo A, Apo B, and Apo A/Apo B on Erectile Dysfunction
Li, X., & Li, D. (2021) · The Journal of Sexual Medicine · doi:10.1016/j.jsxm.2020.12.004 · Cited by 4
Lipoprotein(a): An update on its role in human health and disease
Koutsogianni, A.-D., Liberopoulos, E. N., & Tselepis, A. D. (2021) · Journal of Atherosclerosis Prevention and Treatment · doi:10.53590/japt.02.1028 · Cited by 5
Role of Lipoprotein(a) in Cardiovascular Disease: A Review of Clinical Practice
Minami, Y., Kinoshita, D., Muramatsu, Y., Nagata, T., & Ako, J. (2022) · Journal of Asian Pacific Society of Cardiology · doi:10.15420/japsc.2021.31 · Cited by 5
Nicholls, S. J., & Nelson, A. J. (2024) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2024.2362644 · Cited by 6
“More recent analyses from large cardiovascular outcomes trials of PCSK9 inhibitors have reported that the ability of these agents to lower Lp(a) by up to 30% independently associates with their clinical benefit [65,66].”
BackgroundLipoprotein(a) and Atrial Fibrillation: Mechanistic Insights and Therapeutic Approaches
Zhang, Z., Peng, B., Nuranmubieke, A., Xu, Y., Liu, Y., Tu, T., Lin, Q., Wang, C., Liu, Q., & Xiao, Y. (2024) · International Journal of Medical Sciences · doi:10.7150/ijms.102301 · Cited by 6
“The effect of alirocumab at the maximum dose, whether used as monotherapy or in combination, achieved a 60% decrease in plasma lipoproteins, which is consistent with the effects of evolocumab [46].”
The Role of Lipoprotein(a) in the Progression of Aortic Stenosis
Sherrill, C., Ehrhardt-Humbert, L. C., & Salem, D. N. (2025) · The American Journal of Medicine · doi:10.1016/j.amjmed.2025.02.024 · Cited by 5
Guijarro, C., & Camafort, M. (2019) · Revista Clínica Española (English Edition) · doi:10.1016/j.rceng.2019.05.005 · Cited by 5
Lipoprotein(a) Change After Sleeve Gastrectomy Is Affected by the Presence of Metabolic Syndrome
Paredes, S., Alves, M., Pereira, M. L., Marques, O., & Ribeiro, L. V. P. T. (2019) · Obesity Surgery · doi:10.1007/s11695-019-04212-9 · Cited by 5
Kolovou, V., Katsiki, N., Makrygiannis, S. S., Mavrogieni, S., Karampetsou, N., Manolis, A. J., Melidonis, A. J., Mikhailidis, D. P., & Kolovou, G. D. (2020) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/1074248420943079 · Cited by 5
Association of various lipid parameters with premature coronary artery disease in men
Tyurina, A. V., Афанасьева, О. И., Александровна, К. Е., Tmoyan, N. A., Андреевна, Р. О., Владиславович, Е. М., & Pokrovsky, S. N. (2022) · Russian Journal of Cardiology · doi:10.15829/1560-4071-2022-5058 · Cited by 5
Lipoprotein(a) lowering and cardiovascular risk reduction by PCSK9 inhibitors
Safarova, M. S., & Kullo, I. (2022) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2022.10.010 · Cited by 5
Lai, P., Xu, S., Liu, Z., Ling, J., Tian, K., Yan, J., Chen, D., Zhong, Y., & Xue, J. (2024) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2024.1474472 · Cited by 5
Current perspectives on Lp(a)-lowering therapies: Who may benefit?
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Emerging pharmacological strategies in lipoprotein(a) reduction
Mansoor, T., Ismayl, M., Parikh, S. S., Nambi, V., Virani, S. S., Mehta, A., Jia, X., & Minhas, A. M. K. (2025) · Baylor University Medical Center Proceedings · doi:10.1080/08998280.2025.2524791 · Cited by 4
The prevention of adult cardiovascular disease must begin in childhood: evidence and imperative
Khoury, M., Ware, A. L., & McCrindle, B. W. (2025) · Nature Reviews Cardiology · doi:10.1038/s41569-025-01209-z · Cited by 10
Ancestral Variation in Lp(a): Epidemiology, Isoform Diversity, and Testing
Shah, P., King, S., Trabanino, S., Parsa, S., Chen, T. P., & Rodríguez, F. (2025) · Current Atherosclerosis Reports · doi:10.1007/s11883-025-01365-0 · Cited by 4
Existing and Potential Therapeutic Strategies for Lowering Lipoprotein(a) Levels: An Update
Domański, I., Kozieł, A., Domański, J., & Trocha, M. (2026) · Journal of Clinical Medicine · doi:10.3390/jcm15062179 · Cited by 4
Safety of low lipoprotein(a) levels: the FOURIER trial
Gencer, B., Giugliano, R. P., Ran, X., Mach, F., Stroes, E. S. G., Gouni‐Berthold, I., Češka, R., Владиславович, Е. М., Jukema, J. W., Jensen, H. K., et al. (2026) · European Heart Journal · doi:10.1093/eurheartj/ehag398 · Cited by 4
Self-citationLei, J., Fan, Q., Chen, X., Li, W., Peng, Y., Cai, Y., Liu, X., Liu, C., & Zhang, L. (2024) · Current Neurovascular Research · doi:10.2174/0115672026332171240624100802 · Cited by 4
Lipoprotein (a) Distribution in Aortic Stenosis Patients
Durr, M.-R. R., Burwash, I. G., LAU, L. S. W., Alfraidi, H., Mulloy, A. J., Tavoosi, A., Arangalage, D., Chan, V., Lakhani, M., Aljamaan, A., et al. (2025) · JACC Advances · doi:10.1016/j.jacadv.2025.101662 · Cited by 4
Hu, X., Liu, Y., Yuan, W., Zhang, Z., Li, S., Cheng, A., Yu, Q., Guo, H., Zou, Y., Li, M. L., et al. (2025) · Journal of the American Heart Association · doi:10.1161/jaha.124.041251 · Cited by 4
“While PCSK9 inhibitors have been shown to not only directly reduce lipid components like LDL-C and lipoprotein(a), 32 but also play a role in addressing inflammation, 33 further studies are warranted to explore which patient subgroups may derive the most significant benefit from PCSK9 inhibitor…”
Ray, K. K., Szarek, M. J., Bhatt, D. L., Bittner, V., Fazio, S., Goodman, S. G., Harrington, R. A., Jukema, J. W., White, H. D., Steg, P. G., et al. (2025) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2025.08.043 · Cited by 4
Self-citationZhang, Y., Chai, Z., Chen, M., Li, S., Zhuang, W., Hu, W. W., & Chen, M. (2025) · Precision medicine and engineering. · doi:10.1016/j.preme.2025.100046 · Cited by 5
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To test, or not to test: that is the question for the future of lipoprotein(a)
Ellis, K. L., Chakraborty, A., Moses, E. K., & Watts, G. F. (2019) · Expert Review of Cardiovascular Therapy · doi:10.1080/14779072.2019.1596799 · Cited by 4
“observed in patients with both low LDL-cholesterol and low Lp(a) [111].”
BackgroundArmario, P., Brotons, C., Elosúa, R., de Leciñana, M. A., Castro, A., Clarà, A. B. I., Cortés, O., Rodríguez, Á. D., Herranz, M., Justo, S., et al. (2020) · PubMed Central · Cited by 4
Pharmacological interventions for the treatment of aortic root and heart valve disease
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Altschmiedová, T., Todorovová, V., Vrablı́k, M., & Češka, R. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.849267 · Cited by 4
Self-citationWhen Should We Measure Lipoprotein(a)?
Kostner, K. (2023) · Contemporary cardiology · doi:10.1007/978-3-031-24575-6_17 · Cited by 4
Pax‐8: Molecular biology, pathophysiology, and potential pathogenesis
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“127,128 Therefore, thorough study of the regulatory roles of key molecules in the formation of atherosclerotic lesions is of great significance for the development of new therapeutic strategies for CVD.”
BackgroundXu, L., Wang, L., Wang, Y., Wang, Y., Jiang, Y., Du, P., Cheng, J., Zhang, C., Wang, R., Jiao, T., et al. (2024) · Frontiers in Medicine · doi:10.3389/fmed.2024.1408760 · Cited by 4
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“For example, O ’ Donoghue et al. reported that elevated levels of circulating Lp(a) heighten the likelihood of patients developing cardiovascular disease, regardless of LDL-C levels [40].”
BackgroundComprehensive Assessment of Lipid Markers in Cardiovascular Events Prediction
Inoue, N., Morikawa, S., & Murohara, T. (2024) · International Heart Journal · doi:10.1536/ihj.24-149 · Cited by 5
Changes of lipoprotein(a) levels with endogenous steroid hormones
Tessitore, E., Dobretz, K., Dhayat, N. A., Kern, I., Ponte, B., Pruijm, M. T., Ackermann, D., Estoppey, S., Burnier, M., Martin, P., et al. (2021) · European Journal of Clinical Investigation · doi:10.1111/eci.13699 · Cited by 3
“13,14 Among noncardiovascular drugs, hormonal replacement therapy (HRT) is associated with lower Lp(a) levels in some studies.”
BackgroundSelf-citationLipoprotein(a)—When to Screen and How to Treat
Patel, N., Mittal, N., Choubdar, P. A., & Taub, P. R. (2022) · Current Cardiovascular Risk Reports · doi:10.1007/s12170-022-00698-8 · Cited by 4
Jung, H. W., Kim, C., Hong, S. P., Bae, H., Choi, J. Y., Ryu, J. K., Lee, J., Lee, K., Han, K., Yang, D., et al. (2023) · Journal of Clinical Hypertension · doi:10.1111/jch.14715 · Cited by 3
Zhao, L. Y., Sun, L., Zhang, Z., Yang, K., Li, Z., Wang, M., Zeng, Y., Zhou, X., & Yang, W. (2023) · Lipids in Health and Disease · doi:10.1186/s12944-023-01901-4 · Cited by 4
“reported that a significant reduction in Lp(a) levels was observed in patients using evolocumab (a PCSK9 inhibitor); those with higher baseline Lp(a) levels had greater reductions and tended to benefit from PCSK9 inhibition [37].”
Background
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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