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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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“Although the reduction in the incidence of recurrent cardiovascular events in studies with PCSK9 inhibitors has been shown to depend on both the reduction in LDL cholesterol and Lp(a) concentrations (90).”
Outcomes after coronary angiography in individuals with elevated lipoprotein(a)
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“Acting via ATPCLY (Adenosine triphosphate citrate lyase) inhibition, upstream of Hydroxymethylglutaryl-coenzyme A reductase, its effect on Lp(a) appears comparable to that of statins [61,62].”
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Muvalaplin: A Novel Oral Therapy for Targeted Reduction of Plasma Lipoprotein(a)
Botros, M., Tiji, M., & Lange, R. A. (2026) · Cardiovascular & Haematological Disorders - Drug Targets · doi:10.2174/011871529x418596251201142137 · Cited by 2
Impact of Lipoprotein(a) on Residual Cardiovascular Risk After an Acute Coronary Syndrome
González-Aguado, N., Franco-Hita, R., Larrubia-Valle, J. I., Puyol-Ruiz, F., Mezcua, A. R., García‐Pinilla, J. M., Jiménez-Salva, M., Piserra‐López, A., Pavón, F. J., Pérez-Cabeza, A., et al. (2026) · Journal of Clinical Medicine · doi:10.3390/jcm15051688 · Cited by 2
“Monoclonal antibodies against PCSK9 and small interfering RNA (siRNA) agents are the only approved pharmacologic classes known to reduce Lp(a) levels, demonstrating an approximate reduction of 20–30%, although the underlying mechanisms remain to be fully elucidated [83–85].”
The Lipoprotein(a) Implementation Gap: Bridging Evidence and Clinical Practice
Yang, H. S., Yoon, S., & Hur, M. (2026) · Reviews in Cardiovascular Medicine · doi:10.31083/rcm47152 · Cited by 2
“…LDL-C thresholds in patients with Lp(a) levels above 125 nmol/L, recognizing both the modest Lp(a)-lowering effect and the heightened residual risk [66]; (5) lipoprotein apheresis referral becomes appropriate for patients with Lp(a) levels of 60 mg/dL or higher who experience recurrent…”
InfluentialLipoprotein (a) and Coronary Atherosclerosis in Intracoronary Imaging - YELLOW II – Lp(a) Study
Gurevitz, C., Vengrenyuk, Y., Minatoguchi, S., Yasumura, K., Hooda, A., Krishnan, P., Moreno, P., Narula, J., Sharma, S. K., Rosenson, R. S., et al. (2026) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-026-07850-1 · Cited by 2
“While proprotein convertase subtilisin kexin 9 (PSCK9) targeted therapies decrease Lp(a) by 14–35% on average [9–11], statins tend to increase Lp(a) levels by an average of 8 to 24% [1].”
Lepodisiran: An Updated Review on a Novel and Emerging Lipoprotein (a) Lowering Agent
Urina-Jassir, M., Tong, K., Stanisic, A. V., Frishman, W. H., & Aronow, W. S. (2026) · Cardiology in Review · doi:10.1097/crd.0000000000001228 · Cited by 2
Lorenz, M., Palant, R., Oscherowa, E., Hamoud, W. K.-H., Kirwan, J., Trajkovski, S., Wiebach, J., Fritsche‐Guenther, R., Wu, H., Haritonow, N., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27073079 · Cited by 2
Mansouri, P., & Vafa, R. G. (2026) · Life Sciences · doi:10.1016/j.lfs.2026.124371 · Cited by 4
Jiang, Y., Lin, J., Ma, M., Xu, J., Yu, P., & Wang, H. (2026) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.66159 · Cited by 2
“The fact that Lp(a)—but not LDL-C— independently predicted plaque vulnerability in the overall multivariate model implies that systematic Lp(a) assessment remains valuable, as many patients may harbor clinically occult, Lp(a)-driven unstable plaques despite statin therapy 24, 25) .”
Zantek, N. D., Alquist, C. R., Hofmann, J. C., Klingel, R., Levenbrown, Y., Onwuemene, O. A., Patidar, G. K., Patriquin, C. J., Raval, J. S., Sanchez, A. P., et al. (2026) · Journal of Clinical Apheresis · doi:10.1002/jca.70141 · Cited by 2
Epidemiology of Atherosclerotic Cardiovascular Disease
Hirahatake, K. M., Dicklin, M. R., & Maki, K. C. (2020) · Contemporary cardiology · doi:10.1007/978-3-030-56514-5_5 · Cited by 2
Armario, 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. (2021) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/j.arteri.2020.11.004 · Cited by 2
Lipoprotein(a) and kidney diseases
Pyatchenkov, M. O., Rumyantsev, A. S., Владимирович, З. М., Sherbakov, E. V., & Belskykh, A. N. (2021) · Nephrology (Saint-Petersburg) · doi:10.36485/1561-6274-2021-25-1-31-46 · Cited by 3
Lp(a) as a Cardiovascular Risk Factor
Pirillo, A., & Catapano, A. L. (2023) · Contemporary cardiology · doi:10.1007/978-3-031-24575-6_13 · Cited by 2
Akiyama, T., Ozaki, K., Takano, T., Yoneyama, S., Kubota, N., Okubo, T., Ikegami, R., Hoyano, M., Yanagawa, T., & Inomata, T. (2023) · Internal Medicine · doi:10.2169/internalmedicine.1609-23 · Cited by 2
“Furthermore, patients with high baseline LP-(a) levels enjoy even greater reductions in LP-(a) (4).”
BackgroundAre we seeing the light at the end of the tunnel for high lipoprotein(a)? Lipoprotein(a)
Kayıkçıoğlu, M., Özkan, H. S., & Tokgözoğlu, L. S. (2023) · European Atherosclerosis Journal · doi:10.56095/eaj.v1i3.21 · Cited by 2
Frequency & factors associated with elevated lipoprotein-a among Ghanaian stroke survivors
Gyabaah, S., Adu‐Boakye, Y., Sarfo‐Kantanka, O., Gyan, K. F., Kokuro, C., Agyei, M. K., Akassi, J., Tawiah, P., Norman, B., Ovbiagele, B. I., et al. (2023) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2023.122839 · Cited by 4
Elevated Lp(a): Guidance for Identifying and Managing Patients
Hilleman, D. E., Vacek, J. L., & Backes, J. M. (2024) · Southern Medical Journal · doi:10.14423/smj.0000000000001675 · Cited by 2
Pharmacological methods to lower lipoprotein(a) levels
Wierzbowska, N., Olejnik-Wojciechowska, J., Dąbrowska, A., & Żurawska, K. (2024) · Medical Research Journal · doi:10.5603/mrj.99088 · Cited by 2
“A clinically relevant aspect was the reduction in the risk of death, which proved to be 16% higher for the group with baseline Lp(a) levels above the median compared to the group with Lp(a) levels below the median [20].”
BackgroundEfficacy and safety of drugs in residual cardiovascular risk: A systematic review of the literature
Hernández-Somerson, M. A., Montoya-Agudelo, F., & Huertas-Rodriguez, G. (2024) · International Journal of Cardiology Cardiovascular Risk and Prevention · doi:10.1016/j.ijcrp.2024.200298 · Cited by 2
Frequency of lipoprotein(a) testing and its levels in Pakistani population
Batool, H., Khan, M., Ain, Q., Chughtai, O. R., Khan, M. D., Khan, M. I., & Sadiq, F. (2024) · Global Cardiology Science and Practice · doi:10.21542/gcsp.2024.37 · Cited by 2
“Other drugs including proprotein convertase subti-lase/kexin type 9 inhibitors (PCSK9i) and mipomersen have the potential to lower Lp(a) levels 42,43 .”
BackgroundZhang, K., Li, J., Li, Y., Yan, K., Zhu, P., Tang, X., Yuan, D., Yang, Y., Gao, R., Yuan, J., et al. (2024) · Clinical and Applied Thrombosis/Hemostasis · doi:10.1177/10760296241280711 · Cited by 2
“17,18 The Lp(a)-related risks increase in a linear manner as plasma Lp(a) level elevates to >30 mg/dl. 19 In recent days, the interaction between in fl ammation and Lp(a)-associated risks has aroused widespread attention.”
BackgroundEffect of PCSK9 Inhibitors on Regulators of Lipoprotein Homeostasis, Inflammation and Coagulation
Lunar, P., Meglič, H., Vehar, M., Ugovšek, S., Likozar, A. R., Šebeštjen, M., & Zupan, J. (2025) · Biomedicines · doi:10.3390/biomedicines13020294 · Cited by 2
Emerging Implications of Elevated Lipoprotein(a) Levels in Coronary Artery Bypass Graft Surgery
Patel, S. K., Badross, M. S., Dhingra, N. K., Moroney, M., Casey, J. H., Hassan, S. M. A., Khan, T., Hess, D. A., Koschinsky, M. L., Teoh, H., et al. (2025) · The Annals of Thoracic Surgery · doi:10.1016/j.athoracsur.2025.01.013 · Cited by 2
Key Concepts in Cardiovascular Secondary Prevention: A Case-Based Review
Revankar, S., Shakra, N., DiMaio, J. M., & Agarwala, A. (2025) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2025.03.035 · Cited by 4
Biological and Biosimilar Medicines in Contemporary Pharmacotherapy for Metabolic Syndrome
Górecka, W., Berezovska, D., Mrozińska, M., Nowicka, G., & Czerwińska, M. E. (2025) · Pharmaceutics · doi:10.3390/pharmaceutics17060768 · Cited by 2
“This drug has also been shown to decrease the risk of mortality due to myocardial infarction, coronary heart disease, or the necessity for urgent revascularization by 23% [160].”
Novel Method for Predicting Lp(a) From Genomic Testing Identifies ASCVD Risk Across a Diverse Cohort
Telis, N., Dai, H., Waring, A. A., Kann, D., Wyman, D., White, S., Khuder, B., Tanudjaja, F., Bolze, A., Levy, M. E., et al. (2025) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2025.04.012 · Cited by 2
Experiences of people with elevated lipoprotein(a) and the impact on family and child screening
Eversole, G., Fitzgerald‐Butt, S. M., Halverson, C. M. E., Clary, J. M., & Helm, B. M. (2025) · Journal of clinical lipidology · doi:10.1016/j.jacl.2025.07.011 · Cited by 2
Gender Specificity and Interpretation of Functional Cardiac Imaging: Let's Talk about Sex
Gencer, B., & Mach, F. (2019) · Thrombosis and Haemostasis · doi:10.1055/s-0039-1695010 · Cited by 2
Self-citationJames, R., & Appunni, S. (2019) · Journal of Evidence Based Medicine and Healthcare · doi:10.18410/jebmh/2019/572 · Cited by 2
2019 clinical trials in lipid lowering
Feldman, D. I., Pacor, J., Blumenthal, R. S., & Nasir, K. (2020) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000757 · Cited by 2
Pediatric dyslipidemias: lipoprotein metabolism disorders in children
Ballout, R. A., & Remaley, A. T. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-817962-8.00002-0 · Cited by 3
Lipoprotein a: An emerging risk identifier and evolving clinical target
Tsarouhas, K., Hoursalas, A., Vardavas, A., & Tsitsimpikou, C. (2022) · Public Health Toxicology · doi:10.18332/pht/145601 · Cited by 2
‘Use of lipid-lowering therapy: the guidelines, the drugs or the patient?’
Borghi, C., & Bragagni, A. (2022) · European Heart Journal Supplements · doi:10.1093/eurheartjsupp/suac069 · Cited by 2
“The production of this molecule is largely under genetic control and an increase in its plasma concentration is associated with a progressive increase in cardiovascular risk due to its pro-atherogenic, pro-inflammatory, and pro-thrombotic properties, regardless of the concentration of LDL-C.4 The concept of cumulative…”
BackgroundInfluentialNaami, R., Miller, D. M., Al-Kindi, S. G., & Neeland, I. J. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.1084814 · Cited by 2
Gao, G., Zheng, T., Lan, B., Hui, W., Chen, S., Yuan, Z., Wu, Y., Chiang, J. Y. L., & Chen, T. (2023) · Cardiology Plus · doi:10.1097/cp9.0000000000000036 · Cited by 2
Lp(a) and inflammation: a new insight into atherosclerosis
Pan, H., Hu, K., Wu, Q., Tu, Y., & Guo, Z. (2023) · Clinical and Translational Discovery · doi:10.1002/ctd2.247 · Cited by 2
Lp(a) and risk of cardiovascular disease – A review of existing evidence and emerging concepts
Jasti, M., Islam, S., Steele, N., Ivy, K. N., Maimo, W., & Isiadinso, I. (2023) · Journal of the National Medical Association · doi:10.1016/j.jnma.2023.11.009 · Cited by 2
Liu, H., Li, S., Zhang, Y., Guo, Y., Zhu, C., Wu, N., Gao, Y., Xu, R., Dong, Q., & Li, J. (2024) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.64693 · Cited by 2
“…patients independent of FHx, but it appears to be more effective in those with FHx. Elevated plasma Lp(a) levels have been shown to be associated with an increased risk of CVEs in diverse populations, ranging from the general population to patients with established CAD 3, 5-13, 25-27 25-27) .”
BackgroundSabouret, P. F., Angoulvant, D., Pathak, A., Costa, F., Pezel, T., & Michos, E. D. (2019) · Current Cardiovascular Risk Reports · doi:10.1007/s12170-019-0627-8 · Cited by 2
What’s new on therapies for elevated lipoprotein(a)
Ward, N. C., Schultz, C. J., & Watts, G. F. (2019) · Expert Review of Clinical Pharmacology · doi:10.1080/17512433.2019.1610391 · Cited by 2
Fang, S., Yarmolinsky, J., Gill, D., Bull, C. J., Perks, C. M., Smith, G. D., Gaunt, T. R., & Richardson, T. G. (2022) · medRxiv · doi:10.1101/2022.04.18.22274003 · Cited by 2
Devesa, A., Ibáñez, B., & Fuster, V. (2022) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2022.08.722 · Cited by 2
Development and Multinational Validation of a Novel Algorithmic Strategy for High Lp(a) ScreeningPreprint
Aminorroaya, A., Dhingra, L. S., Oikonomou, E. K., Saadatagah, S., Thangaraj, P., Shankar, S. V., Spatz, E. S., & Khera, R. (2023) · medRxiv · doi:10.1101/2023.09.18.23295745 · Cited by 2
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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