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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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Cites
Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease
Sabatine, M. S., Giugliano, R. P., Keech, A. C., Honarpour, N., Wiviott, S. D., Murphy, S. A., Kuder, J. F., Wang, H., Liu, T., Wasserman, S. M., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1615664 · Cited by 6,138
Self-citationLipoprotein(a) as a cardiovascular risk factor: current status
Nordestgaard, B. G., Chapman, M. J., Ray, K., Borén, J., Andreotti, F., Watts, G. F., Ginsberg, H., Amarenco, P., Catapano, A., Descamps, O. S., et al. (2010) · European Heart Journal · doi:10.1093/eurheartj/ehq386 · Cited by 1,807
(2009) · JAMA · doi:10.1001/jama.2009.1063 · Cited by 1,753
Genetic Variants Associated with Lp(a) Lipoprotein Level and Coronary Disease
Clarke, R., Peden, J. F., Hopewell, J. C., Kyriakou, T., Goel, A., Heath, S. C., Parish, S., Barlera, S., Franzosi, M. G., Rust, S., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0902604 · Cited by 1,671
Effects of extended-release niacin with laropiprant in high-risk patients
The HPS2-THRIVE Collaborative Group (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1300955 · Cited by 1,668
Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction
Kamstrup, P. R. (2009) · JAMA · doi:10.1001/jama.2009.801 · Cited by 1,357
Viney, N. J., van Capelleveen, J. C., Geary, R. S., Xia, S., Tami, J. A., Yu, R. Z., Marcovina, S. M., Hughes, S. G., Graham, M. J., Crooke, R. M., et al. (2016) · The Lancet · doi:10.1016/s0140-6736(16)31009-1 · Cited by 754
Self-citationBurgess, S., Ference, B. A., Staley, J. R., Freitag, D. F., Mason, A. M., Nielsen, S. F., Willeit, P., Young, R., Surendran, P., Karthikeyan, S., et al. (2018) · JAMA Cardiology · doi:10.1001/jamacardio.2018.1470 · Cited by 689
Self-citationTsimikas, S., Viney, N. J., Hughes, S. G., Singleton, W., Graham, M. J., Baker, B. F., Burkey, J. L., Yang, Q., Marcovina, S. M., Geary, R. S., et al. (2015) · The Lancet · doi:10.1016/s0140-6736(15)61252-1 · Cited by 460
Reduction in Lipoprotein(a) With PCSK9 Monoclonal Antibody Evolocumab (AMG 145)
Raal, F. J., Giugliano, R. P., Sabatine, M. S., Koren, M. J., Langslet, G., Bays, H. E., Blom, D. J., Eriksson, M., Dent, R. E., Wasserman, S. M., et al. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2014.01.006 · Cited by 359
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Items 301–400 of 982
Current Clinical Trials for Treating Elevated Lipoprotein(a)
Reyes, C. D. L., Rikhi, R. R., Doherty, S., Hernandez, S., Mirzai, S., Shapiro, M. D., Christof, M., McIntosh, S. W., Wong, N. D., & Block, R. (2025) · Current Cardiovascular Risk Reports · doi:10.1007/s12170-025-00759-8 · Cited by 20
“…such as inhibitors of proprotein convertase subtilisin-kexin type 9 (PCSK9) that reduce the incidence of cardiovascular events primarily by reducing LDL-C while providing a measure of benefit in lowering Lp(a), there are no approved medications spe - cifically for lowering Lp(a) [ 4 , 5 ].”
New Horizons: Revival of Lipoprotein (a) as a Risk Factor for Cardiovascular Disease
Nestel, P. J., Loh, W. J., Ward, N. C., & Watts, G. F. (2022) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgac541 · Cited by 19
Wei, T. L., & Cho, L. (2022) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000856 · Cited by 19
Park, J. S., Cho, K. H., Hong, Y. J., Kim, M. C., Sim, D. S., Kim, J. H., Ahn, Y., & Jeong, M. H. (2023) · Journal of Korean Medical Science · doi:10.3346/jkms.2023.38.e102 · Cited by 18
Rogers, M. A., Bartoli‐Leonard, F., Zheng, K. H., Small, A., Chen, H. Y., Clift, C. L., Asano, T., Kuraoka, S., Blaser, M. C., Perez, K. A., et al. (2023) · Circulation · doi:10.1161/circulationaha.123.066822 · Cited by 22
“14 PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors can reduce circulating Lp(a) abundance by 26.9%, 15 but whether further reduction of circulating Lp(a) provides improvements in cardiovascular disease outcomes is unknown.”
BackgroundInfluentialSelf-citationGuo, C., Cao, H., Shan, G., Zhao, W., Zhang, H., Niu, K., Cui, Z. Q., Tang, N., Liu, K., Pan, L., et al. (2021) · Annals of Translational Medicine · doi:10.21037/atm-20-3899 · Cited by 17
“Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, including evolocumab and alirocumab, have led to modest reductions in Lp(a) and LDL-C, with the most benefit seen in patients with higher absolute values (59,60).”
Li, Q., Chen, Y., Yu, L., Zhu, L., Wang, Z., Jiao, S., Wu, C., Tu, Y., Wu, Y., Guo, Z., et al. (2022) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2022.04.007 · Cited by 19
Hussain, A., & Ballantyne, C. M. (2020) · Annual Review of Medicine · doi:10.1146/annurev-med-100119-013612 · Cited by 19
Recomendaciones preventivas cardiovasculares. Actualización PAPPS 2022
Orozco‐Beltrán, D., Cuixart, C. B., Banegas, J. R., Gil-Guillén, V. F., Cuenca, A. M. C., Rioboó, E. M., Baldó, A. J., Vicuña, J., & Pérez, J. N. (2022) · Atención Primaria · doi:10.1016/j.aprim.2022.102444 · Cited by 64
Genovesi, S., Giussani, M., Lieti, G., Orlando, A., Patti, I., & Parati, G. (2023) · Biomedicines · doi:10.3390/biomedicines11061661 · Cited by 17
Eidensohn, Y., Bhatla, A., Ding, J., Blumenthal, R. S., Martin, S. S., & Marvel, F. A. (2024) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2024.100686 · Cited by 18
“Given the historically low rates of PCSK9 inhibitor utilization, Lp(a) testing may encourage utilization of this class of evidence-based medications, when indicated for LDL-C lowering, by allowing providers to personalize cardiovascular risk assessment for patients [33,34].”
BackgroundZhang, Y., Pei, Z., Chen, B., Qu, Y., Dong, X., Yu, B., Wang, G., Xu, F., Lu, D., He, Z., et al. (2024) · Pharmacological Research · doi:10.1016/j.phrs.2024.107340 · Cited by 17
Zahger, D., Schwartz, G. G., Du, W., Szarek, M. J., Bhatt, D. L., Bittner, V., Budaj, A., Díaz, R., Goodman, S. G., Jukema, J. W., et al. (2024) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2024.06.035 · Cited by 18
Self-citationTherapeutic management of hyperlipoproteinemia (a)
Kosmas, C. E., Sourlas, A., Mallarkey, G., Silverio, D., Garcia, D. Y., Montan, P. D., Guzman, E., & Garcia, M. J. (2019) · Drugs in Context · doi:10.7573/dic.212609 · Cited by 17
Yeang, C., Willeit, P., & Tsimikas, S. (2020) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000713 · Cited by 17
Ying, Q., Chan, D. C., & Watts, G. F. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.603910 · Cited by 17
Bosco, G., Barbagallo, F. D. G., Marco, M. D., Scilletta, S., Miano, N., Pistritto, C., Tiralongo, M., Stefano, C. D., Pennisi, G., Francesco, E. M. D., et al. (2025) · Journal of Translational Medicine · doi:10.1186/s12967-025-07432-z · Cited by 17
“FOU-RIER Outcomes and ODYSSEY OUTCOMES trials showed an Lp(a) reduction of 20–25% with PCSK9-mAb that was associated with a lower incidence of cardiovascular events [17, 18].”
Lipoprotein(a) levels and risk of abdominal aortic aneurysm in the Women's Health Initiative
Chou, E. L., Pettinger, M. B., Haring, B., Mell, M. W., Hlatky, M. A., Wactawski‐Wende, J., Allison, M., Wild, R. A., Shadyab, A. H., Wallace, R. B., et al. (2020) · Journal of Vascular Surgery · doi:10.1016/j.jvs.2020.07.106 · Cited by 16
Владиславович, Е. М., Tmoyan, N. A., Afanasieva, O. I., Afanasieva, M. I., & Pokrovsky, S. N. (2021) · Biomolecules · doi:10.3390/biom11020257 · Cited by 16
“The FOURIER (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in subjects with Elevated Risk) study showed that in patients with significant lower extremities arteries atherosclerotic disease (LEAD) within 2 years of follow-up the risk of CVE was approximately two times higher than in patients with myoca…”
BackgroundCardiovascular Risk Assessment in the Older Athlete
Moorman, A. J., Dean, L. S., Yang, E., & Drezner, J. A. (2021) · Sports Health A Multidisciplinary Approach · doi:10.1177/19417381211004877 · Cited by 18
“In an exploratory analysis of the FOURIER trial of evolocumab in secondary prevention, there was a significant association between achieved Lp(a) level and major CV events.(58) Elevated Lp(a) was not required for enrollment in the PCSK9 inhibitor outcome trials, and targeted studies for patients with high Lp(a) are un…”
BackgroundLipoprotein(a) as Part of the Diagnosis of Clinical Familial Hypercholesterolemia
Langsted, A., & Nordestgaard, B. G. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-01002-0 · Cited by 16
Effect of Alirocumab on Coronary Calcification in Patients With Coronary Artery Disease
Gao, F., Li, Y. P., Ma, X., Wang, Z. J., Shi, D. M., & Zhou, Y. J. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.907662 · Cited by 16
VLDL receptor gene therapy for reducing atherogenic lipoproteins
Krauss, R. M., Lu, J. T., Higgins, J. J., Clary, C. M., & Tabibiazar, R. (2023) · Molecular Metabolism · doi:10.1016/j.molmet.2023.101685 · Cited by 18
Yu, M.-M., Zhao, X., Chen, Y., Tao, X., Ge, J., Jin, H. M., & Zeng, M.-S. (2023) · Cardiovascular Diabetology · doi:10.1186/s12933-023-01857-w · Cited by 17
“It not only produce a strong low-density lipoprotein cholesterol (LDL-C) reduction, but also contribute to a modest reduction of lipoprotein(a) [Lp(a)] [7].”
BackgroundDevelopment and multinational validation of an algorithmic strategy for high Lp(a) screening
Aminorroaya, A., Dhingra, L. S., Oikonomou, E. K., Saadatagah, S., Thangaraj, P., Shankar, S. V., Spatz, E. S., & Khera, R. (2024) · Nature Cardiovascular Research · doi:10.1038/s44161-024-00469-1 · Cited by 16
“…with elevated Lp( a ) can undergo rigorous cardiovascular risk management and initiation or intensification of existing therapies for elevated Lp( a ), with the potential role of proprotein convertase subtilisin/kexin type 9 inhibitors in MACE reduction via lowering Lp( a ) 13–15, 24, 25, 34– 37 .”
Lipoprotein(a)—antisense therapy
Vogt, A. (2019) · Clinical Research in Cardiology Supplements · doi:10.1007/s11789-019-00096-2 · Cited by 15
Current and future role of lipoprotein(a) in preventive cardiology
Berman, A. N., & Blankstein, R. (2019) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000661 · Cited by 16
Regulation of Lipoprotein Homeostasis by Self-Assembling Peptides
Harbour, V., Casillas, C., Siddiqui, Z., Sarkar, B., Sanyal, S., Nguyen, P. K., Kim, K. K., Roy, A., Iglesias-Montoro, P., Patel, S., et al. (2020) · ACS Applied Bio Materials · doi:10.1021/acsabm.0c01229 · Cited by 16
Therapeutic lowering of lipoprotein(a): How much is enough?
Kronenberg, F. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.07.003 · Cited by 16
PCSK9 loss-of-function variants and Lp(a) phenotypes among black US adults
Mefford, M. T., Marcovina, S. M., Bittner, V., Cushman, M., Brown, T. M., Farkouh, M. E., Tsimikas, S., Monda, K. L., López, J. A. G., Muntner, P., et al. (2019) · Journal of Lipid Research · doi:10.1194/jlr.p119000173 · Cited by 16
“duction in Lp(a) concentration at 48 weeks (33).”
BackgroundResultRosenson, R. S., & Goonewardena, S. N. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.04.103 · Cited by 16
The Value of Measuring Lipoprotein(a) in Children
Khoury, M., & Clarke, S. L. (2022) · Circulation · doi:10.1161/circulationaha.122.062592 · Cited by 16
Lipoprotein(a), Residual Cardiovascular Risk, and the Search for Targeted Therapy
Blaha, M. J., & Bhatia, H. S. (2024) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2024.03.370 · Cited by 17
Lipoprotein(a) and risk-weighted apolipoprotein B: a novel metric for atherogenic risk
Rehman, M. B., & Tudrej, B. V. (2024) · Lipids in Health and Disease · doi:10.1186/s12944-024-02307-6 · Cited by 15
Pinto, R. D., Grassi, D., Properzi, G., Desideri, G., & Ferri, C. (2019) · High Blood Pressure & Cardiovascular Prevention · doi:10.1007/s40292-019-00323-7 · Cited by 16
Yu, Z., Hu, L., Sun, C., Wang, Z., Zhang, X., Wu, M., & Liu, L. (2023) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000001419 · Cited by 14
Lipoprotein(a) in Familial Hypercholesterolemia
Jacob, E. O., McIntyre, A. D., Wang, J., & Hegele, R. A. (2023) · CJC Open · doi:10.1016/j.cjco.2023.09.018 · Cited by 15
“For patients with HeFH for whom therapy with PCSK9 inhibitors is contemplated, the moderate Lp(a) lowering ability of these agents 20,21 might be a consideration in those with concomitant Lp(a) elevations.”
BackgroundSong, Z., Zhao, L., Liu, D.-S., Zhao, L.-N., Peng, Q., Li, Z.-Y., Wu, J., Chen, S., Huang, F., Chen, X., et al. (2023) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2023.11.006 · Cited by 15
Rosenson, R. S., Tate, A. M., Grushko, O. G., Damodaran, D., Chen, Q., Boffa, M. B., Koschinsky, M. L., Narula, J., & Goonewardena, S. N. (2025) · Journal of Lipid Research · doi:10.1016/j.jlr.2025.100820 · Cited by 24
Lipoprotein(a) and proprotein convertase subtilisin/kexin type 9 inhibitors
Julius, U., Tselmin, S., Schatz, U., Fischer, S., & Bornstein, S. R. (2019) · Clinical Research in Cardiology Supplements · doi:10.1007/s11789-019-00099-z · Cited by 15
Bourgeois, R., Girard, A. S., Perrot, N., Guertin, J., Mitchell, P. L., Couture, C., Gotti, C., Bourassa, S., Poggio, P., Mass, E., et al. (2020) · CJC Open · doi:10.1016/j.cjco.2020.11.019 · Cited by 15
Parthymos, I., Kostapanos, M. S., Mikhailidis, D. P., & Florentin, M. (2021) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwab052 · Cited by 15
Funabashi, S., Kataoka, Y., Hori, M., Ogura, M., Nakaoku, Y., Nishimura, K., Doi, T., Nishikawa, R., Tsuda, K., Noguchi, T., et al. (2021) · JACC Asia · doi:10.1016/j.jacasi.2021.07.004 · Cited by 15
Marchis, G. M. D., Dittrich, T. D., Malik, R., Zietz, A. V., Kriemler, L. F., Ference, B. A., Dichgans, M., & Georgakis, M. K. (2022) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2022.09.007 · Cited by 14
Cho, K. H., & Hong, Y. J. (2020) · The Korean Journal of Internal Medicine · doi:10.3904/kjim.2020.140 · Cited by 16
“[43] analyzed 25,096 patients having Lp(a) levels in the FOURIER trial and demonstrated that higher levels of Lp(a) were associated with an increased risk of a cardiovascular event irrespective of LDL cholesterol.”
Secondary prevention after CABG: do new agents change the paradigm?
Paquin, A., Poirier, P., Beaudoin, J., & Piché, M. (2020) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000783 · Cited by 15
“These agents are also effective in reducing other atherogenic lipoproteins, including lipoprotein(a) and triglyceride-rich lipoproteins [22,23,25,26].”
BackgroundFuture role of proprotein convertase subtilisin/kexin type 9 inhibitors in preventive cardiology
Mahmood, T. A., & Shapiro, M. D. (2019) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000657 · Cited by 14
Rider, D. A., Chivers, S., Aretz, J., Eisermann, M., Löffler, K., Hauptmann, J., Morrison, E., & Campion, G. (2022) · Toxicological Sciences · doi:10.1093/toxsci/kfac067 · Cited by 14
“Current lipid-modifying agents are largely ineffective at reducing serum Lp(a) levels (van Capelleveen et al., 2016), with monoclonal antibody PCSK9 inhibitors showing modest reductions (Korneva et al., 2021; O’Donoghue et al., 2019; Ray et al., 2019).”
BackgroundMukherjee, D., & Nissen, S. E. (2023) · Current Vascular Pharmacology · doi:10.2174/0115701611267835231210054909 · Cited by 15
LP(a): The new marker of high cardiovascular risk
Averna, M. R., & Cefalu, A. B. (2024) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2024.103845 · Cited by 14
Schwartz, G. G., Szarek, M. J., Jukema, J. W., Cobbaert, C. M., Reijnders, E., Bittner, V., Schwertfeger, M., Bhatt, D. L., Fazio, S., Garon, G., et al. (2025) · Diabetes Care · doi:10.2337/dc24-2110 · Cited by 14
“In the FOURIER trial (34), the PCSK9 inhibitor evolocumab reduced lipoprotein(a) to an extent similar to that of alirocumab in ODYSSEY OUTCOMES, but a relationship between lipoprotein(a) reduction and NOD was not explored.”
Self-citationOtoda, T., Aihara, K., & Takayama, T. (2025) · Biomedicines · doi:10.3390/biomedicines13051053 · Cited by 14
Razavi, A. C., Bhatia, H. S., Blumenthal, R. S., Shapiro, M. D., & Mehta, A. (2025) · Diabetes Obesity and Metabolism · doi:10.1111/dom.16469 · Cited by 16
Afanasieva, O. I., Владиславович, Е. М., Александровна, К. Е., Андреевна, Р. О., Чубыкина, У. В., Egiazaryan, M., Sherstyuk, E. E., Afanasieva, M. I., Utkina, E. A., & Pokrovsky, S. N. (2020) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd7040045 · Cited by 14
“FOURIER study with high-risk patients, was shown that the efficacy of Lp(a) reduction due to Evolocumab administration for 48 weeks depended on the initial Lp(a) concentration and was poorly correlated with changes in LDL-C concentrations [32].”
BackgroundGenetics of Lipoprotein(a): Cardiovascular Disease and Future Therapy
Langsted, A., & Nordestgaard, B. G. (2021) · Current Atherosclerosis Reports · doi:10.1007/s11883-021-00937-0 · Cited by 14
Effect of PCSK9 Inhibitors on Hemostasis in Patients with Isolated Hypercholesterolemia
Basiak, M., Hachuła, M., Kosowski, M., & Okopień, B. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11092542 · Cited by 14
“It is critical to evaluate the plasma concentrations of LDL-C and Lp(a) when using PCSK9 inhibitors, which, in contrast to statins, reduce both [24].”
BackgroundGaine, S. P., Quispe, R., Patel, J., & Michos, E. D. (2022) · Current Cardiovascular Risk Reports · doi:10.1007/s12170-022-00694-y · Cited by 14
Lipoprotein(a): Role in atherosclerosis and new treatment options
Tomić-Naglić, D., Manojlovic, M. S., Pejaković, S., Stepanović, K., & Prodanović, J. (2023) · Biomolecules and Biomedicine · doi:10.17305/bb.2023.8992 · Cited by 15
“A monoclonal antibody that inhibits PCSK9 has also been shown to be effective in lowering Lp(a) levels [75, 76].”
BackgroundMelita, H., Manolis, A. A., Manolis, T. A., & Manolis, A. S. (2022) · PubMed · doi:10.1097/fjc.0000000000001160 · Cited by 13
Xiao, T., Liu, H., Tian, N., Lian, L., Miao, K., Li, Y., Chen, L., Yuan, H., Du, M., Wu, S., et al. (2025) · Liver International · doi:10.1111/liv.70208 · Cited by 13
“Proprotein convertase subtilisin/kexin-9 (PCSK9) inhibitors may decrease circulating Lp(a) levels by approximately 20%, although they are not recommended to reduce plasma Lp(a) levels [34].”
Forzano, I., Florimonte, D., Narciso, V., Canonico, M. E., Castiello, D. S., Manzi, L., Cristiano, S., Spinelli, A. M., Vallone, D. M., D’Alconzo, D., et al. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14238334 · Cited by 17
“Although modest Lp(a) reductions with niacin or CETP inhibitors failed to improve outcomes, emerging data suggest that the more profound reductions achievable with PCSK9 inhibitors may confer incremental benefit [57].”
Mueller, P. A., Yerkes, E., Bergstrom, P., Rosário, S., Hay, J., & Pamir, N. (2022) · Scientific Reports · doi:10.1038/s41598-022-13040-4 · Cited by 13
Song, J., Zhang, X., Wei, M., Bo, Y., Zhou, X., & Tang, B. (2022) · Lipids in Health and Disease · doi:10.1186/s12944-022-01682-2 · Cited by 13
“Conventional LDL-C and apo B reduction therapy had little effect on Lp(a) levels, whereas the proprotein-converting enzyme subtilisin/Kexin 9 (PCSK-9) monoclonal antibodies not only reduced 50–60% LDL-C on average, but also reduced Lp(a) by 25–30% [31, 32].”
BackgroundElevated Lp(a) Levels Correlate with Severe and Multiple Coronary Artery Stenotic Lesions
Hageh, C. A., Chacar, S., Ghassibe‐Sabbagh, M., Platt, D. E., Henschel, A., Hamdan, H., Gauguier, D., Murr, Y. E., Alefishat, E. A., Chammas, E., et al. (2023) · Vascular Health and Risk Management · doi:10.2147/vhrm.s394134 · Cited by 13
Lipoprotein(a): cardiovascular risk and emerging therapies
Fujino, M., & Nicholls, S. J. (2023) · Expert Review of Cardiovascular Therapy · doi:10.1080/14779072.2023.2197593 · Cited by 14
“The two RCTs, FOURIER [32] and ODYSSEY [33], with proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, which are antibodies, also showed an increased risk of CV events, independent of LDL-C levels, with Lp(a) as a ‘residual risk.’”
BackgroundInfluentialPCSK9 Inhibition in Atherosclerotic Cardiovascular Disease
Delialis, D., Dimopoulou, M., Papaioannou, M., Kotsira, G., Maneta, E., Mavraganis, G., Loutos, C., Georgiopoulos, G. A., & Stamatelopoulos, K. S. (2023) · Current Pharmaceutical Design · doi:10.2174/1381612829666230412105238 · Cited by 13
Farina, J., Pereyra, M., Mahmoud, A., Chao, C., Barry, T., Demeter, S. H., Ayoub, C., & Arsanjani, R. (2023) · Pharmaceuticals · doi:10.3390/ph16070919 · Cited by 13
He, J., Yang, M.-F., Song, C., Zhang, R., Yuan, S., Li, J., & Dou, K. (2023) · Journal of Endocrinological Investigation · doi:10.1007/s40618-023-02203-3 · Cited by 13
“Moreover, in research with proprotein convertase subtilisin/kexin type 9 inhibitors, higher reduction of CV risk was observed in patients with higher baseline Lp(a) levels [41, 42].”
Zeng, W., Zhou, F., Zhao, H., Wang, Y., Chen, J., Lu, J., Zheng, D., Kuang, J., Yuan, D., Zhou, J., et al. (2025) · Journal of the American Heart Association · doi:10.1161/jaha.124.035651 · Cited by 13
“39”
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. (2020) · Hipertensión y Riesgo Vascular · doi:10.1016/j.hipert.2020.07.004 · Cited by 13
Wu, B., Zhao, H., Liu, C., Lu, H., Liu, R., Long, J., Zhang, Z., & Zeng, F. (2020) · Postgraduate Medicine · doi:10.1080/00325481.2020.1845517 · Cited by 13
The clinical role of combined serum C1q and hsCRP in predicting coronary artery disease
Jia, Y., Wen, W., Yang, Y., Huang, M., Ning, Y., Jiao, X., Liu, S., Qin, Y., & Zhang, M. (2021) · Clinical Biochemistry · doi:10.1016/j.clinbiochem.2021.04.004 · Cited by 13
Drugs for Prevention and Treatment of Aortic Stenosis: How Close Are We?
Afshar, M. S., Yazdan-Ashoori, S., Engert, J. C., & Thanassoulis, G. (2021) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2021.02.017 · Cited by 14
Langlois, M. R., Nordestgaard, B. G., Langsted, A., Chapman, M. J., Aakre, K. M., Baum, H. H. E., Borén, J., Bruckert, É., Catapano, A. L., Cobbaert, C. M., et al. (2021) · Laboratory Service · doi:10.17116/labs20211001145 · Cited by 13
Advances in Oral Biomacromolecule Therapies for Metabolic Diseases
Jiao, Q., Huang, Y., He, J., & Xu, Y. (2025) · Pharmaceutics · doi:10.3390/pharmaceutics17020238 · Cited by 13
Likozar, A. R., & Šebeštjen, M. (2022) · Atherosclerosis Plus · doi:10.1016/j.athplu.2022.07.001 · Cited by 12
“In patients enrolled in the Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk (FOURIER) trial [24], higher baseline Lp(a) levels were independently associated with increased risk of major CV events, and evolocumab significantly reduced Lp(a) levels by approximately 27%.”
BackgroundResultLoh, W. J., & Watts, G. F. (2022) · Current Opinion in Endocrinology Diabetes and Obesity · doi:10.1097/med.0000000000000789 · Cited by 12
“In the FOURIER trial, evolocumab reduced the risk of CAD death, myocardial infarction and revascularization by 23% in patients with Lp(a) level above the median, whereas 7% risk reduction was observed in patients with Lp(a) level less than the median [63].”
BackgroundInfluentialOrfanos, P., Fonseca, A. F., Hu, X., Gautam, R., Montgomery, G., Studer, R. L., Kaur, J., Saxena, N., & Kaushik, N. (2023) · PLoS ONE · doi:10.1371/journal.pone.0294250 · Cited by 12
“…and HDL-C levels and on specific treatments) [47]; elevated Lp(a) and reference or low Lp(a) thresholds; comorbidities; biomarkers, including HDL-C, LDL-C, TC, HbA1C, and hsCRP; gender distribution; and risk factors for ASCVD (smoking history, history of CAD, MI, stroke, and PAD events) [35,48–50].”
BackgroundInfluentialAssociation of Lipoprotein(a) with arterial stiffness: A Mendelian randomization study
Simistiras, A., Georgiopoulos, G. A., Delialis, D., Mavraganis, G., Oikonomou, E., Maneta, E., Loutos, C., Εvangelou, Ε., & Stamatelopoulos, K. S. (2024) · European Journal of Clinical Investigation · doi:10.1111/eci.14168 · Cited by 12
Hoogeveen, R. C., Diffenderfer, M. R., Lim, E., Liu, C., Ikezaki, H., Guan, W., Tsai, M. Y., & Ballantyne, C. M. (2025) · Nutrients · doi:10.3390/nu17081324 · Cited by 12
Tackling cardiometabolic risk in the Asia Pacific region
Li, J., Yeo, K. K., Tan, K., Ako, J., Krittayaphong, R., Tan, R., Aylward, P. E., Lam, C. S. P., Baek, S. H., Dalal, J. J., et al. (2020) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2020.100096 · Cited by 13
“While PCSK9 inhibitors lower Lp(a), with reports that this contributes to their clinical benefit [74,75], they will continue to be primarily used to lower LDL cholesterol levels.”
BackgroundFunabashi, S., Kataoka, Y., Hori, M., Ogura, M., Doi, T., Noguchi, T., & Harada‐Shiba, M. (2022) · Journal of the American Heart Association · doi:10.1161/jaha.121.025232 · Cited by 12
Wang, L., Liu, L., Zhao, Y., Chu, M., & Teng, J. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.1004264 · Cited by 13
Proprotein Convertase Subtilisin/Kexin Type 9 Inhibition: The Big Step Forward in Lipid Control
Rikhi, R. R., & Shapiro, M. D. (2023) · European Cardiology Review · doi:10.15420/ecr.2023.14 · Cited by 13
Boffa, M. B., & Koschinsky, M. L. (2019) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000641 · Cited by 12
Fras, Z. (2019) · The Anatolian Journal of Cardiology · doi:10.14744/anatoljcardiol.2019.56068 · Cited by 12
“It was reported that in patients with higher than median Lp(a), greater absolute reduction of different major adverse cardiac event (MACE) can be achieved from CV outcome trials using anti-PCSK9 antibodies (FOURIER and ODYSSEY Outcomes) (26, 27).”
BackgroundRizos, C. V., Florentin, M., Skoumas, I., Τζιόμαλος, Κ., Rallidis, L. S., Kotsis, V., Athyros, V., Skalidis, E. I., Kolovou, G. D., Garoufi, A., et al. (2020) · Lipids in Health and Disease · doi:10.1186/s12944-020-01289-5 · Cited by 12
Lipoprotein(a) and aortic valve stenosis: A casual or causal association?
Santangelo, G., Faggiano, A., Bernardi, N., Carugo, S., Giammanco, A., & Faggiano, P. M. (2021) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2021.10.015 · Cited by 13
Moore, M. K., Jones, G. T., McCormick, S., Williams, M. J. A., & Coffey, S. (2024) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwae100 · Cited by 11
Wu, J., Fan, Q., He, Q., Zhong, Q., Zhu, X., Cai, H., He, X., Xu, Y., Huang, Y., & Di, X. (2023) · Medicine · doi:10.1097/md.0000000000036284 · Cited by 14
“[27] Pei et al [28] have experimentally demonstrated the potential clinical therapeutic value of targeting LPA-LPA2 to protect the heart from ischemic injury, warranting further clinical attention.”
BackgroundGhose, T. (2023) · Indian Heart Journal · doi:10.1016/j.ihj.2023.12.010 · Cited by 11
Li, Q., Yin, K., Ma, H., Liu, H.-H., Li, S., Luo, X., Hu, R., Zhang, W., Lv, Z.-S., Niu, X.-L., et al. (2024) · Molecular Therapy · doi:10.1016/j.ymthe.2024.01.008 · Cited by 15
Impact of High Lipoprotein(a) on Long‐Term Survival Following Coronary Artery Bypass Grafting
Yuan, S., Li, F., Zhang, H., Zeng, J., Su, X., Qu, J., Lin, S., Gu, D., Rao, C., Zhao, Y., et al. (2024) · Journal of the American Heart Association · doi:10.1161/jaha.123.031322 · Cited by 13
“8,9 However, we did not analyze the clinical impact of proprotein convertase subtilisin/kexin type 9 inhibitor because the National Medical Products Administration did not approve the use of proprotein convertase subtilisin/kexin type 9 inhibitor in China until 2018.”
BackgroundLeiter, L. A., Hegele, R. A., Brown, V., Bergeron, J., Mackinnon, E. S., & Mancini, G. B. J. (2024) · Reviews in Cardiovascular Medicine · doi:10.31083/j.rcm2505190 · Cited by 12
“…patients with higher baseline Lp(a) levels had greater absolute reductions in Lp(a) and CV risk post-evolocumab treatment, with a 23% reduction in the risk of coronary heart disease death, MI or urgent coronary revascularization compared with only 7% in patients with lower baseline Lp(a) [ 58].”
ResultThe Role of Lipoprotein(a) in Peripheral Artery Disease
Pavlatos, N., & Kalra, D. K. (2024) · Biomedicines · doi:10.3390/biomedicines12061229 · Cited by 14
“Another sub-analysis showed that evolocumab was able to decrease serum Lp(a) levels by a median of 26.9% [84].”
BackgroundInfluentialLipoprotein (a): A new target for pharmacological research and an option for treatment
Pirillo, A., & Catapano, A. L. (2025) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2025.07.021 · Cited by 14
Shah, N. P., Wang, Q., Wolski, K. E., Cho, L., McErlean, E. S., Ruotolo, G., Weerakkody, G. J., Riesmeyer, J. S., Nicholls, S. J., Lincoff, A. M., et al. (2019) · Diabetes Care · doi:10.2337/dc19-1117 · Cited by 11
“Our results are consistent with prior literature that suggests Lp(a) to be a potent harbinger of clinical cardiovascular disease (3,4) but are strengthened by the fact that these results from ACCELERATE were obtained”
ResultLipoprotein (a) and the Risk of Chronic Kidney Disease in Hospitalized Japanese Patients
Tada, H., Yamagami, K., Nishikawa, T., Yoshida, T., Teramoto, R., Sakata, K., Takamura, M., & Kawashiri, M. (2020) · Internal Medicine · doi:10.2169/internalmedicine.4503-20 · Cited by 11
van Niel, J., Geelhoed-Duijvestijn, P. H. L. M., Numans, M. E., Kharagjitsingh, A. V., & Vos, R. C. (2021) · Endocrinology Diabetes & Metabolism · doi:10.1002/edm2.242 · Cited by 11
Okada, T., Miyoshi, T., Doi, M., Nosaka, K., Tsushima, R., Ugawa, S., Takagi, W., Sogo, M., Takahashi, M., & Ito, H. (2022) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd9050153 · Cited by 11
“Third, this study cannot evaluate the effect of evolocumab by itself without statin, although a previous study showed that evolocumab reduced lipoprotein(a) levels in patients resistant or intolerant to statin and/or fibrate therapy [24].”
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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