Association of LPA Variants With Risk of Coronary Disease and the Implications for Lipoprotein(a)-Lowering Therapies: A Mendelian Randomization Analysis
Open accessAbstract
Importance: Human genetic studies have indicated that plasma lipoprotein(a) (Lp[a]) is causally associated with the risk of coronary heart disease (CHD), but randomized trials of several therapies that reduce Lp(a) levels by 25% to 35% have not provided any evidence that lowering Lp(a) level reduces CHD risk. Objective: To estimate the magnitude of the change in plasma Lp(a) levels needed to have the same evidence of an association with CHD risk as a 38.67-mg/dL (ie, 1-mmol/L) change in low-density lipoprotein cholesterol (LDL-C) level, a change that has been shown to produce a clinically meaningful reduction in the risk of CHD. Design, Setting, and Participants: A mendelian randomization analysis was conducted using individual participant data from 5 studies and with external validation using summarized data from 48 studies. Population-based prospective cohort and case-control studies featured 20 793 individuals with CHD and 27 540 controls with individual participant data, whereas summarized data included 62 240 patients with CHD and 127 299 controls. Data were analyzed from November 2016 to March 2018. Exposures: Genetic LPA score and plasma Lp(a) mass concentration. Main Outcomes and Measures: Coronary heart disease. Results: Of the included study participants, 53% were men, all were of white European ancestry, and the mean age was 57.5 years. The association of genetically predicted Lp(a) with CHD risk was linearly proportional to the absolute change in Lp(a) concentration. A 10-mg/dL lower genetically predicted Lp(a) concentration was associated with a 5.8% lower CHD risk (odds ratio [OR], 0.942; 95% CI, 0.933-0.951; P = 3 × 10-37), whereas a 10-mg/dL lower genetically predicted LDL-C level estimated using an LDL-C genetic score was associated with a 14.5% lower CHD risk (OR, 0.855; 95% CI, 0.818-0.893; P = 2 × 10-12). Thus, a 101.5-mg/dL change (95% CI, 71.0-137.0) in Lp(a) concentration had the same association with CHD risk as a 38.67-mg/dL change in LDL-C level. The association of genetically predicted Lp(a) concentration with CHD risk appeared to be independent of changes in LDL-C level owing to genetic variants that mimic the relationship of statins, PCSK9 inhibitors, and ezetimibe with CHD risk. Conclusions and Relevance: The clinical benefit of lowering Lp(a) is likely to be proportional to the absolute reduction in Lp(a) concentration. Large absolute reductions in Lp(a) of approximately 100 mg/dL may be required to produce a clinically meaningful reduction in the risk of CHD similar in magnitude to what can be achieved by lowering LDL-C level by 38.67 mg/dL (ie, 1 mmol/L).
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Genetic studies found a causal link between elevated Lp(a) levels and a higher risk for CVD, and vice versa.
“Consequently, genetic studies found a causal link between elevated Lp(a) levels and a higher risk for CVD diseases,[184–189] and vice versa [190].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [186]
The Results section reports that genetically predicted lower Lp(a) is associated with lower coronary heart disease (CHD) risk, and the introductory passage describes genetic evidence for a likely causal link. The claim states causality without that qualification and broadens CHD to cardiovascular diseases generally. The separately cited “vice versa” clause is not attributed to this source. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSubstantial reductions in Lp(a) levels are necessary to provide a clinically meaningful effect on cardiovascular outcomes.
“However, substantial reductions in Lp(a) levels are necessary to provide a clinically meaningful effect on cardiovascular outcomes [186, 196].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [186]
The Discussion estimates that large absolute Lp(a) reductions are needed for clinically meaningful reductions in coronary heart disease (CHD) risk. It also says further analyses are needed to anticipate effects on stroke, peripheral vascular disease, aortic stenosis, or composite outcomes, so the broader claim about cardiovascular outcomes is not fully supported. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe risk increase associated with elevated Lp(a) was of lower magnitude than the one observed with LDL-C.
“However, the risk increase was of lower magnitude than the one observed with LDL-C [186, 191, 192].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [186]
Randomized trials lowering Lp(a) by 20-30% with niacin or CETP inhibitors have not shown that lowering Lp(a) reduces atherosclerotic cardiovascular disease risk beyond expected from ApoB reduction, but recent PCSK9 inhibitor data suggest a possible role for Lp(a) lowering in reducing cardiovascular risk.
“While randomized trials evaluating therapies that lower Lp(a) by 20-30% (including niacin and CETP inhibitors) have not provided evidence that lowering Lp(a) reduces the risk of ASCVD beyond that which would be expected from the observed reduction in ApoB-containing lipoproteins, recent data with PCSK9 inhibitors have suggested a possible role for Lp(a) lowering in reducing CV risk [76].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [76]
The phenotypic signature of a genetic risk score (GRS) derived from SNPs reliably associated with disease will likely capture multiple signals, including associations arising due to causal pathways leading to disease, trait associations arising due to disease and other elements.
“The phenotypic signature of a genetic risk score (GRS) derived from SNPs reliably associated with disease will likely capture multiple signals, including associations arising due to causal pathways leading to disease, trait associations arising due to disease and other elements 104 .”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [104]
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- Authors
- Burgess, S., Ference, B. A., Staley, J. R., Freitag, D. F., Mason, A. M., Nielsen, S. F., Willeit, P., Young, R., Surendran, P., Karthikeyan, S., Bolton, T. R., Peters, J. E., Kamstrup, P. R., Tybjærg-Hansen, A., Benn, M., Langsted, A., Schnohr, P., Vedel-Krogh, S., Kobylecki, C. J., Ford, I., Packard, C., Trompet, S., Jukema, J. W., Sattar, N., Di Angelantonio, E., Saleheen, D., Howson, J. M. M., Nordestgaard, B. G., Butterworth, A. S., Danesh, J., & for the European Prospective Investigation Into Cancer and Nutrition–Cardiovascular Disease (EPIC-CVD) Consortium
- Affiliations
- University of Cambridge (GB)
- Wayne State University (US)
- University of Copenhagen (DK)
- Innsbruck Medical University (AT)
- Herlev Hospital (DK)
- The Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Copenhagen, Denmark
- Frederiksberg Hospital (DK)
- Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Copenhagen, Denmark
- University of Glasgow (GB)
- Leiden University Medical Center (NL)
- MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
- Center for Non-Communicable Diseases (PK)
- Corresponding author
- Burgess, Stephen
- ORCID
- Burgess, Stephen
- Staley, James R.
- Mason, Amy M.
- Nielsen, Sune F.
- Willeit, Peter
- Young, Robin
- Surendran, Praveen
- Karthikeyan, Savita
- Peters, James E.
- Kamstrup, Pia R.
- Benn, Marianne
- Langsted, Anne
- Schnohr, Peter
- Kobylecki, Camilla J.
- Ford, Ian
- Packard, Chris
- Trompet, Stella
- Jukema, J. Wouter
- Sattar, Naveed
- Saleheen, Danish
- Howson, Joanna M. M.
- Nordestgaard, Børge G.
- Butterworth, Adam S.
- Danesh, John
- Venue
- JAMA Cardiology
- Publisher
- American Medical Association (AMA)
- Published
- 2018-07-01
- Volume
- 3
- Issue
- 7
- Pages
- 619
- ISSN
- 2380-6583 (ISSN-L)
- PMC
- PMC6481553
- OpenAlex
- W2809135070
- Semantic Scholar
- be8a5115894787850744e2f680cf4f00f9c5ffdb
- Cited by
- 689
- References
- 36
- Citations by year
- 2026: 91 · 2025: 86 · 2024: 70 · 2023: 113 · 2022: 84 · 2021: 76 · 2020: 86 · 2019: 71 · 2018: 12
- FWCI
- 63.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- JAMA Cardiology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion, cc-by)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion, cc-by-sa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Leiden Repository (Leiden University) (submittedVersion)
- Explore Bristol Research (submittedVersion, cc-by)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Rivm (National Institute for Public Health and the Environment) (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion)
- Funders
- Amgen
- Pfizer
- AstraZeneca
- Bayer
- Sanofi
- Biogen
- University of Pennsylvania
- Universitetet i Tromsø
- Aarhus Universitet
- NHS Blood and Transplant
- Regeneron Pharmaceuticals
- Wellcome Trust (204623/Z/16/Z, 204623)
- Ionis Pharmaceuticals
- National Institute for Health and Care Research (NF-SI-0617-10113, NF-SI-0512-10165, NF-SI-0512-10135, NF-SI-0617-10149)
- British Heart Foundation (MR/L003120/1, G0800270, SP/09/002, RG/08/014, RG/13/13/30194, RG/08/014/24067)
- University of Oxford
- European Commission (279233)
- University of Glasgow
- Cardiff University
- Institut National de la Santé et de la Recherche Médicale (U1018)
- Universiteit Leiden
- Gentofte Hospital
- Eusko Jaurlaritza
- Umeå Universitet
- Leids Universitair Medisch Centrum
- Rigshospitalet
- National and Kapodistrian University of Athens
- Malmö Högskola
- Universidad de Granada
- Institut Gustave-Roussy
- Medizinische Universität Innsbruck
- Esperion Therapeutics
- Perelman School of Medicine, University of Pennsylvania
- Medical Research Council (SP/09/002, MR/L003120/1, MR/S003746/1, G0800270, MC_UU_12015/1, MR/L003120)
- Det Sundhedsvidenskabelige Fakultet, Københavns Universitet
- Netherlands Heart Institute
- School of Public Health, Imperial College London
- NIHR Cambridge Biomedical Research Centre (MR/L003120/1)
- Daiichi Sankyo Europe
- FP7 Ideas: European Research Council (268834)
- Health Data Research UK
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- lipoprotein(a), coronary heart disease risk, LDL cholesterol, Lp(a)-lowering therapy, genetic score, cardiovascular risk reduction, individual patient data, Mendelian randomization, LDL-C lowering therapy, PCSK9 inhibitors
- MeSH terms
- Hypolipidemic Agents, Coronary Disease, Female, Follow-Up Studies, Humans, Cholesterol, LDL, Male, Middle Aged, Phenotype, Prognosis, Prospective Studies, Risk Factors, Genetic Variation, Biomarkers, Lipoprotein(a), Polymorphism, Single Nucleotide, Mendelian Randomization Analysis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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