Associations of Genetically Predicted Lp(a) (Lipoprotein [a]) Levels With Cardiovascular Traits in Individuals of European and African Ancestry
Open accessAbstract
Background: Lp(a) (lipoprotein [a]) levels are higher in individuals of African ancestry (AA) than in individuals of European ancestry (EA). We examined associations of genetically predicted Lp(a) levels with (1) atherosclerotic cardiovascular disease subtypes: coronary heart disease, cerebrovascular disease, peripheral artery disease, and abdominal aortic aneurysm and (2) nonatherosclerotic cardiovascular disease phenotypes, stratified by ancestry. Methods: We performed (1) Mendelian randomization analyses for previously reported cardiovascular associations and (2) Mendelian randomization–phenome-wide association analyses for novel associations. Analyses were stratified by ancestry in electronic Medical Records and Genomics, United Kingdom Biobank, and Million Veteran Program cohorts separately and in a combined cohort of 804 507 EA and 103 580 AA participants. Results: In Mendelian randomization analyses using the combined cohort, a 1-SD genetic increase in Lp(a) level was associated with atherosclerotic cardiovascular disease subtypes in EA—odds ratio and 95% CI for coronary heart disease 1.28 (1.16–1.41); cerebrovascular disease 1.14 (1.07–1.21); peripheral artery disease 1.22 (1.11–1.34); abdominal aortic aneurysm 1.28 (1.17–1.40); in AA, the effect estimate was lower than in EA and nonsignificant for coronary heart disease 1.11 (0.99–1.24) and cerebrovascular disease 1.06 (0.99–1.14) but similar for peripheral artery disease 1.16 (1.01–1.33) and abdominal aortic aneurysm 1.34 (1.11–1.62). In EA, a 1-SD genetic increase in Lp(a) level was associated with aortic valve disorders 1.34 (1.10–1.62), mitral valve disorders 1.18 (1.09–1.27), congestive heart failure 1.12 (1.05–1.19), and chronic kidney disease 1.07 (1.01–1.14). In AA, no significant associations were noted for aortic valve disorders 1.08 (0.94–1.25), mitral valve disorders 1.02 (0.89–1.16), congestive heart failure 1.02 (0.95–1.10), or chronic kidney disease 1.05 (0.99–1.12). Mendelian randomization–phenome-wide association analyses identified novel associations in EA with arterial thromboembolic disease, nonaortic aneurysmal disease, atrial fibrillation, cardiac conduction disorders, and hypertension. Conclusions: Many cardiovascular associations of genetically increased Lp(a) that were significant in EA were not significant in AA. Lp(a) was associated with atherosclerotic cardiovascular disease in four major arterial beds in EA but only with peripheral artery disease and abdominal aortic aneurysm in AA. Additionally, novel cardiovascular associations were detected in EA.
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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 [188]
The Introduction calls Lp(a) a causal risk factor for atherosclerotic cardiovascular disease, and the Results report higher cardiovascular odds with genetically increased Lp(a), particularly in individuals of European ancestry. The paper does not establish the reverse causal direction—cardiovascular disease causing elevated Lp(a). If “vice versa” instead means that lowering Lp(a) reduces disease risk, the Discussion says the benefit of Lp(a)-lowering drugs was still being evaluated. (LLM, conf=0.83)
Experimental — accuracy not yet measuredElevated lipoprotein(a) concentration is associated with higher risk of CAVS.
“observational and genetic studies have reported that elevated lipoprotein(a) [Lp(a)] concentration is associated with higher risk of CAVS9,10”
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 [10]
The Abstract Results report that higher genetically predicted Lp(a) was associated with aortic valve disorders in individuals of European ancestry, but not significantly in those of African ancestry. The Discussion says those disorders included stenosis and regurgitation; it does not establish a separate association specifically with calcific aortic valve stenosis (CAVS). (LLM, conf=0.86)
Experimental — accuracy not yet measured
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Shah, H., Garacci, E., Behuria, S., Cainzos‐Achirica, M., Kandula, N. R., Kanaya, A. M., & Shah, N. S. (2022) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2022.100453 · Cited by 11 · see citing works
Awad, K., Kamel, M., Mahmoud, A., Farina, J., Badr, A., Pereyra, M., Scalia, I. G., Abbas, M. T., Ali, N. B., Alsidawi, S., et al. (2025) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwaf063 · Cited by 10 · see citing works
Ancestral diversity in lipoprotein(a) studies helps address evidence gaps
Lee, M. P., Dimos, S. F., Raffield, L. M., Wang, Z., Ballou, A. F., Downie, C. G., Arehart, C. H., Correa, A., de Vries, P. S., Du, Z., et al. (2023) · Open Heart · doi:10.1136/openhrt-2023-002382 · Cited by 9 · see citing works
High lipoprotein(a) levels and mitral valve disease: A systematic review
Masson, W. M., Barbagelata, L., OBERTI, P. F., Falconi, M. L., Cobo, A. L., Corral, P., & Nogueira, J. P. (2023) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2023.01.025 · Cited by 7 · see citing works
Lipoprotein(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 · see citing works
Dordonne, S., Mergeay-Fabre, M., Hafsi, N., Ntoutoum, A., Salazar-Cardozo, C., Casse, O., Hounnou, M., Adenis, A. A., Aurelus, J.-M., Misslin, C., et al. (2023) · Journal of Diabetes Research · doi:10.1155/2023/8111521 · Cited by 5 · see citing works
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 · see citing works
Wu, C., Pu, Q., Zou, Y., Jin, J., Lei, Y., Hu, Y., Chen, Z., & Yu, L. (2025) · Scientific Reports · doi:10.1038/s41598-025-15525-4 · Cited by 3 · see citing works
“Additionally, observational and genetic studies have reported that elevated lipoprotein(a) [Lp(a)] concentration is associated with higher risk of CAVS 9,10 , but its association with hemodynamic progression is controversial 11 .”
Metabolic implications of COVID-19 with a focus on lipid profiles and inflammatory markers
Mohamed, F., Gunter, S., Currin, S., Raal, F. J., Kalla, I., & Millen, A. M. E. (2026) · Scientific Reports · doi:10.1038/s41598-026-37439-5 · Cited by 3 · see citing works
Thrombosis, Inflammation, and Lipoprotein(a): Clinical Implications
Safarova, M. S., & Moriarty, P. M. (2023) · Contemporary cardiology · doi:10.1007/978-3-031-24575-6_11 · Cited by 3 · see citing works
Self-citationThe role of lipoprotein(a) in atrial fibrillation: a systematic review
Procyk, G., Grabowski, M., & Gąsecka, A. (2025) · Polskie Archiwum Medycyny Wewnętrznej · doi:10.20452/pamw.16924 · Cited by 3 · see citing works
Jang, A. Y., Lee, J. H., Lee, S., Choe, H. J., Park, S. M., Jeong, I., Kim, B. J., & on behalf of the Lipoprotein(a) Task Force of the Korea Society of Lipid and Atherosclerosis (2025) · Korean Circulation Journal · doi:10.4070/kcj.2025.0388 · Cited by 2 · see citing works
Jang, A. Y., Lee, J. H., Lee, S.-G., Choe, H. J., Park, S. M., Jeong, I., Kim, B. J., & on behalf of the Lipoprotein(a) Task Force of the Korea Society of Lipid and Atherosclerosis (2026) · Journal of Lipid and Atherosclerosis · doi:10.12997/jla.2026.15.1.2 · Cited by 2 · see citing works
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 · see citing works
Safarova, M. S., Santos, R. D., & Moriarty, P. M. (2023) · Elsevier eBooks · doi:10.1016/b978-0-323-88286-6.00034-0 · Cited by 2 · see citing works
Self-citationShi, J., Shringarpure, S., Hinds, D. A., Auton, A., & Holmes, M. V. (2024) · medRxiv · doi:10.1101/2024.07.24.24310950 · Cited by 2 · see citing works
Lp(a) Has Specific Effects on Coronary Artery Disease Independent of LDL-C
Lee, M. P., Koenigsberg, S. H., Anwar, M. Y., Raffield, L. M., Lin, Z., Ballou, A. F., Booth, J. N., Davy-Méndez, T., Kassahun, H., Kent, S. T., et al. (2026) · JACC Advances · doi:10.1016/j.jacadv.2026.102697 · Cited by 1 · see citing works
Outland, E. H., Xin, Y., Dickson, A. L., Mundo, S., Tao, R., Zhong, X. Y., Karakoc, G., Serley, S., Jiang, L., Cox, N. J., et al. (2025) · medRxiv · doi:10.1101/2025.03.07.25323588
Self-citationPeripheral Artery Disease Treatment: Scoping Review with ☸SAIMSARA
SAIMSARA (2026) · SAIMSARA Journal · doi:10.62487/saimsarafa4dc087
Kowalczys, A., Marlęga-Linert, J., Gruchała, M., & Mickiewicz, A. (2026) · Cardiac failure review · doi:10.15420/cfr.2025.46
Lipoprotein(a) and aortic diseases: Epidemiological evidence from observation to causation
Xia, D., Zhang, L., Fang, J., Hu, W., Li, M., Chen, Y., Shu, C., Li, J., & Li, X. (2026) · Journal of clinical lipidology · doi:10.1016/j.jacl.2026.07.014
Lipoprotein(a) in the statin era: from risk marker to therapeutic target
Hong, R., 刘玉华, 李晓春, Liu, H., & 谢东阳 (2026) · Frontiers in Pharmacology · doi:10.3389/fphar.2026.1938864
Lipoprotein(a) Inhibition: Current Evidence, Therapeutic Landscape, and Future Directions
Sabouret, P. F., Giamundo, D. M., Popiołek-Kalisz, J., Spadafora, L., Bernardi, M., Asher, E., Mamas, M. A., Atar, D., & Andò, G. (2026) · Reviews in Cardiovascular Medicine · doi:10.31083/rcm55004
- Authors
- Satterfield, B. A., Dikilitas, O., Safarova, M. S., Clarke, S. L., Tcheandjieu, C., Zhu, X., Bastarache, L., Larson, E. B., Justice, A. E., Shang, N., Rosenthal, E. A., Shah, A. S., Namjou-Khales, B., Urbina, E. M., Wei, W.-Q., Feng, Q., Jarvik, G. P., Hebbring, S. J., de Andrade, M., Manolio, T. A., Assimes, T. L., & Kullo, I. J.
- Affiliations
- Mayo Clinic (US)
- VA Palo Alto Health Care System (US)
- Pennsylvania State University (US)
- Vanderbilt University (US)
- Kaiser Permanente (US)
- Geisinger Health System (US)
- Columbia University (US)
- University of Washington (US)
- Cincinnati Children's Hospital Medical Center (US)
- Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center & Department of Pediatrics, University of Cincinnati College of Medicine, OH (B.-N.K.).
- Vanderbilt University Medical Center (US)
- Marshfield Clinic Research Foundation (US)
- Department of Health Sciences Research (M.d.A.), Mayo Clinic, Rochester, MN.
- National Human Genome Research Institute (US)
- ORCID
- Satterfield, Benjamin A.
- Dikilitas, Ozan
- Safarova, Maya S.
- Clarke, Shoa L.
- Tcheandjieu, Catherine
- Zhu, Xiang
- Bastarache, Lisa
- Larson, Eric B.
- Justice, Anne E.
- Shang, Ning
- Rosenthal, Elisabeth A.
- Shah, Amy Sanghavi
- Urbina, Elaine M.
- Wei, Wei-Qi
- Feng, QiPing
- Jarvik, Gail P.
- Hebbring, Scott J.
- de Andrade, Mariza
- Manolio, Teri A.
- Assimes, Themistocles L.
- Kullo, Iftikhar J.
- Venue
- Circulation: Genomic and Precision Medicine
- Published
- 2021-08
- Volume
- 14
- Issue
- 4
- Pages
- e003354-e003354
- ISSN
- 2574-8300 (ISSN-L)
- PMC
- PMC8634549
- OpenAlex
- W3185131304
- Cited by
- 40
- References
- 59
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 4 · 2023: 12 · 2022: 3 · 2021: 3
- FWCI
- 5.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation Genomic and Precision Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01-BX003362)
- National Heart, Lung, and Blood Institute (K24HL137010)
- National Human Genome Research Institute (U01HG006385, U01HG006379, U01HG004599, U01HG008680, U01HG004424, U01HG004609, U01HG004608, U01HG004438, U01HG004610, U01HG006375, U01HG006380, U01HG006382, U01HG004603, U01HG006378, U01HG006388, U01HG006389)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- lipoprotein(a), Lp(a) levels, atherosclerotic cardiovascular disease, coronary artery disease, cerebrovascular disease, peripheral arterial disease, abdominal aortic aneurysm, congestive heart failure, chronic kidney disease, genetic ancestry, Mendelian randomization
- MeSH terms
- Aged, Aged, 80 and over, Cardiovascular Diseases, Female, United Kingdom, Humans, Male, Middle Aged, Lipoprotein(a), Quantitative Trait, Heritable, Genetic Predisposition to Disease, Black People, White People, Mendelian Randomization Analysis
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