Lp(a) (Lipoprotein[a]) Concentrations and Incident Atherosclerotic Cardiovascular Disease: New Insights From a Large National Biobank
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Objective: Lp(a) (lipoprotein[a]) concentrations are associated with atherosclerotic cardiovascular disease (ASCVD), and new therapies that enable potent and specific reduction are in development. In the largest study conducted to date, we address 3 areas of uncertainty: (1) the magnitude and shape of ASCVD risk conferred across the distribution of lipoprotein(a) concentrations; (2) variation of risk across racial and clinical subgroups; (3) clinical importance of a high lipoprotein(a) threshold to guide therapy. Approach and Results: Relationship of lipoprotein(a) to incident ASCVD was studied in 460 506 middle-aged UK Biobank participants. Over a median follow-up of 11.2 years, incident ASCVD occurred in 22 401 (4.9%) participants. Median lipoprotein(a) concentration was 19.6 nmol/L (25th–75th percentile 7.6–74.8). The relationship between lipoprotein(a) and ASCVD appeared linear across the distribution, with a hazard ratio of 1.11 (95% CI, 1.10–1.12) per 50 nmol/L increment. Substantial differences in concentrations were noted according to race—median values for white, South Asian, black, and Chinese individuals were 19, 31, 75, and 16 nmol/L, respectively. However, risk per 50 nmol/L appeared similar—hazard ratios of 1.11, 1.10, and 1.07 for white, South Asian, and black individuals, respectively. A high lipoprotein(a) concentration defined as ≥150 nmol/L was present in 12.2% of those without and 20.3% of those with preexisting ASCVD and associated with hazard ratios of 1.50 (95% CI, 1.44–1.56) and 1.16 (95% CI, 1.05–1.27), respectively. Conclusions: Lipoprotein(a) concentrations predict incident ASCVD among middle-aged adults within primary and secondary prevention contexts, with a linear risk gradient across the distribution. Concentrations are variable across racial subgroups, but the associated risk appears similar.
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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 [189]
The Introduction (page unavailable) says genetic studies suggest that the association between higher Lp(a) and ASCVD is causal. It describes reduced risk from lowering Lp(a) as a possibility being tested in a trial, not an established causal finding; the paper’s own results show an association rather than prove causation. (LLM, conf=0.85)
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- Authors
- Patel, A. P., Wang, M., Pirruccello, J. P., Ellinor, P. T., Ng, K., Kathiresan, S., & Khera, A. V.
- Affiliations
- Broad Institute (US)
- IBM Research - Cambridge (United States) (US)
- Corresponding author
- Khera, Amit V.
- ORCID
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2021-01
- Volume
- 41
- Issue
- 1
- Pages
- 465-474
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC7769893
- OpenAlex
- W3097307979
- Cited by
- 567
- References
- 50
- Citations by year
- 2026: 135 · 2025: 147 · 2024: 110 · 2023: 89 · 2022: 60 · 2021: 25 · 2020: 1
- FWCI
- 39.95
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion, other-oa)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Heart Association (R01 HL128914, 18SFRN34110082)
- Massachusetts General Hospital
- Broad Institute
- Fondation Leducq (K24HL105780, 18SFRN34110082, 1RO1HL092577, T32HL007208, 14CVD01, R01HL128914)
- Medical Research Council (MC_PC_17228)
- National Heart, Lung, and Blood Institute (1RO1HL092577, R01HL128914, K24HL105780, R01HL092577, T32HL007208)
- National Human Genome Research Institute (K08HG010155, 18SFRN34110082)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- lipoprotein(a), atherosclerotic cardiovascular disease, incident cardiovascular events, racial differences, risk gradient, primary prevention, secondary prevention, middle-aged adults, UK Biobank
- MeSH terms
- Race Factors, Heart Disease Risk Factors, Adult, Aged, Female, United Kingdom, Humans, Male, Middle Aged, Primary Prevention, Prognosis, Time Factors, Biomarkers, Incidence, Lipoprotein(a), Biological Specimen Banks, Risk Assessment, Atherosclerosis, Secondary Prevention
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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