Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (1,018 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A lipoprotein that resembles the low-density lipoproteins but with an extra protein moiety, apoprotein (A) also known as apolipoprotein (A), linked to apolipoprotein b-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Lipoprotein a; Lipoprotein Lp(a); Lipoprotein (a); Lipoprotein (a-).
Where it fits in the MeSH classification
- Broader topics
- Lipoproteins
- Narrower topics
- Apoprotein(a)
Related concepts
- Low-Density Lipoproteins
- Apoprotein
- Apolipoproteins
- Apolipoprotein B-100
Research landscape
PubMed indexes 6,827 records tagged with the MeSH heading “Lipoprotein(a)” (counts retrieved 2026-10-31). 1,706 of them (25.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,505 records.
Reviews account for 1,132 records (16.6%) and meta-analyses for 132. Randomized controlled trials number 399 (5.8%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,505 |
| 2000-2009 | 1,389 |
| 2010-2019 | 1,227 |
| 2020 onward | 1,706 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,132 | 16.6% |
| Meta-analyses | 132 | 1.9% |
| Randomized controlled trials | 399 | 5.8% |
Method: PubMed query "Lipoprotein(a)"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis | 2024 | Research article Design not recorded in structured metadata | 182 | cc by PMID 38233012 · DOI · PMC7616706 |
| Non-genetic influences on lipoprotein(a) concentrations | 2022 | Review article Design not recorded in structured metadata | 125 | cc by PMID 35606076 · DOI · PMC9549811 |
| Independence of Lipoprotein(a) and Low-Density Lipoprotein Cholesterol-Mediated Cardiovascular Risk: A Participant-Level Meta-Analysis | 2025 | Meta-analysis Design not recorded in structured metadata | 98 | cc by PMID 39492722 · DOI · PMC11771346 |
| Lipoprotein(a) and incident venous thromboembolism in pre- and postmenopausal women, and in men | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41903523 · DOI · PMC13266305 |
Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundLipoprotein(a) (Lp(a)) is recognized as a causal factor for coronary heart disease (CHD) but its atherogenicity relative to that of low-density lipoprotein (LDL) on a per-particle basis is indeterminate.
- Closing excerpt
- Therefore, Lp(a) represents a key target for drug-based intervention in a significant proportion of the at-risk population.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (244 words)
BackgroundLipoprotein(a) (Lp(a)) is recognized as a causal factor for coronary heart disease (CHD) but its atherogenicity relative to that of low-density lipoprotein (LDL) on a per-particle basis is indeterminate.ObjectivesThe authors addressed this issue in a genetic analysis based on the fact that Lp(a) and LDL both contain 1 apolipoprotein B (apoB) per particle.MethodsGenome-wide association studies using the UK Biobank population identified 2 clusters of single nucleotide polymorphisms: one comprising 107 variants linked to Lp(a) mass concentration, the other with 143 variants linked to LDL concentration. In these Lp(a) and LDL clusters, the relationship of genetically predicted variation in apoB with CHD risk was assessed.ResultsThe Mendelian randomization-derived OR for CHD for a 50 nmol/L higher Lp(a)-apoB was 1.28 (95% CI: 1.24-1.33) compared with 1.04 (95% CI: 1.03-1.05) for the same increment in LDL-apoB. Likewise, use of polygenic scores to rank subjects according to difference in Lp(a)-apoB vs difference in LDL-apoB revealed a greater HR for CHD per 50 nmol/L apoB for the Lp(a) cluster (1.47; 95% CI: 1.36-1.58) compared with the LDL cluster (1.04; 95% CI: 1.02-1.05). From these data, we estimate that the atherogenicity of Lp(a) is approximately 6-fold (point estimate of 6.6; 95% CI: 5.1-8.8) greater than that of LDL on a per-particle basis.ConclusionsWe conclude that the atherogenicity of Lp(a) (CHD risk quotient per unit increase in particle number) is substantially greater than that of LDL. Therefore, Lp(a) represents a key target for drug-based intervention in a significant proportion of the at-risk population.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38233012 · DOI · PMC7616706
Non-genetic influences on lipoprotein(a) concentrations [2]
Abstract reading summary — source excerpts
- Opening excerpt
- An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease.
- Closing excerpt
- Overall, current evidence supports a role for diet, hormones and related conditions, and liver and kidney diseases in modifying Lp(a) levels.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (241 words)
An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease. However, the extensive variability in Lp(a) levels between individuals and population groups cannot be fully explained by genetic factors, emphasizing a potential role for non-genetic factors. In this review, we provide an overview of current evidence on non-genetic factors influencing Lp(a) levels with a particular focus on diet, physical activity, hormones and certain pathological conditions. Findings from randomized controlled clinical trials show that diets lower in saturated fats modestly influence Lp(a) levels and often in the opposing direction to LDL cholesterol. Results from studies on physical activity/exercise have been inconsistent, ranging from no to minimal or moderate change in Lp(a) levels, potentially modulated by age and the type, intensity, and duration of exercise modality. Hormone replacement therapy (HRT) in postmenopausal women lowers Lp(a) levels with oral being more effective than transdermal estradiol; the type of HRT, dose of estrogen and addition of progestogen do not modify the Lp(a)-lowering effect of HRT. Kidney diseases result in marked elevations in Lp(a) levels, albeit dependent on disease stages, dialysis modalities and apolipoprotein(a) phenotypes. In contrast, Lp(a) levels are reduced in liver diseases in parallel with the disease progression, although population studies have yielded conflicting results on the associations between Lp(a) levels and non-alcoholic fatty liver disease. Overall, current evidence supports a role for diet, hormones and related conditions, and liver and kidney diseases in modifying Lp(a) levels.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35606076 · DOI · PMC9549811
Independence of Lipoprotein(a) and Low-Density Lipoprotein Cholesterol-Mediated Cardiovascular Risk: A Participant-Level Meta-Analysis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundLow-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp[a]) levels are independently associated with atherosclerotic cardiovascular disease (ASCVD).
- Closing excerpt
- ConclusionsThese findings demonstrate the independent and additive nature of Lp(a) and LDL-C levels for ASCVD risk, and that LDL-C lowering does not fully offset Lp(a)-mediated risk.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (268 words)
BackgroundLow-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp[a]) levels are independently associated with atherosclerotic cardiovascular disease (ASCVD). However, the relationship between Lp(a) level, LDL-C level, and ASCVD risk at different thresholds is not well defined.MethodsA participant-level meta-analysis of 27 658 participants enrolled in 6 placebo-controlled statin trials was performed to assess the association of LDL-C and Lp(a) levels with risk of fatal or nonfatal coronary heart disease events, stroke, or any coronary or carotid revascularization (ASCVD). The multivariable-adjusted association between baseline Lp(a) level and ASCVD risk was modeled continuously using generalized additive models, and the association between baseline LDL-C level and ASCVD risk by baseline Lp(a) level by Cox proportional hazards models with random effects. The joint association between Lp(a) level and statin-achieved LDL-C level with ASCVD risk was evaluated using Cox proportional hazards models.ResultsCompared with an Lp(a) level of 5 mg/dL, increasing levels of Lp(a) were log-linearly associated with ASCVD risk in statin- and placebo-treated patients. Among statin-treated individuals, those with Lp(a) level >50 mg/dL (≈125 nmol/L) had increased risk across all quartiles of achieved LDL-C level and absolute change in LDL-C level. Even among those with the lowest quartile of achieved LDL-C level (3.1-77.0 mg/dL), those with Lp(a) level >50 mg/dL had greater ASCVD risk (hazard ratio, 1.38 [95% CI, 1.06-1.79]) than those with Lp(a) level ≤50 mg/dL. The greatest risk was observed with both Lp(a) level >50 mg/dL and LDL-C level in the fourth quartile (hazard ratio, 1.90 [95% CI, 1.46-2.48]).ConclusionsThese findings demonstrate the independent and additive nature of Lp(a) and LDL-C levels for ASCVD risk, and that LDL-C lowering does not fully offset Lp(a)-mediated risk.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39492722 · DOI · PMC11771346
Lipoprotein(a) and incident venous thromboembolism in pre- and postmenopausal women, and in men [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Background and aimsElevated lipoprotein(a) [Lp(a)] levels are an established risk factor for atherosclerotic cardiovascular disease, but the association between Lp(a) and venous thromboembolism (VTE) remains unclear.
- Closing excerpt
- ConclusionsElevated Lp(a) was associated with VTE in premenopausal women and in postmenopausal MHT users, suggesting that hormonal context may influence Lp(a)-associated thrombotic risk.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (265 words)
Background and aimsElevated lipoprotein(a) [Lp(a)] levels are an established risk factor for atherosclerotic cardiovascular disease, but the association between Lp(a) and venous thromboembolism (VTE) remains unclear. Sex and hormonal status may modify the relationship between Lp(a) and VTE.MethodsThe present study included participants from the UK Biobank with available baseline Lp(a) data. Individuals with a history of VTE or cancer, as well as those using anticoagulants, were excluded. Multivariable-adjusted Cox models were used to assess the association between Lp(a) levels ≥125 nmol/L and incident VTE in premenopausal women, postmenopausal women, and men. Subgroup analyses stratified premenopausal women by oral contraceptive (OCP) use and postmenopausal women by menopausal hormone therapy (MHT) use.ResultsAmong 55 302 premenopausal women, 129 045 postmenopausal women, and 189 013 men, the proportions with Lp(a) ≥ 125 nmol/L were 14.0%, 19.0%, and 15.0%, respectively. Over a median (interquartile range) follow-up of 13.6 (12.9-14.4) years, 8186 VTE events occurred (cumulative incidence 2.2%). Lp(a) ≥ 125 nmol/L was associated with incident VTE in premenopausal women [adjusted hazard ratio (aHR) 1.32; 95% confidence interval (CI) 1.04-1.66; P = .02] but not in postmenopausal women (aHR 1.03; 95% CI 0.94-1.13; P = .47; Pinteraction = .03) or men (aHR 1.00; 95% CI 0.92-1.08; P = .94). OCP use did not modify the Lp(a)-VTE association among premenopausal women (Pinteraction = .61). However, among postmenopausal MHT users, Lp(a) ≥ 125 nmol/L was associated with higher VTE risk (aHR 1.48; 95% CI 1.03-2.12; P = .03; Pinteraction = .04).ConclusionsElevated Lp(a) was associated with VTE in premenopausal women and in postmenopausal MHT users, suggesting that hormonal context may influence Lp(a)-associated thrombotic risk.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41903523 · DOI · PMC13266305
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality [5]
- Research article Lipoprotein(a) as a cardiovascular risk factor: current status [6]
- Research article A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies [7]
- Research article Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association [8]
- Research article Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies [9]
- Research article Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials [10]
References
- Björnson E, Adiels M, Taskinen MR, Burgess S, Chapman MJ, Packard CJ, et al.. Lipoprotein(a) Is Markedly More Atherogenic Than LDL: An Apolipoprotein B-Based Genetic Analysis. . 2024. PMID 38233012 · DOI · PMC7616706
- Enkhmaa B, Berglund L. Non-genetic influences on lipoprotein(a) concentrations. . 2022. PMID 35606076 · DOI · PMC9549811
- Bhatia HS, Wandel S, Willeit P, Lesogor A, Bailey K, Ridker PM, et al.. Independence of Lipoprotein(a) and Low-Density Lipoprotein Cholesterol-Mediated Cardiovascular Risk: A Participant-Level Meta-Analysis. . 2025. PMID 39492722 · DOI · PMC11771346
- Ezzat D, Lopez DM, Claggett BL, Li L, Mohammadnia N, Schuermans A, et al.. Lipoprotein(a) and incident venous thromboembolism in pre- and postmenopausal women, and in men. . 2026. PMID 41903523 · DOI · PMC13266305
- Emerging Risk Factors Collaboration, Erqou S, Kaptoge S, Perry PL, Di Angelantonio E, Thompson A, et al.. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA. 2009. PMID 19622820 · DOI · PMC3272390
- Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, et al.. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010. PMID 20965889 · DOI · PMC3295201
- Tsimikas S. A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. J Am Coll Cardiol. 2017. PMID 28183512 · DOI
- Reyes-Soffer G, Ginsberg HN, Berglund L, Duell PB, Heffron SP, Kamstrup PR, et al.. Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association. Arterioscler Thromb Vasc Biol. 2022. PMID 34647487 · DOI · PMC9989949
- Danesh J, Collins R, Peto R. Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies. Circulation. 2000. PMID 10973834 · DOI
- Willeit P, Ridker PM, Nestel PJ, Simes J, Tonkin AM, Pedersen TR, et al.. Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials. Lancet. 2018. PMID 30293769 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.