Lipoprotein(a) Concentration and the Risk of Coronary Heart Disease, Stroke, and Nonvascular Mortality
Open accessAbstract
CONTEXT: Circulating concentration of lipoprotein(a) (Lp[a]), a large glycoprotein attached to a low-density lipoprotein-like particle, may be associated with risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationship of Lp(a) concentration with risk of major vascular and nonvascular outcomes. STUDY SELECTION: Long-term prospective studies that recorded Lp(a) concentration and subsequent major vascular morbidity and/or cause-specific mortality published between January 1970 and March 2009 were identified through electronic searches of MEDLINE and other databases, manual searches of reference lists, and discussion with collaborators. DATA EXTRACTION: Individual records were provided for each of 126,634 participants in 36 prospective studies. During 1.3 million person-years of follow-up, 22,076 first-ever fatal or nonfatal vascular disease outcomes or nonvascular deaths were recorded, including 9336 CHD outcomes, 1903 ischemic strokes, 338 hemorrhagic strokes, 751 unclassified strokes, 1091 other vascular deaths, 8114 nonvascular deaths, and 242 deaths of unknown cause. Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. Analyses excluded participants with known preexisting CHD or stroke at baseline. DATA SYNTHESIS: Lipoprotein(a) concentration was weakly correlated with several conventional vascular risk factors and it was highly consistent within individuals over several years. Associations of Lp(a) with CHD risk were broadly continuous in shape. In the 24 cohort studies, the rates of CHD in the top and bottom thirds of baseline Lp(a) distributions, respectively, were 5.6 (95% confidence interval [CI], 5.4-5.9) per 1000 person-years and 4.4 (95% CI, 4.2-4.6) per 1000 person-years. The risk ratio for CHD, adjusted for age and sex only, was 1.16 (95% CI, 1.11-1.22) per 3.5-fold higher usual Lp(a) concentration (ie, per 1 SD), and it was 1.13 (95% CI, 1.09-1.18) following further adjustment for lipids and other conventional risk factors. The corresponding adjusted risk ratios were 1.10 (95% CI, 1.02-1.18) for ischemic stroke, 1.01 (95% CI, 0.98-1.05) for the aggregate of nonvascular mortality, 1.00 (95% CI, 0.97-1.04) for cancer deaths, and 1.00 (95% CI, 0.95-1.06) for nonvascular deaths other than cancer. CONCLUSION: Under a wide range of circumstances, there are continuous, independent, and modest associations of Lp(a) concentration with risk of CHD and stroke that appear exclusive to vascular outcomes.
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The 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 [191]
The Associations With CHD section (page unavailable) reports a smaller coronary risk association for Lp(a) than for non-HDL cholesterol: adjusted risk ratios of 1.14 and 1.66 per 1-SD increase, respectively. That supports the direction of the comparison, but the paper compares Lp(a) with non-HDL cholesterol, not specifically LDL-C. (LLM, conf=0.86)
Experimental — accuracy not yet measuredStudies over the past decade have confirmed and more robustly demonstrated a risk factor role of Lp(a) for cardiovascular disease.
“Recently, interest in Lp(a) has increased because studies over the past decade have confirmed and more robustly demonstrated a risk factor role of Lp(a) for cardiovascular disease (43-46).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [44]
Higher plasma Lp(a) concentrations are associated with increased atherosclerotic cardiovascular disease risk, but Lp(a) appears to be a much weaker risk factor for most people than LDL-C.
“Higher plasma Lp(a) concentrations are associated with an increased risk of ASCVD, but it appears to be a much weaker risk factor for most people than LDL-C [72,73].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [72]
Lipoprotein(a) has been found in several studies to be an additional risk marker.
“Lp(a) has been found in several studies to be an additional risk marker.49”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [49]
Hyper-Lp(a)-lipoproteinemia is a risk factor for ASCVD.
“[Statement]Hyper-Lp(a)-lipoproteinemia is a risk factor for ASCVD. (Evidence level: E-1a)”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [225]
Lp(a) is an independent risk factor for CAD and stroke.
“Lp(a) is an independent risk factor for CAD and stroke.”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [225]
When the size of apolipoprotein (a) [apo(a)] is small, the concentration of Lp(a) is high, and there is a high risk of CVD.
“When the size of apolipoprotein (a) [apo(a)] is small, the concentration of Lp(a) is high, and there is a high risk of CVD.”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [225]
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- Authors
- The Emerging Risk Factors Collaboration*
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- The Emerging Risk Factors Collaboration*
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2009-07-22
- Volume
- 302
- Issue
- 4
- Pages
- 412
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC3272390
- OpenAlex
- W2104355263
- Semantic Scholar
- 75c90948458f75d1a061098fd357aa90ceef5052
- Cited by
- 1,753
- References
- 107
- Citations by year
- 2026: 97 · 2025: 139 · 2024: 129 · 2023: 125 · 2022: 140 · 2021: 114 · 2020: 116 · 2019: 106 · 2018: 93 · 2017: 100 · 2016: 117 · 2015: 85 · 2014: 85 · 2013: 79 · 2012: 76
- FWCI
- 11.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- VU Research Portal (publishedVersion, other-oa)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- OPUS (Augsburg University) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- AstraZeneca
- GlaxoSmithKline
- Wellcome Trust
- British Heart Foundation (RG/08/014, RG/07/008/23674, RG/08/014/24067)
- Bupa Foundation
- European Commission
- Evelyn Trust
- Merck Sharp and Dohme
- Medical Research Council
- Economic and Social Research Council (ES/G007438/1)
- National Institute on Aging (R03AG021162)
- 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), coronary artery disease, stroke, vascular disease, cardiovascular risk factors, low-density lipoprotein, triglycerides, HDL cholesterol, HDL2, HDL3, prospective cohort, meta-analysis, cardiovascular risk prediction, cardiovascular disease treatment
- MeSH terms
- Cause of Death, Coronary Disease, Humans, Risk Factors, Lipoprotein(a), Stroke
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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