Polygenic Risk Score Identifies Subgroup With Higher Burden of Atherosclerosis and Greater Relative Benefit From Statin Therapy in the Primary Prevention Setting
Open accessAbstract
Background: Relative risk reduction with statin therapy has been consistent across nearly all subgroups studied to date. However, in analyses of 2 randomized controlled primary prevention trials (ASCOT [Anglo-Scandinavian Cardiac Outcomes Trial–Lipid-Lowering Arm] and JUPITER [Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin]), statin therapy led to a greater relative risk reduction among a subgroup at high genetic risk. Here, we aimed to confirm this observation in a third primary prevention randomized controlled trial. In addition, we assessed whether those at high genetic risk had a greater burden of subclinical coronary atherosclerosis. Methods: We studied participants from a randomized controlled trial of primary prevention with statin therapy (WOSCOPS [West of Scotland Coronary Prevention Study]; n=4910) and 2 observational cohort studies (CARDIA [Coronary Artery Risk Development in Young Adults] and BioImage; n=1154 and 4392, respectively). For each participant, we calculated a polygenic risk score derived from up to 57 common DNA sequence variants previously associated with coronary heart disease. We compared the relative efficacy of statin therapy in those at high genetic risk (top quintile of polygenic risk score) versus all others (WOSCOPS), as well as the association between the polygenic risk score and coronary artery calcification (CARDIA) and carotid artery plaque burden (BioImage). Results: Among WOSCOPS trial participants at high genetic risk, statin therapy was associated with a relative risk reduction of 44% (95% confidence interval [CI], 22–60; P <0.001), whereas in all others, the relative risk reduction was 24% (95% CI, 8–37; P =0.004) despite similar low-density lipoprotein cholesterol lowering. In a study-level meta-analysis across the WOSCOPS, ASCOT, and JUPITER primary prevention, relative risk reduction in those at high genetic risk was 46% versus 26% in all others ( P for heterogeneity=0.05). Across all 3 studies, the absolute risk reduction with statin therapy was 3.6% (95% CI, 2.0–5.1) among those in the high genetic risk group and 1.3% (95% CI, 0.6–1.9) in all others. Each 1-SD increase in the polygenic risk score was associated with 1.32-fold (95% CI, 1.04–1.68) greater likelihood of having coronary artery calcification and 9.7% higher (95% CI, 2.2–17.8) burden of carotid plaque. Conclusions: Those at high genetic risk have a greater burden of subclinical atherosclerosis and derive greater relative and absolute benefit from statin therapy to prevent a first coronary heart disease event. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique identifiers: NCT00738725 (BioImage) and NCT00005130 (CARDIA). WOSCOPS was carried out and completed before the requirement for clinical trial registration.
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A polygenic burden of LDL-increasing SNPs can confer monogenic-equivalent risk of cardiovascular disease, with polygenic scores improving clinical models for risk assessment and statin prescription that can reduce coronary heart disease and improve healthcare delivery efficiency.
“This enthusiasm is driven by observations that a polygenic burden of LDL-increasing SNPs can confer monogenic-equivalent risk of cardiovascular disease, with polygenic scores improving clinical models for risk assessment and statin prescription that can reduce coronary heart disease and improve healthcare delivery efficiency5–7.”
From Clinical use of current polygenic risk scores may exacerbate health disparities (2019) · cites this paper as [7]
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Experimental — accuracy not yet measuredIntegrated models of PRS together with other lifestyle and clinical factors have enabled clinicians to more accurately quantify the risk of heart attack.
“Additionally, integrated models of PRS together with other lifestyle and clinical factors have enabled clinicians to more accurately quantify the risk of heart attack for patients;”
From Clinical use of current polygenic risk scores may exacerbate health disparities (2019) · cites this paper as [7]
The Methods (Statistical Analysis; page unavailable) describe models that assess PRS alongside clinical factors, including smoking, and the Results (page unavailable) find that high PRS predicts coronary events after adjustment for traditional risk factors. The paper does not show that integrating PRS with lifestyle and clinical factors improves the accuracy of heart-attack risk estimates, or that clinicians have used such a model for patients. (LLM, conf=0.86)
Experimental — accuracy not yet measuredHigh polygenic risk for CAD may be offset by adherence to a healthy lifestyle or cholesterol-lowering statin therapy.
“For example, we previously showed that a high polygenic risk for CAD may be offset by either of two interventions: adherence to a healthy lifestyle or cholesterol-lowering therapy with statin medications.19–21”
From Genome-wide polygenic scores for common diseases identify individuals with risk equivalent to monogenic mutations (2018) · cites this paper as [21]
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- Authors
- Natarajan, P., Young, R., Stitziel, N. O., Padmanabhan, S., Baber, U., Mehran, R., Sartori, S., Fuster, V., Reilly, D. F., Butterworth, A., Rader, D. J., Ford, I., Sattar, N., & Kathiresan, S.
- Affiliations
- Broad Institute (US)
- From Center for Human Genetic Research and Cardiovascular Research Center, Massachusetts General Hospital, Boston (P.N., S.K.); Program in Medical and Population Genetics, Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge (P.N., S.K.); Department of Medicine, Harvard Medical School, Boston, MA (P.N., S.K.); Department of Public Health and Primary Care, Strangeways Research Laboratory, University of Cambridge, United Kingdom (R.Y., A.B.); Division of Statistical Genetics...
- Corresponding author
- Natarajan, Pradeep
- Young, Robin
- Ford, Ian
- Sattar, Naveed
- Kathiresan, Sekar
- ORCID
- Venue
- Circulation
- Published
- 2017-05-30
- Volume
- 135
- Issue
- 22
- Pages
- 2091-2101
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC5484076
- OpenAlex
- W2590902687
- Cited by
- 570
- References
- 44
- Citations by year
- 2026: 48 · 2025: 57 · 2024: 72 · 2023: 61 · 2022: 62 · 2021: 81 · 2020: 62 · 2019: 57 · 2018: 49 · 2017: 20
- FWCI
- 52.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Funders
- National Institute for Health and Care Research (NF-SI-0512-10165)
- British Heart Foundation (RG/08/014/24067)
- Medical Research Council (MR/L003120/1)
- National Heart, Lung, and Blood Institute (R01HL127564, K08HL114642)
- National Human Genome Research Institute (UM1HG008895)
- 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
- polygenic risk score, statin therapy, primary prevention, coronary artery disease, genetic risk, coronary artery calcification, carotid plaque, subclinical atherosclerosis, relative risk reduction, LDL cholesterol lowering, WOSCOPS, gastric cardia, bioimages, ASCOT, Jupiter, subgroup heterogeneity, cardiovascular risk prediction
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Primary Prevention, Risk Factors, Cohort Studies, Randomized Controlled Trials as Topic, Cost of Illness, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Multifactorial Inheritance, Atherosclerosis, Young Adult, Observational Studies as Topic
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.
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