Genetic Heritability of Ischemic Stroke and the Contribution of Previously Reported Candidate Gene and Genomewide Associations
Abstract
Background and Purpose—: The contribution of genetics to stroke risk, and whether this differs for different stroke subtypes, remainsuncertain. Genomewide complex trait analysis allows heritability to be assessed from genomewide association study (GWAS) data. Previous candidate gene studies have identified many associations with stoke but whether these are important requires replication in large independent data sets. GWAS data sets provide a powerful resource to perform replication studies. Methods—: We applied genomewide complex trait analysis to a GWAS data set of 3752 ischemic strokes and 5972 controls and determined heritability for all ischemic stroke and the most common subtypes: large-vessel disease, small-vessel disease, and cardioembolic stroke. By systematic review we identified previous candidate gene and GWAS associations with stroke and previous GWAS associations with related cardiovascular phenotypes (myocardial infarction, atrial fibrillation, and carotid intima-media thickness). Fifty associations were identified. Results—: For all ischemic stroke, heritability was 37.9%. Heritability varied markedly by stroke subtype being 40.3% for large-vessel disease and 32.6% for cardioembolic but lower for small-vessel disease (16.1%). No previously reported candidate gene was significant after rigorous correction for multiple testing. In contrast, 3 loci from related cardiovascular GWAS studies were significant: PHACTR1 in large-vessel disease ( P =2.63e −6 ), PITX2 in cardioembolic stroke ( P =4.78e −8 ), and ZFHX3 in cardioembolic stroke ( P =5.50e −7 ). Conclusions—: There is substantial heritability for ischemic stroke, but this varies for different stroke subtypes. Previous candidate gene associations contribute little to this heritability, but GWAS studies in related cardiovascular phenotypes are identifying robust associations. The heritability data, and data from GWAS, suggest detecting additional associations will depend on careful stroke subtyping.
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The genetic contribution to stroke is approximately 38%.
“stroke (~38%)184”
From Comorbidity between major depressive disorder and physical diseases: a comprehensive review of epidemiology, mechanisms and management (2023) · cites this paper as [184]
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- Authors
- Bevan, S., Traylor, M., Adib-Samii, P., Malik, R., Paul, N. L. M., Jackson, C., Farrall, M., Rothwell, P. M., Sudlow, C., Dichgans, M., & Markus, H. S.
- Affiliations
- St George's, University of London (GB)
- From the Stroke and Dementia Research Group, St George’s University of London, London, UK (S.B., M.T., P.A.-S., H.S.M.); the Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-University Munich, Germany (R.M., M.D.); the Stroke Prevention Research Unit, Nuffield Department of Neuroscience (N.L.M.P., P.M.R.) and the Department of Cardiovascular Medicine (M.F.), University of Oxford, Oxford, UK (N.L.M.P., P.M.R.); and the Division of Clinical Neurosciences...
- ORCID
- Venue
- Stroke
- Published
- 2012-12
- Volume
- 43
- Issue
- 12
- Pages
- 3161-3167
- ISSN
- 0039-2499 (ISSN-L)
- 1524-4628
- OpenAlex
- W2010457736
- Cited by
- 395
- References
- 62
- Citations by year
- 2026: 14 · 2025: 21 · 2024: 31 · 2023: 27 · 2022: 37 · 2021: 29 · 2020: 33 · 2019: 37 · 2018: 29 · 2017: 30 · 2016: 31 · 2015: 28 · 2014: 32 · 2013: 16
- FWCI
- 14.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Stroke (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (085475/Z/08/Z, 068545/Z/02), 095626, 090532, 085475/B/08/Z)
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
- Keywords
- ischemic stroke, heritability, stroke subtypes, large vessel disease, cerebral small vessel disease, cardioembolic stroke, candidate gene association, PHACTR1, PITX2, ZFHX3, myocardial infarction, atrial fibrillation, carotid intima-media thickness, genetic risk
- MeSH terms
- Homeobox Protein PITX2, Aged, Aged, 80 and over, Atrial Fibrillation, Brain Ischemia, Female, Humans, Male, Microfilament Proteins, Middle Aged, Myocardial Infarction, Phenotype, Risk Factors, Transcription Factors, Databases, Factual, Homeodomain Proteins, Genetic Predisposition to Disease, Stroke, White People, Genome-Wide Association Study, Carotid Intima-Media Thickness
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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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