Genomic Risk Variants at 1p13.3, 1q41, and 3q22.3 Are Associated With Subsequent Cardiovascular Outcomes in Healthy Controls and in Established Coronary Artery Genomic Risk Variants at 1p13.3, 1q41, and 3q22.3 Are Associated With Subsequent Cardiovascular Outcomes in Healthy Controls and in Established Coronary Artery Disease
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Authors
Whalley, Gillian
Ellis, Katrina L.
Frampton, Chris M.
Pilbrow, Anna P.
Troughton, R.W.
Doughty, Robert N.
Ellis, Chris J.
Skelton, Lorraine
Thomson, Judith
Yandle, Tim G.
Richards, A.M.
Cameron, Vicky A.
Ellis, Katrina L.
Frampton, Chris M.
Pilbrow, Anna P.
Troughton, R.W.
Doughty, Robert N.
Ellis, Chris J.
Skelton, Lorraine
Thomson, Judith
Yandle, Tim G.
Richards, A.M.
Cameron, Vicky A.
Author ORCID Profiles (clickable)
Degree
Grantor
Date
2011
Supervisors
Type
Journal Article
Ngā Upoko Tukutuku (Māori subject headings)
Keyword
coronary disease
genetic polymorphisms
genome wide association studies
cardiovascular diseases
outcomes
genetic polymorphisms
genome wide association studies
cardiovascular diseases
outcomes
ANZSRC Field of Research Code (2020)
Citation
Ellis, K. L., Frampton, C. M., Pilbrow, A. P., Troughton, R. W., Doughty, R. N., Whalley, G. A., ... & Cameron, V. A. (2011). Genomic Risk Variants at 1p13. 3, 1q41, and 3q22. 3 Are Associated With Subsequent Cardiovascular Outcomes in Healthy Controls and in Established Coronary Artery DiseaseClinical Perspective. Circulation: Cardiovascular Genetics, 4(6), 636-646.
Abstract
Coronary artery disease (CAD) has multifactorial origins, and although some families are particularly affected, no precise mode of inheritance has been identified. It is likely that this reflects the contribution of numerous genetic components, each conferring a small risk in cumulative interaction with environmental factors to substantively increase disease susceptibility.1 In recent years, significant advances have been made in elucidating the genetic basis of CAD with the completion of several large genome-wide association studies (GWAS) that have looked at the DNA variation across the entire human genome. In a landmark study in 2007, the Wellcome Trust Case Control Consortium identified a region on chromosome 9 (9p21.3) that was the most strongly associated with the risk of developing CAD,2 a finding that has since been replicated in several independent studies.3–6 The 9p21.3 rs1333049 variant is common and may potentially be added to risk profiling in the future. Already it has been reported that adding the 9p21.3 genotype to the traditional risk score significantly improves CAD risk prediction in the community.
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Link to ePress publication
DOI
10.1161/CIRCGENETICS.111.960336
Copyright holder
Copyright © 2011 American Heart Association
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