Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/107552
Title: Genetically determined height and coronary artery disease
Authors: Kathiresan, Sekar
Kee, Frank
König, Inke R.
Nelson, Christopher P.
Hamby, Stephen E.
Saleheen, Danish
Hopewell, Jenna C.
Zeng, Lingyao
Assimes, Themistocles L.
Kanoni, Stavroula
Willenborg, Christina
Burgess, Stephen
Amouyel, Phillipe
Anand, Sonia
Blankenberg, Stefan
Boehm, Bernhard Otto
Clarke, Robert J.
Collins, Rory
Dedoussis, George
Farrall, Martin
Franks, Paul W.
Groop, Leif
Hall, Alistair S.
Hamsten, Anders
Hengstenberg, Christian
Kees Hovingh, G.
Ingelsson, Erik
Kooner, Jaspal
Lehtimäki, Terho
März, Winifred
McPherson, Ruth
Wareham, Nicholas
Willer, Cristen J.
Metspalu, Andres
Nieminen, Markku S.
O'Donnell, Christopher J.
Palmer, Colin N. A.
Peters, Annette
Perola, Markus
Reilly, Muredach P.
Ripatti, Samuli
Roberts, Robert
Salomaa, Veikko
Shah, Svati H.
Schreiber, Stefan
Siegbahn, Agneta
Thorsteinsdottir, Unnur
Veronesi, Giovani
Zalloua, Pierre A.
Erdmann, Jeanette
Deloukas, Panos
Watkins, Hugh
Schunkert, Heribert
Danesh, John
Thompson, John R.
Samani, Nilesh J.
Keywords: DRNTU::Science::Medicine
Issue Date: 2015
Source: Nelson, C. P., Hamby, S. E., Saleheen, D., Hopewell, J. C., Zeng, L., Assimes, T. L., et al. (2015). Genetically determined height and coronary artery disease. New England Journal of Medicine, 372(17), 1608-1618.
Series/Report no.: New England journal of medicine
Abstract: BACKGROUND: The nature and underlying mechanisms of an inverse association between adult height and the risk of coronary artery disease (CAD) are unclear. METHODS: We used a genetic approach to investigate the association between height and CAD, using 180 height-associated genetic variants. We tested the association between a change in genetically determined height of 1 SD (6.5 cm) with the risk of CAD in 65,066 cases and 128,383 controls. Using individual-level genotype data from 18,249 persons, we also examined the risk of CAD associated with the presence of various numbers of height-associated alleles. To identify putative mechanisms, we analyzed whether genetically determined height was associated with known cardiovascular risk factors and performed a pathway analysis of the height-associated genes. RESULTS: We observed a relative increase of 13.5% (95% confidence interval [CI], 5.4 to 22.1; P<0.001) in the risk of CAD per 1-SD decrease in genetically determined height. There was a graded relationship between the presence of an increased number of height-raising variants and a reduced risk of CAD (odds ratio for height quartile 4 versus quartile 1, 0.74; 95% CI, 0.68 to 0.84; P<0.001). Of the 12 risk factors that we studied, we observed significant associations only with levels of low-density lipoprotein cholesterol and triglycerides (accounting for approximately 30% of the association). We identified several overlapping pathways involving genes associated with both development and atherosclerosis. CONCLUSIONS: There is a primary association between a genetically determined shorter height and an increased risk of CAD, a link that is partly explained by the association between shorter height and an adverse lipid profile. Shared biologic processes that determine achieved height and the development of atherosclerosis may explain some of the association. (Funded by the British Heart Foundation and others.).
URI: https://hdl.handle.net/10356/107552
http://hdl.handle.net/10220/38521
DOI: 10.1056/NEJMoa1404881
Rights: © 2015 Massachusetts Medical Society. This paper was published in The New England Journal of Medicine and is made available as an electronic reprint (preprint) with permission of Massachusetts Medical Society. The published version is available at: [http://dx.doi.org/10.1056/NEJMoa1404881]. One print or electronic copy may be made for personal use only. Systematic or multiple reproduction, distribution to multiple locations via electronic or other means, duplication of any material in this paper for a fee or for commercial purposes, or modification of the content of the paper is prohibited and is subject to penalties under law.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:LKCMedicine Journal Articles

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