Copyright © 2004 by the European Society of Cardiology.
Editorial
Coronary artery disease genetics: bigger is better
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, UK
* Correspondence to: K.M. Channon, Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK. Tel.: +44-1865-741166/851085; fax: +44-1865-768844/222077
E-mail address: keith.channon@cardiov.ox.ac.uk
| The first 10% of the full text of this article appears below. |
This editorial refers to "Genetic risk and geneenvironment interaction in coronary artery spasm in Japanese men and women"1 by Y. Murase et al. on page 970
The complexity of coronary artery disease genetics arises from the diversity of clinical phenotypes and from the many biological pathways that contribute to atherosclerotic plaque biology, including lipid metabolism, inflammation, endothelial function, oxidative stress and thrombosis. In addition to environmental factors, inter-individual variation in disease susceptibility or outcome may arise from common polymorphic variation in the genes encoding the proteins that participate in these and other biological pathways. Twin studies suggest that the total genetic contribution to coronary artery disease risk is substantial, but dissecting out the nature of these effects in a complex polygenic trait with
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EHJ 2004 25: 970-977.[Abstract] [Full Text]