Published online before print March 6, 2008, doi: 10.1161/STROKEAHA.107.508515
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(Stroke. 2008;39:1070.)
© 2008 American Heart Association, Inc.
Editorials |
Where Do We Go for Atherothrombotic Disease Genetics?
From the Leibniz-Institute for Arteriosclerosis Research, University of Münster, Department of Molecular Genetics of Cardiovascular Disease, Münster, Germany.
Correspondence to Stefan-Martin Brand-Herrmann, MD, PhD, Leibniz-Institute for Arteriosclerosis Research, University of Münster, Department of Molecular Genetics of Cardiovascular Disease, Domagkstraβe 3, D-48149 Münster, Germany. E-mail brandher@uni-muenster.de
Key Words: atherothrombotic disease • genetics
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
See related articles, pages 1109–1120.
Cardiovascular disease (CVD), including coronary artery disease (CAD) with its fatal clinical outcome myocardial infarction (MI) and stroke, remain the leading cause of deaths in western and nonwestern countries.1,2 In the US, CVD claims more lives than cancer, chronic lower respiratory tract diseases and diabetes mellitus combined, accounting for 
36% of all deaths in 2004 and incurring an estimated direct and indirect cost of 432 billion dollars in 2007.2
Stroke and MI are multifactorial traits with complex pathophysiology. Besides other established factors, family history of disease strongly and independently determines CVD risk.3 There is a nearly 5-fold difference in stroke risk between monocygotic and dizygotic twins,4 and with respect to race, stroke incidence is approximately twice as high in blacks compared to whites.5 Marenberg et al,6 in their study on 20 000 Swedish twins, demonstrated that the relative risk to die from MI, when the other twin already died from this disease, was twice as large for monozygotic compared to dizygotic twins.
Celera Genomics7 and the International Human Genome Project consortium,8 by whole genome shotgun and clone-based sequencing strategies, respectively, proposed 2 versions of the human genome—the diploid genome offering more genetic information than previously anticipated.9 The availability of almost the entire human genome sequence allows for the immediate access to specific target sequences across the human genome. The number of different technologies to explore genetic sequences on a "genome-wide" scale and high-throughput genotyping methods is steadily increasing. Genome-wide approaches are essentially based on
Related Article:
Stroke 2008 39: 1109-1114.