Genetic variants that predispose to heart attack are reported in five studies published online in Nature Genetics. While the effects of these variants on risk of disease are small, further study should provide new biological insight into the mechanisms underlying coronary artery disease, particularly those involving inflammation and lipids.
Four of the studies present genome-wide association studies for heart attack. Jeanette Erdmann and colleagues identify a new susceptibility locus on chromosome 3, in a gene that is highly expressed in the cardiovascular system and may be involved in cell-cell adhesion.
David-Alexandre Tregouet and colleagues report an association with a cluster of variants spanning three genes on chromosome 6. One of these genes encodes apolipoprotein(a), the main protein component of lipoprotein(a), which is a known risk factor for coronary artery disease. The third report from Toshihiro Tanaka and colleagues shows that a variant in a gene called BRAP is associated with risk of myocardial infarction. BRAP binds to two other proteins that this group previously identified as risk factors, and which may be involved in inflammation.
The Myocardial Infarction Genetics Consortium reports three new risk loci and confirms six previously identified loci. Finally, in the fifth study by Daniel Gudbjartsson and colleagues, the authors carried out a genome-wide association for eosinophil numbers. Eosinophils are white blood cells involved in inflammatory processes. Five loci were identified, one of which was also associated with heart attack in six different populations.
Jeanette Erdmann (University of Lubeck, Germany)
David-Alexandre Tregouet (INSERM, Paris, France)
Daniel Gudbjartsson (deCODE Genetics, Reykjavik, Iceland)
Toshihiro Tanaka (Laboratory for Cardiovascular Diseases, Center for Genomic Medicine, RIKEN, Yokohama 230-0045, Japan)
Abstracts available online:
Abstract of Paper 1.
Abstract of Paper 2.
Abstract of Paper 3.
Abstract of Paper 4.
Abstract of Paper 5.
C) Nature Genetics press release.
Message posted by: Trevor M. D'Souza