Myocardial infarction (MI) shows a strong heritability. For a long time the identification of responsible genes has been rather unsuccessful. However, with the advent of genome wide association studies (GWAS) using DNA-array technology a number of significant loci for MI have been identified which were widely replicated. Interestingly, only a small fraction of the hitherto identified genes is also associated with classical risk factors for MI such as hypercholesterolemia or diabetes. Therefore it can be concluded that the MI risk mediated by the newly identified genes involves a number of novel pathophysiological mechanisms. This review summarizes the present state of knowledge in the field and tries to give a perspective on how these findings can be translated into clinical practice and further scientific discovery. Special consideration is given to the association of MI risk with genetic variants in the hemostatic system.
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|Published - 16.12.2010