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pubmed:abstractText |
Prior clinical studies have demonstrated that a family history of coronary artery disease (CAD) is associated with future cardiovascular events. Although there are several Mendelian disorders that are associated with CAD, most common forms of CAD are believed to be multifactorial and the result of many genes with small individual effects. The identification of these genes and their variation would be very helpful for the prediction, prevention, and management of CAD; linkage analysis or candidate gene case-control studies have been largely unsuccessful. On the contrary, recent advances in genomic techniques have generated a large amount of deoxyribonucleic acid (DNA)-based information. The link between CAD and inflammation and biological pathways has been highlighted. In particular, several genome-wide association studies have replicated a novel gene marker on chromosome 9p21. The information gained from genomic studies, in combination with clinical data, is expected to refine personalized approaches to assess risk and guide management for CAD. Genetic risk scores derived from several functional single nucleotide polymorphisms (SNPs) or haplotypes in multiple genes may improve the prediction of CAD. Despite the complexity of CAD genetics, steady progress is expected.
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