Summary Because of new techniques for gene mapping, newmodeling techniques, advances in biocomputing powerand bioinformatics, and the multiple types of clinicalstudies and large patient databases described in thisarticle, we are on the verge of a new understanding ofthe inherited component of CHD. Identifying causativegenes for this disease is likely several years away atbest. Before that time, however, a new understandingwill be reached of the relation between inherited risksand outcomes in cardiovascular disease. With the devel-opment of the SNP Consortium and its associated tech-nology, we also have the promise of a detailed catalogueof disease-modifying genes that may open the door totherapeutic advances. Thus we find ourselves in anexciting time—one that should provide the basis for adeeper understanding of the mechanisms underlyingthe etiology of CHD and that will certainly lead to noveldiagnostic, risk-stratifying, and therapeutic tools withinseveral years. References 1.Wilson PWF, Myers RH, Larson MG, et al. Apoprotein E alleles,dyslipidemia, and coronary heart disease. JAMA 1994;272:1666-71.2.Lander ES, Schork NJ. Genetic dissection of complex traits. Science1994;265:2035-48.3.Davies JL, Kawaguchi Y, Bennett ST, et al. A genome-wide searchfor human type 1 diabetes susceptibility genes. Nature 1994;371:130-6.4.Hanis CL, Boerwinkle E, Chakraborty R, et al. A genome-widesearch for human non-insulin-dependent (type 2) diabetes genesreveals a major susceptibility locus on chromosome 2. NatureGenetics 1996;13:161-6.5.Pericak-Vance MA, Bass MP, Yamaoka LH, et al. Completegenomicscreen in late-onset familial Alzheimer disease: evidence for a newlocus on chromosome 12. JAMA 1997;278:1237-41.American Heart Journal
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