Summary

Although many of these genes demonstrate a significant correlation with polymorphisms and the incidence of CAD or heart failure, the degree of risk is not particularly high in any case (odds ratio typically between 1 and 2). Most investigators agree that the pathogenesis of these diseases is too complex and diverse to be explained on the basis of a SNP. Discrepancies in results of individual studies might be the result of inadequate numbers of subjects enrolled or heterogeneity in the sex and/or racial make of the population studied. However, several studies have shown that the presence of some mutations are linked to others and their effect on disease progression might be additive. Unfortunately, all of the studies published to date involve only a handful of gene mutations on a limited number of subjects enrolled. The costs for performing the DNA analysis prohibits the analysis for more than just of few of these genes at a time. This chapter discussed only a minority of the many polymorphisms that are known to exist among the various proteins and factors known that participate in the disease.

Genes that have been initially targeted are those proteins known to participate in the pathophysiology of cardiac diseases. It might be appropriate for future studies to concentration on the effect of polymorphisms in the success of therapy, both pharmacologic and surgical (e.g., PCI). This justifies the current interest in the genes that modify platelet function, ACE inhibitors, and P-blockers. The work should be further focused in therapies where there is variability in response and/or success (e.g., hypertension). A specific polymorphorism might be an important factor in the lack of success in some instances.

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