Cardiovascular Drugs and Therapy

, Volume 21, Issue 2, pp 121–132

Pharmacogenomics of Renin Angiotensin System Inhibitors in Coronary Artery Disease

Authors

    • School of PharmacyUniversity of Pittsburgh
  • Michael J. Peeters
    • College of PharmacyUniversity of Toledo
Review

DOI: 10.1007/s10557-007-6026-2

Cite this article as:
Tsikouris, J.P. & Peeters, M.J. Cardiovasc Drugs Ther (2007) 21: 121. doi:10.1007/s10557-007-6026-2

Abstract

Renin Angiotensin System (RAS) inhibitors comprise some of the most commonly used medications in coronary artery disease (CAD) and its related syndromes. Unfortunately, significant inter-patient variability seems likely in response to these agents; of which, the influence of genetic determinants is of interest. This review summarizes the available RAS inhibitor pharmacogenomic studies which have evaluated RAS polymorphisms that either elucidate mechanism via surrogate endpoint measurements, or predict efficacy via clinical outcomes in CAD related syndromes.Regardless of the endpoint, none of the RAS genotypes conclusively predicts efficacy of RAS inhibitors. In fact, the results of the pharmacogenomic studies were often in direct conflict with one another. Varied results appear due to methodological limitations (e.g., inadequate study power, genotyping error, methods of endpoint measurement), study conceptualization (e.g., overestimating the contribution of polymorphism to disease, lack of haplotype approach), and differences between studies (e.g., genotype frequency, study subject characteristics, the specific medication and dose used). Thus investigators should consider the various methodological limitations to improve upon the current approach to RAS inhibitor pharmacogenomic research in the vast CAD population.

Key words

pharmacogenomicrenin angiotensin systemACE Inhibitorangiotensin II type-1 receptor blocker

Copyright information

© Springer Science+Business Media, LLC 2007