The Pharmacogenomics of Angiotensin-Converting Enzyme (ACE) Inhibitors ACE inhibitor pharmacogenetics has focused on the insertion/deletion polymorphism (rs4646994), a strong determinant of ACE plasma concentration. However, the GenHAT (Genetics of Hypertension-Associated Treatment) study

did not demonstrate association of this polymorphism with MACE.51 Furthermore, PROGRESS (Perindopril Protection Against Recurrent Stroke Study) did not find an association between the presence of this polymorphism and the risk of MACE, neurological events, or blood pressure response.52 The Rotterdam study reported association of rs699 or Met235Thr in angiotensinogen with myocardial Inhibitors,research,lifescience,medical infarction and stroke among ACE inhibitor users.53 However, in a Chinese population, neither blood pressure response nor atherosclerosis risk appeared to correlate with presence of the variant allele.54 PERGENE Inhibitors,research,lifescience,medical (Perindopril Genetic Association Study) was designed to assess the viability of genetic analysis in the prescription of perindopril and the association

of 52 SNPs with predetermined EUROPA endpoints.55 This study identified two SNPs in the AGTR1 gene and one SNP in the bradykinin 1 receptor associated with perindopril treatment benefit, and a genetic risk score combining these SNPs was able to discriminate Inhibitors,research,lifescience,medical poor responders. Interestingly, five SNPs in linkage disequilibrium with the ID polymorphism (rs4646994) did not appear to influence response to the drug.55 Conclusion In conclusion, the greatest body of work regarding genome-tailored drug prescription has been performed on the oral anticoagulant warfarin. Inhibitors,research,lifescience,medical The use of certain algorithms has demonstrated that tailored prescription after genotyping has Inhibitors,research,lifescience,medical led to more effective control of INR and freedom from adverse events. While much has been elucidated with respect to the pharmacogenetics of commonly prescribed agents in the cardiovascular arena, there remains much work to validate the role of genetic testing in drug prescription. A more complete inventory of the genetic

variation responsible for the efficacy of drug action and the frequency of adverse events would likely yield data that is more reproducible and therefore of greater Pazopanib clinical trial clinical relevance. Funding Statement Funding/Support: Brefeldin_A The author has no funding disclosures. Footnotes Conflict of Interest Disclosure: The author has completed and submitted the Methodist DeBakey Cardiovascular Journal Conflict of Interest Statement and none were reported.
Introduction sellckchem Coronary artery disease (CAD), the number-one killer in the world, is largely preventable. Modification of conventional risk factors such as cholesterol has consistently shown a 30% to 40% reduction in mortality and morbidity.1, 2 Genetic risk factors for CAD, well documented by epidemiological studies, have until recently been elusive.