5% vs. 9.4% of patients (P < .001).36 Cost-effectiveness analyses need to be undertaken to

document broad application of genotype-guided prescription, and they should be done in multiple racial cohorts as variant allele frequencies are disparate among racial groups.30 In the meantime, niche application may be warranted in groups that have high thrombosis risk (e.g., individuals with metallic prosthetic valves) or those who pose elevated bleeding risk (e.g., those who are novel prescribed dual antiplatelet therapy in concert with warfarin). Pharmacogenomics of Hydroxymethylglutaryl (HMG) selleck chem Alisertib coenzyme Inhibitors,research,lifescience,medical A Reductase Inhibitors and Statin-Induced Myopathy Hydroxymethylglutaryl coenzyme A reductase inhibitors or statins are frequently

prescribed drugs that have Inhibitors,research,lifescience,medical been shown to reduce mortality in both primary and secondary prevention settings, as they reduce the frequency of myocardial infarction, cerebrovascular accident, and revascularization procedures by approximately 20% for every 1 mmol/L fall in the level serum low-density Inhibitors,research,lifescience,medical lipoprotein.1 However, there is marked interindividual variability in response to statin administration.37 REGRESS (Regression Growth Evaluation Statin Study) examined the Taq1 B variant in the cholesterol transfer protein and demonstrated that CAD progresses more slowly in individuals with the B2B2 genotype. In B1B1 individuals, however, the response to statin administration is associated with a greater decrease in serum LDL-C. Therefore, while B1B1 individuals carry an elevated baseline coronary risk, this may be offset by an improved response to statins.38 It should be noted that a meta-analysis analyzing patients both with and without antecedent CAD was not able to demonstrate Inhibitors,research,lifescience,medical such an interaction with the statin response.39 Ambiguous data exists with respect to the epsilon2 variant of the apolipoprotein (APO) E gene and statin response.40, 41 A meta-analysis of three GWAS results showed that a SNP in the calmin gene was associated with the response

to statin therapy,42 yet this remains to be confirmed. DNA sequence Inhibitors,research,lifescience,medical variation in APOC1, adjacent to APOE, was also associated with the response to statin Batimastat therapy.42 Kinesin-like protein 6 was associated with improved outcomes in three large randomized controlled trials examining the role of pravastatin treatment.43, 44 This improvement in outcomes appeared to be independent of the lipid-lowering activity of pravastatin. A cross-sectional GWAS found that the relevant SNP (rs20455) was not associated with CAD.45 Moreover, a recent meta-analysis combining 19 similar studies did not demonstrate an association with CAD. However, these studies were not designed to evaluate the pravastatin effect. Statin-induced myopathy is associated with stain administration, although the pathogenesis of this condition is not well understood.