Fig. 3From: Multimorbidity, polypharmacy, and drug-drug-gene interactions following a non-ST elevation acute coronary syndrome: analysis of a multicentre observational studyPatient pharmacogene genotypes. Proportions of genotype-based CYP metaboliser phenotypes (a) and non-CYP pharmacogene genotypes (b) observed across the whole cohort with quality-controlled array genetic data available (n = 1357), except for CYP2B6 (n = 1347), F5 (n = 1346), and CYP2D6 (n = 728). The number of patients with CYP2B6, F5, and CYP2D6 available was less due to exclusion of patients with imputed genotypes outside the predefined imputation acceptance range, and determination of CYP2D6 copy number variation in patients on a CYP2D6 drug substrate (see the ‘Methods’ section). Overall, 713 patients had genotypes available for all analysed genes. EM, extensive (normal) metaboliser; IM, intermediate metaboliser; PM, poor metaboliser; RM, rapid metaboliser; UM, ultra-rapid metaboliser; WT, wild-type; HET, heterozygous; HOM, homozygous for the variant alleleBack to article page