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. 2020 Nov 25;18:367. doi: 10.1186/s12916-020-01827-z

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Study cohort selection process. There were 1470 patients included in the PhACS study, of whom 1456 were discharged alive from their index NSTE-ACS; 1357 had array genetic data available following standard quality control procedures; CYP2D6 genotype was available in 728 after determination of copy number variation in those on CYP2D6 substrates; 698 had non-cardiovascular disease (CVD) drugs at discharge recorded in their case report form (CRF) medication appendix, in addition to CVD drugs explicitly required in the CRF; and in 652 patients (the interaction cohort), CVD drugs, non-CVD drugs, and genetic data were available (although patients not on a CYP2D6 substrate did not require CYP2D6 genotype for inclusion in the interaction cohort)