Abstract
Coronary artery disease (CAD) has a high mortality rate. Despite various therapeutic targets, non-responsiveness to drugs remains a prevalent issue. Pharmacogenomics assesses the way an individual’s genetic attributes affect their likely response to drug therapy. Single-nucleotide polymorphisms play a crucial role in determining these outcomes. This review offers an overview of single-nucleotide polymorphisms investigated in clinical studies and their associations with drug response/nonresponse in the treatment of CAD. A total of 104 studies of whole sets of chromosomes and several genes were explored. A total of 161 polymorphisms exhibited associations with drug response/nonresponse in CAD across diverse ethnic populations. This pool can serve as a pharmacogenomic biomarker for predicting response to drug therapy in patients with CAD.
Graphical abstract
Supplementary data
Author contributions
P Dua contributed to the study design, conduct, data procurement, data analysis, interpretation and drafting and revision of the manuscript. KH Reeta contributed to the study design, analysis, interpretation and critical revision of the manuscript. B Prasher and M Mukerji contributed to the study design, data acquisition and revision of the manuscript. SK Maulik critically reviewed and revised the manuscript. S Seth revised the manuscript. All authors approved the final manuscript and agreed to be accountable for all features of the work in ensuring precision and veracity.
Acknowledgments
The authors are thankful to the Department of Science and Technology, Government of India for providing a fellowship to P Dua under Women Scientist Scheme-A.
Financial disclosure
The authors have no financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Competing interests disclosure
The authors have no competing interests or relevant affiliations with any organization or entity with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Writing disclosure
No writing assistance was utilized in the production of this manuscript.