article · Journal of Health Wellness and Safety Research
Pharmacogenomic profiling is being recognized as a paradigm shift in cardiovascular precision medicine to personalize drug treatment for patients diagnosed with congenital heart disease. The current study followed a scientific approach to prove how genetic differences can cause variations in drug metabolites and influence drug response and toxicity risk among patients with congenital heart disease, most of whom have to take lifelong pharmacotherapy. The current Systematic review provided insights to assess the evidence base and determine any gaps in current knowledge to realize possible benefits through genotype-directed drug treatment among patients diagnosed with congenital heart disease involving human participants. Studies among human participants not related to pharmacogenomics or drug response genetics were excluded. Results showed that many genetic variations, such as those transpiring in cytochrome enzymes, drug receptors, and transport proteins, contribute significantly to the modulation of pharmacokinetic and pharmacodynamic events. Additionally, simulations for economic analysis showed genotype-driven dosing to result in major cost-saving measures amounting to two hundred to seven hundred and sixty-seven United States dollars for each patient mainly by virtue of reduction of adverse drug events, precision dosing expression, and avoidance of inappropriate treatment failure. Notably, while pharmacologic superiority is apparent, many obstacles exist to the implementation stages of this intervention strategy for now, especially among developing economies because of lack of accessibility to testing technology infrastructure, lack of compatibility to electronic medical documentation management systems, and lack of genetic information for use among others. This study thus closes by confirming pharmacogenomics profiling to offer substantial promise toward optimizing treatment safety, efficacy, and result sustainability among patients suffering from congenital heart disease.
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DOI: 10.70382/hujhwsr.v10i3.025
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