The Genetic Blueprint of Cardiovascular Therapy: Pharmacogenomics for Improved Efficacy and Safety

Abstract

Globally, cardio vascular diseases (CVD) remain the primary cause of morbidity and mortality. Pharmacogenomics (PGxs) has profoundly changed how various drug classes are managed in CVDs. For example, genetic polymorphisms in genes such as SLCO1B1 impact how a person responds to statins such as rosuvastatin and atorvastatin, where as the interindividual variability in the reaction to statins (Fluvastatin)used in lipid-lowering therapy can be partly explained by genetic variations in genes encoding drug-metabolizing enzymes such cytochrome P450 and transporters like OATP1B1. Similarly, in antiplatelet therapy, polymorphisms in CYP2C19 affect clopidogrel metabolism, influencing its efficacy in preventing thrombotic events. Genes such as CYP2C9 and VKORC1 are crucial for the metabolism and response to acenocoumarol and warfarin during anticoagulant therapy and monitoring bleeding risk. Genetic variations in CYP2D6 affect the metabolism and effectiveness of propafenone and metoprolol. Understanding the PGx presumptions of these cardiovascular drugs may help develop personalized treatment strategies that lower the possibility of adverse drug reactions, obtain desired therapeutic outcomes, and improve patient compliance and safety with respect to each patient’s unique genetic makeup.

Keywords

• acenocoumarol
• antianginal agents
• anticoagulants
• atorvastatin clopidogrel
• cardiovascular diseases
• cyp450
• metoprolol
• pharmacogenetics
• pharmacogenomics
• propafenone
• warfarin