This present review provides an overview of Acetylsalicylic Acid (ASA), emphasizing its role in cardiovascular disease prevention. ASA’s mechanism involves irreversible inhibition of COX activity, impacting prostaglandin synthesis. The ASA as a crucial lifelong therapy for cardiovascular events, with over 50 million Americans using it. While its clinical benefits are established, the underlying mechanisms, especially in coronary artery disease (CAD) secondary prevention, lack full clarity. The document discusses pharmacokinetics, pharmacodynamics, and optimal doses, including ongoing studies like ADAPTABLE to determine the most effective dosage for secondary prevention. It also touches on pharmacogenomics, highlighting genetic variations influencing ASA response and metabolism, particularly in genes like CYP2C9, UGT1A6, and TBXA2R. Conclusion: The review aims to consolidate information on pharmacological, molecular, genetic, and clinical aspects of ASA’s protective effects in CAD. The expression and saturation of enzymes involved in ASA metabolism can alter individual responses, so understanding the pharmacogenomic profile is important for personalizing treatment and improving clinical outcomes.
No takes yet. Share an insight, caveat, or question.
Luque-Esparza et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: