Stroke is a devastating neurological disorder and a major global public health concern, responsible for significant morbidity and mortality. Among the various types of stroke, cerebral thrombosis, characterized by the formation of blood clots in the cerebral blood vessels, is a predominant cause [1]. Aspirin, a widely prescribed antiplatelet agent, plays a pivotal role in preventing thrombotic events, including those leading to stroke [2]. However, the effectiveness of aspirin therapy exhibits substantial variability among individuals, and a noteworthy proportion of brain stroke patients experience reduced antiplatelet effects, a condition known as aspirin resistance [3]. Understanding the intricate pharmacogenomic factors that contribute to this phenomenon is of paramount importance for tailoring stroke prevention strategies in a more personalized and effective manner. The variability in aspirin responsiveness among brain stroke patients represents a significant clinical challenge. While aspirin's antiplatelet effects are well-documented, the mechanisms underlying aspirin resistance remain complex and multifaceted. This research paper delves into the pharmacogenomic aspects of aspirin resistance in the context of brain stroke, with a specific focus on identifying the genetic factors that underlie this resistance [4-9]. The genetic basis of aspirin resistance has been the subject of extensive investigation in recent years, revealing polymorphisms in genes encoding various platelet function-related enzymes, such as COX-1 and P2Y12, as well as genetic variations in the glycoprotein IIIa (GPIIIa) receptor and the fibrinogen gene [4]. These findings underscore the intricate interplay of genetic factors contributing to aspirin resistance and the pressing need for personalized stroke prevention strategies that account for individual genetic variations. [10-16] This study presents the methodology employed to investigate the pharmacogenomics of aspirin resistance among a cohort of 200 brain stroke patients. Genetic testing was conducted to identify specific polymorphisms associated with platelet function, while assessments of aspirin responsiveness were made through platelet aggregation tests. The study's findings emphasize the significance of genetic factors in influencing the responsiveness of brain stroke patients to aspirin therapy, thereby highlighting the potential for more personalized and effective treatment approaches. In summary, this research contributes to the growing body of knowledge regarding the pharmacogenomic determinants of aspirin resistance in brain stroke patients. By identifying the specific genetic factors associated with resistance, this study underscores the potential for tailoring antiplatelet therapy to individual patient needs, thereby holding promise for improving stroke prevention strategies and reducing the overall burden of morbidity and mortality associated with stroke.

Keywords: Pharmacogenomics, Genetic Factors, Aspirin Resistance, Brain Stroke, Antiplatelet Effects