ROLE OF ANTIPLATELET AGENTS IN THROMBOSIS: A REVIEW

Thrombosis is a major global health concern and a leading cause of morbidity and mortality, particularly in cardiovascular and cerebrovascular diseases such as myocardial infarction, ischemic stroke, deep vein thrombosis, and peripheral arterial disease. Arterial thrombi are primarily platelet-rich and form through mechanisms described by Virchow’s triad: endothelial injury, abnormal blood flow, and hypercoagulable states. Platelets contribute to thrombus formation via adhesion, activation, and aggregation, mediated by glycoprotein receptors and prothrombotic mediators like thromboxane A₂ and adenosine diphosphate. Antiplatelet agents—including cyclooxygenase inhibitors, P2Y₁₂ receptor antagonists, glycoprotein IIb/IIIa inhibitors, phosphodiesterase inhibitors, thrombin receptor antagonists, prostacyclin analogues, and thromboxane-targeted drugs—suppress platelet function at multiple points and are central to managing arterial thrombosis. Clinically, these drugs are used in acute coronary syndromes, post-percutaneous coronary interventions, secondary stroke prevention, and peripheral arterial disease, often in combination as dual therapy for high-risk patients. Formulation strategies, such as enteric coating, modified-release systems, pro-drug design, and novel delivery methods, improve efficacy, safety, and adherence. Despite their benefits, antiplatelet therapies carry risks of bleeding, gastrointestinal effects, and variable patient response, emphasizing the need for careful management and ongoing development of safer, more targeted treatments.