Vakani Jahnavi, Kongi Kavyasudha and Yadala Prapurna Chandra
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, with atherothrombosis as the central pathological mechanism driving coronary artery disease, ischemic stroke, and peripheral arterial disease [1]. Antiplatelet therapy is pivotal in preventing and treating these conditions by targeting platelet adhesion, activation, and aggregation [2]. Aspirin, the earliest and most widely used antiplatelet agent, irreversibly inhibits cyclooxygenase-1, thereby reducing thromboxane A2-mediated platelet activation; however, its benefits are often offset by gastrointestinal toxicity and bleeding risk [3]. The development of P2Y12 receptor inhibitors, such as clopidogrel, prasugrel, and ticagrelor, has revolutionized treatment, particularly in dual antiplatelet therapy (DAPT) following acute coronary syndromes and percutaneous coronary intervention [4]. Additional classes, including glycoprotein IIb/IIIa inhibitors, PAR-1 antagonists, and phosphodiesterase inhibitors, further broaden therapeutic options, though bleeding remains the major limitation [5]. Recent advances emphasize individualized therapy, incorporating genetic testing, platelet function assays, and escalation/de-escalation strategies to balance ischemic protection against hemorrhagic risk. Future perspectives focus on precision medicine, novel targets such as GPVI and PAR-4 receptors, and integration of digital health tools to optimize therapy. This review discusses the pathophysiology, treatment, current strategies, recent advances, and future directions in antiplatelet therapy for Cardiovascular diseases (CVDs) [6].
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