Aspirin is a highly successful antiplatelet drug & still retains its status as the 'front-line' antiplatelet drug; however, increased understanding of platelet biology has led to the development of new antiplatelet drugs that are potentially more effective. Now, more researches in platelet biology has led to this fact that there are more than 90 other metabolic pathways leading to platelet aggregation that are independent of arachidonic acid and therefore not inhibited by aspirin, hence, several more drugs are being developed, aimed at controlling different phases of platelet function such as platelet aggregation & adhesion. The newer drugs now offer potentially greater and more specific control over platelet function. Definitely, these drugs are going to be significantly more expensive than aspirin, and their eventual role in the clinical arena will ultimately depend on both their efficacy and their cost-effectiveness. As we approach the next millennium, it is envisaged that our increased understanding of platelet function, coupled with advances in technology and drug manufacture, will result in even greater improvements in the therapeutic control of platelet thrombus.
Prasugrel; Ticagrelor; Antiplatelet Drug Therapy; Pathophysiology of Platelet Aggregation