Platelets and new antiplatelet drugs

10.2217/14750708.2.3.465 © 2 part of latelets play an important, life-saving role in hemostasis and blood clotting at sites of ascular injury. However, unwanted platelet activation and arterial thrombus formation are mplicated in the onset of myocardial infarction, stroke and other cardiovascular diseases. ifferent mechanisms, such as vascular damage, the development of mural platelet thrombi s a response to injury and the biochemical effects of intraplatelet substances that are eleased in response to damage, may be involved. Thus, antiplatelet therapy has become a ainstay of treatment for these conditions and the benefit of antiplatelet drugs is ocumented across a wide spectrum of clinical conditions. Aspirin has been regarded as the rototype antiplatelet drug and is still the most widely used agent. Aspirin’s antiplatelet ffect is directly due to irreversible inactivation of arachidonic metabolism and suppression of thromboxane A2 synthesis. However, platelet activation occurs via several pathways that do not rely on amplification by released thromboxane A2. Therefore, a number of other compounds have been developed to complement the beneficial effect of aspirin. Four main classes of antiplatelet agents are currently available for clinical use: aspirin, phosphodiesterase inhibitors, thienopyridines and the platelet glycoprotein αIIbβ3 receptor antagonists. This review discusses state-of-the-art antiplatelet therapies and recent advances, using aspirin as the reference standard.