Recent Advances in Antiplatelet Agents

Abstract

Platelet aggregation plays a key role in the pathogenesis of thromboembolic diseases such as myocardial infarction, stroke, unstable angina and peripheral artery disease. Until recently, aspirin was the only antiplatelet agent available to prevent or treat these events. Over the past several years, there has been a substantial expansion in the antiplatelet armamentarium as well as in the understanding of the clinical importance of antiplatelet therapy in limiting the complications of thrombosis. Aspirin was one of the first agents to be adopted and it remains as the standard therapy with the higher amount of available clinical information. Following aspirin, ADP receptor antagonists like ticlopidine and clopidogrel as well as phosphodiesterase inhibitors dipyridamole and cilostazol have been introduced. Glycoprotein (GP) IIb/IIIa receptor antagonists like eptifibatide, tirofiban and abciximab are the newer antiplatelet agents which act at the end of the common pathway of platelet aggregation. Although results of clinical studies with the first oral GPIIb/IIIa antagonists were disappointing, agents of the new generation might expand the potential application of GPIIb/IIIa targeted therapy. This review will highlight recent advances in the development of aspirin, phosphodiesterase inhibitors, ADP receptor antagonists and the platelet glycoprotein IIb/IIIa inhibitors. The emphasis of this paper has been placed on the chemical aspects of these agents.

Dental management of patients receiving anticoagulation or antiplatelet treatment

“…Acetylsalicylic acid -ASA ASA is still the only nonsteroidal anti-inflammatory drug (NSAID) used in the treatment and prevention of thromboembolic diseases (3). The antithrombotic action of ASA depends on the irreversible inhibition of arachidonate cyclo-oxygenase activity in platelets, thereby reducing the extent of thromboxane A2 formation that occurs after activation of phospholipase A2 and release of arachidonic acid (3).…”

“…The antithrombotic action of ASA depends on the irreversible inhibition of arachidonate cyclo-oxygenase activity in platelets, thereby reducing the extent of thromboxane A2 formation that occurs after activation of phospholipase A2 and release of arachidonic acid (3). Thromboxane A2 is a strong platelet agonist, which is an effective inducer of platelet granule secretion as well as platelet aggregation (3). Available evidence suggests that a daily ASA dose of 75-150 mg is recommended for long term prevention of serious vascular events in high risk patients (8).…”

“…Even though several antiplatelet and anticoagulant agents have been developed in recent years, acetylsalicylic acid (ASA) and warfarin are the standard drugs for preventing vascular diseases (3).…”

Anti-platelet aggregation effects of extracts from Arbutus unedo leaves

“…Platelet hyperactivity is thought to play a crucial role in the development of cardiovascular disorders such as strokes and myocardial infarction (Dogne et al 2002;Wong et al, 2010). The high incidence of cardiovascular disorders and the limited tolerability of the main antiplatelet agents currently used (Van De Graaff and Steinhubl, 2001) has stimulated research into the prevention of platelet hyperactivity by several means including medicinal plants (El Haouari and Rosado, 2016).…”

Synthesis and biological evaluation of some dibenzofuran-piperazine derivatives

“…Among these agonists, AA is one of the most powerful agonists for platelet activation 6,7 . Currently, essential antiplatelet drugs used for the prophylaxis and treatment of thromboembolic diseases are aspirin, ridogrel, ticlopidine, clopidogrel, dipyridamole, cilostazol, tirofiban and sibrafiban [8][9][10][11][12] . Nevertheless, these orally administered antiplatelet drugs have certain disadvantages, such as gastric erosion, agranulocytosis, neutropenia, thrombocytopenia, aplastic anemia and thrombotic thrombocytopenic purpura along with inefficient therapy [13][14][15][16] .…”