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Antiplatelet agents inhibit the aggregation of platelets and red blood cells, reducing their ability to connect to the endothelium of blood vessels. By reducing the surface strain of erythrocyte membranes, they facilitate their deformation during the passage through the capillaries and improve the fluidity of blood. Antiplatelet agents are able not only to prevent aggregation but also induce disaggregation of the platelets that have been already aggregated.
Antiplatelet therapy is one of the leading trends in the secondary prevention of ischemic stroke.
The main antiplatelet agents include:
- Acetylsalicylic acid (inhibits cyclooxygenase and thus the elaboration of thromboxane A2 in platelets)
- Dipyridamole (inhibits phosphodiesterase. The action is accompanied by an increase in the adenosine quantity,vasorelaxant and antiplatelet effects)
- Ticlopidine and clopidogrel (Plavix) block ADP and prevent the activation of glycoprotein complexes. They inhibit platelet aggregation caused by ADP and other inducers of adhesion, thus providing strong atiplatelet effect. In the recent years, the leading place among the drugs with the mechanism of platelet antiagreggation belongs to clopidogrel (Plavix). It inhibits the activation of platelets by selective and irreversible binding to specific receptors of ADP (P2Y12), as well as prevents the formation of fibrinogenic bonds. Clopidogrel being a derivative of ticlopidine, is 6 time more effective than the latter.
- Integrins (Eptifibatide, Lamifiban, etc.)- inhibitors of glycoprotein receptors.