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Classification of antiplatelet agents

The figure below shows how antiplatelet drugs can be classified according to their mechanism of action. Drug classes include: ADP antagonists (Thienopyridines), COX-1 inhibitors (the only member of this class is aspirin), phosphodiestherase inhibitors and GPIIb/IIIa antagonists.

Classification of antiplatelet agents

Mechanism of action As shown in the figure, aspirin inhibits platelet cyclooxygenase, a key enzyme in thromboxane A2 (TXA2) generation. Thromboxane A2 triggers reactions that lead to platelet activation and aggregation, aspirin acts as a potent antiplatelet agent by inhibiting generation of this mediator. These effects last for the life of the anucleate platelet, approximately 7 to 10 days.

51:1829-1843 Therapeutic considerations Aspirin is indicated as prophylaxis against transient ischemic attacks. Source: Gasparyan. J Am Coll Cardiol 2008. A related post in this blog reviews some relevant aspects about aspirin pharmacokinetics. It is also used for the treatment of acute coronary syndromes and in the prevention of reoclusion in coronary revascularization procedures. Y. ADP-receptor blockers: thienopyridines Mechanism of action . myocardial infarction and thromboembolic disorders. Since side effects such as GI bleeding and acute renal insufficiency are dose dependent. the recommended antiplatelet dose ranges from 75 mg to 325 mg. A. et al.Aspirin inhibition of COX-1 decreases TXA2 production.

It inhibits adenosine uptake and cyclic GMP phosphodiesterase activity. it is currently used in combination with aspirin or warfarin in the . Phosphodiesterase inhibitors Dipyridamole is acts as vasodilator and antiplatelet agent. thrombocytopenia and thrombotic thrombocytopenic purpura. stroke or established peripheral arterial disease. LWW: 2009. Champe. R. Clopidogrel is approved for prevention of atherosclerotic events following recent myocardial infarction. Source:Harvey. this decreases platelet aggregability. It is approved for secondary prevention of thrombotic strokes in patients intolerant of aspirin and for prevention of stent thrombosis in combination with aspirin. P “Lippincott illustrated reviews: Pharmacology”. It is also approved for use in acute coronary syndromes that are treated with either PCI or coronary artery bypass grafting. leading to a reduced effectiveness of the latter. Like ticlopidine and clopidogrel. It has a better safety profile than ticlopidine. prasugrel requires a loading dose to achieve a maximal antiplatelet effect rapidly. Recent studies have shown that PPIs interact with clopidogrel. 4th edition. Therapeutics Ticlopidine is the oldest thienopyridine currently available. New antiplatelet drugs: Prasugrel is a recently approved ( July 2009) agent in this class. Dipyridamole alone has little antiplatelet effect.Thienopyridines block ADP receptors. Serious adverse effects of ticlopidine therapy are mainly hematologic and include: neutropenia. Thienopyridines act by inhibiting the ADP-dependent pathway of platelet activation. These drugs have no direct effect on prostaglandin metabolism.

Source: www. this class of drugs is not used in an outpatient setting by nonspecialists.prophylaxis of thromboembolic disorders. Therapeutic considerations Abciximab is a chimeric human-murine monoclonal antibody directed against GPIIb/IIIa. GPIIb/IIIa inhibitors The glycoprotein IIb/IIIa inhibitors are used parenterally in patients with acute coronary syndromes by specialists.integrilin. Their action is independent of the aggregation-inducing stimulus. . It is also used in stress testing for myocardial perfusion imaging. eptifibatide and tirofiban are more selective towards the GPIIb/IIIa receptor and have a shorter effect than abciximab. the integrin GPIIb/IIIa antagonists prevent cross-linking of Platelet membrane GPIIb-IIa receptors constitute the final common pathway of platelet aggregation. The peptide derivatives. current indications include unstable angina that does not respond to conventional therapy in patients that undergo percutaneous coronary intervention. Mechanism of action IIb/IIIa receptor binding to fibrinogen.

which has gone through a high technology of biochemical extraction . Not only antithrombolytic. and other peripheral vessel disorders. diabetes neuropathy. pharmacologically plasmin® also has fibrinolytic. angina pectoris. plasminogen activator.with thrombolytic effect that has been proven in vitro and in vivo. and plasmin. .The most serious adverse effects of GPIIB-IIIa antagonists include major bleeding. Study in healthy population shows that plasmin ® is safe. antiplatelet and antiinflamation effect. anticoagulant. Plasmin® (rongshuan jiaonans) is a medicine from China . Plasmin® can decrease blood viscocity and increase erythrocyte deformabulity in animal model. Some preliminary studies show that plasmin® is effective in ischemic stroke. intracerebral hemorrhage and thrombocytopenia. Plasmin® contains many enzymes such as collagenase.