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An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation[1] and inhibit thrombus formation. They are effective in the arterial circulation where classical Vitamin K antagonist anticoagulants have minimal effect.[2]

Antiplatelet drugs are widely used in primary and secondary prevention of thrombotic disease, especially myocardial infarction and ischemic stroke.[1]

Antiplatelet therapy with one or more of these drugs decreases the ability of blood clots to form by interfering with the platelet activation process in primary hemostasis. Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another and to damaged blood vessels' endothelium

1. ANTI PLATELET DR.S.K.SHYAM SUNDAR MEM 1st YEAR PG

2. DRUGS THAT INHIBIT PLATELET AGGREGATION AND THROMBUS FORMATION ARE CALLED ANTI-PLATELET DRUGS.

3. CLASSIFICATION Thromboxane (TXA2) synthesis inhibitor: Low-dose aspirin. Phosphodiesterase inhibitor: Dipyridamole. Purinergic (P2Y12) receptor antagonists: Ticlopidine, clopidogrel, prasugrel, cangrelor, ticagrelor. Glycoprotein (GP) IIb/IIIa receptor antagonists: Abciximab, eptifibatide, tirofiban.

4. TXA2 Synthesis Inhibitor Low-dose aspirin (50–325 mg/day) irreversibly acetylates platelet COX-1 and reduces the production of TXA2. Since platelets cannot synthesize new enzymes, the antiplatelet effect lasts for the lifetime of the platelets, i.e. 7–10 days. In higher doses, aspirin inhibits both TXA2 and PGI2, hence antiplatelet efficacy is reduced. Common adverse effects are gastric irritation and bleeding.

5. Phosphodiesterase Inhibitor Dipyridamole is a vasodilator. It inhibits phosphodiester-ase and increases the concentration of cyclic adenosine monophosphate (cAMP) levelswhich inhibits platelet aggregation. It is occasionally used in combination with warfarin during postoperative period in patients with prosthetic heart valves.

6. P2Y12 Receptor Antagonists Adenosine diphosphate (ADP) released from platelets pro-motes their aggregation.

7. Ticlopidine, clopidogrel and prasugrel are prodrugs and structurally related. They inhibit ADP-mediated platelet aggregation by irreversibly blocking purinergic (P2Y12)receptors on the platelets. The antiplatelet effect persists even after discontinuation of the drugs. They produce synergistic effect when combined with aspirin or GP IIb/IIIaantagonists. They are administered orally.

8. Prasugrel has a faster onset of action and better antiplatelet effect than ticlopidine and clopidogrel. Bleeding is an important adverse effect; risk is more with prasugrel. The other adverse effect of ticlopidine and clopidogrel is diarrhoea. Neutropenia and thrombocytopenia are serious adverse effects of ticlopidine but rare with clopidogrel. Ticagrelor inhibits ADP-mediated platelet aggregation by reversibly blocking plateletP2Y12 receptors. It is rapid acting and more potent. It is administered orally. Nausea, dyspnoea, arrhythmias and bleeding are some of its adverse effects.

9. Glycoprotein IIb/IIIa Receptor Antagonists Activation of GP IIb/IIIa receptors on platelets favours binding of fibrinogen to these receptors resulting in platelet aggregation Abciximab, eptifibatide and tirofiban block GP IIb/IIIa receptors on platelet surface to inhibit final step of platelet aggregation. Abciximab is a monoclonal antibody that binds to GP IIb/IIIa receptor. Eptifibatide is a synthetic drug, which is more specific for GP IIb/IIIa receptor. Tirofiban is a nonpeptide GP IIb/IIIa receptor antagonist. They areuseful as adjunctive therapy in high risk patients with acute coronary syndrome undergoing PCI. The main side effects of these drugs are bleeding and thrombocytopenia.

10. Thrombin Receptor Antagonist Vorapaxar blocks protease-activated receptor 1 (PAR-1) on the surface of platelets, thus produces antiplatelet effect. It is used as an adjunct with aspirin/clopidogrel in patients with MI and peripheral vascular disease. Bleeding is the main side effect.

11. Uses of Antiplatelet Agents Acute coronary syndrome: It includes acute MI and unstable angina. Dual antiplatelet therapy is used – incidence of MI, stroke and mortality is reduced. It decreases occurrence of reocclusion and reduces risk of stent thrombosis. Aspirin in combination with other antiplatelet is used. Patients with unstable angina/NSTEMI should receive low-dose aspirin with P2Y12 blocker (ticagrelor/prasugrel/clopidogrel). In patients with STEMI, the antiplatelet to be used in addition to aspirin depends on reperfusion therapy – primary PCI or fibrinolytics. Aspirin with clopidogrel is used in patients with STEMI treated with fibrinolytics. Aspirin with ticagrelor/prasugrel is preferred in those patients undergoing primary PCI. If no reperfusion therapy is given, then ticagrelor is preferred. For patients at risk of recurrent ischaemic episodes, GP IIb/IIIa antagonist can be added to antiplatelet therapy.

12. Coronary artery disease: Studies have shown that low-dose aspirin reduces the occurrence of subsequent MI, stroke and death in post-MI patients. Clopidogrel can be used as an alternative if aspirin cannot be used. Prosthetic heart valves: Valve thrombosis and thromboembolism are problems associated with prosthetic valves. Aspirin with warfarin reduces these risks. Dipyridamole may be used with warfarin to prevent thromboembolism in patients with prosthetic heart valves.

13. Transient ischaemic attack (TIA): Early initiation of aspirin in patients with TIA reduces risk of recurrent attacks. Peripheral artery disease: Aspirin/clopidogrel may prevent thromboembolism

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