Antiplatelet Therapy

Aspirin
Mechanism Irreversible inhibition of COX-1 ( cyclo oxygenase 1) in platelets. This prevent formation of pro-aggregatory Thromboxane A2 from Arachidonic acid. This action lasts through out platelet life span (7-10 days).

Adverse effects
In Gastro intestinal tract it inhibits production of prostaglandins that protect gastric mucosa. Dyspepsia Nausea Gastric mucosal ulceration and bleeding. Avoid in pregnancy and breast feeding.

Clopidogrel and Prasugrel

Mechanism These drugs have active derivatives that bind irreversibly to purinergic P2 receptors on platelets. They reduce the binding of ADP; one of the initiators of platelet activation. Clopidogrel is an alternative to Aspirin for secondary prevention of vascular disease when Aspirin is not tolerated. Prasugrel can be used in place of clopidogrel.

Adverse effects
Increase the risk of bleeding. The efficacy of clopidogrel may be reduced when taken with the proton pump inhibitor Omeprazole.

Dipyridamole
Mechanism Inhibits the enzyme Phosphodiesterase which degrades cyclic nucleotides. In the platelets this increases intracellular concentration of cAMP and reduces activation and expression of cell surface GPIIb/IIIa receptors, leading to inhibition of platelet aggregation. Used in secondary prevention of stroke in combination with Aspirin.

Adverse effects
Gastrointestinal upset. Myalgia Dizziness Flushing Hypotension and Tachycardia.

Glycoprotein IIb/IIIa Receptor Antagonists

Mechanism Abciximab is a monoclonal antibody to the GPIIb/IIIa receptors. Abciximab irreversibly binds to GPIIb/IIIa receptors and blocks the binding of fibrinogen, reducing platelet aggregation by more than 90%.

Adverse effects
Bleeding is the main risk. Throbocytopenia may occur. Nausea Vomiting Hypotension Bradycardia