antiplatelet
An antiplatelet stops the tiny cell fragments called platelets from clumping together. When a vessel wall is injured or a fatty plaque cracks, platelets are the first responders that pile up and stick together to plug the gap. In a diseased artery that same clumping can form a clot that blocks blood flow; an antiplatelet keeps the platelets slippery so the dangerous plug does not form.
These drugs interfere with platelet activation and aggregation by different routes. Aspirin irreversibly inhibits the enzyme cyclooxygenase, cutting production of thromboxane A2, a platelet-activating signal. Clopidogrel, prasugrel and ticagrelor block the platelet P2Y12 receptor for ADP. Because they act on the arterial, platelet-driven side of clotting, antiplatelets are mainstays for preventing heart attacks and ischaemic strokes, and dual antiplatelet therapy is standard after a coronary stent.
Like anticoagulants, their main hazard is bleeding, particularly in the stomach and gut where aspirin also irritates the lining, and the risk is amplified when antiplatelet and anticoagulant drugs are combined. Aspirin's effect lasts the platelet's lifetime of about a week because the inhibition is irreversible, which is why it is often stopped several days before major surgery.
After receiving a coronary stent, a patient takes aspirin plus ticagrelor, dual antiplatelet therapy, to keep platelets from clotting on the new metal scaffold while the artery heals.
A bare stent is highly thrombogenic, so dual antiplatelet cover is essential in the months after.
Antiplatelets and anticoagulants are often confused; antiplatelets mainly prevent clots in fast-flowing arteries, while anticoagulants mainly prevent clots in slow-flowing veins and the heart.