Antiplatelets

The body forms clots two ways. In fast-flowing arteries, injury (like a ruptured cholesterol plaque) exposes surfaces that platelets stick to and pile onto — a platelet-rich "white clot." In slow-flowing veins, the coagulation cascade builds a fibrin-and-red-cell "red clot."

This is why antiplatelets and anticoagulants are not interchangeable. Antiplatelets (aspirin, clopidogrel) target the arterial, platelet-driven clots behind heart attacks and most strokes. Anticoagulants (warfarin, heparin, DOACs) target the venous, cascade-driven clots of DVT/PE and atrial fibrillation. Confusing the two is a classic — and dangerous — error.

Platelets are activated through several signals; the drugs block different ones. Aspirin irreversibly blocks the enzyme COX-1, so platelets can’t make thromboxane A₂, a key aggregation signal — and because a platelet can’t remake the enzyme, the effect lasts the platelet’s whole ~7–10-day lifespan. Clopidogrel, prasugrel, and ticagrelor block the P2Y12 (ADP) receptor, a different activation pathway.

A crucial detail: clopidogrel and prasugrel are prodrugs — inactive until the liver converts them. Clopidogrel depends on the enzyme CYP2C19, and patients who are "poor metabolizers" activate too little drug and stay at risk (its boxed warning). Ticagrelor is *not* a prodrug — it blocks P2Y12 directly and reversibly, so it works regardless of CYP2C19.

After a coronary stent, patients take dual antiplatelet therapy (DAPT) — aspirin *plus* a P2Y12 blocker — because a bare metal scaffold in an artery is intensely clot-prone until the vessel lining grows over it. Stopping either drug too early lets a clot form right at the stent — stent thrombosis — which often causes a large, sometimes fatal heart attack.

That is why "don’t stop your antiplatelet before you talk to your cardiologist" is a life-or-death teaching point, and why any procedure requiring the drug to be held must be coordinated with the prescribing team.