antiplatelets

Antiplatelets are drugs that inhibit platelet activation and aggregation to reduce arterial thrombosis. They act on platelets rather than the coagulation factors in plasma.

Major categories include aspirin; P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor); glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, tirofiban); and other agents such as dipyridamole, cilostazol, and vorapaxar. Aspirin irreversibly inhibits COX-1 in platelets, reducing thromboxane A2. P2Y12 inhibitors block ADP-mediated platelet activation. GP IIb/IIIa inhibitors prevent the final aggregation step by blocking fibrinogen binding. Dipyridamole and cilostazol raise intracellular cAMP in platelets, reducing activation. Vorapaxar blocks thrombin-mediated platelet activation through PAR-1.

Used to prevent arterial thrombosis in coronary disease, after acute coronary syndromes, and after stent placement; also employed for secondary prevention of ischemic stroke or TIA and in some peripheral artery disease.

Bleeding is the principal risk; GI bleeding and intracranial hemorrhage are possible, with higher risk from combination therapy or in older patients. They are not effective for preventing venous clots. Some patients show reduced response to certain agents (for example clopidogrel).

Commonly, low-dose aspirin (75–100 mg daily) is used; P2Y12 inhibitors are prescribed for defined durations after ACS or PCI, depending on risk and procedure. Therapy may be paused for surgery to minimize bleeding risk; bleeding risk must be balanced against thrombotic risk.