ATEROMA

Aspirin reversibly inhibits platelet activation by inhibiting the cyclooxygenase-1 enzyme and blocking TXA2 synthesis. The P2Y12 receptor inhibitors block ADP activation of the platelet. The P2Y12 receptor is required for G12 protein–mediated activation of the GpIIb/IIIa receptor. This results in decreased platelet degranulation and aggregation. Clopidogrel requires a 2-step metabolism by hepatic cytochrome enzymes for biotransformation to its active form, whereas prasugrel undergoes a single-step conversion to its active metabolite. Ticagrelor and cangrelor are direct-acting reversible antagonists of the P2Y12 receptor. Abciximab, eptifibatide, and tirofiban are direct inhibitors of the GpIIb/ IIIa receptors and thereby inhibit platelet aggregation. Vorapaxar is an oral protease–activated receptor (PAR)–1 antagonist that inhibits thrombin-induced platelet activation by reversible binding of the PAR-1 receptor on platelets. Cangrelor, abciximab, eptifibatide, and tirofiban are intravenous antiplatelet medications. Because these are often used together with an oral antiplatelet regimen for treating acute coronary syndrome, they are included in the figure. Aspirin Vorapaxor Drug administration type Oral intravenous Clopidogrel Prasugrel Ticagrelor Cangrelor Abciximab Eptifibatide Tirofiban Binds cyclooxigenase 1 and inhibits thromboxane A 2 (TXA 2 ) synthesis Binds protease-activated receptor (PAR)-1 and inhibits thrombin induced platelet activation Binds to P2Y12 receptor and inhibits adenosine diphosphate (ADP) induced platelet activation Binds to glycoprotein llb/llla (Gpllb/IIIa) receptor and inhibits aggregation 73 ATEROMA - Resúmenes