Belong to class of antithrombotic agents.
Focus on preventing arterial rather than venous thrombogenesis, but are useful in certain types of venous thrombotic disease.
Useful in acute and chronic clinical processes.
Function to counteract platelet aggregation at sites of arterial endothelial injury or unstable atherosclerotic plaques.
Purpose is to prevent arterial obstruction or occlusion and downstream micro embolism into the systemic circulation.
Platelet function inhibition has an important process and life-threatening condition such as strokes, peripheral arterial disease, acute coronary syndromes and acute myocardial infarction.
Main antiplatelet inhibitory functions are blockade of arachidonic acid cascade in the platelet membrane and inhibition of the adenosine diphosphate (ADP) aggregation pathway.
Aspirin irreversibly inhibits cyclooxygenase 1 (COX-1), an enzyme responsible for the formation of thromboxane A2, a potent inducer and amplifier of platelet activation and aggregation.
Aspirin is the prototypic antiplatelet drug.
Other antiplatelet agents act through the arachidonate pathway such as direct inhibitors of thromboxane A2 or inhibitors of thromboxane receptors.
ADP pathway blockade can be accomplished by inhibition of phosphodiesterase 5, by direct inhibition of the P2Y12 platelet receptor.
Phosphodiesterase inhibition can occur with dipyridamole.
P2Y12 can be inhibited by thienopyridines or cyclopentyl-triazolo-pyrimidinic compounds.
Thienopyridines include ticlopidine, clopidogrel, and prasurgel.
Cyclopentyl-triazolo-pyrimidinic compounds include ticagrelor and cangrelor.
Women treated with antiplatelet drugs experience more bleeding complications than men, probably because they are generally older, have worse renal function, and more comorbidities.