Aspirin resistance: Fact or fiction? A point of view

Figure 1 Pathways of platelet aggregation. Platelets can be activated in response to collagen, von Willebrand factor (vWF) and tissue factor when there is injury to the endothelial lining. A host of other stimuli, such as adenosine diphosphate (ADP), 5-hydroxytryptamine (5-HT), epinephrine and thromboxane A₂ (TXA₂), can initiate aggregation via specific receptors. The end-point is the rise in cytosolic Ca²⁺ which induces platelet activation/aggregation. Externalization of glycoprotein (Gp)IIb/IIIa receptors causes fibrin bands to bind to different platelets. Aspirin interferes with the conversion of arachidonic acid (AA) to TXA₂ and inhibits the rise in cytosolic Ca²⁺ and subsequent platelet aggregation.