Platelet aggregation enhancement

"Platelet aggregation enhancement" denotes an increase in the ability or tendency of platelets to clump together after activation, a process fundamental for normal blood clotting (hemostasis) and tissue repair. However, excessive enhancement of this process increases the risk of thrombotic events such as myocardial infarction and stroke. Platelet aggregation is mediated by surface receptors (notably integrin GPIIb/IIIa, P2Y12, and GPVI), soluble agonists (ADP, thromboxane A2, collagen, thrombin), and bridging molecules like fibrinogen and von Willebrand factor. Therapeutic agents usually target these receptors and pathways rather than the aggregate process itself.

Other names

Platelet activation enhancementenhanced platelet aggregationincreased platelet aggregation

Inhibition of cyclooxygenase (aspirin) reduces thromboxane A2 production. Blockade of P2Y12 receptor (clopidogrel, prasugrel, ticagrelor) blocks ADP-mediated activation. Blockade of GPIIb/IIIa receptor (abciximab) prevents fibrinogen-mediated aggregation.