Platelet function in intravascular device implant-induced intimal injury

Abstract

Platelets are involved in the rapid response to intimal injury in which the underlying thrombogenic subendothelial matrix is exposed, leading to platelet adhesion, secretion, aggregation, and initiation of arterial thrombus formation. The platelet activation pathway involves a multistep process of distinct receptors, adhesive ligands, release of mediators, receptor-ligand interactions, and recruitment of more platelets to the site of injury. The balance between blood fluidity and intimal injury-induced arterial thrombosis is maintained by an intact endothelium that controls vessel tone, synthesizes inhibitors and activators of platelet function, and thereby allows the free flow of blood cell elements. An intravascular device implant causes intimal injury, which is accompanied by decreased antithrombotic potential of the endothelial cells and increased release of prothrombotic substances. A trigger for the formation of intimal injury-induced thrombus formation may be due to endothelial dysfunction and/or the loss of endothelial cell barrier between the subendothelial matrix and flowing blood, which allows initiation of platelet activation. A thorough understanding of the platelet regulatory mechanisms is necessary to develop effective antiplatelet therapy to prevent the complications of thrombosis following revascularization procedures using percutaneous coronary intervention. This review summarizes the temporal events following intravascular device implants, including endothelial cell injury, platelet activation, receptor-mediated signaling events, platelet-rich thrombus formation, and the redundant platelet pathways, all of which may be potential therapeutic targets.