1. Figure 1 Mechanism of thrombus formation during ST-segment
elevation myocardial infarction, and targets of currently available antithrombotic agents
Figure 1 | Mechanism of thrombus formation during ST-segment elevation myocardial infarction, and targets of currently available antithrombotic agents. After plaque rupture, adhesion of platelets to the subendothelium during the rolling phase is mediated by the interaction between the glycoprotein (GP) Ib/V/IX receptor complex located on the platelet surface and von Willebrand factor (vWF), and between collagen exposed at the site of vascular injury and platelet collagen receptors. Binding of collagen to these receptors triggers intracellular mechanisms that induce the release of activating factors, mainly thromboxane A2 (TXA2), ADP, and thrombin. These factors enhance the interactions among adherent platelets and promote further recruitment and activation of circulating platelets. Platelet activation by these mediators has as the final pathway the conversion of the platelet GP IIb/IIIa receptor, the main receptor mediating platelet aggregation, into its active form. Activated GP IIb/IIIa receptors bind to fibrinogen and vWF, leading to platelet aggregation and thrombus formation mediated by platelet–platelet interactions. Vascular injury also exposes subendothelial tissue factor, which forms a complex with factor VIIa and sets off a chain of events that culminates in formation of the prothrombinase complex. Prothrombin is converted to thrombin, which subsequently converts fibrinogen to fibrin, generating a fibrin-rich clot, and further activates platelets by binding to protease-activated receptors (PAR1) on the platelet membrane. However, only a modest amount of thrombin is produced as a result of the coagulation cascade, and the surface of activated platelets is the main source of circulating thrombin. Antiplatelet and anticoagulant agents work by inhibiting key receptors and factors involved in this cascade of events. COX, cyclooxygenase; TP, thromboxane prostanoid.
Franchi, F. et al. (2017) Antithrombotic therapy for patients with STEMI undergoing primary PCI
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