Plaque Rupture and Clot Formation

Following plaque rupture, a clot (a partially occlusive or completely occlusive thrombus), forms on top of the ruptured plaque. The thrombogenic contents of the plaque are exposed to blood elements. Exposure of collagen and tissue factor induce platelet adhesion and activation, which promote the release of platelet-derived vasoactive substances including adenosine diphosphate (ADP) and thromboxane A2 (TXA2)6 These produce vasoconstriction and potentiate platelet activation. Furthermore, during platelet activation, a change in the conformation in the glycoprotein IIb/IIIa surface receptors of platelets occurs which cross-links platelets to each other through fibrinogen bridges. This is considered the final common pathway of platelet aggregation. Inclusion of platelets gives the clot a white appearance. Simultaneously, the extrinsic coagulation cascade pathway is activated as a result of exposure of blood components to the thrombogenic lipid core and endothelium, which are rich in tissue factor. This leads to the production of thrombin (factor lla), which converts fibrinogen to fibrin through enzymatic activity.6 Fibrin stabilizes the clot and traps red blood cells, which gives the clot a red appearance. Therefore, the clot is composed of cross-linked platelets and fibrin strands.6

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