Activaton of Coagulation Cascade in Acute Coronary Syndrome

Abstract

The acute coronary syndrome (ACS) arise from procoagulant changes in complex plaques, which trigger both platelet activation and coagulation pathways. These two pathways intersect at a number of points that form positive-feedback loops to sustain and accelerate thrombus formation. A key initiating event in the pathology of ACS is atheromatous plaque disruption, in which the exposure of thrombogenic material triggers simultaneous activation of primary and secondary hemostatic pathways. Platelets are activated on exposed subendothelial collagen and blood coagulation is triggered via exposure of tissue factor (TF). In the pathogenesis of the ACS, blood clotting activation has a crucial role. The coagulation processes are currently believed to be mostly cell surface-based, including three overlapping phases: initiation, when tissue factor-expressing cells and microparticles are exposed to plasma; amplification, whereby small amounts of thrombin induce platelet activation and aggregation, and promote activation of factors (F)V, FVIII and FXI on platelet surfaces; and propagation, in which the Xase (tenase) and prothrombinase complexes are formed, producing a burst of thrombin and the cleavage of fibrinogen to fibrin. Fibrin is an important contributor to thrombogenesis. This review discuss the activation of the coagulation cascade in thrombus formation in ACS.