As a normal response of the body, chemical mediators would bereleased thus activating thrombosis promoting repair of the rupturedplaque wherein endothelium would be replaced with fibrotic tissues whichcontributes to narrowing of the artery and loss of its elasticity which mayeventually result in another episode of occlusion (figure 3). Thistransformation of an atherosclerotic plaque to an unstable lesion followsthe different stages in platelet activation and aggregation. Rupture or ulceration of an atherosclerotic plaque exposes the subendothelial matrix(primarily composed of collagen and tissue factor) to circulating blood.This particular event will result to platelet adhesion through the binding of platelet glycoprotein (GP) Ib to von Willerbrand factor and GP VI bindingto collagen. Platelet activation ensues leading to a (1) change in shape of the platelet (from smooth discoid to spiculated form) which increases thesurface area on which thrombin generation can occur, (2) degranulation of the platelet alpha and dense granules, releasing thromboxane A
,serotonin and other platelet aggregatory and chemoattractant agents; and(3) increased expression of GP IIb/IIIa which enhances affinity tofibrinogen. Lastly platelet aggregation takes place wherein fibrinogenbinds to activated platelet GP IIb/IIIa, creating a growing plateletaggregate. This process continuously happening which decreases thearterial lumen in the long run. In line with this, secondary hemostasishappens wherein plasma coagulation system is activated. Tissue factor will cause the activation of Factor X changing it to Factor Xa which leadsto formation of thrombin (factor IIa) which play a central role in arterialthrombosis: (1) thrombin converts fibrinogen to fibrin (2) thrombinpowerfully stimulates platelet aggregation; and (3) it activates factor XIIIleading to cross – linking and stabilization of fibrin clot. Thrombinmolecules will eventually incorporated to coronary thrombi forming thenidus of rethrombosis.