After the clot has been formed, the activated platelets incorporated in the clot rearrange and contract their intracellular actin/myosin cytoskeleton. The intracellular actin network is connected to the internal part of the integrin αIIbβ3 fibrinogen receptor. Following coagulation, the external part of αIIbβ3 will have bound to the fibrin network of the clot, and therefore, as a result of platelet contractile force on the fibrin network, the formed clot will compact on itself and hence reduce its total volume. The mechanism is termed clot retraction, and it is considered that its main physiological function is to clear the obstructed vessel for renewed blood flow . Disrupting the fibrin binding capability of platelets with the use of integrin αIIbβ3 inhibitors results in a complete loss of clot retraction [69, 70]. Commonly used integrin ?IIb?3 inhibitors are abciximab, eptifibatide and tirofiban. Clot retraction can also be inhibited by the use of cytochalsin E, a cell permeable metabolite of fungal origin that prevents intracellular actin rearrangement [71-73].