Thrombin generation in a disrupted atheroma. After plaque rupture, local inflammation leads to exposure of TF to the surrounding blood, initiating thrombin generation. Activated platelets release active components from the cytosol, which induces the externalization of phosphatidylserine through the flip-flop mechanism. Platelets exerts a regulatory function by serving as a source of inflammatory mediators and interacting with circulating white cells. Local blood flow changes in the culprit artery increase in situ prothrombotic conditions. Local fibrinolysis release thrombin-bound fibrin and contribute to thrombus growth.