<unk>  occurs most often during the first 2 weeks following AMI. AMI patients most at risk display the 3 characteristics of Virchow's triad: Stagnation of blood The risk of<unk>  formation increases as infarction size increases. A larger infarction means a larger area of tissue injury, which may be akinetic or dyskinetic, resulting in stagnation of ventricular blood. Endothelial injury Monocytes and macrophages play important roles in healing after myocardial infarction. With the absence of monocytes and macrophages, chances of<unk>  formation are very high. Failure to clear cellular debris from the infarct compromises the endothelial lining of the<unk>  ventricle and exposes the damaged tissue to the blood. The response is to build a<unk>  composed of fibrin, red blood cells and platelets. Hypercoagulable state For several days after AMI, the levels of tissue factor and D-dimer, which are involved in coagulation, are high, which increases the risk of<unk>  formation.<unk>  may be good for the heart when tissues are severely damaged because it acts to thicken the wall, thus protecting it against rupture.
Left ventricular thrombus
Spontaneous coronary artery dissection
Unstable angina
Libman–Sacks endocarditis
Acute pericarditis
Isolated atrial amyloidosis
Cardiac myxoma
Primary ventricular fibrillation