This 78-year-old male experienced a posterior myocardial infarction six years prior to this admission. Recently, he had begun to experience occasional angina. Four days prior to death, he experienced anterior chest pain and discomfort which he regarded as not too distressing. However, EKGs showed a classic acute anterior myocardial infarction in addition to the healed posterior infarct. His bloodwork also showed an elevated troponin. The patient progressively deteriorated with signs of left ventricular failure and died with arrhythmias and pulmonary edema. Pertinent laboratory data are:

# Aspartate Aminotransferase (AST) 60 IU/L.# Total Creatine Phosphokinase (CPK) 165 IU/L. All of the activity was due to CPK III (MM) isoenzyme fraction; no CPK (MB) activity was detectable.# Troponin I 38 µg/L.  == Autopsy Findings ==Examination of the At autopsy his heart showed a healed posterior infarct. The right coronary artery was completely occluded but partially recanalized. The left main coronary artery had severe atherosclerotic stenosis and a thrombus filling the lumen. The entire anterolateral aspect of the left ventricle was soft with variegated areas appearing hyperemic or pale. There was extensive mural thrombosis and reactive pericarditis.

File:IPLab3AcuteMyocardialInfarction1IPLab3AcuteMyocardialInfarction1a.JPG|This is a gross photo of the heart at autopsy after the left ventricle was opened. Note the thrombotic material (T) that is present within the left ventricular lumen over the area of infarction. On the cut edge of the left ventricular free wall you can see the areas of hemorrhage and the pale myocardium indicative of an acute myocardial infarction (arrows).File:IPLab3AcuteMyocardialInfarction1bf.jpg|This is a low-power photomicrograph of infarcted heart. There is a layer of surviving myocardial tissue (1) along the epicardium and then a blue line (2) which represents the accumulation of inflammatory cells at the border of the infarct. There is thrombotic material (3T) adherent to the endocardial surface.File:IPLab3AcuteMyocardialInfarction2IPLab3AcuteMyocardialInfarction2bs.jpg|This is a higher-power photomicrograph which shows more clearly the viable tissue along the epicardium (1Epi), the blue line of inflammatory cells (2arrows), and with the infarcted myocardium (3)below.File:IPLab3AcuteMyocardialInfarction3IPLab3AcuteMyocardialInfarction3b.jpg|This is a photomicrograph of the edge of the infarct with normal tissue on above and infarcted tissue below the left (1). The accumulation line of inflammatory cells (2) is at the edge of the infarcted tissue (3arrow).File:IPLab3AcuteMyocardialInfarction4IPLab3AcuteMyocardialInfarction4b.jpg|This is a higher-power photomicrograph of infarcted tissue just below the edge line of the infarctinflammatory cells. The accumulation of inflammatory cells is on the left (1) myocytes have lost their nuclei and the infarcted tissue cytoplasm has a granular appearance indicating that this is on the right (2). Note that intact cells can be seen in the infarct but there are no nucleicoagulation necrosis.File:IPLab3AcuteMyocardialInfarction5IPLab3AcuteMyocardialInfarction5b.jpg|This is a high-power photomicrograph of another area he inflammatory cells present at the border zone between normal and infarcted tissue. Many of this section. There are several hypereosinophilic the inflammatory cells within this section have begun to die and break down (arrowsnote blue tinge to tissue)but viable nutrophils and some lymphocutes and macrophages are visible.