IPLab:Lab 3:Acute Myocardial Infarction

Clinical Summary

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. The patient progressively deteriorated with left ventricular failure and died with arrhythmias and pulmonary edema. Pertinent laboratory data are:

1. Aspartate Aminotransferase (AST) 60 IU/L.
2. 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.
3. Troponin I 18 µg/L.

Autopsy Findings

Examination of the 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.

Images

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  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 (3) adherent to the endocardial surface.

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  This is a higher-power photomicrograph which shows more clearly the viable tissue along the epicardium (1), the blue line of inflammatory cells (2), and the infarcted myocardium (3).

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  This is a photomicrograph of the edge of the infarct with normal tissue on the left (1). The accumulation of inflammatory cells (2) is at the edge of the infarcted tissue (3).

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  This is a higher-power photomicrograph of the edge of the infarct. The accumulation of inflammatory cells is on the left (1) and the infarcted tissue is on the right (2). Note that intact cells can be seen in the infarct but there are no nuclei.

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  This is a high-power photomicrograph of another area of this section. There are several hypereosinophilic cells within this section (arrows).

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  This is a low-power photomicrograph of a mural thrombus (1) adherent to the endocardial surface (arrows).

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  This is a photomicrograph of the lines of Zahn. Pale areas (1) represent platelets with some fibrin and the darker lines (2) represent RBCs and leukocytes enmeshed in fibrin strands.

Study Questions

• Are the serum enzyme results consistent with the time course of this clinical history?

The infarct occurred approximately 4 days prior to death. His CPK-MB levels would be expected to have gone down by now. His AST is slightly elevated and his LDH is moderately elevated with a high LDH1:LDH2 ratio. These findings are consistent with the clinical history.

• Why do mural thrombi often form in infarcted hearts?

The endocardium is usually the most severely damaged after an arterial occlusion since it is at the end of the circulation of the heart. Thus, with the infarcted tissue in the endocardium there is an acute inflammatory reaction which initiates coagulation and thrombus formation.

• What is the primary cell type in this inflammatory reaction?

At this stage it is primarily neutrophils, but there area a few macrophages. Usually, neutrophils enter an infarct by 12-24 hours and macrophages enter the lesion by 72 hours post-MI. By 3-7 days the lesion is primarily macrophages and by 10 days there are macrophages, fibroblasts, and endothelial cells (granulation tissue). The healing reaction in this patient may have been slower than normal because of his poor condition.