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

• 
  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.
• 
  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).
• 
  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).
• 
  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.
• 
  This is a high-power photomicrograph of another area of this section. There are several hypereosinophilic cells within this section (arrows).
• 
  This is a low-power photomicrograph of a mural thrombus (1) adherent to the endocardial surface (arrows).
• 
  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.

Additional Resources

Related IPLab Cases

Myocardial infarction is necrosis of myocardial tissue which occurs as a result of a deprivation of blood supply, and thus oxygen, to the heart tissue. Blockage of blood supply to the myocardium is caused by occlusion of a coronary artery.

Angina pectoris is chest pain produced by myocardial ischemia, it worsens upon exertion.

Arrhythmias are abnormal heart rhythms.

Pulmonary edema refers to the accumulation of fluid in the pulmonary alveolar and tissue spaces as a result of changes in capillary permeability and/or increases in capillary hydrostatic pressure.

AST is a NON-SPECIFIC marker of myocardial infarction (i.e., it is also elevated in other conditions, such as liver disease and skeletal muscle injury). AST levels peak at 48--72 hours following the infarction. A normal AST level would be less than 37 IU/L.

An elevated total CPK (a collective measure of all CPK isoenzymes) is a NONSPECIFIC marker for myocardial infarction. However, an elevation in the level of CPK-MB isoenzyme is a more specific marker for myocardial infarction. The CPK-MM isoenzyme is specific for skeletal muscle. CPK levels begin to rise 4-8 hours following an infarction, usually peak within the first 24-48 hours, and then return to baseline within 3-4 days. A normal CPK level is 35 to 250 IU/L.

Troponin I is a muscle contractile protein that is increased in serum after myocardial necrosis, it is a sensitive and specific marker of acute MI, and better than CK-MB as a cardiac injury marker. Normally troponin I values are less than 10 µg/L but values can rise 5 to 50 times after an acute myocardial infarction.

Recanalization is the process of the forming of channels through an organized thrombus so that blood flow is restored.

A thrombus is a solid mass resulting from the aggregation of blood constituents within the vascular system.

Mural thrombosis is the formation of multiple thrombi along an injured endocardial wall.

Pericarditis is inflammation of the pericardium - often with deposition of fibrin.

Mural thrombosis is the formation of multiple thrombi along an injured endocardial wall.

An occlusion is a blockage.