IPLab:Lab 3:Acute Myocardial Infarction
This 78-year-old male experienced a posterior myocardial infarctionMyocardial 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. six years prior to this admission. Recently, he had begun to experience occasional anginaAngina pectoris is chest pain produced by myocardial ischemia, it worsens upon exertion.. 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 infarctionMyocardial 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. in addition to the healed posterior infarct. The patient progressively deteriorated with left ventricular failure and died with arrhythmiasArrhythmias are abnormal heart rhythms. and pulmonary edemaPulmonary 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.. Pertinent laboratory data are:
- Aspartate Aminotransferase (AST) 60 IU/L.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.
- Total Creatine Phosphokinase (CPK) 165 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. All of the activity was due to CPK III (MM) isoenzyme fraction; no CPK (MB) activity was detectable.
- Troponin ITroponin 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. 38 µg/L.
Examination of the heart showed a healed posterior infarct. The right coronary artery was completely occluded but partially recanalizedRecanalization is the process of the forming of channels through an organized thrombus so that blood flow is restored.. The left main coronary artery had severe atherosclerotic stenosis and a thrombusA thrombus is a solid mass resulting from the aggregation of blood constituents within the vascular system. filling the lumen. The entire anterolateral aspect of the left ventricle was soft with variegated areas appearing hyperemic or pale. There was extensive mural thrombosisMural thrombosis is the formation of multiple thrombi along an injured endocardial wall. and reactive pericarditisPericarditis is inflammation of the pericardium - often with deposition of fibrin..
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.
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.
The endocardium is usually the most severely damaged after an arterial occlusionAn occlusion is a blockage. 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 thrombusA thrombus is a solid mass resulting from the aggregation of blood constituents within the vascular system. formation.
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.
- Helft G, Worthley SG. Anti-thrombotic, anti-platelet and fibrinolytic therapy: current management of acute myocardial infarction. Heart Lung Circ 2001;10(2):68-74.
Related IPLab Cases
- Lab 1: Heart: Myocardial Infarction (Coagulative Necrosis)
- Lab 3: Heart: Healed Myocardial Infarction
- Lab 4: Heart: Mural Thrombus
- Lab 4: Coronary Artery: Thrombosis
- Lab 4: Lung: Pulmonary Congestion and Edema