Pathology: Myocardial Infarction
1. Discuss myocardial infarction and its pathogenesis.
2. Describe the sequence of changes involved in myocardial infarction.
3. List the major physiologic and morphologic complications of myocardial infarction.
4. Describe management of myocardial infarction.
5. Discuss patient teaching of myocardial infarction.
Myocardial infarction (MI), commonly known as a heart attack, is an irreversible necrosis of the heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a ...view middle of the document...
The damage in the myocardium is essentially the result of a tissue response that includes apoptosis (cell death) and inflammatory changes. Therefore, the heart of patients who suddenly die from an acute coronary event may show little or no evidence of damage response to the myocardium at autopsy. The typical MI initially manifests as coagulation necrosis that is ultimately followed by myocardial fibrosis. Contraction-band necrosis is also seen in many patients with ischemia. This is followed by reperfusion, or it is accompanied by massive adrenergic stimulation, often with concomitant myocytolysis. The left coronary artery system covers more territory than does the right coronary artery system; therefore, a MI in this system is most likely to produce extensive injury, with impairment of function, pulmonary congestion, and low cardiac output. Thus, the pathogenesis can include:
• Occlusive intracoronary thrombus - a thrombus overlying a plaque causes 75% of myocardial infarctions, with superficial plaque erosion present in the remaining 25%.
• Vasospasm - with or without coronary atherosclerosis and possible association with platelet aggregation.
• Emboli - from left sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale. ("The internet pathology," 2011)
The molecular events during MI relate to the initial ischemic event, reperfusion, and subsequent inflammatory response. Up to 6 hours following the initial ischemic event, most cell loss occurs via apoptosis. After that, necrosis predominates. Ischemic endothelial cells express adhesion molecules that attract neutrophils that subsequently migrate into damaged myocardium.
Evolution of Morphologic Changes in Myocardial Infarction:
Time Gross Features Light Microscopic Findings
0-½ hr None ultra structural changes (reversible with reperfusion up to approximately 20 minutes ischemic time)
½-4hr None Usually none; variable waviness of fibers at border
4-12hr Occasionally dark mottling Beginning coagulation necrosis; edema; hemorrhage
12-24hr Dark mottling Ongoing coagulation necrosis; pyknosis of nuclei; marginal contraction band necrosis; beginning neutrophilic infiltrate
1-3 days Mottling with yellow-tan infarct center Coagulation necrosis, with loss of nuclei and striations; interstitial infiltrate of neutrophils
3-7 days Hyperemic border; central yellow-tan softening Beginning disintegration of dead myofibers, with dying neutrophils; early phagocytosis of dead cells by macrophages at infarct border
7-10 days Maximally yellow-tan and soft, with depressed red-tan margins Well-developed phagocytosis of dead cells; early formation of fibro-vascular granulation tissue at margins
10-14 days Red-gray depressed infarct borders Well-established granulation tissue with new blood vessels and collagen deposition
2-8wk Gray-white scar, progressive from...