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File:IPLab3HealedMyocardialInfarction8.jpg|This is a higher-power photomicrograph of a trichrome-stained section of heart containing an old healed MI. The scar tissue (mature fibrous connective tissue) is stained blue.
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== Study Questions ==
* <spoiler text="Why does this 37-year-old woman have such severe coronary atherosclerosis?">Diabetes mellitus is a major risk factor for developing premature atherosclerosis.</spoiler>
* <spoiler text="Why are there areas of acute myocardial injury in the section of myocardium from the patient with the old healed myocardial infarction?">This finding is very common in areas adjacent to an old infarction. If you remember from previous cases, there were areas of vacuolar change adjacent to the acute infarct. The areas adjacent to an infarct may still be alive but they will be at risk for additional ischemic insult. In this current case, the patient had several serious medical problems which may have caused hypotension and poor perfusion to the heart. Thus, the areas of risk could have been damaged leading to acute myocardial necrosis.</spoiler>
* <spoiler text="What is the time course of the normal inflammatory response after a myocardial infarction?">Few morphologic changes occur in the heart until approximately 6 to 12 hours after coronary occlusion. Subtle changes such as hypereosinophilia, coagulation necrosis and wavy fiber change can be seen during this early time period. If there is reperfusion of the myocardium there may be contraction band necrosis as well.
By two to three days there is an acute inflammatory cell infiltrate comprising primarily neutrophils.
At 5 to 10 days macrophages come in to phagocytose the necrotic myocardial tissue. As the dead tissue is being phagocytosed by macrophages, fibroblasts and blood vessels begin to grow into the area of infarction and form granulation tissue.
Fibroblasts lay down collagen and by two to three months the infarct is replaced by matured collagenous "scar" tissue.</spoiler>
{{IPLab 3}}
[[Category: IPLab:Lab 3]]