Myocardial Infarctions

• Occur when there is evidence of:
  – Myocardial injury is defined as elevated levels of cardiac troponin values.
  – Ischemia is occurs when there is an imbalance between oxygen supply and demand.
• Infarctions usually occur in the left ventricle, and damage may extend to the right ventricle or even the atria.
• The evolution of myocardial infarctions comprises processes of inflammation and repair in response to myocardial injury and ischemia.
  – Sustained ischemia leads to the death of cardiomyocytes and the release of their contents into the extracellular matrix.
  – The release of cell contents into the ECM triggers the inflammatory response, which is dominated by neutrophils.
  – Eventually, the necrotic cell debris is removed.
  – Collagen deposition and scar formation occurs.
• The healing process requires a balance between the processes of inflammation and tissue repair.
  – When these processes are out of balance, adverse remodeling can lead to heart failure, arrhythmias, and other complications.
  Review complications

• A common site of blockage is in the left anterior descending coronary artery.
• The “zone of perfusion” for this artery, which, due to the blockage, is now also the “area at risk” of ischemia and infarction.
  – Blockage in other coronary arteries puts different areas at risk.
• When blockage leads to significant ischemia, the area at risk becomes the area of infarction, which is characterized by a necrotic core and a surounding border zone

Evolution of myocardial infarction

• First, we illustrate some normal, healthy cardiac cells:
  – Branching, striated cells with intercalated discs and nuclei.

First 12 hours of myocardial infarction, cell death occurs.
– Coagulation necrosis begins, and cells spill their contents into the surrounding ECM.
– Microscopic changes include the appearance of “wavy fibers,” which are elongated myocardiocytes; their striations and nuclei become less apparent.
– The sarcolemma begins to malfunction, allowing the cell contents to spill.
– Results in edema and hemorrhaging, which further pushes the myocytes apart.
– Serum levels of key biomarkers, creatine kinase-MB (CK-MB) and cardiac troponin I, begin to rise.
– Arrhythmia, which is the direct result of cardiomyocyte cell dysfunction, is the most common cause of death in the early hours after myocardial infarction.

12-24 hours after infarction, the inflammatory process dominates.
– Coagulation necrosis continues, and neutrophils and other pro-inflammatory leukocytes infiltrate and digest the necrotic tissues.
– Dark mottling of the myocardium may become visible.
– Creatine kinase-MB and cardiac troponin levels peak at approximately 24 hours after infarction.

3 days post-infarction, the processes of inflammation repair and tissue repair begins.
– This is marked by a shift from pro-inflammatory cells to apoptotic neutrophils and phagocytic macrophages.
– Macrophages phagocytose the dying neutrophils as well as the necrotic tissue debris.
– In a gross image, we would see the development of a hyperemic border with a yellow-tan center at the area of the infarct.
– Pericarditis most commonly occurs around days 2 and 3 after infarct; it may be characterized by chest pain or an audible friction rub upon auscultation.

7 days post-infarct, phagocytic debris removal continues and granulation tissue begins to appear.
– Granulation tissue comprises proliferating myofibroblasts, loose collagen fibers, and newly forming capillaries and vascular tissues.
– In a gross image, show that we would see a hyperemic border with central softening, with a yellow appearance.
– Because of this softening in the myocardium, the risk of cardiac rupture is highest around days 4-7; rupture can involve a free wall, as we’ve shown in our illustration, or in a septum or papillary muscle.
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10-14 days Granulation tissue starts to replace the yellow necrotic tissue; collagen deposition for scar formation begins.

Weeks 2-8: grayish-white scar tissue develops from out outside border inwards towards the core.
– Dressler syndrome may develop; this is a delayed form of pericarditis thought to be caused by an autoimmune reaction.

3-6 months: a mature scar characterized by dense collagen occupies the area of infarction.
– True ventricular aneurysm is a potential late complication, in which the thin, scarred area of the heart wall bulges during systole; this can lead to heart failure, arrhythmias, or other complications.