Myocardial Infarctions: Pathophysiology
Myocardial Infarctions
Occur when there is evidence of:
Myocardial injury is defined as elevated levels of cardiac troponin values.
Ischemia 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 surrounding border zone
Myocardial Infarctions: Timeline and Progression
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.
This 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:
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 resolution 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-infarction: 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 post-infarction: Granulation tissue starts to replace the yellow necrotic tissue.
Collagen deposition for scar formation begins.
2-8 Weeks: 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.
