Lecure 22: Pathology of MI Flashcards
Three classes of causes of ischemic heart disease
Conditions that influence supply of blood (90% of all cases due to obstructive atherosclerosis), conditions that influence O2 availability, increased O2 demand
Define myocardial infarction
Frank cardiac necrosis due to ischemia
MI is a result of…
Acute change in plaque –> thrombotic occlusion
MI sequence of events
- Intraplaque hemorrhage, etc –> 2. Platelets adhere to subendothelial collagen/plaque and activate, forming microthrombi –> 3. Vasospasm by mediators –> 4. Coagulation pathway activated –> 5. Thrombus expands, occluding vessel lumen
When coronary lumen is partially occluded, EKG finding? Fully occluded?
Non-ST segment elevation; ST-segment elevation MI
Where do we find coronary arteries (layer). Major coronary arteries (3) and what it supplies
Epicardium; Left anterior descending (anterior left ventricle/septum); Left circumflex (lateral left ventricle); Right coronary artery (right heart, posterior regions)
Two classes of MI
Subendocardial or transmural
What region of the heart is most vulnerable to ischemia?
Endocardium
How does the wavefront of necrosis during MI spread? (zones)
Subendocardium –> subepicardium
Define a transmural infarct
Ischemic necrosis involves full or nearly full thickness of the ventricular wall due to sustained obstruction (no intervention)
Do you see ST elevation with transmural infarct?
Yes
A subendocardial infarct is limited…
To inner 1/3 - 1/2 ventricular wall
Identify and describe both types of subendocardial infarct
Regional: transient/partial obstruction relieved before necrosis extends to full thickness; Circumferential: prolonged, severe hypotension superimposed on sub-critical coronary stenosis
Do you see ST elevation with subendocardial infarct?
No
Multifocal microinfarction involves what kind of vessels and usually presents as?
Pathology of smaller vessels; outcome is SCD due to fatal arrhythmia or ischemic dilated cardiomyopathy
Cells and MI: Caught early (describe)
Potentially reversible: low ATP, failure of Na-K pump, cellular swelling
Cells and MI: Caught late (timing and describe)
Non-reversible (20-30 minutes): disruption of sarcolemma, intracellular molecules leak out into blood (diagnostic)
What molecules leak out due to loss of sarcolemma integrity? Which is the best marker?
Troponin I, CK-MB, Myoglobin; Troponin I (levels stay high for many hours)
How fast does it take to deplete 50% ATP?
10 min
How long after an MI needs to pass before we can visualize pathology?
12 hours
What do we see in early infarct (4-24 hours)
Dark mottling due to stagnate blood
What do we see several days (1-3 days) into infarct?
Coagulative necrosis (loss of nuclei and striations) with neutrophils, grossly: yellow center
What do we see between 3-14 days after an infarct?
Macrophages (phagocytosis)/fibroblasts and granulation tissues at margins, grossly: yellow-tan coloring and red borders
What do we see after two weeks - several months after an infarct?
Dense collagen and no more inflammatory cells, grossly: gray-white scar
What happens after two months post-infarct?
Complete scar
Histologically, what can we see in
Wavy appearance of myoctyes
What is a special stain for early infarct?
C5b-9, which provides evidence of ischemia
Complications of MI (7)
Loss of contractile function, arrhythmia, myocardial rupture, aneurysms/thrombi, pericarditis (due to inflammation), papillary muscle rupture, heart failure
Describe myocardial rupture (where [3 in order of occurrence], when)
Rupture of ventricle wall –> cardiac tamponade OR rupture of septum –> left to right shunting OR papillary muscle rupture; 2-4 days post MI, but up to 2 weeks
What happens when papillary muscles rupture?
Sudden incompetence of mitral valve –> regurgitation –> DEATH
Why can MI lead to ventricular aneurysm? What is a complication?
Weakening of wall –> mural thrombus
Pericarditis can be of two flavors…
Acute (several days) or delayed (weeks to months later)
Does pericarditis tend to occur with subendocardial or transmural MI?
Transmural
What increases your risk of post-MI complications?
Large infarct (shock, arrhythmias, CHF), location, and wall thickness involved
How do we decrease severity of MI?
Reperfusion, as early as possible!
Consequence of reperfusion and possible mechanisms (4)
Reperfusion injury (oxidative stress, intracellular Ca2+ overload aggravated by ROS, inflammation due to now invading neutrophils, complement activation)
Histological findings of reperfuson injury
- Hemorrhage (leakage from injured vessels) and 2. Eosinophilic contraction bands in lethally injured cells (due to sudden influx of Ca2+)
