Lecure 22: Pathology of MI

Question 1

Three classes of causes of ischemic heart disease

Answer 1

Conditions that influence supply of blood (90% of all cases due to obstructive atherosclerosis), conditions that influence O2 availability, increased O2 demand

Question 2

Define myocardial infarction

Answer 2

Frank cardiac necrosis due to ischemia

Question 3

MI is a result of…

Answer 3

Acute change in plaque –> thrombotic occlusion

Question 4

MI sequence of events

Answer 4

1. 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

Question 5

When coronary lumen is partially occluded, EKG finding? Fully occluded?

Answer 5

Non-ST segment elevation; ST-segment elevation MI

Question 6

Where do we find coronary arteries (layer). Major coronary arteries (3) and what it supplies

Answer 6

Epicardium; Left anterior descending (anterior left ventricle/septum); Left circumflex (lateral left ventricle); Right coronary artery (right heart, posterior regions)

Question 7

Two classes of MI

Answer 7

Subendocardial or transmural

Question 8

What region of the heart is most vulnerable to ischemia?

Answer 8

Endocardium

Question 9

How does the wavefront of necrosis during MI spread? (zones)

Answer 9

Subendocardium –> subepicardium

Question 10

Define a transmural infarct

Answer 10

Ischemic necrosis involves full or nearly full thickness of the ventricular wall due to sustained obstruction (no intervention)

Question 11

Do you see ST elevation with transmural infarct?

Answer 11

Yes

Question 12

A subendocardial infarct is limited…

Answer 12

To inner 1/3 - 1/2 ventricular wall

Question 13

Identify and describe both types of subendocardial infarct

Answer 13

Regional: transient/partial obstruction relieved before necrosis extends to full thickness; Circumferential: prolonged, severe hypotension superimposed on sub-critical coronary stenosis

Question 14

Do you see ST elevation with subendocardial infarct?

Answer 14

No

Question 15

Multifocal microinfarction involves what kind of vessels and usually presents as?

Answer 15

Pathology of smaller vessels; outcome is SCD due to fatal arrhythmia or ischemic dilated cardiomyopathy

Question 16

Cells and MI: Caught early (describe)

Answer 16

Potentially reversible: low ATP, failure of Na-K pump, cellular swelling

Question 17

Cells and MI: Caught late (timing and describe)

Answer 17

Non-reversible (20-30 minutes): disruption of sarcolemma, intracellular molecules leak out into blood (diagnostic)

Question 18

What molecules leak out due to loss of sarcolemma integrity? Which is the best marker?

Answer 18

Troponin I, CK-MB, Myoglobin; Troponin I (levels stay high for many hours)

Question 19

How fast does it take to deplete 50% ATP?

Answer 19

10 min

Question 20

How long after an MI needs to pass before we can visualize pathology?

Answer 20

12 hours

Question 21

What do we see in early infarct (4-24 hours)

Answer 21

Dark mottling due to stagnate blood

Question 22

What do we see several days (1-3 days) into infarct?

Answer 22

Coagulative necrosis (loss of nuclei and striations) with neutrophils, grossly: yellow center

Question 23

What do we see between 3-14 days after an infarct?

Answer 23

Macrophages (phagocytosis)/fibroblasts and granulation tissues at margins, grossly: yellow-tan coloring and red borders

Question 24

What do we see after two weeks - several months after an infarct?

Answer 24

Dense collagen and no more inflammatory cells, grossly: gray-white scar

Question 25

What happens after two months post-infarct?

Answer 25

Complete scar

Question 26

Histologically, what can we see in

Answer 26

Wavy appearance of myoctyes

Question 27

What is a special stain for early infarct?

Answer 27

C5b-9, which provides evidence of ischemia

Question 28

Complications of MI (7)

Answer 28

Loss of contractile function, arrhythmia, myocardial rupture, aneurysms/thrombi, pericarditis (due to inflammation), papillary muscle rupture, heart failure

Question 29

Describe myocardial rupture (where [3 in order of occurrence], when)

Answer 29

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

Question 30

What happens when papillary muscles rupture?

Answer 30

Sudden incompetence of mitral valve –> regurgitation –> DEATH

Question 31

Why can MI lead to ventricular aneurysm? What is a complication?

Answer 31

Weakening of wall –> mural thrombus

Question 32

Pericarditis can be of two flavors…

Answer 32

Acute (several days) or delayed (weeks to months later)

Question 33

Does pericarditis tend to occur with subendocardial or transmural MI?

Answer 33

Transmural

Question 34

What increases your risk of post-MI complications?

Answer 34

Large infarct (shock, arrhythmias, CHF), location, and wall thickness involved

Question 35

How do we decrease severity of MI?

Answer 35

Reperfusion, as early as possible!

Question 36

Consequence of reperfusion and possible mechanisms (4)

Answer 36

Reperfusion injury (oxidative stress, intracellular Ca2+ overload aggravated by ROS, inflammation due to now invading neutrophils, complement activation)

Question 37

Histological findings of reperfuson injury

Answer 37

1. Hemorrhage (leakage from injured vessels) and 2. Eosinophilic contraction bands in lethally injured cells (due to sudden influx of Ca2+)