MI Pathology

Question 1

Ischemia

Answer 1

Injury resulting from hypoxia induced by reduced blood flow

Question 2

Effects of impaired inflow of blood

Answer 2

Reduced oxygen, reduced nutrients

Question 3

Effects of impaired outflow of blood

Answer 3

Insufficient removal of metabolites

Question 4

Ischemic heart disease

Answer 4

A group of syndromes that result from inadequate blood supply to meet the oxygen demands of the heart resulting from ischemia.

90% caused by coronary artery disease

Question 5

Principal presentations of ischemic heart disease

Answer 5

Angina
MI
Chronic IHD w/HF
Sudden Cardiac Death - regional ischemia causes fatal ventricular arrhythmia

Question 6

MI

Answer 6

Irreversible myocardial muscle damage caused by prolonged cardiac ischemia.
Discrete focus of ischemic muscle necrosis.

Question 7

Circumflex artery supplies

Answer 7

Lateral edge of left ventricle

Question 8

LAD supplies

Answer 8

Front and bottom of left ventricle. Anterior edge of IVSeptum

Question 9

RCA supplies

Answer 9

Blood to the right atrium, ventricle, and bottom of left ventricle, and posterior edge of septum. Also, PAPILLARY MUSCLE

Question 10

Progression of MI

Answer 10

Starts in the subendocardium and in the central portion of the area at risk. Progresses as a wavefront of necrosis moves from subendo to subepicardium

Question 11

Transmural infarct

Answer 11

Ischemic necrosis involves full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery.

Question 12

What causes transmural infarcts

Answer 12

Acute plaque change and superimposed thrombus with sustained obstruction.

Question 13

Common complications of transmural infarcts

Answer 13

Pericarditis or ventricular rupture

Question 14

Subendocardial infarct

Answer 14

ischemic necrosis limited to the inner 1/3 or 1/2 of the ventricular wall. Subendocardial zone is the least perfused and most vulnerable to any reduction in flow.

Question 15

Regional subendocardial infarct

Answer 15

transient obstruction of a coronary artery which is relieved before the necrosis extends across the full thickness of the myocardium.

Question 16

Circumferential subendocardial infarct

Answer 16

Due to prolonged severe hypotension.

Question 17

Multifocal microinfarction

Answer 17

Due to pathology only involving smaller intramural vessels.

Can be from microemboli, vasculitis, vascular spasm (cocaine/adrenaline)

Question 18

Outcome of multifocal microinfarcts

Answer 18

Sudden cardiac death due to fatal arrhythmia, ischemic dilated cardiomyopathy.

Question 19

What do the cellular consequences of myocardial ischemia depend on?

Answer 19

Severity and duration of the blood flow deprivation

Question 20

Characteristics of early ischemia

Answer 20

Switch from aerobic to anaerobic metabolism, decreased ATP and accumulation of lactate. Glycogen depletion. ATP deficiency leads to failure of NA K pump, so water rushes in. Mild cellular and mitochondrial swelling.

This is potentially reversible

Question 21

Characteristics of late ischemia

Answer 21

This occurs after 20-30 minutes of ischemia. Disruptions in the sarcolemma occur and intracellular molecules leak out (biomarkers).

Amorphous densities in the mitochondria.

This is non-reversible

Question 22

Effect of ischemia on mitochondria

Answer 22

Creation of amorphous densities

Question 23

Curve of ATP concentration vs minutes

Answer 23

Decreasing exponentially

Question 24

Curve of lactate concentration vs minutes

Answer 24

Increasing sigmoidally

Question 25

When is myocardial injury reversible

Answer 25

20-30 minutes after onset of severe ischemia. After that, dead myocardium starts to accumulate.

Question 26

When is myocardial loss of viability after MI complete?

Answer 26

6-12 hours after onset of severe ischemia

Question 27

``` Cellular consequences of myocardial ischemia over the course of: Seconds Minutes 20-30 Minutes 1 hour ```

Answer 27

Seconds: Onset of ATP depletion (cessation of aerobic metabolism Minutes: Decrease in contractility due to depletion of atp 20-30 Minutes: irreversible cell injury 1 Hour is microvascular injury

Question 28

Is MI apparent on gross exam?

Answer 28

Yes, but only after 12 hours or so

Question 29

Gross features 12-24 hours post MI

Answer 29

Dark Mottling due to coagulative necrosis. Reddish blue discoloration. Looks like red jello.

Question 30

Gross features3-7 days

Answer 30

Hyperemic border due to granulation tissue, central yellow-tan softening due to inflammatory infiltrates.

Question 31

Gross features >2 months

Answer 31

Complete scarring (grey-white)

Question 32

Microscopic features 12-24 hours post MI

Answer 32

Coagulative necrosis with wavy fibers

Question 33

Microscopic features 3-7 d

Answer 33

Neutrophils, macrophages and removal of necrotic tissue. Some granulation tissue (very congested vessels)

Question 34

Microscopic features >2 months

Answer 34

Fibrous tissue and collagenous scar stained blue with trichrome.

Question 35

Can you see histologic changes very early after infarction?

Answer 35

Not on H and E, but if you stain for complement you can!

Question 36

Features of coagulative necrosis

Answer 36

Loss of nuclei

Question 37

When are neutrophils most common?

Answer 37

1-3 days post MI

Question 38

When are macrophages most common?

Answer 38

3-7 days post MI

Question 39

Granulation tissue

Answer 39

Very congested vasculature, las lymphoid cells, fibroblasts, lots of capillaries even wtihout blood cells

Question 40

Does >2 months look like 10 years after MI?

Answer 40

Yes.

Question 41

Old MI Scar

Answer 41

Dense collagen fibrous tissue, no inflammatory infiltrates.

Question 42

Myocardial rupture

Answer 42

Due to softening and weakening of necrotic and inflamed myocardium. Rupture of free wall (most common) causes hemopericardium and cardiac tamponade. Happens in the first 2 weeks post MI Rupture of the Ventricular septum (L->R shunt can cause death) Papillary muscle rupture

Question 43

True aneurysms

Answer 43

Occur weeks->months post MI. Can cause incompetent mitral valve or mural thrombi.

Question 44

MI induced pericarditis

Answer 44

Happens with transmural thrombi only. Can cause fibrinous or fibrinohemorrhagic pericarditis.

Question 45

Dressler Syndrome

Answer 45

Autoimmune mediated pericarditis months after MI

Question 46

Proposed mechanisms of reperfusion injury

Answer 46

1. Oxidative stress from reoxygenation (ROS cause injuries) 2. Intracellular calcium overload (causes bands) 3. Inflammation (brings neutrophils) 4. Complement activation

Question 47

Common pathologic findings in reperfusion injury

Answer 47

Hemorrhage (due to leakage from weakened ischemic vessels) Contraction bands in lethally injured cells (exaggerated contraction of sarcomeres due to flooding of new plasma calcium)