Pathology of Myocardia Ischemia and Infarction

Question 0

Can chronic ischemia lead to improved collateral blood flow?

Answer 0

yes.

Question 1

What is the cell-level result of MI?

Answer 1

Coagulative necrosis.

Question 2

When are changes from ischemia still entirely reversible?

Answer 2

20-40 minutes after it begins.

Question 3

What are the signs/symptoms of vasospasm induced (Printzmetal’s) ischemia?

Answer 3

Intermittent angina that isn’t acute, but occurs during rest. Often wakes people from sleep.

Question 4

What does it take to get a complete transmural infarction?

Answer 4

Usually the complete occlusion of an epicardial artery.

Question 5

Which myocytes die first?

Answer 5

The subendocardial myocytes die first, and necrosis progresses outward in a wavefront. (reaching maximum extent at 4-6 hours)

Question 6

What’s one way to get infarcted myocardial tissue without occluding an epicardial artery?

Answer 6

Shock can cause subendocardial infarction.

Question 7

Earliest change in ischemic myocytes visible by light microscopy?

Answer 7

Thin, wavy (stretched) myocytes.

Question 8

When post-MI is most coagulative necrosis visible?

Answer 8

6-24 hours.

Question 9

When, post-MI, is most PMN infiltration visible?

How about macrophages?

Answer 9

PMNs: 6hrs - 3 days.
Macs: 6hrs - 10 days (until clearance of all debris)

Question 10

When, post-MI, is granulation tissue at maximum levels?

Answer 10

2-4 weeks.

Question 11

When, post-MI, does a scar form?

Answer 11

8-10 weeks

Question 12

Vague timeline of changes in gross appearance of heart tissue post-MI?

Answer 12

Within 12hrs: no visible change.
Dark mottling from trapped deox. blood (12-24 hours)
It gets paler.
Then with granulation tissue, develops hyperemia. (3-10 days)

Question 13

How can you see very early ischemia (<12-24 hrs) in gross pathology of the heart?

Answer 13

TTC stain - stains LDH.
Only intact cells will still have LDH, and thus stain red.
Infarcted areas will be lighter.

Question 14

3 outcomes of reperfusion, at the cellular level?

Answer 14

Rescue of ischemic myocytes.
Altered pattern of necrosis: contraction banding.
Reperfusion injury

Question 15

What is thought to be the mechanism behind reperfusion injury?
How does it look different, grossly?

Answer 15

It’s thought to be mediated by the generation of free radicals. Can spread damage to healthy tissue.
Grossly, hemorrhage will be visible, due to damage to endothelial cells.

Question 16

Why can impaired contractility after reperfusion be an unreliable measure of damage from MI?

Answer 16

Myocytes may be initially stunned or hibernating, and thus not contracting well.

Question 17

What is contraction band necrosis? Why does it happen? How can you be sure these aren’t normal cells?

Answer 17

A form of necrosis that occurs with reperfusion of “doomed” myocytes. Membrane damage -> Ca++ builds up cytosol -> contractile elements contract.
These cells don’t have nuclei.

Question 18

How can MI lead to embolus generation?

Answer 18

Aneurysms and other alterations in flow, and dysfunctional endocardial cells can lead to thrombus generation that throws emboli.

Question 19

What might cause you to hear a “rub” in a patient several days post transmural MI?

Answer 19

Acute fibrinous pericarditis. This can cause chest pain… and a friction rub, but usually resolves spontaneously.

Question 20

How can an MI lead to cardiac tamponade?

Answer 20

If a free wall of the ventricle is perforated, hemopericardium can cause tamponade.