Pathology of Myocardia Ischemia and Infarction Flashcards
Can chronic ischemia lead to improved collateral blood flow?
yes.
What is the cell-level result of MI?
Coagulative necrosis.
When are changes from ischemia still entirely reversible?
20-40 minutes after it begins.
What are the signs/symptoms of vasospasm induced (Printzmetal’s) ischemia?
Intermittent angina that isn’t acute, but occurs during rest. Often wakes people from sleep.
What does it take to get a complete transmural infarction?
Usually the complete occlusion of an epicardial artery.
Which myocytes die first?
The subendocardial myocytes die first, and necrosis progresses outward in a wavefront. (reaching maximum extent at 4-6 hours)
What’s one way to get infarcted myocardial tissue without occluding an epicardial artery?
Shock can cause subendocardial infarction.
Earliest change in ischemic myocytes visible by light microscopy?
Thin, wavy (stretched) myocytes.
When post-MI is most coagulative necrosis visible?
6-24 hours.
When, post-MI, is most PMN infiltration visible?
How about macrophages?
PMNs: 6hrs - 3 days.
Macs: 6hrs - 10 days (until clearance of all debris)
When, post-MI, is granulation tissue at maximum levels?
2-4 weeks.
When, post-MI, does a scar form?
8-10 weeks
Vague timeline of changes in gross appearance of heart tissue post-MI?
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)
How can you see very early ischemia (<12-24 hrs) in gross pathology of the heart?
TTC stain - stains LDH.
Only intact cells will still have LDH, and thus stain red.
Infarcted areas will be lighter.
3 outcomes of reperfusion, at the cellular level?
Rescue of ischemic myocytes.
Altered pattern of necrosis: contraction banding.
Reperfusion injury
What is thought to be the mechanism behind reperfusion injury?
How does it look different, grossly?
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.
Why can impaired contractility after reperfusion be an unreliable measure of damage from MI?
Myocytes may be initially stunned or hibernating, and thus not contracting well.
What is contraction band necrosis? Why does it happen? How can you be sure these aren’t normal cells?
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.
How can MI lead to embolus generation?
Aneurysms and other alterations in flow, and dysfunctional endocardial cells can lead to thrombus generation that throws emboli.
What might cause you to hear a “rub” in a patient several days post transmural MI?
Acute fibrinous pericarditis. This can cause chest pain… and a friction rub, but usually resolves spontaneously.
How can an MI lead to cardiac tamponade?
If a free wall of the ventricle is perforated, hemopericardium can cause tamponade.
