Myocardial Infarction Flashcards
Myocardial ischemia
a condition of reversible inadequate blood supply to the heart due to fixed coronary stenosis, coronary vasospasm, increased myocardial demand, intraplaque hemmorhage, etc..
Stunned myocyte
myocytes injured by acute ischemia, they look normal microscopically, but need time to repair before they work normally again. Caused by myocytes acumulating calcium, oxygen derived free radicals, and damage to cytoplasmic proteins and organelles. Takes time to reverse.
What does chronic ischemia cause myocytes to do?
Causes myocytes to hunker down, catabolize (break down) their contractile proteins and revert to a primitive state limited to survival functions.
Myocardial infarction
irreversible necrosis of heart muscles due to prolonged ischemia greater than 20 minutes.
What exactly is chronic ischemia
Repeated episodes of ischemia too brief to cause infarction or inadequate perfusion that is low enough to injure but not to kill.
90% of MIs due to what
coronary atherosclerosis
0-12 hours, what phase and what findings for unreperfused myocardial infarction.
Acute phase, no findings
12-24 hours, what phase and what findings
Acute, progressive pallor
2-3 days
Acute, Yellow and softened
4-7 days
Subacute, Red border
1-6 weeks
Gradual replacement of yellow infarct by red granulation tissue
6-12 weeks
Gradual white scarring
Microscopic pathology of classical unreperfused acute MI
1-3 days: thin wavy myocytes
Coagulation necrosis, contraction band necrosis,
Day 2- lymphocyte proliferation
Day 3- Macrophages
Day 4- fibroblasts
Day 11-12: angiogenesis and fibroblast proliferation.
Contraction band necrosis
seen in the periphery of an infarct, results from the influx of calcium through damaged cell membranes.
Acute phase of reperfused MI
1-3 days, contraction band necrosis and hemorrhage
Earliest subacute phase of Reperfused MI
Lymphocytes presesnt, granulation tissue formed, then collagen
No-reflow phenomenon and hemorrhage
Examples of reperfusion injury. Basically in a reperfusion injury, cell membranes that have been rendered permeable by ischemia may allow excess calcium into the cells with reperfusion. Also, oxygen brought in by the restored blood flow may give rise to injurious oxygen free radicals. May also bring in overzealous inflammaotory cells.
Ischemic Preconditioning
Brief episodes of ischemia render the myocytes less vulnerable to infarct due to the induction of protective proteins
Transmural infarction
Full thickening of the heart wall. Often associated with occlusive thrombosis superimposed on an atherosclerotic plaque.
Coagulation necrosis components
hypereosinophilia, loss of striations, nuclear changes (pyknosis etc…) Coag necrosis is the major characteristic of unreperfused MI
Contraction band necrosis
hypereosinophilic bands of hypercontracted sarcomeres. A result of calcium influx through damaged cell membranes (hence the contraction band necrosis. Usually seen along the periphery. Seen often with reperfusion injury
Reperfusion MI occurs when:
When blood flow to ischemic cardiac myocytes is restored via angioplasty, thrombolytic therapy, coronary bypass, etc… You can save cells if you do it early enough. If not, it alters the appearnace and thats all
Reperfusion causes them to be
smaller, patchier, with hemorrhage
No-reflow phenomenon
seen in reperfusion when an attempt to restore blood flow to an ischemic area fails because of some obstruction casued by capillary swelling, thrombus, embolisms, etc…
