Myocardial Ischemia and Infarction Flashcards
reversible inadequate blood supply
ischemia
What is myocardial ischemia due to?
fixed coronary stenosis increased myocardial demand coronary vasospasm intraplaque hemorrhage superimposed thrombosis **any combo of these factors
myocytes that look normal by microscopy but do not work
stunned myocytes
fatal arrhythmia may precede ______
irreversible injury to myocytes/infarct
T or F: fatal arrythmias can occur prior to in infarct
T
Stunned myocytes are (reversible or irreversible)
reversible
What causes stunned myocytes
ischemia
T or F: stunned myocytes can initiate an arrhythmia
T
myocyte with cytoplasm cleared of contractile proteins
hibernating myoctes (breaks doen the contractile protein for fuel to stay alive)
chronically ishemic myocyte
hibernating myocytes
acutely ischeic myocte
stunned myocytes
growth into or enlargement of arteries in areas of chronic ischemia
collateral coronary arteries
- *not unique to the heart
- **neovascualrization and enlargement of existing ones
myocytolysis
cleared cytoplasm of hibernating myocyte
Hibernating myocyte is a reversible or irreversible cellular change
reversible; just need to make new contractile proteins
T or F: rapid ischemia will result in collateral coronary arteries
F: ischemia must occur slowly
irreversible necrosis of heart muscle from prolonged ischemia
myocardial infarction
a myocyte can go without blood/O2 for ___ mins
20 mins
In an MI, the infarction is thought to occur in a wavefront starting ____ (where) and not complete until ___ (time) after it started
subendocardial region
6 hrs
MI involving full thickness of heart wall
transmural MI
90% of transmural MIs are assc with
occlusive thrombosis superimposed on atherosclerotic plaque with an acute change (disruption of an unstable vulnerable plaque by ulceration or rupture)
Surgery causes _____ state. How does this relate to artherlosclerosis?
hypercoagulable
- *imp for people that have artherlosclerotic disease = inc risk of MI, stroke, and death with surgery
- **superimposed thrombosis on artherlosclerosis
What arteries does artherlosclerosis favor?
cerebral and coronary arteries
MI involving the inner portion of the heart wall
subendocardial MI
more likely to be patchy infarcts with episodic extension
subendocardial MI
Can subendocardial MIs be detected with ECG?
not all the time
need greater than 1/3 of the wall thickness affected??
gross pathology in unreperfused MI after... 0-12 hrs 12-24 hrs 2-3 days 4-7 days 1-6 weeks 6-12 weeks
0-12 hrs: none
12-24 hrs: progressive pallor
2-3 days: yellow
4-7 days: red boarder (granulation tissue)
1-6 weeks: yellow –> red (granulation tissue) *thinning of wall @ infarct and thickening at other parts of wall
6-12 weeks: gradual white scarring –> thinned wall
microscopic pathology at acute phase of MI: 1-3 hrs
4-12 hrs
thin wavy myocytes coagualtion necrosis (hypereosinophillia + loss of striations + nuclear pyknosis --> karyorrhexis, karyolysis, loss)
thin wavy myocytes
1-3 hrs after acute MI (irreversible)
hypereosinophillia + loss of striations + nuclear pyknosis –> karyorrhexis, karyolysis, loss
coagulation necrosis
*visible 4-12 hrs after acute MI event
loss of striations
coagulation necrosis (4-12 hrs post acute MI)
follows myocyte necrosis and is first visible 6-12 hrs most MI, usually assc with edema and sometime hemorrhage; peaks at 3 days
neutrophillic infiltration
neutrophils move in _____(time) after MI and peak ____ (time)
6-12 hrs
3 days
neutrophillic infiltration is assc with
edema and sometimes hemorrhage
dense hypereosinophillic transverse bands of hyper-contracted sacromeres across dead myocytes
contraction brand necrosis
hypercontracted sarcomeres
contraction brand necrosis
When does contraction brand necrosis appear pos unreperfused MI
1-3 days
infiltration by lymphocytes at day ___
macrophages appear at day ___
fibroblasts appear at day ___
***they first appear at the periphery!!
2
3
4
What is the order of cellular infiltration post MI?
neutrophils lymphocytes macrophages fibroblasts (+/- eosinophils and plasma cells)
ingrowth of capillaries (angiogeneis) and proliferation of fibroblasts
granulation tissue
for an unreperfused MI, granulation tissue at day ___ at what part of the heart tissue?
11
periphery
What pigments are found in macrophages post MI (also color)
lipofusion and hemosiderin
brown
will pigment laiden macrophages be around at day 12?
yes
Reperfusion effects after MI (1-9)
- smaller then it would have been
- more patchy
- hemorrage into it
- more contraction band necrosis
- accelerated inflammation and repair
- diffusion of infalmmation and repair
- fewer neutrophils
- more macrophages
- more interstitial fibrosis (between myocytes)
characteristic feature of reperfusion
hemorrhages
Why is there more contraction in reperfusion?
reperfusion brings in more Ca but there is No ATP to release the contraction (due to lack of blood flow/O2)
dark mottling and hemorrhage
acute phase (days 1-3) immediately following reperfusion
dark mottling + brown (hemosiderin from broken down blood)
earliest subacut phase (days 4-5)
Shrunken red + brown + bits of gray-white
days 6-10
early subacute
reperfused
Brown + intermingled gray-white
days 11-14
mid subacute
reperfused
Progressive white, intermingled normal
weeks 2-7
late subacute
reperfused
Acute phase of reperfused MI
contraction band necrosis with hemorrhage
immediately following reperfusion
Coagulation necrosis (center of big infarct)
Neutrophilic infiltration (acute inflammation) following myocyte necrosis, first visible 2 hours following reperfusion, decreased with reperfusion
when flow is restored in major CA that had been occuleded but there is not re-flow
no-reflow phenomenon
What causes no reflow phenomenon?
edema or microthrombi in capilaries
= disease in microvasculatore
disease in microvasculature
no reflow phenomenon
subacute phase of reperfused MI
acceleration of repair and scar formation
Lymphocytes (+/- eosinophils, +/- plasma cells)–>
Then granulation tissue–> collagen
Accelerated inflammation and repair:
reperfusion can lead to healing of a large infact by ___ and small infarts by ___
12-7 weeks
2 weeks
patches of preserved myocardium commonly interspereed scar may cause
re-entrant ventricular arrhythmias
downside of reperfusion?
re-entrant ventricular arrhythmias
What is the earliest finding of an unreperfused MI?
thin wavy myocytes
In unreperfused MI, the granulation tissue is gradually replaced by ____
acellular fibrous collagen scar
