Myocardial Ischemia and Infarction

Question 1

reversible inadequate blood supply

Answer 1

ischemia

Question 2

What is myocardial ischemia due to?

Answer 2

fixed coronary stenosis
increased myocardial demand
coronary vasospasm 
intraplaque hemorrhage
superimposed thrombosis
**any combo of these factors

Question 3

myocytes that look normal by microscopy but do not work

Answer 3

stunned myocytes

Question 4

fatal arrhythmia may precede ______

Answer 4

irreversible injury to myocytes/infarct

Question 5

T or F: fatal arrythmias can occur prior to in infarct

Answer 5

T

Question 6

Stunned myocytes are (reversible or irreversible)

Answer 6

reversible

Question 7

What causes stunned myocytes

Answer 7

ischemia

Question 8

T or F: stunned myocytes can initiate an arrhythmia

Answer 8

T

Question 9

myocyte with cytoplasm cleared of contractile proteins

Answer 9

hibernating myoctes (breaks doen the contractile protein for fuel to stay alive)

Question 10

chronically ishemic myocyte

Answer 10

hibernating myocytes

Question 11

acutely ischeic myocte

Answer 11

stunned myocytes

Question 12

growth into or enlargement of arteries in areas of chronic ischemia

Answer 12

collateral coronary arteries

• *not unique to the heart
• **neovascualrization and enlargement of existing ones

Question 13

myocytolysis

Answer 13

cleared cytoplasm of hibernating myocyte

Question 14

Hibernating myocyte is a reversible or irreversible cellular change

Answer 14

reversible; just need to make new contractile proteins

Question 15

T or F: rapid ischemia will result in collateral coronary arteries

Answer 15

F: ischemia must occur slowly

Question 16

irreversible necrosis of heart muscle from prolonged ischemia

Answer 16

myocardial infarction

Question 17

a myocyte can go without blood/O2 for ___ mins

Answer 17

20 mins

Question 18

In an MI, the infarction is thought to occur in a wavefront starting ____ (where) and not complete until ___ (time) after it started

Answer 18

subendocardial region

6 hrs

Question 19

MI involving full thickness of heart wall

Answer 19

transmural MI

Question 20

90% of transmural MIs are assc with

Answer 20

occlusive thrombosis superimposed on atherosclerotic plaque with an acute change (disruption of an unstable vulnerable plaque by ulceration or rupture)

Question 21

Surgery causes _____ state. How does this relate to artherlosclerosis?

Answer 21

hypercoagulable

• *imp for people that have artherlosclerotic disease = inc risk of MI, stroke, and death with surgery
• **superimposed thrombosis on artherlosclerosis

Question 22

What arteries does artherlosclerosis favor?

Answer 22

cerebral and coronary arteries

Question 23

MI involving the inner portion of the heart wall

Answer 23

subendocardial MI

Question 24

more likely to be patchy infarcts with episodic extension

Answer 24

subendocardial MI

Question 25

Can subendocardial MIs be detected with ECG?

Answer 25

not all the time | need greater than 1/3 of the wall thickness affected??

Question 26

``` gross pathology in unreperfused MI after... 0-12 hrs 12-24 hrs 2-3 days 4-7 days 1-6 weeks 6-12 weeks ```

Answer 26

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

Question 27

microscopic pathology at acute phase of MI: 1-3 hrs | 4-12 hrs

Answer 27

``` thin wavy myocytes coagualtion necrosis (hypereosinophillia + loss of striations + nuclear pyknosis --> karyorrhexis, karyolysis, loss) ```

Question 28

thin wavy myocytes

Answer 28

1-3 hrs after acute MI (irreversible)

Question 29

hypereosinophillia + loss of striations + nuclear pyknosis --> karyorrhexis, karyolysis, loss

Answer 29

coagulation necrosis | *visible 4-12 hrs after acute MI event

Question 30

loss of striations

Answer 30

coagulation necrosis (4-12 hrs post acute MI)

Question 31

follows myocyte necrosis and is first visible 6-12 hrs most MI, usually assc with edema and sometime hemorrhage; peaks at 3 days

Answer 31

neutrophillic infiltration

Question 32

neutrophils move in _____(time) after MI and peak ____ (time)

Answer 32

6-12 hrs | 3 days

Question 33

neutrophillic infiltration is assc with

Answer 33

edema and sometimes hemorrhage

Question 34

dense hypereosinophillic transverse bands of hyper-contracted sacromeres across dead myocytes

Answer 34

contraction brand necrosis

Question 35

hypercontracted sarcomeres

Answer 35

contraction brand necrosis

Question 36

When does contraction brand necrosis appear pos unreperfused MI

Answer 36

1-3 days

Question 37

infiltration by lymphocytes at day ___ macrophages appear at day ___ fibroblasts appear at day ___ ***they first appear at the periphery!!

Answer 37

2 3 4

Question 38

What is the order of cellular infiltration post MI?

Answer 38

``` neutrophils lymphocytes macrophages fibroblasts (+/- eosinophils and plasma cells) ```

Question 39

ingrowth of capillaries (angiogeneis) and proliferation of fibroblasts

Answer 39

granulation tissue

Question 40

for an unreperfused MI, granulation tissue at day ___ at what part of the heart tissue?

Answer 40

11 | periphery

Question 41

What pigments are found in macrophages post MI (also color)

Answer 41

lipofusion and hemosiderin | brown

Question 42

will pigment laiden macrophages be around at day 12?

Answer 42

yes

Question 43

Reperfusion effects after MI (1-9)

Answer 43

1. smaller then it would have been 2. more patchy 3. hemorrage into it 4. more contraction band necrosis 5. accelerated inflammation and repair 6. diffusion of infalmmation and repair 7. fewer neutrophils 8. more macrophages 9. more interstitial fibrosis (between myocytes)

Question 44

characteristic feature of reperfusion

Answer 44

hemorrhages

Question 45

Why is there more contraction in reperfusion?

Answer 45

reperfusion brings in more Ca but there is No ATP to release the contraction (due to lack of blood flow/O2)

Question 46

dark mottling and hemorrhage

Answer 46

acute phase (days 1-3) immediately following reperfusion

Question 47

dark mottling + brown (hemosiderin from broken down blood)

Answer 47

earliest subacut phase (days 4-5)

Question 48

Shrunken red + brown + bits of gray-white

Answer 48

days 6-10 early subacute reperfused

Question 49

Brown + intermingled gray-white

Answer 49

days 11-14 mid subacute reperfused

Question 50

Progressive white, intermingled normal

Answer 50

weeks 2-7 late subacute reperfused

Question 51

Acute phase of reperfused MI

Answer 51

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

Question 52

when flow is restored in major CA that had been occuleded but there is not re-flow

Answer 52

no-reflow phenomenon

Question 53

What causes no reflow phenomenon?

Answer 53

edema or microthrombi in capilaries | = disease in microvasculatore

Question 54

disease in microvasculature

Answer 54

no reflow phenomenon

Question 55

subacute phase of reperfused MI

Answer 55

acceleration of repair and scar formation Lymphocytes (+/- eosinophils, +/- plasma cells)--> Then granulation tissue--> collagen Accelerated inflammation and repair:

Question 56

reperfusion can lead to healing of a large infact by ___ and small infarts by ___

Answer 56

12-7 weeks | 2 weeks

Question 57

patches of preserved myocardium commonly interspereed scar may cause

Answer 57

re-entrant ventricular arrhythmias

Question 58

downside of reperfusion?

Answer 58

re-entrant ventricular arrhythmias

Question 59

What is the earliest finding of an unreperfused MI?

Answer 59

thin wavy myocytes

Question 60

In unreperfused MI, the granulation tissue is gradually replaced by ____

Answer 60

acellular fibrous collagen scar