Ischemic Heart Disease--Nichols

Front 1

Cardiac myocytes deprived of blood supply start dying after how many minutes?

Back 1

20

Front 2

Death of the myocytes in a ____________________
myocardial infarction starts in the __________ zone, spreads in a wavefront to the ____________ zone and is usually complete after about _____________.

Back 2

Transmural (full thickness)
Subendocardial--> subpericaridal zone
3 hours

Front 3

What is the ECG evidence of ischemia?

Back 3

ST-segment depression
T wave inversion

Front 4

How long does it take for dead myocytes to show microscopic manifestations of their death?

What is the one exception?

Back 4

4 hours

Dead thin wavy myocytes my be visible as early as a half hour after infarction.

Front 5

What are the three components of coagulative necrosis of dead myocytes in classic (UNREPERFUSED) myocardial infarction?

Back 5

1. Loss of normal cytoplasmic striations
2. Cytoplasmic hypereosinophilia
3. Nuclear changes (pyknosis, karyorrhexis, karyolysis, loss)

Front 6

What is shown here?
What is this the earliest evidence of?
How early can you see it?

Back 6

Thin wavy myocytes: sometimes present,
sometimes the earliest microscopic evidence
of myocardial infarction, as early as 30 minutes
after it has occurred

Front 7

What is shown here?
What has not occurred yet?

Back 7

Cardiac myocyte coagulative necrosis in the narrow window after hypereosinophilia (and loss of striations, not evident here only because myocytes sectioned on end) have signaled necrosis, but before neutrophils have responded to the necrosis
�

Front 8

What is shown here?
When does this usually occur?

Back 8

Acute neutrophilic response to acute myocardial
infarction. This typically reaches maximum around 2 days.

Front 9

What is the karrorrhectic debris shown here? How does it arise? About how old would this infarct be?

Back 9

Since they only live for a day or 2, neutrophils
in an acute myocardial infarction begin contributing their breakdown debris after a few days and they yield much more karyorrhexic debris than cardiac
myocytes, so extensive nuclear dust (as seen here) is a feature of infarcts 3-6 days old.

Front 10

Describe the myocytolysis shown here.

Back 10

Thin subendocardial layer of cardiac myocytes that can get enough oxygen and nutrients from the cardiac luminal blood before it is pumped out to survive an infarct, survive, not prosper; they commonly catabolize their cytoplasmic contractile proteins (as seen here). Clearing of contractile proteins = MYOCYTOLYSIS.
�

Front 11

What is show in the image here?
What are the viable myocytes with myoctyolysis also called?

Back 11

Here is a higher power view of the same infarct showing some of the viable myocytes with myocytolysis, which is also referred to as hibernating myocardium, and non-viable (dead) myocytes with
coagulation necrosis (showing loss of striations, hypereosinophilia and loss of nuclei).

Front 12

Why are the neutrophils in the subendocardial region? What else enters in this manner?

Back 12

Because they come in from the edges (usually not including the subendocardial edge).

lymphocytes, macrophages and fibroblasts, who follow in the subacute healing phase.

Front 13

In classic (unreperfused) myocardial infarction, what enters in the early subacute phase (days 4-10)?

What happens in days 2-4?

Back 13

Infiltration by lymphocytes (bosses), first few at day 2 (sometimes), macrophages (garbage collectors), first few at day 3, fibroblasts (collagen engineers), first few at day 4, (+ / - eosinophils, plasma cells), beginning at the periphery
�

Front 14

What is this? About how many weeks after the infarct is this?

What types of cells do you see?

Back 14

This is a subacute (healing phase) myocardial infarction at 2-3 weeks with numerous fibroblasts and multiple new-grown blood vessels (neovascularization), which tend to come about the same time as fibroblasts, later than lymphocytes and
macrophages.

Front 15

Is this an early or late subacute infarct? How can you tell?

Back 15

This is a very late subacute infarct, almost completely converted to a scar. Just a few lymphocytes still hanging around (surveying the work of the macrophages and fibroblasts they bossed around).
�

Front 16

Lead V1-V4 correspond to what wall and coronary artery?

Back 16

Anterior, LAD

Front 17

Leads II, III, and AVF. What wall and coronary artery?

Back 17

Inferior, right

Front 18

Leads I, aVL, V5-V6. What wall and coronary artery?

Back 18

Lateral, left circumflex

Front 19

How many hours does it take for dead cardiac muscle to show macroscopic (gross) manifestations of death?

Back 19

12 hours

Front 20

Acute inflammation (neutrophils), clean-up (macrophages) and repair (fibroblasts) all come in from the edge of a myocardial infarction because why?
�

Back 20

There is no blood supply to bring them there (that's why it's infarcted.

Front 21

True or false.

The bigger the infarct, the longer it takes to heal and be converted to an acellular fibrous scar.

How long does a really big one take?

Back 21

True

3 months

Front 22

Classic myocardial infarction. Three locations.

Which is acute (hrs old), which is subacute (days old), and which is healed (weeks to years old?

Back 22

Answers.

Front 23

What is a transmural infarction?

Back 23

Involves the full thickness of the heart wall.

Front 24

What are 90% of transmural infarctions associated with?

Back 24

90% associated with occlusive thrombosis superimposed on atherosclerotic plaque with an acute change (disruption of an unstable vulnerable plaque by rupture or erosion)
�

Front 25

What does subendocardial infarction involve?
What will it look like?

Back 25

Involving inner portion of heart wall more likely to be patchy and to have episodic extension becoming more common than transmural.
�

Front 26

What are the nine effects of REPERFUSION?

Back 26

Myocardial Infarction: Reperfusion Effects
1. Smaller than it would have been
2. More patchy than it would have been
3. Hemorrhage into it
4. More contraction band necrosis
5. Accelerated inflammation and repair
6. Diffusion of inflammation and repair
7. Fewer neutrophils
8. More macrophages
9. More interstitial fibrosis

Front 27

What is the microscopic pathology of subacute phase (4-10 days old) reperfused myocardial infarction?

What changes in repair do you see?

Back 27

Lymphocytes (+/- eosinophils, +/- plasma cells), then granulation tissue, collagen. Accelerated inflammation and repair: appears about 1 day older at 2 days
2 days older at 4 days
4 days older at 6 days

Front 28

Describe the microscopic pathology of subacute phase reperfused myocardial infarction days 11-the end.

How much can healing be accelerated?

Back 28

Healing of a large infarct can be accelerated from 12 to 7 weeks, a small one done by 2

Patches of preserved myocardium commonly interspersed with scar(may make re-entrant ventricular arrhythmias more common)

Front 29

This myocardium has 3 zones: delineate, describe and diagnose each.

Back 29

Zone 1 = hypereosinophilia + loss of nuclei = coagulative necrosis
Zone 2 = vacuolated (cleared) cytoplasm = myocytolosis
Zone 3 = interstitial edema and viable myocytes

Front 30

A 55-year-old black male banker with a body mass index of 31 and 48 pack-year history of smoking ending 17 years ago has a 15-year history of diabetes
mellitus treated with metformin, hypercholesterolemia treated with atorvastatin, and hypertension treated with amlodipine and benazepril.

He volunteers to mow his mother’s lawn, collapses while doing so and is found dead.
Autopsy shows the following in his heart: What is the most likely cause of death?

Back 30

Myocardial infarction --> less than 4 hours old

Front 31

What is this? How is it normally?

Back 31

Front 32

What is this?

Back 32

Thin wavy myocytes
All dead and dead for a while --> nuclei have faded away.

Front 33

What is this?

Back 33

Amyloidosis = confluent and hyaline (smooth and featureless)

Front 34

This 37-year-old white female with a 22-year history of insulin-dependent diabetes was hospitalized 10 hours prior to death with chest pain and shortness of breath. Three months before, she had begun to experience progressive weakness and for the previous 3 weeks, she had increasing dyspnea on exertion and worsening of a chronic cough.

Describe and make two diagnoses. Why would fibrosis cause malignant ventricular arrhythmias? What is this called?

Back 34

Left ventricle = concentric hypertrophy > 1.4 cm, numerous irregular patches of white scarring

Hypertrophic heart disease
Scars from old MI
Non conducting tissue --> electrical signal bounces off and sends in all directions to myocytes that pass it on before normal signal. MALIGNANT RE-ENTRANT VENTRICULAR TACHYCARDIA

Front 35

There is a myocardial infarction between the arrows.
How old is it? How can you tell?

Back 35

5 days old
3 zones (innermost = yellow, mid = tan, outer = grey-tan)
Outer zone = young granulation tissue, many macrophages, not red because neovascularization comes later

Front 36

There is a cardiac rupture at the big arrow.
Where is it located relative to the infarct?
Why is it located there?
Why is it most likely at the time that it occurred relative to the infarct?

Back 36

Cardiac rupture
Edge of infarct = surviving muscle pulling on necrotic muscle

Necrotic muscle disintegrating into debris field --> consistency of water balloon on fifth day.

Front 37

When do you see thin wavy myocytes?

Back 37

MI first visible as early as 30 minutes = earliest finding

Front 38

What do you see with coagulation necrosis? When do you see it?

Back 38

MI
Hypereosinophilia + loss of striations + nuclear pyknosis, then karyorrhexis, karyolysis, loss first visible at 4-12 hours

Front 39

When do you see neutrophilic infiltration?

Back 39

MI (acute inflammation)
Follows myocyte necrosis
6-12 hours

Front 40

What is it?

Back 40

E = decreased neutrophil infiltration

Front 41

What is the answer

Back 41

(A) Cardiac rupture!

Front 42

Cardiac rupture is more common in which patients (5 things)?

When does it generally occur?

Back 42

Females (2x)
Elderly (>70)
Hypertension history
First MI
Anterior wall infarct

Occurs on the fifth day

Front 43

A 68-year-old white male bartender in Memphis, TN, with a history of smoking presents in February with worsening dyspnea and cough over several days.

Differential?

Back 43

HF due to IHD (silent MI)
Pneumonia (bacterial or viral)
PE
Autoimmune and idiopathic lung disease

Front 44

On further questioning, the dyspnea is on exertion and he has a chronic cough. He awakes at night sweaty, chilly, short of breath and coughing, but he has long had repeated nighttime awakening. He feels sick, has a stuffy nose, sore throat, muscle aches and joint aches, but his answers to questions are all vague and
he does not know what day it is. What could it be?

Back 44

Shock = confusion
Influenza = ill, malaise, nasal congestions, sore throat, muscle aches, and cough

Front 45

He appears ill and is obese. His temperature is 38, heart rate 110, blood pressure 110/60, respirations 29 and saturation 93%. His heart has an irregular rhythm, but no murmurs. He has bilateral basal pulmonary crackles. His abdomen is mildly distended, but not tender. He has mild ankle edema. His skin is cool and moist.

Now what do you think it could be?

Back 45

Causes of atrial fibrillation:

Heart failure, pneumonia, PE
Fever = infection
Ankle edema and bibasilar crackles = HF
Cool, moist skin = shock

Front 46

His BNP is 400 (normal <100), hemoglobin 14 (nl 13-17), WBC count 21.6 (nl 4.5-11) with 78% segs, platelets 190 (nl 150-400), Na 135 (nl 135-145), and K 4.8 (nl 3.5-5).

Now what do you think?

Back 46

Elevated BNP = HEART FAILURE
Elevated white blood cell count and neutrophilia = infectious pneumonia

Heart failure due to undiagnosed IHD and influenza pneumonia with sepsis --> precipitated HF

Front 47

What is the effect of sepsis on HF?

Back 47

Vasodilation and increased metabolism --> increased HR and CO to meet increased demand

If coronary atherosclerosis limits blood flow, increased demand on pump can cause it to fail.

Front 48

True or false.

Warm skin can differentiate shock from other types.

Back 48

Sometimes...but don't count on it!