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Cardio Week 4 > Lecture 43: Ischemic Dirsorders of the Myocardium > Flashcards

Lecture 43: Ischemic Dirsorders of the Myocardium Flashcards

1
Q

What are the two types of ischemia?

A
  1. non-lethal
  2. lethal
    Ischemia = inadequate blood flow that leads to inadequate O2 and inadequate removal of waste
    Reperfusion can alter these events
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2
Q

What does lethal ischemia lead to?

A

Coagulative necrosis

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3
Q

What is ischemia caused by?

A
  1. reduced blood flow

2. increased myocardial demand

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4
Q

What is the most important cause of ischemic heart disease?

A

Atherosclerosis

Clinically important atherosclerosis affects epicardial coronary arteries

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5
Q

What is the layer most susceptible to ischemic injury?

A

Subendocardium because flow is from epicardial to endocardial, and is subjected to most resistance due to shear forces

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6
Q

Whats the collateral circulation like in the coronaries?

A

They are minimal but can form when there is a coronary occlusion

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7
Q

What are the earliest changes to myocardium in ischemia?

A
  1. switch from aerobic to anaerobic metabolism
  2. cessation of contraction
  3. altered electrical activity
  4. relaxation of myofibrils, allowing stretch of myocytes by still contracting adjacent myocardium
    Changes are reversible for up to 20-40 minutes
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8
Q

How long can myocardial tissue live without perfusion?

A

20 minutes

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9
Q

What happens if myocardium ischemic for >40 minutes?

A

First coagulative necrosis starting with most susceptible layer (subendocardium)
Necrosis followed by phagocytosis (polys then macrophages)
Healing by replacement with granulation tissue progressing to a scar

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10
Q

When you reperfuse myocardium, what modifications may the myocardium undergo?

A
  1. stunning
  2. precondition
  3. hibernation
  4. contraction band necrosis
  5. Reperfusion injury
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11
Q

When there is an occluded artery, what is the first part of myocardium to necrose?

A

The subendocarium

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12
Q

What are the clinical consequences of MI?

A
  1. silent angina
  2. stable angina pectoris (when pain is felt with increased workload/activity and is relieved with rest)
  3. Prinzmetal’s (variant) angina
    • Cardiac pain occurring during sleep
    • caused by vasospasm
  4. acute coronary syndromes (unstable angina)
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13
Q

What does stenosis of >75% lead to? >90%?

A

Angina during exercise

Angina during rest

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14
Q

What are the types of acute coronary syndromes?

A
  1. unstable (crescendo) angina
  2. acute MI
  3. sudden cardiac death
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15
Q

What are the susceptible plaques?

A 
30-60% narrowing
Thin fibrous caps
Morell ipid
Less SMC
More inflammation
Disruption leads to superimposed thrombus
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16
Q

What does incomplete obstruction by thrombus lead to?

A

Unstable angina
Subendocardial MI
Sudden death

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17
Q

What does complete obstruction lead to?

A

Transmural MI

Sudden death

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18
Q

What can happen to non-lethal thrombi?

A
  1. becomes organized and incorporated into the plaque

2. lysed either spontaneously or with medical intervention

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19
Q

What is the difference in consequence between total occlusion and less than total occlusion?

A

Total occlusion = transmural MI
Not total occlusion = subendocardial infarction
Shock can cause subendothelial infarction

20
Q

Why is there ST depression in subendocardial MI but ST elevation in trasmural MI?

A

Because movement of current in systole is from normal  ischemic tissue
Movement of currrent in diastole is from ischemic  normal
In systole for the transmural MI, current is going towards the lesion from BOTH SIDES so it is traveling towards the lead right above the lesion (it’s as if the current was traveling to same portion of the heart)
When it is just subendocardium however, the current will go from epidcardium to endocardium (so even though the current is converging, it will ultimately go in direction AWAYfrom the lead placed on the skin)
The green arrows = flow of current during DIASTOL, which makes sense because in diastole, flow moves from ischemic to normal
PT segment is also elevated/depressed during non-transmural/transmural injury respectively during diastole

21
Q

What are the initial microscopic changes in acute MI?

A

Thin wavy (stretched) myocytes
Occurs in minutes
IMMEDIATELY after infarct
Non-contractile myocardium

22
Q

What is the second microscopic change after acute MI?

A

6-24 hours
Coagulative necrosis
hypereosinophilia

23
Q

What is the third stage of change

After acute MI?

A

Poly infiltration
6hr-3 days
Top left

24
Q

What is the 4th stage of change

After acute MI?

A 
Infiltration of macrophages
7 days (top right)
25
Q

What is the 5th stage of change?

A

Granulation tissue (sprouting of new vessels)
Bottom left
2-4 weeks

26
Q

What is the 6th stage of MI change?

A

Collagen scar

8-10 weeks (bottom right)

27
Q

What is granulation tissue?

A

Combination of new vessels and fibroblasts

28
Q

How do the acute changes of MI progress?

A

From the periphery towards the center
Therefore the most advanced changes (furthest stage) is observed at the periphery
Necrotic (coagulatively necrotic, first stage) may persist in center for weeks or indefinitely

29
Q

What are the key characteristics of the microscopic changes for acute MI?

A

Starts at periphery and is dependent on blood supply
Changed most advanced then on periphery
Edges may not be well defined
Necrotic muscle maypersist in center of necrosis indefinitely

30
Q

What are gross features of the gross MI?

A
  1. no gross changes in first 12 hours
  2. dark mottling (trapped deox blood) 12-24 hours
  3. tan-yellow pallor 1-3 days due to necrosis
  4. hyperemic border with softened yellow, depressed pale necrotic center = 3-10 days
  5. gray-red depressed periphery (advancing granulation tissue) 10-14 days
  6. grey-white scar progressing from periphery to center
31
Q

What GROSS changes of the heart post-MI do we observe from 12-24 hours?

A 
Dark mottling
Trapped deoxygenated blood (thrombus)
Red = normal (because has TTZ)
White = infarcted (because no TTZ
Since it has no LDH)
32
Q

What is triphenyl tetrazolium chlorid (TTZ)? what changes in the MI heart can we see grossly with TTZ stain?

A

Stains for lactic dehydrogenase (LDH)
Red stain = myocardial cells intact because still retain LDH
NON-red stain = myocardial cells died prior to death and released all of its LDH

33
Q

What GROSS changes of the heart do we observe 1-3 days post MI?

A

tan-yellow pallor 1-3 days due to necrosis

34
Q

What GROSS changes of the heart do we observe 3-10 days post-MI?

A

Hyperemic border with softened yellow, depressed pale necrotic center = 3-10 days

35
Q

What GROSS changes of the heart do we observe 10-14 days post-MI?

A

gray-red depressed periphery (advancing granulation tissue) 10-14 days

36
Q

What GROSS changes of the heart do we observe weeks to months post-MI?

A

grey-white scar progressing from periphery to center

37
Q

What does reperfusion after ischmic injury accomplish?

A
  1. rescues non-lethally injured myocytes
  2. alters pattern of necrosis of dying cells and leads to CONTRACTION BAND necrosis
  3. can cause additional injury (reperfusion injury)
38
Q

How can reperfusion can injury?

A 
Caused by oxygen free radicals
Oxygen-derived free radicals can injure
Endothelium of microvessels, resulting
In hemorrhage converting ischemic
Infarct (white) to hemorrhagic (red) infarct
39
Q

What is preconditioning?

A

When you reperfuse myocardial tissue and tissue becomes less susceptible to subsequent lethal ischemia

40
Q

How can evaluating impaired contractility overestimate irreversibly injured myocardium?

A

Because hibernating and stunned myocardium can recover with reperfusion
They just cant contract at that time

41
Q

What are the characteristics of contraction band necrosis?

A

Scrunched up sarcomeres together
Caused by reperfusion of already lethally impaired myocytes prior to coagulative necrosis
Injured myocytes have leaky membranes that allow calcium ion influx and hypercontraction of myofibrils (which is why you see all these abnormal bands)
Notice that picture below has NO nuclei but scrunched up bands
These myocytes are non-functional

42
Q

What are the complications of MI?

A
  1. mural thrombus +/- embolization at regions of infarction
  2. dysrhythmias
  3. contractile dysfunction
    i. diastolic failure
    ii. systolic failure
  4. MV dysfunction
    i. mitral valve ring dilation
    ii. papillary muscle dysfunction
    iii. changed configuration of valveapparatus
  5. pericarditis (transmural MI only)
  6. Ventricular rupture of free wall, IV septum or papillary muscle
  7. aneurysm
  8. remodeling
    i. infarct expansion
    ii. distortion by scar
    iii. hypertrophy of remaining myocardium
    iv. chamber dilation
    v. interference with mitral valve apparatus
  9. possible role of TGF-beta and ACEi and ARBs
43
Q

What causes acute fibrinous pericarditis?

A

Acute pericarditis is caused by pericardial effusion and Dressler’s syndrome (development of antibodies to antigens in the heart that will then lead to autoimmune pericarditis
Seen as bread and butter (fibrinous) gross appearance

44
Q

When do you get perforation of the free wall of left ventricle?

A

3-6 days after MI
Occurs where the polys are going to be
At the edge of the dead tissue because it starts from the periphery

45
Q

What causes aneurysm formation?

A

A complication of transmural myocardial infarction

Due to progressive outward bulging and thinning of infarcted area

46
Q

What are the histological features of myocardial aneurysm?

A

Stained different color than myocardium because wall is fibrous

Cardio Week 4 (12 decks)

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