Path 1: Atherosclerosis and Ischemic Heart Dz Flashcards

1
Q
A

Aortic Dissection

The right carotid artery is compressed by blood dissecting upward from a tear with aortic dissection. Blood may also dissect to coronary arteries. Thus patients with aortic dissection may have symptoms of severe chest pain (for distal dissection) or may present with findings that suggest a stroke (with carotid dissection) or myocardial ischemia (with coronary dissection).

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1
Q
  1. Was there a rupture in this case?
  2. Where is the blood?
A

Aortic Dissection

  1. Yes. This was an aortic dissection with a rupture.
  2. The blood is in the media.

Microscopically, the tear (arrow) in this aorta extends through the media, but blood also dissects along the media (asterisk).

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2
Q
  1. Explain how a plaque is formed.
  2. What is the process leading from plaque disruption to severe fixed coronary obstruction (chronic ischemic heart dz)?
  3. Plaque disruption can lead to what two types of thrombi?
  4. What are some of the major complications of a plaque?
A

Coronary Atherosclerosis:

1. You got this!

2. Healing

3. Mural thrombi with variable obstruction AND occlusive thrombi

  • *4.** Complications:
    1. Critical stenosis of lumen
    2. Acute thrombosis
    3. Hemorrhage into plaque
    4. Aneurysm and rupture of wall
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2
Q

What are the components of an atherosclerotic plaque?

A

Coronary Atherosclerosis: Atherosclerotic plaque is composed of varying proportions of:

Cells: smooth muscle cells, fibroblasts, macrophages, leukocytes

Connective tissue: collagen, elastic fibers, proteoglycans

Lipid: intracellular and extracellular

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3
Q
  1. What is this?
  2. What are the white streaks?
A

Aortic Atherosclerosis

  1. Atheroembolism ??
  2. Cholesterol clepts
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4
Q
  1. The histologic appearance of a myocardial infarct is dependent on the ___ of the infarct.
  2. Predict the time frame for each stage in the photo.
A

Histology of MI

  1. The histologic appearance of a myocardial infarct is dependent on the age of the infarct. Thus, infarcts can be “dated” by the microscopic characteristics, as outlined in Table
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4
Q
  1. What major event is occuring here?
  2. What is the time frame for when this occurs?
  3. What kind of cells are predominant now?
  4. What are those red horizontal streaks?
A

Histology of MI

  1. Repair
  2. About 5-7 days (towards end of 1st week, but max granulation tissue at 10 days-2 weeks)
  3. Mononuclear cells like monocytes are now infiltrating. The neutrophils were the first responders but by now they have already undergone apoptosis.
  4. The streaks are capillaries at the periphery of the infacrt. The caps cause dark red boarders at about 1 week old = neovascularization!
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5
Q
  1. What is this?
  2. What are some RF’s for aortic dissection?
A

Aortic Dissection

  1. Cross section of aorta. Blood clot formed–> aortic dissection –> blood clot now compressing the lumen. Note how the blood is dissection through the media and adventitia –> can lead to tamponade.
  2. RF’s
    - HTN
    - CT disorders like Marfan’s syndrome –> mutation in fibrillin protein, which associates with elastic fibers
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6
Q
  1. What are the two white spaces and why are they there?
  2. What does this indicate?
A

Coronary Atherosclerosis:

  1. A thrombi formed in the darkish space on the left. Then, over time, the body tries to organize the thrombi and macrophages try to remove it = forms another lumen as they chomp away!
  2. Two lumens would imply prior thrombosis and RECANALIZATION.
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7
Q
  1. What is this?
A

Aortic Atherosclerosis

  1. Infra-renal abdominal aortic aneurysm. Atherosclerosis commonly affects the infra-renal abdominal aorta, but may affect any region.
    - May see ulceration/plaque rupture, which may not be symptomatic
    - Diseased aorta can develop into an aneurysm, an abnormal localized dilatation of the aortic wall
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8
Q

How many days post MI?

A

Histology of MI

  • Days 3-7
  • Hyperemic border due to hemorrhage
  • No cross striations
  • hemorragic necrosis (RBCs in there??
  • Reperfusion myocardium??
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8
Q
  1. What kind of cells do you see here?
  2. How many days post MI?
A

Histology of MI

  1. PMNs! Neutrophils! Infiltrate infected myocardium.
  2. About 1-3 days?
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9
Q
  1. What is the difference between type A and type B aortic dissections?
A
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10
Q
  1. What is this?
  2. What causes the pale tissue?
  3. What is significant about the rim of the palor area?
  4. If this is a bird’s eye view looking down into the heart, occlusion in what coronary artery most likely caused this necrotic tissue?
A

Acute MI

  1. Left and right ventricles
  2. Necrosed tissue does not receive blood and thus turns pale.
  3. The rim of the palor area is dark red. This is granulation tissue that will form new vessels = neovascularization. This occurs as the body tries to repair the damaged tissue.
  4. Infarct is in the L anterior wall and in the anterior 2/3 of the interventricular septal wall. Therefore, occlusion was mostly likely in the LAD.

- 5-7 days (UTAH)

1-3 weeks (KAYA)

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10
Q
  1. What is this?
  2. What can this lead to?
A

Aortic Dissection

  1. Aortic dissection moving back towards the heart.
  2. Hemopericardium and tamponade.

Aortic dissection can lead to hemopericardium (blood dissects through the media proximally), which can lead to tamponade.

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11
Q
  1. What is this!?
  2. What coronary artery was this?
  3. When is the heart most susceptible to this complication?
A

Complications of MI

1. Ventricular rupture (myocardium)

  • Results from weakening of myocardium (due to necrosis and progressive removal of necrotic tissue) following transmural myocardial infarction
  • Occurs most frequently 3-5 days following MI
  • Three types seen in next slides.
    2. LAD because apex affected
    3. Around 3-5 days is when the myocardium is weakest because macrophages come and collect debris BEFORE collagen is deposited. Therefore the walls are fragile and can break.
  • could cause a cardiac tamponade
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13
Q
A

Normal Heart: Coronary Artery

  • muscular (thick media of smooth muscles)
  • large open lumen
  • epicardial fat
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13
Q
  1. What is this?
A

Remote MI

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13
Q
  1. What kind of rupture is this?
A

Complications of MI

  1. Rupture of papillary muscle of mitral valve: Acute valvular insufficiency
    - MI affected mitral valve –> valve incompetence
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13
Q
  1. Characterize these three aortas as normal, moderate athero, or severe athero.
  2. What do you call a thrombi that breaks off from the atherosclerosis?
A

Aortic Atherosclerosis

  1. Top= Severe (ruptured); Middle= moderate; Bottom= normal
  2. Atheroembolus.
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15
Q
A

Coronary Atherolerosis

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16
Q
  1. What kind of rupture is this?
A

Complications of MI

  1. Rupture of LV free wall: Hemopericardium and cardiac tamponade
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17
Q

What days is the heart most susceptible to rupture, especially AFTER a previous MI just 3 weeks prior?

A

Complications of MI

Days 3-5

In cross section, the point of rupture of the myocardium is shown with the arrow. In this case, there was a previous myocardial infarction 3 weeks before, and another myocardial infarction occurred, rupturing through the already thin ventricular wall 3 days later.

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18
Q
  1. How would you characterize an old MI?
  2. Where is the old MI in this photo?
A

​Remote MI

  1. An old myocardial infarct is characterized by scar tissue, in which the normal myocardium is replaced by fibrous connective tissue. Typically, the scar tissue is firm, white, and the ventricular wall thinned as compared to the uninvolved myocardium.
  2. LV??
18
Q
  1. What kind of necrosis was this?
  2. What do you notice about the nuclei?
  3. How long does this take to show?
A

Histology of MI

  1. Coagulative Necrosis
  2. In coagulative necrosis, there is a loss of nuclei! Left with the ghost of cytoplasm.
  3. This takes about 12 + hours to show and is well developed after 24 hours.
    - earliest change you can see under scope
19
Q

What major event occured here? What kind of clot is forming?

A

Coronary Atherosclerosis:

- Rupture of plaque –> exposed collagen –> thrombus formation with fibrin (pink)

  • Fibrin clot narrowing the lumen
20
Q
A

Aortic Atherosclerosis

22
Q
A

Normal Heart: Aortic valve with thin, delicate cusps. Note orifices of coronary arteries.

22
Q
A

Complications of MI

  • fibrous pericarditis ???
24
Q
A

Coronary Atherosclerosis: Coronary Artery

  • Yellow atherosclerotic plaque
  • Thrombus caused by rupture
26
Q

ID:

  • Ascending Aorta
  • Epicardial Fat
  • LAD
  • RV
  • LV
A

Normal Heart: External view of normal heart with epicardial fat containing coronary artery (LAD) and smooth visceral pericardium

27
Q
A

Normal Heart

28
Q
  1. What is this?
  2. What kind of symptoms would you expect to see in aortic dissection?
  3. Where does blood usually go in a dissection? Is it the same thing as a rupture?
A

Aortic Dissection

  1. Dissection of the ascending aorta.
  2. Tearing pain that radiates to the back.
  3. A rupture and dissection are not the same thing. In a dissection, blood can somehow get into the intima layer and dissect the layers forming a pseudo-canal. This can lead to a rupture.

There is a tear (arrow) located 7 cm above the aortic valve and proximal to the great vessels in this aorta with marked atherosclerosis. This is an aortic dissection.

30
Q
  1. Describe which areas of the heart you would see necrosis if there was occlusion in the following coronary arteries:

A. LCX

B. LAD

C. RCA

  1. T/F: Majority of the population has left sided dominant circulation and thus, most MIs are due to LAD obstruction.
A

Acute MI

1. MI: Distribution based on large vessel occlusion (common):

A. Left circumflex artery (see A in figure below):

a. 15-20%
b. Lateral left ventricle (LV free wall) except apex

B. Left anterior descending coronary artery (see B in figure below):

a. 40-50% (MOST COMMON)
b. anterior wall of left ventricle, anterior septum (2/3 of anterior portion), and apex

C. Right coronary artery (see C in figure below):

a. 30-40%
b. Posterior-inferior left ventricle, posterior septum (1/3 of posterior portion), post-inf. right ventricle

2. False. While is it TRUE that most MIs are caused by occlusion in the LAD (“widow maker”), majority of people are R-dominant circulation.

31
Q
A

Normal Heart: Normal histology of myocardium

  • cross striations
  • nuclei @ center of cell (vs. skeletal muscles)
32
Q

What is this vessel and what areas of the heart does it supply?

A

Coronary Atherosclerosis: LAD coronary artery

  • opened longitudinally with thrombus
  • dark area of necrosis
  • LAD supplies anterior wall and apex
34
Q
A

Acute MI

  • necrosis and hyperemia (surrounding red border)
35
Q

Summary Slide

A
36
Q
  1. Where was the infarct located and what coronary artery was occluded?
  2. What caused the posterior LV wall to be thin?
  3. About how many hours/days/weeks post MI would you see this?
A

Remote MI

  1. The infarct is located in the posterior 1/3 of the septum, as well as the LV posterior wall and LV lateral (free) wall. This would indicate an occlusion mostly likely occured in the RCA and/or LCX.
  2. The necrosed myocardium underwent the healing process whereby collagen creates a scar. The scar tissue over time will contract and create a thin, white tough scar.
  3. 2 months- 1 year
37
Q
  1. What is this?
  2. What is the palor area?
  3. About how many hours post MI would you see this?
A

Acute MI

  1. Left Ventricle
  2. Palor area = necrosed muscle
  3. You would see this only after 8-12 hours of the Acute MI (if the patient is still alive).
39
Q
A

Coronary Atheroscelrosis: Coronary artery

  • lumen occluded by thrombus
40
Q
A

Aortic Dissection

Here, the dissection went into the muscular wall. In any case, an aortic dissection is an extreme emergency and can lead to death in a matter of minutes. The blood can dissect up or down the aorta. Blood dissecting up around the great vessels can close off the carotids. Blood can dissect down to the coronaries and shut them off.

41
Q

How many days post MI?

A

Histology of MI

  • 1-2 days
  • Have dark red contraction bands extending across muscle fibers (will be lost soon)
  • Nuclei almost gone
  • Beginning of acute inflammation
42
Q
A

Aortic Atherosclerosis

  • cholesterol clefts and foam cells
43
Q
  1. What are the two major types of Acute MI?
  2. What are the major differences between them?
A
  • *Two major types:**
  • *1. Subendocardial (10%): Necrosis limited to inner 1/3 to 1/2 of myocardium**
  • may be due to global reduction in perfusion or single vessel occlusion
  • *2. Transmural (90%): Necrosis involves entire (or virtually entire) myocardial wall thickness**
  • usually single vessel occlusion
44
Q
A

Complications of MI

  1. Left Ventriular wall anerysm? and thickness?
45
Q
A

Normal Heart: Coronary Artery

46
Q
  1. What is occuring here?
  2. What kind of thrombi can form?
  3. What are some other complications of this condition?
  4. Is the affected area contractile?
  5. What causes the LA to look like that?
A

Complications of MI

  1. Ventricular aneurysm: Weakened ventricle leads to out pouching of a thinned ventricle
  2. Stasis of blood may lead to “mural” thrombus within aneurysm. The mural thrombi attaches to the endocardium wall but can break off and enter circulation and cause a stroke if enters carotid artery.
  3. Heart failure, arrythmias.
  4. Ventricular aneurysm due to remote MI is composed of fibrous tissue which is non-contractile.
  5. The LA is dilated because the LV dilates and affects the mitral valve (becomes incompetent) so blood backs up and stretches out the LA.
48
Q
  1. What kind of rupture is this?
  2. What kind of symptoms would you expect to see?
A

Complications of MI

  1. Rupture of IV septum: Left to right shunt
  2. SOB because blood goes from LV –> RV –> lungs. This can lead to hypoxia as the O2 rich blood gets shunted away from leaving the heart through the aorta. You would also hear a systolic murmur.
48
Q
  1. What is this?
A

​Complications of MI

  1. A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow. Note how the aneurysm bulges out. The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm.
49
Q

How many days post MI?

A

Histology of MI

- Looks like a alot of neutrophils inflitrating…probably around 12-24 hours (or 1-3 days)?

50
Q
  1. What is the role of the PMNs in this photo?
  2. How many days post MI?
A

Histology of MI

  1. Phagocytize the damaged cells.
  2. Days 3-7 or 7-10??
52
Q
  1. What is going on in this picture?
  2. Can you date it? What makes it difficult?
A

Histology of MI

  1. Scar tissue formation (collagen).
  2. Infarct could have been 2 months ago - years ago. It’s hard to date “healed” tissue.
54
Q
A

Coronary Atherosclerosis: Plaque formation over time in LAD

  • thickening of walls
55
Q
A

Normal Heart: Normal tricuspid valve with thin leaflets and chordae tendonae attached to papillary muscles

56
Q
  1. What is this?
  2. What dz is it most likely caused by?
  3. What is a double lumen?
  4. Why is dissection bad?
A

Aortic Dissection

  1. Dissection of blood within the wall of the aorta, resulting in a blood filled channel
  2. Associated with hypertension, disorders of connective tissue, others
  3. Blood from the dissection may cause a second, distal tear in the intima, resulting in a “double lumen” aorta
  4. May cause catastrophic and often fatal hemorrhage

This aorta has been opened longitudinally to reveal an area of fairly limited dissection that is organizing. The red-brown thrombus can be seen in on both sides of the section as it extends around the aorta. The intimal tear would have been at the left. This creates a “double lumen” to the aorta. This aorta shows severe atherosclerosis which, along with cystic medial necrosis and hypertension, is a risk factor for dissection.

57
Q
  1. Identify each layer of this aorta.
A

Aortic Atherosclerosis

  1. Layers from left to right

Inner: Plaque and hemorrhage

Spikey layer: Cholesterol under intima

Smoothish looking layer: Media (smooth muscle)

Out: Adventitia

58
Q
  1. What is the white streak in the upper left corner?
  2. What is the pink stuff?
A

Coronary Atherosclerosis: Zoomed in view of Fibrin clot

  1. Needle Cleft (“Cholesterol cleft”) = clear space where lipid in the extracellular space was cleared out by slide fixation.
  2. Pink= collagen from the plaque and ECM
    - leukocytes
    - bottom pink is thrombus
59
Q

What stains purple and what stains pink?

A

Coronary Atherosclerosis: Coronary artery

  • now lumen is 90% occluded due to plaque
  • note border of where wall is in relation to plaque
  • H and E staining.
  • Purple (H)= minerals and hardening/calcification, nuclei
  • Pink (E)= muscles and fat, intra/excellular proteins