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2 Path Unit > 10/23 Ischemic Heart Disease > Flashcards

10/23 Ischemic Heart Disease Flashcards

1
Q

What is the number one cause of death in the U.S.?

A

Heart Disease

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2
Q

Dominant cause of ischemic heart disease is?

A

insufficient coronary perfusion (due to narrowing of epicardial coronary arteries)

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3
Q

T/F Most ischemic heart disease has an asymptomatic phase?

A

T

[sudden cardiac death is first symptom in 50%!]

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4
Q

When do coronaries fill? Tachycardia does what to this

A
  • diastole

- Reduces filling

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5
Q

Review coronary anatomy!

A
  • LMA->LCX (plus OM1 & 2)
  • LMA->LAD (Plus D1, D2)
  • RCA->PL and PD
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6
Q

total occlusion of what branch takes out 15% of Left Ventricle? 35%? 50%?

A
  • LCX (left circumflex)
  • RCA
  • LAD
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7
Q

Plaques are found at which location in LCA? Which location in RCA?

A
  • proximal LAD and LCX

- Entire length of RCA

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8
Q

Soft plaques are made of?

A

necrosis

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9
Q

Hard plaques are made of?

A

fibrocalcific substance

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10
Q

Coronary occlusion grading follows what scale? When is it considered symptomatic?

A

-Less than 25% occluded= Grade 1
-26-50%=Grade 2
…and so on
-Grade 4 is considered “severe” and has symptoms

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11
Q

Severe left main artery disease has what prognosis?

A

high rate of sudden death. [usually occurs w/ severe 3-vessel disease]

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12
Q

Little white chunks in a coronary artery seen on X-ray is called what?

A

plaque calcification

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13
Q

T/F collateral arteries dilate and grow when stimulated by downstream ischemia?

A

T. [non-functional normally though]

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14
Q

T/F chronic coronary lesions typically can vasospasm or hemorrhage?

A

F, chronic are typically stable, slowly enlarging.

-Acute are rapidly enlarging, prone to rupture at any grade, thrombose, hemorrhage, and vasospasm (endothelial injury)

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15
Q

Am I typical of chronic or acute coronary lesions: unstable angina?

A

acute

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16
Q

Am I typical of chronic or acute coronary lesions: asymptomatic ischemic heart disease

A

Both!

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17
Q

Am I typical of chronic or acute coronary lesions: stable angina

A

chronic

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18
Q

Am I typical of chronic or acute coronary lesions: myocardial infarction

A

acute

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19
Q

Am I typical of chronic or acute coronary lesions: Heart failure

A
  • chronic heart failure in chronic coronary lesions, while…
  • acute heart failure in acute coronary lesions
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20
Q

Am I typical of chronic or acute coronary lesions: sudden death

A

acute

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21
Q

what 3 fates can occur after a CORONARY plaque rupture?

A
  • healing
  • embolism
  • thrombosis (most common & clinically significant! More than embolism.)
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22
Q

what 3 fates can occur after a CORONARY plaque rupture which leads to THROMBOSIS?

A
  • organization (Most common!!)
  • embolization
  • obstruction
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23
Q

Plaque progression is which? a)more fat deposited OR b)repeated episodes of plaque rupture, thrombosis, organization

A

B.

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24
Q

T/F plaque instability can occur an any stage of narrowing?

A

T

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25
Q

Hemorrhage within a plaque may lead to?

A

-acute coronary syndrome (possibly by inducing vasospasm)

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26
Q

concentric plaques are nice, because they prevent?

A

vasospasm

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27
Q

Ischemia is defined as?

A
  • myocytes remain viable
  • sublethal

[may produce angina, arrhythmia, or heart failure!]

28
Q

acute ischemia looks like what on histo?

A

normal myocytes OR with contraction bands

29
Q

chronic ischemia looks like what on histo?

A

vacuolated myoctyes w/ decreased contractile elements

30
Q

Infarction is defined as?

A

-non-salvageable myocytes

31
Q

Acute infarction looks like what on histo?

A

coagulative necrosis w/ contraction bands, apoptosis, wavy fibers. Depending on time afterward: neutrophils, macrophages, granulation tissue, scarring

32
Q

_________ myocardium is most susceptible to ischemia

A

subendocardial

33
Q

As ischemia/infarction progress, they expand in what directions?

A

radially outward, and transmurally toward the epicardium

34
Q

How many hours of severely reduced perfusion result in permanent damage?

A

this is weird but…

-“at least 2 to 4 hours” (“necrosis is usually complete within 6”)

35
Q

What is the wavefront phenomenon?

A

progression of MI from subendocardial to transmural

36
Q

What type of MI result in relatively discreet infarcts and occur in very specific locations?

A

acute MI associated with coronary artery occlusion

37
Q

What type of MI is circumferentially distributed around the LV?

A

acute MI associated with global hypoperfusion

38
Q

What type of infarcts are found in embolic disease?

A

focal acute MI that may not be subendocardial and are not in specific coronary distribution

39
Q

What type of MI is STEMI?

A

transmural

40
Q

What type of MI is non STEMI?

A

subendocardial

41
Q

Is transmural or subendocardial more common?

A

transmural [involves half of myocardial thickness]

42
Q

How does a subendocardial MI occur?

A

rapid lyses of coronary thrombus or prolonged hypo perfusion of heart

43
Q

When do macrophages start cleaning up an MI inflammation? granulation tissue?

A

8-11 days

11-14 days

44
Q

When does collagen deposition take place?

A

day 14+

45
Q

When does death of neutrophils take place?

A

5-7 days

46
Q

What does a week one MI infarct look like?

A

begins dark mottling
yellow-tan from increasing neutrophils/necrosis
border of infarct stays hyperemic

47
Q

What is karyorrhectic debris symbolic of in MI recovery?

A

neutrophils starting to die

48
Q

What does a week two MI infarct look like?

A

center is maximally yellow tan and soft with a depressed red/gray border of granulation

49
Q

Which direction of clean up takes place?

A

outside in,

50
Q

What cells are a main component of granulation tissue that you should be able to point out

A

fibroblasts (residual chronic inflammatory cells too)

51
Q

What does a week 3-4 MI look like microscopically?

A

fibrosis with numerous fibroblasts, pink collagen, and very sparse chronic inflammatory cells

52
Q

What color is collagen in trichrome?

A

blue

53
Q

Review the following list of complications of MI

A

arrhythmias, contractile dysfunction, rupture, RV infarct, expansion, extension, aneurysms in the ventricle, thrombus, progressive late heart failure, pericarditis

54
Q

What are the 4 main outcomes of electrical failure following MI?

A

acute arrhythmias
non-lethal
arrest- resuscitated
sudden death

55
Q

What are the 3 outcomes of pump failure following MI?

A

acute HF
cardiogenic shock [>40% LV loss]
chronic HF

56
Q

When is myocardial rupture most common?

A

3-7 days post MI, correlates with maximal degradation`

57
Q

Is a free wall rupture fatal?

A

rapidly

58
Q

Papillary muscle rupture commonly leads to what?

A

acute mitral regurg

59
Q

Is the free wall rupture most common?

A

Yes- anterolateral wall

60
Q

What are the risk factors of myocardial rupture?

A 
> 60 years old
Female>male
chronic hypertension
No LV hypertrophy
FIRST MI !!!!!!!!!![no scars that block]
61
Q

Is there high mortality in rupture of ventricular septum?

A

Yes- this is why we repair it. Acute L>R shunt

62
Q

What location does papillary muscle rupture occur most?

A

post-medial

63
Q

Is infarct extension or infarct expansion more commonly associated with mural thrombus and poorer prognosis?

A

Infarct expansion

64
Q

What are the 3 main consequences of aneurysm in the myocardial wall?

A

-arrhythmias
-mural thrombus
-chronic heart failure
[no rupture after 1 mo]

65
Q

What is chronic ischemic heart disease also known as? What is commonly seen 6 (for review)?

A
  1. ischemic cardiomyopathy
  2. progressive heart failure, previous coronary arterial interventions, LV hypertrophy and dilatation, discreet scars, thickened endocardium, thrombus often.
66
Q

What syndrome is pericarditis following MI? how many days after MI? occur only after transmural MI?

A

Dressler’s, day 2 or 3, yes

2 Path Unit (14 decks)

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