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Y2 - Path - Exam 4 > 4: Ischemic heart disease > Flashcards

4: Ischemic heart disease Flashcards

1
Q

2 key causes of Ischemic heart diease?

Which of the two accounts for the majority of the cases?

A
  • Reduced Perfusion (*>90% of cases due to obstructive atherosclerotic lesions in coronary arteries)
  • Increased myocardial demand
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2
Q

Which pathological cause of ischemic heart disease is associated w/ the following causes?

  • Coronary emboli, myocardial vessel inflammation, spasm
  • Hypoxemia, systemic hypotension
A

These cause REDUCED PERFUSION –> resulting in ischemic heart disease

(recall: >90% of cases due to obstructive atherosclerotic lesions in coronary arteries)

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3
Q

Which pathological cause of ischemic heart disease is associated w/ the following causes?

  • Due to increased contractility, HR, ventricular wall tension/thickness (myocardial hypertrophy)
A

Due to increased myocardial demand

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4
Q

Percentage occlusion of coronary artery assoc with the 3 stages of ischemic disease?

  1. asymptomatic
  2. stable angina
  3. unstable angina
A
  1. asymptomatic - <70% occlusion
  2. stable angina - >70% occlusion
  3. unstable angina - >90% occlusion
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5
Q

four key clinical presentations of Ischemic heart disease?

A
  • angina pectoris (chest pain)
  • congestive hear failure
  • myocardial infarction
  • sudden cardiac death
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6
Q

definition: intermittent chest pain caused by transient, reversible myocardial ischemia

(15 sec-15 min)

A

angina pectoris

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7
Q

what is the pathological cause of Angina (chest pain)?

A

pain is a consequence of the ischemia-induced release of adenosine & bradykinin

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8
Q

type of ischemic heart disease assoc with the following description?

  • Predictable chest pain associated with exertion
  • Crushing/squeezing, substernal chest pain radiating down left arm/jaw
  • Pain relieved by rest, drugs (nitoglycerin)
A

Typical/stable ischemic heart disease– most common

  • reversible w/ medications (nitroglycerin)
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9
Q

type of ischemic heart disease assoc with the following description?

  • Coronary artery spasm, can affect normal vessels
  • Responds to vasodilators (relieved/reversible w/ medications)
A

Prinzmetal/variant – uncommon

(Responds to vasodilators (relieved/reversible w/ medications))

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10
Q

type of ischemic heart disease assoc with the following description?

  • increasingly frequent pain, occurs at rest
A

Unstable ischemic heart disease

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11
Q

type of ischemic heart disease assoc with the following description?

  • necrosis of heart muscle due to ischemia
  • Epi: 10% occur <40 y/o; M>F
  • Causes: atherosclerosis, vasculitis, amyloid, sickle cell disease
A

Myocardial infarction;

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12
Q

what is thought to cause “women being protected against MI during reproductive years?”

A

HORMONES are thought to have PROTECTIVE EFFECT

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13
Q

Describe the pathogenesis of myocardial infarction?

A
  1. Preexisting atherosclerotic occlusion
  2. New, superimposed thrombosis
  3. +/- vasospasm/ vasoconstriction
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14
Q

Preexisting atherosclerotic occlusion:

where does it occur?

A
  • LAD, LCX – first cm from aorta takeoff
    • (left anterior descending)
    • (left circumflex artery)
  • RCA – along entire length
    • (right coronary artery)
  • “critical stenosis” - if fibrous cap is eroded and ruptures –> completely occludes the lumen
  • Collateral perfusion
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15
Q

define: critical stenosis

A

critical narrowing of an artery (stenosis) that results in a significant reduction in maximal flow capacity in a distal vascular bed

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16
Q

New, superimposed thrombus:

process of superimposed thrombsis

A
  • Eroded/ruptured plaque
  • Platelets adhere, aggregate, and are activated
  • Coagulation is activated
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17
Q

+/- vasospasm / vasoconstriction:

describe this third stage of pathogenesis of ischemic heart disease

A
  • Compromised lumen diameter
  • Increases local shear forces –> further damaging the fibrous cap –> plaque disruption
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18
Q

review the acute plaque changes

A
  1. atherosclerosis –>
  2. plaque disruption –> healing –> severe fixed coronary obstruction (chronic ischemic heart disase)
  3. Plaque disruption –?
    • mural thrombus w/ variable obstruction/ emboli
    • occlusive thrombus
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19
Q

factors contributing to acute plaque change –> MI?

A
  • vulnerable plaques
  • adrenergic stimulation

*In the majority of cases, culprit lesions in myocardial infarction patients were NOT critically stenotic OR symptomatic before plaque rupture

(slide 11)

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20
Q

what are: large atheromatous cores or thin fibrous caps

A

VULNERABLE / UNSTABLE PLAQUES:

these are more prone to rupturing

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21
Q

how does adrenergic stimulation affect/contribute to acute plaque change?

A
  • Adrenergic stimulation adds to plaque stress
  • Causes of adrenergic stimulation:
    • Surge in adrenergic stimulation associated with waking and rising
    • Intense emotional stress
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22
Q

what are the 3 REVERSIBLE changes in the myocardial response to ischemia?

A
  1. Aerobic metabolism ceases ↓ATP ↑lactic acid
  2. Loss of contractility
  3. Ultra-structural changes on cellular level
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23
Q

what are the 2 irreversible changes in the Myocardial Response to Ischemia?

A

Irreversible changes occur in 20-40 minutes of prolonged ischemia

  • Coagulative necrosis of myocytes
  • Microvascular thrombosis
24
Q

which aspect of the artery is MOST SUSCEPTIBLE to infarction?

A

SUBENDOCARDIAL ZONE is most susceptible;

susceptible to developing ischemia due to being FURTHEST AWAY from coronary artery

(endocardial zone is typically spared during periods of ischemia)

25
Q

which type of infarcts involve full thickness of ventricle?

What is seen on ECG?

A
  • TRANSMURAL INFARCTS involve full thickness of ventricle
  • Yields ST segment elevations on ECG (aka STEMI)

Slide 14

26
Q

which type of infarcts involve limited to inner third or myocardium?

What is seen on ECG?

A
  • SUBENDOCARDIAL INFARCTS; limited to inner 1/3 or myocardium
  • Typically show ST segment depressions (aka non-STEMI or NSTEMI

Slide 14

27
Q

Left anterior descending (LAD) artery occlusion:

  • what is it?
  • where does it occur?
  • what % of MIs?
  • nickname for this occlusion?
A
  • type of heart attack that’s caused by a 100% blockage of the left anterior descending (LAD) artery
  • Location: Anterior LV wall, anterior 2/3rds of septum, apex
  • 40-50% of MI; accounts for most of the causes of MIs
  • “widow maker”
28
Q

Right coronary artery (RCA) occlusion

  • where does it occur?
  • what % of MIs?
A
  • Location: RV and posterior 1/3rd of septum and posterior LV (if PDA arises from
    RCA)
  • 30-40% of MIs (2nd most common)
29
Q

Left circumflex artery (LCX) occlusion:

  • location
  • % of MIs
A
  • Lateral LV wall
  • 15-20% of Myocardial Infarction
30
Q

which artery perfuses 1/3rd of septum and posterior LV artery?

what’s its course?

A

Posterior descending artery;

  • Arises from RCA (90%) or LCX –> dominant vessel
  • PDA is often a branch off of Right Coronary Artery; but CAN be a branch
    off of Left Coronary (Left Circumflex Artery) – termed “Left Dominant
    Circulation”
31
Q

how does the gross appearance of a myocardial infarct differ from hours:

  • <4 hours
  • 4-12 hours
A
  • <4 hours – no changes appreciated
    • If preceded death by 2-3 hours, area can be highlighted by immersing tissue in triphenyltetrazolium chloride
  • • 4-12 hours – occasional dark mottling (dark discoloration, on myocardium)
32
Q

when do microscopic changes of myocardial infarct appear?

what are these changes?

A
  • microscopic changes usually require >4 hrs
  • changes:
    • EM changes in first 4 hrs (sarcolemmal disruption, mitochondrial amorphous densities)
    • Early coagulation necrosis
    • Edema
    • Hemorrhage

Slide 22

33
Q

the image is of a triphenyltetrazolium chloride stain;

where is the ischemia?

A

Lateral Left Ventricle experienced ischemia:

due to Left Circumflex branch being occluded –> ischemia (can’t pick up the stain)

34
Q

what are the gross findings of myocardial infarct at 12-24 HOURS?

A

Dark mottling (red-blue discoloration)

35
Q

what are the microscopic findings of myocardial infarct at 12-24 HOURS?

A
  • Coagulation necrosis
  • Pyknotic nuclei (shrunken and dark)
  • Myocyte hypereosinophilia
  • Contraction band necrosis
  • Early neutrophilic infiltrate
36
Q

gross anatomical changes in a 24-72 hour myocardial infarct?

A

Mottling with yellow-tan infarct center

37
Q

MICROSCOPIC anatomical changes in a 24-72 hour myocardial infarct?

A
  • Coagulative necrosis
    • Loss of myocyte nuclei
    • Loss of muscle cross-striations
  • Brisk neutrophilic infiltrate
38
Q

gross anatomical changes of a 3-7 day old myocardial infarct?

A
  • Gross changes are most prominent at 3-7 days
  • Hyperemic border, central yellow-tan softening
  • Central softening (feels gelatinous/ soft to touch), depression due to removal of dead tissue
39
Q

microscopic anatomical changes of a 3-7 day old myocardial infarct?

A
  • Dead myofibers removed
  • Neutrophils disappearing
  • Macrophage infiltration
40
Q

gross anatomical appearance of 7-14 day old myocardial infarct

A
  • Maximally yellow-tan and soft (7-10 days)
  • Red-gray (10-14 days)
41
Q

microscopic anatomical appearance of 7-14 day old myocardial infarct?

A
  • Granulation tissue at margins (7-10 days)
  • 10-14 days:
    • Well-established granulation tissue
    • New blood vessel formation (angiogenesis)
    • Collagen deposition (pink on histo slide is the new collagen being deposited)
42
Q

gross and micoscopic anatomical features of 2-8 week old myocardial infarct?

A
  • Gross: Gray-white scar
  • Microscopic:
    • Increased collagen deposition
    • Decreased cellularity
    • Macrophages are leaving the area
43
Q

gross and micoscopic anatomical features of a >2 month old myocardial infarct?

A
  • Gross - Scarring complete
  • Microscopic - Dense collagenous scar

area is all scar tissue; nonfunctional tissue (can’t determine how old it is, but we know it’s older than 2 months)

44
Q

what is REPERFUSION, and what can be done to stimulate this?

A
  • Restoration of blood flow, which improves long and short-term survival
    • **Goal is to reperfuse early**
  • Thrombolysis (tissue plasminogen activator), angioplasty, or coronary arterial bypass graft
45
Q

what is reperfusion injury?

what are the pathological changes that result locally upon reperfusion?

A
  • Late restoration of blood flow to ischemic tissue can incite local damage
  • Changes
    • Mitochondrial dysfunction – mitochondrial contents are released and promotes apoptosis
    • Myocyte hypercontracture
    • Free radicals form and cause myocyte damage
    • Leukocytes aggregate and may occlude microvasculature
    • Platelets and complement are activated
46
Q

how do hemorrhagic lesions occur after reperfusion injury?

A
  • vasculature is injured during ischemia –> bleeding after flow is reestablished
  • brown bc it’s experienced hemorrhage
47
Q

JUST ONE CRUEL AND UNUSUAL HISTO QUESTION BC PROFS SUCKKK:

what does this histo image show?

A
  • Contraction band necrosis – intensely eosinophilic stripes (closely-packed sarcomeres)
  • dark pink vertical lines; buildup of calcium –> contraction bands form due to excess excitation (can’t relax, stuck in contracted state
48
Q

how do we diagnose a myocardial infarction?

A
  • clinical symptoms (**but 10-15% of pts may be asymptomatic)
    • Severe, crushing substernal chest pain
    • Radiation to neck, jaw, epigastrium, left arm
    • Diaphoresis, nausea, vomiting
  • labs
  • EKG changes/ abnormalities
    • STEMI and ST segment depression
49
Q

what do irreversibly damaged myocytes release?

A

intracellular macromolecules

(such as Creatinine Kinase enzyme, Troponin free int he cytoplasm)

50
Q

what are the 3 key biomarkers for myocardial ifnarctions?

  • Which are most sensitive and specific?
  • Which is best to identify subsequent MIs?
A
  • Troponin I and T are MOST sensitive and specific
  • CK-MB is more helpful to identify subsequent MIs
51
Q

key consequences of myocardial infarction?

A
  • Arrhythmias: risk for V. fib is greatest in first hour
  • Mural thrombus: impaired contractility leads to stasis, endocardial damage creates thrombogenic surface
  • Myocardial rupture
  • Papillary muscle dysfunction –> post-infarct mitral regurgitation
  • Pericarditis: 2nd or 3rd day after transmural infarct (full thickness of wall)
  • Ventricular aneurysm: dilation/ballooning outward; can occur in the ventricle
52
Q

myocardial rupture:

epidemiology, adn causes

A
  • Epi: 1-5% of MIs and fatal
    • Left ventricular free wall most common –> leads to hemopericardium, cardiac tamponade
    • Occurs 3-7 days after infarction
  • Ventricular septum –> leads to VSD
  • Papillary muscle rupture –> leads to MR
53
Q

the gross image is of what?

A

post-MI ventricular aneurysm;

Wall is dilated; there’s a dilation of the wall (myocytes have been
degraded by macrophages; –> so the area is more prone to formation
of aneurysm)

54
Q

Chronic Ischemic Heart Disease:

  • define?
  • classic type of patient?
A
  • Progressive heart failure secondary to ischemic myocardial damage – ischemic cardiomyopathy
  • Patient:
    • Prior infarction(s) & compensatory mechanisms fail (hypertrophy of residual viable
      myocytes)
    • Severe coronary artery disease (microinfarcts and replacement fibrosis without clinical evidence of a frank infarct)
55
Q

Chronic ischemic heart disease:

morphology

A
  • LV dilation and hypertrophy, areas of gray-white scars
  • myocyte hypertrophy, diffuse subendocardial myocyte vacuolization, fibrosis
56
Q

histological features in subendocardial zone after a myocardial infarct?

A

diffuse subendocardial myocyte vacuolization

Y2 - Path - Exam 4 (13 decks)

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