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C2 Modules CLINICAL > Carotid Imaging > Flashcards

Carotid Imaging Flashcards

1
Q

What is carotid artery?

A

Hardening of arteries

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2
Q

Where is carotid artery located?

A

On each side of neck pulse

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3
Q

What are the 3 imaging approaches?

A
  1. Anatomic criteria
  2. Morphological criteria
  3. Pathophysiological criteria
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4
Q

What is Grading stenosis?

A

All individuals with TIA or non-disabling stroke should have carotid imaging within 7 days of event or 24 hours

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5
Q

What are high-risk plaque features?

A
  1. Thin fibrous caps
  2. Intra-plaque haemorrhage
  3. Large lipid-rich necrotic cores
  4. Neurovascularisation
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6
Q

What did 3D TOF pulse sequence distinguish?

A

Between intact and thick versus thin and rupture caps

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7
Q

What is there 89% agreement between?

A

3D TOF and histology

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8
Q

What does contrast enhancement MRI with gadolinium demonstrate?

A

Preferential enhancement of fibrous tissue

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9
Q

What is there strong association with?

A

Recent and recurrent cerebrovascular event

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10
Q

What has some studies reported?

A

A moderate relationship between the degree of stenosis and likelihood of events

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11
Q

What can ultrasound and CT look at?

A

Some other plaque characteristics - is there evidence of irregularities on lining of the plaque suggestive of rupture

  • there is haemorrhage within it
  • Stenotic and anatomical criteria
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12
Q

What was the Dutch study?

A

Atherosclerosis is much common as you get older

- more common in men

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13
Q

What are the screening carotids?

A
  1. In over 80’s, moderate disease present in 7.5% of men and 5% of women
  2. Severe disease present in 3.1% of men and 0.9% of women
  3. CEA in asymptomatic individuals felt to reduce risk of stroke by 3.5% compared to best medical therapy
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14
Q

What are the risk of endarterectomy procedure?

A

region of 2-3%

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15
Q

What does damage within plaque cause?

A

Destabilisation process

Bleeding within structure itself [atherosclerotic plaque]

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16
Q

What is the consequence of bigger plaques?

A

More inflammation and more likely for the plaque to destablise
The blood can’t diffuse all the way down to the deep aspect of cord –> becomes deeper necrosis –> further inflammation

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17
Q

What is imaging validated against?

A

The endarterectomy specimen

the specimen is removed by surgery

18
Q

For Fibrous cap, what is there a strong association with?

A

Recent and recurrent cerebrovascular events

19
Q

What is plaque haemorrhage?

A
  1. Degradation of haemorrhage into methaemoglobin
  2. This shortens the relaxation time of T1, resulting in bright signal on T1 (such as fast-spin echo)
  3. Validated against histology
20
Q

What is Neovascularisation?

A
  1. May be imaged using dynamic contrast-enhanced (DCE) MRI
  2. T1-weighted technique using repeated measurement of contrast intensity
  3. Post-contrast concentration and Ktrans reflect the degree of neovascularsation
21
Q

Why is repeated imaging of plaque important?

A

To see the overall movement of gadolinium is over the course of time after the injection

22
Q

What is USPIO?

A
  1. Ultrasmall supermagnetic particles of iron oxide - enhanced MRI
  2. These particles are taken up by macrophages via scavenger receptors
  3. Results in T2-weighted susceptibility effect (reduced signal)
23
Q

What are the advantages of MRI?

A
  1. Excellent spatial resolution
    (micrometres)
  2. Longitudinal imaging [No radiation]
  3. Availability
24
Q

What are the disadvantages of MRI?

A
  1. Tolerability

2. Unable to detect micro-calcification

25
Q

How does PET scanner work?

A

Symptomatic carotid disease
1. Injected with radio-tracer

  1. Targets physiological processes of interest
    - accumulates in those regions
  2. Label with proton rich typically 18 F
  3. Collected up areas of high physiological activity where it decays
  4. Protons are released from that nucleus and encounters electrons in neighbouring tissues
  5. Results in gamma burst - detected
  6. Co-register with CT components of PET CT scanner - match up areas of hot spot - match up anatomically
26
Q

What is a key process of plaque destabilisation?

A

Inflammation

Enzymes are causing matrix metalloproteinases cap to break down

27
Q

What does microcalcification cause?

A

Mechanical destabilisation

28
Q

What are the two tracers?

A
  1. FDG

2. Sodium flouride [NaF]

29
Q

What is FDG?

A

Analogue of glucose

Taken up where there is metabolic activity

30
Q

Fluorodeoxyglucose (FDG)

A
  1. 18F-FDG taken up in cells via glucose transporter types (GLUT) one and three (upregulated in atherogenesis)
  2. Undergoes phosphoyrlation to 18F-FDG-6-phosphate
  3. 18F-FDG-6-phosphate lacks 2’-hydroxyl-group, so cannot enter glycosis/kreb’s cycle
31
Q

What does FDG uptake correlate with?

A

CD68 on excised histology after CEA

32
Q

FDG uptake…

A
  1. Higher in culprit plaques versus non-culprit
  2. Higher in those with high-risk plaque features
  3. Correlates with cardiovascular risk factors
33
Q

What is FDG uptake associated with?

A
  1. Increased microembolic signals on transcranial Doppler

2. Increased risk of reccurent events

34
Q

PET tracer uptake

A

Standardised uptake value (SUV):
SUV = activity / (injected activity * weight)

Tissue-to-background ratio (TBR):
TBR = SUV in ROI / SUV in venous phase

35
Q

Sodium fluoride (NaF)

A
  1. 18F-NaF identifies sites of active microcalcification

2. Radiolabelled fluoride exchanged for hydroxyl group in hydroxyapatite forming fluoroapatite

36
Q

Newer tracers

A

FDG is sensitive but non-specific.
68Ga-DOTATATE targets somatostatin receptor subtype-2 (SST2).
Outperformed FDG in pilot studies.1

37
Q

PET in research

A

Highly sensitive, allowing small sizes.
Can directly measure effect of intervention on pathophysiology and is increasingly used in drug trials.
e.g. FDG-PET has demonstrated the pleiotropic effect of statins.1

38
Q

What are the advantages of Hybrid PET/MRI?

A

Combine morphology and pathophysiology.
Improved soft tissue contrast.
Reduced radiation.

39
Q

What are disadvantages of Hybrid PET/MRI?

A

Cost.
Availability.
Tolerability.
Attenuation correction.

40
Q

What is carotid dissection

A

1-2% of all ischaemic strokes.
10-25% of ischaemic strokes in under 50 years of age.

Unilateral headache occurs in approx. 2/3 of cases.
Horner’s syndrome is another warning sign.

CADISS study had a recurrence of 1-2% at 3 months.

Management with either antiplatelet or anticoagulant.

C2 Modules CLINICAL (26 decks)

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