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
How does PET scanner work?
Symptomatic carotid disease 1. Injected with radio-tracer 2. Targets physiological processes of interest - accumulates in those regions 3. Label with proton rich typically 18 F 4. Collected up areas of high physiological activity where it decays 5. Protons are released from that nucleus and encounters electrons in neighbouring tissues 6. Results in gamma burst - detected 7. Co-register with CT components of PET CT scanner - match up areas of hot spot - match up anatomically
26
What is a key process of plaque destabilisation?
Inflammation | Enzymes are causing matrix metalloproteinases cap to break down
27
What does microcalcification cause?
Mechanical destabilisation
28
What are the two tracers?
1. FDG | 2. Sodium flouride [NaF]
29
What is FDG?
Analogue of glucose | Taken up where there is metabolic activity
30
Fluorodeoxyglucose (FDG)
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
What does FDG uptake correlate with?
CD68 on excised histology after CEA
32
FDG uptake...
1. Higher in culprit plaques versus non-culprit 2. Higher in those with high-risk plaque features 3. Correlates with cardiovascular risk factors
33
What is FDG uptake associated with?
1. Increased microembolic signals on transcranial Doppler | 2. Increased risk of reccurent events
34
PET tracer uptake
Standardised uptake value (SUV): SUV = activity / (injected activity * weight) Tissue-to-background ratio (TBR): TBR = SUV in ROI / SUV in venous phase
35
Sodium fluoride (NaF)
1. 18F-NaF identifies sites of active microcalcification | 2. Radiolabelled fluoride exchanged for hydroxyl group in hydroxyapatite forming fluoroapatite
36
Newer tracers
FDG is sensitive but non-specific. 68Ga-DOTATATE targets somatostatin receptor subtype-2 (SST2). Outperformed FDG in pilot studies.1
37
PET in research
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
What are the advantages of Hybrid PET/MRI?
Combine morphology and pathophysiology. Improved soft tissue contrast. Reduced radiation.
39
What are disadvantages of Hybrid PET/MRI?
Cost. Availability. Tolerability. Attenuation correction.
40
What is carotid dissection
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.