Carotid artery atherosclerosis

Pathophysiology

• Exact mechanisms by which it causes ischaemic strokes are not well-known
• Two mechanisms:
  • Embolisation - felt to be the predominant cause
  • Hypoperfusion - only occurs in patients with severe multi-vessel occlusive disease in carotids and vertebrals
• Severity of carotid artery stenosis is strongly associated with stroke risk - currently the most important predictor of benefit, along with ulcerated appearance on imaging
• The term 'vulnerable' plaque is often used to denote an unstable plaque, or one that would be prone to complications. Associated factors:
  • Higher degree of stenosis
  • Older age
  • HTN
  • Increased creatinine
  • Smoking history >10 pack years
  • Hx of contralateral TIA/stroke
  • Low gray-scale median
  • Increased plaque area
  • Absence of discrete white areas without acoustic shadowing

Risk factors:

• Old age
• Total cholesterol
• SBP
• Smoking
• Vascular disease
• Diabetes
• Male

Presentation

• Vast majority are completely asymptomatic
  • Cervical bruit is only physical finding
  • Very non-specific and insensitive
• Some have had a TIA/crescendo TIA
• Some have had a stroke (evidence of infarct on cerebral imaging)

Imaging

• Carotid duplex USS - >90% accuracy compared to angiography
  • Degree of stenosis and also character of the plaque
• If further information required, CT/MR angiography is useful (CT maybe gives more information but requires contrast)
  • High bifurcation
  • Unusual lesion
  • Before re-operative CEA
  • Vertebrobasilar insufficiency
  • Intracerebral arterial disease
  • Symptomatic patients (to assess for infarction)
    • MRI more accurate early on in stroke
• Mild: <50%
• Moderate: 51-69%
• Severe: 70-99%
• Occluded: 100%

Overall treatment approach once significant carotid stenosis is found:

• Symptomatic - target for intervention
• Asymptomatic - institution of medical therapy and consideration of intervention
  • Estimate risk of stroke based on clinical scenario and plaque phenotype
    • Patient characteristics
      • Prior neurologic symptoms - especially ipsilateral symptoms within past 6 months, and especially within the first month
      • Prior silent emboli/asymptomatic infarcts
      • Contralateral carotid occlusion
      • Renal insufficiency
      • Smoking
    • Plaque characteristics
      • Degree of stenosis is the most reliable imaging predictor of stroke risk. Symptomatic patients with high-grade stenosis (70-99%) can be assumed to have a causal relationship, but relationship not as strong with moderate (50-69%) stenosis. Lesions <50% are unlikely to cause strokes in the future.
      • Plaque progression (i.e. progressive increase)
      • Vulnerable plaques:
        • Plaque heterogeneity with increased echolucency
        • Evidence of surface irregularity (ulcerations)
        • Thin or disrupted dibrous cap with adjacent echolucent plaque area
        • Increased inflammatory infiltrate (MRI or PET)
  • Assess patient-specific benefit (functional capacity, life expectancy)
    • Life expectancy. Symptomatic patients with high-grade stenosis can be considered for intervention with a life expectancy of at least 2-3 years. Asymptomatic patients should be expected to survive 3-5 years to be considered.
    • Age. Not associated with increased risk of adverse outcomes after CEA, but does increase risk of CAS.
    • Gender. Greater benefit from CEA in men. Women more often require patching after CEA due to having smaller carotids.
    • Functional status should be sufficient that a further neurological event would result in serious deterioration in functional or cognitive ability. Proceed only very carefully with mild to moderate dementia.
    • Cardiac history - consider regional anaesthetic for CEA
    • Pulmonary disease - not as important as cardiac
  • Intervention-specific risk (procedure and operator-related)

Indications for intervention (note that the greater the stenosis, the greater the justification for intervention)

• Symptomatic
  • 50-99% stenosis (there was some question of a 70-99% cut-off for women, but this is not mentioned in Rutherford's)
  • CEA preferred, but CAS is still better than nothing
  • Intervene within two weeks of stroke or TIA if possible
  • If only moderate stenosis is present, evaluate patients carefully to be sure there is no other source of emboli
• Asymptomatic
  • 60-99% stenosis - men and women
  • CEA preferred
  • Intervene only if combined stroke and death rate is <3%

Contraindications

• Absolute:
  • Total chronic occlusion of the ICA
• Relative:
  • Prior neck irradiation
  • Tracheostomy
  • Prior radical neck dissection
  • Contralateral vocal cord paralysis
  • Atypical lesion location (high or low) that is surgically inaccessible
  • Severe recurrent carotid stenosis
  • Unacceptably high medical risk
  • Severe disability precluding the preservation of useful function
  • Drowsy (decreased GCS) - can't survive by themselves for 24 hours
    • Modified Rankin score >=3
  • Infarction >1/3 of MCA territory (risk of haemorrhagic transformation)

CEA vs CAS

• CREST trial (2010) found no significant difference in related mortality/morbidity at 4 year mark. However, CAS has a higher periprocedural stroke risk, and CEA has a higher periprocedural MI risk.
  • Has been criticised to say that CEA is actually much better if you only consider stroke and death as primary endpoints
• Neurologic symptoms - CEA has much better results, ESPECIALLY in the first week after a stroke
• Hostile neck - poor tissue planes, increased risk of infection

Specific scenarios

• Carotid bifurcation stenosis <50%
  • Medical management alone if symptomatic
  • No clear support for medical management if asymptomatic
• Contralateral carotid occlusion
  • Higher risk from intervention
  • Still intervene in symptomatic patients
  • Weigh up risks/benefits in asymptomatic patients
• In-stent restenosis/recurrence after CEA
  • Early re-stenosis is likely to be a proliferative lesion (intimal hyperplasia) - data suggests a relatively benign course. Late re-stenosis is more likely to be recurrent atherosclerotic disease.
  • Consider reintervention in symptomatic patients with recurrence/ISR of >50%, or >70% asymptomatic
  • Reintervention can be CEA or CAS, but CAS is preferred
  • Risks are higher compared with initial procedure
• Radiation-induced stenosis
  • Good results with either CAS or CEA