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Cerebral atherosclerotic steno-occlusive disease encompasses
- Extracranial carotid occlusive atherosclerotic disease
- Intracranial steno-occlusive atherosclerotic disease (ICAD).
Symptomatic carotid occlusions
- Have a high risk of ipsilateral stroke (2%-6% per year), while asymptomatic patients have a much lower risk.
- ICAD is a leading cause of ischemic stroke globally, with up to 40% of patients experiencing recurrent ischemia within 2 years of diagnosis.
Pathophysiology
- Stages of cerebral haemodynamic impairment
- Stage I hemodynamic failure
- Reduced arterial response to vasodilatory stimuli (decreased cerebrovascular reserve)
- Normal Oxygen extraction fraction
- Stage II hemodynamic failure, or “misery perfusion,”
- Loss of cerebrovascular reserve
- Increase in OEF
- Stage III hemodynamic failure
- True ischemia
- Loss of cerebrovascular reserve
- No further increase in OEF
- Complete ICA occlusion --> Reduction in CPP in the distal cerebral circulation (depending on the extent of extracerebral and cerebral collaterals) --> Autoregulatory cerebral vasodilation + increase in Oxygen Extraction Fraction --> If CPP drops even further after ICA occlusion such that cerebral autoregulatory capacity is exhausted and CBF is reduced, the cerebral metabolic rate can be maintained by an increase in OEF. --> CPP is reduced to the point that both cerebral autoregulatory vasodilation and increased OEF compensatory mechanisms are depleted (true ischaemia)
- The St. Louis Carotid Occlusion Study
- Which showed that patients with cerebral hemodynamic insufficiency demonstrated by increased oxygen extraction fraction (OEF) on PET were at the greatest risk of stroke after medical management for atherosclerotic carotid occlusion
Current state of affairs
- Imaging technologies introduced since the 1985 EC/IC trial can identify flow-dependent ischemia.
- Xenon-CT, TCD, SPECT, and MRI and CT perfusion may be used in combination with acetazolamide challenge to evaluate cerebrovascular reserve and reactivity
- As cerebral perfusion pressure decreases in severe atherosclerotic occlusive disease, cerebral autoregulation is unable to maintain adequate CBF to meet metabolic demands.
- In this state of “misery perfusion”, oxygen extraction fraction (OEF) of available blood flow will increase.
- Abnormal OEF, as quantified by PET, is an independent predicator of subsequent stroke.
- Patients with abnormal response to acetazolamide challenge (p.244) and/or with elevated OEF are therefore potential candidates for cerebral revascularization.
Treatment
- Medical management
- Dual antiplatelet therapy
- Risk factor optimization
- High-dose statins.
- Endovascular stenting
- The SAMMPRIS trial found endovascular treatment of ICAD inferior to aggressive medical management.
- Recent advancements have led to a resurgence in revascularization procedures with lower morbidity rates.
- Wingspan Stent System: Demonstrated lower periprocedural (2.6%) and 1 year morbidity (8.5%) compared to SAMMPRIS.
- Extracranial-intracranial (EC-IC) bypass. (See Bypass)
- Cerebral revascularization is established for moyamoya syndrome and disease but remains controversial for atherosclerotic occlusive disease.
- Bypass Candidates:
- Identified as those with failed angioplasty
- Stenting
- Unfavourable anatomy for endovascular treatment.
- EC-IC Bypass:
- Fell out of favor for steno-occlusive atherosclerotic cerebrovascular disease after the EC-IC bypass study in 1985 and the COSS study in 2011, which showed no benefit over medical therapy.
- Japanese EC-IC Trial:
- Contradicted other studies by showing a decrease in major strokes in the bypass group at 2 years.
- Carotid Occlusion Surgery Study (COSS)
- Which questioned the efficacy of flow augmentation for atherosclerotic vessel occlusion,
- Stopped prematurely due to high perioperative stroke rates.
- High 30-day stroke rate in the COSS trial was seen as an outlier compared to other centers.
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