Background and Purpose Carotid artery dissections comprise approximately 10% - 25% of acute ischaemic strokes, particularly in younger populations. The early recognition and management of severe flow limiting internal carotid artery (ICA) dissections in a setting of acute ischaemia is particularly important to minimise the risk of complete vessel occlusion, thromboembolic complications, and/or progression of ischaemia to infarction. We describe our experience in 7 patients presenting with long-segment, flow limiting ICA dissections presenting with hyperacute ischaemic symptoms.

Methods A multicentre retrospective study was initiated of all patients presenting with ICA dissections and acute stroke symptoms, hyperacute ischaemia (<8 hours from symptom onset) with National Institute of Health Stroke Scale (NIHSS) scores > 4 at presentation. Inclusion criteria included arbitrary ICA dissection length of > 2cm, severe >70% stenosis and/or flow limitation by conventional angiography and/or CT/MR perfusion imaging, Patients underwent medical and/or endovascular management at the discretion of the attending physician. Patient demographics, presentations, medical comorbidities (hypertension, diabetes, hyperlipidemia), medical treatment (IV tPA/anticoagulation/antiplatelets), endovascular procedures (carotid stenting/intra-arterial thrombolysis/thrombectomy), complications and post-treatment course with technical/clinical outcomes (modified Rankin Scores (mRS) at 90-days) were analysed. Good functional outcome was defined as mRS 0–2 at 90 days.

Results Seven patients (1F/6M, mean age: 46 (21-80) presented in the hyperacute phase (mean symptom onset to presentation time of 201.4 (60-480) minutes) with acute ischaemic symptoms (slurred speech, aphasia, facial droop, hemiplegia/hemiparesis) and mean baseline NIHSS score of 15.5 (5-21). ICA dissection length (> 2 cm) and stenosis (90%–100%) were confirmed with cross-sectional CT/MR angiography. Tandem intracranial thromboembolic occlusions were noted in 4/7 patients. Flow limitation was documented in 7/7 patients with a penumbra of hypoperfused tissue seen in 6 patients. Four patients underwent endovascular stent reconstruction of the ICA utilising both intracranial and carotid stents, and after receiving IV tPA (n=3) without improvement. Conversely, three patients were medically managed with antiplatelet therapy alone (n=1) or antiplatelets post-IV tPA therapy (n=2). All endovascular stenting patients received dual antiplatelet therapy for > 6 months or a short term GP2b/3a inhibitor (24 hours) followed by dual antiplatelets. No technical complications (in-stent thrombosis/stenosis, distal or new territory thromboemboli, early reperfusion haemorrhage, or delayed haemorrhagic infarct) were encountered during/following endovascular vessel reconstruction. Endovascular stenting in younger patients was associated with lower infarct volumes and better functional outcomes at 90-days (3/4 versus 1/3) despite higher baseline NIHSS scores and longer delays in treatment. Conversely, in the medically managed group, 2 patients progressed to middle cerebral artery occlusions with large hemispheric infarcts. A single patient that underwent endovascular ICA reconstruction presented with an eloquent internal capsule and corona radiate infarct even prior to intervention.

Conclusions We describe our experience with both the medical and endovascular management of severe flow limiting dissections presenting with hyperaacute ischaemia. Our preliminary data suggests the safety and feasibility of stent reconstruction in long segment carotid dissections presenting with hyperacute ischaemia, with favourable outcomes over IV tpA and/or antiplatelets alone.

Disclosures O. Rahman: None. A. Honmarand: None. M. Soltanolkotabi: None. M. Hurley: None. A. Shaibani: None. S. Ansari: None.