Karissa Arthur, MD
European Stroke Organisation Conference
September 1–3, 2021
Cervical Artery Dissection: Christopher Traenka, University Hospital Basel
Dr. Traenka discussed carotid artery dissection (CeAD) in this talk. He first discussed CeAD and sports. Patients with CeAD obtained during stroke should refrain from any sports activities for at least one month, and this period may need to be prolonged considering the patient’s clinical course. When resuming activities, patients should start at low intensity and gradually increase activity. Most patients will go back to full activity in 6-12 months.
Next, Dr. Traenka discussed acute recanalization therapies. Endovascular therapy (EVT) in CeAD has scarce data and no data from randomized controlled trials. Two studies found that patients with carotid artery stent had improved recanalization but no improvement in functional outcome. However, the patients in these studies were not randomized, and patients who received EVT were more severe at onset. Overall, in cases with LVO and CeAD, EVT should be considered.
Dr. Traenka then discussed antithrombotic therapy in CeAD. The TREAT-CAD2 studied aspirin versus vitamin K antagonist in patients with CeAD and found that there were more composite clinical outcomes and MRI outcomes in the aspirin group, but noninferiority of aspirin was not achieved. Notably, all ischemic strokes (7 overall) occurred in the aspirin group, and 5/7 occurred on day 1. Dr. Traenka concluded that aspirin is not non-inferior to vitamin K antagonists, but the evidence to support aspirin as standard is weak. He proposed that in patients with pure local symptoms without hemodynamic compromise, aspirin can be used. However, in patients with ischemia (clinical or MRI proven), anticoagulation with vitamin K antagonists should be used. DOACs are not recommended due to lack of robust data. In the future, improved diagnostics may help to individualize treatment.
Extracranial Carotid Aneurysms: Causes, Stroke Risk and Treatment: Gert J De Borst, UMC Utrecht
In this talk, Dr. De Borst discussed the treatment and outcomes of extracranial carotid aneurysms. Extracranial carotid aneurysms are rare, compromising <1% of peripheral arterial aneurysms and 0.4% of all carotid interventions. However, 1 in 6 patients with extracranial carotid aneurysms have bilateral aneurysms, and 1 in 5 have aneurysms elsewhere, usually intracranial. The mean age of presentation is 50, with a male:female incidence of 2:1. Most extracranial carotid aneurysms are found incidentally and are asymptomatic. Others present with local cervical compression or thrombo-embolic events, though rupture at presentation is rare.
There are no evidence-based guidelines for treatment of these aneurysms. Often, asymptomatic aneurysms are treated conservatively and followed over time, whereas symptomatic aneurysms are often treated surgically. Surgical options include aneurysm resection, partial aneurysmectomy, flow diverting stents, coiling or embolization, or bare metal stents. Recent literature reviews reflect the paucity of data on outcomes of cervical artery aneurysms. One review in 2015 found only 6 series on surgical treatment, with no series of conservative or endovascular management. The pooled stroke rate in this review was 4.6%, mortality rate was 2.3%, and cranial nerve palsy rate was 18%.
Dr. De Borst ended his talk discussing a worldwide carotid aneurysm registry (CAR). The registry includes patients with single or bilateral fusiform or saccular aneurysm located between the aortic arch and carotid syphon, and includes all treatment modalities. The objectives are to define the natural course of these aneurysms, understand optimal imaging techniques, identify risk factors for complications, document outcomes of treatment, and follow long-term outcomes. They currently have just below 500 patients enrolled.
In Vivo Imaging and Blood Biomarkers of Carotid Plaque Inflammation: Peter Kelly, Mater University Hospital
Dr. Kelly described in vivo imaging and blood biomarkers of carotid plaque inflammation. The best studied imaging modality to assess unstable plaque is FDG-PET. In DUCASS, 60 patients with stroke or TIA within 14 days were enrolled, and all had carotid stenosis >50% ipsilateral to the stroke. Ipsilateral FDG-PET uptake was greater in patients with recurrent stroke, and mean maximum standardized uptake value (SUV max) was higher in patients with recurrent stroke. This study was validated with BIOVASC, which found that the risk of 90-day recurrent stroke increased each time the SUV max increased by 1 point. Dr. Kelly also described a systematic review of FDG-PET in the literature and relationship to recurrent stroke; howeverc there was a lack of data besides the beforementioned studies in addition to an unpublished study from Sant Pau Barcelona. The pooled hazard ratio for recurrent stroke per 1 unit SUV max increase was 2.19 (CI 1.41-3.39, p < 0.001).
Dr. Kelly discussed the SCAIL (symptomatic carotid atheroma inflammation lumen-stenosis) score. This score ranges from 0-5, and contains values for FDG uptake values and stenosis as follows: SUVmax <2 g/mL, 0 points; SUVmax 2-2.99 g/mL, 1 point; SUVmax 3-3.99 g/mL, 2 points; SUVmax ≥4 g/mL, 3 points and stenosis <50%, 0 points; 50%-69%, 1 point; ≥70%, 2 points. They found that the SCAIL score independently predicted recurrent stroke after PET imaging. In conclusion, SCAIL score may be used to select patients for revascularization in less straightforward cases such as mild carotid stenosis, women, younger patients, TIA, or late presentations.
Finally, Dr. Kelly discussed blood inflammatory markers and stroke. Blood inflammatory markers may be targets for new medications for stroke prevention, and may be markers of risk to select patients for more aggressive treatment. Currently data shows that IL-1, IL-6, and high sensitivity CRP may be useful as biomarkers; however, there are no randomized controlled trials studying their use. Two current trials are looking at colchicine in stroke, with analysis of benefit in carotid stenosis.
Carotid Plaque Composition and Implications for Stroke Aetiologies: Johanna Ospel, University Hospital Basel
Dr. Ospel discussed carotid plaque composition in her talk. Large artery atherosclerosis is a cause of 25% of ischemic stroke, but this classification only includes stenosis >50%. This is problematic as in the NASCET and ESCT trials, 40% of patients with stroke at follow up had <50% stenosis. Dr. Ospel argued that it is time to update the TOAST criteria, as these criteria are based on DSA imaging, which only takes into account the vessel lumen and does not define high-risk plaque features.
There are several ways to imaging the carotid arteries. DSA was used in the early trials, but its drawbacks include radiation, contrast use, it is invasive, and it only evaluates the lumen. Ultrasound is radiation-free and inexpensive, but is operator dependent and can have shadow effects. CTA is fast, inexpensive, not operator dependent, and has high availability, but it uses radiation and has low utility in assessing vessel wall. Finally, MRA has no radiation, is not operator dependent, and offers more information on plaque components; however, it is expensive, less readily available, is prone to motion artifact, and many patients have a contraindication to MRI.
There are several high-risk carotid features. Increased plaque volume is associated with increased vulnerability, though this measurement requires post-processing and is impractical in clinical practice. Increased plaque thickness >3mm can be evaluated on CTA and is more commonly seen with ipsilateral stroke. Surface irregularity is associated with increased risk of future stroke, but there are no standardized definitions of this irregularity. The presence of calcium is associated with lower risk of stroke, and lack of calcification is associated with higher risk. Intraplaque hemorrhage is associated with increased risk of stroke, and this can be evaluated with MRA and appears as hyperintense T1 signal. Absence of intraplaque hemorrhage has also been associated with lower risk of stroke even if high grade stenosis is present. Other high-risk features include: neovascularization, change in morphology over time, doughnut sign, and carotid web.
Dr. Ospel concluded by describing what she terms symptomatic non-stenotic carotid disease, defined by ipsilateral infarcts and high-risk carotid plaque with <50% stenosis.
Hemodynamic Stroke: Differences Between Anterior and Posterior Circulation: Katharina (Karin) Klijn, Radboud University Medical Center
Dr. Klijn described hemodynamic strokes in her talk. Hemodynamic strokes are caused by hypoperfusion rather than thromboembolism or local vasculopathy. In the Heart-Brain Study, more cortical infarcts were found ipsilateral to side of carotid occlusion, and there was lower flow in carotid artery. Carotid artery occlusion is also found in 9% of ischemic stroke patients. In the posterior circulation, 1/3 of patients have vertebrobasilar stenosis.
Dr. Klijn described several warning signs of hemodynamic origin. One such sign is limb-shaking, which are short, 1-5 minute episodes usually involving an entire arm or leg or both that are not epileptic in origin. 40% of these patients experience paresis after an attack. There is an association with limb-shaking events and lower CO2 reactivity and presence of collaterals. There are also eye signs and symptoms, including chronic ischemia with venous stasis retinopathy, gradual worsening of vision, neovascularization papil, glaucoma, pain, rubeosis iridis, blindness. Other signs of hemodynamic origin of stroke include symptom onset when: rising from supine, exercising, transitioning from cold to warm temperatures, eating, coughing, having taken antihypertensive, bleeding, or having anemia.
In the workup of hemodynamic origin of stroke, one should check for orthostasis. Imaging may show borderzone infarcts (especially internal border zone). Opthalmologic investigation may be done in select patients to look for chronic ischemia. If occlusion of carotid is found in the acute setting, the occlusion should be confirmed several days later to rule out severe stenosis rather than occlusion.
The VERiTAS study found that in patients with symptomatic >50% bilateral vertebrobasilar stenosis, 25% had low flow state and these patients had 3x higher risk of stroke. Patients with TIA or minor stroke and carotid artery occlusion also have increased risk of stroke. Treatment of hemodynamic stroke includes: antiplatelets and aggressive control of vascular risk factors. Unproven treatments that may be considered in select patients include: bed rest, tapering antihypertensives, endarterectomy of contralateral ICA stenosis of ipsilateral external carotid artery, and angioplasty/stent of vertebral or subclavian artery stenosis.
