Alain Viguier

Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial: results up to 4 years from a randomised, multicentre trial

BACKGROUND Carotid stenting is a potential alternative to carotid endarterectomy but whether this technique is as safe as surgery and whether the long-term protection against stroke is similar to that of surgery are unclear. We previously reported that in patients in the Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial, the rate of any stroke or death within 30 days after the procedure was higher with stenting than with endarterectomy. We now report the results up to 4 years. METHODS In this follow-up study of a multicentre, randomised, open, assessor-blinded, non-inferiority trial, we compared outcome after stenting with outcome after endarterectomy in 527 patients who had carotid stenosis of at least 60% that had recently become symptomatic. The primary endpoint of the EVA-3S trial was the rate of any periprocedural stroke or death (ie, within 30 days after the procedure). The prespecified main secondary endpoint was a composite of any periprocedural stroke or death and any non-procedural ipsilateral stroke during up to 4 years of follow-up. Other trial outcomes were any stroke or periprocedural death, any stroke or death, and the above endpoints restricted to disabling or fatal strokes. This trial is registered with ClinicalTrials.gov, number NCT00190398. FINDINGS 262 patients were randomly assigned to endarterectomy and 265 to stenting. The cumulative probability of periprocedural stroke or death and non-procedural ipsilateral stroke after 4 years of follow-up was higher with stenting than with endarterectomy (11.1%vs 6.2%, hazard ratio [HR] 1.97, 95% CI 1.06-3.67; p=0.03). The HR for periprocedural disabling stroke or death and non-procedural fatal or disabling ipsilateral stroke was 2.00 (0.75-5.33; p=0.17). A hazard function analysis showed the 4-year differences in the cumulative probabilities of outcomes between stenting and endarterectomy were largely accounted for by the higher periprocedural (within 30 days of the procedure) risk of stenting compared with endarterectomy. After the periprocedural period, the risk of ipsilateral stroke was low and similar in both treatment groups. For any stroke or periprocedural death, the HR was 1.77 (1.03-3.02; p=0.04). For any stroke or death, the HR was 1.39 (0.96-2.00; p=0.08). INTERPRETATION The results of this study suggest that carotid stenting is as effective as carotid endarterectomy for middle-term prevention of ipsilateral stroke, but the safety of carotid stenting needs to be improved before it can be used as an alternative to carotid endarterectomy in patients with symptomatic carotid stenosis.

Isolated Acute Nontraumatic Cortical Subarachnoid Hemorrhage

SUMMARY: Our aim was to review the etiologic background of isolated acute nontraumatic cSAH. While SAH located in the basal cisterns originates from a ruptured aneurysm in approximately 85% of cases, a broad spectrum of vascular and even nonvascular pathologies can cause acute nontraumatic SAH along the convexity. Arteriovenous malformations or fistulas, cortical venous and/or dural sinus thrombosis, and distal and proximal arteriopathies (RCVS, vasculitides, mycotic aneurysms, Moyamoya, or severe atherosclerotic carotid disease) should be sought by noninvasive imaging methods or/and conventional angiography. Additionally, PRES may also be a source of acute cSAH. In elderly patients, cSAH might be attributed to CAA if numerous hemorrhages are demonstrated by GRE T2 images. Finally, cSAH is rarely observed in nonvascular disorders, such as abscess and primitive or secondary brain tumors.

Long-Term Follow-Up Study of Endarterectomy Versus Angioplasty in Patients With Symptomatic Severe Carotid Stenosis Trial

Background and Purpose— We aimed at comparing the long-term benefit–risk balance of carotid stenting versus endarterectomy for symptomatic carotid stenosis. Methods— Long-term follow-up study of patients included in Endarterectomy Versus Angioplasty in Patients With Symptomatic Severe Carotid Stenosis (EVA-3S), a randomized, controlled trial of carotid stenting versus endarterectomy in 527 patients with recently symptomatic severe carotid stenosis, conducted in 30 centers in France. The main end point was a composite of any ipsilateral stroke after randomization or any procedural stroke or death. Results— During a median follow-up of 7.1 years (interquartile range, 5.1–8.8 years; maximum 12.4 years), the primary end point occurred in 30 patients in the stenting group compared with 18 patients in the endarterectomy group. Cumulative probabilities of this outcome were 11.0% (95% confidence interval, 7.9–15.2) versus 6.3% (4.0–9.8) in the endarterectomy group at the 5-year follow-up (hazard ratio, 1.85; 1.00–3.40; P=0.04) and 11.5% (8.2–15.9) versus 7.6% (4.9–11.8; hazard ratio, 1.70; 0.95–3.06; P=0.07) at the 10-year follow-up. No difference was observed between treatment groups in the rates of ipsilateral stroke beyond the procedural period, severe carotid restenosis (≥70%) or occlusion, death, myocardial infarction, and revascularization procedures. Conclusions— The long-term benefit–risk balance of carotid stenting versus endarterectomy for symptomatic carotid stenosis favored endarterectomy, a difference driven by a lower risk of procedural stroke after endarterectomy. Both techniques were associated with low and similar long-term risks of recurrent ipsilateral stroke beyond the procedural period. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00190398.

Asymptomatic cerebral embolic signals in patients with acute cerebral ischaemia and severe aortic arch atherosclerosis

Abstract Severe aortic arch atheroma (AAA) is a strong risk factor for ischaemic stroke, but it is unclear whether AAA is a source of cerebral emboli or simply a marker of cerebral atherosclerosis. The purpose of this study was to find out the prevalence of asymptomatic cerebral embolic signals (ES) in patients with acute cerebral ischaemia, AAA and no other potential source of cerebral embolism. Forty patients with anterior circulation ischaemic stroke or transient ischaemic attack (TIA) were prospectively studied using transesophageal echocardiography (TEE) and transcranial Doppler (TCD) scanning within seven days of symptom onset. Patients with a cardiac source of embolism or carotid stenosis > 50 % were excluded. ES were detected in 14.3 % (2/14) of patients with AAA ≥ 4 mm and in no patients with AAA < 4 mm or no AAA (p=0.14). The findings suggest that ES may be associated with severe AAA but their prevalence is low in this setting.

Acute Convexity Subarachnoid Hemorrhage Related to Cerebral Amyloid Angiopathy: Clinicoradiological Features and Outcome

BACKGROUND The specificities of acute convexity subarachnoid hemorrhage (cSAH) related to cerebral amyloid angiopathy (CAA) and its evolution are not well known. We aimed to describe the clinicoradiological pattern, the magnetic resonance imaging (MRI) evolution, and the risk of recurrent bleeding in such patients. METHODS Among consecutive patients with an acute nontraumatic cSAH, subjects with available MRI who meet the modified Boston criteria for probable CAA were included. Review of medical records, MRI findings, and follow-up data was performed. RESULTS Twenty-three patients (14 women; mean age ± standard deviation: 75.9 ± 7.3 years) were included. cSAH was revealed by transient focal neurological episodes (TFNEs) in 18 of 23 (78.3%) patients. In all patients, acute cSAH appeared as a sulcal fluid-attenuated inversion recovery hyperintensity and GRE T2 hypointensity. Cortical superficial siderosis and cortical microbleeds, respectively, were observed in 21 (91.3%) and 20 (86.9%) patients. Twenty patients (87%) had available follow-up data with a mean duration of 29.8 ± 20.2 months. Recurrent TFNEs occurred in 40% of patients. Acute cSAH evolved into cortical superficial siderosis in all patients. New subarachnoid bleedings defined by recurrent acute cSAH (n = 8) or extension of siderosis (n = 14) were detected in 83.3% of the patients. Lobar intracerebral hemorrhage (ICH) occurred in 7 patients (35%). CONCLUSION CAA-related cSAH has a specific pattern defined by a high prevalence of TFNEs and cortical superficial siderosis, with a high risk of recurrent bleeding, either cSAH or lobar ICH. The systematic evolution from cSAH to focal cortical superficial siderosis reveals data on siderosis physiopathology.

Risk factor profile by etiological subtype of ischemic stroke in the young

BACKGROUND AND PURPOSE Studies of risk factors for ischemic stroke in the young have generally considered ischemic stroke as a whole. The purpose of the present study was to evaluate the association of traditional cardiovascular risk factors with etiological subtypes of ischemic stroke in young adults. METHODS Retrospective review of data from patients aged 16-54 years consecutively treated for first-ever ischemic stroke in an academic stroke unit. Definite causes of stroke were classified using the ASCO (A for atherothrombosis, S for small vessel disease, C for cardiac source, O for other cause) classification system. We used multinomial logistic regression analysis to evaluate associations of age, gender, smoking, hypertension, diabetes and blood lipids with each etiological subtype. RESULTS A total of 400 patients were included: 244 men (61.1%), 156 women (38.9%); mean age (SD) 44.5 (8.5) years. A definite cause of stroke could be identified in 202 (50.5%) patients. Definite causes of stroke included: atherothrombosis, 72 (18.0%) patients; cardioembolism, 37 (9.25%) patients; small vessel disease, 28 (7.0%) patients; other definite cause, 65 (16.25%) patients including 44 patients with carotid or vertebral artery dissection. Atherothrombosis was associated with age, smoking, diabetes, hypertension and low HDL-cholesterol. Small vessel disease was associated with age and hypertension. Cardioembolism was associated with age. CONCLUSION The risk factor profile differs between etiological subtypes of ischemic stroke in young adults. Our findings emphasize the impact of smoking, diabetes, hypertension and low HDL-cholesterol as risk factors for atherothrombosis, and of hypertension as a risk factor for small vessel disease in young adults.

Cervical artery stenoses in sickle cell disease.

97.8%; A2Hb 2.2%, and AHb undetectable. Despite thrombolysis, blood transfusion exchanges, and anti-edematous treatment, the patient’s condition deteriorated. A decompressive craniectomy was performed on the 4th day. At 6 months, the patient remained hemiparetic and was unable to walk, but his dysphasia had markedly improved. The modified Ranking score was 4. Screening for thrombophilia (protein C and S, factor VII, antithrombin III and lipoprotein (a) plasma levels, search for antiphospholipid antibodies, factor V Dear Sir, Ischemic stroke is a common complication of sickle cell disease (SCD). Approximately 1 in10 patients with this disease has a stroke before the age of 20 years, and 20% have evidence of brain infarction on MRI [1–3] . It is the primary cause of stroke in children [2] . Ischemic stroke in these patients is usually associated with an intracranial internal carotid (IC) fork stenosis or occlusion. Here we report a patient with SCD, ischemic stroke and multiple stenoses of the extracranial carotid and vertebral arteries.

Ischemic cerebral attacks due to a pseudo-aneurysm of the internal carotid artery with Listeria monocytogenes

Sirs: Mycotic aneurysms of the internal carotid artery are extremely rare. They may be linked to a local infection spreading by contiguity, complicate an operation or septicaemia. We report a case of an aneurysm following septicaemia caused by Listeria monocytogenes. A 73-year old man was admitted for a sudden, rapidly regressive paresis of the right upper limb. He had no inflammatory syndrome on admission. CT of the brain was normal. The cervical Doppler sonogram showed an atheromatous stenosis assessed at 70% on the left internal carotid artery. Two days later, he was febrile and was given amoxicillin + clavulanic acid on the assumption of a pneumopathy. He then experienced repeated transient ischemic attacks in the left carotid territory, despite heparin in association with aspirin and clopidogrel. A painful, non-pulsing, inflammatory lateral cervical mass progressively developed. Two weeks after admission, he suffered an ischemic stroke in the posterior area of the left middle cerebral artery. At the same time, the mass had considerably increased and induced a BernardHorner sign and dysphonia. A high fever had recurred. Cervical CT showed a mass surrounding the left carotid sinus, with a thick, irregular shell, and with contrast enhancement. A pool of contrast medium was visible inside the mass and was connected to the carotid lumen (Fig. 1). Blood cultures were positive for Listeria monocytogenes serovar 4. We concluded that this was a case of thrombosed, mycotic pseudoaneurysm. Intravenous amoxicillin was initiated and the patient was operated on five days later. The operation consisted of evacuating the pseudo-aneurysm, which communicated with the lumen of the internal carotid artery, via an opening at the level of the atheromatous plaque. Then, the carotid sinus was resected, an internal carotid-carotid bypass was performed using a saphenous vein graft, and the external carotid artery was reimplanted. On the removed piece, the rupture on the internal carotid wall was clearly visible (Fig. 2). Listeria monocytogenes was also isolated on the operative piece. The evolution was favourable, with no recurrence within three years. The thoracoabdomino-pelvic scan and arterial Doppler sonogram of the lower limbs showed no other aneurysms. Listeria monocytogenes is a ubiquitous saprophytic bacterium which can be found in up to 5% of gastrointestinal tracts of healthy adults [13]. A bacteraemia can occur in immunocompetent patients, but the infection is limited to the development of granulomae in contact with vascular epithelia. An arterial lesion on a large vessel with Listeria monocytogenes remains exceptional. 20 cases have been reported in the literature [2, 4, 7, 10]. Such patients are usually male, elderly, and with cardiovascular risk factors, but no immunodeficiency. The abdominal aorta and arteries of the lower limbs are the most frequent sites. This is the first report of a Listeria monocytogenes N. Boulloche Æ T. Slaoui Æ A. Viguier M. Rigal Æ V. Larrue Dept. of Neurology CHU Rangueil Toulouse, France

Magnetic resonance imaging of arterial stroke mimics: a pictorial review

Acute ischaemic stroke represents the most common cause of new sudden neurological deficit, but other diseases mimicking stroke happen in about one-third of the cases. Magnetic resonance imaging (MRI) is the best technique to identify those ‘stroke mimics’. In this article, we propose a diagnostic approach of those stroke mimics on MRI according to an algorithm based on diffusion-weighted imaging (DWI), which can be abnormal or normal, followed by the results of other common additional MRI sequences, such as T2 with gradient recalled echo weighted imaging (T2-GRE) and fluid-attenuated inversion recovery (FLAIR). Analysis of the signal intensity of the parenchyma, the intracranial arteries and, overall, of the veins, is crucial on T2-GRE, while anatomic distribution of the parenchymal lesions is essential on FLAIR. Among stroke mimics with abnormal DWI, T2-GRE demonstrates obvious abnormalities in case of intracerebral haemorrhage or cerebral amyloid angiopathy, but this sequence also allows to propose alternative diagnoses when DWI is negative, such as in migraine aura or headaches with associated neurological deficits and lymphocytosis (HaNDL), in which cortical venous prominence is observed at the acute phase on T2-GRE. FLAIR is also of major interest when DWI is positive by better showing evocative distribution of cerebral lesions in case of seizure (involving the hippocampus, pulvinar and cortex), hypoglycaemia (bilateral lesions in the posterior limb of the internal capsules, corona radiata, striata or splenium of the corpus callosum) or in posterior reversible encephalopathy syndrome (PRES). Other real stroke mimics such as mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes (MELAS), Susac’s syndrome, brain tumour, demyelinating diseases and herpes simplex encephalitis are also included in our detailed and practical algorithm.Key points• About 30% of sudden neurological deficits are due to non-ischaemic causes.• MRI is the best technique to identify stroke mimics.• Our practical illustrated algorithm based on DWI helps to recognise stroke mimics.