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Background: Small, randomized trials of patients with cervical artery dissection showed conflicting results regarding optimal stroke prevention strategies. We aimed to compare outcomes in patients with cervical artery dissection treated with antiplatelets versus anticoagulation., Methods: This is a multicenter observational retrospective international study (16 countries, 63 sites) that included patients with cervical artery dissection without major trauma. The exposure was antithrombotic treatment type (anticoagulation versus antiplatelets), and outcomes were subsequent ischemic stroke and major hemorrhage (intracranial or extracranial hemorrhage). We used adjusted Cox regression with inverse probability of treatment weighting to determine associations between anticoagulation and study outcomes within 30 and 180 days. The main analysis used an as-treated crossover approach and only included outcomes occurring with the above treatments., Results: The study included 3636 patients (402 [11.1%] received exclusively anticoagulation and 2453 [67.5%] received exclusively antiplatelets). By day 180, there were 162 new ischemic strokes (4.4%) and 28 major hemorrhages (0.8%); 87.0% of ischemic strokes occurred by day 30. In adjusted Cox regression with inverse probability of treatment weighting, compared with antiplatelet therapy, anticoagulation was associated with a nonsignificantly lower risk of subsequent ischemic stroke by day 30 (adjusted hazard ratio [HR], 0.71 [95% CI, 0.45-1.12]; P =0.145) and by day 180 (adjusted HR, 0.80 [95% CI, 0.28-2.24]; P =0.670). Anticoagulation therapy was not associated with a higher risk of major hemorrhage by day 30 (adjusted HR, 1.39 [95% CI, 0.35-5.45]; P =0.637) but was by day 180 (adjusted HR, 5.56 [95% CI, 1.53-20.13]; P =0.009). In interaction analyses, patients with occlusive dissection had significantly lower ischemic stroke risk with anticoagulation (adjusted HR, 0.40 [95% CI, 0.18-0.88]; P interaction =0.009)., Conclusions: Our study does not rule out the benefit of anticoagulation in reducing ischemic stroke risk, particularly in patients with occlusive dissection. If anticoagulation is chosen, it seems reasonable to switch to antiplatelet therapy before 180 days to lower the risk of major bleeding. Large prospective studies are needed to validate our findings., Competing Interests: Disclosures Disclosures provided by Dr Nguyen in compliance with American Heart Association annual Journal Editor Disclosure Questionnaire are available at https://www.ahajournals.org/editor-coi-disclosures. Dr Arnold reports compensation from Boehringer Ingelheim, AstraZeneca, Bayer, Bristol-Myers Squibb, Covidien, Daiichi Sankyo, Novartis, Sanofi, Pfizer, Medtronic, Novo Nordisk, and Amgen for consultant services. Dr Lester reports a provisional patent for Methods and compositions for disrupting tau aggregates. Dr Touze reports compensation from Elsevier for other services and employment by Caen. J.E. Kaufman reports grants from Goldschmidt Jacobson-Stiftung. Dr Traenka reports travel support from Bayer Healthcare. Dr Aguiar de Sousa reports compensation from Daiichi Sankyo, Bayer, AstraZeneca, Johnson & Johnson, and Fundação Bial for other services; compensation from the University of British Columbia for data and safety monitoring services; compensation from Organon & Co for consultant services. Dr Rosa reports grants from Merck Sharp & Dohme Corporation. Dr Field reports compensation from HLS Therapeutics, AstraZeneca Canada, and Roche for consultant services; service as a board member for Destine Health; and compensation from the Canadian Medical Protective Association for expert witness services; and grants from Bayer. Dr Leker reports compensation from Medtronic, Ischemaview, Bayer, Abbott Diabetes Care, Biogen, Janssen Biotech, and Boehringer Ingelheim for other services. Dr Nolte reports compensation from Daiichi Sankyo Europe GmbH, Boehringer Ingelheim, Pfizer, Bristol-Myers Squibb, and Alexion Pharmaceuticals for consultant services; and compensation from AstraZeneca, Abbott Canada, Deutsches Zentrum für Neurodegenerative Erkrankungen, Novartis, Portola Pharmaceuticals, Deutsches Zentrum für Herz-Kreislaufforschung, and Novartis for other services. Dr Poppe reports grants from Foundation Brain Canada, Heart and Stroke Foundation of Canada, and Stryker; and compensation from Roche for other services. Dr Liebeskind reports compensation from Medtronic, Genentech, Cerenovus, Stryker, and Rapid Medical Ltd, for consultant services. B. Mac Grory reports grants from the National Institutes of Health; employment by Duke University Medical Center; compensation from Bayer for other services; grants from the American Heart Association, Duke Bass Connections, and the Duke Office of Physician Scientist Development. Dr Al Kasab reports compensation from Stryker for other services and employment by Medical University of South Carolina. Dr Kicielinski reports compensation from Stryker, Penumbra Inc, Medtronic, and MicroVention Inc, for other services; travel support from MicroVention Inc; and employment by Medical University of South Carolina and Elsevier. Dr de Havenon reports stock options in TitinKM and Certus; grants from the National Institutes of Health; and compensation from Novo Nordisk for consultant services. Dr Siegler reports grants from Philips and employment by the University of Chicago. Dr Willey reports compensation from Edwards Lifesciences Corporation and Abbott Fund for end point review committee services; compensation from Uptodate for other services; and compensation from the Abbott Laboratories for consultant services. Dr Sharma reports a provisional patent for a stroke etiology classifier algorithm and grants from the National Institutes of Health Clinical Center. Dr Martins reports compensation from Pfizer, Medtronic, Servier Affaires Medicales, Daiichi Sankyo, Bayer, Novo Nordisk, Novartis, Penumbra Inc, and Boehringer Ingelheim for other services. Dr Simpkins reports grants from the National Institutes of Health. Dr Stretz reports grants from Massachusetts General Hospital. Dr Furie reports compensation from Janssen Biotech for consultant services. The other authors report no conflicts

Background and Purpose: The efficacy of endovascular therapy in patients with acute ischemic stroke due to tandem occlusion is comparable to that for isolated intracranial occlusion in the anterior circulation. However, the optimal management of acute cervical internal carotid artery lesions is unknown, especially in the setting of carotid dissection, but emergency carotid artery stenting (CAS) is frequently considered. We investigated the safety and efficacy of emergency CAS for carotid dissection in patients with acute stroke with tandem occlusion in current clinical practice., Methods: We retrospectively analyzed a prospectively maintained database composed of 2 merged multicenter international observational real-world registries (Endovascular Treatment in Ischemic Stroke and Thrombectomy in Tandem Lesion). Data from endovascular therapy performed in the treatment of tandem occlusions related to acute cervical carotid dissection between January 2012 and January 2019 at 24 comprehensive stroke centers were analyzed., Results: The study assessed 136 patients with tandem occlusion due to dissection, including 65 (47.8%) treated with emergency CAS and 71 (52.2%) without. The overall rates of favorable outcome (90-day modified Rankin Scale score, 0-2) and successful reperfusion (modified Thrombolysis in Cerebral Infarction, 2b-3) were 58.0% (n=76 [95% CI, 49.6%-66.5%]) and 77.9% (n=106 [95% CI, 71.0%-85.0%]), respectively. In subgroup analyses, the rate of successful reperfusion (89.2% versus 67.6%; adjusted odds ratio, 2.24 [95% CI, 1.33-3.77]) was higher after CAS, whereas the 90-day favorable outcome (54.3% versus 61.4%; adjusted odds ratio, 0.84 [95% CI, 0.58-1.22]), symptomatic intracerebral hemorrhage (sICH; 10.8% versus 5.6%; adjusted odds ratio, 1.59 [95% CI, 0.79-3.17]), and 90-day mortality (8.0% versus 5.8%; adjusted odds ratio, 1.00 [95% CI, 0.48-2.09]) did not differ. In sensitivity analyses of patients with successful intracranial reperfusion, CAS was not associated with an improved clinical outcome., Conclusions: Emergency stenting of the dissected cervical carotid artery during endovascular therapy for tandem occlusions seems safe, whatever the quality of the intracranial reperfusion.

Background and Purpose: Dissection is an increasingly recognized cause of ischemic stroke, which occurs spontaneously or after trauma, in relatively young patients. We hypothesized that there might be a predisposing factor weakening the vascular wall and that arterial tortuosity might be higher in patients with dissection., Methods: We consecutively enrolled cervical artery dissection (CerAD) patients who had undergone magnetic resonance angiography. Age- and sex-matched healthy subjects who underwent magnetic resonance angiography in a routine health examination were used as controls. The tortuosity was measured semiautomatically from the carotid artery and vertebral artery (VA) arteries. Tortuosity index was defined as: [(arc/chord)-1×100] in each arteries. Independent risk factors associated with CerAD were investigated using multivariable analysis. Subgroup analysis according to the dissected artery was performed., Results: There were no differences in vascular risk factors between the 75 CerAD patients and the 75 controls. The tortuosity indexes of the contralesional VA (16.3±6.8 versus 12.1±4.5, respectively; P<0.001) and carotid artery (8.8±4.0 versus 7.3±2.9, respectively; P=0.01) were higher in patients with CerAD compared with those of control subjects. VA tortuosity (odds ratio, 1.175; P=0.001) was independently associated with the presence of CerAD. In subgroup analysis, VA tortuosity was significantly higher in 57 patients with VA dissection than in controls (P<0.001), and carotid artery tortuosity was marginally higher in 18 patients with carotid artery dissection (P=0.05)., Conclusions: CerAD is associated with tortuous cervical arteries, which may implicate weakened cervical vascular structure in these patients., (© 2016 American Heart Association, Inc.)

Background and Purpose: Isolated Horner syndrome without associated cranial nerve palsies or ischemic symptoms is an important presentation of spontaneous internal carotid artery dissection (sICAD). Ultrasound is often used as a screening method in these patients because cervical MRI is not always available on an emergency basis. Current knowledge on ultrasound findings in patients with sICAD presenting with isolated Horner syndrome is limited., Methods: Patients were recruited from prospective cervical artery dissection databases of 3 tertiary care centers. Diagnosis of sICAD was confirmed by cervical MRI and MR angiography or digital subtraction angiography in all patients. Data on Doppler sonography and color duplex sonography examinations performed within 30 days of symptom onset were analyzed., Results: We identified 88 patients with Horner syndrome as the only sign of sICAD. Initial ultrasound examination was performed in 72 patients after a mean time interval from symptom onset to examination of 11 (SD 8) days. The overall frequency of false-negative ultrasound findings was 31% (22 of 72 patients). It showed stenosis >or=80% or occlusion in 34 (47%) patients, and stenosis

Background and Purpose: MR is widely used to depict still ischemic but viable tissue in acute stroke. However, the relationship between the apparent diffusion coefficient (ADC) and energy failure from reduced oxygen supply are unknown in man., Methods: Acute carotid-territory stroke patients were studied prospectively with both diffusion tensor-imaging and back-to-back steady-state 15O-PET. Substantial numbers of voxels with oxygen extraction fraction >0.70 (ie, significant ongoing hypoxia) were identified in 3 patients (imaged at 7, 16 and 21 hours after stroke onset). In this voxel population, the quantitative relationships between the ADC and cerebral metabolic rate of oxygen (CMRO2), and ADC and cerebral blood flow (CBF), were assessed., Results: The ADC remained essentially unchanged until CBF reached values approximately 20 mls/100g per min, beyond which it declined linearly. In contrast, except when severely reduced, the ADC was a poorer predictor of CMRO2. For both CBF and CMRO2, however, the relationship with ADC became steeper with longer times since onset, ie, the same ADC reflected lower perfusion and CMRO2 with elapsed time., Conclusions: Despite the small sample and late times from stroke onset, the findings indicate that the degree of restricted water diffusion reliably reflects the severity of oxygen deprivation below the penumbral threshold but is less strongly related to metabolic disruption, which may explain why the ADC does not reliably predict tissue outcome. However, the same degree of diffusion restriction may correspond to greater severity of tissue disruption with elapsing time, which has relevance for stroke therapy. Time elapsed since stroke onset should be taken into account when interpreting ADC declines and in voxel-based infarct prediction models.

Background and Purpose: It is unclear whether stroke in patients with spontaneous dissection of the cervical internal carotid artery (ICAD) is due to thromboembolism or impaired hemodynamics. This study investigated the mechanism of stroke in ICAD by examining brain imaging and cerebrovascular findings of such patients., Methods: We retrospectively evaluated the prospectively collected brain CT, MR, and ultrasound findings of 141 consecutive patients with 143 ICADs causing ischemic stroke. Eleven patients were not included because they had an inappropriate temporal bone window (n=6) or were treated with thrombolysis (n=5). Thus, the data of 130 patients (76 men, 54 women) with 131 ICADs were analyzed., Results: All patients had territorial infarcts; 6 patients (5%) also had border-zone infarct patterns. Territorial infarcts affected the middle cerebral artery (MCA) in 130 of 131 cases (99%) and the anterior cerebral artery (ACA) in 1 case (1%). Additional vascular territories were affected in 8 patients with MCA infarcts (ACA, n=5 [4%]; posterior cerebral artery, n=3 [2%]). The pattern (hemodynamic versus thromboembolic) and extent of infarction were not influenced by vascular findings (MCA stenosis or occlusion, ACA occlusion, degree of obstruction in the dissected ICA, pattern of cross-flow in 115 patients with >80% ICA stenosis or occlusion)., Conclusions: This study suggests that thromboembolism, not hemodynamic infarction, is the essential stroke mechanism in ICAD.

Background and Purpose: Carotid artery dissection (CAD) is a common cause of stroke in young patients. Clots formed at the low-flow zone in the false arterial lumen may give rise to distal emboli, and the mural hematoma may eventually occlude the artery. Anticoagulation is currently the accepted treatment, but it is unknown which patients will improve spontaneously, which will respond to anticoagulation, and which will have an exacerbation of ischemic symptoms despite therapy. Endovascular treatment of CAD may be an attractive alternative to anticoagulation, and methods of identifying patients who stand to benefit from such therapy need to be established., Methods: We present here 3 cases of spontaneous symptomatic CAD in which endovascular stenting procedures were performed on the basis of a paradigm aimed at identifying potentially salvageable but at-risk brain tissue by combining clinical with MRI (diffusion and perfusion) and angiographic data., Results: Diffusion-perfusion MRI mismatches and/or evidence of cerebral ischemia on angiographic parenchymography were identified in all patients. They did not respond to anticoagulation, were therefore treated with endovascular stents, and had excellent outcomes., Conclusions: Endovascular stent placement may be an immediate, effective, and safe method of restoring vessel lumen integrity. It may be considered for selected patients who are clinically symptomatic despite anticoagulant treatment and in whom neuroimaging methods suggest that the neurological signs originate from a viable, hypoperfused, ischemic penumbra.

Background and Purpose: The natural history of aneurysmal forms of cervical artery dissection (CAD) is ill defined. The aims of this study were to assess (1) clinical and anatomic outcome of aneurysmal forms of extracranial internal carotid artery (ICA) and vertebral artery (VA) dissections and (2) factors associated with aneurysmal forms of CAD., Methods: Seventy-one consecutive patients with CAD were reviewed. Aneurysmal forms of CAD were identified from all available angiograms by 2 neuroradiologists. The frequency of arterial risk factors, of multiple vessel dissections, and of artery redundancies was compared in patients with and without aneurysm. Patients with aneurysm were invited by mail to undergo a final clinical and radiological evaluation., Results: Of the 71 patients, 35 (49.3%) had a total of 42 aneurysms. Thirty aneurysms were located on a symptomatic artery (ICA, 23; VA, 7) and 12 on an asymptomatic artery (ICA, 10; VA, 2). Patients with aneurysm had multiple dissections of cervical vessels (18/35 versus 7/36; P:=0.005) and arterial redundancies (20/35 versus 11/36; P:=0.02) more frequently than patients without aneurysm. They were also more often migrainous (odds ratio=2.7 [95% CI, 0.8 to 8.5]) and tobacco users (odds ratio=2.2 [95% CI, 0.7 to 6.3]). Clinical and anatomic follow-up information was available for 35 (100%) and 33 patients (94%), respectively. During a mean follow-up of >3 years, no patient had signs of cerebral ischemia, local compression, or rupture. At follow-up, 46% of the aneurysms involving symptomatic ICA were unchanged, 36% had disappeared, and 18% had decreased in size. Resolution was more common for VA than for ICA aneurysms (83% versus 36%). None of the aneurysms located on an asymptomatic ICA had disappeared., Conclusions: Although aneurysms due to CAD frequently persist, patients carry a very low risk of clinical complications. This favorable clinical outcome should be kept in mind before potential harmful treatment is contemplated.