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Cervical artery dissection is a major cause of stroke in young people (aged <50 years). Historically, clinicians have preferred using oral anticoagulation with vitamin K antagonists for patients with cervical artery dissection, although some current guidelines—based on available evidence from mostly observational studies—suggest using aspirin. If proven to be non-inferior to vitamin K antagonists, aspirin might be preferable, due to its ease of use and lower cost. We aimed to test the non-inferiority of aspirin to vitamin K antagonists in patients with cervical artery dissection. We did a multicentre, randomised, open-label, non-inferiority trial in ten stroke centres across Switzerland, Germany, and Denmark. We randomly assigned (1:1) patients aged older than 18 years who had symptomatic, MRI-verified, cervical artery dissection within 2 weeks before enrolment, to receive either aspirin 300 mg once daily or a vitamin K antagonist (phenprocoumon, acenocoumarol, or warfarin; target international normalised ratio [INR] 2·0–3·0) for 90 days. Randomisation was computer-generated using an interactive web response system, with stratification according to participating site. Independent imaging core laboratory adjudicators were masked to treatment allocation, but investigators, patients, and clinical event adjudicators were aware of treatment allocation. The primary endpoint was a composite of clinical outcomes (stroke, major haemorrhage, or death) and MRI outcomes (new ischaemic or haemorrhagic brain lesions) in the per-protocol population, assessed at 14 days (clinical and MRI outcomes) and 90 days (clinical outcomes only) after commencing treatment. Non-inferiority of aspirin would be shown if the upper limit of the two-sided 95% CI of the absolute risk difference between groups was less than 12% (non-inferiority margin). This trial is registered with ClinicalTrials.gov, NCT02046460. Between Sept 11, 2013, and Dec 21, 2018, we enrolled 194 patients; 100 (52%) were assigned to the aspirin group and 94 (48%) were assigned to the vitamin K antagonist group. The per-protocol population included 173 patients; 91 (53%) in the aspirin group and 82 (47%) in the vitamin K antagonist group. The primary endpoint occurred in 21 (23%) of 91 patients in the aspirin group and in 12 (15%) of 82 patients in the vitamin K antagonist group (absolute difference 8% [95% CI −4 to 21], non-inferiority p=0·55). Thus, non-inferiority of aspirin was not shown. Seven patients (8%) in the aspirin group and none in the vitamin K antagonist group had ischaemic strokes. One patient (1%) in the vitamin K antagonist group and none in the aspirin group had major extracranial haemorrhage. There were no deaths. Subclinical MRI outcomes were recorded in 14 patients (15%) in the aspirin group and in 11 patients (13%) in the vitamin K antagonist group. There were 19 adverse events in the aspirin group, and 26 in the vitamin K antagonist group. Our findings did not show that aspirin was non-inferior to vitamin K antagonists in the treatment of cervical artery dissection. Swiss National Science Foundation, Swiss Heart Foundation, Stroke Funds Basel, University Hospital Basel, University of Basel, Academic Society Basel.

Introduction: Cervical artery dissection is a major cause of stroke in the young. The optimal choice and duration of antithrombotic treatment for stroke prevention are debated, particularly beyond 3 months after symptom onset. Patients and methods: TREAT-CAD (TREATment of Cervical Artery Dissection) was a randomized controlled trial with blinded outcome assessment comparing non-inferiority of aspirin to anticoagulation (Vitamin-K-antagonists) in participants with symptomatic, Magnetic-Resonance-(MR)-imaging-verified cervical artery dissection. TREAT-CAD could not establish non-inferiority of aspirin to anticoagulation at 3 months. Thereafter participants could continue antithrombotic medication and obtained a standardized assessment of clinical and MR-Imaging outcomes between 3 and 6 months. As crossover to the other treatment arm was possible, we performed an as-treated analysis as main analysis. The main outcomes were new clinical (ischemic stroke, intracranial/major extracranial bleeding, or death) and new MR-Imaging outcomes (ischemic or hemorrhagic brain lesions). Results: Among the 122 participants in the as-treated analysis, 3/93 (3.2%) aspirin-treated participants had new clinical (n = 1) and MRI-outcomes (n = 2) between 3 and 6 months while 1/29 (3.4%) anticoagulated participants had an MRI-outcome (n = 1). All outcome events were hemorrhagic while ischemic events were absent. No deaths occurred. This yields an absolute difference of 0.2% (95% CI −8.0% to 7.5%, p = 1.0). Discussion and conclusion: During the extended follow-up period of a controlled randomized trial comparing aspirin to anticoagulation in cervical artery dissection, outcomes between 3 and 6 months after randomization occurred rarely, similarly often in both groups and were exclusively hemorrhagic events. Thus, studies balancing benefits versus harms of antithrombotic treatment beyond 3 months are warranted. Registration: ClinicalTrials.gov: NCT02046460. https://clinicaltrials.gov/ct2/show/NCT02046460. Graphical abstract

Abstract BACKGROUND: Dissection of the carotid and vertebral arteries is an important cause of stroke in young patients. OBJECTIVE: The objective of this study is to compare antithrombotic treatments in patients with carotid and vertebral dissections. METHODS: Three hundred seventy patients with carotid and vertebral artery dissections were included. Univariate and multivariate analyses were conducted to analyze the association between treatment and new or recurrent events and clinical outcome. RESULTS: Mean follow-up was 24.3 months. In patients with spontaneous dissection, 55% received antiplatelets, 29.4% anticoagulation, and 12.6% combined treatment. New or recurrent ischemic and hemorrhagic events occurred in 9.6% of patients on antiplatelets, 10.4% on anticoagulation, and 13.3% on combined treatment. For traumatic dissection, 58.3% received antiplatelets, 26.9% anticoagulation, and 10.2% combined treatment. New or recurrent ischemic and hemorrhagic events occurred in 6.9% on antiplatelets, 11.1% on anticoagulation, and 20% on combined treatment. In patients with intracranial dissection, 63.1% were started on antiplatelets, 19.7% on anticoagulation, and 14.5% on combined treatment. Ischemic and hemorrhagic events occurred in 8.5% on antiplatelet treatment, 15.4% on anticoagulation, and 18.2% on combined treatment. In patients with extracranial dissection, 54.4% were on antiplatelets, 28.9% on anticoagulation, and 11.2% on combined treatment. Ischemic and hemorrhagic events occurred in 10.1% on antiplatelet treatment, 9.3% on anticoagulation, and 13.8% on combined treatment. The association between antithrombotic treatment and ischemic/hemorrhagic events and clinical outcome was not significant for all subtypes of dissection. CONCLUSION: The rate of new or recurrent events is similar with antiplatelet and anticoagulation treatment in treating intracranial and extracranial carotid and vertebral artery dissection.

When a tear occurs in one of the major arteries in the neck and allows blood to enter the wall of the artery and split its layers, the result is either stenosis or aneurysmal dilatation of the vessel. This process was long thought to be a rare cause of stroke, particularly in the absence of trauma, and the diagnosis was usually not made until the postmortem examination. 1 – 3 It was not until the late 1970s, when Fisher et al. 1 and Mokri et al. 2 described dissections of carotid and vertebral arteries as detected by modern diagnostic approaches, that dissections began to . . .

Purpose of Review We aimed to summarize recent findings in cervical (CeAD) and intracranial artery dissection (IAD) research. Recent Findings Considered a disease of the young- and middle-aged, an analysis on the largest CeAD-population to date ( n  = 2391) revealed that about 1 of 14 CeAD-patients was aged ≥60 years. Distinct genetic variants were associated with CeAD. However, in clinical practice, genetic investigations are not helpful due to the small effect size. Despite the paucity of data from randomized-controlled trials in CeAD-stroke patients, both intravenous thrombolysis and endovascular treatment should be considered as acute treatment in such patients. Future research is needed to clarify which patients benefit most from each treatment modality. Whether to use antiplatelets or anticoagulants in stroke prevention in CeAD-patients is still a matter of debate. One randomized-controlled feasibility trial has been published, and another trial designed to show non-inferiority of aspirin to vitamin-K-antagonists is underway and will be terminated in late 2018. Non-vitamin-K-oral anticoagulants should not be used in CeAD outside a properly designed trial, as experience with these drugs in CeAD-patients is limited. With many IAD patients developing intracranial hemorrhage, antithrombotic therapy should be used with caution. Summary Knowledge about CeAD and IAD has advanced substantially. Nevertheless, further research is mandatory, in particular regarding pathophysiology, acute treatment, and stroke-preventive therapy, as well as long-term outcome and prognosis.

Background Vertebrobasilar dissecting aneurysm (VBDA) has high morbidity and mortality rates, and it is an important cause of stroke in young and middle-aged adults. Previous studies have shown that aneurysm wall inflammation is a major factor contributing to the high risk of aneurysm growth and rupture. Metformin inhibits inflammation and may be a suitable candidate drug for VBDA. Here, we report the protocol for a study designed to evaluate the ability of metformin to reduce the degree of aneurysm wall inflammation in patients with VBDA, as measured by high-resolution vessel wall imaging (HR-VWI). Methods The study is a multicentre, prospective, randomised, controlled, and blinded clinical trial. Sixty patients with unruptured VBDA who meet the inclusion/exclusion criteria will be recruited competitively from three hospitals in China. Patient recruitment began in May 2024 and is expected to end in December 2025. The patients will be randomised (1:1) to treatment or placebo ( n  = 30 in each group), receiving either 250-mg metformin or placebo orally twice per day for 6 months. The primary outcome will be the change in VBDA wall inflammation measured by HR-VWI. The secondary outcomes will be changes in VBDA morphology, typical imaging signs, and inflammatory biomarkers. Discussion Previous studies on metformin for the treatment of intracranial aneurysms have been performed in animals. However, prospective clinical studies in humans are lacking. Therefore, this study will provide insights into the anti-inflammatory effects of metformin in inhibiting VBDA growth and rupture and may reveal a new treatment modality for unruptured VBDA. The protocol has been approved by the Ethics Committee of Beijing Tiantan Hospital (approval no. KY2023-188–02). All patients will be required to provide written informed consent prior to participation. The results of the study will be disseminated through peer-reviewed journals and at relevant academic conferences. Trial registration NCT06405971. Registered on May 9, 2024.

Background: American and European guidelines support antiplatelet agents and anticoagulants as reasonable treatments of cervical artery dissection (CAD), though randomized clinical trials are lacking. The utility of novel oral anticoagulants (NOAC), effective in reducing embolic stroke risk in non-valvular atrial fibrillation (NVAF), has not been reported in patients with CAD. We report on the use, safety, and efficacy of NOACs in the treatment of CAD. Methods: We retrospectively identified patients diagnosed with CAD at a single academic center between January 2010 and August 2013. Patients were categorized by their antithrombotic treatment at hospital discharge with a NOAC (dabigatran, rivaroxaban, or apixaban), traditional anticoagulant (AC: warfarin or treatment dose low-molecular weight heparin), or antiplatelet agent (AP: aspirin, clopidogrel, or aspirin/extended-release dypyridamole). Using appropriate tests, we compared the baseline medical history, presenting clinical symptoms and initial radiographic characteristics among patients in the 3 treatment groups. We then evaluated for the following outcomes: recurrent stroke, vessel recanalization, and bleeding complications. p values <0.05 were considered significant. Results: Of the 149 included patients (mean age 43.4 years; 63.1% female; 70.5% vertebral artery CAD), 39 (26.2%), 70 (47.0%), and 40 (26.8%) were treated with a NOAC, AC, and AP, respectively. More patients with severe stenosis or occlusion were treated with NOAC than with AC or AP (61.8 vs. 60.0 vs. 22.5%, p = 0.002). Other baseline clinical and radiographic findings, including the presence of acute infarction and hematoma, did not differ between the 3 treatment groups. One hundred and thirty-five (90.6%) patients had clinical follow-up (median time 7.5 months) and 125 (83.9%) had radiographic follow-up (median time 5 months) information. There were 2 recurrent strokes in the NOAC group and 1 in each of the AC and AP groups (p = 0.822). There were more major hemorrhagic events in the AC group (11.4%) compared to the NOAC (0.0%) and AP (2.5%) groups (p = 0.034). Three patients treated with NOAC and none treated with AC or AP had a worsened degree of stenosis on follow-up imaging (8.6 vs. 0.0 vs. 0.0%, p = 0.019). Conclusion: Compared to traditional anticoagulants for CAD, treatment with NOACs is associated with similar rates of recurrent stroke, fewer hemorrhagic complications, but greater rates of radiographic worsening. These data suggest that NOACs may be a reasonable alternative in the management of CAD. Prospective validation of these findings is needed.

Carotid and vertebral artery dissections are estimated to account for ∼20% of strokes in patients under 45-years-old. This meta-analysis compared the efficacy and safety of treatment with anticoagulants versus antiplatelet agents to determine the optimal therapy. We searched 4 electronic databases for clinical trials published from January 1, 1980 to August 25, 2021 that included patients who received anticoagulant or antiplatelet therapy for carotid and/or vertebral artery dissections. The curative effect was judged by recanalization evaluated by imaging. The primary outcomes were all cause death and ischemic stroke; secondary outcomes included hemorrhage and transient ischemic attack (TIA). Patients who received only a single drug treatment were divided into antiplatelet or anticoagulant groups; all received conservative treatment without surgical intervention. For this investigation, we pooled the available studies to conduct a meta-analysis, which included 7 articles with 1126 patients. The curative effect of vascular recanalization was not significantly different between the 2 treatment groups (odds ratio [OR] = 0.913, 95% confidence interval [CI]: 0.611-1.365, P = .657); similarly, no significant differences were found regarding the primary outcomes all cause death (OR = 1.747, 95%CI: 0.202-15.079, P = .612) and ischemic stroke (OR = 2.289, 95%CI: 0.997-5.254, P = .051). Patients treated with anticoagulants were more likely to experience TIA (OR = 0.517, 95%CI: 0.252-1.060, P = .072) and hemorrhage (OR = 0.468, 95%CI: 0.210-1.042, P = .063), but the differences were not statistically significant. Overall, there were no statistically significant differences between anticoagulant therapy and antiplatelet therapy for the treatment of carotid and vertebral artery dissections.

Background Arterial dissection is a rare complication of pregnancy and puerperium. There have been reports of aortic, coronary and cervical artery dissection in association with preeclampsia, however, vertebral artery dissection is rarely reported particularly in the antenatal setting in the presence of a Hypertensive Disorder of Pregnancy (HDP).The general annual incidence of symptomatic spontaneous cervicocephalic arterial dissection is 0.0026 % and a data registry reported that 2.4 % of these occurred in the post-partum period. The actual incidence of vertebral artery dissection in HDP is unknown as the current literature consists of case series and reports only with most documenting adverse outcomes. Given the presence of collateral circulation, unilateral vertebral artery dissections may go unrecognised and may be more common than suspected. Case presentation We present a case series of four patients with vertebral artery dissection in association with HDP, two of which occurred in the antenatal setting and two in the post-partum setting. All our patients had favourable outcome with no maternal neurological deficit and live infants. Our discussion covers the proposed pathophysiology of vertebral artery dissection in HDP and the management of it. Conclusion Our case series highlights the need to consider VAD an important differential diagnosis when assessing pregnant women with headache and neck pain particularly in the context of HDP

Clazosentan prevents vasospasms after aneurysmal subarachnoid hemorrhage (SAH). However, clinical data on patients with SAH with ruptured vertebral artery dissecting aneurysms (VADAs) are limited. We report the case of a 49-year-old male patient with mild-grade (WFNS grade 1) thick and diffuse (modified Fisher grade 3) SAH who underwent endovascular trapping of a ruptured VADA, resulting in a poor functional outcome with a modified Rankin Scale score of 4 due to severe symptomatic vasospasm refractory to clazosentan, requiring repeated rescue endovascular therapies and chronic communicating hydrocephalus. A retrospective analysis of the clot density in the basal and Sylvian cisterns, assessed by the Hounsfield unit (HU) values of serial CT scans, in this patient showed persistent higher values, distinct from another VADA case that showed a decline in HU values with a good clinical course. These results imply the limited effectiveness of clazosentan in cases of thick and diffuse SAH after a ruptured VADA, even in good-clinical-grade patients treated with less invasive modalities. The HU values may become a simple quantitative marker for predicting symptomatic vasospasms and chronic hydrocephalus.