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Age was reported to be an effect-modifier in four randomised controlled trials comparing carotid artery stenting (CAS) and carotid endarterectomy (CEA), with better CEA outcomes than CAS outcomes noted in the more elderly patients. We aimed to describe the association of age with treatment differences in symptomatic patients and provide age-specific estimates of the risk of stroke and death within narrow (5 year) age groups. In this meta-analysis, we analysed individual patient-level data from four randomised controlled trials within the Carotid Stenosis Trialists' Collaboration (CSTC) involving patients with symptomatic carotid stenosis. We included only trials that randomly assigned patients to CAS or CEA and only patients with symptomatic stenosis. We assessed rates of stroke or death in 5-year age groups in the periprocedural period (between randomisation and 120 days) and ipsilateral stroke during long-term follow-up for patients assigned to CAS or CEA. We also assessed differences between CAS and CEA. All analyses were done on an intention-to-treat basis. Collectively, 4754 patients were randomly assigned to either CEA or CAS treatment in the four studies. 433 events occurred over a median follow-up of 2·7 years. For patients assigned to CAS, the periprocedural hazard ratio (HR) for stroke and death in patients aged 65–69 years compared with patients younger than 60 years was 2·16 (95% CI 1·13–4·13), with HRs of roughly 4·0 for patients aged 70 years or older. We noted no evidence of an increased periprocedural risk by age group in the CEA group (p=0·34). These changes underpinned a CAS-versus CEA periprocedural HR of 1·61 (95% CI 0·90–2·88) for patients aged 65–69 years and an HR of 2·09 (1·32–3·32) for patients aged 70–74 years. Age was not associated with the postprocedural stroke risk either within treatment group (p≥0·09 for CAS and 0·83 for CEA), or between treatment groups (p=0·84). In these RCTs, CEA was clearly superior to CAS in patients aged 70–74 years and older. The difference in older patients was almost wholly attributable to increasing periprocedural stroke risk in patients treated with CAS. Age had little effect on CEA periprocedural risk or on postprocedural risk after either procedure. None.

The risk of periprocedural stroke or death is higher after carotid artery stenting (CAS) than carotid endarterectomy (CEA) for the treatment of symptomatic carotid stenosis. However, long-term outcomes have not been sufficiently assessed. We sought to combine individual patient-level data from the four major randomised controlled trials of CAS versus CEA for the treatment of symptomatic carotid stenosis to assess long-term outcomes. We did a pooled analysis of individual patient-level data, acquired from the four largest randomised controlled trials assessing the relative efficacy of CAS and CEA for treatment of symptomatic carotid stenosis (Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis trial, Stent-Protected Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy trial, International Carotid Stenting Study, and Carotid Revascularization Endarterectomy versus Stenting Trial). The risk of ipsilateral stroke was assessed between 121 days and 1, 3, 5, 7, 9, and 10 years after randomisation. The primary outcome was the composite risk of stroke or death within 120 days after randomisation (periprocedural risk) or subsequent ipsilateral stroke up to 10 years after randomisation (postprocedural risk). Analyses were intention-to-treat, with the risk of events calculated using Kaplan-Meier methods and Cox proportional hazards analysis with adjustment for trial. In the four trials included, 4775 patients were randomly assigned, of whom a total of 4754 (99·6%) patients were followed up for a maximum of 12·4 years. 21 (0·4%) patients immediately withdrew consent after randomisation and were excluded. Median length of follow-up across the studies ranged from 2·0 to 6·9 years. 129 periprocedural and 55 postprocedural outcome events occurred in patients allocated CEA, and 206 and 57 for those allocated CAS. After the periprocedural period, the annual rates of ipsilateral stroke per person-year were similar for the two treatments: 0·60% (95% CI 0·46–0·79) for CEA and 0·64% (0·49–0·83) for CAS. Nonetheless, the periprocedural and postprocedural risks combined favoured CEA, with treatment differences at 1, 3, 5, 7, and 9 years all ranging between 2·8% (1·1–4·4) and 4·1% (2·0–6·3). Outcomes in the postprocedural period after CAS and CEA were similar, suggesting robust clinical durability for both treatments. Although long-term outcomes (periprocedural and postprocedural risks combined) continue to favour CEA, the similarity of the postprocedural rates suggest that improvements in the periprocedural safety of CAS could provide similar outcomes of the two procedures in the future. None.

ABSTRACTObjectivesPoststroke depression (PSD) is a public health issue, affecting one-third of stroke survivors, and is associated with multiple negative consequences. Reviews tried to identify PSD risk factors with discrepant results, highlighting the lack of comparability of the analyzed studies. We carried out a meta-analysis in order to identify clinical risk factors that can predict PSD. DesignPubMed and Web of Science were searched for papers. Only papers with a strictly defined Diagnostic and Statistical Manual of Mental Disorders depression assessment, at least 2 weeks after stroke, were selected. Two authors independently evaluated potentially eligible studies that were identified by our search and independently extracted data using standardized spreadsheets. Analyses were performed using MetaWin®, the role of each variable being given as a risk ratio (RR). ResultsEighteen studies were included in the meta-analysis. Identified risk factors for PSD with RR significantly above 1 were previous history of depression (RR 2.19, confidence interval (CI) 1.52–3.15), disability (RR 2.00, CI 1.58–2.52), previous history of stroke (RR 1.68, CI 1.06–2.66), aphasia (RR 1.47, CI 1.13–1.91), and female gender (RR 1.35, CI 1.14–1.61). Fixed effects model leads to identification of two more risk factors: early depressive symptoms with an RR of 2.32 (CI 1.43–3.79) and tobacco consumption (RR 1.40, CI 1.09–1.81). Time bias was found for alcohol consumption. Sample size was significantly involved to explain the role of “alcohol consumption” and “cognitive impairment.” ConclusionFive items were significantly predictive of PSD. It might be of clinical interest that depressive-related risk factors (such as past depressive episodes) were having the largest impact.

Background Daily manual tasks require cognitive-motor interactions. There is limited research on cognitive-motor dual-tasks involving the upper extremity. In this study we used a manual visuomotor dual-task to measure post-stroke cognitive-motor impairments. Given previous evidence of impaired cognitive-motor interaction in stroke we hypothesized that the presence of enhanced dual-task cognitive load will impact motor performance in stroke patients. We also hypothesized that this dual-task effect would be greater in stroke patients compared to healthy controls. We also explored whether cognitive-motor impairments observed in these single- and dual-task conditions would relate to deficits in manual dexterity. Methods 30 chronic stroke participants (29.77 ± 35.39 months post-stroke) with mild-to-moderate hemiparesis without cognitive impairment (global screening test) and 30 age-matched healthy subjects performed a visuomotor grip force-tracking task in single- and dual-task conditions, requiring divided attention (resisting visual distraction) and working memory (mental addition of transiently displayed numbers). Gaze was simultaneously recorded to probe cognitive performance through saccades. Dexterity impairments were separately quantified using a kinetic device. Results Stroke patients had increased visuomotor tracking error but did not show significantly increased change in visuomotor tracking error during the dual-task, with no significant difference between single task condition vs. divided attention or vs. working memory dual-task conditions. In contrast, age-matched healthy controls did show the expected difference with significantly higher dual-task force-tracking error. The between-group analysis only revealed a significant group difference (Stroke vs. Control) with stroke patients producing twice as much tracking error in both single and dual-task conditions. Stroke participants showed significantly reduced dual-task saccade modulation, with a reduced difference in saccades to displayed numbers (similar in both groups) vs. to distractors (higher in stroke) (median ± IQR: stroke 14.6 ± 18.75%; controls: 26.4 ± 32.41%). Non-inhibited saccades to distractors explained certain dexterity group differences (force control and timing of finger movements). Conclusion The visuomotor force-tracking error, although increased, did not show enhanced cognitive-motor interaction in stroke. However, the task-related saccade analysis did detect impaired divided attention post-stroke, that may contribute to impaired dexterity, particularly in tasks requiring on-line sensorimotor integration. Upper limb dual-tasking practice may be relevant for engaging attention and enhancing post-stroke activities in daily life. Trial registration ClinicalTrials.gov ID NCT05454748.

Objective To compare the efficacy of Dextrain Manipulandum™ training of dexterity components such as force control and independent finger movements, to dose-matched conventional therapy (CT) post-stroke. Methods A prospective, single-blind, pilot randomized clinical trial was conducted. Chronic-phase post-stroke patients with mild-to-moderate dexterity impairment (Box and Block Test (BBT) > 1) received 12 sessions of Dextrain or CT. Blinded measures were obtained before and after training and at 3-months follow-up. Primary outcome was BBT-change (after–before training). Secondary outcomes included changes in motor impairments, activity limitations and dexterity components. Corticospinal excitability and short intracortical inhibition (SICI) were measured using transcranial magnetic stimulation. Results BBT-change after training did not differ between the Dextrain (N = 21) vs CT group (N = 21) (median [IQR] = 5[2–7] vs 4[2–7], respectively; P = 0.36). Gains in BBT were maintained at the 3-month post-training follow-up, with a non-significant trend for enhanced BBT-change in the Dextrain group (median [IQR] = 3[− 1–7.0], P = 0.06). Several secondary outcomes showed significantly larger changes in the Dextrain group: finger tracking precision (mean ± SD = 0.3 ± 0.3N vs − 0.1 ± 0.33N; P < 0.0018), independent finger movements (34.7 ± 25.1 ms vs 7.7 ± 18.5 ms, P = 0.02) and maximal finger tapping speed (8.4 ± 7.1 vs 4.5 ± 4.9, P = 0.045). At follow-up, Dextrain group showed significantly greater improvement in Motor Activity Log (median/IQR = 0.7/0.2–0.8 vs 0.2/0.1–0.6, P = 0.05). Across both groups SICI increased in patients with greater BBT-change (Rho = 0.80, P = 0.006). Comparing Dextrain subgroups with maximal grip force higher/lower than median (61.2%), BBT-change was significantly larger in patients with low vs high grip force (7.5 ± 5.6 vs 2.9 ± 2.8; respectively, P = 0.015). Conclusions Although immediate improvements in gross dexterity post-stroke did not significantly differ between Dextrain training and CT, our findings suggest that Dextrain enhances recovery of several dexterity components and reported hand-use, particularly when motor impairment is moderate (low initial grip force). Findings need to be confirmed in a larger trial. Trial registration ClinicalTrials.gov NCT03934073 (retrospectively registered)

Background The evaluation process of French medical students will evolve in the next few years in order to improve assessment validity. Script concordance testing (SCT) offers the possibility to assess medical knowledge alongside clinical reasoning under conditions of uncertainty. In this study, we aimed at comparing the SCT scores of a large cohort of undergraduate medical students, according to the experience level of the reference panel. Methods In 2019, the authors developed a 30-item SCT and sent it to experts with varying levels of experience. Data analysis included score comparisons with paired Wilcoxon rank sum tests and concordance analysis with Bland & Altman plots. Results A panel of 75 experts was divided into three groups: 31 residents, 21 non-experienced physicians (NEP) and 23 experienced physicians (EP). Among each group, random samples of N  = 20, 15 and 10 were selected. A total of 985 students from nine different medical schools participated in the SCT examination. No matter the size of the panel (N = 20, 15 or 10), students’ SCT scores were lower with the NEP group when compared to the resident panel (median score 67.1 vs 69.1, p  < 0.0001 if N = 20; 67.2 vs 70.1, p  < 0.0001 if N  = 15 and 67.7 vs 68.4, p  < 0.0001 if N  = 10) and with EP compared to NEP (65.4 vs 67.1, p  < 0.0001 if N = 20; 66.0 vs 67.2, p  < 0.0001 if N = 15 and 62.5 vs 67.7, p  < 0.0001 if N = 10). Bland & Altman plots showed good concordances between students’ SCT scores, whatever the experience level of the expert panel. Conclusions Even though student SCT scores differed statistically according to the expert panels, these differences were rather weak. These results open the possibility of including less-experienced experts in panels for the evaluation of medical students.

Background Identification of intraplaque haemorrhage using magnetic resonance imaging (MRI) is expensive, technically demanding and sometimes uncomfortable. Photoacoustic imaging (PAI) is a new non-invasive technique combining multi-wavelength infrared laser light and ultrasound (US) imaging, able to discriminate blood and other components in the tissues. The measurement by the multi-spectral PAI is likely to be more applicable and therefore could be complementary to MRI. Objectives Validate a portable multimodal and multi-wavelength PAI system, for the identification of intraplaque haemorrhage and compare with MRI. Materials and Methods Patients underwent carotid MRI, and US. Photoacoustic acquisitions are performed and analysed a posteriori blindly of the status of the subjects and results of MRI/US. All patients gave written informed consent. Histology of plaque will be performed as gold standard. Results We included 15 patients (71 ± 5 years old) with carotid stenosis grade of >70% (NASCET). PAI imaging was feasible in all patients. On raw images, only clutter signal can be observed. After adequate post processing, carotid wall with the intima media and plaques were clearly visible with PAI. PAI signal from the lumen can be observed, also strong PAI signals are visible inside the plaque in a reproducible manner. Correspondence between MRI and PAI will be analysed later. Conclusion The use of the PAI technique for carotid plaque assessment is feasible, and PAI signal are observed inside the plaque. Further analyses are needed to assess the reflected PAI signal inside the plaque, for haemorrhage detection in the future.

Whether arterial stiffness is a surrogate end-point for cardiovascular and renal disease has never been directly demonstrated by a controlled clinical trial. Our main hypothesis is a better prevention of outcomes in high risk hypertensives with PWV normalization driven strategy than with usual blood pressure driven therapeutic strategy based on European Society of Hypertension—European Society of Cardiology (ESH—ESC) guidelines. The strategy for preventing cardiovascular and renal events based on arterial stiffness study is a multicenter open-label randomized controlled trial with blinded endpoint evaluation comparing a therapeutic strategy targeting the normalisation of Pulse Wave Velocity (PWV group) versus a classical therapeutic strategy only implementing the ESH—ESC Guidelines (conventional group), for reducing cardiovascular and renal events. Patients with primary hypertension, aged 55–75 years, and at medium-to-very high cardiovascular risk will be included and followed-up for 4 years. In the PWV group, treatment will be adjusted to carotid-femoral PWV measured every 6 months. In the conventional group, PWV will be measured at baseline and every 2 years, but its value will be blinded to the investigator in charge of the patient. In the PWV group, the therapeutic strategy will preferably use a combination of Angiotensin-converting Enzyme Inhibitor (ACEI) [or Angiotensin Receptor Blockers (ARB)] and calcium channel blockers, as well as maximal recommended doses of ACEIs and ARBs. The primary combined endpoint includes stroke and coronary events (myocardial infarction, angioplasty, bypass), fatal or not, peripheral artery disease (angioplasty, bypass, amputation), hospitalization for heart failure, aortic dissection, chronic kidney disease (doubling of creatinine, dialysis), and sudden death. Twenty-five research centers will include a total of 1500 patients, in order to show a 20% reduction in the primary combined endpoint - the incidence of which is estimated at 10% per year - in the PWV group compared to the conventional group.

Aim To validate a photoacoustic imaging (PAI) system, for the identification of intraplaque hemorrhage, comparing it with MRI and histology (gold standard). Methods 25 patients with carotid stenosis>70% and clinical indication to tromboendoarterectomy were recruited. Angio-MRI for intraplaque hemorrhage assessment (Cube sequence) was performed. PAI clips (5 seconds, Frame rate 1000/sec, 3 to 15 per patient) were acquired. Each clip was scored for the presence of PAI signal by means of an integrated scoring system (semiquantitative, from 0 to 12). Semiquantitative grading scales were used to assess plaque histological features of hemorrhage and vulnerability. Results 18 patients had no missing MRI, PAI and histology data and were included in this analysis. Mean age was 73 ± 8 years, 60% men, 80% Caucasians, 92% hypertensives, 60% with a previous stroke. At histology, only 3 plaques out of 21 showed no signs of intraplaque hemorrhage, 4 showed small hemorrhage, while 14 (67%) showed large hemorrhages. PAI score (best cut-off ≥ 4) correctly classified 14 out of 18 patients (Sensitivity = 73.3%, specificity = 100%, AUC = 0.867). MRI performance was substantially similar, with 12 patients correctly classified (sensitivity = 60%, specificity = 100%, AUC = 0.800), with a non-significant difference in AUC compared to PAI ( p = 0.420). Conclusions In this first in-vivo human study, PAI is able to identify histological intraplaque hemorrhage with an excellent specificity and acceptable sensitivity, equivalent to MRI. The very high specificity, with a low number of false positives, make PAI a good candidate for evaluation of plaques prior to surgery to i.e. reinforce the decision to perform surgery.

Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke. We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602. Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19–2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95% CI 1·20–1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82–3·29) for intracranial haemorrhage and 1·23 (1·08–1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95% CI 3·08–6·72] for intracranial haemorrhage vs 1·47 [1·19–1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36–9·05] vs 1·43 [1·07–1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69–15·81] vs 1·86 [1·23–2·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48–84] per 1000 patient-years vs 27 intracranial haemorrhages [17–41] per 1000 patient-years; and for ≥20 cerebral microbleeds, 73 ischaemic strokes [46–108] per 1000 patient-years vs 39 intracranial haemorrhages [21–67] per 1000 patient-years). In patients with recent ischaemic stroke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazard (aHR) for subsequent intracranial haemorrhage than for ischaemic stroke, but the absolute risk of ischaemic stroke is higher than that of intracranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden. British Heart Foundation and UK Stroke Association.