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Background COVID‐19 is associated with an increased stroke risk. Moreover, outcome at discharge was worse in patients with large‐vessel occlusion stroke with concomitant COVID‐19 receiving endovascular treatment (ET). We aimed to investigate the impact of concomitant COVID‐19 on later functional outcome in patients with large‐vessel occlusion stroke treated with ET. Methods We analyzed patients from the GSR‐ET (German Stroke Registry–Endovascular Treatment), an observational multicenter registry of patients with large‐vessel occlusion stroke receiving ET. Baseline characteristics, procedural parameters, discharge parameters, and functional outcome at 90 days were compared between patients with concomitant COVID‐19 and propensity score–matched controls (ratio, 1:4; matched for age, sex, prestroke modified Rankin Scale score, and stroke severity), and multivariable ordinal regression analysis was performed. Results Among 4010 patients receiving ET between February 2020 and December 2021, 72 (1.8%) had concomitant COVID‐19. Compared with 224 matched patients without COVID‐19, they (n=56) were more severely affected, with a higher median National Institutes of Health Stroke Scale (NIHSS) score after 24 hours (NIHSS score, 14.5 [interquartile range {IQR}, 9–22] versus 12 [IQR, 6–18.75]; P=0.015), and NIHSS score and modified Rankin Scale score at discharge (NIHSS score, 12 [IQR, 6.75‐16.75] versus 6 [IQR, 2–13]; P=0.001; and modified Rankin Scale score, 5 [IQR, 4–5] versus 4 [IQR, 2–5]; P=0.023), but functional outcome at 90‐day follow‐up was similar (modified Rankin Scale score, 4 [IQR, 4–6] versus 4 [IQR, 2–6]; P=0.34). After adjustment for prespecified confounders, COVID‐19 was associated with worse functional outcome at discharge (common odds ratio [OR], 0.40 [95% CI, 0.19–0.80]; P=0.011), but not at 90‐day follow‐up (common OR, 0.72 [95% CI, 0.32–1.60]; P=0.43). Conclusions COVID‐19 affected short‐term, but not 90‐day, functional outcome in patients with large‐vessel occlusion stroke treated with ET. Hence, ET should not be withheld in patients with concomitant COVID‐19.

Abstract Background Oral anticoagulation (OAC) is the mainstay of secondary prevention in ischemic stroke patients with atrial fibrillation (AF). However, in AF patients with large vessel occlusion stroke treated by endovascular therapy (ET) and acute carotid artery stenting (CAS), the optimal antithrombotic medication remains unclear. Methods This is a subgroup analysis of the German Stroke Registry—Endovascular Treatment (GSR-ET), a prospective multicenter cohort of patients with large vessel occlusion stroke undergoing ET. Patients with AF and CAS during ET were included. We analyzed baseline and periprocedural characteristics, antithrombotic strategies and functional outcome at 90 days. Results Among 6635 patients in the registry, a total of 82 patients (1.2%, age 77.9 ± 8.0 years, 39% female) with AF and extracranial CAS during ET were included. Antithrombotic medication at admission, during ET, postprocedural and at discharge was highly variable and overall mortality in hospital (21%) and at 90 days (39%) was high. Among discharged patients (n = 65), most frequent antithrombotic regimes were dual antiplatelet therapy (DAPT, 37%), single APT + OAC (25%) and DAPT + OAC (20%). Comparing DAPT to single or dual APT + OAC, clinical characteristics at discharge were similar (median NIHSS 7.5 [interquartile range, 3–10.5] vs 7 [4–11], p = 0.73, mRS 4 [IQR 3–4] vs. 4 [IQR 3–5], p = 0.79), but 90-day mortality was higher without OAC (32 vs 4%, p = 0.02). Conclusions In AF patients who underwent ET and CAS, 90-day mortality was higher in patients not receiving OAC. Registration: https://www.clinicaltrials.gov ; Unique identifier: NCT03356392.

The N-terminally truncated pyroglutamate Aβ3−42 (AβpE3−42) and Aβ4−42 peptides are known to be highly abundant in the brain of Alzheimer's disease (AD) patients. Both peptides show enhanced aggregation and neurotoxicity in comparison to full-length Aβ, suggesting that these amyloid peptides may play an important role in the pathogenesis of AD. The aim of the present work was to study the direct effect of the combination of AβpE3−42 and Aβ4−42 on ongoing AD-related neuron loss, pathology, and neurological deficits in transgenic mice. Bigenic mice were generated by crossing the established TBA42 and Tg4-42 mouse models expressing the N-truncated Aβ peptides AβpE3−42 and Aβ4−42, respectively. After generation of the bigenic mice, detailed phenotypical characterization was performed using either immunostainings to evaluate amyloid pathology or quantification of neuron numbers using design-based stereology. The elevated plus maze was used to study anxiety levels. In order to evaluate sensori-motor deficits, the inverted grid, the balance beam and the string suspension tasks were applied. We could demonstrate that co-expression of AβpE3−42 and Aβ4−42 accelerates neuron loss in the CA1 pyramidal layer of young bigenic mice as seen by reduced neuron numbers in comparison to single transgenic homozygous mice expressing either AβpE3−42 or Aβ4−42. This observation coincides with the robust intraneuronal Aβ accumulation observed in the bigenic mice. In addition, loss of anxiety and motor deficits were enhanced in an age-dependent manner. The sensori-motor deficits correlate with the abundant spinal cord pathology, as demonstrated by robust intracellular Aβ accumulation within motor neurons and extracellular Aβ deposition. Our observations demonstrate that a combination of AβpE3−42 and Aβ4−42 has a stronger effect on ongoing AD pathology than the peptides alone. Therefore, AβpE3−42 and Aβ4−42 might represent excellent potential therapeutic targets and diagnostic markers for AD.