11 research outputs found

    Intravenous thrombolysis in acute central retinal artery occlusion – A prospective interventional case series

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    <div><p>Background</p><p>No evidence-based therapy exists for non-arteritic central retinal artery occlusion (NA-CRAO). Retinal ischemic tolerance is low; irreversible damage occurs within four hours of experimental NA-CRAO. In previous randomized trials evaluating intra-arterial or intravenous thrombolysis (IVT) in NA-CRAO, only one patient was treated this early. In December 2013, the Departments of Neurology & Stroke and Ophthalmology at University Hospital Tuebingen, Germany, decided to treat patients using IVT within 4.5 hours of NA-CRAO, the therapeutic window established for ischemic stroke.</p><p>Materials and methods</p><p>Consecutive NA-CRAO patients with severe visual loss received IVT after exclusion of intracranial hemorrhage. Follow-up was conducted at day 5 (d5) and day 30 (d30). Visual outcomes were compared to the conservative standard treatment (CST) arm of the EAGLE-trial.</p><p>Results</p><p>Until August 2016, 20 patients received IVT within 4.5 hours after NA-CRAO with a median onset-to-treatment time of 210 minutes (IQR 120–240). Visual acuity improved from baseline mean logarithm of the minimum angle of resolution 2.46±0.33 (SD) (light perception) to 1.52±1.09 (Snellen equivalent: 6/200) at d5 (p = 0.002) and 1.60±1.08 (Snellen equivalent: 6/240) at d30. Compared to the EAGLE CST-arm, functional recovery to reading ability occurred more frequently after IVT: 6/20 (30%) versus 1/39 (3%) at d5 (p = 0.005) and at d30 5/20 (25%) versus 2/37 (5%) (p = 0.045). Two patients experienced serious adverse events (one angioedema and one bleeding from an abdominal aortic aneurysm) but recovered without sequelae.</p><p>Conclusions</p><p>IVT within 4.5 hours after symptom onset may represent an effective treatment of NA-CRAO. Randomized trials are warranted to evaluate efficacy and safety of early IVT in acute NA-CRAO.</p></div

    Additional file 1: Table S1. of Point-of-care testing for emergency assessment of coagulation in patients treated with direct oral anticoagulants

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    Patient characteristics in the study groups. Table S2. Baseline laboratory results of patients in the study groups. Table S3. Diagnostic accuracy of HemochronŽ Signature aPTT and ACT-LR POCT cards for dabigatran. (DOC 87 kb

    Patient flow.

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    <p>BCVA = best corrected visual acuity, CRAO = central retinal artery occlusion, IVT = intravenous thrombolysis, INR = international normalized ratio, LogMAR = logarithm of the minimum angle of resolution.</p

    Intravenous thrombolysis in acute central retinal artery occlusion – A prospective interventional case series - Fig 2

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    <p><b>Evolution of best corrected visual acuity over time (BCVA):</b> (A) mean BCVA of our intravenous thrombolysis (IVT) cohort (N = 20) and of the conservative standard treatment (CST) group of the EAGLE-trial [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0198114#pone.0198114.ref007" target="_blank">7</a>]. (B) individual BCVA of our IVT-cohort and (C) of the EAGLE CST-arm. Functional blindness (LogMAR >1.3) and functional recovery (LogMAR ≤0.5) are indicated by a gray and blue background, respectively. LogMAR = logarithm of the minimum angle of resolution.</p

    Categorical presentation of best corrected visual acuity.

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    <p>Categorical presentation of best corrected visual acuity (according to the current version of the WHO International Classification of Diseases [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0198114#pone.0198114.ref014" target="_blank">14</a>]) at baseline and at day 30 of our intravenous thrombolysis cohort and of the conservative standard treatment group of the EAGLE-trial [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0198114#pone.0198114.ref007" target="_blank">7</a>]. We defined favorable outcome as mild or no visual impairment (LogMAR ≤0.5, indicated in blue). Unfavorable outcome includes moderate or severe visual impairment (LogMAR >0.5 to ≤1.3) and functional blindness (LogMAR >1.3). LogMAR = logarithm of the minimum angle of resolution.</p

    TRoponin of Unknown origin in STroke evaluated by multi-component cardiac Magnetic resonance Imaging - The TRUST-MI study

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    AimsIncreased high-sensitive cardiac troponin I (hs-cTnI) levels are common in patients with acute ischemic stroke. However, only a minority demonstrates culprit lesions on coronary angiography, suggesting other mechanisms, e.g., inflammation, as underlying cause of myocardial damage. Late Gadolinium Enhancement (LGE)-cardiac magnetic resonance (CMR) with mapping techniques [T1, T2, extracellular volume (ECV)] allow the detection of both focal and diffuse myocardial abnormalities. We investigated the prevalence of culprit lesions by coronary angiography and myocardial tissue abnormalities by a comprehensive CMR protocol in troponin-positive stroke patients.Methods and resultsPatients with troponin-positive acute ischemic stroke and no history of coronary artery disease were prospectively enrolled. Coronary angiography and CMR (LGE, T1 + T2 mapping, ECV) were performed within the first days of the acute stroke. Twenty-five troponin-positive patients (mean age 62 years, 44% females) were included. 2 patients (8%) had culprit lesions on coronary angiography and underwent percutaneous coronary intervention. 13 patients (52%) demonstrated LGE: (i) n = 4 ischemic, (ii) n = 4 non-ischemic, and (iii) n = 5 ischemic AND non-ischemic. In the 12 LGE-negative patients, mapping revealed diffuse myocardial damage in additional 9 (75%) patients, with a high prevalence of increased T2 values.ConclusionsOur data show a low prevalence of culprit lesions in troponin-positive stroke patients. However, > 50% of the patients demonstrated myocardial scars (ischemic + non-ischemic) by LGE-CMR. Mapping revealed additional myocardial abnormalities (mostly inflammatory) in the majority of LGE-negative patients. Therefore, a comprehensive CMR protocol gives important insights in the etiology of troponin which might have implications for the further work-up of troponin-positive stroke patients.</p
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