Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/33038
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dc.contributor.authorSharobeam, Angelos-
dc.contributor.authorLin, Longting-
dc.contributor.authorLam, Christina-
dc.contributor.authorGarcia-Esperon, Carlos-
dc.contributor.authorGawarikar, Yash-
dc.contributor.authorPatel, Ronak-
dc.contributor.authorLee-Archer, Matthew-
dc.contributor.authorWong, Andrew-
dc.contributor.authorRoizman, Michael-
dc.contributor.authorGilligan, Amanda K-
dc.contributor.authorLee, Andrew-
dc.contributor.authorTan, Kee Meng-
dc.contributor.authorDay, Susan-
dc.contributor.authorLevi, Christopher-
dc.contributor.authorDavis, Stephen M-
dc.contributor.authorParsons, Mark-
dc.contributor.authorYan, Bernard-
dc.date2023-
dc.date.accessioned2023-06-07T02:47:23Z-
dc.date.available2023-06-07T02:47:23Z-
dc.date.issued2023-05-29-
dc.identifier.citationStroke and Vascular Neurology 2023en_US
dc.identifier.issn2059-8696-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/33038-
dc.description.abstractThe optimal time to commence anticoagulation in patients with atrial fibrillation (AF) after ischaemic stroke or transient ischaemic attack (TIA) is unclear, with guidelines differing in recommendations. A limitation of previous studies is the focus on clinically overt stroke, rather than radiologically obvious diffusion-weighted imaging ischaemic lesions. We aimed to quantify silent ischaemic lesions and haemorrhages on MRI at 1 month in patients commenced on early (<4 days) vs late (≥4 days) anticoagulation. We hypothesised that there would be fewer ischaemic lesions and more haemorrhages in the early anticoagulant group at 1-month MRI. A prospective multicentre, observational cohort study was performed at 11 Australian stroke centres. Clinical and MRI data were collected at baseline and follow-up, with blinded imaging assessment performed by two authors. Timing of commencement of anticoagulation was at the discretion of the treating stroke physician. We recruited 276 patients of whom 208 met the eligibility criteria. The average age was 74.2 years (SD±10.63), and 79 (38%) patients were female. Median National Institute of Health Stroke Scale score was 5 (IQR 1-12). Median baseline ischaemic lesion volume was 5 mL (IQR 2-17). There were a greater number of new ischaemic lesions on follow-up MRI in patients commenced on anticoagulation ≥4 days after index event (17% vs 8%, p=0.04), but no difference in haemorrhage rates (22% vs 32%, p=0.10). Baseline ischaemic lesion volume of ≤5 mL was less likely to have a new haemorrhage at 1 month (p=0.02). There was no difference in haemorrhage rates in patients with an initial ischaemic lesion volume of >5 mL, regardless of anticoagulation timing. Commencing anticoagulation <4 days after stroke or TIA is associated with fewer ischaemic lesions at 1 month in AF patients. There is no increased rate of haemorrhage with early anticoagulation. These results suggest that early anticoagulation after mild-to-moderate acute ischaemic stroke associated with AF might be safe, but randomised controlled studies are needed to inform clinical practice.en_US
dc.language.isoeng-
dc.subjectAnticoagulantsen_US
dc.subjectAtrial Fibrillationen_US
dc.subjectIschemic Attack, Transienten_US
dc.subjectMagnetic Resonance Imagingen_US
dc.subjectStrokeen_US
dc.titleEarly anticoagulation in patients with stroke and atrial fibrillation is associated with fewer ischaemic lesions at 1 month: the ATTUNE study.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleStroke and Vascular Neurologyen_US
dc.identifier.affiliationMelbourne Brain Centre at Royal Melbourne Hospital, Parkville, Victoria, Australia.en_US
dc.identifier.affiliationUniversity of New South Wales South Western Sydney Clinical School, Liverpool, New South Wales, Australia.en_US
dc.identifier.affiliationDepartment of Neurology, John Hunter Hospital, Newcastle, New South Wales, Australia.en_US
dc.identifier.affiliationDepartment of Neurology, Calvary Public Hospital, Canberra, Australian Capital Territory, Australia.en_US
dc.identifier.affiliationThe University of Queensland School of Medicine, Herston, Queensland, Australia.en_US
dc.identifier.affiliationDepartment of Neurology, Northern Hospital Epping, Epping, Victoria, Australia.en_US
dc.identifier.affiliationDepartment of Neurology, Royal Brisbane and Women's Hospital, Herston, Queensland, Australiaen_US
dc.identifier.affiliationNeurologyen_US
dc.identifier.affiliationNeurosciences Clinical Institute, Epworth Healthcare, Richmond, Virginia, Australiaen_US
dc.identifier.affiliationFlinders University College of Medicine and Public Health, Adelaide, South Australia, Australia.en_US
dc.identifier.affiliationDepartment of Neurology, Gold Coast University Hospital, Southport, Queensland, Australia.en_US
dc.identifier.affiliationThe University of Sydney Northern Clinical School, St Leonards, New South Wales, Australia.en_US
dc.identifier.affiliationepartment of Neurology and Neurophysiology, Liverpool Hospital, Liverpool, New South Wales, Australiaen_US
dc.identifier.affiliationUniversity of New South Wales South Western Sydney Clinical School, Liverpool, New South Wales, Australia.en_US
dc.identifier.doi10.1136/svn-2023-002357en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0001-5833-7632en_US
dc.identifier.orcid0000-0001-8843-5890en_US
dc.identifier.pubmedid37247875-
local.name.researcherGilligan, Amanda K
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptNeurology-
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