Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/22835
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dc.contributor.authorSajeev, Jithin K-
dc.contributor.authorKalman, Jonathan M-
dc.contributor.authorDewey, Helen-
dc.contributor.authorCooke, Jennifer C-
dc.contributor.authorTeh, Andrew W-
dc.date.accessioned2020-03-23T22:10:38Z-
dc.date.available2020-03-23T22:10:38Z-
dc.date.issued2020-03-
dc.identifier.citationJACC. Clinical electrophysiology 2020; 6(3): 251-261-
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/22835-
dc.description.abstractAtrial fibrillation (AF) is well-recognized in the pathophysiology of left atrial thrombogenesis and resultant cardioembolic stroke. Subclinical AF is believed to account for a significant proportion of embolic stroke. However, recent randomized control trials failed to demonstrate a significant benefit for oral anticoagulation, in an unselected population with embolic stroke of undetermined source. This has reinvigorated the focus on finding robust markers to identify patients at risk of cardioembolic stroke. Several nonfibrillatory atrial electrical markers, along with structural and biochemical abnormalities, have been associated with ischemic stroke, independently of AF. An increasingly complex relationship exists among vascular risk factors, atrial remodeling, and thrombogenesis. Identifying robust markers of an underlying atrial myopathy may allow for early identification of patients at risk for cardioembolic stroke. This review outlines the inconsistencies in the evidence for AF as the prerequisite for left atrial thrombogenesis and embolic stroke. It will highlight the current evidence and controversies for adverse atrial remodeling, independent from rhythm, as a plausible mechanism for left atrial thrombogenesis and ischemic stroke.-
dc.language.isoeng-
dc.subjectESUS-
dc.subjectatrium-
dc.subjectmyopathy-
dc.subjectStroke-
dc.subjectthrombogenesis-
dc.titleThe Atrium and Embolic Stroke: Myopathy Not Atrial Fibrillation as the Requisite Determinant?-
dc.typeJournal Article-
dc.identifier.journaltitleJACC. Clinical electrophysiology-
dc.identifier.affiliationDepartment of Neuorosciences, Eastern Health, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Cardiology, Royal Melbourne Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationUniversity of Melbourne, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Cardiology, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationMonash University, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Cardiology, Eastern Health, Melbourne, Victoria, Australiaen
dc.identifier.doi10.1016/j.jacep.2019.12.013-
dc.identifier.pubmedid32192674-
dc.type.austinJournal Article-
dc.type.austinReview-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptCardiology-
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