{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T02:32:04Z","timestamp":1792549924216,"version":"4.5.0"},"reference-count":98,"publisher":"Wiley","issue":"24","license":[{"start":{"date-parts":[[2024,11,8]],"date-time":"2024-11-08T00:00:00Z","timestamp":1731024000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>Stroke is a leading cause of death and disability worldwide. Atrial myopathy, including fibrosis, is associated with an increased risk of ischaemic stroke, but the mechanisms underlying this association are poorly understood. Fibrosis modifies myocardial structure, impairing electrical propagation and tissue biomechanics, and creating stagnant flow regions where clots could form. Fibrosis can be mapped non\u2010invasively using late gadolinium enhancement magnetic resonance imaging (LGE\u2010MRI). However, fibrosis maps are not currently incorporated into stroke risk calculations or computational electro\u2010mechano\u2010fluidic models. We present multiphysics simulations of left atrial (LA) myocardial motion and haemodynamics using patient\u2010specific anatomies and fibrotic maps from LGE\u2010MRI. We modify tissue stiffness and active tension generation in fibrotic regions and investigate how these changes affect LA flow for different fibrotic burdens. We find that fibrotic regions and, to a lesser extent, non\u2010fibrotic regions experience reduced myocardial strain, resulting in decreased LA emptying fraction consistent with clinical observations. Both fibrotic tissue stiffening and hypocontractility independently reduce LA function, but, together, these two alterations cause more pronounced effects than either one alone. Fibrosis significantly alters flow patterns throughout the atrial chamber, and particularly, the filling and emptying jets of the left atrial appendage (LAA). The effects of fibrosis in LA flow are largely captured by the concomitant changes in LA emptying fraction except inside the LAA, where a multifactorial behaviour is observed. This work illustrates how high\u2010fidelity, multiphysics models can be used to study thrombogenesis mechanisms in patient\u2010specific anatomies, shedding light onto the links between atrial fibrosis and ischaemic stroke.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16399-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Left atrial (LA) fibrosis is associated with arrhythmogenesis and increased risk of ischaemic stroke; its extent and pattern can be quantified on a patient\u2010specific basis using late gadolinium enhancement magnetic resonance imaging.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Current stroke risk prediction tools have limited personalization, and their accuracy could be improved by incorporating patient\u2010specific information such as fibrotic maps and haemodynamic patterns.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We present the first electro\u2010mechano\u2010fluidic multiphysics computational simulations of LA flow, including fibrosis and anatomies from medical imaging.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Mechanical changes in fibrotic tissue impair global LA motion, decreasing LA and left atrial appendage (LAA) emptying fractions, especially in subjects with higher fibrosis burdens.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Fibrotic\u2010mediated LA motion impairment alters LA and LAA flow near the endocardium and the whole cavity, ultimately leading to more stagnant blood regions in the LAA.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp287011","type":"journal-article","created":{"date-parts":[[2024,11,8]],"date-time":"2024-11-08T12:15:41Z","timestamp":1731068141000},"page":"6789-6812","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Multiphysics simulations reveal haemodynamic impacts of patient\u2010derived fibrosis\u2010related changes in left atrial tissue mechanics"],"prefix":"10.1113","volume":"602","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7492-5741","authenticated-orcid":false,"given":"Alejandro","family":"Gonzalo","sequence":"first","affiliation":[{"name":"Department of Mechanical Engineering University of Washington  Seattle WA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6341-4014","authenticated-orcid":false,"given":"Christoph M.","family":"Augustin","sequence":"additional","affiliation":[{"name":"Gottfried Schatz Research Center, Division of Biophysics Medical University of Graz  Graz Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Savannah F.","family":"Bifulco","sequence":"additional","affiliation":[{"name":"Department of Bioengineering University of Washington  Seattle WA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5399-4094","authenticated-orcid":false,"given":"\u00c5shild","family":"Telle","sequence":"additional","affiliation":[{"name":"Department of Bioengineering University of Washington  Seattle WA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaacoub","family":"Chahine","sequence":"additional","affiliation":[{"name":"School of Cardiology University of Washington  Seattle WA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmad","family":"Kassar","sequence":"additional","affiliation":[{"name":"School of Cardiology University of Washington  Seattle WA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"Guerrero\u2010Hurtado","sequence":"additional","affiliation":[{"name":"Department of Aerospace and Biomedical Engineering Universidad Carlos III de Madrid  Legan\u00e9s Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eduardo","family":"Dur\u00e1n","sequence":"additional","affiliation":[{"name":"Dept. 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