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In this work, we aimed to understand how differences in atrial anatomy affect AF inducibility and dynamics, both without and with fibrosis, through in silico models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Atrial wall anatomies from late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) were used to generate personalised models. Detailed intra- and inter-atrial structures (pectinate muscles, Bachmann\u2019s bundle, fossa ovalis, coronary sinus, and fibre orientations) were mapped onto patient-specific atrial anatomies through a novel strategy using universal atrial coordinates and a highly detailed reference model. Patient-specific endomysial fibrosis was incorporated based on LGE-MRI. We quantified AF and macro-reentrant atrial tachycardia (MRAT) initiation rates in models with and without fibrosis, comparing reentry dynamics using renewal theory.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We generated personalised models of 10 patients, all but one with low-fibrotic content (Utah stages\u2009\u2264\u20092). Anatomical variability did not significantly affect AF initiation rates in both non-fibrotic (54.0\u2009\u00b1\u200913.7%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.43) and fibrotic models (53.5\u2009\u00b1\u200915.3%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.37). For AF\u2009+\u2009MRAT, initiation rates varied significantly among fibrotic models (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.04) but not among non-fibrotic ones (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.14). Reentry formation rates varied significantly across anatomies both with and without fibrosis (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.04). With fibrosis, reentry destruction rates also varied significantly (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.02). The number of simultaneous reentries varied significantly across patient anatomies (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001 without fibrosis,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05 with fibrosis), with fibrosis altering reentry counts in 2 patients (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.02).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Atrial anatomy influenced patient-specific variability in AF reentry dynamics, while fibrosis played a limited modifying role in this low-fibrotic cohort.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s10439-026-04265-9","type":"journal-article","created":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T17:03:12Z","timestamp":1783616592000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Analysis of the Effect of Anatomical Variability on Atrial Fibrillation Dynamics Through a Novel Framework for Personalised Atrial Model Generation"],"prefix":"10.1007","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9850-392X","authenticated-orcid":false,"given":"Victor Gon\u00e7alves","family":"Marques","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1803-8237","authenticated-orcid":false,"given":"Ali","family":"Gharaviri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7432-0424","authenticated-orcid":false,"given":"Simone","family":"Pezzuto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4238-5319","authenticated-orcid":false,"given":"Eduard","family":"Guasch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8115-5906","authenticated-orcid":false,"given":"Llu\u00eds","family":"Mont","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8804-235X","authenticated-orcid":false,"given":"Pietro","family":"Bonizzi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3738-7328","authenticated-orcid":false,"given":"Stef","family":"Zeemering","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1532-3315","authenticated-orcid":false,"given":"Ulrich","family":"Schotten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,9]]},"reference":[{"key":"4265_CR1","doi-asserted-by":"publisher","first-page":"752","DOI":"10.1161\/CIRCRESAHA.117.311081","volume":"122","author":"J Heijman","year":"2018","unstructured":"Heijman, J., J.-B. 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