{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T10:35:28Z","timestamp":1791974128454,"version":"4.4.0"},"reference-count":64,"publisher":"Oxford University Press (OUP)","issue":"8","license":[{"start":{"date-parts":[[2024,4,22]],"date-time":"2024-04-22T00:00:00Z","timestamp":1713744000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000266","name":"UK Engineering and Physical Sciences Research Council","doi-asserted-by":"publisher","award":["2421745"],"award-info":[{"award-number":["2421745"]}],"id":[{"id":"10.13039\/501100000266","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["FS\/CRTF\/21\/24144"],"award-info":[{"award-number":["FS\/CRTF\/21\/24144"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["RE\/18\/3\/34214"],"award-info":[{"award-number":["RE\/18\/3\/34214"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["FS\/17\/22\/32644"],"award-info":[{"award-number":["FS\/17\/22\/32644"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["RE\/13\/1\/30181"],"award-info":[{"award-number":["RE\/13\/1\/30181"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Swiss National Supercomputing Centre, Switzerland","award":["icp005"],"award-info":[{"award-number":["icp005"]}]},{"name":"Swiss National Supercomputing Centre, Switzerland","award":["icp013"],"award-info":[{"award-number":["icp013"]}]},{"name":"Swiss National Supercomputing Centre, Switzerland","award":["icp019"],"award-info":[{"award-number":["icp019"]}]},{"name":"University of Oxford Advanced Research Computing"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,7,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Lethal arrhythmias in hypertrophic cardiomyopathy (HCM) are widely attributed to myocardial ischaemia and fibrosis. How these factors modulate arrhythmic risk remains largely unknown, especially as invasive mapping protocols are not routinely used in these patients. By leveraging multiscale digital twin technologies, we aim to investigate ischaemic mechanisms of increased arrhythmic risk in HCM.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Computational models of human HCM cardiomyocytes, tissue, and ventricles were used to simulate outcomes of Phase 1A acute myocardial ischaemia. Cellular response predictions were validated with patch-clamp studies of human HCM cardiomyocytes (n = 12 cells, N = 5 patients). Ventricular simulations were informed by typical distributions of subendocardial\/transmural ischaemia as analysed in perfusion scans (N = 28 patients). S1-S2 pacing protocols were used to quantify arrhythmic risk for scenarios in which regions of septal obstructive hypertrophy were affected by (i) ischaemia, (ii) ischaemia and impaired repolarization, and (iii) ischaemia, impaired repolarization, and diffuse fibrosis. HCM cardiomyocytes exhibited enhanced action potential and abnormal effective refractory period shortening to ischaemic insults. Analysis of \u223c75 000 re-entry induction cases revealed that the abnormal HCM cellular response enabled establishment of arrhythmia at milder ischaemia than otherwise possible in healthy myocardium, due to larger refractoriness gradients that promoted conduction block. Arrhythmias were more easily sustained in transmural than subendocardial ischaemia. Mechanisms of ischaemia\u2013fibrosis interaction were strongly electrophysiology dependent. Fibrosis enabled asymmetric re-entry patterns and break-up into sustained ventricular tachycardia.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>HCM ventricles exhibited an increased risk to non-sustained and sustained re-entry, largely dominated by an impaired cellular response and deleterious interactions with the diffuse fibrotic substrate.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvae086","type":"journal-article","created":{"date-parts":[[2024,4,22]],"date-time":"2024-04-22T08:25:56Z","timestamp":1713774356000},"page":"914-926","source":"Crossref","is-referenced-by-count":14,"title":["Mechanisms of ischaemia-induced arrhythmias in hypertrophic cardiomyopathy: a large-scale computational study"],"prefix":"10.1093","volume":"120","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7695-2046","authenticated-orcid":false,"given":"James 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UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4096-3173","authenticated-orcid":false,"given":"Raffaele","family":"Coppini","sequence":"additional","affiliation":[{"name":"Department of NeuroFarBa, University of Florence , Florence , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rafael","family":"Sachetto","sequence":"additional","affiliation":[{"name":"Department of Computer Science, Federal University of S\u00e3o Jo\u00e3o del-Rei , S\u00e3o Jo\u00e3o del-Rei, Minas Gerais , Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5287-9016","authenticated-orcid":false,"given":"Hugh","family":"Watkins","sequence":"additional","affiliation":[{"name":"Radcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford , Oxford , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1239-9608","authenticated-orcid":false,"given":"Betty","family":"Raman","sequence":"additional","affiliation":[{"name":"Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Radcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford , Oxford , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1634-3601","authenticated-orcid":false,"given":"Alfonso","family":"Bueno-Orovio","sequence":"additional","affiliation":[{"name":"Department of Computer Science, University of Oxford , Oxford , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,4,22]]},"reference":[{"key":"2024070215232898800_cvae086-B1","first-page":"644","article-title":"Enhanced American College of Cardiology\/American Heart Association strategy for prevention of sudden cardiac 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