Result: Simulation-based digital twinning of activation and repolarisation sequences from the ECG across healthy and diseased hearts.

Title:
Simulation-based digital twinning of activation and repolarisation sequences from the ECG across healthy and diseased hearts.
Authors:
Coleman JA; Department of Computer Science, University of Oxford, Oxford, United Kingdom., Camps J; Department of Engineering, Universitat Pompeu Fabra, Barcelona, Spain., Hasaballa AI; Department of Computer Science, University of Oxford, Oxford, United Kingdom., Bueno-Orovio A; Department of Computer Science, University of Oxford, Oxford, United Kingdom. Electronic address: alfonso.bueno@cs.ox.ac.uk.
Source:
Computers in biology and medicine [Comput Biol Med] 2025 Nov; Vol. 198 (Pt B), pp. 111222. Date of Electronic Publication: 2025 Oct 22.
Publication Type:
Journal Article
Language:
English
Journal Info:
Publisher: Elsevier Country of Publication: United States NLM ID: 1250250 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0534 (Electronic) Linking ISSN: 00104825 NLM ISO Abbreviation: Comput Biol Med Subsets: MEDLINE
Imprint Name(s):
Publication: New York : Elsevier
Original Publication: New York, Pergamon Press.
MeSH Terms:
Electrocardiography*/methods , Models, Cardiovascular* , Action Potentials* , Arrhythmias, Cardiac*/physiopathology , Arrhythmias, Cardiac*/diagnostic imaging , Signal Processing, Computer-Assisted* , Cardiomyopathy, Hypertrophic*/physiopathology , Cardiomyopathy, Hypertrophic*/diagnostic imaging , Heart Ventricles*/physiopathology , Heart Ventricles*/diagnostic imaging, Humans ; Computer Simulation ; Male ; Female ; Adult ; Middle Aged
Contributed Indexing:
Keywords: Digital twin; ECG; Hypertrophic cardiomyopathy; Modelling; Personalisation; Simulation; T wave
Entry Date(s):
Date Created: 20251023 Date Completed: 20251115 Latest Revision: 20251115
Update Code:
20251116
DOI:
10.1016/j.compbiomed.2025.111222
PMID:
41130161
Database:
MEDLINE

Further Information

Abnormal patterns of ventricular repolarisation are thought to contribute to lethal arrhythmias in various cardiac conditions, including inherited and acquired channelopathies, cardiomyopathies, and ischaemic heart disease. However, methods to detect these repolarisation abnormalities are limited. In this study, we introduce and assess a novel simulation-based method to infer ventricular activation and repolarisation times from the 12-lead electrocardiogram (ECG) and magnetic resonance-derived ventricular anatomical reconstruction, applicable for the first time to both healthy controls and cases with abnormal repolarisation. First, ventricular activation times were reconstructed through iterative refinement of early activation sites and conduction velocities, until the model and target QRS complexes matched. Then, ventricular repolarisation times were reconstructed through iterative refinement of ventricular action potential durations and an action potential shape parameter until the model and target T waves matched, including regularisation. Repolarisation inference was evaluated against 18 benchmark simulations with known repolarisation times, including both control and hypertrophic cardiomyopathy (HCM) cases with abnormal repolarisation. Inferred repolarisation times showed good agreement with the ground truth in control and HCM (Spearman r=0.63±0.11 and 0.65±0.19, respectively), with the inferred model T waves closely matching the target T waves (r=0.81±0.05 and 0.78±0.08, respectively). The method further demonstrated flexibility in reconstructing the macroscopic patterns of delayed repolarisation across a range of abnormal ventricular repolarisation sequences, demonstrating applicability to a wide range of pathological scenarios. Simulation-based inference can accurately reconstruct repolarisation times from the 12-lead ECG in cases with both normal and abnormal repolarisation patterns.
(Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.