ArticleeLife2024
Clinical phenotypes in acute and chronic infarction explained through human ventricular electromechanical modelling and simulations.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- In silico optimization of regenerative cell therapy in the infarcted human ventricles to mitigate arrhythmic burden.Stem cell reports · 2026Article
- Cardiac remodelling in type 2 diabetes: Pathophysiological mechanisms and opportunities for multiscale computational modelling and simulation.The Journal of physiology · 2026Review
- Electromechanical modelling and simulation of human-induced pluripotent stem cell-derived cardiomyocytes predict drug-induced contractility effects.The Journal of physiology · 2026Article
- T-World Virtual Human Cardiomyocyte. II. Organ-Scale Simulations and Applications.Circulation research · 2026Article
- Quantitative systems toxicology: modelling to mechanistically understand and predict drug safety.Nature reviews. Drug discovery · 2026Review
- BioModels' model of the year 2024.Frontiers in systems biology · 2026Article
- Harnessing 12-lead ECG and MRI data to personalise repolarisation profiles in cardiac digital twin models for enhanced virtual drug testing.Medical image analysis · 2025Article
- Cardiac conduction system regeneration prevents arrhythmias after myocardial infarction.Nature cardiovascular research · 2025Article
- Article
- Quantitative assessment of the usability of electromechanical human-based modelling and simulation to replace Langendorff isolated rabbit heart experiments in the preclinical setting.Frontiers in pharmacology · 2025Article
- Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Sudden death after myocardial infarction (MI) is associated with electrophysiological heterogeneities and ionic current remodelling. Low ejection fraction (EF) is used in risk stratification, but its mechanistic links with pro-arrhythmic heterogeneities are unknown. We aim to provide mechanistic explanations of clinical phenotypes in acute and chronic MI, from ionic current remodelling to ECG and EF, using human electromechanical modelling and simulation to augment experimental and clinical investigations. A human ventricular electromechanical modelling and simulation framework is constructed and validated with rich experimental and clinical datasets, incorporating varying degrees of ionic current remodelling as reported in literature. In acute MI, T-wave inversion and Brugada phenocopy were explained by conduction abnormality and local action potential prolongation in the border zone. In chronic MI, upright tall T-waves highlight large repolarisation dispersion between the border and remote zones, which promoted ectopic propagation at fast pacing. Post-MI EF at resting heart rate was not sensitive to the extent of repolarisation heterogeneity and the risk of repolarisation abnormalities at fast pacing. T-wave and QT abnormalities are better indicators of repolarisation heterogeneities than EF in post-MI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.