ArticleThe Journal of physiology2012
Three-dimensional mechanisms of increased vulnerability to electric shocks in myocardial infarction: altered virtual electrode polarizations and conduction delay in the peri-infarct zone.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Heart Digital Twins Predict Features of Invasive Reentrant Circuits and Ablation Lesions in Scar-Dependent Ventricular Tachycardia.Circulation. Arrhythmia and electrophysiology · 2025Article
- The effect of non-local coupling of fibroblasts on pacing dynamics in a 2D tissue: a simulation study.Scientific reports · 2025Article
- Confocal microscopy-based estimation of intracellular conductivities in myocardium for modeling of the normal and infarcted heart.Computers in biology and medicine · 2022Article
- OptoGap is an optogenetics-enabled assay for quantification of cell-cell coupling in multicellular cardiac tissue.Scientific reports · 2021Article
- Factors Promoting Conduction Slowing as Substrates for Block and Reentry in Infarcted Hearts.Biophysical journal · 2019Article
- Personalized Cardiac Computational Models: From Clinical Data to Simulation of Infarct-Related Ventricular Tachycardia.Frontiers in physiology · 2019Article
- Virtual electrophysiological study as a tool for evaluating efficacy of MRI techniques in predicting adverse arrhythmic events in ischemic patients.Physics in medicine and biology · 2018Article
- Personalized virtual-heart technology for guiding the ablation of infarct-related ventricular tachycardia.Nature biomedical engineering · 2018Article
- Modeling the Electrophysiological Properties of the Infarct Border Zone.Frontiers in physiology · 2018Review
- Imaging-Based Simulations for Predicting Sudden Death and Guiding Ventricular Tachycardia Ablation.Circulation. Arrhythmia and electrophysiology · 2017Review
- Optogenetic defibrillation terminates ventricular arrhythmia in mouse hearts and human simulations.The Journal of clinical investigation · 2016Article
- Computational rabbit models to investigate the initiation, perpetuation, and termination of ventricular arrhythmia.Progress in biophysics and molecular biology · 2016Review
- Arrhythmia risk stratification of patients after myocardial infarction using personalized heart models.Nature communications · 2016Article
- Article
- Computational Representations of Myocardial Infarct Scars and Implications for Arrhythmogenesis.Clinical Medicine Insights. Cardiology · 2016Review
- Image-based reconstruction of three-dimensional myocardial infarct geometry for patient-specific modeling of cardiac electrophysiology.Medical physics · 2015Article
- Three-dimensional cardiac computational modelling: methods, features and applications.Biomedical engineering online · 2015Review
- Accuracy of prediction of infarct-related arrhythmic circuits from image-based models reconstructed from low and high resolution MRI.Frontiers in physiology · 2015Article
- Methodology for image-based reconstruction of ventricular geometry for patient-specific modeling of cardiac electrophysiology.Progress in biophysics and molecular biology · 2014Article
- Images as drivers of progress in cardiac computational modelling.Progress in biophysics and molecular biology · 2014Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Defibrillation efficacy is decreased in infarcted hearts, but the mechanisms by which infarcted hearts are more vulnerable to electric shocks than healthy hearts remain poorly understood. The goal of this study was to provide insight into the 3D mechanisms for the increased vulnerability to electric shocks in infarcted hearts. We hypothesized that changes in virtual electrode polarizations (VEPs) and propagation delay through the peri-infarct zone (PZ) were responsible. We developed a micro anatomically detailed rabbit ventricular model with chronic myocardial infarction from magnetic resonance imaging and enriched the model with data from optical mapping experiments. We further developed a control model without the infarct. The simulation protocol involved apical pacing followed by biphasic shocks. Simulation results from both models were compared.The upper limit of vulnerability(ULV) was 8 V cm(-1) in the infarction model and 4 V cm(-1) in the control model. VEPs were less pronounced in the infarction model, providing a larger excitable area for postshock propagation but smaller transmembrane potential gradients to initiate new wavefronts. Initial post-shock transmural activation occurred at a later time in the infarction model, and the PZ served to delay propagation in subsequent beats. The presence of the PZ was found to be responsible for the increased vulnerability.
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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.