ArticleBiophysical journal2011
Susceptibility to arrhythmia in the infarcted heart depends on myofibroblast density.
Article in Biophysical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 107 citations in OpenAlex.
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- The Hodgkin-Huxley-Katz Prize Lecture: Heart digital twins: A new paradigm in arrhythmia medicine.The Journal of physiology · 2026Article
- Models of cardiomyocyte-non-myocyte electrical interactions.The Journal of physiology · 2026Review
- Atrial fibroblast metabolic reprogramming in atrial fibrillation: a candidate mechanism within multicellular atrial cardiomyopathy.Frontiers in cardiovascular medicine · 2026Review
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
- Computational modeling of cardiac electrophysiology and arrhythmogenesis: toward clinical translation.Physiological reviews · 2024Review
- Identifying sex similarities and differences in structure and function of the sinoatrial node in the mouse heart.Frontiers in medicine · 2024Article
- Functional significance of myocardial activity atEuropean journal of nuclear medicine and molecular imaging · 2023Article
- The physics of heart rhythm disorders.Physics reports · 2022Article
- Mechanisms of ventricular arrhythmias elicited by coexistence of multiple electrophysiological remodeling in ischemia: A simulation study.PLoS computational biology · 2022Article
- Role of Scar and Border Zone Geometry on the Genesis and Maintenance of Re-Entrant Ventricular Tachycardia in Patients With Previous Myocardial Infarction.Frontiers in physiology · 2022Article
- Mechanisms of arrhythmia termination during acute myocardial ischemia: Role of ephaptic coupling and complex geometry of border zone.PloS one · 2022Article
- Machine Learning Identification of Pro-arrhythmic Structures in Cardiac Fibrosis.Frontiers in physiology · 2021Article
- Variability in electrophysiological properties and conducting obstacles controls re-entry risk in heterogeneous ischaemic tissue.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2020Article
- Sensitivity and Uncertainty Analysis of Two Human Atrial Cardiac Cell Models Using Gaussian Process Emulators.Frontiers in physiology · 2020Article
- Factors Promoting Conduction Slowing as Substrates for Block and Reentry in Infarcted Hearts.Biophysical journal · 2019Article
- Article
- Concise Review: Reduction of Adverse Cardiac Scarring Facilitates Pluripotent Stem Cell-Based Therapy for Myocardial Infarction.Stem cells (Dayton, Ohio) · 2019Review
- Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Personalized Cardiac Computational Models: From Clinical Data to Simulation of Infarct-Related Ventricular Tachycardia.Frontiers in physiology · 2019Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Fibroblasts are electrophysiologically quiescent in the healthy heart. Evidence suggests that remodeling following myocardial infarction may include coupling of myofibroblasts (Mfbs) among themselves and with myocytes via gap junctions. We use a magnetic resonance imaging-based, three-dimensional computational model of the chronically infarcted rabbit ventricles to characterize the arrhythmogenic substrate resulting from Mfb infiltration as a function of Mfb density. Mfbs forming gap junctions were incorporated into both infarct regions, the periinfarct zone (PZ) and the scar; six scenarios were modeled: 0%, 10%, and 30% Mfbs in the PZ, with either 80% or 0% Mfbs in the scar. Ionic current remodeling in PZ was also included. All preparations exhibited elevated resting membrane potential within and near the PZ and action potential duration shortening throughout the ventricles. The unique combination of PZ ionic current remodeling and different degrees of Mfb infiltration in the infarcted ventricles determines susceptibility to arrhythmia. At low densities, Mfbs do not alter arrhythmia propensity; the latter arises predominantly from ionic current remodeling in PZ. At intermediate densities, Mfbs cause additional action potential shortening and exacerbate arrhythmia propensity. At high densities, Mfbs protect against arrhythmia by causing resting depolarization and blocking propagation, thus overcoming the arrhythmogenic effects of PZ ionic current remodeling.
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