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Updated: Jul 14, 2026
A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
Published on: February 17, 2023
Organization of ventricular fibrillation in the human heart
Kirsten H W J Ten Tusscher1, Rok Hren, Alexander V Panfilov
1Department of Theoretical Biology, Utrecht University, Utrecht, The Netherlands. khwjtuss@hotmail.com
Insights
Sudden cardiac death, often caused by ventricular fibrillation (VF), is more organized in humans than in animals. This difference, linked to action potential duration, may impact treatment strategies for this dangerous arrhythmia.
Area of Science:
- Cardiovascular physiology
- Computational biology
- Cardiac electrophysiology
Background:
- Sudden cardiac death (SCD) is a leading cause of mortality, primarily due to ventricular fibrillation (VF).
- Previous research suggested VF in animal hearts is disorganized, driven by numerous reentrant waves.
- Clinical data indicate human VF may possess a distinct organizational structure.
Purpose of the Study:
- To investigate the organization of ventricular fibrillation (VF) in the human heart using a detailed computational model.
- To compare the organizational characteristics of human VF with those observed in large animal hearts.
- To identify factors influencing the spatial organization of VF in the human heart.
Main Methods:
- Development of a detailed computational model of the human ventricles, incorporating cell electrophysiology, anatomy, and anisotropic fiber direction.
- Simulation of ventricular fibrillation (VF) within the human heart model.
- Analysis of the number and behavior of reentrant sources driving VF in the simulation.
- Investigation of the impact of parameters like anisotropy ratio, tissue excitability, and restitution on VF organization.
Main Results:
- Simulated human VF exhibited characteristics consistent with clinical observations.
- Human VF was found to be driven by a significantly lower number of reentrant sources (approx. 10) compared to large animal hearts (approx. 50).
- Minimum action potential duration was identified as the strongest determinant of the number of reentrant sources driving VF, differing notably between human and animal hearts.
Conclusions:
- Human ventricular fibrillation (VF) demonstrates a simpler spatial organization than VF in large animal hearts.
- Differences in minimum action potential duration are proposed as a key factor contributing to the distinct organization of human VF.
- These findings have potential implications for the development of novel therapeutic and preventative strategies for human VF.
Abstract:
Sudden cardiac death is a major cause of death in the industrialized world, claiming approximately 300,000 victims annually in the United States alone. In most cases, sudden cardiac death is caused by ventricular fibrillation (VF). Experimental studies in large animal hearts have shown that the uncoordinated contractions during VF are caused by large numbers of chaotically wandering reentrant waves of electrical activity. However, recent clinical data on VF in the human heart seem to suggest that human VF may have a markedly different organization. Here, we use a detailed model of the human ventricles, including a detailed description of cell electrophysiology, ventricular anatomy, and fiber direction anisotropy, to study the organization of human VF. We show that characteristics of our simulated VF are qualitatively similar to the clinical data. Furthermore, we find that human VF is driven by only approximately 10 reentrant sources and thus is much more organized than VF in animal hearts of comparable size, where VF is driven by approximately 50 sources. We investigate the influence of anisotropy ratio, tissue excitability, and restitution properties on the number of reentrant sources driving VF. We find that the number of rotors depends strongest on minimum action potential duration, a property that differs significantly between human and large animal hearts. Based on these findings, we suggest that the simpler spatial organization of human VF relative to VF in large animal hearts may be caused by differences in minimum action potential duration. Both the simpler spatial organization of human VF and its suggested cause may have important implications for treating and preventing this dangerous arrhythmia in humans.
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