Key result
A novel 3D discrete finite element methodology successfully simulated fibrosis-mediated conduction delays and reentrant electrical activations in an image-derived model of non-ischemic cardiomyopathy.
Why the study?
Patients with nonischemic cardiomyopathy and interstitial fibrosis often suffer from life-threatening arrhythmias, which the authors aimed to simulate.
A novel 3D electrophysiological modeling methodology incorporating topologically consistent interstitial fibrosis networks successfully simulates ventricular arrhythmias in non-ischemic cardiomyopathy.
Should not yet alter clinical management in non-ischemic cardiomyopathy; extends computational arrhythmia modeling and remains hypothesis-generating pending validation.
OBJECTIVE: Interstitial fibrosis is a pathological expansion of the heart's inter-cellular collagen matrix. It is a potential complication of nonischemic cardiomyopathy (NICM), a class of diseases involving electrical and or mechanical dysfunction of cardiac tissue not caused by atherosclerosis. Patients with NICM and interstitial fibrosis often suffer from life threatening arrhythmias, which we aim to simulate in this study. METHODS: Our methodology builds on an efficient discrete finite element (DFE) method which allows for the representation of fibrosis as infinitesimal splits in a mesh. We update the DFE method with a local connectivity analysis which creates a consistent topology in the fibrosis network. This is particularly important in nonischemic disease due to the potential presence of large and contiguous fibrotic regions and therefore potentially complex fibrosis networks. RESULTS: In experiments with an image-based model, we demonstrate that our methodology is able to simulate reentrant electrical events associated with cardiac arrhythmias. These reentries depended crucially upon sufficient fibrosis density, which was marked by conduction slowing at high pacing rates. We also created a 2D test-case which demonstrated that fibrosis topologies can modulate transient conduction block, and thereby reentrant activations. CONCLUSION: Ventricular arrhythmias due to interstitial fibrosis in NICM can be efficiently simulated using our methods in medical image based geometries. Furthermore, fibrosis topology modulates transient conduction block, and should be accounted for in electrophysiological simulations with interstitial fibrosis. SIGNIFICANCE: Our study provides methodology which has the potential to predict arrhythmias and to optimize treatments non-invasively for nonischemic cardiomyopathies.
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Balaban et al. (2020) studied Non-ischemic dilated cardiomyopathy (n=1). 3D Discrete Finite Element (DFE) modeling of interstitial fibrosis vs. Control model with no fibrosis was evaluated. A novel 3D discrete finite element methodology successfully simulated fibrosis-mediated conduction delays and reentrant electrical activations in an image-derived model of non-ischemic cardiomyopathy.
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