An Efficient Finite Element Approach for Modeling Fibrotic Clefts in the Heart

Costa, Caroline Mendonça; Campos, Fernanda; Prassl, Anton J.; Santos, Rodrigo Weber dos; Sánchez‐Quintana, Damian; Ahammer, Helmut; Hofer, Eberhard P.; Plank, Gernot

doi:10.1109/tbme.2013.2292320

Cited by 37 publications

(34 citation statements)

References 32 publications

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“…There are several attempts to model the interaction of waves within regions of heterogeneous cardiac tissue, where cells are partially disconnected [59–61]. Their main results are a decrease of the macroscopic conduction velocity [51, 62] and a decrease of excitability which may preclude spiral breakup [26].…”

Section: Discussionmentioning

confidence: 99%

Reentry and Ectopic Pacemakers Emerge in a Three-Dimensional Model for a Slab of Cardiac Tissue with Diffuse Microfibrosis near the Percolation Threshold

Alonso¹,

Santos²,

Bär³

2016

PLoS ONE

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Arrhythmias in cardiac tissue are generally associated with irregular electrical wave propagation in the heart. Cardiac tissue is formed by a discrete cell network, which is often heterogeneous. Recently, it was shown in simulations of two-dimensional (2D) discrete models of cardiac tissue that a wave crossing a fibrotic, heterogeneous region may produce reentry and transient or persistent ectopic activity provided the fraction of conducting connections is just above the percolation threshold. Here, we investigate the occurrence of these phenomena in three-dimensions by simulations of a discrete model representing a thin slab of cardiac tissue. This is motivated (i) by the necessity to study the relevance and properties of the percolation-related mechanism for the emergence of microreentries in three dimensions and (ii) by the fact that atrial tissue is quite thin in comparison with ventricular tissue. Here, we simplify the model by neglecting details of tissue anatomy, e. g. geometries of atria or ventricles and the anisotropy in the conductivity. Hence, our modeling study is confined to the investigation of the effect of the tissue thickness as well as to the comparison of the dynamics of electrical excitation in a 2D layer with the one in a 3D slab. Our results indicate a strong and non-trivial effect of the thickness even for thin tissue slabs on the probability of microreentries and ectopic beat generation. The strong correlation of the occurrence of microreentry with the percolation threshold reported earlier in 2D layers persists in 3D slabs. Finally, a qualitative agreement of 3D simulated electrograms in the fibrotic region with the experimentally observed complex fractional atrial electrograms (CFAE) as well as strong difference between simulated electrograms in 2D and 3D were found for the cases where reentry and ectopic activity were triggered by the micro-fibrotic region.

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Section: Discussionmentioning

confidence: 99%

Reentry and Ectopic Pacemakers Emerge in a Three-Dimensional Model for a Slab of Cardiac Tissue with Diffuse Microfibrosis near the Percolation Threshold

Alonso¹,

Santos²,

Bär³

2016

PLoS ONE

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“…In addition, a 2D sheet with w isth progressively widening from 0.2 to 4 mm was built to study the effects of geometrical asymmetries on formation and conduction of PVCs. The scar tissue was represented as being necrotic, i.e., by imposing no-flux boundary condition at its interface [27]. Isotropic tissue conductivity was assigned to the tissue with a value of 0.14 S/m [28] to dissect out the role of the isthmus' width on PVC formation.…”

Section: D Sheets With Idealized Scarmentioning

confidence: 99%

“…Finally, fibrosis was modeled by removing FEs representing myocardium from the geometrical models. While more sophisticated techniques exist [27], overall behavior would be qualitatively similar since wave propagation would still have to travel tortuous pathways.…”

Section: Study Limitationsmentioning

confidence: 99%

Microscopic Isthmuses and Fibrosis Within the Border Zone of Infarcted Hearts Promote Calcium-Mediated Ectopy and Conduction Block

et al. 2018

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Ventricular tachycardia (VT) secondary to myocardial infarction (MI) remain a major cause of sudden death in adults. Premature ventricular complexes (PVCs), the first initiating beats of a portion of these arrhythmias, arise from triggered activity in the infarct border zone (BZ). At the cellular scale, spontaneous calcium release (SCR) events are a known cause of triggered activity and have been reported in cells that survive MI. At the tissue scale, fibrosis has been shown to play an important role in creating the substrate for VT. However, the interplay between SCR-mediated triggered activity and fibrosis upon VT formation in infarcted hearts has not been fully investigated. Here, we conduct in-silico experiments to assess how macroscopic and microscopic anatomical properties of the BZ can create a substrate for SCR-mediated VT formation. To study this question, we employ a stochastic subcellular-scale model of SCR events and action potential to simulate different cardiac preparations. Within 2D sheet models with idealized infarct scars and BZ we show that the probability of PVCs is higher, 55%, in preparations with thin conducting isthmuses (0.2 mm) transcending the scar. In an anatomically-detailed model of the rabbit ventricles with a realistic representation of intramural scars, we show that the heart's protective source-sink mismatch prevents ectopy. Furthermore, we demonstrate that fibrosis disrupts this antiarrhythmic mechanism making PVCs more likely. PVC probability is highest (≥25%) when fibrosis accounts for 60 and 90% of the BZ in the 2D sheet and the 3D anatomical model, respectively. Above these thresholds, PVC occurrence decreases because of: (1) the reduced number of myocytes in the BZ; (2) conduction block. Block is caused either by disconnection of BZ cells from the myocardium or due to source-sink mismatches at regions of rapid tissue expansion. Moreover, while outward propagation to healthy tissue may fail, PVCs traveling inward through the scar might encounter more favorable loading conditions. These PVCs may exit to the myocardium and reenter back at the region of block. Overall, our findings indicate that thin isthmuses and strands of myocytes interspersed with fibrosis can be arrhythmogenic. Ablation of these microscopic structures may prevent VT formation.

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“…The results of the effects of fibrosis texture in anisotropic tissue presented here are obtained for the fibrosis represented as a set of the finite size inexcitable obstacles. If, however, the interstitial fibrosis is modelled using approach 26 as an internal boundary condition, the thickness of the obstacle will be zero. Therefore, although rescaling will still work here, it should show that such decoupling along the fibers will always increase the pre-existing anisotropy.…”

Section: Discussionmentioning

confidence: 99%

Anisotropic conduction in the myocardium due to fibrosis: the effect of texture on wave propagation

Nezlobinsky

Solovyova

Panfilov

2020

Sci Rep

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Cardiac fibrosis occurs in many forms of heart disease. It is well established that the spatial pattern of fibrosis, its texture, substantially affects the onset of arrhythmia. However, in most modelling studies fibrosis is represented by multiple randomly distributed short obstacles that mimic only one possible texture, diffuse fibrosis. An important characteristic feature of other fibrosis textures, such as interstitial and patchy textures, is that fibrotic inclusions have substantial length, which is suggested to have a pronounced effect on wave propagation. In this paper, we study the effect of the elongation of inexcitable inclusions (obstacles) on wave propagation in a 2D model of cardiac tissue described by the TP06 model for human ventricular cells. We study in detail how the elongation of obstacles affects various characteristics of the waves. We quantify the anisotropy induced by the textures, its dependency on the obstacle length and the effects of the texture on the shape of the propagating wave. Because such anisotropy is a result of zigzag propagation we show, for the first time, quantification of the effects of geometry and source-sink relationship, on the zigzag nature of the pathway of electrical conduction. We also study the effect of fibrosis in the case of pre-existing anisotropy and introduce a procedure for scaling of the fibrosis texture. We show that fibrosis can decrease or increase the preexisting anisotropy depending on its scaled texture.

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An Efficient Finite Element Approach for Modeling Fibrotic Clefts in the Heart

Cited by 37 publications

References 32 publications

Reentry and Ectopic Pacemakers Emerge in a Three-Dimensional Model for a Slab of Cardiac Tissue with Diffuse Microfibrosis near the Percolation Threshold

Reentry and Ectopic Pacemakers Emerge in a Three-Dimensional Model for a Slab of Cardiac Tissue with Diffuse Microfibrosis near the Percolation Threshold

Microscopic Isthmuses and Fibrosis Within the Border Zone of Infarcted Hearts Promote Calcium-Mediated Ectopy and Conduction Block

Anisotropic conduction in the myocardium due to fibrosis: the effect of texture on wave propagation

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