Computer simulations of cardiac defibrillation: a look inside the heart

Trayanova, Natalia A.; Eason, James; Aguel, Felipe

doi:10.1007/s00791-002-0082-8

Cited by 102 publications

(87 citation statements)

References 53 publications

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“…Local activation and repolarisation times and APD were measured during the 7th paced beat, at a basic cycle length of 250 ms. In addition, to better study arrhythmogenesis in the rabbit ventricles, the dynamics of the scroll-wave filaments, the organising centres of re-entrant activity, was analysed using an algorithm published previously (Trayanova et al, 2002;Larson et al, 2003). Pseudoelectrocardiograms (ECG) (Plonsey and Barr, 2000), were computed at a node marked E2 in Fig.…”

Section: Discussionmentioning

confidence: 99%

“…This study used a 3D geometrically accurate rabbit ventricular model (Vetter and McCulloch, 1998) that incorporated realistic fibre architecture and representation of the blood within the ventricular cavities and the perfusing bath (Trayanova et al, 2002). The finite element mesh consisted of 829 021 tetrahedral elements, with a spatial resolution of 500 μm.…”

Section: Computational Modelmentioning

confidence: 99%

“…As a result, the upper limit of vulnerability (ULV), which is defined as the highest shock strength (SS) above which no arrhythmia is induced, can be used to approximate the defibrillation threshold as part of the clinical procedure of programming the implantable cardioverter/defibrillators. Recently, the use of an anatomically based computational model of stimulation/defibrillation has provided significant insight into the mechanisms of cardiac vulnerability to electric shocks and defibrillation in normal (Trayanova et al, 2002;Aguel et al, 2003;Rodriguez et al, 2005), and diseased hearts (Rodriguez et al, 2004). These simulations have supplied information with high spatial and temporal resolution regarding the shock-induced electrical events within the depth of the myocardial wall, not accessible by current experimental techniques.…”

Section: Introductionmentioning

confidence: 99%

“…This is achieved by investigating the mechanisms of cardiac vulnerability to electric shocks using an anatomically accurate three-dimensional (3D) rabbit ventricular model (Vetter and McCulloch, 1998;Trayanova et al, 2002), which for the first time incorporates transmural heterogeneities in electrophysiological properties and gap-junctional coupling.…”

Section: Introductionmentioning

confidence: 99%

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The role of transmural ventricular heterogeneities in cardiac vulnerability to electric shocks

Maharaj

Blake

Trayanova

et al. 2008

Progress in Biophysics and Molecular Biology

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Transmural electrophysiological heterogeneities have been shown to contribute to arrhythmia induction in the heart; however, their role in defibrillation failure has never been examined. The goal of this study is to investigate how transmural heterogeneities in ionic currents and gap-junctional coupling contribute to arrhythmia generation following defibrillation strength shocks. This study used a 3D anatomically realistic bidomain model of the rabbit ventricles. Transmural heterogeneity in ionic currents and reduced sub-epicardial intercellular coupling were incorporated based on experimental data. The ventricles were paced apically, and truncated-exponential monophasic shocks of varying strength and timing were applied via large external electrodes. Simulations demonstrate that inclusion of transmural heterogeneity in ionic currents results in an increase in vulnerability to shocks, reflected in the increased upper limit of vulnerability, ULV, and the enlarged vulnerable window, VW. These changes in vulnerability stem from increased post-shock dispersion in repolarisation as it increases the likelihood of establishment of re-entrant circuits. In contrast, reduced sub-epicardial coupling results in decrease in both ULV and VW. This decrease is caused by altered virtual electrode polarisation around the region of sub-epicardal uncoupling, and specifically, by the increase in (1) the amount of positively polarised myocardium at shock-end and (2) the spatial extent of post-shock wavefronts.

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Section: Discussionmentioning

confidence: 99%

Section: Computational Modelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The role of transmural ventricular heterogeneities in cardiac vulnerability to electric shocks

Maharaj

Blake

Trayanova

et al. 2008

Progress in Biophysics and Molecular Biology

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“…The model is the first to use bi-domain simulation (in which the electrical field outside the cells is reconstructed as well as the potentials across the cell membranes), with detailed fibre geometry and detailed cellular electrophysiology. (61,62) Such simulations require enormous computing resources, currently available only on large supercomputers (which is the main reason why the simulation is restricted to a slice of the ventricle-computations of the whole canine ventricle would, at present, be too demanding).…”

Section: Calcium Balance: the Hilgemann-noble Modelmentioning

confidence: 99%

Modelling the heart: insights, failures and progress

Noble

2002

BioEssays

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SummaryMathematical models of the heart have developed over a period of about 40 years. Cell types in all regions of the heart have been modelled and they are now being incorporated into anatomically detailed models of the whole organ. This combination is leading to the creation of the first 'virtual organ,' which is being used in drug discovery and testing, and in simulating the action of devices, such as cardiac defibrillators. Simulation is a necessary tool of analysis in attempting to understand biological complexity. We often learn as much from the failures as from the successes of mathematical models. It is the iterative interaction between experiment and simulation that is important. Examples are given where this process has been instrumental in some of the major advances in the field.

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Systems biology of the heart

Noble

2005

Encyclopedia of Genetics, Genomics, Proteomics and Bioinformatics

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Models of the heart have been developed since 1960, starting with the discovery and modeling of potassium channels. The first models of calcium balance were made in the 1980s and have now reached a high degree of physiological detail. During the 1990s, these cell models have been incorporated into anatomically detailed tissue and organ models. Systems biology of the heart is now well developed and is proving increasingly useful in unraveling complicated physiological functions and in understanding disease states.

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Computer simulations of cardiac defibrillation: a look inside the heart

Cited by 102 publications

References 53 publications

The role of transmural ventricular heterogeneities in cardiac vulnerability to electric shocks

The role of transmural ventricular heterogeneities in cardiac vulnerability to electric shocks

Modelling the heart: insights, failures and progress

Systems biology of the heart

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