14,053 research outputs found
Nonlinear physics of electrical wave propagation in the heart: a review
The beating of the heart is a synchronized contraction of muscle cells
(myocytes) that are triggered by a periodic sequence of electrical waves (action
potentials) originating in the sino-atrial node and propagating over the atria and
the ventricles. Cardiac arrhythmias like atrial and ventricular fibrillation (AF,VF)
or ventricular tachycardia (VT) are caused by disruptions and instabilities of these
electrical excitations, that lead to the emergence of rotating waves (VT) and turbulent
wave patterns (AF,VF). Numerous simulation and experimental studies during the
last 20 years have addressed these topics. In this review we focus on the nonlinear
dynamics of wave propagation in the heart with an emphasis on the theory of pulses,
spirals and scroll waves and their instabilities in excitable media and their application
to cardiac modeling. After an introduction into electrophysiological models for action
potential propagation, the modeling and analysis of spatiotemporal alternans, spiral
and scroll meandering, spiral breakup and scroll wave instabilities like negative line
tension and sproing are reviewed in depth and discussed with emphasis on their impact
in cardiac arrhythmias.Peer ReviewedPreprin
Negative tension of scroll wave filaments and turbulence in three-dimensional excitable media and application in cardiac dynamics
Scroll waves are vortices that occur in three-dimensional excitable media. Scroll waves have been observed in a variety of systems including cardiac tissue, where they are associated with cardiac arrhythmias. The disorganization of scroll waves into chaotic behavior is thought to be the mechanism of ventricular fibrillation, whose lethality is widely known. One possible mechanism for this process of scroll wave instability is negative filament tension. It was discovered in 1987 in a simple two variables model of an excitable medium. Since that time, negative filament tension of scroll waves and the resulting complex, often turbulent dynamics was studied in many generic models of excitable media as well as in physiologically realistic models of cardiac tissue. In this article, we review the work in this area from the first simulations in FitzHugh-Nagumo type models to recent studies involving detailed ionic models of cardiac tissue. We discuss the relation of negative filament tension and tissue excitability and the effects of discreteness in the tissue on the filament tension. Finally, we consider the application of the negative tension mechanism to computational cardiology, where it may be regarded as a fundamental mechanism that explains differences in the onset of arrhythmias in thin and thick tissue
Data-Driven Modeling and Prediction of Complex Spatio-Temporal Dynamics in Excitable Media
Spatio-temporal chaotic dynamics in a two-dimensional excitable medium is (cross-) estimated using a machine learning method based on a convolutional neural network combined with a conditional random field. The performance of this approach is demonstrated using the four variables of the Bueno-Orovio-Fenton-Cherry model describing electrical excitation waves in cardiac tissue. Using temporal sequences of two-dimensional fields representing the values of one or more of the model variables as input the network successfully cross-estimates all variables and provides excellent forecasts when applied iteratively
Multiple mechanisms of spiral wave breakup in a model of cardiac electrical activity
It has become widely accepted that the most dangerous cardiac arrhythmias are
due to re- entrant waves, i.e., electrical wave(s) that re-circulate repeatedly
throughout the tissue at a higher frequency than the waves produced by the
heart's natural pacemaker (sinoatrial node). However, the complicated structure
of cardiac tissue, as well as the complex ionic currents in the cell, has made
it extremely difficult to pinpoint the detailed mechanisms of these
life-threatening reentrant arrhythmias. A simplified ionic model of the cardiac
action potential (AP), which can be fitted to a wide variety of experimentally
and numerically obtained mesoscopic characteristics of cardiac tissue such as
AP shape and restitution of AP duration and conduction velocity, is used to
explain many different mechanisms of spiral wave breakup which in principle can
occur in cardiac tissue. Some, but not all, of these mechanisms have been
observed before using other models; therefore, the purpose of this paper is to
demonstrate them using just one framework model and to explain the different
parameter regimes or physiological properties necessary for each mechanism
(such as high or low excitability, corresponding to normal or ischemic tissue,
spiral tip trajectory types, and tissue structures such as rotational
anisotropy and periodic boundary conditions). Each mechanism is compared with
data from other ionic models or experiments to illustrate that they are not
model-specific phenomena. The fact that many different breakup mechanisms exist
has important implications for antiarrhythmic drug design and for comparisons
of fibrillation experiments using different species, electromechanical
uncoupling drugs, and initiation protocols.Comment: 128 pages, 42 figures (29 color, 13 b&w
Influence of cardiac tissue anisotropy on re-entrant activation in computational models of ventricular fibrillation
The aim of this study was to establish the role played by anisotropic diffusion in (i) the number of filaments and epicardial phase singularities that sustain ventricular fibrillation in the heart, (ii) the lifetimes of filaments and phase singularities, and (iii) the creation and annihilation dynamics of filaments and phase singularities. A simplified monodomain model of cardiac tissue was used, with membrane excitation described by a simplified 3-variable model. The model was configured so that a single re-entrant wave was unstable, and fragmented into multiple re-entrant waves. Re-entry was then initiated in tissue slabs with varying anisotropy ratio. The main findings of this computational study are: (i) anisotropy ratio influenced the number of filaments Sustaining simulated ventricular fibrillation, with more filaments present in simulations with smaller values of transverse diffusion coefficient, (ii) each re-entrant filament was associated with around 0.9 phase singularities on the surface of the slab geometry, (iii) phase singularities were longer lived than filaments, and (iv) the creation and annihilation of filaments and phase singularities were linear functions of the number of filaments and phase singularities, and these relationships were independent of the anisotropy ratio. This study underscores the important role played by tissue anisotropy in cardiac ventricular fibrillation
A study of early afterdepolarizations in a model for human ventricular tissue
Sudden cardiac death is often caused by cardiac arrhythmias. Recently, special attention has been given to a certain arrhythmogenic condition, the long-QT syndrome, which occurs as a result of genetic mutations or drug toxicity. The underlying mechanisms of arrhythmias, caused by the long-QT syndrome, are not fully understood. However, arrhythmias are often connected to special excitations of cardiac cells, called early afterdepolarizations (EADs), which are depolarizations during the repolarizing phase of the action potential. So far, EADs have been studied mainly in isolated cardiac cells. However, the question on how EADs at the single-cell level can result in fibrillation at the tissue level, especially in human cell models, has not been widely studied yet. In this paper, we study wave patterns that result from single-cell EAD dynamics in a mathematical model for human ventricular cardiac tissue. We induce EADs by modeling experimental conditions which have been shown to evoke EADs at a single-cell level: by an increase of L-type Ca currents and a decrease of the delayed rectifier potassium currents. We show that, at the tissue level and depending on these parameters, three types of abnormal wave patterns emerge. We classify them into two types of spiral fibrillation and one type of oscillatory dynamics. Moreover, we find that the emergent wave patterns can be driven by calcium or sodium currents and we find phase waves in the oscillatory excitation regime. From our simulations we predict that arrhythmias caused by EADs can occur during normal wave propagation and do not require tissue heterogeneities. Experimental verification of our results is possible for experiments at the cell-culture level, where EADs can be induced by an increase of the L-type calcium conductance and by the application of I blockers, and the properties of the emergent patterns can be studied by optical mapping of the voltage and calcium
Reentry produced by small-scale heterogeneities in a discrete model of cardiac tissue
Reentries are reexcitations of cardiac tissue after the passing of an excitation wave which can cause
dangerous arrhythmias like tachycardia or life-threatening heart failures like fibrillation. The heart is formed by a
network of cells connected by gap junctions. Under ischemic conditions some of the cells lose their connections,
because gap junctions are blocked and the excitability is decreased. We model a circular region of the tissue where
a fraction of connections among individual cells are removed and substituted by non-conducting material in a twodimensional
(2D) discrete model of a heterogeneous excitable medium with local kinetics based on electrophysiology.
Thus, two neighbouring cells are connected (disconnected) with a probability f (1 - f). Such a region is assumed to be
surrounded by homogeneous tissue. The circular heterogeneous area is shown to act as a source of new waves which
reenter into the tissue and reexcitate the whole domain. We employ the Fenton-Karma equations to model the action potential for the local kinetics of the discrete nodes to study the statistics of the reentries in two dimensional networks
with different topologies. We conclude that the probability of reentry is determined by the proximity of the fraction of
disrupted connections between neighboring nodes (Peer ReviewedPostprint (published version
Nonlinear diffusion & thermo-electric coupling in a two-variable model of cardiac action potential
This work reports the results of the theoretical investigation of nonlinear
dynamics and spiral wave breakup in a generalized two-variable model of cardiac
action potential accounting for thermo-electric coupling and diffusion
nonlinearities. As customary in excitable media, the common Q10 and Moore
factors are used to describe thermo-electric feedback in a 10-degrees range.
Motivated by the porous nature of the cardiac tissue, in this study we also
propose a nonlinear Fickian flux formulated by Taylor expanding the voltage
dependent diffusion coefficient up to quadratic terms. A fine tuning of the
diffusive parameters is performed a priori to match the conduction velocity of
the equivalent cable model. The resulting combined effects are then studied by
numerically simulating different stimulation protocols on a one-dimensional
cable. Model features are compared in terms of action potential morphology,
restitution curves, frequency spectra and spatio-temporal phase differences.
Two-dimensional long-run simulations are finally performed to characterize
spiral breakup during sustained fibrillation at different thermal states.
Temperature and nonlinear diffusion effects are found to impact the
repolarization phase of the action potential wave with non-monotone patterns
and to increase the propensity of arrhythmogenesis
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