53 research outputs found
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
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
Spiral-wave Dynamics Depends Sensitively on nhomogeneities in Mathematical Models of Ventricular Tissue
Every sixth death in industrialised countries occurs because of cardiac
arrhythmias like ventricular tachycardia (VT) and ventricular fibrillation
(VF). There is growing consensus that VT is associated with an unbroken spiral
wave of electrical activation on cardiac tissue but VF with broken waves,
spiral turbulence, spatiotemporal chaos and rapid, irregular activation. Thus
spiral-wave activity in cardiac tissue has been studied extensively.
Nevertheless many aspects of such spiral dynamics remain elusive because of the
intrinsically high-dimensional nature of the cardiac-dynamical system. In
particular, the role of tissue heterogeneities in the stability of cardiac
spiral waves is still being investigated. Experiments with conduction blocks in
cardiac tissue yield a variety of results: some suggest that blocks can
eliminate VF partially or completely, leading to VT or quiescence, but others
show that VF is unaffected by obstacles. We propose theoretically that this
variety of results is a natural manifestation of a fractal boundary that must
separate the basins of the attractors associated, respectively, with VF and VT.
We substantiate this with extensive numerical studies of Panfilov and Luo-Rudy
I models, where we show that the suppression of VF depends sensitively on the
position, size, and nature of the inhomogeneity.Comment: 9 pages, 5 figures
Spiral-Wave Turbulence and Its Control in the Presence of Inhomogeneities in Four Mathematical Models of Cardiac Tissue
Regular electrical activation waves in cardiac tissue lead to the rhythmic contraction and expansion of the heart that ensures blood supply to the whole body. Irregularities in the propagation of these activation waves can result in cardiac arrhythmias, like ventricular tachycardia (VT) and ventricular fibrillation (VF), which are major causes of death in the industrialised world. Indeed there is growing consensus that spiral or scroll waves of electrical activation in cardiac tissue are associated with VT, whereas, when these waves break to yield spiral- or scroll-wave turbulence, VT develops into life-threatening VF: in the absence of medical intervention, this makes the heart incapable of pumping blood and a patient dies in roughly two-and-a-half minutes after the initiation of VF. Thus studies of spiral- and scroll-wave dynamics in cardiac tissue pose important challenges for in vivo and in vitro experimental studies and for in silico numerical studies of mathematical models for cardiac tissue. A major goal here is to develop low-amplitude defibrillation schemes for the elimination of VT and VF, especially in the presence of inhomogeneities that occur commonly in cardiac tissue. We present a detailed and systematic study of spiral- and scroll-wave turbulence and spatiotemporal chaos in four mathematical models for cardiac tissue, namely, the Panfilov, Luo-Rudy phase 1 (LRI), reduced Priebe-Beuckelmann (RPB) models, and the model of ten Tusscher, Noble, Noble, and Panfilov (TNNP). In particular, we use extensive numerical simulations to elucidate the interaction of spiral and scroll waves in these models with conduction and ionic inhomogeneities; we also examine the suppression of spiral- and scroll-wave turbulence by low-amplitude control pulses. Our central qualitative result is that, in all these models, the dynamics of such spiral waves depends very sensitively on such inhomogeneities. We also study two types of control schemes that have been suggested for the control of spiral turbulence, via low amplitude current pulses, in such mathematical models for cardiac tissue; our investigations here are designed to examine the efficacy of such control schemes in the presence of inhomogeneities. We find that a local pulsing scheme does not suppress spiral turbulence in the presence of inhomogeneities; but a scheme that uses control pulses on a spatially extended mesh is more successful in the elimination of spiral turbulence. We discuss the theoretical and experimental implications of our study that have a direct bearing on defibrillation, the control of life-threatening cardiac arrhythmias such as ventricular fibrillation
Competing mechanisms of stress-assisted diffusivity and stretch-activated currents in cardiac electromechanics
We numerically investigate the role of mechanical stress in modifying the
conductivity properties of the cardiac tissue and its impact in computational
models for cardiac electromechanics. We follow a theoretical framework recently
proposed in [Cherubini, Filippi, Gizzi, Ruiz-Baier, JTB 2017], in the context
of general reaction-diffusion-mechanics systems using multiphysics continuum
mechanics and finite elasticity. In the present study, the adapted models are
compared against preliminary experimental data of pig right ventricle
fluorescence optical mapping. These data contribute to the characterization of
the observed inhomogeneity and anisotropy properties that result from
mechanical deformation. Our novel approach simultaneously incorporates two
mechanisms for mechano-electric feedback (MEF): stretch-activated currents
(SAC) and stress-assisted diffusion (SAD); and we also identify their influence
into the nonlinear spatiotemporal dynamics. It is found that i) only specific
combinations of the two MEF effects allow proper conduction velocity
measurement; ii) expected heterogeneities and anisotropies are obtained via the
novel stress-assisted diffusion mechanisms; iii) spiral wave meandering and
drifting is highly mediated by the applied mechanical loading. We provide an
analysis of the intrinsic structure of the nonlinear coupling using
computational tests, conducted using a finite element method. In particular, we
compare static and dynamic deformation regimes in the onset of cardiac
arrhythmias and address other potential biomedical applications
A note on stress-driven anisotropic diffusion and its role in active deformable media
We propose a new model to describe diffusion processes within active
deformable media. Our general theoretical framework is based on physical and
mathematical considerations, and it suggests to use diffusion tensors directly
coupled to mechanical stress. A proof-of-concept experiment and the proposed
generalised reaction-diffusion-mechanics model reveal that initially isotropic
and homogeneous diffusion tensors turn into inhomogeneous and anisotropic
quantities due to the intrinsic structure of the nonlinear coupling. We study
the physical properties leading to these effects, and investigate mathematical
conditions for its occurrence. Together, the experiment, the model, and the
numerical results obtained using a mixed-primal finite element method, clearly
support relevant consequences of stress-assisted diffusion into anisotropy
patterns, drifting, and conduction velocity of the resulting excitation waves.
Our findings also indicate the applicability of this novel approach in the
description of mechano-electrical feedback in actively deforming bio-materials
such as the heart
Scroll-Wave Dynamics in Human Cardiac Tissue: Lessons from a Mathematical Model with Inhomogeneities and Fiber Architecture
Cardiac arrhythmias, such as ventricular tachycardia (VT) and ventricular fibrillation (VF), are among the leading causes of death in the industrialized world. These are associated with the formation of spiral and scroll waves of electrical activation in cardiac tissue; single spiral and scroll waves are believed to be associated with VT whereas their turbulent analogs are associated with VF. Thus, the study of these waves is an important biophysical problem. We present a systematic study of the combined effects of muscle-fiber rotation and inhomogeneities on scroll-wave dynamics in the TNNP (ten Tusscher Noble Noble Panfilov) model for human cardiac tissue. In particular, we use the three-dimensional TNNP model with fiber rotation and consider both conduction and ionic inhomogeneities. We find that, in addition to displaying a sensitive dependence on the positions, sizes, and types of inhomogeneities, scroll-wave dynamics also depends delicately upon the degree of fiber rotation. We find that the tendency of scroll waves to anchor to cylindrical conduction inhomogeneities increases with the radius of the inhomogeneity. Furthermore, the filament of the scroll wave can exhibit drift or meandering, transmural bending, twisting, and break-up. If the scroll-wave filament exhibits weak meandering, then there is a fine balance between the anchoring of this wave at the inhomogeneity and a disruption of wave-pinning by fiber rotation. If this filament displays strong meandering, then again the anchoring is suppressed by fiber rotation; also, the scroll wave can be eliminated from most of the layers only to be regenerated by a seed wave. Ionic inhomogeneities can also lead to an anchoring of the scroll wave; scroll waves can now enter the region inside an ionic inhomogeneity and can display a coexistence of spatiotemporal chaos and quasi-periodic behavior in different parts of the simulation domain. We discuss the experimental implications of our study
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