Modeling Cardiac Defibrillation

Trayanova, Natalia A.; Aguel, Felipe; Larson, Claire; Haro, Carlos

doi:10.1016/b0-7216-0323-8/50034-8

Cited by 14 publications

(4 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Clayton [ 28 ] presents a detailed analysis on how numerous metrics (including number of filaments, lifetimes, number of births, deaths, and divisions) are affected by membrane kinetics and geometry. Arevalo et al [ 35 ] and Trayanova et al [ 34 ] present postshock filament distributions, and some filament dynamics are described, although not in detail. All of the above studies use representations of the heart that do not include fine-scale structure .…”

Section: Introductionmentioning

confidence: 99%

Filament Dynamics during Simulated Ventricular Fibrillation in a High-Resolution Rabbit Heart

Pathmanathan

Gray

2015

BioMed Research International

View full text Add to dashboard Cite

The mechanisms underlying ventricular fibrillation (VF) are not well understood. The electrical activity on the heart surface during VF has been recorded extensively in the experimental setting and in some cases clinically; however, corresponding transmural activation patterns are prohibitively difficult to measure. In this paper, we use a high-resolution biventricular heart model to study three-dimensional electrical activity during fibrillation, focusing on the driving sources of VF: “filaments,” the organising centres of unstable reentrant scroll waves. We show, for the first time, specific 3D filament dynamics during simulated VF in a whole heart geometry that includes fine-scale anatomical structures. Our results suggest that transmural activity is much more complex than what would be expected from surface observations alone. We present examples of complex intramural activity, including filament breakup and reattachment, anchoring to the thin right ventricular apex; rapid transitions among various filament shapes; and filament lengths much greater than wall thickness. We also present evidence for anatomy playing a major role in VF development and coronary vessels and trabeculae influencing filament dynamics. Overall, our results indicate that intramural activity during simulated VF is extraordinarily complex and suggest that further investigation of 3D filaments is necessary to fully comprehend recorded surface patterns.

show abstract

Section: Introductionmentioning

confidence: 99%

Filament Dynamics during Simulated Ventricular Fibrillation in a High-Resolution Rabbit Heart

Pathmanathan

Gray

2015

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…The mechanisms by which an electric shock terminates cardiac arrhythmias have been the subject of a large body of research (for review, see1). These studies have been driven by the understanding that a significant reduction in shock energy can only be achieved by full appreciation of the mechanisms by which a shock interacts with the heart and then exploiting them to devise novel low-voltage therapeutic approaches.…”

mentioning

confidence: 99%

Atrial defibrillation voltage: Falling to a new low

Trayanova

2011

Heart Rhythm

Self Cite

View full text Add to dashboard Cite

The mechanisms by which an electric shock terminates cardiac arrhythmias have been the subject of a large body of research (for review, see 1 ). These studies have been driven by the understanding that a significant reduction in shock energy can only be achieved by full appreciation of the mechanisms by which a shock interacts with the heart and then exploiting them to devise novel low-voltage therapeutic approaches.The research has demonstrated that the response of the myocardium to the shock involves simultaneous occurrence of positive and negative membrane polarization [2][3][4] . Detailed analysis of the etiology of this "virtual electrode polarization" (VEP) has demonstrated that tissue structure is responsible for its formation of VEP as well as for its shape, location, polarity, and intensity. The effect of tissue structure is two-fold. First, discontinuities in tissue structure (i.e. conductivities) force current to cross the membranes of neighboring cells, giving rise to VEP. Intercellular and interlaminar clefts 5,6 , or tissue lesions 7 are possible factors in this process. Second, continuous tissue structure such as ventricular shape and fiber architecture also give rise to VEP 8 .Action potential duration in the myocardium can be either extended by positive VEP or shortened by negative VEP, and strong negative VEP can completely abolish the action potential, creating a new, post-shock excitable area 9 . Propagation through the post-shock excitable area has proven to directly determine the outcome of a defibrillation shock. A shock succeeds in extinguishing fibrillatory wavefronts if excitations manage to traverse the newly-created post-shock excitable area before the rest of the myocardium recovers from refractoriness. Decreasing the post-shock excitable area could thus increase the likelihood of defibrillation success and lower the defibrillation voltage 10 ; however, this has proven difficult since the post-shock excitable areas are often hidden deep in the ventricular wall 10,11 .When the shock happens to affect resting cells (those that are part of the pre-shock, fibrillatory wavefront's excitable gap), positive VEPs immediately depolarize these cells; these cells become "secondary sources" emitting new wavefronts, rapidly overwhelming any effects of negative VEP. The targeted activation of cells in the fibrillatory wavefront's excitable gap by electric shocks thus has the potential to eliminate the reentrant circuit by rendering tissue refractory. Furthermore, since this is an excitation process (by positive VEP), the external current needs to only bring cells to the excitation threshold, requiring less energy as compared to de-excitation (by negative VEP) where an activated cell is forced into premature recovery.Address for correspondence: Johns Hopkins University, 3400 N. Charles St., Hackerman Hall Room 216, Baltimore, MD 21218, office phone: 410-516-4375, office fax: 410-516-5294, ntrayanova@jhu.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted...

show abstract

“…The numerical accuracy of the discretizations considered was assessed using a single-cell problem (24)(25)(26)(27)(28)(29)(30) and the method of manufactured solutions. As seen in Tables 2-4, all the discretizations provide converging numerical solutions.…”

Section: Numerical Accuracymentioning

confidence: 99%

“…The classical models (monodomain, bidomain) have been successfully used to study the propagation of the electrochemical wave in cardiac tissue (e.g., [14][15][16]), the initiation of excitation waves (e.g., [17][18][19][20][21]), the development of cardiac arrhythmias (e.g., [14,17,18]), the effect of defibrillation (e.g., [22][23][24][25][26][27][28]), and the effect of various drugs (e.g., [29][30][31][32]). …”

Section: Introductionmentioning

confidence: 99%

A Cell-Based Framework for Numerical Modeling of Electrical Conduction in Cardiac Tissue

et al. 2017

View full text Add to dashboard Cite

In this paper, we study a mathematical model of cardiac tissue based on explicit representation of individual cells. In this EMI model, the extracellular (E) space, the cell membrane (M), and the intracellular (I) space are represented as separate geometrical domains. This representation introduces modeling flexibility needed for detailed representation of the properties of cardiac cells including their membrane. In particular, we will show that the model allows ion channels to be non-uniformly distributed along the membrane of the cell. Such features are difficult to include in classical homogenized models like the monodomain and bidomain models frequently used in computational analyses of cardiac electrophysiology. The EMI model is solved using a finite difference method (FDM) and two variants of the finite element method (FEM). We compare the three schemes numerically, reporting on CPU-efforts and convergence rates. Finally, we illustrate the distinctive capabilities of the EMI model compared to classical models by simulating monolayers of cardiac cells with heterogeneous distributions of ionic channels along the cell membrane. Because of the detailed representation of every cell, the computational problems that result from using the EMI model are much larger than for the classical homogenized models, and thus represent a computational challenge. However, our numerical simulations indicate that the FDM scheme is optimal in the sense that the computational complexity increases proportionally to the number of cardiac cells in the model. Moreover, we present simulations, based on systems of equations involving ∼117 million unknowns, representing up to ∼16,000 cells. We conclude that collections of cardiac cells can be simulated using the EMI model, and that the EMI model enable greater modeling flexibility than the classical monodomain and bidomain models.

show abstract

Modeling Cardiac Defibrillation

Cited by 14 publications

References 44 publications

Filament Dynamics during Simulated Ventricular Fibrillation in a High-Resolution Rabbit Heart

Filament Dynamics during Simulated Ventricular Fibrillation in a High-Resolution Rabbit Heart

Atrial defibrillation voltage: Falling to a new low

A Cell-Based Framework for Numerical Modeling of Electrical Conduction in Cardiac Tissue

Contact Info

Product

Resources

About