EFFECT OF CARDIAC TISSUE ANISOTROPY ON THREE-DIMENSIONAL ELECTRICAL ACTION POTENTIAL PROPAGATION

2010 ◽  
Vol 24 (17) ◽  
pp. 1847-1853 ◽  
Author(s):  
ZHI ZHU HE ◽  
JING LIU
Keyword(s):  
Action Potential ◽  
Computational Models ◽  
Cardiac Tissue ◽  
Three Dimensional ◽  
Propagation Model ◽  
Spatial Inhomogeneity ◽  
Cardiac Tissues ◽  
Action Potential Propagation ◽  
Self Similar ◽  
Tissue Anisotropy

A three-dimensional (3D) electrical action potential propagation model is developed to characterize the integrated effect of cardiac tissue structure using a homogenous function with a spatial inhomogeneity. This method may be more effective for bridging the gap between computational models and experimental data for cardiac tissue anisotropy. A generalized 3D eikonal relation considering anisotropy and a self-similar evolution solution of such a relation are derived to identify the effect of anisotropy and predict the anisotropy-induced electrical wave propagation instabilities. Furthermore, the phase field equation is introduced to obtain the complex three-dimensional numerical solution of the new correlation. The present results are expected to be valuable for better understanding the physiological behavior of cardiac tissues.

scholarly journals Cardiac alternans induced by fibroblast-myocyte coupling: mechanistic insights from computational models

2009 ◽  
Vol 297 (2) ◽  
pp. H775-H784 ◽  
Author(s):  
Yuanfang Xie ◽  
Alan Garfinkel ◽  
James N. Weiss ◽  
Zhilin Qu
Keyword(s):  
Action Potential ◽  
Computational Models ◽  
Cardiac Tissue ◽  
Experimental Studies ◽  
Outward Current ◽  
Transient Outward Current ◽  
Two Dimensional ◽  
Background Current ◽  
Cardiac Alternans ◽  
Main Components

Recent experimental studies have shown that fibroblasts can electrotonically couple to myocytes via gap junctions. In this study, we investigated how this coupling affects action potential and intracellular calcium (Cai) cycling dynamics in simulated fibroblast-myocyte pairs and in two-dimensional tissue with random fibroblast insertions. We show that a fibroblast coupled with a myocyte generates a gap junction current flowing to the myocyte with two main components: an early pulse of transient outward current, similar to the fast transient outward current, and a later background current during the repolarizing phase. Depending on the relative prominence of the two components, fibroblast-myoycte coupling can 1) prolong or shorten action potential duration (APD), 2) promote or suppress APD alternans due to steep APD restitution (voltage driven) and also result in a novel mechanism of APD alternans at slow heart rates, 3) promote Cai-driven alternans and electromechanically discordant alternans, and 4) promote spatially discordant alternans by two mechanisms: by altering conduction velocity restitution and by heterogeneous fibroblast distribution causing electromechanically concordant and discordant alternans in different regions of the tissue. Thus, through their coupling with myocytes, fibroblasts alter repolarization and Cai cycling alternans at both the cellular and tissue scales, which may play important roles in arrhythmogenesis in diseased cardiac tissue with fibrosis.

Genesis of the monophasic action potential: role of interstitial resistance and boundary gradients

2004 ◽  
Vol 286 (4) ◽  
pp. H1370-H1381 ◽  
Author(s):  
Joseph V. Tranquillo ◽  
Michael R. Franz ◽  
Björn C. Knollmann ◽  
Alexandra P. Henriquez ◽  
Doris A. Taylor ◽  
...  
Keyword(s):  
Action Potential ◽  
Time Course ◽  
Cardiac Tissue ◽  
Mechanical Load ◽  
Critical Role ◽  
Applied Pressure ◽  
Three Dimensional ◽  
Membrane Dynamics ◽  
Monophasic Action Potential ◽  
Tissue Properties

The extracellular potential at the site of a mechanical deformation has been shown to resemble the underlying transmembrane action potential, providing a minimally invasive way to access membrane dynamics. The biophysical factors underlying the genesis of this signal, however, are still poorly understood. With the use of data from a recent experimental study in a murine heart, a three-dimensional anisotropic bidomain model of the mouse ventricular free wall was developed to study the currents and potentials resulting from the application of a point mechanical load on cardiac tissue. The applied pressure is assumed to open nonspecific pressure-sensitive channels depolarizing the membrane, leading to monophasic currents at the electrode edge that give rise to the monophasic action potential (MAP). The results show that the magnitude and the time course of the MAP are reproduced only for certain combinations of local or global intracellular and interstitial resistances that form a resting tissue length constant that, if applied over the entire domain, is smaller than that required to match the wave speed. The results suggest that the application of pressure not only causes local depolarization but also changes local tissue properties, both of which appear to play a critical role in the genesis of the MAP.

Effects of early afterdepolarizations on reentry in cardiac tissue: a simulation study

2007 ◽  
Vol 292 (6) ◽  
pp. H3089-H3102 ◽  
Author(s):  
Ray B. Huffaker ◽  
James N. Weiss ◽  
Boris Kogan
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Genetic Diseases ◽  
Three Dimensional ◽  
New Wave ◽  
Early Afterdepolarizations ◽  
Heart Rates ◽  
Torsades Des Pointes ◽  
Repolarization Reserve ◽  
Inward Currents

Early afterdepolarizations (EADs) are classically generated at slow heart rates when repolarization reserve is reduced by genetic diseases or drugs. However, EADs may also occur at rapid heart rates if repolarization reserve is sufficiently reduced. In this setting, spontaneous diastolic sarcoplasmic reticulum (SR) Ca release can facilitate cellular EAD formation by augmenting inward currents during the action potential plateau, allowing reactivation of the window L-type Ca current to reverse repolarization. Here, we investigated the effects of spontaneous SR Ca release-induced EADs on reentrant wave propagation in simulated one-, two-, and three-dimensional homogeneous cardiac tissue using a version of the Luo-Rudy dynamic ventricular action potential model modified to increase the likelihood of these EADs. We found: 1) during reentry, nonuniformity in spontaneous SR Ca release related to subtle differences in excitation history throughout the tissue created adjacent regions with and without EADs. This allowed EADs to initiate new wavefronts propagating into repolarized tissue; 2) EAD-generated wavefronts could propagate in either the original or opposite direction, as a single new wave or two new waves, depending on the refractoriness of tissue bordering the EAD region; 3) by suddenly prolonging local refractoriness, EADs caused rapid rotor displacement, shifting the electrical axis; and 4) rapid rotor displacement promoted self-termination by collision with tissue borders, but persistent EADs could regenerate single or multiple focal excitations that reinitiated reentry. These findings may explain many features of Torsades des pointes, such as perpetuation by focal excitations, rapidly changing electrical axis, frequent self-termination, and occasional degeneration to fibrillation.

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