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Register a new userSpiral- and scroll-wave dynamics in mathematical models for canine and human ventricular tissue with varying Potassium and Calcium currents
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We conduct a systematic,direct-numerical-simulation study,in mathematical models for ventricular tissue,of the dependence of spiral-and scroll-wave dynamics on $G_{Kr}$, the maximal conductance of the delayed rectifier Potassium current($I_{Kr}$) channel,and the parameter $gamma_{Cao}$,which determines the magnitude and shape of the current $I_{CaL}$ for the L-type calcium-current channel,in both square and anatomically realistic,whole-ventricle simulation domains using canine and human models. We use ventricular geometry with fiber-orientation details and employ a physiologically realistic model for a canine ventricular myocyte. We restrict ourselves to an HRD-model parameter regime, which does not produce spiral- and scroll-wave instabilities because of other,well-studied causes like a very sharp action-potential-duration-restitution (APDR) curve or early after depolarizations(EADs) at the single-cell level. We find that spiral- or scroll-wave dynamics are affected predominantly by a simultaneous change in $I_{CaL}$ and $I_{Kr}$,rather than by a change in any one of these currents;other currents do not have such a large effect on these wave dynamics in this parameter regime of the HRD model.We obtain stability diagrams in the $G_{Kr} -gamma_{Cao}$ plane.In the 3D domain,the geometry of the domain supports the confinement of the scroll waves and makes them more stable compared to their spiral-wave counterparts in 2D domain. We have also carried out a comparison of our HRD results with their counterparts for the human-ventricular TP06 model and have found important differences. In both these models,to make a transition,(from broken-wave to stable-scroll states or vice versa) we must simultaneously increase $I_{Kr}$ and decrease $I_{CaL}$;a modification of only one of these currents is not enough to effect this transition.
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Ventricular tachycardia (VT) and ventricular fibrillation (VF) are lethal rhythm disorders, which are associated with the occurrence of abnormal electrical scroll waves in the heart. Given the technical limitations of imaging and probing, the in situ visualization of these waves inside cardiac tissue remains a challenge. Therefore, we must, perforce, rely on in-silico simulations of scroll waves in mathematical models for cardiac tissue to develop an understanding of the dynamics of these waves in mammalian hearts. We use direct numerical simulations of the Hund-Rudy-Dynamic (HRD) model, for canine ventricular tissue, to examine the interplay between electrical scroll-waves and conduction and ionic inhomogeneities, in anatomically realistic canine ventricular geometries with muscle-fiber architecture. We find that millimeter-sized, distributed, conduction inhomogeneities cause a substantial decrease in the scroll wavelength, thereby increasing the probability for wave breaks; by contrast, single, localized, medium-sized ($simeq $ cm) conduction inhomogeneities, exhibit the potential to suppress wave breaks or enable the self-organization of wave fragments into stable, intact scrolls. We show that ionic inhomogeneities, both distributed or localised, suppress scroll-wave break up. The dynamics of a stable rotating wave is not affected significantly by such inhomogeneities, except at high concentrations of distributed inhomogeneities, which can cause a partial break up of scroll waves. Our results indicate that inhomogeneities in the canine ventricular tissue are less arrhythmogenic than inhomogeneities in porcine ventricular tissue, for which an earlier in silico study has shown that the inhomogeneity-induced suppression of scroll waves is a rare occurrence.
Spiral waves of excitation in cardiac tissue are associated with life-threatening cardiac arrhythmias. It is, therefore, important to study the electrophysiological factors that affect the dynamics of these spiral waves. By using an electrophysiologically detailed mathematical model of a myocyte (cardiac cell), we study the effects of cellular parameters, such as membrane-ion-channel conductances, on the properties of the action-potential (AP) of a myocyte. We then investigate how changes in these properties, specifically the upstroke velocity and the AP duration (APD), affect the frequency $omega$ of a spiral wave in the mathematical model that we use for human-ventricular tissue. We find that an increase (decrease) in this upstroke-velocity or a decrease (increase) in the AP duration increases (decreases) $omega$. We also study how other intercellular factors, such as the fibroblast-myocyte coupling, diffusive coupling strength, and the effective number of neighboring myocytes, modulate $omega$. Finally, we demonstrate how a spiral wave can drift to a region with a high density of fibroblasts. Our results provide a natural explanation for the anchoring of spiral waves in highly fibrotic regions in fibrotic hearts.
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