scholarly journals Deriving the Bidomain Model of Cardiac Electrophysiology From a Cell-Based Model; Properties and Comparisons

2022 ◽  
Vol 12 ◽  
Author(s):  
Karoline Horgmo Jæger ◽  
Aslak Tveito
Keyword(s):  
Cardiac Electrophysiology ◽  
Cardiac Tissue ◽  
Close Relation ◽  
Bidomain Model ◽  
Normal Range ◽  
Intracellular Space ◽  
A Cell ◽  
Conductive Properties ◽  
Insight Into ◽  
Conduction Properties

The bidomain model is considered to be the gold standard for numerical simulation of the electrophysiology of cardiac tissue. The model provides important insights into the conduction properties of the electrochemical wave traversing the cardiac muscle in every heartbeat. However, in normal resolution, the model represents the average over a large number of cardiomyocytes, and more accurate models based on representations of all individual cells have therefore been introduced in order to gain insight into the conduction properties close to the myocytes. The more accurate model considered here is referred to as the EMI model since both the extracellular space (E), the cell membrane (M) and the intracellular space (I) are explicitly represented in the model. Here, we show that the bidomain model can be derived from the cell-based EMI model and we thus reveal the close relation between the two models, and obtain an indication of the error introduced in the approximation. Also, we present numerical simulations comparing the results of the two models and thereby highlight both similarities and differences between the models. We observe that the deviations between the solutions of the models become larger for larger cell sizes. Furthermore, we observe that the bidomain model provides solutions that are very similar to the EMI model when conductive properties of the tissue are in the normal range, but large deviations are present when the resistance between cardiomyocytes is increased.

scholarly journals From Millimeters to Micrometers; Re-introducing Myocytes in Models of Cardiac Electrophysiology

2021 ◽  
Vol 12 ◽  
Author(s):  
Karoline Horgmo Jæger ◽  
Andrew G. Edwards ◽  
Wayne R. Giles ◽  
Aslak Tveito
Keyword(s):  
Cardiac Electrophysiology ◽  
Cardiac Tissue ◽  
Cardiac Conduction ◽  
Bidomain Model ◽  
Wave Dynamics ◽  
Alternative Approach ◽  
Biophysical Processes ◽  
Averaged Models ◽  
The Cost ◽  
Present Understanding

Computational modeling has contributed significantly to present understanding of cardiac electrophysiology including cardiac conduction, excitation-contraction coupling, and the effects and side-effects of drugs. However, the accuracy of in silico analysis of electrochemical wave dynamics in cardiac tissue is limited by the homogenization procedure (spatial averaging) intrinsic to standard continuum models of conduction. Averaged models cannot resolve the intricate dynamics in the vicinity of individual cardiomyocytes simply because the myocytes are not present in these models. Here we demonstrate how recently developed mathematical models based on representing every myocyte can significantly increase the accuracy, and thus the utility of modeling electrophysiological function and dysfunction in collections of coupled cardiomyocytes. The present gold standard of numerical simulation for cardiac electrophysiology is based on the bidomain model. In the bidomain model, the extracellular (E) space, the cell membrane (M) and the intracellular (I) space are all assumed to be present everywhere in the tissue. Consequently, it is impossible to study biophysical processes taking place close to individual myocytes. The bidomain model represents the tissue by averaging over several hundred myocytes and this inherently limits the accuracy of the model. In our alternative approach both E, M, and I are represented in the model which is therefore referred to as the EMI model. The EMI model approach allows for detailed analysis of the biophysical processes going on in functionally important spaces very close to individual myocytes, although at the cost of significantly increased CPU-requirements.

scholarly journals Accelerating mono-domain cardiac electrophysiology simulations using OpenCL

2015 ◽  
Vol 1 (1) ◽  
pp. 413-417
Author(s):  
Eike M. Wülfers ◽  
Zhasur Zhamoliddinov ◽  
Olaf Dössel ◽  
Gunnar Seemann
Keyword(s):  
Cardiac Electrophysiology ◽  
Cardiac Tissue ◽  
Ionic Currents ◽  
Domain Model ◽  
Electrical Excitation ◽  
Simulation Domain ◽  
Speed Up ◽  
Cross Platform ◽  
Atrial Myocyte ◽  
Intel Xeon

AbstractUsing OpenCL, we developed a cross-platform software to compute electrical excitation conduction in cardiac tissue. OpenCL allowed the software to run parallelized and on different computing devices (e.g., CPUs and GPUs). We used the macroscopic mono-domain model for excitation conduction and an atrial myocyte model by Courtemanche et al. for ionic currents. On a CPU with 12 HyperThreading-enabled Intel Xeon 2.7 GHz cores, we achieved a speed-up of simulations by a factor of 1.6 against existing software that uses OpenMPI. On two high-end AMD FirePro D700 GPUs the OpenCL software ran 2.4 times faster than the OpenMPI implementation. The more nodes the discretized simulation domain contained, the higher speed-ups were achieved.

Engineered cardiac tissue analyzed using the mechanical bidomain model

2018 ◽  
Vol 98 (5) ◽  
Author(s):  
Kharananda Sharma ◽  
Bradley J. Roth
Keyword(s):  
Cardiac Tissue ◽  
Bidomain Model

scholarly journals Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Srinivas Tapa ◽  
Lianguo Wang ◽  
Samantha D. Francis Stuart ◽  
Zhen Wang ◽  
Yanyan Jiang ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Cardiac Electrophysiology ◽  
Neural Control ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Sympathetic Nerve Stimulation ◽  
Post Surgery ◽  
Dopamine Beta Hydroxylase ◽  
Perfused Hearts ◽  
Insight Into

Abstract Myocardial infarction (MI) can result in sympathetic nerve loss in the infarct region. However, the contribution of hypo-innervation to electrophysiological remodeling, independent from MI-induced ischemia and fibrosis, has not been comprehensively investigated. We present a novel mouse model of regional cardiac sympathetic hypo-innervation utilizing a targeted-toxin (dopamine beta-hydroxylase antibody conjugated to saporin, DBH-Sap), and measure resulting electrophysiological and Ca2+ handling dynamics. Five days post-surgery, sympathetic nerve density was reduced in the anterior left ventricular epicardium of DBH-Sap hearts compared to control. In Langendorff-perfused hearts, there were no differences in mean action potential duration (APD80) between groups; however, isoproterenol (ISO) significantly shortened APD80 in DBH-Sap but not control hearts, resulting in a significant increase in APD80 dispersion in the DBH-Sap group. ISO also produced spontaneous diastolic Ca2+ elevation in DBH-Sap but not control hearts. In innervated hearts, sympathetic nerve stimulation (SNS) increased heart rate to a lesser degree in DBH-Sap hearts compared to control. Additionally, SNS produced APD80 prolongation in the apex of control but not DBH-Sap hearts. These results suggest that hypo-innervated hearts have regional super-sensitivity to circulating adrenergic stimulation (ISO), while having blunted responses to SNS, providing important insight into the mechanisms of arrhythmogenesis following sympathetic nerve loss.

scholarly journals Case report: MRI findings of acute uremic encephalopathy in a 1-year-old boy

2021 ◽  
pp. 20210057
Author(s):  
Amar Ajay Chotai ◽  
Dipayan Mitra
Keyword(s):  
Emergency Department ◽  
Renal Function ◽  
Case Report ◽  
Extracellular Potassium ◽  
Neurological Abnormality ◽  
Normal Range ◽  
Mri Findings ◽  
Intracellular Space ◽  
History Of ◽  
Function Profile

We present a 1-year-old boy who presented to the emergency department with a 7-day history of diarrhoea and vomiting. The initial renal function profile demonstrated a urea of 55 mmol l−1 (normal range between 5 and 20 mmol l−1), creatinine 695 micromol/L (normal range between 62–106 micromol/L) and potassium 9.1 mmol l−1 (normal range between 3.5–5.0 mmol l−1), with a profound metabolic acidosis. Upon examination, there were no significant findings, specifically no neurological abnormality. He was prescribed back-to-back Salbutamol nebulisers, to increase the shift of extracellular potassium into the intracellular space, followed by i.v. calcium gluconate, with some improvement in potassium levels. A further 5 mmol of sodium bicarbonate was given, as well as a stat dose of 1 mg/kg furosemide, and per rectal calcium resonium. He was then commenced on an infusion with 10% dextrose with insulin. He was subsequently found to be in urinary retention and a catheter was inserted, which drained 1700 ml. A subsequent renal function profile, 24 hours after admission, demonstrated improvement with urea 39 mmol l−1, creatinine 300 micromol/L and potassium 3.0 mEq/L.

scholarly journals Mathematical analysis and 2-scale convergence of a heterogeneous microscopic bidomain model

2018 ◽  
Vol 28 (05) ◽  
pp. 979-1035 ◽  
Author(s):  
Annabelle Collin ◽  
Sébastien Imperiale
Keyword(s):  
Mathematical Analysis ◽  
Cardiac Electrophysiology ◽  
Convergence Theory ◽  
Bidomain Model ◽  
Periodic Homogenization ◽  
Homogenization Procedure ◽  
Uniform Estimates ◽  
Bidomain Equations ◽  
Homogenization Process

The aim of this paper is to provide a complete mathematical analysis of the periodic homogenization procedure that leads to the macroscopic bidomain model in cardiac electrophysiology. We consider space-dependent and tensorial electric conductivities as well as space-dependent physiological and phenomenological nonlinear ionic models. We provide the nondimensionalization of the bidomain equations and derive uniform estimates of the solutions. The homogenization procedure is done using 2-scale convergence theory which enables us to study the behavior of the nonlinear ionic models in the homogenization process.

scholarly journals Controlled Construction of Stable Network Structure Composed of Honeycomb-Shaped Microhydrogels

Life ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 38 ◽  
Author(s):  
Masayuki Hayakawa ◽  
Satoshi Umeyama ◽  
Ken Nagai ◽  
Hiroaki Onoe ◽  
Masahiro Takinoue
Keyword(s):  
Cell Communication ◽  
Model Systems ◽  
Stable Component ◽  
Photosensitive Polymer ◽  
A Cell ◽  
External Stimuli ◽  
Structural Instabilities ◽  
Insight Into ◽  
Stable Network ◽  
Microfluidic Technique

Recently, the construction of models for multicellular systems such as tissues has been attracting great interest. These model systems are expected to reproduce a cell communication network and provide insight into complicated functions in living systems./Such network structures have mainly been modelled using a droplet and a vesicle. However, in the droplet and vesicle network, there are difficulties attributed to structural instabilities due to external stimuli and perturbations. Thus, the fabrication of a network composed of a stable component such as hydrogel is desired. In this article, the construction of a stable network composed of honeycomb-shaped microhydrogels is described. We produced the microhydrogel network using a centrifugal microfluidic technique and a photosensitive polymer. In the network, densely packed honeycomb-shaped microhydrogels were observed. Additionally, we successfully controlled the degree of packing of microhydrogels in the network by changing the centrifugal force. We believe that our stable network will contribute to the study of cell communication in multicellular systems.

Hyperhomocysteinemia’s effect on antioxidant capacity in rats

Open Medicine ◽  
2010 ◽  
Vol 5 (5) ◽  
pp. 620-626 ◽  
Author(s):  
Christian Filip ◽  
Elena Albu ◽  
Nina Zamosteanu ◽  
M. Irina ◽  
Mihaela Silion ◽  
...  
Keyword(s):  
Antioxidant Defense ◽  
Plasma Concentrations ◽  
Total Antioxidant Status ◽  
Reactive Species ◽  
Type I ◽  
Defense System ◽  
Normal Range ◽  
Sod Activity ◽  
Intracellular Space ◽  
Antioxidant Defense Systems

AbstractHyperhomocysteinemia represents elevated homocysteine (Hcys) concentrations in blood above the normal range. In humans, the normal range of homocysteine is 5.0–15.9 mM/ml. High levels of homocysteine disturb the normal epithelial functions and correlate with cardiovascular diseases even at slightly increased concentrations. In homocysteine metabolism, vitamins play an important role. The mechanism through which homocysteine triggers these effects is not yet elucidated, but the involvement of reactive species may be the answer. It is not known whether the intra- or extracellular antioxidant system is more affected by elevated homocysteine levels. We studied the effects of hyperhomocysteinemia on the intra- and extracellular antioxidant defense systems in two different types of diet in rats. Type I was food with low folic acid and vitamin B12 content and type II was food with normal amounts of these two vitamins. Hyperhomocysteinemia was experimentally induced by oral administration of methionine 2 mg/kg body weight, single daily dose, for a 15-day period. Plasma concentrations of homocysteine were measured using an HPLC method. In the response of the intracellular antioxidant defense system against hyperhomocysteinemia, we determined the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in red blood cells, using RANDOX kits for manual use. For the extracellular response we determined the plasma total antioxidant status (TAS) also using a RANDOX kit for manual use. Our data show that methionine load induces hyperhomocysteinemia despite normal vitamin supply in rats. SOD activity rose with simultaneous decrease in GPx activity independently of diet; this might suggest that the intracellular defense system was disturbed by the rise in homocysteine level. TAS decrease suggests that the extracellular antioxidant defense was also affected. We assume that hyperhomocysteinemia is directly linked to reactive species generation and the intracellular space seems to be more affected than the extracellular one.

scholarly journals Numerical Simulations of Fractionated Electrograms and Pathological Cardiac Action Potential

2002 ◽  
Vol 4 (3) ◽  
pp. 167-181 ◽  
Author(s):  
Simona Sanfelici
Keyword(s):  
Numerical Simulations ◽  
Cardiac Tissue ◽  
Time Discretization ◽  
Ionic Currents ◽  
Bidomain Model ◽  
Approximation Process ◽  
Point Of Interest ◽  
Intracellular Conductivity ◽  
Membrane Ionic Currents ◽  
Fractionated Electrograms

The aim of this work is twofold. First we focus on the complex phenomenon of electrogram fractionation, due to the presence of discontinuities in the conduction properties of the cardiac tissue in a bidomain model. Numerical simulations of paced activation may help to understand the role of the membrane ionic currents and of the changes in cellular coupling in the formation of conduction blocks and fractionation of the electrogram waveform. In particular, we show that fractionation is independent ofINAalterations and that it can be described by the bidomain model of cardiac tissue. Moreover, some deflections in fractionated electrograms may give nonlocal information about the shape of damaged areas, also revealing the presence of inhomogeneities in the intracellular conductivity of the medium at a distance.The second point of interest is the analysis of the effects of space–time discretization on numerical results, especially during slow conduction in damaged cardiac tissue. Indeed, large discretization steps can induce numerical artifacts such as slowing down of conduction velocity, alteration in extracellular and transmembrane potential waveforms or conduction blocks, which are not predicted by the continuous bidomain model. Several possible numerical and physiological explanations of these effects are given. Essentially, the discrete system obtained at the end of the approximation process may be interpreted as a discrete model of the cardiac tissue made up of isopotential cells where the effective intracellular conductivity tensor depends on the space discretization steps; the increase of these steps results in an increase of the effective intracellular resistance and can induce conduction blocks if a certain critical value is exceeded.

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