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JOURNAL OF COMPUTER SCIENCE AND ENGINEERING, VOLUME 15, ISSUE 2, OCTOBER 2012

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Application of 2-D Network Simplification to Modellingand Simulation of the Cardiac Electrical ActivityUsing Bidomain Approach
Isaiah A. Adejumobi and Oluwaseun I. Adebisi
Abstract-This work is an application of 2-D network simplification to modelling and simulation of cardiac electrical activity using the bidomain approach. The electrical activity of the heart is governed by differential equations consisting of partial differential equations (PDEs) coupled to a system of ordinary differential equations (ODEs).Theseequations are challenging to solve numerically and implement owing to their non-linearity and stiffness. Explicit forward Euler method and 2-D network modelling were respectively used for the time and space discretizations of the derived bidomain model. We implemented and simulated the discretized model to obtain the time characteristic of the transmembrane potential, Vm in the normal cardiac tissue. We also observed the effects of changing the values of extracellular and intracellular resistances e, ion Vm; changing which resulted in its time dilation and gradual to near complete collapse. These are signs of cardiac electrical abnormalities. This work has not only revealed the nature of propagating cardiac electrical signal based on 2-D network simplification of the bidomain model but has also revealed that increase in values of electrical coupling between the cells in the 2-D network domain can significantly impact on the propagating cardiac electrical signal. Index Terms: bidomain approach, cardiac electrical activity, 2-D network simplification, transmembrane potential

1 INTRODUCTION
The electrical activity is very important for the heart to perform its functions. It is particularly responsible for the periodic contraction and relaxation of the heart which pumps blood throughout the body [1]. However, abnormal cardiac electrical activities have been posing great threats globally, causing many premature deaths. Mathematical models and computer simulations are rapidly becoming vital tools for investigating the heart conditions and the potential side effects of drugs on cardiac rhythms [2], [3]. They offer a realistic means of understanding the underlying mechanisms of heart functions and many other biological systems without carrying out physical experiments. coupled systems of partial differential equations (PDEs) and ordinary differential equations (ODEs) [1], [4]. These equations are usually non-linear and stiff, hence, pose computational challenges. Nevertheless, we adopted the bidomain approach in the present work due its ability to give a realistic simulation of cardiac electrical activity. It consists of a system of two degenerate non-linear partial differential equations coupled to a system of ordinary differential equations. Hence, to handle the computational complexities posed by the bidomain model, we have considered 2-D network simplification of the model in this work where the cardiac tissue is represented by interconnected network of cells, each individually described by a given system of cell model. This work is an application of 2-D network simplification to modelling and simulation of cardiac electrical activity using the bidomain approach. The electrical property of interest is the cardiac action potential. Our focus is to increase the value electrical coupling between the cells in the 2-D network domain and study the resulting effects on the cardiac action potential.

The cardiac electrophysiological models are governed by differential equations consisting of

I.A. Adejumobi is with Electrical Department, Federal University Nigeria. O.I. Adebisi is with Electrical Department, Federal University Nigeria.

and Electronics Engineering of Agriculture, Abeokuta, and ElectronicsEngineering of Agriculture, Abeokuta,

1.1Cardiac Action Potential Action potential is an important basic electrical property of the heart. It is a time characteristic of

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the transmembrane potential which is usually followed by a recovering of the resting condition. It shows different shapes and amplitudes according to the different kind of excitable media to which the cells belong to, and in the large muscle cells makes it possible the simultaneous contraction of the whole cell [5]. An action potential propagates across the heart in a heterogeneous way, keeping the same shape and amplitude all along an entire neural or muscular fibre. Cardiac cells are characterized by a negative transmembrane potential at rest and show two kinds of action potentials: the quick (or fast) and the slow response [5], [6]. The quick response action potential is typical in the myocardium fibres (both atrial and ventricular) and in the Purkinje fibres, which are fibres specialized in the conduction. The quick response action potential is usually identified by five different phases namely: phase 0 (depolarization phase), phase 1 (partial repolarization phase), phase 2 (plateau phase), phase 3 (repolarization) and phase 4 (resting membrane potential phase). Depolarization phase occurs due to the opening of the fast sodium ion (Na+) channels, causing a rapid increase in the membrane conductance to Na+ and therefore a rapid influx of Na+ into the cell. The partial repolarization phase occurs a result of the inactivation of the fast Na+ channels. The transient outward of potassium ion (K+) causes the small downward deflection of the action potential. The balance between the slow inward calcium ion (Ca++) currents and the outward K+ currents causes the plateau phase. Usually, the ventricular contraction persists throughout the action potential, so the long plateau produces a long action potential to ensure a forceful contraction of substantial duration. Rapid repolarization is caused by the outward K+ current. Na+ channelrecovery starts during the relative refractory period. These phases are shown in fig. 1.

Fig. 1: Quick (fast) response action potential [6]

The slow response action potential is typical of the Sinoatrial Node (SA), the natural pacemaker of the heart, and the Atrioventricular Node (AV), the tissue meant to transfer pulse from atria to ventricles. The slow response action potential is identified by a less negative resting membrane potential phase, a smaller slope and amplitude depolarization phase, an absence of the partial repolarization phase and by a relative refractory period that continues during resting membrane potential phase. The slow response action potential is shown in fig. 2.

0 3 4

Fig. 2: Slow response action potential [6]

The electrical activity of the heart as a whole is therefore characterized by a complex multiscale structure, ranging from the microscopic activity of ion channels in the cellular membrane to the macroscopic properties of the anisotropic propagation of the excitation and recovery fronts in the whole heart and the most complete model that gives the description of such a complex process is the anisotropic bidomain model.

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2 MATHEMATICAL MODEL FOR CARDIAC ELECTRICAL ACTIVITY


The electrical wave propagation in the thoracic volume is governed by three fundamental electrical laws [1], [ 7], [ 8]: The electrical charge conservation law The electrical conduction law (Ohms law) The consequence to the electromagnetic induction law

. =

(5

Equation (5) is generally called the continuity equation [9], [10]. For a good conductor, the volume charge density is zero, = 0, since the amount of positive and negative charges are equal [11]. Hence, if thoracic volume is assumed to be volume of conductor, equation (5) can be modified as: . = 0 (6 Equation (6) is called the electrical charge conservation law. Relatingthe current density j with the electric field E in volt per metre (V/m), the electric field E with the electric potential in volt (V) and current density j with the electric potential , the following fundamental laws emerge [9], [10]: the electric conduction law (Ohms law), electromagnetic induction law and modified Ohms law represented by: j = E E = (8 j = (9 (7

The law of conservation of charge states that an outward flow of positive charges must be balanced by a decrease of positive chargeswithin the close surface [9], [10]. Hence, this requires that: = . = (1

Where I is the current in Ampere (A) j is the current density in Ampere per square meter (A/m2) Q is the charge in Coulomb (C) S is the surface area in square meter (m2) t is the time in seconds (s) Applicationof divergence theoremwhich the surface integral to the volume integral to (1) gives (2) [9], [10]:

. =

. v

(2

Representing the enclosed charge Q by the volume integral of the charge density, (1) and (2) can be modified as: . v = ( ) v (3

Where is the conductivity in siemens per metre (S/m). The adopted bidomain modelassumes the cardiac tissue as a homogenized two-phase Ohmic conducting medium with one phase representing the intracellular space and the other, extracellular space. The phases are linked by a network of resistors and capacitors representing the ion channels and the capacitive current driven across the cell membrane due to a difference in potential respectively as shown in fig. 3.

Where is the volume charge density in coulomb per cubic meter (C/m3). Keeping the surface constant, the derivatives in (1), (2) and (3) becomes partial derivative and may appear within the integral as: . v = ( ) v (4

Since (4) is true for any volume no matter how small [9], [10]then;

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Extending the cell model formulated by Hodgkin and Huxley as reported in Matthias [12] with its electric circuit equivalence diagram as shown in fig. 4 to our reference model gives: = + , (15 Where is the membrane capacitance in per area unit. Imis the membrane current in ampere (A) Iappis the excitation current in ampere (A) Iion is the ionic current in ampere (A)

Fig. 3: Schematic model of the bidomain space [12]

Considering a post homogenization process, the intracellular and extracellular domains can be assumed to be superimposed to occupy the whole heart volume H [1], [13], [14], [15] and also applies to the cell membrane. Hence, the average intracellular and extracellular current densities, and , conductivity tensors and and electric potentials and are defined in H. Application of (6) to the heart volume gives: . = . = (10

Where is the surface to volume ratio of the cell membrane per meter (m-1) is the cell membrane current in ampere (A) From (10), (11) is obtained: . + = 0 (11

Fig.4: Cell model equivalent circuit diagram;ionic currents are parallel-connected tomembrane capacitor[12]

The use of (13) and (15) in (10) yields: . + . = ( + , ) in (16

Putting(9) in (10) yields: . = . (12

The ionic variable w satisfies a system of ODE of the type given by (17): = , in (17 Where g is a vector-valued function.

The transmembrane potential, , defined as difference in potential between intracellular and extracellular spaces is represented by: (13

Where is the intracellular electric potential in volt (V) is the extracellular electric potential in volt (V) Substitution of (13) in (12), gives: . ( + ) = . (14

The bidomain model described by (14), (16) and (17) depicts a non-linear elliptic equation for the extracellular potential coupled with the parabolic differential equation for the transmembrane potential Vm as well as an ordinary differential equation representing the ionic current w.

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Equations (14) and (16) describe the propagation of the electrical signal through the cardiac tissue while (17) describes the electrochemical reaction in the cell. The bidomain model described by (14), (16) and (17) has to be coupled to an ionic model and complemented with appropriate initial and boundary conditions for complete description of electrical wave propagation in the cardiovascular system.

current flows across the boundary between the intracellular and extracellular domains, that is: . = . (21

Where n is the normal vector to the domain boundary.

2.1 Ionic Model Some of the ionic models that have been to obtain the expressions forIionand g include [16]:FitzHughNagumo model, Aliev-Panfilov Model, Roger McCulloch Model and MitchellSchaeffer model. However, we considered FitzHugh-Nagumo (FHN) model because it qualitatively gives the representation of the most basic features of the action potential coupled with its straightforwardness as well as wider theoretical and computational applications. Thevariantof the FHN model adoptedis represented by (18) and (19) [17].
= 1 1 3 3 = 2 + (19 (18

2.3 Discretization The bidomain equations described by (14), (16) and (17) are non-linear. For easy handling and manipulation, these equations need to be linearized (discretized). Also, the bidomain equations are both time and space dependent, therefore they must be separately linearized. Various explicit and implicit time discretization techniques exist for linearizing differential equations, though, implicit method offers greater stability than explicit method but the latter is a very simple and straightforward method and problem of instability can be reduced by making the time step size very small. Hence, we employed explicit forward Euler time discretization scheme to linearize (16) and (17), which contain time derivatives.Equations (14) and (16) are spacediscretized using 2-D discrete (network) modelling. The final discretized equations are given by (22), (23) and (24).
1

Where 1 , 2 , , are positive constant parameters respectively called excitation rate constant, recovery rate constant, recovery decay constant and excitation decay constant. They are typical assumed to be positive constant. 1 controls the sharpness of the action potential which determines its mobility while2 controls the action potential duration.

+1

+ +

(22

With and assumed unity; Gi, the intracellular admittance matrix equivalent to . , and t, timestep size. +1 = + 2 + (23
= + 1

2.2 Initial and Boundary Conditions The bidomain equations described by (14), (16) and (17) are subjected to the initial conditions given by (20):
, , 0 = , , 0 = (20

. (24

Where Ge, the extracellular admittance matrix equivalent to . .

The boundary conditionimposed on this (14), (16) and (17) is that of a sealed boundary where no

2.3.1. Construction of Admittance MatricesGi and Ge Owing to the adoption of 2-D discrete (network) modelling, we were able replace Del operators on the intracellular and extracellular conductivity tensors i and e with intracellular and extracellular admittances Gi and Ge. Gi and Ge were constructed by considering node arrays Nx-by-Ny

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defined in the 2-D network domain to be linked by network of resistors arranged along x- and ydirection with ex, ey, ix, and iy representing the extracellular and intracellular resistance values along these directions.These resistors arrays were then transformed into matrices in the implementation code. This procedure is illustrated here using 2 by 3 nodes in figure 5 as an example and the result was generalized to the Nx by Ny nodes considered in this work. Each resistor was represented by five indices; the xi and yi indices of one the nodes to which the resistor was connected, the xj and yj indices of the other nodes to which the resistor was connected and resistor value . These five-index arrays are presented in table 1. The two separate indices representing each node (cell) to which the resistor was connected were then converted into a single index (encircled numbers in fig.5) which now represented the first node (x'i) to which the resistor was connected and the second node (y'j) to which the resistor was connected. It is these two singleindexed arrays that were stored in the matrices of Gi and Ge to represent the positions pij where the resistors are to be placed in the admittance matrices. This is presented in table 2.

1 1

2 3

2 2

2 3

y y

TABLE 2 TWO SINGLE-INDEXED ARRAYS


x'i 1 2 4 5 1 2 3 y'j 2 3 5 6 4 5 6

Scanning through the network of resistors in fig.5 from left to right and right to left, it was observed that the resistor values were equal in both directions, that is, 12 is equal to 21 and so on. Based on this, size of the admittance matrices Gi snd Ge is 6 by 6 matrices that is (2 x 3 by 2 x 3). The final matrix elements positions pij and their values are respectively shown in the matrices below. 11 21 31 41 51 61 12 22 32 42 52 62 13 14 23 24 33 34 43 44 53 54 63 64 15 25 35 45 55 65 0 0 0 0 16 26 36 46 56 66

, =

1 1, 1

1,2

1,3

y x
2,1 4 2,2 5

y
x

0 0 0 , = 0 0 0 0 Where gx is 1

0 0 0 0 0 0 0 0 0 0 0 and gy is 1

2,3 6

Fig. 5: Network of Resistors Connecting the Nodes

The admittance matrices finally obtained represented homogeneous but anisotropic system since the resistors appeared the same everywhere but current flows in the two different directions x and y due to difference in the resistances in the x and y directions were different.

TABLE 1 FIVE-INDEX ARRAYS


xi 1 1 2 2 1 yi 1 2 1 2 1 xj 1 1 2 2 2 yj 2 3 2 3 1 x x x x y

3 APPLICATION OF COMPUTER
The discretized equations were implemented in Java programming language (Java 6.0 version). Java is an object-oriented programming language. We adopted Java basically because of its enriched mathematical library and well designed Graphical User Interface (GUI) for displaying graphical representation of results. Another benefit of Java is

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its portability across various operating systems. A flow chart for the implementation algorithms is shown in fig. 6 below. Simulation experiments were carried out on a 4GB RAM, Intel (R) Core (TM) i7 CPU M620 @ 2.67GHz and 32-bit operating system computer. Running time of one simulation experiment ranged between 3 and 7minutes for unchanged and changed intracellular and extracellular resistances.

Start

Input parameters

Define arrays

Impose initial conditions on Vm and w

Construct admittance matrices Gi and Ge

Keep matrix Gi

Sum matrices Gi and Ge

Invert the sum of matrices Gi and Ge

Construct the right hand side of equation (24)

Solve for e at timestep n (24)

Next timestep

Solve Vm at timestep n+1(22) Solve w at timestep n+1 (23)

Plot results Vm against Time

Stop
Fig. 6: Flow chart for the bidomain code

4 SIMULATION ANALYSIS

RESULTS

AND

In this section of the work we present the results of our simulations. We performed simulation experiment using the developed 2-D Java programme based on the linearized bidomain equations given by (22), (23) and (24) and the parameters in table 3.

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TABLE 3 VALUES OF BASIC PARAMETERS [17]


Parameter Symbol Value Excitation rate constant 1 0.2 Recovery rate constant 2 0.2 Excitation decay constant 0.7 Recovery decay constant 0.8 Time step size t 0.01 Extracellular resistance in x1.0 direction Extracellular resistance in y- 3.0 direction Intracellular resistance in x- 1.0 direction Intracellular resistance in y- 3.0 direction Resting transmembrane -1.2 potential Initial value of ionic variable wo -0.62 The selected cells 8, 10, 15, 17 of the 50-by-50 nodes (cells) specified in 2-D network domain produced the propagated electrical waves in the normal cardiac tissue as shown in fig. 7a to d respectively with depolarization, partial repolarization, plateau, repolarization and resting membrane potential phases identified using the values 0, 1, 2, 3, and 4 in fig. 7b for clarity. This electrical signal produced is called the action potential (time characteristic of transmembrane potential), with the highest period observed in this work around 600ms. Fig. 7a to d are typically of the same wave pattern, consistent with the theoretical standard and the experimental findings from other researchers [1], [18, [19].

1 0

2 3 4

(b)

(c)

(d)
Fig. 7: Electrical wave propagation in the normal cardiac tissue: (a) at cell 8, (b) at cell 10, (c) at cell 15, (d) at cell 17

(a)

In order tostudy the effects ofincreasing the value of electrical coupling between the cells in the

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2-D network domain on the propagated cardiac signal, the extracellular and the intracellular resistances ex, ey, ix, and iy connecting different cells along x and y directions in the 2-D network domain were subjected to five levels of increment. The values of ex, ey, ix, and iygiven as 1, 3, 1 and 3 respectively were increased by a factors of 1.5, 2, 2.5, 3 and 10.During the simulations, time dilation effect in which the cardiac signals witnessed extended excitation cycles was observed when the extracellular and intracellular resistances ex, ey, ix, and iy along the x and y directions in the 2-D network domain were increased by factors of 1.5, 2, 2.5, 3 and10 respectively. Also, it was observed that the slopes of cardiac signals witnessed gradual collapse which became more obvious when ex, ey, ix, and iy were increased by factors of 3 and 10.The implication of this slope collapse is that the cardiac signals were not able to return to the resting state especially under the incremental factor of 10 for the period around 2 seconds which when compared to the excitation values in fig. 7 is an over-excitation period and is an indication of abnormal electrical wave propagation in the cardiac tissue. The obtained propagated cardiac signals for each incremental value are presented in fig. 8, 9, 10, 11, 12.

(b)

(c)

(a) (d)
Fig. 8: Electrical wave propagation due to increment in ex, ey, ix, and iy by factor of 1.5: (a) at cell 8, (b) at cell 10, (c) at cell 15, (d) at cell 17

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(a) (d)
Fig. 9: Electrical wave propagation due to increment in ex, ey, ix, and iy by factor of 2: (a) at cell 8, (b) at cel 10, (c) at cell 15, (d) at cell 17

(b)

(a)

(c) (b)

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(c)

(b)

(d)
Fig. 10: Electrical wave propagation due to increment in ex, ey, ix, and iy by factor of 2.5: (a) at cell 8, (b) atcell 10, (c) at cell 15, (d) at cell 17

(c)

(d) (a)
Fig. 11: Electrical wave propagation due to increment in ex, ey, ix, and iy by factor of 3: (a) at cell 8, (b) at cell10, (c) at cell 15, (d) at cell 17

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(a)

(d)
Fig. 12: Electrical wave propagation due to increment in ex, ey, ix, and iy by factor of 10: (a) at cell 8, (b) at cell10, (c) at cell 15, (d) at cell 17

5 CONCLUSION
In this work, we applied 2-D network simplification to the modelling and simulation of cardiac electrical activity using bidomain approach. Apart from the fact that our adoption of 2-D network simplification of the bidomain model enabled to avoid excessive computations, we have also been able to provide some insights into the electrical behaviour of human heart, revealing the nature of the electrical wave propagation pattern in the normal cardiac tissue.This work further revealed that increase in the intracellular and extracellular resistances coupling different cells in the 2-D network domain beyond certain limit can cause time dilation effect and collapse of the cardiac electrical waves with the overall effect of a delayed repolarization.If this persists for a long time, it may result in sudden cardiac death. Research is still on-gong on the application of continuum modelling (specifically finite element method) to analysis of cardiac electrical activity using bidomain approach. This model takes care of the pitfall our adopted network (discrete) modelling which uses cell counts below the actual cell counts of the heart.

(b)

6 REFERENCES
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[2] J.A. DiMasi, R.W. Hansen and H.G. Grabowski, The Price of Innovation: New Estimates of Drug Development Costs, J. Health Econ., vol. 22, no. 2,pp. 151185, 2003. [3] R.J. Spiteri and R.C. Dean,On The Performance of an Implicit-Explicit Runge Kutta Method in Models of Cardiac Electrical Activity, IEEE Trans. Biomed. Eng., vol. 55, no. 5,pp. 14881495, 2008. [4] Y. Belhamadia, Recent Numerical Methods in Electrocardiology, in: D. Campolo (Ed.), New Development in Biomedical Engineering,http://www.intechopen.com/book, 2010. [5] L. Gerardo-Giorda, Modelling and Numerical Simulation of Action Potential Patterns in Human Atrial Tissues. Technical Report TR2008-004, Mathematics and Computer science, Emory University, Atlanta, USA, 2008. [6] R.E. Klabunde, Cardiovasculas Physiology Concepts.New York, NY: Lippincott William and Wilkin, 2011. [7] A.D. Alin, M.M. Alexandru, M. Mihaela and M.I. Corina, Numerical simulation in electrocardiography, Rev. Roum. Sci. Techn. lectrotechn. et nerg., vol. 56, pp. 209218, 2011. [8] C.S. Henriquez, Simulating The Electrical Behaviour of Cardiac Tissue Using The Bidomain Model,Crit. Rev. Biomedical Engineering,vol. 21, pp. 1-77, 1993. [9] J.A. Edminister, Electromagnetics. New Delhi, India: Tata McGraw-Hill Publishing Company Limited, 2006. [10] W.H. Hayt and J.A. Buck, Engineering electromagnetics.New Delhi, India:McGrawHill Education Private Limited, 2006. [11] S.R. Reddy, Electromagnetic theory. Chennai, India: V. Ramesh Publisher, 2002. [12] G. Matthias, 3D bidomain equation for muscle fibers, masters thesis, Fredrich-AlexanderUniversitt Erlangen-Nrnberg, Germany, 2011. [13] E.J. Vigmond, R.W. dosSantos, A.J. Prassl, M. Deo and G. Plank, Solvers for The Cardiac Bidomain Equations, Prog. Biophys. Mol. Biol., vol. 96, pp. 3-18, 2008. [14] M. Boulakia, M.A. Fernandez, J.-F. Gerbeau, and N. Zemzemi, Mathematical modelling of electrocardiograms: A numerical study, Ann Biomed Eng., vol. 38, pp. 1071-1097, 2009.

[15] M. Boulakia, M.A. Fernandez, J.-F. Gerbeau, and N. Zemzemi, towards the numerical simulation of electrocardiograms, in: F.B. Sachse and G. Seemann (Eds.), Functional Imaging and Modeling of the Heart, SpringerVerlag, pp. 240-249, 2007. [16] Boulakia, M., Fernandez, M.A., Gerbeau, J.-F. andN.Zemzemi, A coupled system of PDEs and ODEs arising in electrocardiograms modelling. Appl. Math. Res. Exp. (abn 002): 28, 2008. [17] O.F. Niels, Bidomain model of cardiac excitation, http://pages.physics.cornell.edu, 2003. [18] F.H. Nigel, Efficient simulation of action potential propagation in a bidomain, doctoral dissertation, Duke University, Durhan, Northern Carolina, USA, 1992. [19] B.M. Rocha, F.O. Campros, G. Planck, R.W. dos-Santos, M. Liebmann, and G.C. Haase, Simulation of electrical activity in the heart with graphical processing units, SFB Report No. 2009-016, Austria, 2009. Isaiah A. Adejumobi obtained his B.Eng., M.Eng. and Ph.D degrees in Electrical Engineering from University of Ilorin, Ilorin, Nigeria in 1987, 1992 and 2003 respectively. He started his academic career form University of Ilorin in August 1990 where he worked for about fifteen and half years before moving to his present place of work; Federal Society University of of Agriculture and a Abeokuta, registered Dr Nigeria. He is a Corporate Member of Nigeria Engineering in Nigeria. Engineering for Council for the Regulation of Engineering Academically Adejumobi has led some joint researches in electrical and related disciplines. He has over thirty journal publications both locally and internationally. He is currently working on a joint research on Cardiac Electrical Activities, a research that was motivated due in to the increasing He is cardiovascular Engineering. Oluwaseun I. Adebisi obtained his B.Eng. degree in Electrical and Electronics Engineering from problems Nigeria.

currently an Associate Professor of Electrical

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Federal University of Agriculture, Abeokuta, Nigeria. He is currently a Junior Research Fellow in the Department of Electrical and Electronics

Engineering in the University. His research interest is on Modelling of Cardiac Electrical Activities.

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