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IntroductionCardiac muscle can respond to long term increase in demand placed upon it or advancement of age by cellular hypertrophy. Hypertrophy is a major cause of cardiac disease.Hypertrophy induces an increased action potential duration (APD) and calcium transient duration. It reduces the calcium transient amplitude. The electrical restitution properties of cells often dictate spatial behaviours and their instabilities. The relationship between APD of successive pulses APD n and their corresponding diastolic intervals is given by APD n+1 = f (SI -DI n ) where f is the restitution relationship for single cell. It is known that if as MethodsA computer model of rat left ventricular cell was constructed by modifying an already existing model [2]. The main modifications included were as following.For exchanger current [9]. A 30% increase in cell capacitance [10], 30% increase in cell size [11,12] was also implemented. Hypertrophy induced T-type calcium current was also considered. Steady state kinetics were obtained from [13]. The time constants and formulation for the current were taken from [14]. Both control and hypertrophic models were integrated using a simple forward Euler method with a time step of 0.1 µs which gave stable solutions.The virtual strand was 8 mm long. Electrotonic interaction between cells was simulated through diffusive coupling and 1D models were developed by incorporating single cell models into a parabolic partial differential equation (PDE) of the formwhere I ion is the total cellular ionic current, V is the cell membrane voltage, C is cell capacitance, and D is the diffusion constant. The space step was 0.1 mm. No flux boundary conditions were imposed at each end of the strand. Diffusion constant was set to a value of 0.1 cm 2 /s. Periodic waves were stimulated in the strand by applying a periodic SI to 7 nodes situated at one end of the strand. Stimulus duration was 5 ms. Strength of SI was 0.6 pA in