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A discrete model has been developed which reproduces the intercellular electrophysiological processes within a block of myocardial tissue. The behaviour of individual elements is introduced in the form of the digitised physiologic and premature action potentials which are comprehended as series of jumps between discrete polarisation levels. For each cellular element, the model introduces the ercitation threshold as the minimum electric flow in the surrounding which can ercite the cell, and the sensitivity towards the electrotonic interactions which can advance or slow down the depolarisation and repolarisation processes of the cell. The ercitation threshold and the electrotonic sensitivity are dependent on the current polarity of the element. The numerical solution of the model is based on discrete planning of asynchronous events. The time increments are dynamically computed according to the chosen precision of the discrete polarity levels. The model enables efficient simulation of the electrophysiological properties in 3-dintensional models of the myocardial tissue. The paper presents a detailed fonnal description of the model.

A computer model of cardiac excitation and recovery processes reproduced chaotic behavior of the simulated tissue to investigate the way that different parameters influence the degree of modeled disorganization. The model included abnormal shapes of action potential curves corresponding to premature excitation, excitation transmission based on transmembrane voltages, and the electronic interactions between neighboring cells. The model was used to examine a one-dimensional cable of simulated cells. The degree of the simulated chaos was examined in the dependence on the shapes of action potential curves, on the threshold of transmembrane voltages initiating an excitation wave, and on the degree of the electrotonic interactions of neighboring cells. The maximum disorganization was achieved when combining the negative influence of all parameters. Changing the shape of the action potential curves had a greater preventive influence on the modeled chaos than variation of the other parameters. >

A computer model reproduced atrio-ventricular (AV) reentrant tachycardia and its termination by overdrive on-circuit pacing. The model simulated activation waves radiating along a one-dimensional circular pathway, the portions of which represent the atrial, AV nodal, His-Purkinje, ventricular, and bypass parts of the tachycardia circuit. The modeled pathway was composed of 289 elements, and the model distinguished only the depolarized and resting states of constituent elements and introduced differential refractoriness and conduction velocity for each element. Cycle length dependence of AV nodal decremental conduction is also introduced. The experiments with the model examined the capability of overdrive on-circuit pacing to terminate the tachycardia. The results of the study suggest that the usual impression of a regular recovery wave and of a regular excitable window moving uniformly along the macro-reentrant circuit is incorrect. >

A computer simulation model of cardiac rhythm and heart-pacemaker interactions has been used to examine the possibility of short atrial-ventricular (AV) delay DDD pacing to prevent junctional reentry tachycardia. The experiments compared the actions of two pacemaker models: a clinically realistic DDD mode operating with quasi-Wenckebach prolongation of the AV delay, and a modification of the DDD mode which is programmed according to atrial and ventricular refractoriness of the heart and the conduction delays of pathological bypass tracts. The pathological phenomena modeled in the experiments simulate different possibilities of tachycardia initiation. The computational results prove that many possible mechanisms of initiation of junctional reentry tachycardia are beyond the prophylactic capabilities of current sophisticated DDD pacemakers. The results also show that the suggested pacing mode improves antitachycardia prophylaxis even when responding to complex pathological episodes of natural cardiac activity. >

A computer model simulating both excitation and recovery processes within a block of heart muscle tissue has been developed. It incorporates blocks of tissue consisting of several thousand elements and introduces phenomena which are omitted in other heart models. These include the specific shapes of action potential curve corresponding to excitation of cells which have not been fully recovered. Results of simulation studies are presented in the form of three-lead orthogonal electrocardiograms (ECGs). Another model was used to reproduce the electronic interactions between neighboring cells during recovery phases. It also improves the concept of the modeled excitation and treats the depolarization as an self-initiating process depending only on membrane voltage between coupled cells. Both models have been used in various computational series. The results presented include models of destabilizing the tissue due to fast sequential stimulation models of repolarization changes in ischemia and infarction, and models of 'reflection' mechanisms. >