Computer Model Of Excitation Research Articles

Mechanisms in T-wave alternans caused by intraventricular block

It is recognized that 2:1 intraventricular (IV) block can result in T-wave alternans but is usually assumed that it would also affect QRS waveform. Block in a local region is not, however, varied activation sequence of the same muscle mass because the blocked region is not activated and is not part of the mass that is activated in cycles without block. Also, the block region may have electrocardiogram (ECG) effects when its state differs from other regions. In view of those considerations, the ECG effects of IV block were evaluated by using a computer model of excitation and recovery. ECGs were calculated from differences between the excited state and various degrees of recovery. Results provided evidence that boundaries associated with regions of block rather than regions having varied activation sequence were the major factors in T-wave alternans caused by IV block. Effects of the boundaries included cancellation of the effects of IV block on QRS complexes. Findings suggest that IV block cannot be excluded as a mechanism of T-wave alternans in the absence of QRS alternans.

Computer model of excitation and recovery in the anisotropic myocardium: I. Rectangular and cubic arrays of excitable elements

A computer model of propagated excitation and recovery in anisotropic cardiac tissue is presented that consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. The model's performance was first tested in a two-dimensional configuration with uniform anisotropy; this method allowed comparison of simulated isochrones of excitation and extracellular electrograms with the results of experimental in vitro studies of cardiac tissue. Next the model was used to study propagated excitation in a three-dimensional region representing the anisotropic properties of the ventricular wall, with attention to the effects produced by variable fiber direction from “endocardium” to “epicardium”.

Computer model of excitation and recovery in the anisotropic myocardium: III. Arrhythmogenic conditions in the simplified left ventricle

A computer model of propagated excitation and recovery in anisotropic cardiac tissue has been described in the first two reports of this series. The model consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. As described in the previous two reports, the model's performance was tested in rectangular and cubic arrays of excitable elements and in the “normal” three-dimensional simplified left ventricle with anisotropy. The present report deals with arrhythmogenic conditions in the simplified left ventricle with anisotropy and ventricular-gradient properties; specifically, we studied activation and recovery in the presence of an ischemic region and under various stimulation protocols. The aim of these simulations was to elucidate the role of reentry in the genesis of ventricular tachycardia. Our simulations produced reentrant activation as a result of appropriate endocardial stimulation.

Computer model of excitation and recovery in the anisotropic myocardium: II. Excitation in the simplified left ventricle

A computer model of propagated excitation and recovery in anisotropic cardiac tissue was described in the first report of this series. The model consists of a large number of excitable elements whose subthreshold interactions are governed by the anisotropic bidomain theory but whose suprathreshold behavior (action potential) is largely preassigned. As described in the first report, the model's performance was tested in rectangular and cubic arrays of excitable elements. This second report deals with three-dimensional simulations in a simplified left ventricle with anisotropy; specifically, the activation process in the “normal” ventricle is described (exemplified by the activation sequences started from various endocardial, intramural, and epicardial sites). To further substantiate our model's validity, we compare simulated epicardial and body-surface potential distributions with experimental findings in isolated canine hearts and with clinical evidence provided by electrocardiographic body-surface mapping.