The Mechanism of Simulated Torsade de Pointes in a Computer Model of Propagated Excitation

Abstract

Mechanism of Torsade de Pointes. A computer model that simulated propagation, nonuniform cycle length dependent recovery of excitability, and slow propagation during incomplete recovery in cardiac muscle has been shown to exhibit behavior similar to torsade de pointes. The conditions required in the model resembled those in long QT syndromes with regionally prolonged ventricular repolarization. In the model, premature excitation of a path with relatively short refractory periods resulted in sequential reentry of that path from a region with longer refractory periods. Sites of reentry become progressively more distal to the site of initiation. The episodes terminated spontaneously when reentrant excitation reached the end of unclosed paths or collided in closed paths. Each reentry site moved away from its initial position in the short recovery path because the distance traversed by propagation in that path exceeded the distance at which reentry occurred via the longer recovery region. The migrating sites of reentry resulted in changing QRS waveform in calculated electrocardiograms including changing QRS polarity when calculated from appropriate sites. Variations of the basic behavior occurred with nonuniform distribution of refractory periods within relatively short and long refractory period regions and included unidirectional progression of reentry sites and multiple circuits of reentry in closed paths. Termination of serial reentry at times other than those when activation reached the end of unclosed paths or collided in closed paths also occurred with nonuniform distribution of refractory periods. Findings provide a plausible explanation for the changing QRS waveform, spontaneous termination, and association of torsade de pointes with long QT syndromes but do not elucidate the mechanism of initiation of the tachyarrhythmia.