Mechanisms in simulated torsade de pointes.

ABSTRACT

A mechanism of torsade de pointes consisting of moving sites of reentrant excitation has been proposed on the basis of findings with a computer model. Substantial additions to that mechanism are now proposed based on further studies with the same model. The model simulated propagation, cycle length-dependent recovery of excitability, and slow propagation during incomplete recovery. Regions of relatively short and long recovery were assigned because of evidence of regional prolongation of recovery in long QT syndromes in which torsade de pointes is frequent. As previously reported, premature excitation in the short recovery region initially propagated independently, then entered the long recovery region and reentered the short recovery region distal to the site of origin. Reentrant excitation initiated a similar series of events, and serial reentry at systematically changing locations resulted in changing patterns of excitation compatible with the changing QRS waveform in torsade de pointes. Episodes terminated when reentrant excitation reached the end of unclosed short recovery paths, collided in closed paths, or encountered refractoriness in the presence of nonuniform short recovery. In this study, it was shown that excitation preceding reentry had important effects on the mechanism. These included reversal of the direction of serial reentry, bidirectional serial reentry, reentry at multiple sites from the same parent conditions, and occurrence of reentry without the requirement of slow propagation. Evidence for a Doppler shift of cycle lengths in regions from which serial reentry was receding or approaching was obtained. Sustained serial reentry was also demonstrated and is a possible mechanism for polymorphic ventricular tachycardia. Findings further define a possible mechanism of torsade de pointes.