The sequence of a short and long cycle length has been observed frequently to precede the onset of torsade de pointes in patients. The purpose of this study was to determine the mechanism of that relation by means of a computer model of propagated excitation. The model included cycle length-dependent refractoriness and slow propagation during incomplete recovery and has been used previously to document that changing QRS waveform and limited duration of torsade de pointes episodes can be explained by moving sites of reentrant excitation. In this study, a short-long cycle-length sequence due to a ventricular premature response and compensatory pause was shown to prolong the period during which simulated torsade de pointes could be initiated. A premature response that failed to initiate the arrhythmia in the absence of that sequence did so after the sequence. Both the premature ventricular response and compensatory pause of the short-long cycle-length sequence contributed to prolongation of the torsade period, but by different mechanisms. The compensatory pause prolonged refractory periods and increased their disparity by a direct effect of cycle length. The ventricular premature response had similar effects, but these were indirect and due to the activation sequence of the response. When such a response was followed by a supraventricular response, the ventricular cycle length included atrioventricular conduction time and was longer than that with a series of responses of either supraventricular or ventricular origin. In addition to elucidating the mechanism of the short-long cycle sequence relation to torsade de pointes, the findings suggest that long cycles of whatever nature or the sequence of ventricular and supraventricular responses of whatever cycle length may facilitate initiation of the arrhythmia.