Abstract

Triggered activity (TA) has recently received increased attention as a mechanism responsible for cardiac arrhythmias. However, few studies have shown TA in the intact heart. In an ouabain-treated dog's heart we have shown: (a) overdrive acceleration, (b) a concordant relationship between the postpacing interval (PI) and pacing cycle length (CL), and (c) a discordant relationship between the PI and number of paced beats necessary to induce TA. These findings appear to agree with the distinctive characteristics of TA arrhythmias elucidated in previous in vitro studies and suggest TA rather than a reentrant tachycardia. In addition, it is possible that this heart preparation could be considered as a suitable model for the study of TA arrhythmias. These results were obtained using a programmed stimulation protocol in this dog model: (1) Following single programmed ventricular stimulation during sinus rhythm, a repetitive ventricular response (RVR) of more than 3 beats occurred in only 20% of hearts. The relationship between PI and the coupling interval (CI) of the extrastimulus was concordant in 80% (12/15) and discordant in 13% (2/15) of all experiments. The PI-CI relationship was influenced by the mutual relationship between the stimulating, recording, and originating sites of TA. (2) RVR of more than 3 beats was induced by consecutive overdrive ventricular stimulation during sinus rhythm (78%). In addition, the PI-pacing CL relationship was concordant (100%). (3) The transient termination of sustained VT that occurred spontaneously after administration of a large dose of ouabain was seen in only 15% of the cases after a single programmed premature ventricular stimulation. The return cycle-CI relationship was biphasic in 75% (15/20) experiments and discordant in 25% (5/20) of the experiments. (4) The termination of spontaneous sustained VT by overdrive ventricular stimulation occurred in only 8% of the cases. Transient overdrive acceleration of VT occurred after overdrive pacing (53%). In contrast, overdrive suppression occurred in only 13%. Thus, the characteristics of TA arrhythmias observed in the whole heart preparations differed, in some respects, from those obtained by in vitro studies. These quantitative observations could suggest a differentiation, based on probability, between TA and the reentrant mechanism that would respond to programmed stimulation in a similar manner. The differentiation between reentrant and triggered ventricular tachycardia can be made with reasonable assurance using these programmed stimulation techniques.

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