Termination of ventricular tachycardia in the human heart. Insights from three-dimensional mapping of nonsustained and sustained ventricular tachycardias.
BACKGROUND
To define the electrophysiological basis for the termination of ventricular tachycardia (VT), three-dimensional cardiac mapping and analysis of the terminal beats of nonsustained VT and beats of sustained VT were performed in six patients with healed myocardial infarcts.


RESULTS
Termination of VT was due to activation from multiple initiation sites that were discordant from those responsible for the maintenance of sustained VT in 45% of cases, to repetitive activation from single sites that were discordant from those responsible for the maintenance of sustained VT in 24% of cases, or to activation from sites concordant with the sites of repetitive activation during sustained VT in 31% of cases. Sustained VT was characterized by occasional shifting of initiation sites, even after the tachycardia entered the stable monomorphic phase. Mapping was of sufficient density to define the mechanisms for 21 terminating beats of VT. In 5 cases, termination was due to intramural reentry, which initiated with the total activation time of the preceding beat of 204 +/- 11 milliseconds (ms) but terminated primarily because of a decrease in total activation time (144 +/- 23 ms, P = .03) that was associated with the development of intramural conduction block or with significant changes in the activation sequence along the reentrant circuit. In 16 cases, terminal beats were initiated by a focal mechanism on the basis of the absence of intervening electrical activity from the termination of the preceding beat to the initiation of the terminating beat (172 +/- 9 ms). Focal activation was associated with less conduction delay of the preceding beat (115 +/- 6 ms) than terminating reentrant beats (P < .001) and usually terminated suddenly without oscillations in cycle length or total activation time.


CONCLUSIONS
Termination of VT is associated with alterations in initiation sites that are most often discordant from those maintaining sustained VT and is due to either reentrant or focal mechanisms.
Pogwizd
S M
SM
Cardiovascular Division, Washington University School of Medicine, St Louis, Mo 63110, USA.
Chung
M K
MK
Cain
M E
ME
D004562:Electrocardiography; D004594:Electrophysiology; D006321:Heart / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D017202:Myocardial Ischemia / Q000503:physiopathology; D017180:Tachycardia, Ventricular / Q000503:physiopathology*; D013997:Time Factors