Pogwizd S M, Chung M K, Cain M E
Cardiovascular Division, Washington University School of Medicine, St Louis, Mo 63110, USA.
Circulation. 1997 Jun 3;95(11):2528-40. doi: 10.1161/01.cir.95.11.2528.
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.
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.
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.
为明确室性心动过速（VT）终止的电生理基础，对6例陈旧性心肌梗死患者进行了三维心脏标测，并分析了非持续性VT的终末搏动和持续性VT的搏动。
VT的终止在45%的病例中是由于来自多个起始部位的激动，这些起始部位与维持持续性VT的部位不一致；在24%的病例中是由于来自单个部位的反复激动，这些部位与维持持续性VT的部位不一致；在31%的病例中是由于来自与持续性VT期间反复激动部位一致的部位的激动。持续性VT的特征是起始部位偶尔发生变化，即使在心动过速进入稳定的单形性阶段后也是如此。标测密度足以明确21次VT终止搏动的机制。在5例中，终止是由于壁内折返，其起始于前一个搏动的总激动时间为204±11毫秒（ms），但主要因总激动时间缩短（144±23 ms，P = 0.03）而终止，这与壁内传导阻滞的发生或沿折返环的激动顺序的显著变化有关。在16例中，终末搏动是由局灶机制起始的，这是基于从前一个搏动终止到终末搏动起始之间没有中间电活动（172±9 ms）。局灶性激动与前一个搏动的传导延迟（115±6 ms）相比，比终末折返性搏动要少（P < 0.001），并且通常突然终止，周期长度或总激动时间没有振荡。
VT的终止与起始部位的改变有关，这些改变最常与维持持续性VT的部位不一致，并且是由于折返或局灶机制。
