Chung M K, Pogwizd S M, Miller D P, Cain M E
Cardiovascular Division, Washington University School of Medicine, St Louis, Mo 63110, USA.
Circulation. 1997 Jun 3;95(11):2517-27. doi: 10.1161/01.cir.95.11.2517.
Elucidation of the electrophysiological mechanisms of nonsustained ventricular tachycardia (VT) in humans is required to define the relationship between nonsustained VT and sustained VT. This goal requires, at least in part, analysis of transmural ventricular activation in patients with both sustained and nonsustained VTs.
We analyzed three-dimensional intraoperative cardiac maps of extrastimuli and beats during 44 nonsustained VTs and the initiating beats of 6 sustained VTs from six patients with healed myocardial infarcts who were undergoing arrhythmia surgery. The coupling interval, total activation time, and diastolic interval of each extrastimulus and beat of nonsustained VT were compared with counterparts during sustained VT. Sites activated last during extrastimuli initiating nonsustained or sustained VTs occurred in the same region, and activation times were comparable. However, the site of earliest activation during the initial or subsequent beats of nonsustained VT was discordant from the site activated earliest during the first and subsequent beats of sustained VT in 74% of cases. The mean variance in coupling interval, but not total activation time or diastolic interval, was significantly greater for VT that terminated before the 10th cycle than for VT that sustained. When analyzed from the last extrastimulus up to the fifth VT cycle, the standard deviation of the coupling interval, but not of the total activation time, was greater for nonsustained than for sustained VTs. Electrode density was sufficient to define an arrhythmia mechanism for 36 beats of nonsustained VT. Twenty-one (58%) initiated in the subendocardium, midmyocardium, or epicardium by a macroreentrant mechanism, and 15 (42%) initiated in the subendocardium by a focal mechanism.
Compared with sustained VT, nonsustained VT initiates at discordant sites, is characterized by oscillations in coupling interval but not in total activation time, and initiates by either a macroreentrant or a focal mechanism.
为明确非持续性室性心动过速(VT)与持续性室性心动过速之间的关系,需要阐明人类非持续性室性心动过速的电生理机制。这一目标至少部分需要分析持续性和非持续性室性心动过速患者的跨壁心室激动情况。
我们分析了6例陈旧性心肌梗死且正在接受心律失常手术患者的44次非持续性室性心动过速及6次持续性室性心动过速的起始搏动过程中的三维术中心脏图。将非持续性室性心动过速每次额外刺激和搏动的耦合间期、总激动时间及舒张间期与持续性室性心动过速时的相应参数进行比较。引发非持续性或持续性室性心动过速的额外刺激过程中最后被激动的部位位于同一区域,且激动时间相近。然而,在74%的病例中,非持续性室性心动过速初始或后续搏动过程中最早激动的部位与持续性室性心动过速首次及后续搏动过程中最早激动的部位不一致。在第10个心动周期之前终止的室性心动过速,其耦合间期的平均方差显著大于持续性室性心动过速,而总激动时间和舒张间期的平均方差则无显著差异。从最后一次额外刺激直至第5个室性心动过速周期进行分析时,非持续性室性心动过速耦合间期的标准差大于持续性室性心动过速,而总激动时间的标准差则无此差异。电极密度足以明确36次非持续性室性心动过速搏动的心律失常机制。21次(58%)由大折返机制起源于心内膜下、心肌中层或心外膜,15次(42%)由局灶机制起源于心内膜下。
与持续性室性心动过速相比,非持续性室性心动过速起源部位不一致,其特征为耦合间期而非总激动时间存在波动,且由大折返或局灶机制起源。