Osswald S, Wilber D J, Lin J L, Du D, Holden H B, Ruskin J N, Garan H
Harvard Medical School, Massachusetts General Hospital, Boston 02114, USA.
J Cardiovasc Electrophysiol. 1997 Jan;8(1):11-23. doi: 10.1111/j.1540-8167.1997.tb00604.x.
Distinct surface ECG morphologies (ECGMs), from one episode to the next, of recurrent monomorphic ventricular tachycardia (VT) in the same patient complicate endocardial catheter mapping and the success of ablative therapy. This study investigates the incidence and mechanisms of multiple ECGMs during recurrent monomorphic VTs in a canine model of experimental myocardial infarction (MI).
Computerized ECG analysis and simultaneous endocardial and epicardial activation mapping with a 64 bipolar electrode array were used to analyze the relation between site of VT origin, local activation sequence, and surface ECGM in 72 VT episodes induced in 9 of 17 dogs with experimental MI. Pairwise comparisons of all VTs induced in the same animal were done in drug-free state (47 VTs) and after intravenous procainamide (25 VTs). In drug-free state, VT pairs with similar surface ECGMs manifested endocardial breakthrough sites (BSs) within a distance < 10 mm in 46 (100%) of 46 VT pairs compared to 43 (45%) of 95 VT pairs with different surface ECGMs (P < 0.0001). Of all 89 VT pairs with endocardial BSs within < 10 mm, similar endocardial activation patterns were found in 34 (74%) of 46 pairs with similar ECGMs in contrast to 6 (14%) of 43 pairs with different ECGMs (P < 0.001). Similar comparisons of VT pairs induced after intravenous procainamide administration showed that the endocardial BSs were located within < 10 mm in 9 (75%) of 12 VT pairs with similar and in 17 (49%) of 95 with different surface ECGMs, respectively (P = NS).
In the same heart, similar surface ECGMs of recurrent VT are highly predictive of closely spaced endocardial BSs in drug-free state, but not after procainamide administration. Nearly half of the VTs with different surface ECGMs still originate from closely spaced endocardial BSs but commonly manifest a change in the endocardial activation spread from this site. Thus, assumptions about different mechanisms and sites of VT origin based on different surface ECGMs should be made with caution.
同一患者复发性单形性室性心动过速（VT）发作时，每次发作的体表心电图形态（ECGM）不同，这使得心内膜导管标测和消融治疗的成功率变得复杂。本研究在实验性心肌梗死（MI）犬模型中，调查复发性单形性VT期间多种ECGM的发生率及机制。
使用计算机化心电图分析以及带有64个双极电极阵列的同步心内膜和心外膜激动标测，分析17只患有实验性MI的犬中9只犬诱发的72次VT发作的VT起源部位、局部激动顺序与体表ECGM之间的关系。在无药状态（47次VT）和静脉注射普鲁卡因酰胺后（25次VT），对同一动物诱发的所有VT进行两两比较。在无药状态下，46对具有相似体表ECGM的VT对中，46对（100%）的心内膜突破点（BSs）距离<10 mm，而95对具有不同体表ECGM的VT对中，有43对（45%）的心内膜突破点距离<10 mm（P<0.0001）。在所有心内膜BSs距离<10 mm的89对VT中，46对具有相似ECGM的VT对中有34对（74%）的心内膜激动模式相似，而43对具有不同ECGM的VT对中只有6对（14%）的心内膜激动模式相似（P<0.001）。对静脉注射普鲁卡因酰胺后诱发的VT对进行类似比较，结果显示，12对具有相似体表ECGM的VT对中有9对（75%）的心内膜BSs距离<10 mm，95对具有不同体表ECGM的VT对中有17对（49%）的心内膜BSs距离<10 mm（P=无显著差异）。
在同一心脏中，复发性VT相似的体表ECGM在无药状态下高度预测心内膜BSs距离相近，但在注射普鲁卡因酰胺后则不然。近一半具有不同体表ECGM的VT仍起源于心内膜BSs距离相近的部位，但通常表现为从此部位开始的心内膜激动传播发生改变。因此，基于不同体表ECGM对VT起源的不同机制和部位所做的假设应谨慎。
