Bardy G H, Ungerleider R M, Smith W M, Ideker R E
Circulation. 1983 Jan;67(1):52-9. doi: 10.1161/01.cir.67.1.52.
A dog model of torsades de pointes (TdP) was developed. Twenty 18-30-kg dogs had cardiopulmonary bypass instituted to maintain stable temperature, perfusion pressure and oxygenation. Quinidine, 30 mg/kg, was then administered and burst ventricular pacing was used to induce arrhythmias. The left anterior descending coronary artery was occluded for 15 minutes and repeat pacing studies were performed. Maps of epicardial activation were made from 27 simultaneously recorded electrograms obtained from 1-mm bipolar electrodes secured to the epicardium with a nylon mesh sock. Arrhythmias in five dogs met criteria for the diagnosis of TdP: All had the characteristic undulating QRS morphology typically associated with TdP, all occurred in the setting of QT prolongation and all ended spontaneously. The epicardial maps demonstrated that each change in QRS morphology was associated with a change in the site of epicardial breakthrough. Those QRS complexes during the transition from one morphology to the next were associated with fusion cycles in which both the old and new sites of epicardial breakthrough were present. In essence, two or more competing activation sequences were vying for control of epicardial depolarization. This conclusion was strengthened by our ability to simulate TdP in the surface ECG and in epicardial maps by simultaneously pacing from two widely separated ventricular sites at slightly different, varying rates.
建立了尖端扭转型室性心动过速（TdP）的犬模型。20只体重18 - 30千克的犬接受体外循环以维持稳定的体温、灌注压和氧合。随后给予30毫克/千克的奎尼丁，并采用心室短阵猝发刺激诱发心律失常。左前降支冠状动脉闭塞15分钟，然后重复进行起搏研究。通过用尼龙网袜固定在心肌外膜上的1毫米双极电极同步记录27个电信号，绘制心肌外膜激动图。五只犬的心律失常符合TdP的诊断标准：所有犬均具有与TdP典型相关的特征性波动QRS形态，均发生在QT间期延长的情况下，且均自发终止。心肌外膜图显示，QRS形态的每一次改变都与心肌外膜激动突破点的改变相关。从一种形态转变为另一种形态过程中的那些QRS波群与融合周期相关，在融合周期中同时存在心肌外膜激动突破的旧位点和新位点。本质上，两个或更多相互竞争的激动序列争夺对心肌外膜去极化的控制。通过在体表心电图和心肌外膜图中从两个相距很远的心室部位以略有不同、变化的速率同时起搏来模拟TdP的能力，进一步强化了这一结论。
