Romero Ayala L C, Medrano G A, Cárdenas Loaeza M, Clemente A C
Arch Inst Cardiol Mex. 1987 Jan-Feb;57(1):67-72.
Studies on twenty dogs were performed. With open thorax, aconitine was injected into the thickness of the interventricular septum. D2 and direct derivations were registered in the epicardium of the right atrium, on right and left septal surfaces and in the His bundle. As the experiment ended, the heart was taken out to determine the placement of the electrodes and the site of application of aconitine. "Torsades de pointes" were obtained in 15 dogs, with a rotation of 180 degrees during the episode. The rotation of A QRS occurred with a beat of intermediate direction which corresponded to a ventricular capture of a sinus beat or a ventricular echo after that beat, and a sequence of activation of AHV established in various beats, the first of which had a prolonged AH (p less than 0.01). The consecutive change of direction of QRS happened when that sequence of activation disappeared, and there was an A-V dissociation as in the beginning of the episode. In conclusion, in this experimental model, the Torsades de pointes were produced by double mechanism, an increased focus of automatism and a macro-re-entry that involves the two branches of the His bundle, the A-V node and the atrium.
对20只狗进行了研究。在开胸状态下,将乌头碱注入室间隔厚度处。在右心房的心外膜、左右间隔表面和希氏束记录D2和直接导联。实验结束时,取出心脏以确定电极的位置和乌头碱的应用部位。15只狗出现了“尖端扭转型室速”,发作期间有180度的扭转。QRS波的扭转与中间方向的搏动同时发生,这对应于窦性搏动的心室夺获或该搏动后的心室回波,并且在不同搏动中建立了AHV激活序列,其中第一个搏动的AH延长(p<0.01)。当该激活序列消失时,QRS波方向连续改变,并且存在与发作开始时一样的房室分离。总之,在这个实验模型中,尖端扭转型室速由双重机制产生,即自律性增加和涉及希氏束两个分支、房室结和心房的大折返。