Janse M J, Wilms-Schopman F J, Coronel R
Department of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, The Netherlands.
J Cardiovasc Electrophysiol. 1995 Jul;6(7):512-21. doi: 10.1111/j.1540-8167.1995.tb00424.x.
It is not known whether ventricular fibrillation (VF) is always caused by multiple wavelet reentry, or if it could also be caused by a single wandering reentrant wavefront. Activation mapping of the entire ventricles during VF is practically impossible.
We studied VF in a two-dimensional sheet of left ventricular subepicardial tissue of isolated, Langendorff-perfused pig hearts. Left and right endocardial cryoablation via probes filled with liquid nitrogen caused coagulation necrosis of the right ventricle, interventricular septum, and most of the left ventricular wall, leaving a thin subepicardial layer intact. Left ventricular epicardial activation patterns were constructed based on simultaneous recording of 128 unipolar extracellular electrograms. Regular pacing through a central electrode before and after freezing revealed that, following cryoablation, the activation pattern no longer showed evidence of involvement of the Purkinje system, and that it was compatible with propagation through a two-dimensional anisotropic tissue sheet. VF was induced by burst pacing. When the mass of surviving subepicardium was < 10 g, no VF could be induced; when it was between 10 and 20 g, VF was nonsustained; when it was > 20 g, VF was sustained. Unipolar extracellular electrograms during VF before and after cryablation could not be distinguished from each other; however, epicardial activation patterns were markedly different. In the intact left ventricle, up to six different wavefronts were simultaneously present during a 100-msec time window. In the "frozen heart," during a period of about 0.5 seconds, at most two wandering reentrant waves were simultaneously present; sometimes only one reentrant wave was seen in a 100-msec time window.
The extracellular waveform during VF can be caused by different forms of reentry: multiple wavelet reentry (on the order of six different wavefronts), two independent wandering reentrant waves, and a single wandering reentrant wave.
目前尚不清楚心室颤动（VF）是否总是由多个小波折返引起，或者它是否也可能由单个游走性折返波前引起。在VF期间对整个心室进行激活标测实际上是不可能的。
我们在离体的、Langendorff灌注的猪心脏的左心室心外膜下组织二维薄片中研究VF。通过充满液氮的探针进行左、右心内膜冷冻消融，导致右心室、室间隔和大部分左心室壁发生凝固性坏死，仅留下一层薄的心外膜下组织完好无损。基于128个单极细胞外电图的同步记录构建左心室心外膜激活模式。在冷冻前后通过中央电极进行常规起搏显示，冷冻消融后，激活模式不再显示浦肯野系统受累的证据，并且与通过二维各向异性组织薄片的传播相一致。通过短阵快速起搏诱发VF。当存活的心外膜下组织质量<10 g时，无法诱发VF；当质量在10至20 g之间时，VF为非持续性；当质量>20 g时，VF为持续性。冷冻消融前后VF期间的单极细胞外电图彼此无法区分；然而，心外膜激活模式明显不同。在完整的左心室中，在100毫秒的时间窗口内同时存在多达六个不同的波前。在“冷冻心脏”中，在约0.5秒的时间段内，最多同时存在两个游走性折返波；有时在100毫秒的时间窗口内仅看到一个折返波。
VF期间的细胞外波形可由不同形式的折返引起：多个小波折返（约六个不同的波前）、两个独立的游走性折返波和一个单一的游走性折返波。
