Valderrábano M, Lee M H, Ohara T, Lai A C, Fishbein M C, Lin S F, Karagueuzian H S, Chen P S
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Circ Res. 2001 Apr 27;88(8):839-48. doi: 10.1161/hh0801.089259.
The intramural dynamics of ventricular fibrillation (VF) remain poorly understood. Recent investigations have suggested that stable intramural reentry may underlie the mechanisms of VF. We performed optical mapping studies of VF in isolated swine right ventricles (RVs) and left ventricles (LVs). Nine RV walls were cut obliquely in their distal edge exposing the transmural surface. Six LV wedge preparations were also studied. Results showed that intramural reentry was present. In RV, 28 of 44 VF episodes showed reentry; 15% of the activation pathways were reentrant. Except for 4 episodes, reentry was transmural, involving subendocardial structures as the papillary muscle (PM) or trabeculae. In LV, reentry was observed in 27 of 27 VF episodes; 23% of the activations were part of reentrant pathways (P<0.05 compared with RV). All LV reentrant pathways were truly intramural (confined to the wall) and were frequently located at the PM insertion. In both ventricles, reentry was spatially and temporally unstable. Histological studies showed abrupt changes in fiber orientation at sites of reentry and wave splitting. Connexin 40 immunostaining demonstrated intramyocardial Purkinje fibers at sites of reentry in the PM root and around endocardial trabeculae. Our results confirm that reentry is frequent-but unstable-in the myocardial wall during VF. In RV, reentry is mostly transmural and requires participation of subendocardial structures. The LV has a greater incidence of reentry and is intramural. Anisotropic anatomic structures played key roles in the generation of wave splitting and in the maintenance of reentry.
室颤（VF）的壁内动力学仍未得到充分理解。最近的研究表明，稳定的壁内折返可能是室颤机制的基础。我们对分离的猪右心室（RV）和左心室（LV）进行了室颤的光学标测研究。9个右心室壁在其远端边缘斜切，暴露透壁表面。还研究了6个左心室楔形标本。结果显示存在壁内折返。在右心室，44次室颤发作中有28次显示折返；15%的激动途径是折返性的。除4次发作外，折返是透壁的，涉及心内膜下结构如乳头肌（PM）或小梁。在左心室，27次室颤发作中有27次观察到折返；23%的激动是折返途径的一部分（与右心室相比，P<0.05）。所有左心室折返途径均为真正的壁内折返（局限于心室壁），且常位于乳头肌附着处。在两个心室中，折返在空间和时间上都是不稳定的。组织学研究显示，折返部位的纤维方向突然改变以及波分裂。连接蛋白40免疫染色显示，在乳头肌根部和心内膜下小梁周围的折返部位存在心肌内浦肯野纤维。我们的结果证实，在室颤期间，折返在心肌壁内频繁发生但不稳定。在右心室，折返大多是透壁的，需要心内膜下结构的参与。左心室的折返发生率更高，且是壁内折返。各向异性的解剖结构在波分裂的产生和折返的维持中起关键作用。
