Hauer R N, de Bakker J M, de Wilde A A, Straks W, Vermeulen J T, Janse M J
Heart-Lung Institute, University Hospital, Utrecht, The Netherlands.
Circulation. 1991 Jul;84(1):267-78. doi: 10.1161/01.cir.84.1.267.
DC shock catheter ablation for the treatment of ventricular tachycardia (VT) may induce VT episodes that disappear within days.
A 30-J cathodal shock was delivered to the endocardial left ventricular wall in 15 closed-chest dogs. All dogs had VT during the first day after ablation. Eleven of these dogs were studied on the first day. Extensive epicardial and endocardial activation mapping in vivo, in Langendorff-perfused hearts, and in tissue blocks in a tissue bath localized the site of origin of VT to subendocardial Purkinje fibers in a border zone surrounding the central necrotic ablation lesion. Intracellular recording showed that this zone consisted of a subendocardial superficial layer (SSL) of cells with abnormal characteristics, a resting membrane potential (RMP) of -58 +/- 11 mV (mean +/- SD), and an action potential amplitude (APA) of 61 +/- 20 mV. In addition, the steepness of phase 0 of the action potential was markedly reduced. In three dogs abnormal automaticity was found in a very small area. Immediately below the SSL, cells were normal with an RMP of -78 +/- 5 mV and an APA of 107 +/- 8 mV. Histology confirmed a thin SSL with edematous and necrotic cells, hemorrhage, and infiltration. The other four dogs were studied at 1 week after ablation when VT was absent. Microelectrode impalement in the SSL was either impossible or showed nearly normal action potential characteristics. Histological examination showed a markedly thickened fibrotic subendocardial layer at places where impalement was impossible. Normal subendocardium was found in other areas of the border zone.
Our results indicate that VT after DC shock ablation originates from cells with abnormal automaticity in the superficial subendocardial border zone around the central ablation lesion. Within 1 week edematous and necrotic cells in this border zone are replaced by a fibrotic layer, and this transition is associated with the disappearance of VT.
直流电休克导管消融术治疗室性心动过速（VT）可能诱发数天内消失的VT发作。
对15只开胸犬的心内膜左心室壁施加30焦耳的阴极电击。所有犬在消融术后第一天均出现VT。其中11只犬在第一天接受研究。在体内、Langendorff灌注心脏以及组织浴中的组织块上进行广泛的心外膜和心内膜激动标测，将VT的起源部位定位至围绕中央坏死消融灶的边缘区内的心内膜下浦肯野纤维。细胞内记录显示，该区域由具有异常特征的心内膜下浅层（SSL）细胞组成，静息膜电位（RMP）为-58±11mV（平均值±标准差），动作电位幅度（APA）为61±20mV。此外，动作电位0期的斜率明显降低。在三只犬中，在非常小的区域发现了异常自律性。在SSL下方紧邻处，细胞正常，RMP为-78±5mV，APA为107±8mV。组织学证实SSL较薄，伴有细胞水肿、坏死、出血和浸润。另外四只犬在消融术后1周进行研究，此时VT已消失。在SSL处进行微电极刺入要么无法进行，要么显示出几乎正常的动作电位特征。组织学检查显示，在无法刺入的部位，心内膜下纤维化层明显增厚。在边缘区的其他区域发现了正常的心内膜。
我们的结果表明，直流电休克消融术后的VT起源于中央消融灶周围心内膜下浅层边缘区具有异常自律性的细胞。在1周内，该边缘区的水肿和坏死细胞被纤维化层取代，这种转变与VT的消失相关。
