Misaki T, Tsubota M, Watanabe G, Watanabe Y, Matumoto Y, Ishida K, Iwa T, Okada R
Department of Surgery, Toyama Medical and Pharmaceutical University, Japan.
Circulation. 1994 Jul;90(1):264-71. doi: 10.1161/01.cir.90.1.264.
The mechanism of ventricular tachycardia (VT) after correction of tetralogy of Fallot (TF) is poorly understood. The purpose of this study was to examine the histopathology of the arrhythmogenic area detected by intraoperative mapping.
The patients were three men who underwent radical surgery for TF at age 3, 3, or 5 years, respectively. VT developed at 8, 9, or 11 years, respectively, after surgery, and shock developed during VT in every case. The ECG revealed monomorphic VT in two cases and polymorphic VT in one case. Induction of VT resulted in a wide left-axis deviation-pattern QRS with cycle lengths varying between 260 and 330 milliseconds. The VT origin was identified at the right ventricular outflow tract (RVOT). A radical operation was performed with the patient under cardiopulmonary bypass. On epicardial mapping, delayed activation of the RVOT was recorded during sinus rhythm, and clockwise circus movement of the macroreentry current during VT on the right ventricular free wall was documented in each case. The VTs were treated successfully by surgical resection and cryoablation of the myocardium. In every patient, histology of the myocardial specimens showed degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets. These lesions corresponded anatomically to the area of myocardium in which delayed activation was evident during epicardial mapping.
The results of this study indicate that patients with VT after radical correction of the TF have abnormal histopathological findings at the site of the prior right ventriculotomy scar. These lesions were noted within the region of delayed activation found during epicardial mapping and were found to be a part of the reentrant circuit.
法洛四联症（TF）矫正术后室性心动过速（VT）的机制尚不清楚。本研究的目的是检查术中标测检测到的致心律失常区域的组织病理学。
患者为3名男性，分别在3岁、3岁或5岁时接受了TF根治手术。VT分别在术后8、9或11年发生，且每例患者在VT发作期间均出现休克。心电图显示2例为单形性VT，1例为多形性VT。诱发VT导致QRS波呈宽左轴偏移型，周长在260至330毫秒之间变化。VT起源于右心室流出道（RVOT）。在体外循环下对患者进行了根治性手术。在心外膜标测中，窦性心律时记录到RVOT延迟激活，每例均记录到VT发作时右心室游离壁上大折返电流的顺时针环形运动。通过手术切除和心肌冷冻消融成功治疗了VT。在每例患者中，心肌标本的组织学检查均显示有变性、脂肪变性、纤维化、炎性细胞浸润和散在的心肌小岛。这些病变在解剖学上与心外膜标测中延迟激活明显的心肌区域相对应。
本研究结果表明，TF根治矫正术后发生VT的患者，在先前右心室切开瘢痕部位有异常的组织病理学表现。这些病变在心外膜标测中发现的延迟激活区域内被观察到，并且被发现是折返环路的一部分。
