Imaging and pathological evaluation of deep intramural ventricular tachycardia after combined bipolar and ethanol ablation

Imaging and pathological evaluation of deep intramural ventricular tachycardia after combined bipolar and ethanol ablation
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双极和乙醇联合消融后深部壁内室性心动过速的影像学和病理学评估

DOI:
10.1016/j.jacep.2020.08.040
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发表时间:
2020
期刊:
JACC Clin Electrophysiol
影响因子:
--
通讯作者:
Hasebe N.
Hasebe N.
中科院分区:
--
文献类型:
--
作者:
Sakamoto N;Komatsu Y;Otsu K;Kamikokura Y;Hontani M;Sugiyama E;Minoshima A;Tanabe Y;Sekiguchi Y;Tanino M;Sato N;Kawamura Y;Nogami A;Aonuma K;Hasebe N.

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66岁男性肥厚性心肌病经历室性心动过速(VT)风暴。对比计算机断层成像显示左侧基底-前心室肥厚心肌的深部晚期强化(图1A)。我们通过联合左心室双极射频导管消融(RFCA)和乙醇消融(EA)成功终止了壁内室速。双极RFCA在左心室和室间隔进行(左心室心内膜:THERMOCOOL SMARTTOUCH SF, Biosense Webster, Inc., Diamond Bar, California;心外膜:abblaze, Japan Lifeline Co., Ltd;右心室:FlexAbility, St. Jude Medical, Inc., Saint Paul, Minnesota)。双极电压图显示,心外膜低压区和成功的双极RFCA位点均位于晚期增强区域(图1B)。在EA进入高侧支后,VT终止。EA术后1个月的低密度ct显示部分心肌梗死区域(补充图1)。无静脉血栓复发;然而,患者在2年后死于急性胆管炎。尸检的组织病理学结果显示左心室心内膜、心外膜和右心室双极RFCA病变明显为肉眼纤维化病变,但未扩展到壁内心肌(图1C)。在显微镜下,病变的壁内心肌表现为几乎均匀的纤维化病变,几乎没有残余的心肌(图1D)。RFCA和EA联合形成了一个包括VT底物的跨壁纤维化病变(补充图1)。据我们所知,本报告是第一个比较双极RFCA和EA联合治疗肥厚性心肌病的壁内室速起源的影像学和病理评价。
A66-year-old man with hypertrophic cardiomyopathy had experienced ventricular tachycardia (VT) storms. Contrast computed tomography imaging revealed a deep intramural late enhancement in the hypertrophic myocardium of the basal-anterior left ventricle (Figure 1A). We successfully terminated the intramural VT by combined left ventricular bipolar radiofrequency catheter ablation (RFCA) and ethanol ablation (EA). Bipolar RFCA was performed on the left ventricle and ventricular septum(left ventricular endocardium: THERMOCOOL SMARTTOUCH SF, Biosense Webster, Inc., Diamond Bar, California; epicardium: Ablaze, Japan Lifeline Co., Ltd.; right ventricle: FlexAbility, St. Jude Medical, Inc., Saint Paul, Minnesota). Bipolar voltage maps showed that both epicardial lowvoltage areas and successful bipolar RFCA sites were located in the area of late enhancement (Figure 1B). The VT was terminated after EA into the high lateral branch. Low-density areas on computed tomography imaging performed 1 month after the EA showed some of the myocardial infarction areas (Supplemental Figure 1). No VT recurred; however, the patient died of acute cholangitis after 2 years.Histopathological findings from the postmortem examination revealed that the left ventricular endocardial, epicardial, and right ventricular side of the bipolar RFCA lesions, apparent as a gross fibrotic lesion, did not extend to the intramural myocardium (Figure 1C). Under microscopic examination, however, the intramural myocardium of the lesions appeared as an almost uniform fibrotic lesion with little residual myocardium (Figure 1D). Combined RFCA and EA had created a transmural fibrotic lesion including a VT substrate (Supplemental Figure 1). To our knowledge, this report is the first comparing imaging and pathological evaluation of the origin of intramural VT treated by combined bipolar RFCA and EA in hypertrophic cardiomyopathy.