Electrophysiology Section, Cardiovascular, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA; Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Electrophysiology Section, Cardiovascular, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
JACC Clin Electrophysiol. 2020 Feb;6(2):231-240. doi: 10.1016/j.jacep.2019.09.014. Epub 2019 Dec 18.
This study sought to evaluate the prevalence, mapping features, and ablation outcomes of non-scar-related ventricular tachycardia (NonScar-VT) and Purkinje-related VT (Purkinje-VT) in patients with structural heart disease.
VT in structural heart disease is typically associated with scar-related myocardial re-entry. NonScar-VTs arising from areas of normal myocardium or Purkinje-VTs originating from the conduction system are less common.
We retrospectively analyzed 690 patients with structural heart disease who underwent VT ablation between 2013 and 2017.
A total of 37 (5.4%) patients (16 [43%] with ischemic cardiomyopathy, 16 [43%] with nonischemic dilated cardiomyopathy, and 5 [14%] others) demonstrated NonScar/Purkinje-VTs, which represented the clinical VT in 76% of cases. Among the 37 VTs, 31 (84%) were Purkinje-VTs (28 bundle branch re-entrant VT). The remaining 6 (16%) VTs were NonScar-VTs and included 4 idiopathic outflow tract VTs. A total of 16 patients had prior history of VT ablations: empirical scar substrate modification was performed in 6 (38%) patients and residual inducibility of VT had not been assessed in 7 (44%). In all 37 patients, the NonScar/Purkinje-VT was successfully ablated. After a median follow-up of 18 months, the targeted NonScar/Purkinje-VT did not recur in any patients, and 28 (76%) of patients were free from any recurrent VT episodes.
NonScar/Purkinje-VTs can be identified in 5.4% of patients undergoing VT ablation in the setting of structural heart disease. Careful effort to induce, characterize, and map these VTs is important because substrate-based ablation strategies would fail to eliminate these types of VT.
本研究旨在评估结构性心脏病患者中非瘢痕相关室性心动过速（NonScar-VT）和浦肯野相关室性心动过速（Purkinje-VT）的发生率、映射特征和消融结果。
结构性心脏病中的 VT 通常与瘢痕相关的心肌折返有关。源自正常心肌区域的 NonScar-VTs 和源自传导系统的 Purkinje-VTs 则较为少见。
我们回顾性分析了 2013 年至 2017 年间接受 VT 消融治疗的 690 例结构性心脏病患者。
共有 37 例（5.4%）患者（16 例[43%]为缺血性心肌病，16 例[43%]为非缺血性扩张型心肌病，5 例[14%]为其他）表现为 NonScar/Purkinje-VTs，占所有 VT 的 76%。在 37 例 VT 中，31 例（84%）为浦肯野折返性 VT（28 例为束支折返性 VT）。其余 6 例（16%）为 NonScar-VTs，包括 4 例特发性流出道 VT。共有 16 例患者有 VT 消融的既往病史：6 例（38%）患者行经验性瘢痕基质改良，7 例（44%）患者未评估 VT 的残余可诱导性。在所有 37 例患者中，NonScar/Purkinje-VT 均成功消融。在中位随访 18 个月后，所有患者均未出现靶向性 NonScar/Purkinje-VT 复发，28 例（76%）患者无任何复发性 VT 发作。
在结构性心脏病患者行 VT 消融治疗中，可识别出 5.4%的 NonScar/Purkinje-VT。仔细诱发性 VT、对其进行特征描述和映射非常重要，因为基于基质的消融策略无法消除这些类型的 VT。
