Division of Cardiology, Queen's University, Kingston, Ontario, Canada; Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
Heart Rhythm. 2019 Aug;16(8):1174-1181. doi: 10.1016/j.hrthm.2019.02.016. Epub 2019 May 11.
In patients with ischemic ventricular tachycardia (VT), substrate may be "protected" by the posteromedial papillary muscle (PMPM), explaining failure of endocardial-only ablation.
We sought to characterize the arrhythmogenic substrate and ablation approach in patients with ischemic VT mapped to the inferior left ventricle in which endocardial ablation failed because of inaccessible substrate underlying the PMPM.
We included 10 patients with recurrent ischemic VT, evidence of inferior scar, and failed endocardial ablation. In all patients, epicardial mapping was performed via a percutaneous (n = 9) or surgical (n = 1) approach, and VT elimination was achieved by ablation opposite to the PMPM. Clinical characteristics, electrocardiographic characteristics, and procedural data were analyzed.
In all patients, intracardiac echocardiography showed hyperechoic scar below the PMPM, and 5 exhibited a pattern characterized by subendocardial basal scar that became intramural and epicardial at distal segments. In 4 patients, VT remained inducible despite endocardial scar isolation, manifested by the absence of electrograms, dissociated potentials, and/or exit block. Eleven inducible VTs were mapped to the epicardium underlying the PMPM: 8 had a right bundle branch block configuration with variable transition, while 3 exhibited left bundle branch block with negative concordance. An inferior QS pattern was present in 10 of 11 VTs. Noninducibility was achieved in 8 patients, and 7 patients remained arrhythmia-free after a mean follow-up of 27 ± 23 months.
In patients with inferior ischemic scar, VT may arise from the area underneath the PMPM, limiting endocardial ablation. Intracardiac echocardiography accurately defines the substrate distribution, and an epicardial approach may eliminate VT. A pattern of "basal-endocardial/apical-epicardial" ischemic involvement is described.
在缺血性室性心动过速（VT）患者中，由于后内侧乳头肌（PMPM）下方的基质可能“受到保护”，因此心内膜消融可能会失败。
我们旨在研究由于 PMPM 下方的不可及基质而导致心内膜消融失败的缺血性 VT 患者的标测和消融方法。
我们纳入了 10 名因心内膜消融失败而出现缺血性 VT 复发、下壁瘢痕证据和心内膜消融失败的患者。在所有患者中，通过经皮（9 例）或外科（1 例）途径进行心外膜标测，通过消融 PMPM 对面的组织来消除 VT。分析了临床特征、心电图特征和手术数据。
在所有患者中，心腔内超声显示 PMPM 下方存在回声增强的瘢痕，其中 5 例表现出一种特征性的模式，即心内膜下基底瘢痕在远段变为心壁内和心外膜。在 4 例患者中，尽管进行了心内膜瘢痕隔离，但 VT 仍可诱发，表现为无心电图、分离电位和/或出口阻滞。11 种可诱发的 VT 在心外膜下 PMPM 下被标测到：8 种呈右束支传导阻滞构型，有可变的过渡，而 3 种呈左束支传导阻滞伴负性一致。11 种 VT 中 10 种呈现下壁 QS 模式。8 例患者实现了非诱发，7 例患者在平均 27±23 个月的随访后保持无心律失常。
在下壁缺血性瘢痕患者中，VT 可能起源于 PMPM 下方的区域，限制了心内膜消融。心腔内超声准确地定义了基质的分布，心外膜途径可以消除 VT。描述了一种“基底心内膜/尖部心外膜”缺血性受累的模式。
