Noninvasive epicardial and endocardial electrocardiographic imaging of scar-related ventricular tachycardia.

Noninvasive epicardial and endocardial electrocardiographic imaging of scar-related ventricular tachycardia.
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DOI:
10.1016/j.jelectrocard.2016.07.026
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发表时间:
2016-11
影响因子:
1.3
通讯作者:
Sapp, John L.
Sapp, John L.
中科院分区:
医学4区
文献类型:
--
作者:
Wang, Linwei;Gharbia, Omar A.;Horacek, B. Milan;Sapp, John L.

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大多数危及生命的室性心动过速(VT)是由异质性瘢痕基质和狭窄的存活组织链维持的。瘢痕相关性室性心动过速的有效治疗方法是通过导管消融术改变潜在的瘢痕基质。如果在持续性室性心动过速期间可以进行激动序列和夹带标测,则通常可以识别回路的出口和峡部。然而,在有创导管标测的情况下,只有血流动力学稳定的单形性VT才能以这种方式标测。对于大多数耐受性差的室性心动过速或多发性室性心动过速患者,不可能对折返环进行仔细检查。快速标测不稳定室性心动过速的非侵入性方法可能有助于改进关键消融部位的识别。对于接受瘢痕相关室性心动过速导管消融术的患者,在消融术前进行CT扫描,并在诱导室性心动过速期间采集120导联体表心电图(ECG)。这些数据用于无创ECG成像,以计算重建两个心室的心外膜和内膜上的电位。从重建的电描记图中提取VT电路的激活时间和相位图。分析了导管标测获得的瘢痕基质,以及通过成功终止室性心动过速的消融部位确认的室性心动过速出口。重建的折返回路正确显示了心外膜和心内膜的激动源,与消融术确认的出口部位位置一致。折返回路的时间动态,特别是由激活等时线的拥挤和锯齿形传导所指示的传导减慢,与通过导管电压图获得的瘢痕基底配合良好。此外,结果表明,一些折返回路涉及心外膜层和心内膜层,并且只能通过同时标测两个层来正确解释。本研究探讨了心电图成像的潜力不稳定折返电路的心跳到心跳映射。它表明,同时心外膜和心内膜标测可以改善折返回路及其出口的3D空间结构的描绘。它还表明,相位映射的使用可以揭示缓慢传导的区域与疤痕内和周围的可疑异质区域很好地搭配。
The majority of life-threatening ventricular tachycardias (VTs) are sustained by heterogeneous scar substrates with narrow strands of surviving tissue. An effective treatment for scar-related VT is to modify the underlying scar substrate by catheter ablation. If activation sequence and entrainment mapping can be performed during sustained VT, the exit and isthmus of the circuit can often be identified. However, with invasive catheter mapping, only monomorphic VT that is hemodynamically stable can be mapped in this manner. For the majority of patients with poorly tolerated VTs or multiple VTs, a close inspection of the reentry circuit is not possible. A noninvasive approach to fast mapping of unstable VTs can potentially allow an improved identification of critical ablation sites. For patients who underwent catheter ablation of scar-related VT, CT scan was obtained prior to the ablation procedure and 120-lead body-surface electrocardiograms (ECGs) were acquired during induced VTs. These data were used for noninvasive ECG imaging to computationally reconstruct electrical potentials on the epicardium and on the endocardium of both ventricles. Activation time and phase maps of the VT circuit were extracted from the reconstructed electrograms. They were analyzed with respect to scar substrate obtained from catheter mapping, as well as VT exits confirmed through ablation sites that successfully terminated the VT. The reconstructed reentry circuits correctly revealed both epicardial and endocardial origins of activation, consistent with locations of exit sites confirmed from the ablation procedure. The temporal dynamics of the reentry circuits, particularly the slowing of conduction as indicated by the crowding and zig-zag conducting of the activation isochrones, collocated well with scar substrate obtained by catheter voltage maps. Furthermore, the results indicated that some reentry circuits involve both the epicardial and endocardial layers, and can only be properly interpreted by mapping both layers simultaneously. This study investigated the potential of ECG-imaging for beat-to-beat mapping of unstable reentrant circuits. It shows that simultaneous epicardial and endocardial mapping may improve the delineation of the 3D spatial construct of a reentry circuit and its exit. It also shows that the use of phase mapping can reveal regions of slow conduction that collocate well with suspected heterogeneous regions within and around the scar.
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