Optimal Ablation Techniques for Ventricular Tachycardia Management

Figures

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  Figure 1:. Purkinje-related ventricular tachyarrhythmias in ICM. A: Purkinje triggers manifested as closely coupled premature ventricular complexes (PVCs; arrows) for polymorphic VT or VF initiation. B: Purkinje fibers arborized along the infarct border may also serve as either a localized microreentrant or part of a macroreentrant circuit using the subendocardial scar substrate for monomorphic VT. This may manifest as frequent monomorphic PVCs (arrows). ICM: ischemic cardiomyopathy; VF: ventricuventricular fibrillation; VT: ventricular tachycardia.

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  Figure 2:. Endoepicardial mapping in patients with NICM. Endocardial and epicardial bipolar electrogram recordings were performed in a patient with NICM. The LV endocardial voltage showed minimal abnormal low-voltage areas, while the LV epicardial voltage showed extensive low-voltage scar located near the basal lateral LV. The endocardial and epicardial bipolar voltage color gradient is depicted. The purple areas represent normal tissue (endocardial amplitude ≥ 1.5 mV or epicardial amplitude > 1.0 mV) whereas dense scar is depicted in red (amplitude < 0.5 mV). The border zone is defined as areas with the color gradient being between red and purple. Activation mapping during sustained VT demonstrated an early, mid-diastolic potential located at the LV lateral epicardium (arrow). Overdrive pacing at this site showed entrainment with concealed fusion, consistent with an epicardial isthmus site. LV: left ventricular; MV: mitral valve; NICM: nonischemic cardiomyopathy; VT: ventricular tachycardia.

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  Figure 3:. Identification of VT-conducting channel. A: Catheter mapping in a patient with a large anterior myocardial infarction. The spontaneous VT has a left bundle branch block–right inferior (LBB-RI) QRS morphology. The endocardial bipolar voltage map showed a large anterior scar. The color gradient adjustments of the bipolar voltage correspond with 0.5 mV to 1.6 mV, 0.35 mV to 0.55 mV, and 0.21 mV to 0.31 mV. A potential VT-related conduction channel can be identified at a color threshold range of 0.21 mV to 0.31 mV. Recordings from inside this channel during differential pacing demonstrate progressively late potentials from the border zone into the scar area. Pacing from within this channel with decremental late potentials/LAVAs resulted in a perfect pacemap suggestive of a potential VT isthmus site. B: With right ventricular pacing at different rates, delayed and fractionated signals were recorded within the channel. Decremental prolongation of the pacing stimuli-to-potential intervals were noted with increasing pacing rates, suggestive of local conduction delay into the channel. C: With right ventricular premature stimulation, decremental multicomponent and fractionated local…

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  Figure 4:. Pacemap localization of VT circuit. A: A schema of a “figure-of-eight” reentrant VT circuit. During sinus rhythm, when pacing at the exit side of the mid-isthmus line, the activation wavefront propagates in two directions, but more rapidly to the exit site, resulting in near-identical RS morphologies as that of clinical VTs with an ECG average correction (ECG-AC) of 100%. When pacing at the entrance side of the mid-isthmus, the wavefront propagates more rapidly to the entrance and away from the exit, resulting in different ventricular activation patterns and paced QRS morphologies, with a poor ECG correlation (ECGAG: 10%). B: Left: An example of a VT circuit visualized using a “pacemapping” map superimposed on the three-dimensional electroanatomic maps. The color gradient corresponds with the degree of ECG correlation as compared with the clinical VT (> 97% pacemap QRS match: red; < 33% QRS match: purple). Middle: A pacemapping map showing a good (97%) correlation zone, corresponding with the VT exit. Close to this zone, a poor (27%) correlation zone with an abrupt transition within a short distance is seen. In another direction, an abrupt transition is observed between the good…

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  Figure 5:. Differences in scar area and late potentials between ICM and NICM substrates. A: With high-density electroanatomical maps of patients with ICM, the dense scar was twice as large on the endocardium as compared with on the epicardium. Such predilection for endocardial scar was not as prominent in patients with NICM, with nearly equal extents of scar on the endocardium and epicardium present. Less dense scar (solid bars) was observed in patients with NICM. The open bars indicate the border zone. B: Patients with ICM had more late potentials and evidence of slow conduction than patients with NICM. This difference was driven by a greater number of very late potentials (vLPs) (solid bars) in ICM. BZ: border zone; DS: dense scar; ICM: ischemic cardiomyopathy; mLP: moderate late potentials; NICM: nonischemic cardiomyopathy. Modified from Nakahara S, Tung R, Ramirez RJ, et al. Characterization of the arrhythmogenic substrate in ischemic and non-ischemic cardiomyopathy. J Am Coll Cardiol. 2010;55(21):2355–2365. Used with permission.

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  Figure 6:. A VT ablation approach in patients with NICM. This figure represents a flow chart and a potential approach in patients with NICM who undergo catheter ablation for VT. The ECG criteria during sinus rhythm that predict the presence of LV basal lateral scar include an R-wave in lead V1 ≥ 0.15 mV and an S-wave in lead V6 ≥ 0.15 mV.76 This can be distinguished from patients with prior inferior/inferolateral myocardial infection by (1) lateral lead QRS fragmentation, (2) a lack of inferior Q waves, and (3) a lead V6 S/R ratio of ≥ 0.25.77 These findings may be useful in predicting the presence of LV scar and in determining the risk of VT in patients with NICM. The ECG criteria predictive of an epicardial exit during ventricular arrhythmias (ie, PVCs, VTs) are summarized in Table 2. Epicardial mapping may be considered in selected patients when (1) the 12-lead ECG of the VT suggests an epicardial origin; (2) there is evidence of epicardial substrate on imaging studies (eg, MRI, intracardiac echocardiography); (3) there is unipolar electrogram voltage abnormality; and (4) there is failure of prior endocardial ablation. The important decision steps are highlighted in yellow. AIV: anterior…

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  Figure 7:. VT recurrence rate by acute ablation results. In patients with post-infarction VT, successful late potential abolition and post-procedural VT non-inducibility constitute significant endpoints after catheter ablation. Complete late potential abolition or elimination reduces VT recurrence to exceptionally low rates and compares favorably with post-procedural non-inducibility of VT. Persistence of late potentials/LAVAs or persistent inducibility predict a poor outcome. LAVAs: local abnormal ventricular activities; LP: late potential; VT: ventricular tachycardia.

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  Figure 8:. Recurrence of post-infarction VT after catheter ablation. The blue bars represent studies that used a limited substrate ablation approach. The green bars represent studies that evaluated early intervention with a limited substrate ablation. The black bars represent studies utilizing an extensive substrate-based modification ablation approach. The pooled data are depicted as red bars. *Studies that included a subgroup of patients with NICM. RRR: relative risk reduction; VT: ventricular tachycardia. Adapted from Al-Ahmad AA, Callans DJ, Hsia HH, et al. Hands-On Ablation: The Experts’ Approach. 2nd ed. Minneapolis, MN: Cardiotext Publishing, LLC; 2017. Used with permission from Cardiotext Publishing.