Substrate-based approaches in ventricular tachycardia ablation

Abstract

Catheter ablation for ventricular tachycardia (VT) in patients with structural heart disease is now part of standard care. Mapping and ablation of the clinical VT is often limited when the VT is noninducible, nonsustained or not haemodynamically tolerated. Substrate-based ablation strategies have been developed in an aim to treat VT in this setting and, subsequently, have been shown to improve outcomes in VT ablation when compared to focused ablation of mapped VTs. Since the initial description of linear ablation lines targeting ventricular scar, many different approaches to substrate-based VT ablation have been developed. Strategies can broadly be divided into three categories: 1) targeting abnormal electrograms, 2) anatomical targeting of conduction channels between areas of myocardial scar, and 3) targeting areas of slow and/or decremental conduction, identified with "functional" substrate mapping techniques. This review summarises contemporary substrate-based ablation strategies, along with their strengths and weaknesses.

Keywords: Functional substrate mapping; ILAM; Ventricular arrhythmias; Ventricular tachycardia.

Graphical abstract

Fig. 1

Schematic of Scar-Related VT Channels. Putative VT isthmus shown in solid black arrow. Focal ablation to part of this circuit may terminate VT but allow for different VT circuits to form via alternate exits from the scar (black interrupted arrows). Non-putative channels in the scar may be present (red arrow) and are not targeted as part of a clinical VT ablation. However, with ongoing remodelling over time, these channels may precipitate re-entry. Ablation of all channels, not just putative channels, likely explains the better outcomes with substrate-based approaches.

Fig. 2

Anatomical-Based Substrate Ablation. 72-year-old male with ischaemic cardiomyopathy from previous anteroseptal infarct. Panel A: Voltage mapping using tradition range of 0.5–1.5 mV shows a large area of scar core over the anteroseptum with no definite channel. Adjusting the voltage window to 0.1–1.0 mV reveals a channel between two areas of dense scar that was not seen using the traditional cutoff values. Panel B: A pre-procedural cardiac CT with ADAS processing demonstrates a border-zone channel between two areas of scar core at the mid septum. Panel C: Activation map of the clinical VT, demonstrating conduction through the conducting channel identified with both ADAS and voltage mapping. ADAS = automated detection of arrhythmogenic substrate, VT = ventricular tachycardia.

Fig. 3

EGM-Based Substrate Ablation. 54-year-old with sarcoidosis and VT originating from the RV free wall. Panel A: Voltage mapping demonstrates extensive scar over the RV free wall with no clear channel. LPs have been individually tagged (blue). LPs can be seen over an extensive area, predominantly within the scar area. Panel B: LAVAs have been individually tagged (burgundy). LAVA distribution here is primarily within scar border-zones. Panel C: All abnormal signals have been tagged (blue = LP, burgundy = LAVA, white = fractioned and double potentials). Abnormal signals cover virtually the entire region of abnormal voltage; substrate omogenization in this instance would require extensive ablation. Panel D: Mapped VT circuit. Critical isthmus site occurs in an area of very low voltage (<0.1 mV). All EGM types are found in this area, although the PPV for each type across the entire map is low. LP = late potential, LAVA = local abnormal ventricular activation, FS = fractionated signal, MDP = mid-diastolic potential, VT = ventricular tachycardia.

Fig. 4

Pace-Mapping-Based Substrate Ablation. 53-year-old male with tetralogy of Fallot and previous VT ablation, with line from superior tricuspid annulus to posterior pulmonary valve. Panel A: Bipolar voltage map demonstrating very low voltage (<0.05 mV) in the area of previous ablation. Panel B: No local signals area seen in the area of previous ablation. Given the clinical VT morphology was similar to VT ablated in the original procedure, a pace-mapping approach was undertaken. Pace-mapping at high output (20 mA at 10 ms pulse width) along the previous ablation line was performed. A single site of capture was identified (blue tag). Panel C: Pace-mapping shows a long stim-QRS (>200 ms) with an excellent (98.7%) morphology map to the clinical VT. Panel D: VT activation mapping reveals no local signals in the area of interest. However, ablation at the site of pace-mapping rendered the VT non-inducible. In this instance, pace-mapping at high-out likely captured an epicardial component of the circuit that could not be mapped endocardially.

Fig. 5

Pace-Mapping Correlation Map. 28-year-old with desmin cardiomyopathy. Following ablation of clinical VT (VT1), VT2 was easily inducible but not haemodynamically tolerated. Panel A: A Pace-mapping demonstrated an acute transition from excellent correlation (a) to poor correlation (c), consistent with an isthmus channel (white interrupted arrow). Panel B: The channel identified with pace-map correlation was localised between the mitral annulus and the initial ablation set. Extending the ablation set to join the mitral annulus rendered VT2 noninducible. LAT = local activation time, PM = pace-map, VT = ventricular tachycardia.

Fig. 6

ILAM-Based Substrate Ablation. 76-year-old with ischaemic cardiomyopathy. Endocardial VT ablation was performed, revealing a common isthmus at the mid-apical septum. Panel A: ILAM demonstrates a primary deceleration zone (maximum isochronal crowding) at the mid-apical septum. Panel B: VT activation mapping demonstrates the primary deceleration zone corresponds to the mid-isthmus. Ablation in this area rendered the VT non-inducible.