Cardiac Magnetic Resonance for Ventricular Tachycardia Ablation and Risk Stratification

Abstract

Ventricular tachycardia is the most frequent cause of sudden cardiovascular death in patients with structural heart disease. Radiofrequency ablation is the treatment cornerstone in this population. Main mechanism for structural heart disease-related ventricular tachycardia is re-entry due to presence of slow conduction area within the scar tissue. Electroanatomical mapping with high density catheters can elucidate the presence of both scar (voltage maps) and slow conduction (activation maps). Despite the technological improvements recurrence rate after ventricular tachycardia ablation is high. Cardiac magnetic resonance has demonstrated to be useful to define the location of the scar tissue in endocardium, midmyocardium and/or epicardial region. Furthermore, recent studies have shown that cardiac magnetic resonance can analyse in detail the ventricular tachycardia substrate in terms of core scar and border zone tissue. This detailed tissue analysis has been proved to have good correlation with slow conduction areas and ventricular tachycardia isthmuses in electroanatomical maps. This review will provide a summary of the current role of cardiac magnetic resonance in different scenarios related with ventricular tachycardia in patients with structural heart disease, its limitations and the future perspectives.

Keywords: SCAR; ablation; cardiac magnetic resonance; electroanatomical mapping; ventricular tachycardia.

Figure 1

(A) Raw images of cardiac magnetic resonance (CMR) in a patient with chronic anterior myocardial infarction. The bright area seen is due to late gadolinium enhancement (LGE). Automatic segmentation of endocardium and epicardium with detection of the core scar is shown in red (intensity of LGE >60% of the area with maxim intensity signal of LGE), healthy tissue is shown in blue (intensity of LGE <40% of the area with maxim intensity signal of LGE) and the border zone is shown in yellow (areas with intermediate LGE intensity). (B) Three-dimensional reconstruction of CMR is shown from endocardium (layer 10%) to epicardium (layer 90%) with large anterior transmural myocardial infarction, with area of channels (white) of intermediate tissue (yellow) crossing the core scar (red).

Figure 2

Adapted from Andreu et al. (29). Panel 1: Pattern distribution of hyperenhancement in cardiac magnetic resonance images. (A) Endocardial hyperenhancement in left ventricle the anterior wall. (B) Transmural hyperenhancement in the left ventricle posterior wall and endocardial hyperenhancement of the posteroseptal wall. (C) Mid-myocardial hyperenhancement in the anteroseptal wall. (D) Epicardial hyperenhancement in the left ventricle lateral wall. Panel 2: Cardiac magnetic resonance and electroanatomical map of two patients with mid-myocardial hyperenhancement at the successful ablation site. (A,B) Endocardial ablation of premature ventricular contractions originating from the right ventricle. (A) The distance to the boundary of the hyperenhancement region was shorter in the right ventricle than in the left ventricle. (B) Radiofrequency ablation of the right ventricle was performed. (C,D) Endocardial ablation of the left ventricle. (C) In this case, the distance to the boundary of the hyperenhancement region was shorter from the left ventricle than from the right ventricle. (D) A previous unsuccessful radiofrequency ablation was attempted in the right ventricle. After mapping, the left ventricle the maximum precocity of the left ventricle septum was obtained, and radiofrequency ablation eliminated premature ventricular contraction.

Figure 3

Adapted from Quinto et al. (31). Upper panel: Example of transmural channel in pixel signal intensity (PSI) map of three-dimensional late gadolinium enhancement-cardiac magnetic resonance (LGE-CMR) reconstruction of the left ventricle. The core scar is shown in red, border zone in yellow, and healthy tissue in blue. A clear transmural large anteroapical scar with a channel of border zone in the apical-lateral is seen from the endocardial layers (20–30%) to the epicardial (80–90%). The bottom panel shows the Kaplan-Meier curve for ventricular tachycardia-free survival according to the presence of septal substrate, transmural channels, and midmural channels.

Figure 4

Examples of correlation of three-dimensional pixel signal intensity (PSI) maps reconstruction from late gadolinium enhancement-cardiac magnetic resonance (LGE-CMR) (red: core scar, yellow: border zone, blue: healthy tissue: blue) with different electroanatomical (EAM) maps. (A) From left to right: EAM high density voltage map showing anterolateral scar (core scar: grey, border zone: red, healthy tissue: purple), ventricular tachycardia with a figure-of-eight circuit using border zone inside the scar (black line in the voltage map) with diastolic electrograms during ventricular tachycardia (VT); and PSI LGE-CMR map with clear conducting channel (blue line) at the same region as compared to the EAM voltage and activation map. (B) Left panel shows sinus rhythm isochronal activation map with an area of isochronal crowding (white circle) suggesting an area of deceleration zone. Right panel shows LGE-PSI map with an area of a very ramified channel (blue lines) inside a scar in the same area of deceleration zone in sinus rhythm EAM map. (C) Epicardial high density voltage map (left panel) and late potentials map (centre panel) with two small scars (right panel, grey area), intermediate tissue between scars, and area (red) of late potentials corresponding to border zone between scars. Right panel shows epicardial LGE-CMR PSI map (layer 80%) with the same two scars detected in the voltage map.

Figure 5

Adapted from Roca-Luque et al. (30). Pace-map electroanatomical map (EAM) of right ventricle (RV) (anterior view) with the highest concordance with ventricular tachycardia morphology (92%) in the anterior RV septum. Ablation as unsuccessful from both right and left ventricle. EAM is merged with pre-procedural cardiac tomography (CT) scan and a septal artery is observed irrigating the area of best pace-map. Centre panel shows only CT scan with septal artery irrigating an area of intramural eptal scar (red) corresponding to the area of best pace-map. Bottom panels show septal alcolholisation of the culprit area according pre-procedural imaging The wire inside septal artery (grey arrows) is shown in front of catheter tip (white star) in the RV septum. After alcholisation at that region (bottom right panel) ventricular tachycardia stops.

Figure 6

Adapted from Sánchez-Somonte et al. (54). (A) Late gadolinium enhancement-cardiac magnetic resonance (LGE-CMR) reconstruction of the left ventricle (LV) with a posteroseptal scar (core in red, BZ in white, and healthy myocardium in blue). A white line is drawn over the surface, representing a conducting channel. We can see the substrate evolution through different layers, from the endocardium (10–30%) to the epicardium (70–90%), with a defined channel in different layers. (B) LGE-CMR reconstruction of the LV with an anterior scar. In this case the scar is very homogeneous (mainly composed of core tissue) compared with the scar in panel (A) and it has no conducting channels. (C) LGE-CMR reconstruction of the LV without scar. BZ, 5 border zone; LGE-CMR, 5 late gadolinium enhanced cardiac magnetic resonance; LV, 5 left ventricle. Upper right panel shows cumulative incidence functions for appropriate therapies depending on scar mass >10 g and the present channels. At 6-year follow-up, 37.65% of patients with channels and scar mass > 10 g reached the primary end point compared with 2.78% of patients without channels and scar mass < 10 g.