Catheter Ablation of Scar-mediated Ventricular Tachycardia: Are Substrate-based Approaches Replacing Mapping?

Abstract

Scar-mediated ventricular tachycardia (VT) is a recognized cause of morbidity and mortality in patients with ischemic cardiomyopathy and other cardiomyopathies such as nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and cardiac sarcoidosis. Implantable cardioverter-defibrillator (ICD) therapy improves survival but does not prevent the onset of recurrent VT or associated morbidity from ICD shocks. While randomized controlled trials have demonstrated advantages of scar-mediated VT ablation in comparison with antiarrhythmic drugs, procedural success has remained overall modest at between 50% and 70%. Standard scar-mediated VT ablation has relied on the use of activation and entrainment mapping during sustained VT to identify critical isthmuses for ablation. Substrate-based approaches have emerged as options to address hemodynamically unstable VT and have focused on identifying electrograms characteristic of critical isthmuses (eg, late potentials, local abnormal ventricular activities, conducting channels) within dense scar during sinus rhythm. Scar homogenization, a more recent approach, relies minimally on mapping and focuses on complete substrate modification. Core isolation, on the other hand, another recent development, relies heavily on mapping to identify regions within scar that are "cores" for arrhythmogenicity and then concentrates ablation to these areas. At this time, scar-mediated VT ablation appears to be at a crossroads wherein evolving substrate-based approaches are exploring whether to rely less or increasingly more on mapping. This review will therefore discuss the evolution of substrate-based, scar-mediated VT ablation and in the process try to answer whether there is still a role for mapping.

Keywords: Catheter ablation; dilated cardiomyopathy; electroanatomic mapping; ischemic heart disease; ventricular tachycardia.

Figure 1:

3D electroanatomic RV endocardial voltage map of a patient with ARVC created using CARTO^® (Biosense Webster, Diamond Bar, CA, USA). Dense scar is defined as that less than 0.5 mV and is depicted in red. Late potentials are marked with turquoise-colored tags. Inset electrogram from the ablation catheter distal tip (MAP 1–2) displays a markedly delayed late potential at a site within dense scar (yellow arrow). High-output (45–50 W), open-irrigated ablation targeted all late potentials and any detectable signal within the dense scar and are marked with red tags (shades of red depict ablation duration).

Figure 2:

3D electroanatomic RV epicardial voltage map created using CARTO^® (Biosense Webster, Diamond Bar, CA, USA) of the same patient with ARVC described in Figure 1. Dense scar is defined as that less than 0.5 mV and is depicted in red. Late potentials are marked with turquoise-colored tags and reveal a branching pattern of conducting channels within epicardial scar. Inset electrogram from the ablation catheter distal tip (MAP 1–2) displays a continuous, low-amplitude signal within a conducting channel (yellow arrow). Dechanneling was performed using high-output (45–50 W), open-irrigated ablation and sites are marked with red tags (shades of red depict ablation duration).

Figure 3:

3D electroanatomic RV epicardial voltage map created using CARTO^® (Biosense Webster, Diamond Bar, CA, USA) at one year later of the same patient with ARVC described in Figure 1. Dense scar is defined as that less than 0.5 mV and is depicted in red. The presentation of recurrent monomorphic VT at one year after the first ablation is an example of either the progression of ARVC or the limitations of less-complete, substrate-based ablation approaches. Endocardial (not shown here) and epicardial scar homogenization using high-output (45–50 W), open-irrigated ablation was performed and sites are marked with red tags (shades of red depict ablation duration).