Volumetric source imaging for the non-invasive localization of septal ventricular tachycardia circuits
J Reventos-Presmanes, E Guillen, M Correas, J Vicente, I Hernandez-Romero, C Fambuena, M S Guillem, A M Climent, P Bhagirath, T Rosseel, A Porta-Sanchez, I Roca-LuqueAbstract
Background
Conventional electroanatomic mapping (EAM) is the gold-standard for guiding ventricular tachycardia (VT) ablation, but it is often limited to the endocardium and can struggle to characterize global activation, particularly for deep intramural or septal circuits. A novel non-invasive volumetric source imaging (VSI) approach [1] reconstructs 3D transmural activation, offering a potential solution. However, its clinical performance in localizing these challenging septal VTs has not been systematically validated.
Purpose
To validate the diagnostic performance of VSI for localizing septal VT circuits using invasive EAM as the gold-standard, and to evaluate its ability to identify the culprit arrhythmogenic channel on late gadolinium enhancement cardiac magnetic resonance (LGE-CMR).
Methods
In this single-centre retrospective study, we included patients referred for catheter ablation with septal VTs confirmed by EAM who underwent both pre-procedural LGE-CMR and periprocedural electrocardiographic imaging. Non-invasive VSI reconstructions, derived from a 128-lead body surface vest, were generated for each mapped VT based on activation or pace mapping. The critical components of the VT circuit were localized on both VSI and EAM using the 17-segment AHA model. For each segment, we computed the percentage of time it remained activated relative to the VT cycle length (%VT-CL) and compared segments with VT origin to those with passive activity. The ability of VSI to identify the specific arrhythmogenic channel seen on LGE-CMR was also assessed.
Results
A total of 22 patients were included (95.5% male, age 60.0 ± 15.6 years; 45.5% non-ischemic cardiomyopathy). Among this cohort, 23 septal VTs (mean cycle length 387.8 ± 94.5 ms) were successfully mapped using EAM. VSI enabled the non-invasive and single-beat visualization of septal VT circuits (Figure 1), identifying the septal pathway even in cases where invasive EAM was incomplete (Figure 2). On a segmental basis, VSI localized septal VT origins with a 78.8% sensitivity, 96.7% specificity, 66.7% positive predictive value, and 98.7%, negative predictive value. Segments containing critical parts of the VT circuit showed significantly higher percentages of VT-CL compared to those with passive activity (80.1 ± 25.3% vs 43.7 ± 32.7%, p < 0.01). Furthermore, VSI correctly identified the culprit arrhythmogenic channel in 14 of 16 cases (87.5%) where a septal origin was associated with a channel on LGE-CMR, out of a total of 36 channels assessed.
Conclusion
By providing a complete 3D, transmural view of activation, non-invasive VSI could overcome the 2D surface-based limitations of other mapping techniques to accurately localize deep septal VT circuits. This provides a potential novel diagnostic and planning tool to guide ablation strategy, particularly when activation mapping is precluded by non-sustained or hemodynamically unstable VT.