Endo-epicardial electrical disarray in arrhythmogenic cardiomyopathy with ventricular arrhythmias
Johanna B Tonko1, Gema Cabero-Vidal2, Samuel Ruipérez-Campillo3
1Centre for Translational Electrophysiology, Institute for Cardiovascular Science, University College London, London, United Kingdom; Department for Cardiology, St. Bartholomew's Hospital, London, United Kingdom.
Insights
Vector field heterogeneity (VFH) quantifies electrical disorganization in arrhythmogenic cardiomyopathy (ACM). VFH reveals hidden substrate in normal-appearing areas, improving ACM substrate mapping.
Area of Science:
- Cardiology
- Electrophysiology
- Biomedical Engineering
Background:
- Arrhythmogenic cardiomyopathy (ACM) is a hereditary heart condition causing ventricular arrhythmias (VA).
- The burden of VA can be severe, even when structural changes are not obvious on standard imaging.
- Identifying the electrical substrate is crucial for managing ACM patients.
Purpose of the Study:
- To measure local electrical propagation disorganization using vector field heterogeneity (VFH) in ACM patients.
- To determine if VFH can detect subclinical electrical abnormalities missed by conventional voltage mapping.
Main Methods:
- Retrospective analysis of high-density endo-epicardial substrate maps from 23 ACM patients.
- Calculation of directional vector maps and VFH from unipolar electrograms.
- Comparison of VFH across different voltage regions (normal, border zone, scar) and deceleration zones (DZs).
Main Results:
- VFH was significantly higher in scar regions (OV <0.3 mV) compared to normal or border zones.
- Epicardial VFH was higher than endocardial VFH in border zones, while endocardial VFH was higher in normal areas.
- Highest VFH values were found in DZs and in normal-voltage areas adjacent to low-voltage substrate, indicating hidden electrical disorganization.
Conclusions:
- VFH effectively identifies increased electrical propagation heterogeneity in ACM, particularly in scar and DZs.
- VFH unmasks subclinical electrical abnormalities in areas with normal voltage adjacent to scar, suggesting microstructural changes or transmural disease.
- VFH can complement existing substrate mapping techniques for a more comprehensive assessment of ACM.
Background:
Arrhythmogenic cardiomyopathy (ACM) is a hereditary condition frequently presenting with ventricular arrhythmias (VA). VA burden may be disproportionate to detectable structural alterations.
Objective:
To quantify local disorganization of electrical propagation using the vector field heterogeneity (VFH) metric in patients with ACM and to assess whether VFH may unmask subclinical substrate missed in conventional voltage maps.
Methods:
High-density endo-epicardial substrate maps acquired with a 16-pole grid catheter in patients with ACM were retrospectively reviewed. Directional vector maps of electrical propagation were computed offline from 4 × 4 unipolar arrays. VFH, ranging from 0 (perfect planar wave) to 1 (maximal disorganization), was estimated as a quantitative measure of local propagation heterogeneity. VFH values were compared between endo- and epicardial maps and across omnipolar voltage (OV)-defined regions: normal (OV >1.5 mV), border zone (0.3-1.5 mV), scar (<0.3 mV), as well as isochronal deceleration zones (DZs).
Results:
Overall, 23 patients were included. VFH differed significantly across voltage categories (P < .001) with highest VFH observed in regions OV <0.3 mV (epi 0.57 [0.28] vs endo 0.56 [0.30]). In border zone regions, epicardial VFH exceeded endocardial VFH (0.41 [0.42] vs 0.39 [0.45]), whereas in normal OV areas, endocardial VFH was higher than epicardial VFH (epi 0.17 [0.27] vs endo 0.29 [0.34]). Highest VFH were recorded at sites of DZs (0.59 [0.25]), with a trend toward increased electrical disarray during sensed extras (0.62 [0.28], P = .88). Notably, in epicardial regions with normal-voltage directly adjacent to low-voltage substrate, VFH was significantly elevated compared with overall normal-voltage areas (0.26 [0.32] vs 0.17 [0.27], P < .001).
Conclusion:
In patients with ACM, VFH identified a significantly increased heterogeneity in electrical propagation at sites of scar and DZs, but also in normal-voltage areas adjacent to low-voltage areas and on the endocardium. This could indicate microstructural alterations and/or transmural disease progression that are missed in traditional assessments but unmasked by VFH, and could complement existing substrate mapping approaches in ACM.
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