Electrocardiographic Imaging of Repolarization Abnormalities in Structural Heart Disease for Characterisation of Arrhythmogenic Phenotypes

BACKGROUND: Electrocardiographic Imaging (ECGI) enables non-invasive assessment of 3-dimensional activation and repolarization sequences. Whether ECGI allows to detect repolarization abnormalities in relation to myocardial scar and differentiate arrhythmogenic phenotypes has not been systematically investigated. OBJECTIVE: To compare ECGI-derived activation time (AT) and activation-recovery interval (ARI) metrics in sinus rhythm in patients with structural heart disease (SHD) and evaluate their relationship to myocardial scar and VT status. METHODS: Patients who underwent 252-electrode CT-ECGI and delayed-enhancement MRI were reviewed and categorised according to presence of myocardial scar, left ventricular ejection fraction (LVEF) and history of re-entrant VT. Reconstructed unipolar activation and repolarization maps, and derived ARI maps, were co-registered with 3D MRI scar models. ARI duration, ARI dispersion and AT dispersion were estimated at ventricular and segmental levels and compared across groups and tissue types. RESULTS: 71 patients were included: 39 patients with scar+/VT+ (28.3% ischemic, LVEF 41.2±17.5%), 14 patients with scar+/VT- (37.5% ischemic, LVEF 33.3±10.6%), 9 patients with impaired LVEF/VT- (LVEF 21.9±5.6%) and 9 controls (LVEF 59.2±7.1%). In sinus rhythm, ARI duration and dispersion differed significantly between groups and tissue types (all p<0.05). Segmental ARI was longest over scar regions and dispersion higher in transmural (22.0ms 26.3) and subepicardial scar (20.6ms 22.8, compared to subendocardial (16.5ms 16.1) and non-scarred myocardium (15.8ms 20.3, p<0.001). ARI dispersion within scar regions was significantly higher in the scar+/VT+ compared to scar+/VT- cohort (β = -8.4ms, p=0.009). Activation dispersion was significantly increased at sites of scar compared to normal myocardium (β = -5.3ms, p<0.001) but showed only a trend toward distinguishing VT status (p=0.059). Severe LV dysfunction, even in the absence of overt myocardial scar, was also associated with significantly prolonged ARI and elevated dispersion metrics compared to controls. CONCLUSION: ECGI-derived activation-recovery interval alterations in SHD are associated with scar presence, transmurality and VT history. Segmental ARI dispersion in association with myocardial scar may potentially serve as a complementary non-invasive marker of arrhythmogenic risk.