Electrocardiographic imaging of repolarization abnormalities in structural heart disease for characterization of...

Electrocardiographic imaging (ECGI) enables noninvasive 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.

This study aimed to compare ECGI-derived activation time and activation-recovery interval (ARI) metrics in sinus rhythm in patients with structural heart disease (SHD) and evaluate their relationship to myocardial scar and ventricular tachycardia (VT) status.

Patients who underwent 252-electrode computed tomography-ECGI and delayed-enhancement magnetic resonance imaging were reviewed and categorized according to the presence of myocardial scar, left ventricular ejection fraction (LVEF), and history of reentrant VT. Reconstructed unipolar activation and repolarization maps and derived ARI maps were coregistered with 3-dimensional magnetic resonance imagin scar models. ARI duration, ARI dispersion, and activation time dispersion were estimated on ventricular and segmental levels and compared across groups and tissue types.

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 < .05). Segmental ARI was longest over scar regions and dispersion higher in transmural (22.0 ms [IQR 26.3]) and subepicardial scar (20.6 ms [IQR 22.8]) than subendocardial scar (16.5 ms [IQR 16.1]) and non-scarred myocardium (15.8 ms [IQR 20.3]; P < .001). ARI dispersion within scar regions was significantly higher in the scar+/VT+ than the scar+/VT- cohort (β = -8.4 ms; P = .009). Activation dispersion was significantly increased at sites of scar compared with normal myocardium (β = -5.3 ms; P < .001) but showed only a trend toward distinguishing VT status (P = .059). Severe left ventricular dysfunction, even in the absence of overt myocardial scar, was also associated with significantly prolonged ARI and elevated dispersion metrics compared with controls.

ECGI-derived ARI 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.