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Comparative Study
. 2021 May 4;10(9):e020153.
doi: 10.1161/JAHA.120.020153. Epub 2021 Apr 21.

Electrocardiographic Imaging of Repolarization Abnormalities

Affiliations
Comparative Study

Electrocardiographic Imaging of Repolarization Abnormalities

Laura R Bear et al. J Am Heart Assoc. .

Abstract

Background Dispersion and gradients in repolarization have been associated with life-threatening arrhythmias, but are difficult to quantify precisely from surface electrocardiography. The objective of this study was to evaluate electrocardiographic imaging (ECGI) to noninvasively detect repolarization-based abnormalities. Methods and Results Ex vivo data were obtained from Langendorff-perfused pig hearts (n=8) and a human donor heart. Unipolar electrograms were recorded simultaneously during sinus rhythm from an epicardial sock and the torso-shaped tank within which the heart was suspended. Regional repolarization heterogeneities were introduced through perfusion of dofetilide and pinacidil into separate perfusion beds. In vivo data included torso and epicardial potentials recorded simultaneously in anesthetized, closed-chest pigs (n=5), during sinus rhythm, and ventricular pacing. For both data sets, ECGI accurately reconstructed T-wave electrogram morphologies when compared with those recorded by the sock (ex vivo: correlation coefficient, 0.85 [0.52-0.96], in vivo: correlation coefficient, 0.86 [0.52-0.96]) and repolarization time maps (ex-vivo: correlation coefficient, 0.73 [0.63-0.83], in vivo: correlation coefficient, 0.76 [0.67-0.82]). ECGI-reconstructed repolarization time distributions were strongly correlated to those measured by the sock (both data sets, R2 ≥0.92). Although the position of the gradient was slightly shifted by 8.3 (0-13.9) mm, the mean, max, and SD between ECGI and recorded gradient values were highly correlated (R2=0.87, 0.75, and 0.86 respectively). There was no significant difference in ECGI accuracy between ex vivo and in vivo data. Conclusions ECGI reliably and accurately maps potentially critical repolarization abnormalities. This noninvasive approach allows imaging and quantifying individual parameters of abnormal repolarization-based substrates in patients with arrhythmogenesis, to improve diagnosis and risk stratification.

Keywords: ECG; electrocardiographic imaging; electrocardiography; electrophysiology mapping; repolarization.

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Conflict of interest statement

Dr Cluitmans is employed part‐time by Philips Research. The remaining authors have no disclosures to report.

Figures

Figure 1
Figure 1. (A) In vivo and (B) ex vivo experimental setups.
Figure 2
Figure 2. Recorded (top) and ECGI reconstructed (bottom) epicardial electrograms with repolarization times (vertical lines) for a representative case using torso tank data.
Electrograms are presented for electrodes marked on the recorded repolarization map during dofetilide+pinacidil perfusion, at (1) baseline (blue) with no drug perfusion; (2) with dofetilide‐only (green) perfusion in non‐LAD coronaries, which prolongs RT; and (3) with the additional perfusion of pinacidil (red) in the LAD (white dashed line) which shortens RT. ECGI indicates electrocardiographic imaging; LAD, left anterior descending artery; and RT, repolarization time.
Figure 3
Figure 3. Comparison of recorded and ECGI repolarization times.
A, Recorded and ECGI reconstructed RT maps at baseline (blue) with no drug perfusion, with dofetilide‐only (green) perfusion in non‐LAD coronaries, and with additional perfusion of pinacidil (red) in the LAD (white dashed line). B, “Kernel” probability distributions fitted to recorded and ECGI activation (light gray) and RTs (dark gray) for these RT maps with the detected peaks of RT distributions (white square). ECGI indicates electrocardiographic imaging; LAD, left anterior descending artery; and RT, repolarization time.
Figure 4
Figure 4. Linear regression plots of recorded and ECG‐derived mean repolarization time (mean RT; top left), std RT (top right), total RT dispersion (TRTD; bottom left), and kernel probability distribution peak timings (bottom right) from both in vivo (blue) and ex vivo (red) data.
For all plots, there was no significant difference between regression fits for 5 in vivo and 9 ex vivo data sets (P>0.10). Data collected from 146 cardiac sequences.
Figure 5
Figure 5. Evaluation of ECGI reconstructed RT gradients.
A, Recorded and ECGI reconstructed RT gradient maps at baseline (blue) with no drug perfusion, with dofetlide‐only (green) perfusion in non‐LAD coronaries, and with additional perfusion of pinacidil (red) in the LAD (black dashed line). B, Distribution of RT gradients with mean, max and SD from recorded/ECGI reconstructions respectively. ECGI indicates electrocardiographic imaging; LAD, left anterior descending artery; and RT, repolarization time.
Figure 6
Figure 6. Linear regression plots of repolarization time gradient (ΔRT) statistics including mean ΔRT (left), max ΔRT (middle) and std ΔRT (right) from both in vivo (blue) and ex vivo (red) data sets.
For all plots, there was no significant difference between regression fits for 5 in vivo and 9 ex vivo data sets (P>0.10). Data collected from 146 cardiac sequences. ECGI indicates electrocardiographic imaging; LAD, left anterior descending artery; and RT, repolarization time.
Figure 7
Figure 7. Evaluation of ECGI reconstructed electrograms, RT and RT gradients (ΔRT) for a representative in vivo data set during left ventricular apical pacing.
A, Recorded (top) and ECGI (bottom) reconstructed epicardial electrograms with RTs (vertical lines). Electrograms are located at electrodes marked on the recorded and ECG (B) RT maps with (C) ΔRT maps below. ECGI indicates electrocardiographic imaging; and RT, repolarization time.

Comment in

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