Electric Field-Based Spatial Analysis of Noncontact Unipolar Electrograms to Map Regional Activation-Repolarization Intervals

Vermoortele, Dylan; Amoni, Matthew; Ingelaere, Sebastian; Sipido, Karin R.; Willems, Rik; Claus, Piet

doi:10.1016/j.jacep.2023.02.004

Cited by 2 publications

(4 citation statements)

References 25 publications

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“…Using a recently developed algorithm, we mapped the local repolarization time from spatially dense electrograms of noncontact electroanatomical maps of the LV. 19 Contact mapping defined the infarct, BZ, and remote regions, which were translated to polar maps to aid visualization (Figure 1A). The local ARIs, as a measure of repolarization time, were plotted on the polar map (Figure 1B, left).…”

Section: Resultsmentioning

confidence: 99%

“…Mapping data were processed to calculate the local activation-recovery interval (ARI) for each local electrogram and reconstruct a spatially dense map using the E-field method. 19…”

Section: Methodsmentioning

confidence: 99%

“…Mapping data were processed to calculate the local activation-recovery interval (ARI) for each local electrogram and reconstruct a spatially dense map using the E-field method. 19 After 1 to 3 days of recovery, animals were euthanized for tissue harvesting and cellular experiments.…”

Section: In Vivo Cardiac Electrophysiologymentioning

confidence: 99%

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Heterogeneity of Repolarization and Cell-Cell Variability of Cardiomyocyte Remodeling Within the Myocardial Infarction Border Zone Contribute to Arrhythmia Susceptibility

Amoni

Vermoortele

Ekhteraei-Tousi

et al. 2023

Circ: Arrhythmia and Electrophysiology

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BACKGROUND: After myocardial infarction, the infarct border zone (BZ) is the dominant source of life-threatening arrhythmias, where fibrosis and abnormal repolarization create a substrate for reentry. We examined whether repolarization abnormalities are heterogeneous within the BZ in vivo and could be related to heterogeneous cardiomyocyte remodeling. METHODS: Myocardial infarction was induced in domestic pigs by 120-minute ischemia-reperfusion injury. After 1 month, remodeling was assessed by magnetic resonance imaging, and electroanatomical mapping was performed to determine the spatial distribution of activation-recovery intervals. Cardiomyocytes were isolated and tissue samples collected from the BZ and remote regions. Optical recording allowed assessment of action potential duration (di-8-Anepps, stimulation at 1 Hz, 37 °C) of large cardiomyocyte populations while gene expression in cardiomyocytes was determined by single nuclear RNA sequencing. RESULTS: In vivo, activation-recovery intervals in the BZ tended to be longer than in remote with increased spatial heterogeneity evidenced by a greater local SD (3.5±1.3 ms versus remote: 2.0±0.5 ms, P =0.036, n pigs =5). Increased activation-recovery interval heterogeneity correlated with enhanced arrhythmia susceptibility. Cellular population studies (n cells =635–862 cells per region) demonstrated greater heterogeneity of action potential duration in the BZ (SD, 105.9±17.0 ms versus remote: 73.9±8.6 ms; P =0.001; n pigs =6), which correlated with heterogeneity of activation-recovery interval in vivo. Cell-cell gene expression heterogeneity in the BZ was evidenced by increased Euclidean distances between nuclei of the BZ (12.1 [9.2–15.0] versus 10.6 [7.5–11.6] in remote; P <0.0001). Differentially expressed genes characterizing BZ cardiomyocyte remodeling included hypertrophy-related and ion channel–related genes with high cell-cell variability of expression. These gene expression changes were driven by stress-responsive TFs (transcription factors). In addition, heterogeneity of left ventricular wall thickness was greater in the BZ than in remote. CONCLUSIONS: Heterogeneous cardiomyocyte remodeling in the BZ is driven by uniquely altered gene expression, related to heterogeneity in the local microenvironment, and translates to heterogeneous repolarization and arrhythmia vulnerability in vivo.

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Section: Resultsmentioning

confidence: 99%

“…Mapping data were processed to calculate the local activation-recovery interval (ARI) for each local electrogram and reconstruct a spatially dense map using the E-field method. 19…”

Section: Methodsmentioning

confidence: 99%

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Heterogeneity of Repolarization and Cell-Cell Variability of Cardiomyocyte Remodeling Within the Myocardial Infarction Border Zone Contribute to Arrhythmia Susceptibility

Amoni

Vermoortele

Ekhteraei-Tousi

et al. 2023

Circ: Arrhythmia and Electrophysiology

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“…Holland and Arnsdorf (1977) showed with the solid angle theory that the EGM properties change depending on the electrode location and the geometry of the infarcted tissue. Recent studies have argued that local potential differences, as observed by a bipolar electrode, or any pair in an array configuration, can be described as projections of an electrical field vector (Vermoortele et al, 2023). The effect of the catheter orientation (and, thus, the bipolar electrodes) on iEGMs has been addressed in the study by Gaeta et al (2020), and the effects of anisotropy on the potential field were studied in Colli Franzone et al, 1982.…”

Section: )mentioning

confidence: 99%

Impact of electrode orientation, myocardial wall thickness, and myofiber direction on intracardiac electrograms: numerical modeling and analytical solutions

2023

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Intracardiac electrograms (iEGMs) are time traces of the electrical potential recorded close to the heart muscle. We calculate unipolar and bipolar iEGMs analytically for a myocardial slab with parallel myofibers and validate them against numerical bidomain simulations. The analytical solution obtained via the method of mirrors is an infinite series of arctangents. It goes beyond the solid angle theory and is in good agreement with the simulations, even though bath loading effects were not accounted for in the analytical calculation. At a large distance from the myocardium, iEGMs decay as 1/R (unipolar), 1/R2 (bipolar and parallel), and 1/R3 (bipolar and perpendicular to the endocardium). At the endocardial surface, there is a mathematical branch cut. Here, we show how a thicker myocardium generates iEGMs with larger amplitudes and how anisotropy affects the iEGM width and amplitude. If only the leading-order term of our expansion is retained, it can be determined how the conductivities of the bath, torso, myocardium, and myofiber direction together determine the iEGM amplitude. Our results will be useful in the quantitative interpretation of iEGMs, the selection of thresholds to characterize viable tissues, and for future inferences of tissue parameters.

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Electric Field-Based Spatial Analysis of Noncontact Unipolar Electrograms to Map Regional Activation-Repolarization Intervals

Cited by 2 publications

References 25 publications

Heterogeneity of Repolarization and Cell-Cell Variability of Cardiomyocyte Remodeling Within the Myocardial Infarction Border Zone Contribute to Arrhythmia Susceptibility

Heterogeneity of Repolarization and Cell-Cell Variability of Cardiomyocyte Remodeling Within the Myocardial Infarction Border Zone Contribute to Arrhythmia Susceptibility

Impact of electrode orientation, myocardial wall thickness, and myofiber direction on intracardiac electrograms: numerical modeling and analytical solutions

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