3-Dimensional ventricular electrical activation pattern assessed from a novel high-frequency electrocardiographic imaging technique: principles and clinical importance

Figure 1. Ex-vivo experimental setup. (a) The Langendorff-perfused pig heart suspended in a human torso-shaped tank with 256 electrodes embedded in the torso surface and 108-electrode epicardial sock with plunge needle electrodes. (b) A schematic interpretation of the sock placed over the ventricle, 3 plunge electrode needles with four contacts (4 mm distance) inserted into the ventricles, LAD—left anterior descending artery, RCA—right coronary artery, CFX—circumflex artery. (c) Comparison of the geometry of the experimental setup with an example of the human torso.

Figure 2. HFECGI theory validation using ex-vivo data. (a) Comparison of different activation maps on the sock—high-frequency activation times computed from torso records (HFAT), epicardial activation times computed from epicardial sock contacts (SEAT), and differential (DIFF) activation map computed as difference SEAT-HFAT. The red color in DIFF map means endo → epi direction, gray color means epi → endo direction (see Fig. 3). Marks 1,2,3 identify the position of needles. P marks identify the position of LV epicardial pacing. (b) Transmural depolarization wavefront propagation using signals from needle electrodes. Each needle electrode contained 4 contacts, marked by color (blue = close to epicardium; red = close to endocardium). The vertical color lines in the needles potentials indicate related activation time being the maximum negative derivative in each signal. If the blue contact is not shown, its position was outside the epicardial tissue. The gray signal represents epicardial potential measured on the sock contact in close proximity to the needle. The black signal represents high-frequency envelopes projected on epicardium to the needle position. The gray and black vertical marks…

Figure 3. Ex-vivo comparison of the difference between epicardial sock, needle contacts, and high-frequency activation times. (a) Differential activation maps SEAT-HFAT, difference SEAT-HFAT near the needle (thin edges bars), and the difference between the near-epi and near-endo activation in the needle contacts (thick edges bars). Positive values indicate the direction of endo-to-epi activation (shades of red in differential maps); negative values indicate the direction of epi-to-endo activation (shades of gray in differential maps). There is a high correlation (c = 0.93) between the difference values and 100% agreement in the direction of propagation in the differential map and needle’s contacts. (b) Comparison of the first and the last activation in the epicardial sock map, and in the high-frequency map. The first activation time on the sock was equal to zero Thus dark blue bars (last sock activation time) define the total activation time (TAT). The difference between cyan and red bars (last and first HF activation) defines high-frequency total activation time (HFTAT).

Figure 4. ECGI and HFECGI parameters in LBBB, IVCD, RBBB and normal patients. (a) Pt—patient, CC—correlation coefficient between EAT and HFAT in virtual points, QRSd—QRS duration, TAT, HFTAT—total activation time, DLR, HFDLR—interventricular electrical delay. (b) Relative magnitudes of parameters in IVCD patients compared to LBBB patients (mean LBBB = 1), *p < 0.05, **p < 0.01. HFECGI parameters HFTAT and HFDLR indicate significantly lower dyssynchrony in IVCD patients. Mean values and standard deviation.

Figure 5. Three-dimensional activation pattern interpretation. High-frequency activation times (HFAT), epicardial activation times (EAT), and differences (DIFF) in four exemplary patients: Left bundle branch block (LBBB, patient #3), right bundle branch block (RBBB, patient #14), intraventricular conduction disturbance (IVCD, patient #1) and normal synchronous heart (NORMAL, patient #11). (a) HFAT, DIFF, and EAT maps. Each map is shown from three projections (anterior, left, and inferior). (b) The red and gray arrows indicate the direction of electrical activation propagation derived from the EAT-HFAT plot in the second row; the size of the arrow corresponds to the endo-epi time delay. Numbers show the approximate timing of electrical activation.

Figure 6. High-frequency electrocardiographic imaging. (a) Block diagram that compares the electrocardiographic imaging (ECGI) technique and high-frequency (HF) electrocardiographic imaging (HFECGI) technique. (b) Estimation and interpretation of epicardial activation time (EAT), HF activation time (HFAT), and their difference (DIFF). EAT is computed as the delay between the QRS onset and the maximal negative slope of epicardial potential. It corresponds to the time when the depolarization wave reaches the epicardium. HFAT is defined as the delay between the QRS onset and the center of mass (hatched area) computed from HFQRS projected on the epicardium. In this way, HFAT reflects the time when the largest amount of myocardial cells is depolarized simultaneously—activation at approximately halfway on the depolarization path across the wall. DIFF then indicates the delay between the midwall and epicardial activation.

Figure 7. High-frequency ECG spatial sensitivity. The HF signal amplitude at a given time is the sum of simultaneously depolarized myocardial cells. Single HF source contribution is determined by the distance of the myocardial cell from the body surface electrode. The contribution decreases approximately with the square of the distance. (a) The black color shows areas with the largest contribution, light grey with the lowest contribution. For a given geometry, in the case of the V1 electrode, the right ventricular signal is 10 times stronger than the left ventricular signal. In the case of the V6 electrode, the right ventricular signal contribution is approximately 5 times weaker than the left ventricular signal (free wall) contribution. (b) Comparison of the measured HF amplitude of two different equivalent sources (S1, S2) in five body surface electrodes with different distances (E1-5). The closer the electrode is to the sources (E1), the better it can distinguish them—a higher difference between the amplitude of the near and far source. (c) Example of the mid septum activation (red circle) contribution to V1 (RV), V3 (apex), and V5 (LV free wall) electrodes. The lowest mid septum…

Figure 8. Interpretation of difference between ECGI and HFECGI-derived activation times. (a) High-frequency activation time (HFAT) and epicardial activation time (EAT) maps (anterior view) of patient #3 (LBBB). The red color indicates earlier activation, and the blue color indicates later activation. (b) Schematic representation of ventricular dyssynchrony based on EAT and HFAT. (c) DIFF map; red tones indicate EAT > HFAT and gray tones HFAT > EAT. (d) Interpretation of DIFF values. In area 1 HFAT is smaller (sooner) than EAT (marked by red arrow), representing a dominant propagation directed from the endocardium to the epicardium. In area 2 the prevailing direction of propagation is opposite because EAT precedes HFAT (marked by the gray arrow). In areas with similar EAT and HFAT values (area 3), the dominant direction of propagation is along the wall, or there are turbulences in depolarization propagation.