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. 2016 Aug 24;11(8):e0160999.
doi: 10.1371/journal.pone.0160999. eCollection 2016.

Comparison of Electric- And Magnetic-Cardiograms Produced by Myocardial Ischemia in Models of the Human Ventricle and Torso

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Free PMC article

Comparison of Electric- And Magnetic-Cardiograms Produced by Myocardial Ischemia in Models of the Human Ventricle and Torso

Erick A Perez Alday et al. PLoS One. .
Free PMC article

Abstract

Myocardial ventricular ischemia arises from a lack of blood supply to the heart, which may cause abnormal repolarization and excitation wave conduction patterns in the tissue, leading to cardiac arrhythmias and even sudden death. Current diagnosis of cardiac ischemia by the 12-lead electrocardiogram (ECG) has limitations as they are insensitive in many cases and may show unnoticeable differences to normal patterns. As the magnetic field provides extra information on cardiac excitation and is more sensitive to tangential currents to the surface of the chest, whereas the electric field is more sensitive to flux currents, it has been hypothesized that the magnetocardiogram (MCG) may provide a complementary method to the ECG in ischemic diagnosis. However, it is unclear yet about the differences in sensitivity regions of body surface ECG and MCG signals to ischemic conditions. The aim of this study was to investigate such differences by using 12-, 36- ECG and 36-MCG computed from multi-scale biophysically detailed computational models of the human ventricles and torso in both control and ischemic conditions. It was shown that ischemia produced changes in the ECG and MCG signals in the QRS complex, T-wave and ST-segment, with greater relative differences seen in the 36-lead ECG and MCG as compared to the 12-leads ECG (34% and 37% vs 26%, respectively). The 36-lead ECG showed more averaged sensitivity than the MCG in the change of T-wave due to ischemia (37% vs 32%, respectively), whereas the MCG showed greater sensitivity than the ECG in the change of the ST-segment (50% vs 40%, respectively). In addition, both MCG and ECG showed regional-dependent changes to ischemia, but with MCG showing a stronger correlation between ischemic region in the heart. In conclusion, MCG shows more sensitivity than ECG in response to ischemia, which may provide an alternative method for the diagnosis of ischemia.

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Multi-scale computer models of the human ventricles and torso.
(A) Computational model of the human ventricles showing (i) AP, (ii) anatomically accurate structure, and (iii) myofibre orientations derived from DTMRI imaging. (B) Heart-torso model (i), and positions of the electrodes/sensors in the surface of the body (ii). (C) Simulated body-field maps and (D) example single electrode signals, for ECG (i) and MCG (ii). The white arrows show the direction of the electric potential, while the green circled arrows show the direction of the magnetic field, consistent with the right hand rule (C).
Fig 2
Fig 2. Simulated action potentials under control and ischemic conditions.
Simulated action potentials (APs) under control conditions (Black line), phase A (blue line) and phase B (red line) of ischemia. (A) Endocardium. (B) Myocardium cell. (C) Epicardium.
Fig 3
Fig 3. Simulated 12-leads ECG and MCG under control and ischemic conditions.
Simulated time courses of 12-lead ECGs (superior), MCGs (from leads D3 to D6; bottom) under control (blue line) and ischemic conditions (Phase A with variant locations; gray lines). Experimental data (red) was included in the MCG for comparison purposes. Simulated 12-lead ECG and MCG were normalized to the maximum amplitude of each lead, and superimposed over experimental recordings from a healthy subject.
Fig 4
Fig 4. Simulated 36-lead ECG and MCG under control and ischemic conditions.
Simulated 36-lead ECG (top panels) and MCG (bottom panels) in control (blue line) and ischemic (grey line) conditions. In control conditions, ECG and MCG were normalized and superimposed with experimental data [18] (red line), simulated data (blue line) during control and ischemic conditions (Phase A with variant locations; grey lines). The numbers and letters represent the electrode/sensor position (Fig 1B-ii). Simulated 36-lead ECG and MCG were normalized to the maximum amplitude of each lead, and superimposed over experimental recordings from a healthy subject.
Fig 5
Fig 5. Averaged relative differences of 12- and 36-lead ECG and 36-MCG.
Averaged relative differences of the QRS complex, ST- segment and T-wave of the12-lead ECG (pink bar), 36-lead ECG (red bar) and MCG (blue bar) between the ischemic (Phase A & B with variant locations) and control condition.
Fig 6
Fig 6. Relative differences of each of the 36-leads ECG and MCG between ischemic and control conditions.
Computed relative differences for each of the 36-leads ECG (red) and MCG (blue) with control conditions for the QRS complex, ST-segment, and T-wave.
Fig 7
Fig 7. Maps of major differences of BSP and MCG between ischemic and control conditions.
Maps of major differences of BSP (top panels) and MCG (bottom panels) between ischemia and control conditions for the QRS complex, ST-segment, and T-wave, during both early (Phase A) and late (Phase B) ischemic phases. The contour lines correspond to small variations in the small difference range, in both frontal (front) and posterior (back) part of the torso.
Fig 8
Fig 8. Maps of the major difference of BSP and MCG between control and localized ischemic condition.
Maps of the major difference of BSP and MCG between control and varied localized ischemic condition during the ST-segment. Ischemic region was considered in four different ventricular locations (labeled in red): Superior left ventricle (A), inferior left ventricle (B), superior right ventricle (C), inferior right ventricle (D). The contour lines correspond to small variations in the small difference range.

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Grant support

This work was supported by CONACyT and EPSRC project grant. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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