Differences in the upslope of the precordial body surface ECG T wave reflect right to left dispersion of repolarization in the intact human heart

Summary Objectives: In this paper, we present a unified electrodynamic heart model that permits simulations of the body surface potentials generated by the heart in motion. The inclusion of motion in the heart model significantly improves the accuracy of the simulated body surface potentials and therefore also the 12-lead ECG. Methods: The key step is to construct an electromechanical heart model. The cardiac excitation propagation is simulated by an electrical heart model, and the resulting cardiac active forces are used to calculate the ventricular wall motion based on a mechanical model. The source-field point relative position changes during heart systole and diastole. These can be obtained, and then used to calculate body surface ECG based on the electrical heart-torso model. Results: An electromechanical biventricular heart model is constructed and a standard 12-lead ECG is simulated. Compared with a simulated ECG based on the static electrical heart model, the simulated ECG based on the dynamic heart model is more accordant with a clinically recorded ECG, especially for the ST segment and T wave of a V1-V6 lead ECG. For slight-degree myocardial ischemia ECG simulation, the ST segment and T wave changes can be observed from the simulated ECG based on a dynamic heart model, while the ST segment and T wave of simulated ECG based on a static heart model is almost unchanged when compared with a normal ECG. Conclusions: This study confirms the importance of the mechanical factor in the ECG simulation. The dynamic heart model could provide more accurate ECG simulation, especially for myocardial ischemia or infarction simulation, since the main ECG changes occur at the ST segment and T wave, which correspond with cardiac systole and diastole phases.

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The repolarization pattern of ARVC patients, healthy gene carriers and controls as analyzed with a 252-leads Body Surface Mapping Vest

European Heart Journal ◽

10.1093/ehjci/ehaa946.0337 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

V Kommata ◽

M.I Elshafie ◽

M Perez ◽

R Augustine ◽

C Blomstrom-Lundquist

Keyword(s):

Body Surface ◽

Funding Source ◽

Surface Mapping ◽

Pattern Type ◽

T Wave ◽

Gene Carriers ◽

Surface Ecg ◽

Back Panel ◽

The Right

Abstract Background Repolarization abnormalities have a central role on the diagnosis of ARVC according to recent HRS consensus document from 2019 stating that T wave inversion in the right precordial leads is a major criteria if it appears in V1-V3 or a minor criteria if it appears in only V1-V2. Purpose The aim of our study was to investigate whether repolarization patterns as recorded by a Body Surface Mapping (BSM) system consisting of a vest with 252 ECG leads, could differentiate ARVC patients and even gene carriers from normal individuals. Our hypothesis is that the method can potentially identify repolarization disturbances earlier or better than conventional 12-lead ECG. Method 12 definite ARVC patients, 20 healthy gene carriers and 8 family members who tested negative for the family mutation (controls) were included. All patients underwent 12-lead ECG, including right precordial leads (V4R) and BSM recordings. Repolarization (T-wave polarity and concordance with QRS complex vector) was analyzed qualitatively in all BSM recordings, the results of which were displayed on a color code map (fig.1). Results The mean age was 49.6, 43.6 and 38.8 years in ARVC patients, healthy gene carriers and controls, respectively. The number of males in the three groups were 8/12, 8/20 and 5/8, respectively. All 8 controls had similar repolarization patterns with negative and concordant T waves on the right back panel, and T waves that successively changed from negative concordant (green) to positive disconcordant (red) and finally positive concordant (blue) on the left front panel (pattern 1). All 12 ARVC patients had different repolarization patterns as compared to the controls. Two of these patients had no apparent repolarization changes on conventional 12 lead ECG. The pattern type 2 repolarization, as defined by same pattern as the controls at the right back panel but different pattern at the front left panel was seen in 3/12 ARVC patients. The remaining 9 ARVC patients had different repolarization patterns both on the front and on the back panel (pattern 3). Among gene carriers, 15 had a normal repolarization pattern (pattern 1) and 5 demonstrated an abnormal repolarization pattern (4 had pattern type 2 and one pattern 3) despite normal surface ECG. Conclusions Using BSM recordings, abnormal repolarization patterns can be detected in all ARVC patients, even in those without repolarization changes on conventional surface ECG. The observation that 25% of gene carriers had divergent repolarization patterns, may indicate an early stage of the disease, and be used as an early diagnostic marker of the disease. Further and larger studies are warranted to confirm these observations. Repolarisation patterns recorded by BSM Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Selanders Stiftelse

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Measurement of T wave variability in body surface ECG

Journal of Electrocardiology ◽

10.1016/j.jelectrocard.2016.07.014 ◽

2016 ◽

Vol 49 (6) ◽

pp. 883-886 ◽

Cited By ~ 2

Author(s):

Mathias Baumert

Keyword(s):

Body Surface ◽

T Wave ◽

Surface Ecg

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Faculty Opinions recommendation of Myocardial ischaemia in patients with coronary endothelial dysfunction: insights from body surface ECG mapping and implications for invasive evaluation of chronic chest pain.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.13266956.14620054 ◽

2011 ◽

Author(s):

Juan-Carlos Kaski ◽

Peter Ong

Keyword(s):

Chest Pain ◽

Endothelial Dysfunction ◽

Body Surface ◽

Myocardial Ischaemia ◽

Surface Ecg ◽

Invasive Evaluation ◽

Coronary Endothelial Dysfunction

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Transmural repolarization does not underlie the T-wave in the human heart. Correlation between in vivo data and computer simulations

Heart Rhythm ◽

10.1016/j.hrthm.2005.02.314 ◽

2005 ◽

Vol 2 (5) ◽

pp. S101-S102 ◽

Cited By ~ 1

Author(s):

Chantal E. Conrath ◽

Ronald Wilders ◽

Ruben Coronel ◽

Jacques M. De Bakker ◽

Peter Taggart ◽

...

Keyword(s):

Computer Simulations ◽

Human Heart ◽

T Wave

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Reduction of repolarization reserve unmasks the proarrhythmic role of endogenous late Na+ current in the heart

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00467.2009 ◽

2009 ◽

Vol 297 (3) ◽

pp. H1048-H1057 ◽

Cited By ~ 42

Author(s):

Lin Wu ◽

Sridharan Rajamani ◽

Hong Li ◽

Craig T. January ◽

John C. Shryock ◽

...

Keyword(s):

Torsade De Pointes ◽

Polymorphic Ventricular Tachycardia ◽

Isolated Hearts ◽

T Wave ◽

Dispersion Of Repolarization ◽

Transmural Dispersion Of Repolarization ◽

Repolarization Reserve ◽

Monophasic Action Potentials ◽

Transmural Dispersion

Reduction of repolarization reserve increases the risk of arrhythmia. We hypothesized that inhibition of K+ current ( IK) to decrease repolarization reserve would unmask the proarrhythmic role of endogenous, physiological late Na+ current (late INa). Monophasic action potentials (MAP) and 12-lead electrocardiogram were recorded from female rabbit isolated hearts. To block IK and reduce repolarization reserve, E-4031, 4-aminopyridine, and BaCl2 were used; to block endogenous late INa, tetrodotoxin (TTX) and ranolazine were used. E-4031 (1–60 nM) concentration-dependently prolonged MAP duration (MAPD90) and increased duration of the T wave from Tpeak to Tend (Tpeak-Tend), transmural dispersion of repolarization (TDR), and beat-to-beat variability (BVR) of MAPD90. E-4031 caused spontaneous and pause-triggered polymorphic ventricular tachycardia [ torsade de pointes (TdP)]. In the presence of 60 nM E-4031, TTX (0.6–3 μM) and ranolazine (5–10 μM) shortened MAPD90, decreased TDR, BVR, and Tpeak-Tend ( n = 9–20, P < 0.01), and abolished episodes of TdP. In hearts treated with BaCl2 or 4-aminopyridine plus E-4031, TTX (0.6–3 μM) shortened MAPD90 and decreased Tpeak-Tend. Ranolazine could not reverse the effect of E-4031 to inhibit human ether-a-go-go-related gene (HERG) K+ current; thus, the reversal by ranolazine of effects of E-4031 was likely due to inhibition of late INa and not to antagonism of the HERG-blocking action of E-4031. We conclude that endogenous, physiological late INa contributes to arrhythmogenesis in hearts with reduced repolarization reserve. Inhibition of this current partially reverses MAPD prolongation and abolishes arrhythmic activity caused by IK inhibitors.

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Atrial septal defect patients with greater shunts show susceptibility for ventricular arrhythmias

Heart Vessels and Transplantation ◽

10.24969/hvt.2020.206 ◽

2020 ◽

Vol 4 (Issue 3) ◽

Cited By ~ 2

Author(s):

Osman Can Yontar

Keyword(s):

Ventricular Arrhythmia ◽

Atrial Septal Defect ◽

Septal Defect ◽

Ventricular Repolarization ◽

Systolic Pulmonary Artery Pressure ◽

T Wave ◽

Dispersion Of Repolarization ◽

Increased Risk ◽

Shunt Group ◽

Ventricular Arrhythmogenesis

Objective: Ventricular arrhythmia episodes are not infrequent in patients with atrial septal defect (ASD). Disturbance in cardiac volume and pressures may lead to enlargement and fibrosis in heart. An interatrial volume displacement through septal defect, briefly interatrial shunt, is the major reason for this complication. Prolongation of the interval between the peak and end of the T wave (Tpeak to Tend, Tp-e) on the 12-lead electrocardiogram (ECG), is utilized as a marker of ventricular arrhythmogenesis during last years. The aim of this study was to assess if there is an impact of shunt ratio on ventricular repolarization in patients with ASD by using Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. Methods: Patient records of Samsun Training and Research Hospital were retrospectively analyzed. Electrocardiograms of 133 patients, who were diagnosed as ASD between January 2016 and December 2019 were obtained and scanned. ECG intervals were measured. Shunt ratios, right ventricle diameters and volumes were also acquired. Patients were grouped into two by their calculated shunt ratio, ratio of ≥2.0 is accepted as a high shunt group and <2.0 as a low shunt group. Results: Both groups’ baseline characteristics were similar. Right ventricular dimensions and systolic pulmonary artery pressure were higher in high shunt group. Furthermore, ASD patients with higher shunt ratio had significantly higher ECG measurements than controls, Tp-e: 103.0 (22.1) vs 76.2 (10.2); Tp-e/QT: 0.25 (0.03) vs 0.21 (0.02); Tp-e/QTc: 0.22 (0.03) vs, 0.17 (0.02); for all p<0.001). Of all ECG parameters; Tp-e (r=0.631, p<0.001), Tp-e/QT (r=0.531, p<0.001) and Tp-e/QTc (r=0.614, p<0.001) had moderate correlation with shunt ratio. Conclusion: T wave peak-to-end interval is a measure of transmural dispersion of repolarization and accepted as a surrogate for increased ventricular arrhythmogenesis risk. Our findings show that ASD patients whose shunt ratio are ≥2.0 show increased risk for arrhythmias. Key words: atrial septal defect, electrocardiogram, ventricular arrhythmia, risk, ventricular repolarization

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