BACKGROUND: T-wave morphology changes have been linked to heterogeneity of ventricular repolarization and increase of arrhythmia vulnerability. Therefore, century-long debates around the genesis of T wave become even more relevant. Here are some interesting questions for the debates: (1) why T waves are usually concordant with QRS complex? (2) Is there a significant and consistent transmural dispersion of repolarization across heart wall? (3) What kind of T-wave morphology changes can be induced by either transmural or apical-basal dispersion of repolarization? METHOD: The previously developed GE's cell-to-electrocardiogram (ECG) model (GE Healthcare, Milwaukee, WI) was used to study the relation between cellular behavior and the T-wave morphology. The study focused on 2 types of repolarization dispersions: (1) Transmural (from endocardium to epicardium) and (2) Apical-basal (from apex to base of ventricles). More specifically, the transmural dispersions were created by adjusting the slow and fast delayed potassium rectifier current (Iks, Ikr) and transient outward current (Ito), on endocardial, midmyocardial (M cell) and epicardial cells separately. The apical-basal dispersion was adjusted according to the coordinates along the axis from the base to the apex of the ventricle. The contribution of M cell toward T-wave morphology were studied by adjusting the M cell's repolarization time in the range of shorter to longer than those of endocardial repolarization time. RESULTS: In the global transmural dispersion cases, QT interval is prolonged from 350 to 450 milliseconds, T-peak to T-end interval (TpTe) is prolonged from 50 to 130 milliseconds, and T-wave notches appeared when the heterogeneity is increased. In the localized transmural dispersion cases, significant T-wave morphology features such as TpTe, T-wave notches appeared in very limited precordial leads. In the global apical-basal dispersion cases, main T-wave change is on the amplitude, and T waves in several precordial leads and lead II turn to positive from negative. And the localized apical-basal dispersion does not generate significant T-wave morphology changes. CONCLUSIONS: The cell-to-ECG model provides a unique way to study electrophysiology and to link physiologic factors to ECG morphology changes. The simulation results suggest that the apical-basal dispersion of repolarization contributes to positive T wave more than the transmural dispersion. The contribution of localized transmural dispersion to surface ECG is very much localized to certain precordial leads.
BACKGROUND: T-wave morphology changes have been linked to heterogeneity of ventricular repolarization and increase of arrhythmia vulnerability. Therefore, century-long debates around the genesis of T wave become even more relevant. Here are some interesting questions for the debates: (1) why T waves are usually concordant with QRS complex? (2) Is there a significant and consistent transmural dispersion of repolarization across heart wall? (3) What kind of T-wave morphology changes can be induced by either transmural or apical-basal dispersion of repolarization? METHOD: The previously developed GE's cell-to-electrocardiogram (ECG) model (GE Healthcare, Milwaukee, WI) was used to study the relation between cellular behavior and the T-wave morphology. The study focused on 2 types of repolarization dispersions: (1) Transmural (from endocardium to epicardium) and (2) Apical-basal (from apex to base of ventricles). More specifically, the transmural dispersions were created by adjusting the slow and fast delayed potassium rectifier current (Iks, Ikr) and transient outward current (Ito), on endocardial, midmyocardial (M cell) and epicardial cells separately. The apical-basal dispersion was adjusted according to the coordinates along the axis from the base to the apex of the ventricle. The contribution of M cell toward T-wave morphology were studied by adjusting the M cell's repolarization time in the range of shorter to longer than those of endocardial repolarization time. RESULTS: In the global transmural dispersion cases, QT interval is prolonged from 350 to 450 milliseconds, T-peak to T-end interval (TpTe) is prolonged from 50 to 130 milliseconds, and T-wave notches appeared when the heterogeneity is increased. In the localized transmural dispersion cases, significant T-wave morphology features such as TpTe, T-wave notches appeared in very limited precordial leads. In the global apical-basal dispersion cases, main T-wave change is on the amplitude, and T waves in several precordial leads and lead II turn to positive from negative. And the localized apical-basal dispersion does not generate significant T-wave morphology changes. CONCLUSIONS: The cell-to-ECG model provides a unique way to study electrophysiology and to link physiologic factors to ECG morphology changes. The simulation results suggest that the apical-basal dispersion of repolarization contributes to positive T wave more than the transmural dispersion. The contribution of localized transmural dispersion to surface ECG is very much localized to certain precordial leads.
Authors: Julia Ramírez; Michele Orini; Ana Mincholé; Violeta Monasterio; Iwona Cygankiewicz; Antonio Bayés de Luna; Juan Pablo Martínez; Esther Pueyo; Pablo Laguna Journal: J Am Heart Assoc Date: 2017-05-19 Impact factor: 5.501