Electrocardiographic T Wave and its Relation With Ventricular Repolarization Along Major Anatomical Axes

Abstract

Background— The genesis of the electrocardiographic T wave is incompletely understood and subject to controversy. We have correlated the ventricular repolarization sequence with simultaneously recorded T waves. Methods and Results— Nine pig hearts were Langendorff-perfused (atrial pacing, cycle length 650 ms). Local activation and repolarization times were derived from unipolar electrograms sampling the ventricular myocardium. Dispersion of repolarization time was determined along 4 anatomic axes: left ventricle (LV)–right ventricle (RV), LV:apico-basal, LV:anterior-posterior, and LV:transmural. The heart was immersed in a fluid-filled bucket containing 61 electrodes to determine T p (T peak in lead of maximum integral), T p T e (T p to T end ), and T p T e _total (first T peak in any lead to last T end in any lead). Repolarization was nonlinearly distributed in time. RT 25 (time at which 25% of sites were repolarized, 288±26 ms) concurred with T p . T p T e was 38±8 ms, and T p T e _total was 75±9 ms. T p T e _total correlated with dispersion of repolarization time in the entire heart (73±18 ms), but not with dispersion of repolarization times along individual axes (LV–RV, 66±17 ms; LV:apico-basal, 51±18 ms; LV:anterior-posterior, 51±27 ms; mean LV:transmural, 14±7 ms; all n=9). Conclusions— We provide a correlation between local repolarization and T wave in a pseudo-ECG. Repolarization differences along all anatomic axes contribute to the T wave. T p T e _total represents total dispersion of repolarization. At T p , ≈25% of ventricular sites have been repolarized.

Experimental Validation of Noninvasive Epicardial and Endocardial Activation Imaging

“…7,27 Also in the in situ setting, we were able to reliably map ventricular paced activation. The EDL inverse was highly accurate (85%) in discriminating endocardial from epicardial origin of activation, despite the positional error (18 [15][16][17][18][19][20][21][22][23][24][25][26][27] mm) being larger than the average wall thickness (≈5 mm for the right ventricle and 10 mm for the left ventricle). This can be explained by the fact that the surface at which activation originates does not only affect the socalled initial vector of the ECG, but also changes the shape and direction of the transmural activation wavefront later in the QRS complex.…”

“…15,25 However, low transmural dispersion will also augment the relative error introduced by the limited resolution of our triangulated ventricular geometry. To remove this effect from the initial estimate, we used an artificially high transmural conduction velocity set to 100× the velocity along the wall for the anisotropic part of the propagation model.…”

“…Figure 5 shows the QRS complexes of a BSM recorded during sinus rhythm, together with the calculated activation map and the catheter-derived activation times (4 endocardial and 15 epicardial sites). The absolute differences between calculated and measured activation times were 11±5 ms (54 mainly posterior sites) and 5±3 ms (19 lateral and posterior sites; Figure 5) for the 2 catheter mappings, (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27) mm. In Figure 6, examples of QRS complexes and calculated activation times are shown for endocardial ( Figure 6A) and epicardial stimulation ( Figure 6B).…”

“…Locations of the needle electrodes within the heart were determined from the observed needle path after dissection of the heart. For more detailed methods, see Meijborg et al 15 We analyzed recordings of sinus rhythm or atrial-paced, atrioventricular-conducted rhythm (both further referred to as sinus rhythm) and of spontaneous ventricular ectopic activations. …”

Action potential duration gradients in the heart ventricles and the cardiac electric field during ventricular repolarization (a model study)

“…In the period of repolarization, the voltage gradients in the heart ventricles resulted from the differences in action potential duration (APD) and the differences in activation times between the different parts of the ventricles [1]. Experiments revealed transmural, apicobasal, left-to-right and anteriorposterior APD gradients in the heart ventricles with the magnitude of these gradients being different in various species or conditions [2][3][4][5][6]. All these gradients could contribute to the T-wave; however, there is no consensus on which one is the most significant in the development of the T-wave.…”