Elsevier

Journal of Electrocardiology

Volume 41, Issue 6, November–December 2008, Pages 575-580
Journal of Electrocardiology

The meaning of the Tp-Te interval and its diagnostic value

https://doi.org/10.1016/j.jelectrocard.2008.07.030Get rights and content

Abstract

Background

The interval between T peak (Tp) and T end (Te) has been proposed as a measure of transmural dispersion of repolarization, but experimental and clinical studies to validate Tp-Te have given conflicting results. We have investigated the meaning of Tp-Te and its diagnostic potential.

Methods

We used a digital model of the left ventricular wall to simulate the effect of varying action potential durations on the timing of Tp and Te. Furthermore, we used the vectorcardiogram to explain the relationships between Tp locations in the precordial electrocardiogram leads.

Results

Prolongation or ischemic shortening of action potentials in our model did not result in substantial Tp shifts. The phase relationships revealed by the vectorcardiogram showed that Tp-Te in the precordial leads is a derivative of T loop morphology.

Conclusion

Tp-Te is the resultant of the global distribution of the repolarization process and is a surrogate diagnostic parameter.

Introduction

Increased dispersion of repolarization, the disturbance of the normal orderly pattern of ventricular recovery, is generally thought to predispose to ventricular arrhythmias. It is, therefore, most desirable to be able to read the subtle signs in the ST-T that might foretell trouble. QT dispersion was hailed as such a sign but finally had to be dismissed as an erroneous concept.1, 2 Now the interval between the peak of the T wave (Tp) and the end of the T wave (Te) is being proposed with the same intent.

The idea was born in the realm of left ventricular cellular electrophysiology. Haws and Lux3 measured that the end of repolarization (EOR) as estimated from pericardial unipolar electrograms approximately coincided with the end of a single given intracellular action potential (AP). The relation between intracellular APs and the electrocardiographic T wave was investigated in greater detail by Yan and Antzelevitch4 with the use of left ventricular wedge preparations. They recorded APs separately from the subendocardial, midmyocardial, and subepicardial layers synchronously with a bipolar “pseudo” electrocardiogram (ECG) straddling the preparation. The APs from the midmyocardium had the longest duration, presumably produced by the M cells earlier described by Sicouri and Antzelevitch.5 The peak of T in the pseudo ECG aligned with the end of the epicardial AP, the earliest completion of repolarization in the ventricular wall, and the end of T aligned with the end of the midmyocardial AP, the total conclusion of repolarization. The Tp-Te interval was, therefore, taken to be a reflection of the transmural dispersion of repolarization (TDR). When an ECG was constructed from the potential differences between the APs, it matched the actually recorded pseudo ECG.

It is quite a step from the wedge preparation to the in vivo experiment, where TDR is measured in the whole heart and its imprint on the ECG is examined in a regular surface ECG. In some studies (eg, Bai et al6), the findings of Antzelevitch were confirmed, but contrary results emerged from other studies. Xia et al7 report that, in pigs, the earliest EOR as well as the latest EOR are both found in the endocardium. In the precordial leads, Te more or less coincides with the latest endocardial EOR and Tp with the earliest endocardial EOR. Tp-Te, therefore, is not a measure of transmural but of global (apico-basal) dispersion of repolarization. In their experiments, there is no role for M cells, which might even be absent from the porcine myocardium altogether. Similar conclusions are reached by Opthof et al.8 In open chest dogs, they performed endocardial, epicardial, and intramural mapping of repolarization times, defined as the sum of activation time and activation-recovery interval. The mean difference in local repolarization times between endocardium and epicardium was only 2.7 milliseconds in normal dogs, increasing to 14.5 milliseconds in so-called memory dogs, pretreated with 3 weeks of ventricular pacing. Tp-Te in the surface ECG (lead II) measured 42 milliseconds in both groups and therewith clearly exceeded any TDR but appeared tightly correlated with global dispersion of repolarization, defined as the difference between earliest and latest moment of repolarization at any myocardial recording site. No midmyocardial zone of latest repolarization was found. In all dogs, epicardial repolarization lagged behind endocardial repolarization, and Tp in lead II coincided with the average EOR of the right ventricle.

Matters are compounded by the fact that measurement of Tp-Te is far from straightforward and coherent instructions for its measurement are lacking. The problems arise as soon as the T wave deviates from the standard form. Must a flat ST-T be simply ignored? What to do with a biphasic T? What if the T wave gradually changes sign across the leads? Is the maximum ST-T negativity equivalent to a Tp?

However unsettled the issues still are, clinical studies have already appeared that say that increased Tp-Te is associated with a heightened tendency to, or an enhanced inducibility of, ventricular tachycardia and, consequently, may be seen as a sign of a harmful dispersion of repolarization.9, 10 Oddly enough, a shorter Tp-Te (averaged over V4-V6) went along with increased cardiovascular mortality in a study by Smetana et al.11

The present study is an attempt to explain and perhaps reconcile these conflicting findings. We investigated the meaning of Tp-Te and its diagnostic potential by 2 different methods. Firstly, a digital model of the left ventricular wall served to simulate the effect of varying AP durations on the timing of Tp. Secondly, the vectorcardiogram (VCG) was called to assistance for understanding the behavior of Tp-Te in the precordial ECG leads.

Section snippets

The digital ventricular model

Our model has been described previously.12 Briefly, it represents a stylized apico-basal slice of the left ventricle, containing 1961 hexagonal cells in a single sheet (Fig. 1). To each of the 12 cell layers from endocardium to epicardium, an AP is assigned of specified shape and duration. The timing of the APs follows a simulated excitation sequence, with a difference of 72 milliseconds between the earliest and the latest excitation of the cells. Between subendocardium and subepicardium, the

Model simulation of pathologic conditions

Fig. 2 shows the effect of 3 “ischemic” areas on the ECG produced in an observation point about 3 cm from the epicardial wall, at an angle of 78° with the long axis of the ventricular slice (about the direction of lead V2). In the midmyocardium, shortening of the AP by even up to 80 milliseconds and expanding the number of “ischemic” layers to encompass the whole midmyocardium does not produce a time shift of Tp, although its amplitude is reduced by almost a third. In the subepicardial

Discussion

The literature regarding the presence of a midmyocardial zone of increased AP duration is controversial. In our model, such a zone is embedded. Although the model complies with the M cell concept,13 it contradicts the premise that local TDR is responsible for an increase in Tp-Te in the local ECG. In the model, Tp-Te does not react to even extensive ischemia in a sector of the midmyocardium. According to Antzelevitch et al,13 the end of epicardial repolarization coincides with Tp, but, in the

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    The Tp-e interval is only a parameter that shows the distribution of the repolarization process. Therefore, the Tp-e interval may reflect the transmural distribution of repolarization [7]. The increase in Tp-e/QT ratio and Tp-e interval in a standard ECG has been determined in many studies as an indicator of cardiac arrhythmia risk and has been defined and used as an electrocardiographic index of ventricular arrhythmogenesis [8].

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