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Exp Clin Cardiol. 2001 Winter; 6(4): 179–182.
PMCID: PMC2858996
Experimental Cardiology

Value of QT dispersion in evaluating spatial dispersion of ventricular repolarization during acute myocardial ischemia

Chuan Yong Li, BS MS PhD,1 Lin Zhuang Jia, BS MS,1 and Lexin Wang, MD PhD2



To study the value of epicardial QT interval dispersion in predicting ischemia-induced heterogeneity of ventricular repolarization.


Ischemia was produced by total occlusion of the obtuse branch of the circumflex coronary artery in seven open-chest sheep. A 64-channel electrocardiogram (ECG) was acquired from the epicardium before and after coronary artery occlusion. Wavelet transformation was used to determine the characteristic points of the epicardial ECGs, and to measure the QT interval and activation-recovery interval (ARI) and their dispersions.


The average QT interval and ARI from the epicardial ECG were not changed by acute myocardial ischemia (P=0.07 and P=0.13, respectively). QT dispersion remained unchanged during ischemia (P=0.17), whereas ARI dispersion was significantly increased by acute ischemia (59.9±24.0 ms versus 126.3±32.1 ms, P<0.001).


These findings indicate that epicardial QT dispersion is less sensitive than ARI dispersion in estimating repolarization heterogeneity induced by acute myocardial ischemia.

Keywords: Activation-recovery interval dispersion, Heterogeneity, Ischemia, QT dispersion, Ventricular repolarization

Great effort has been made to develop a sensitive and reliable method to assess ventricular repolarization. QT dispersion on body surface electrocardiogram (ECG) has been used to predict heterogeneity of ventricular repolarization and incidence of fatal ventricular arrhythmias in patients with acute myocardial ischemia (14). Although some studies showed that QT dispersion on body surface ECG represents repolarizarion inhomogeneity evaluated by monophasic action potentials (5,6), other studies questioned the value of QT dispersion in representing the repolarization heterogeneity (711). Using a dog heart in an artificial volume conductor, Macleod et al (7) and Lux et al (8) measured epicardial and body surface ECG, and found that epicardial and body surface QT dispersion cannot reflect local repolarization changes caused by temperature difference. Wang (9) recorded 64 epicardial ECGs and 12-lead surface ECG simultaneously in sheep, and found that body surface QT dispersion does not adequately reflect the spatial dispersion of ventricular repolarization measured from the epicardium. Furthermore, some clinical studies showed that QT dispersion is not a good predictor of arrhythmia risk for patients (10,11).

The physiological meaning of QT dispersion from the epicardial ECG is unclear. The aim of this study was to investigate whether QT dispersion measured from the epicardium is related to the dispersion of the activation recovery interval (ARI), an index of ventricular repolarization (12,13), during acute myocardial ischemia.


Data acquisition:

Seven sheep were anesthetized with pentobarbital (30 mg/kg intravenous infusion, followed by 2 to 3 mg/min intravenous infusion). Transmural ischemia was induced by permanent occlusion of the obtuse marginal branch of the left circumflex coronary artery. This regional ischemia increases the spatial heterogeneity of the recovery time of the heart (14). Unipolar ECGs were recorded from the epicardium using a 64-electrode sock (Cardiovascular Research and Training Institute, University of Utah, USA). The 64-channel ECGs were obtained at 1 Ks/s by using a 120-channel data acquisition system. The recordings were made before and 10 min after the coronary artery ligation.

QT and ARI measurements:

QRS and T waves were extracted from an epicardial ECG that was processed by a wavelet transformation (15,16). The purpose of the wavelet transformation is to analyze the signal at various resolutions by decomposing it into wavelets that are well localized both in time and in frequency domains. It can characterize the local regularity of the signal, and this feature can be used to distinguish ECG waves from serious noise, artefacts and baseline drift, and to enhance the different ECG waves by transformation at a different scale. A quadratic spline wavelet at a 21 scale behaves as a band pass filter suitable for the QRS complex, while that at a 25 scale behaves as a band pass filter suitable for the T wave (17). Thus, a quadratic spline wavelet was used, and the wavelet transformation of the epicardial ECG at a 21 scale was used to extract the QRS complex and that at a 25 scale to extract the T wave (Figure 1). The QT interval was defined as the interval between the beginning of the Q wave and the end of the T wave. The ARI interval was defined as the time interval between activation time (the point with the most negative slope on the QRS complex) and the recovery time (the point with the most positive slope in the T wave) (12,13). For each sheep, QT or ARI was represented by the average value of 64 ECG channels. The algorithm based on wavelet transformation was developed to automatically determine QT and ARI intervals channel by channel.

Figure 1
Quadratic spline wavelet transformation of an electrocardiogram (ECG) at different scales. (a) Original ECG; (b) Transformation at a 21 scale; (c) Transformation at a 25 scale

QT and ARI dispersion was defined as the difference between the maximum and the minimum values in each sheep. MatLab (The MathWorks, Inc, USA) was used to implement all the programming and computing of this study.

Statistical analysis:

Control and ischemic animals were compared by two-tailed Student’s t test, with P<0.05 being considered statistically significant.


QT and ARI intervals:

Figure 2 shows the average values of QT interval and ARI in each animal. The mean QT interval of the seven sheep increased from 300.5±41.8 ms to 327.2±39.6 ms during ischemia (P=0.07), whereas the aver-age value of ARI increased from 240.8±31.8 ms to 257.3±34.2 ms (P=0.13). Table 1 lists the longest QT interval and ARI before and during ischemia.

Figure 2
QT interval (A) and activation-recovery interval (ARI) (B) in control and ischemic groups
Longest QT interval and activation-recovery interval (ARI) before and during ischemia in sheep

Dispersions of QT interval and ARI:

QT dispersion was increased in only three of the seven animals (Figure 3). The average of the pooled QT dispersion values in the seven animals was 48.0±6.7 ms before and 55.9±12.6 ms after coronary occlusion (P=0.17). ARI dispersion increased during ischemia in all animals (Figure 3). The average ARI dispersion in the seven animals increased from 59.9±24.0 ms to 126.3±32.1 ms (P<0.001).

Figure 3
QT interval (A) and activation-recovery interval (ARI) (B) dispersion in control and in ischemic groups


This study has shown that ARI dispersion is increased by acute myocardial ischemia, indicating an increased heterogeneicity of ventricular repolarization. However, the degree of change in epicardial QT dispersion is largely variable among animals, and the average QT dispersion in the seven animals remained unchanged during ischemia. This suggests that epicardial QT dispersion is not sensitive in detecting the ischemia-induced alterations in ventricular repolarization. This may partially explain why body surface QT dispersion is not always associated with the inhomogeneity of ventricular depolarization (911).

The epicardial QT interval is measured in the same way as the body surface QT interval, which is from the beginning of the QRS complex to the end of the T wave. The physiological meaning of the QT interval acquired from unipolar epicardial ECG is poorly understood, but it is generally considered to approximate the time from the earliest depolarization of the ventricular myocardium to its latest repolarization. Although prolongation of the QT interval or an increase in QT dispersion may reflect increased inhomogeneity of myocardial re-polarization, it can also be caused by a nonuniform increase in action potential duration. QT intervals from the same epicardial sites are longer than the actual duration of repolarization; therefore, QT dispersion may not reflect the nonuniformity of ventricular recovery time. This is supported by the reports of Macleod et al (7) and Lux et al (8) that epicardial QT intervals have no association with actual ventricular recovery time.

Epicardial ARI is another measure of ventricular recovery time. The activation and recovery time of ARI represents the beginning and the end of action potential; therefore, the value of ARI is close to the action potential duration measured from the same epicardial sites (12,13). ARI is also closely correlated with ventricular refractory time (12). The significant increase in ARI dispersion seen in our study is consistent with the ample evidence that acute ischemia enhances heterogeneity of ventricular repolarization (18,19), an important mechanism of arrhythmogenesis.

In conclusion, epicardial ARI dispersion is increased by acute myocardial ischemia. Ventricular repolarization heterogeneity induced by ischemia is less likely to be detected by epicardial QT interval dispersion. The potential clinical implication of the study is that ARI dispersion, rather than QT dispersion, should be the preferred index for future clinical studies of ventricular heterogeneity and associated arrhythmic risk in ischemic patients.


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