A complementary index for quantification of cardiac electrical dispersion: transmural dispersion of repolarization.

To the Editor,

We read the article titled “Influence of the left ventricular types on QT intervals in hypertensive patients” by Kunisek et al. (1) published in the January issue of Anatol J Cardiol with great interest. In this well-designed research, the authors investigated the effects of left ventricular hypertrophy (LVH) types on cardiac repolarization parameters and severity of ventricular arrhythmias using 12-lead ECG and ambulatory ECG monitoring in hypertensive subjects. In conclusion, they reported that the repolarization parameters of QT interval (QTI) duration, corrected QT interval (QTc), and QT dispersion (QTd) are not affected by the degree and type of LVH. Meanwhile, they found that QTd was significantly and QTI non-significantly increased in male patients with severe concentric and eccentric hypertrophy. In addition, they revealed that QTI was significantly prolonged in subjects with complex ventricular arrhythmias (Lown III-V) compared with that in subjects with simple ventricular arrhythmias (Lown I-II).

Heterogeneity in the duration of the cardiac repolarization phase causes electrical instability, leading to arrhythmias. As used in this study, QTd is the most frequently used parameter to detect ventricular inhomogeneity. The reproducibility of QTI measurements is low both in manual and automatic measurements, and the inter-and intra-observer variability of QTd is very high.

There are three myocyte types having different electrophysiological properties in the ventricular myocardium: endocardial, epicardial, and midmyocardial M cells. Midmyocardial M cells typically have the longest repolarization phase. The repolarization phase of midmyocardial M cells continues until the end of the T wave. On the other hand, the repolarization phase of epicardial cells ends at the peak of the T wave. The time between the peak and end of the T wave is known as the Tp–e interval, as an index of transmural dispersion of repolarization (TDR) (2). In addition, the Tp-e/QT ratio has also been used as an electrical dispersion index of the myocardium, showing the arrhythmic risk. The role of TDR in evaluation of the arrhythmic risk has been demonstrated in coronary artery disease and in the Brugada, short QT, and long QT syndromes. Previously, we showed that the Tp-e interval was increased in patients with obstructive sleep apnea and chronic arsenic exposure via drinking water (3, 4). Increased TDR has also been demonstrated in subjects with hypertension and ventricular hypertrophy (5). Regarding these observations, increased left ventricular mass causes repolarization heterogeneity, leading to increased TDR. This situation suggests that the thickened layer of the heart is mostly the midmyocardial layer, which leads to prolongation of the Tp–e interval. In their study, Kunisek et al. (1) divided the study population into nine groups according to the severity and type of LVH. Alterations in left ventricular geometry may influence TDR. We believe that if it was measured in this study, TDR may have been found to be increased in some groups. Thus, considering all the data about QTI, QTd, and TDR, the study may have completely illuminated the effects of LVH types on the electrical heterogeneity of the myocardium in many respects.