Transmural dispersion of repolarization and atrial electromechanical coupling: complementary indices for quantifying cardiac electrical heterogeneity in patients with conversion disorder.

Abstract

Dear editor We read with great interest the article entitled “P-wave and QT dispersion in patients with conversion disorder” by Izci et al1 in Therapeutics and Clinical Risk Management. In this well designed research, Izci et al studied QT dispersion (QTd) and P-wave dispersion (Pd) in patients with conversion disorder (CD). In conclusion, they reported that corrected QT (QTc) and QTd values were significantly altered in patients with CD when compared to healthy controls, but that there was no significant difference in terms of Pd. It has been postulated that the relationship between somatoform disorders and CD is related to altered autonomic functions.2 These changes may affect the refractory period and conduction velocity of the heart. In line with these assumptions, heterogeneity in the duration of the ventricular repolarization phase leading to arrhythmias may also be seen in patients with CD. As in this study, QTd is the most frequently used parameter to detect ventricular inhomogeneity. However, reproducibility of QT interval measurements is low in both manual and automatic measurements and interobserver and intraobserver variability of QTd is very high.3,4 Quantifying the inhomogeneity of the myocardium, transmural dispersion of repolarization (TDR) has also been used since the beginning of the 2000s in addition to QTd.5 There are three types of myocyte, ie, endocardial, epicardial, and midmyocardial M cells, each having different electrophysiological properties in the ventricular myocardium. Mid-myocardial M cells have typically the longest repolarization phase. The repolarization phase of the midmyocardial M cells continues until the end of the T-wave. However, the repolarization phase of the 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, and is an index of the TDR.5 In addition, the Tp-e/QT ratio has also been used as an electrical dispersion index for the myocardium, showing arrhythmic risk. The role of the TDR in evaluation of 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.6 On the other hand, the basic electrophysiological characteristics of the atrium that predispose to atrial arrhythmias are prolongation of intra-atrial and interatrial conduction times and heterogeneous propagation of sinus impulses. Pd is an accepted marker of atrial depolarization heterogeneity and the altered propagation of sinus impulses found to be associated with increased risk of atrial fibrillation. Although prolonged Pd values were found to be correlated with atrial fibrillation, it is controversial whether Pd is related to heterogeneity of atrial conduction or to other factors. Furthermore, reproducibility of P-wave measurements is low in both manual and automatic measurements and interobserver and intraobserver variability is very high. Atrial electromechanical coupling (AEC) can be assessed by electrocardiography-integrated tissue Doppler imaging and provides a means to determine the atrial mechanical and electrical event. Analysis of AEC by tissue Doppler imaging allows precise analysis of AEC between different regions. Moreover, measurement of AEC may suggest an inhomogeneous propagation of sinus impulses in different cardiac sites. Autonomic dysregulation and altered sympathovagal balance, as in somatoform disorders, may account for heterogeneity in atrial conduction properties. Measurement of AEC has been done in patients with psoriasis, ankylosing spondylitis, hyperthyroidism, end-stage renal disease, and hypertension.7–9 Regarding these observations, autonomic imbalance may cause atrial depolarization and sinus impulse propagation abnormalities leading to altered AEC. Our opinion is that, if AEC intervals had been measured in this study, they may have been found to be altered in patients with CD. Further, regarding the forementioned observations, if Izci et al had measured the Tp-e interval and Tp-e/QT ratio in their study, they might have found an increased TDR in their patients with CD. Considering all the data about Pd, AEC, QTd, and TDR, their study might have revealed the effects of CD on electrical heterogeneity of the myocardium more completely in many respects.