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

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          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.

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          Most cited references 22

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          P-wave dispersion: a novel predictor of paroxysmal atrial fibrillation.

           Polychronis E Dilaveris (corresponding) ,  John E Gialafos (2006)
          The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with a clinical history of paroxysmal AF show a significantly increased P-wave duration in 12-lead surface electrocardiograms (ECG) and signal-averaged ECG recordings. The inhomogeneous and discontinuous atrial conduction in patients with paroxysmal AF has recently been studied with a new ECG index, P-wave dispersion. P-wave dispersion is defined as the difference between the longest and the shortest P-wave duration recorded from multiple different surface ECG leads. Up to now the most extensive clinical evaluation of P-wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensives, in patients with coronary artery disease and in patients undergoing coronary artery bypass surgery. P-wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, no electrophysiologic study has proven up to now the suspected relationship between the dispersion in the atrial conduction times and P-wave dispersion. The methodology used for the calculation of P-wave dispersion is not standardized and more efforts to improve the reliability and reproducibility of P-wave dispersion measurements are needed. P-wave dispersion constitutes a recent contribution to the field of noninvasive electrocardiology and seems to be quite promising in the field of AF prediction.
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            Transmural dispersion of repolarization and ventricular tachyarrhythmias.

            Myocardial transmural dispersion of repolarization (TDR) has been associated with reentrant arrhythmias in animal studies but a clinical association has not yet to been demonstrated. The present study examines the relationship between TDR and ventricular tachyarrhythmias in human subjects. This study consisted of 65 patients with non-sustained ventricular tachycardia, sustained ventricular tachycardia, ventricular fibrillation or unexplained syncope with organic heart disease. The control group included 65 patients with paroxysmal supraventricular tachycardia. The 12 ECG was recorded at a recording rate of 100 mm/sec. The interval from the peak to the end of the T wave in the precordial (ECG), referred to as TpTe was assumed to be representative of TDR. Patients were divided into three groups based on the ability to induce VT at the time of electrophysiologic study: VT inducible group (n=37), VT non-inducible group (n=25) and control group (n=65). V4 TpTe/ radical RR was significantly prolonged in the VT inducible group, as compared to the VT non-inducible group (n=25) and the control group (118.9 +/- 26.1 vs. 103.9 +/- 25.7, 104.1 +/- 22.6 ms, P<.05). Patients who develop VT spontaneously (n=13) during a mean follow-up period of 25 months, displayed significantly prolonged V3 TpTe/ radical RR, compared to patients who did not develop VT spontaneously or the control group (132.5 +/- 37.4 vs. 109.8 +/- 26.3, 107.1 +/- 24.1 ms, P <.05). Prolonged TDR is associated with inducibility as well as spontaneous development of VT in higher risk patients. TDR may be a useful index for predicting ventricular tachyarrhythmias.
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              Dispersion of QT interval in patients with and without susceptibility to ventricular tachyarrhythmias after previous myocardial infarction.

              The aim of this study was to estimate the value of QT dispersion measurement from the standard 12-lead electrocardiogram (ECG) in identifying patients susceptible to reentrant ventricular tachyarrhythmias after a previous myocardial infarction. Variability in QT interval duration on the different leads of the 12-lead ECG has been proposed as an indicator of risk for ventricular arrhythmias in different clinical settings, but the value of QT dispersion measurement in identifying patients at risk for reentrant ventricular tachyarrhythmias after myocardial infarction is not known. The QT interval duration, QT dispersion and clinical and angiographic variables were compared between 30 healthy subjects; 40 patients with a previous myocardial infarction but no history of arrhythmic events or inducible ventricular tachycardia during programmed electrical stimulation; and 30 postinfarction patients with a history of cardiac arrest (n = 12) or sustained ventricular tachycardia (n = 18) and inducible, sustained monomorphic ventricular tachycardia by electrical stimulation. Dispersion of the corrected QT interval (QTc) differed significantly between the study groups and was significantly increased in patients with susceptibility to ventricular tachyarrhythmias ([mean +/- SD] 104 +/- 41 ms) compared with that in both healthy subjects (38 +/- 14 ms, p < 0.001) and postinfarction patients with no susceptibility to arrhythmias (65 +/- 31 ms, p < 0.001). Maximal QT interval duration was also prolonged in the group with arrhythmias compared with that in the other groups (p < 0.001). Multivariate analysis, including clinical and angiographic variables, QT dispersion and maximal QT interval, showed that QT dispersion was the independent factor that most effectively identified the patient groups with and without susceptibility to ventricular tachyarrhythmias (p < 0.001). Increased QT dispersion is related to susceptibility to reentrant ventricular tachyarrhythmias, independent of degree of left ventricular dysfunction or clinical characteristics of the patient, suggesting that the simple, noninvasive measurement of this interval from a standard 12-lead ECG makes a significant contribution to identifying patients at risk for life-threatening arrhythmias after a previous myocardial infarction.

                Author and article information

                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                20 July 2015
                : 11
                : 1077-1080
                [1 ]Department of Cardiology, Golcuk Military Hospital, Kocaeli, Turkey
                [2 ]Department of Cardiology, GATA Haydarpasa Hospital, Medipol University, Istanbul, Turkey
                [3 ]Department of Cardiology, Medipol University, Istanbul, Turkey
                [1 ]Department of Psychiatry, Istanbul Bilim University, School of Medicine, Istanbul, Turkey
                [2 ]Department of Emergency, Faculty of Medicine Hospital, Zonguldak Bulent Ecevit University, Zonguldak, Turkey
                [3 ]Department of Cardiology, Kartal Kosuyolu High Specialization Training and Research Hospital, Istanbul, Turkey
                [4 ]Department of Psychiatry, Erenköy Training and Research Hospital for Psychiatry, Istanbul, Turkey
                [5 ]Department of Emergency, Kartal Training and Research Hospital, Istanbul, Turkey
                Author notes
                Correspondence: Alptug Tokatli, Golcuk Asker Hastanesi, Kardiyoloji Servisi, 12 Donanma Street, Golcuk, Kocaeli 41910, Turkey, Tel +90 26 2426 0271, Fax +90 26 2414 1111, Email alptugtokatli@ 123456gmail.com
                Correspondence: Filiz İzci, İstanbul Bilim Üniversitesi, Tıp Fakültesi, Psikiyatri ABD, Abide-i Hürriyet Cad 164. Şişli, I˙stanbul, Turkey, Tel +90 21 2224 4966, Fax +90 21 2291 1245, Email filizizci@ 123456yahoo.com
                © 2015 Tokatli et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.




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