ELECTROPHYSIOLOGY
Relationship between transmural dispersion of repolarization, Tpeak–Tend interval, and ventricular arrhythmias: reply
Department of Cardiology
Second University of Naples
Naples
Second University of Naples
Via Leonardi Bianchi
Naples 8100
Italy
Tel: +33 093382841171
Fax: +33 9817064277
E-mail address: ammendolaernesto{at}libero.it
Department of Cardiology
Second University of Naples
Naples
Department of Cardiology
Monadi Hospital
Naples
Department of Cardiology
Monadi Hospital
Naples
Department of Cardiology
Monadi Hospital
Naples
Department of Cardiology
Monadi Hospital
Naples
Department of Cardiology
Second University of Naples
Naples
We thank Dr Swenne and his colleagues for their interest in our manuscript.1
Transmural dispersion of repolarization (TDR) in the heart has been linked to a variety of arrhythmic manifestations.2 Three electrophysiologically distinct cell types have been identified in the ventricular myocardium: endocardial, epicardial, and M cells. Differences in the time course of repolarization of these three ventricular myocardial cell types contribute prominently to inscription of the electrocardiographic T-wave.3 In isolated ventricular wedge preparations, the peak of the T-wave was shown to coincide with epicardial repolarization and the end of the T-wave with repolarization of the M cells, so that Tpeak–Tend provides a measure of TDR.4 Some studies have suggested that although Tpeak–Tend interval on the surface ECG may not be absolutely equivalent to TDR, this interval may provide an index of TDR and thus be helpful in forecasting risk for the development of life-threatening arrhythmias.3–7 The method for Tpeak–Tend interval measurement must also be established. Some authors measured Tpeak–Tend interval from the earliest Tpeak to the latest Tend on the 12-lead ECG;8 others selected special leads such as II, V5, an average of all leads, or ambulatory ECG to analyse Tpeak–Tend interval.9–11 Further studies are clearly required in order to define the measurement of this ECG interval, which is better correlated with TDR in humans.
Our data showed that epicardial left-ventricular (LV) pacing alone increases ventricular heterogeneity of repolarization and the risk of malignant ventricular arrhythmias compared with biventricular pacing (BiV), probably because of reversal of the physiological endocardial-to-epicardial ventricular activation.
In the BELIEVE study,12 in which 74 heart failure patients who were randomized to left-ventricular only or to bi-ventricular pacing were followed for 1 year, sudden cardiac death occurred in only two patients and comparable numbers of ventricular arrhythmia episodes were observed in LV and BiV groups. This study was not able to detect any evidence for a proarrhythmic effect of left-ventricular pacing, perhaps because most patients were treated with amiodarone.
We believe that further studies are needed to assess the influence of left-ventricular pacing on myocardial dispersion of repolarization and to evaluate whether LV pacing affects the prevalence of ventricular arrhythmias.
 |
References |
|---|
 Top References |
|---|
[1] Santagelo L, Ammendola E, Russo V, Cavallaro C, Vecchione F, Garofalo S, et al. Europace 2006; 8: 502–5.
[2] Antzelevitch C. Tpeak–Tend interval as an index of transmural dispersion of repolarization. Eur J Clin Invest 2001; 31: 555–7.[CrossRef][Web of Science][Medline]
[3] Yan GX and Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long QT syndrome. Circulation 1998; 98: 1928–36.
[4] Di Diego JM, Nesterenko VV, Antzelevitch C. Epicardial activation of left ventricular wall prolongs QT interval and transmural dispersion of repolarization: implications for biventricular pacing. Circulation 2004; 109: 2136–42.
[5] Antzelevitch C, Shimizu W, Yan GX, et al. The M cell: its contribution to the ECG and to normal and abnormal electrical function of the heart. J Cardiovasc Electrophysiol 1999; 10: 1124–52.[Web of Science][Medline]
[6] Milberg P, Reinsch N, Wasmer K, et al. Transmural dispersion of repolarization as a key factor of arrhythmogenicity in a novel intact heart model of LQT3. Cardiovasc Res 2005; 65: 397–404.
[7] Shimizu M, Ino H, Okeie K, et al. T-peak to T-end interval may be a better predictor of high-risk patients with hypertrophic cardiomyopathy associated with a cardiac troponin I mutation than QT dispersion. Clin Cardiol 2002; 25: 335–9.[Web of Science][Medline]
[8] Xia Y, Liang Y, Kongstad O, et al. Tpeak–Tend interval as an index of global dispersion of ventricular repolarization: evaluations using monophasic action potential mapping of the epi- and endocardium in swine. J Interv Card Electrophysiol 2005; 14: 79–87.[CrossRef][Web of Science][Medline]
[9] Lubinski A, Lewicka-Nowak E, Kempa M, et al. New insight into repolarization abnormalities in patients with congenital longQT syndrome: the increased transmural dispersion of repolarization. Pacing Clin Electrophysiol 1998; 21: 172–5.[CrossRef][Medline]
[10] Davey PP. QT interval measurement: Q to TApex or Q to TEnd? J Int Med 1999; 246: 145–149.[CrossRef][Web of Science][Medline]
[11] Nakagawa M, Takahashi N, Watanabe M, et al. Gender differences in ventricular repolarization: terminal Twave interval was shorter in women than in men. Pacing Clin Electrophysiol 2003; 26: 59–64.[CrossRef][Medline]
[12] Gasparini M, Bocchiardo M, Lunati M, et al. Comparison of 1-year effects of left ventricular and biventricular pacing in patients with heart failure who have ventricular arrhythmias and left bundle-branch block: the Bi vs Left Ventricular Pacing: An International Pilot Evaluation on Heart Failure Patients with Ventricular Arrhythmias (BELIEVE) multicenter prospective randomized pilot study. Am Heart J 2006; 152: 155–7.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||