CRT
Biventricular pacing and transmural dispersion of the repolarization
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Tel: +31 71 526 1972
Fax: +31 84 221 8904
E-mail address: c.a.swenne{at}lumc.nl
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
Department of Cardiology
Leiden University Medical Center
PO Box 9600
2300 RC Leiden
The Netherlands
In 2003, Medina-Ravell et al.1
published a study that suggested that biventricular pacing could be arrhythmogenic in a subset of patients because of the reversal of the normal endocardial-to-epicardial activation sequence by left-ventricular epicardial pacing. As epicardial action potentials are briefer than endocardial action potentials, transmural dispersion of the repolarization (TDR) is larger with an epicardial-to-endocardial activation sequence than with an endocardial-to-epicardial activation sequence. Medina-Ravell et al. demonstrated this in an isolated arterially perfused rabbit left-ventricular wedge preparation. They also showed, in a quasi-ECG derived from this preparation, that TDR was faithfully reflected by the Tpeak-end interval and that Tpeak-end was larger with epicardial pacing than with endocardial pacing of the preparation. Their conclusion that a similar effect occurs in intact hearts in humans was substantiated by the observation that in 29 heart failure patients with a biventricular pacemaker, the Tpeak-end interval was larger during left-ventricular epicardial pacing than during right-ventricular endocardial pacing. However, no Tpeak-end values with sinus rhythm and with biventricular pacing were reported, due to measurement difficulties.
With interest, we read the recently published study by Santangelo et al.2 They describe how left-ventricular, right-ventricular, and bi-ventricular pacing in heart failure patients influences a number of ECG indexes of ventricular dispersion of the repolarization, among others the Tpeak-end interval. Compared with sinus rhythm, the Tpeak-end interval increased with left-ventricular epicardial and with right-ventricular endocardial pacing, but it decreased with bi-ventricular pacing. The observations by Santangelo et al. confirm nicely the findings of our recent study3 in which we evaluated, in a similar way, the effect of left-, right-, and bi-ventricular pacing on a set of ECG indexes thought to represent ventricular dispersion of repolarization, among which was Tpeak-end. We also found the briefest Tpeak-end interval to occur with biventricular pacing.
What should be the conclusion from these observations? Medina-Ravell et al.1 conclude that, in their patients, epicardial left-ventricular pacing increases TDR with respect to right-ventricular pacing, because the Tpeak-end interval is the largest with left-ventricular pacing. Santangelo et al.2 conclude, among others, on the basis of the behaviour of the Tpeak-end interval, that left-ventricular and right-ventricular pacing increase TDR with respect to sinus rhythm, whereas bi-ventricular pacing decreases TDR. The implications of such a conclusion would be that any single-lead ventricular pacing, be it sole endocardial right-ventricular or sole epicardial left-ventricular pacing, would be undesirable because it increases TDR. It also implies that the thus-created disadvantageous situation can be turned to being advantageous by simultaneous biventricular pacing. Would that mean that the inversion of the endocardial-to-epicardial activation by epicardial left-ventricular pacing is undone by simultaneous right-ventricular pacing? The BELIEVE study,4 in which 74 heart failure patients who were randomized to left-ventricular only or to bi-ventricular pacing were followed for 1 year, was not able to detect any evidence for a proarrhythmic effect of left-ventricular pacing.
Our conclusion, supported by computer simulations3 is that the Tpeak-end interval in the ECG of intact humans is not reflecting TDR, in contrast to the Tpeak-end interval in the quasi-ECG made in the left-ventricular wedge-preparation. The surface ECG made from a whole heart and the quasi-ECG derived from a preparation of the left-ventricular free wall are not analogous because surface ECG electrodes record, from a distance, electrical activity in the whole heart; in the above studies, cancellation plays a prominent role.5 The quasi-ECG is, however, recorded close to a small preparation in which cancellation plays virtually no role. The peak in the T-wave in the surface ECG reflects septal repolarization rather than, e.g., repolarization of the endocardium in the case of left-ventricular epicardial pacing.
Although it may well be true that in intact human hearts with left-ventricular and with biventricular pacing, TDR may be locally increased under the left-ventricular epicardial electrode, this is not reflected in the Tpeak-end interval on the surface ECG.
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[1] Medina-Ravell VA, Lankipalli RS, Yan GX, Antzelevitch C, Medina-Malpica NA, Medina-Malpica OA, et al. Effect of epicardial or biventricular pacing to prolong QT interval and increase transmural dispersion of repolarization: does resynchronization therapy pose a risk for patients predisposed to long QT or torsade de pointes? Circulation 2003; 107: 740–6.
[2] Santangelo L, Ammendola E, Russo V, Cavallaro C, Vecchione F, Garofalo S, et al. Influence of biventricular pacing on myocardial dispersion of repolarization in dilated cardiomyopathy patients. Europace 2006; 8: 502–5.
[3] van Huysduynen BH, Swenne CA, Bax JJ, Bleeker GB, Draisma HH, van Erven L, et al. Dispersion of repolarization in cardiac resynchronization therapy. Heart Rhythm 2005; 2: 1286–93.[CrossRef][Web of Science][Medline]
[4] Gasparini M, Bocchiardo M, Lunati M, Ravazzi PA, Santini M, Zardini 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.
[5] Burgess MJ, Millar K, Abildskov JA. Cancellation of electrocardiographic effects during ventricular recovery. J Electrocardiol 1969; 2: 101–7.[Medline]
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