(Circulation. 1997;95:401-404.)
© 1997 American Heart Association, Inc.
Articles |
Depolarization-Repolarization Inhomogeneity After Repair of Tetralogy of Fallot
The Substrate for Malignant Ventricular Tachycardia?
the Royal Brompton Hospital, National Heart and Lung Institute, Imperial College, London, UK.
Correspondence to Prof Andrew N. Redington, Royal Brompton Hospital/National Heart and Lung Institute, Sydney St, London SW3 6NP, UK.
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Abstract |
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Background We have previously shown that QRS prolongation (
180 ms) is a risk marker for sustained ventricular tachycardia (VT) late after repair of tetralogy of Fallot (rTOF). We have now examined the dispersion of QT and its components QRS and JT, in an attempt to determine whether any association exists between these measurements and the presence of VT in these patients.
Methods and Results QRS duration and QT/QRS/JT dispersion were measured manually from standard ECGs in 10 syncopal rTOF patients (21.4±4.6 years after repair; group 1) with QRS180 ms and with documented VT and were compared with 9 rTOF patients with QRS 180 ms and no VT (group 2), 40 rTOF patients with QRS <180 ms and no clinical arrhythmias (group 3), and 40 nontetralogy control subjects (20 with right bundle-branch block [group 4] and 20 with normal ECG patterns [group 5]). Mean QT dispersion (62±36 ms) in the tetralogy patients was greater than in the nontetralogy control subjects (34±10 ms, P<.001). There were significant differences in all measured parameters between groups 1 and 3 and more importantly between groups 1 and 2. QRS dispersion in group 1 also correlated with QRS duration but not with JT dispersion.
Conclusions Our data suggest that both depolarization and repolarization abnormalities are associated with VT after rTOF. Furthermore, increased QT, QRS, and JT dispersions, combined with a QRS180 ms, refine risk stratification for VT in these patients.
Key Words: tetralogy of Fallot • arrhythmia • syncope • electrocardiography
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Introduction |
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Sustained ventricular tachycardia (VT) and sudden death late after repair of tetralogy of Fallot is widely reported1 2 and may be the most common cause of sudden death in childhood.3 We have previously shown that QRS prolongation
180 ms on the resting ECG identifies patients at risk of malignant ventricular arrhythmias after repair of tetralogy of Fallot (rTOF).4 We have suggested that this prolongation of QRS—an ECG reflection of abnormal and delayed depolarization—may play a role in the creation of a reentry circuit for ventricular tachycardia in these patients. Abnormalities of repolarization as measured by QT dispersion, however, have been reported more frequently in groups susceptible to VT. These include those individuals with long QT syndrome,5 hypertrophic cardiomyopathy,6 and chronic heart failure.7
In this study, we have examined the dispersion of QT and its components QRS and JT after rTOF in an attempt to determine whether any association exists between these measurements and the presence of VT in these patients.
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Methods |
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We have examined 12-lead ECGs in five different groups. Table 1
gives their ages and follow-up characteristics. Group 1 consisted of all 10 patients with documented sustained VT from a large data set (
180 patients) of adult survivors after rTOF currently being followed in our institution (Royal Brompton Hospital, National Heart and Lung Institute, Imperial College, London, UK). Nine patients had required resuscitation during a syncopal episode (near-miss sudden death); the remaining patient presented with palpitations and dizziness. Seven patients had clinically documented VT, and all 10 had easily inducible sustained VT during electrophysiological study. The last ECG before the onset of arrhythmia was analyzed in this group. Group 2 consisted of all 9 rTOF patients who had a maximum QRS duration 180 ms but had not sustained a symptomatic ventricular arrhythmia. Nine patients from group 1 and 3 patients from group 2 were included in our previous report4 ; the remaining patients and ECGs have since become available to us. Group 3, again from the same set of patients who underwent rTOF, included 40 patients selected to be matched for age, sex, and length of follow-up compared with group 1. Selection was made without knowledge of any other parameters. All had QRS duration <180 ms and no history of clinical arrhythmias (all in group 3 had a pattern consistent with right bundle-branch block [rSR' pattern in V1 and delayed S in I and V6]). Their mean QRS duration and length of follow-up from repair were not significantly different from our previously published report for the entire group,4 suggesting no selection bias. Finally, we examined the ECGs of 40 nontetralogy control subjects with no history of arrhythmia or syncope. Twenty were adult patients with an atrial septal defect, all with a right bundle-branch block ECG pattern. These patients were selected from a previously published cohort8 to provide the closest age and sex matching with group 1. The remaining 20 were normal control subjects with normal ECG patterns (group 5) who were age and sex matched with group 1.
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Simultaneous, standard 12-lead acquisition ECGs were used. All patients were in sinus rhythm. No patients were on antiarrhythmic drugs or drugs known to affect QRS complex and or QT interval during or before acquisition of the ECG analyzed in the study.
Analyses of QT and its component QRS and JT intervals were performed by one blinded observer on these 12-lead ECGs obtained in the traditional ECG lead position and recorded at 25 mm/s. QT and QRS measurements were made manually as previously described.4 9 10 The end of the T wave was taken at its return to the T-p baseline. Care was taken to avoid U waves in any measurement, and when U waves were present, the end of T wave was taken as the nadir between T and U.7 11 Three consecutive cycles were measured in each of the standard 12 leads, and a mean value was calculated from the three values. The JT interval was then calculated by subtracting QRS from QT (means) in individual leads. When the end of the QRS complex or T wave could not be identified, the lead was not included. A minimum of seven leads, at least three precordial, was required for QT/QRS/JT dispersion to be calculated.7 12 13 Repeatability of these measurements was tested by two independent observers blinded from the clinical data who analyzed a random sample of 12 (12%) ECGs. The QT/QRS/JT dispersion was defined as the difference between the maximum and minimum QT/QRS/JT intervals occurring in any of the 12 ECG leads.
Data were analyzed by use of ANOVA with Bonferroni's correction for multiple comparisons. Linear regression analysis was also performed by the least squares method.
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Results |
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Repeated measurements of QT/QRS/JT dispersion on 135 leads from 12 randomly chosen ECGs were performed twice by two blinded observers. The percentage differences in QT/QRS/JT dispersion measurements for the same ECG ranged from 2% to 5% for within-observer and 2% to 6% for between-observer variabilities.
There was no difference in RR interval between groups. As expected, there were significant differences in QT interval and QRS duration between groups 4 and 5 (Table
s 1 and 2). QRS, JT, and QT dispersions were similar, however. Patients from group 3 differed from normal control subjects in terms of their QT interval and QRS duration and in the dispersion of QT but not QRS and JT. There were further differences in all measured parameters (QT interval, QT/QRS/JT dispersion) between groups 1 and 3 (Table 3). Table 3 also shows significant differences in the dispersion of QT and its components QRS and JT between groups 1 and 2, which is of greater importance because these two groups have the same degree of QRS prolongation. There were significant correlations between QRS duration or QT interval and the dispersion of QT/QRS/JT in patients with VT (Table 4) and in all patients from our study with rTOF (Table 5). In the VT group, QRS dispersion correlated well with QRS duration (r=.72, P<.02) but less well with the dispersion of QT (r=.61, P=.06), and there was no correlation between the dispersion of QRS and JT (r=.5, P=.13).
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A QT interval >500 ms, a QT dispersion >75 ms, a QRS dispersion >35 ms, or finally a JT dispersion >65 ms, as a single marker, would have positively identified only patients with sustained VT from this study population. Furthermore, the combination of a QRS duration 180 ms with an additional QT dispersion >60 ms, a QRS dispersion >35 ms, or finally a JT dispersion>60 ms (Table 3) would be 98.3% sensitive and 100% specific for identification of patients with sustained VT.
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Discussion |
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The pathogenesis of sustained VT, thought to account for the majority of sudden death after rTOF, remains unclear, and there is no easy way of identifying patients at risk. We have previously shown depolarization abnormalities in the form of QRS prolongation and demonstrated how they relate to the mechanical properties of the right ventricle after rTOF.4 QRS duration showed a strong correlation with cardiothoracic ratio, and patients with QRS prolongation demonstrated normal, nonrestrictive, right ventricular diastolic physiology.14 When QRS duration >180 ms, these patients would appear to be at risk of malignant ventricular arrhythmias and sudden death. It is unclear, however, whether QRS duration is a surrogate risk factor in that if the right ventricle dilates and the patient develops VT, he or she is more likely to be hemodynamically compromised and die. It is also unclear whether mechanical events alone cause the electrical abnormalities demonstrated. Furthermore, the exact degree of QRS prolongation, particularly in more contemporary follow-up series, that predicts VT may be variable; therefore, further refinement of risk stratification may be useful.
There is good evidence to suggest that VT may result from mechanical changes in the left ventricle. Dilatation or stretch leads to a wider dispersion of repolarization and increased excitability and may potentiate the likelihood of reentry arrhythmia.15 16 Furthermore, changes in ventricular volume load can exaggerate the electrical inhomogeneity of the myocardium that normally exists owing to asymmetry of ventricular geometry and wall stress and thus predispose to reentry arrhythmia.17 Other investigators, looking at a number of conditions with reentry VT,6 7 18 including rTOF,19 have shown that QT dispersion provides information about regional variations in ventricular repolarization.5 These investigators have focused on repolarization rather than depolarization abnormalities and have largely ignored QRS dispersion, which was equally important in our group of patients and sheds light on potential mechanisms. QRS dispersion is likely to represent inhomogeneity of depolarization in the same way that QT dispersion has been taken to represent inhomogeneity of repolarization.
We have examined both QRS and JT dispersions after rTOF in an attempt to identify the possible association between inhomogeneity of depolarization and repolarization and the occurrence of VT. Our study shows that both depolarization and repolarization abnormalities exist in patients with rTOF that are significantly greater in patients with sustained VT. These abnormalities, as expressed by QRS and JT dispersions, respectively, were not linearly related in the ventricular arrhythmia group, suggesting that these are not simply related phenomena but that there might be an independent association. Furthermore, analysis of QT and its components made it possible to differentiate tetralogy patients with documented VT from those with a similar degree of QRS prolongation but no clinical arrhythmia. It may be that both abnormal conduction and increased dispersion of refractoriness are required for ventricular arrhythmogenesis in these patients. There is considerable evidence that abnormal conduction, as evidenced by the prolongation in QRS and the rSR' pattern almost invariably seen after rTOF does not result wholly from proximal right bundle-branch block.20 21 Interestingly, there was a significant correlation between QRS duration and QRS dispersion in our patients with rTOF, suggesting that the QRS prolongation and the propensity to ventricular arrhythmias may reflect inhomogeneity of depolarization throughout the right ventricle. There were also significant differences in QT dispersion between the tetralogy patients (QRS <180 ms, no clinical arrhythmias) and the nontetralogy control subjects, although of smaller magnitude. Because QT interval changes are dynamic, serial measurements within these rTOF groups may provide further information on disease progression, altered susceptibility to malignant arrhythmias, and the effects of treatment. Finally, it would be naive to assume that other postoperative factors such as myocardial scarring, postoperative hemodynamics, and individual variation will not play additional roles in the pathogenesis of arrhythmia in these patients. Our data cannot be interpreted as the only mechanism of sudden death but must represent the most common.
In terms of the methodology used, the RR interval did not differ between groups. In view of previous criticism of the most commonly used Bazett's formula that may overcorrect for differences in heart rate,22 we elected not to give rate-corrected values. We included 20 nontetralogy control subjects with an unoperated atrial septal defect and right bundle-branch block pattern because all the tetralogy patients had similar rSR' patterns. This emphasizes our point that it is the prolongation and not the precise pattern of the QRS complex, seen at different degrees in both of these groups, that reflects right ventricular size and represents a mechanoelectrical interaction with potential arrhythmogenic effects for these patients. This hypothesis is further supported by our recent report of surgical closure of atrial septal defects in adults in whom QRS duration shortened after acute volume off-loading of the right ventricle.8 There are potential problems in accurate measurement of the QT interval and QRS complex, particularly in identifying the end of the QRS and T wave.11 12 Whether computer analysis of the QT interval is more accurate than manual measurement and whether one computer algorithm is superior to another are not yet settled.23 24 With careful measurements by experienced physicians and with exclusion of a relatively small number of "unsuitable" leads, however, acceptably low within- and between-observer measurement variabilities can be obtained.25 There is no doubt, however, that the clinical utility and application of these measurements in the clinical setting could be improved further by the use of standardized, validated computerized techniques with automatic measurements for each lead.
We speculate that both depolarization and repolarization abnormalities contribute to the pathogenesis of ventricular arrhythmia in patients after rTOF. A QRS duration of 180 ms remains the simplest, most practical way of identifying those at risk. The dispersion of QT and its components QRS and JT refines risk stratification for these patients. However, we agree with the previous suggestion26 that a large-scale, long-term follow-up study of the wider utility of these measurements is needed before specific therapeutic options for the treatment of individual patients can be evaluated.
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Acknowledgments |
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We are grateful to Prof Stuart Cobbe for his helpful comments, to Dr Jane Somerville and other medical and surgical colleagues for allowing us to study their patients, and to Dr Mark Rosenthal for advice on statistics. Finally, we are indebted to Dr Kostas A. Gatzoulis for his suggestions regarding data analysis and reproducibility testing.
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Footnotes |
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Reprint requests to Dr Michael A. Gatzoulis, Toronto Congenital Cardiac Centre for Adults, Toronto Hospital, 200 Elizabeth St, Toronto, Canada M5G 2C4.
Received March 4, 1996; revision received September 5, 1996; accepted September 7, 1996.
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