Q J Med 2004; 97: 7-13
© Association of Physicians 2004; all rights reserved.
Review |
Predicting late sudden death from ventricular arrhythmia in adults following surgical repair of tetralogy of Fallot
From the Department of Cardiology, Queen Elizabeth Hospital, Birmingham, and 1Department of Cardiology, Northern General Hospital, Sheffield, UK
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Summary |
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 Top Summary IntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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Tetralogy of Fallot was the first complex congenital cardiac defect to undergo open repair. The life expectancy and quality of life of those surviving surgery is now good, although late survival is compromised by the occurrence of sudden death. The emergence of successful methods for both the prevention of arrhythmias (including valve replacements and electrophysiological ablation) and the treatment of arrhythmias when they occur (including implantable defibrillators), has meant the identification of those at risk is of even greater importance. This paper reviews the predictive methods currently available to the practising physician caring for these increasingly common patients.
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Introduction |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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The overall incidence of tetralogy of Fallot approaches 10% of the 4–6 per 1000 live-born with congenital heart disease. Early definitive repair of tetralogy of Fallot is now advocated, with an actuarial survival rate of almost 90% at 30 years.1 Survival into adulthood is both expected and of high quality. The large majority of patients who undergo corrective surgery within the first two years of life lead normal lives without significant cardiac or vascular symptoms.2 But although the long-term outcome is good, survival is not the same as for age- and sex-matched controls.3 Through continued surveillance in specialist units, the devastating occurrence of sudden death has been recognized as a late complication of surgical correction of tetralogy of Fallot. The incidence of such an event appears to be between 1.5 and 4.5 deaths per 1000 patient years, most commonly occurring 4 years or more after repair.4 Physicians responsible for the on-going care of patients with surgically-corrected tetralogy of Fallot have the difficult task of identifying those at risk of sudden death. Although much effort has been spent in establishing the relationship between ventricular arrhythmia and sudden death in tetralogy of Fallot, the risk of this complication should be placed in the context of survival of other groups of patients following corrective surgery for congenital heart defects. In particular, mortality is higher in corrected transposition of the great arteries, with sudden death the most common cause of death.5
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Clinical factors predicting risk of VT/sudden death |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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Clinical features give some indication of risk. The condition of tetralogy of Fallot is in itself a risk factor for sudden death, since this occurs in unoperated patients (sudden death also affects the natural history of other congenital defects affecting the right ventricular outflow tract, such as double-outlet right ventricle).6 The co-existence of other defects, including the aberrant origin of the left anterior descending coronary artery in 3–5% cases, increases the possibility of late sudden death.7 Risk is modified by early surgical correction if performed under the age of 5 years, leaving the individual with good right ventricular function. In a study of 163 subjects surviving 30 days after operation, the 30-year actuarial survival rate in those aged < 5 years at the time of complete repair was 90%, compared to 76% in those aged 12 years or older.3 Risk is affected by the type of repair performed: use of a right ventriculotomy is associated with the highest rate of ventricular dysrhythmia, and the presence of a ventricular septal patch is a second potential source of re-entrant arrhythmia.8 Fibrous–fatty substitution occurs at the site of surgical scarring, and may provide a substrate for abnormalities of depolarization and repolarization. The quality of surgical correction affects long-term susceptibility to sudden death, with residual outflow obstruction and pulmonary regurgitation of particular importance. Post-operative cardiac catheterization identifies patients at risk of ventricular arrhythmias (RVSP > 60 mmHg) and patients at risk of sudden death (residual RV to PA outflow tract gradient > 40 mmHg).9,10 Post-operative complications increase the frequency of late events. Transient complete heart block in the immediate post-operative period, despite return to sinus rhythm before discharge, is associated with a five-fold increase in late sudden death—presumably because of injury to the conduction system.11
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Electrocardiographic predictors of VT/sudden death |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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Routine ECG
Electrocardiographic indicators of increased risk of ventricular arrhythmia and sudden death have been identified in predominantly retrospective cohort studies. The assumption behind many of these studies is that there is a cause-and-effect relationship between ventricular arrhythmia and sudden death.6 Ventricular ectopic beats are common enough to occur in 19% of standard 12-lead ECGs in corrected tetralogy of Fallot, and are associated with an increase in the rate of sudden death compared to those without ventricular ectopic beats. In a series of 233 patients followed up for a median of 5.2 years, 38% of those with ventricular premature extrasystoles died, compared with 2% of those without (ventricular premature extrasystoles were present in all of those who died suddenly).12 QRS duration > 180 ms has 100% sensitivity for sustained VT and sudden death, whereas a QRS duration < 180 ms has a negative predictive value of 100% for these events.13 Prolonged QRS duration is associated with pulmonary regurgitation and right ventricular enlargement, which may be important modulating factors in the pathogenesis of sudden death.14 A high rate of increase in QRS duration (mean 3.5 ms/year) calculated using consecutive standard 12-lead ECGs also identifies those at risk of VT and sudden death, although the risk ratio for such a finding is low (1.05, 95%CI 1.02–1.09).15 One interpretation of such data is that the initial surgical injury to the myocardium acts as a substrate for arrhythmia and induces an increase in QRS duration. Right ventricular dilatation and QRS lengthening then modify the risk of sudden death.
Ambulatory Holter monitoring
Ambulatory ECG monitoring has allowed greater detection of ventricular ectopics and non-sustained ventricular tachycardia. It has been suggested that aggressive pharmacological suppression of ventricular ectopics (from > 10 PVCs per hour to < 10 PVCs per hour) may reduce the rate of sudden death.9 However, there are two problems with such an approach. Firstly, the detection of ventricular ectopics and non-sustained ventricular tachycardia is common, and such findings on 24-h or 48-h monitors are a poor predictor of sudden death.16 Ventricular arrhythmias on serial 24-h Holter monitors appear to be stable over time, and do not deteriorate.17 Secondly, the pharmacological suppression of ventricular ectopy may in itself increase risk of arrhythmia.18 Routine ambulatory monitoring seems to be of limited value in the absence of other evidence of increasing risk of arrhythmia.
Signal-averaged ECG analysis
Signal-averaging of ECGs (SAECG), repolarization (QT and JT) analysis, and heart rate variability (HRV) analysis are all methods that have been used to try to refine risk prediction. Studies have frequently used surrogate markers to identify those considered to be at greatest risk of arrhythmic death, including the presence of frequent ventricular ectopy and non-sustained ventricular tachycardia on Holter monitoring. However, it should be remembered that these markers may lack accuracy in predicting sudden death. Signal averaging of ECGs is a method of detecting abnormalities in ventricular depolarization, and successfully predicts risk of ventricular arrhythmias in ischaemic heart disease.19 In tetralogy of Fallot, root mean square voltage in the last 40 ms is lower, and low-amplitude signal duration of the terminal filtered QRS complex is higher, in those with symptomatic spontaneous VT or resuscitated VF, compared to those without VT.20 However, SAECG cannot distinguish between patients with corrected Fallot who have non-sustained and sustained VT on Holter and normal controls.21 The clinical utility of SAECG as an independent predictor of ventricular arrhythmia still needs to be confirmed in a prospective study in tetralogy.
Analysis of repolarization
Heterogeneity of repolarization is a hallmark of ventricular tachyarrhythmia, and has been studied using analysis of QT/JT duration and dispersion. Increased QT dispersion has been documented in patients who have had a right ventriculotomy, distinguishing them from controls, subjects with uncorrected tetralogy and from subjects with transatrial surgery and no ventriculotomy.22 The study of both QT and JT dispersion calculated on standard 12-lead ECGs provides added value in predicting those at risk of symptomatic sustained VT and near-miss sudden death who have QRS prolongation.23 The combination of a QRS duration > 180 ms plus QT dispersion > 60 ms or JT dispersion > 60 ms was 98% sensitive and 100% specific for patients with sustained ventricular tachycardia. These depolarization and repolarization abnormalities contribute to arrhythmogenesis in adults, but are not detectable in children.24
Heart rate variability
Electrical stability of the heart is partly dependent on autonomic function. Cardiac autonomic control can be assessed by the measurement of baroreflex sensitivity and heart rate variability (HRV). There is considerable evidence to show that low levels of these markers of cardiac autonomic control are strongly and independently associated with an adverse prognosis in ischaemic heart disease. Reduced HRV appears to be a feature following repair of tetralogy of Fallot, and is associated with widening of the QRS.25 The reduction in HRV correlates with RV dilatation and RV pressure, but not with RV function. There is some evidence that more marked pulmonary regurgitation is associated with a progressive reduction in HRV.26 A greater reduction in the standard deviation of normal-to-normal RR intervals (SDNN), which is a measurement of overall HRV, is associated with sustained VT and with abnormalities in the myocardial adrenergic system assessed by reduced uptake of 123I metaiodobenzylguanidine during tomographic imaging.27 Again, however, prospective evaluation is required to show whether reduced HRV is a clinically useful independent predictor for late sudden death, since the absolute difference in SDNN between those with (103 ± 34.8) and without (127 ± 25.4) VT is small.
Exercise testing for arrhythmia
Arrhythmias are found in approximately 25% of subjects attending for exercise testing, but most of these arrhythmias are identified during rest or in recovery. Suppression of ventricular ectopic activity during stress is a non-specific finding, and has no prognostic value (as in patients with coronary artery disease). The incidence of arrhythmia during stress may be as high as 73.3%, although this rate is variable.28 Ventricular arrhythmias are more commonly induced during stress in those who are older at the time of their repair, and in those with the longest period of follow-up between repair and stress, implying a time-dependent effect.29 Exercise-induced arrhythmias also occur more commonly in those with a high RV systolic pressure (> 60 mmHg).30 It is not known whether the induction of ventricular arrhythmia during stress is an independent risk factor for sudden death.
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Electrophysiology in the prediction of VT/sudden death |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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Ventricular arrhythmias develop in unoperated patients with tetralogy of Fallot, most likely because of fibrosis at the pulmonary infundibulum, and in operated patients, because of fibrosis at the right ventriculotomy scar. Re-entrant circuits have been identified in electrophysiological mapping studies at both sites.31 Radiofrequency ablation of these re-entrant circuits has been successful in the treatment of sustained VT resistant to pharmacotherapy.32 However, even though induced VT may correspond with clinical sustained VT, EP studies by themselves do not appear to be able to identify patients at risk of sudden death.33 Both false-positive studies (inducible VT in those without mortality on follow-up) and false-negative studies (non-inducible VT in those with subsequent sustained VT) occur often enough to reduce the predictive utility of the test.34 Thus, invasive EP is a therapeutic option reserved for use once an accurate non-invasive means of identifying those at high risk of sudden death has been developed.
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Haemodynamic factors predicting the risk of sudden death |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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Persistent haemodynamic abnormalities are associated with late sudden death, including elevated right ventricular systolic pressure > 60 mmHg and increased pulmonary outflow gradient > 40 mmHg on right heart catheterization, right ventricular volume overload, and right ventricular dysfunction.35 Such haemodynamic abnormalities may affect risk of sudden death in two ways: (a) the patient with moderate-to-severe haemodynamic abnormalities will tolerate fast VT less well; (b) it has been postulated that abnormalities in right ventricular and pulmonary valve function may directly modulate the arrhythmic risk through some form of ‘mechanoelectrical interaction’.13 In particular, patients with severe pulmonary regurgitation secondary to RV outflow patching appear to be at high risk. This is analogous to the predisposition of patients with dilated left ventricles due to long-standing aortic regurgitation to the development of ventricular arrhythmias. This modulation of arrhythmic potential by the haemodynamic effect of pulmonary regurgitation is of particular interest, since this may be amenable to surgical correction. In a retrospective study, QRS duration stabilized in patients undergoing pulmonary valve replacement for severe regurgitation and/or RV outflow tract obstruction late after repair of tetralogy of Fallot, but continued to lengthen in similar subjects who did not undergo replacement.36 Replacement of the pulmonary valve was also associated with a reduction in the incidence of ventricular tachycardia at a mean follow-up of 4.7 years. The reduction in ventricular arrhythmia following intervention for pulmonary regurgitation mirrored trends seen in earlier studies.37,38
Radionuclide angiography
Routine cardiac catheterization to identify haemodynamic changes associated with a relatively rare arrhythmic outcome does not seem a viable option, so what methods should be used in patient assessment? Radionuclide ventricular angiography can identify higher right ventricular volumes in those with VT compared to subjects without documented arrhythmias, but does not appear to be useful in assessing differences in function.39,40 Pulmonary regurgitation results in volume overload of the right ventricle, with the long-term development of right ventricular dilatation. RV dilatation is associated with QRS prolongation and arrhythmia. In turn, both radionuclide and echocardiographic studies have demonstrated a link between moderate–severe pulmonary regurgitation and sustained ventricular tachycardia/sudden death.41 As further evidence of this link, it is thought that the higher rate of VT in those with a transannular patch, which allows for free pulmonary regurgitation, may be due to the long-term effect of this regurgitation on the RV.
Echocardiography
Echocardiography has obvious benefits in post-operative assessment of tetralogy of Fallot in that it is non-invasive and readily available. Simple measurements of RV size have been used to identify associations with sustained VT and sudden death, although most studies have been retrospective case control studies in which the outcome variable has been dichotomized and there is considerable overlap between groups. Hence, relative increases in: M-mode dimensions of the RV from the parasternal long axis,42 2D measurements of RV long axis length relative to the LV,13 2D measurements of the ratio of the maximum short diameters of the RV:LV,43 and 2D measurements of end-diastolic volume using a biplane Simpsons method, have all been associated with the presence of ventricular arrhythmia.21 However, clear differences in RV size and function between those suffering VT and sudden death using M-mode and 2D measurements have not been demonstrated consistently.41 The complex 3D shape of the RV limits the efficacy of transthoracic assessment of RV size and function. There is no simple geometric shape that approximates to the RV chamber that is wrapped around the LV, so quantitative assessment is difficult and reproducibility is reduced. Two more recent approaches may overcome these practical problems. Firstly, transthoracic 3D echo may improve the accuracy and reproducibility of assessment of RV size, volume and function, and be more useful in long-term follow-up. Increases in RV volume calculated from transthoracic 3D echos correlate with QRS prolongation and compare well with MRI.44 Secondly, the myocardial performance index is a Doppler technique that gives an index of global ventricular function through assessment of ejection and isovolumetric relaxation and contraction times. However, the predictive value of such assessment has yet to be proven.45
Alternative approaches have concentrated on the use of Doppler echocardiography. Pulsed Doppler assessment of the presence of antegrade pulmonary artery flow (A wave) in late diastole throughout inspiration and expiration, has been used to differentiate between restrictive and non-restrictive function of the RV.46 Restrictive physiology of the RV is associated with later beneficial reduction in pulmonary regurgitation, superior exercise performance, less ventricular dilation, and less QRS prolongation, whereas non-restrictive physiology in association with pulmonary regurgitation may identify a group of subjects at highest risk of RV dilatation, with a consequent increase in risk of sudden death. VT and sudden death occur almost solely in those with at least moderate PR, but echo assessment of PR is of limited use, because of its semi-quantitative nature.15 The newer development of tissue Doppler may improve quantitative assessment of RV function, and reduce the problems of load-dependence that are inherent in the velocity measurements of PR and PA flow.47
Magnetic resonance imaging
Inter-observer variability in standard M-mode, 2D and pulsed Doppler measurements increases the number of patients with corrected tetralogy of Fallot required in follow-up studies of RV function and PR as predictors of arrhythmic events. MRI has substantial capability for anatomical and functional evaluation of corrected tetralogy of Fallot, with the added advantage of reduced inter-observer variability.48 Velocity-mapping MRI successfully differentiates between restrictive RV physiology and can grade pulmonary regurgitation.49 Tomographic MRI has been used to document the changes in RV volume and mass believed to underlie the progressive increase in QRS duration predictive of arrhythmia.14 It is likely that the use of MRI in routine evaluation will increase, but as yet it does not have a defined role in prediction of ventricular arrhythmia.
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Conclusion |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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In spite of the number of techniques available, no single risk factor has yet been identified to predict VT and sudden death convincingly in corrected tetralogy of Fallot. Large prospective studies would be required to identify such factors, involving a population in which 70–80 deaths might be expected to provide adequate statistical power.50 Follow-up of subjects with tetralogy of Fallot for evaluation of susceptibility to ventricular arrhythmia requires consideration of clinical history, details of operative procedures undertaken, post-procedural catheterization data, ECG data and ongoing non-invasive haemodynamic assessment. Once an at-risk patient is identified, the optimum management strategy remains unclear, with the probable exception that anti-arrhythmic medication in the long-term may present an inadequate solution. However, the development of successful catheter ablation, the availability of automatic implantable cardio-defibrillators, and the potential reduction in arrhythmia propensity following pulmonary valve replacement, mean that therapeutic strategies are available.51 Further study is needed to define their use.
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Footnotes |
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Address correspondence to Dr R.P. Steeds, Consultant Cardiologist, Queen Elizabeth Hospital, Metchley Park Road, Edgbaston, Birmingham B15 2TH. e-mail: rick.steeds{at}uhb.nhs.uk
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References |
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TopSummaryIntroductionClinical factors predicting risk...Electrocardiographic predictors...Electrophysiology in the...Haemodynamic factors predicting...ConclusionReferences |
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