International Journal of Cardiology, 30 (1991) 143-150 0 1991 Elsevier Science Publishers B.V. (Biomedical Division) 0167-5273/91/$03.50 ADONIS 0167527391OOQ51A

143

CARD10 01187

Review

Late ventricular arrhythmias occurring after repair of tetralogy of Fallot : do they matter? J.E. Deanfield Thoracic Unit, The Hospital for Sick Children, London, U.K.

(Received 30 January 1990; revision accepted 3 September 1990)

Key words: Ventricular arrhythmia;

Tetralogy of Fallot

Introduction Surgery has transformed the outlook for patients with tetralogy of Fallot from a condition in which less than a quarter of patients could be expected to survive past the first decade [l] to one in which late survival approaches that of the general population matched for age, sex and race [2]. As a result, attention has been focused on the late complications of the survivors which prevent surgery from being described as a “cure”. The most dramatic of these is sudden death, which has occurred in small numbers of patients in almost every large series with long post-operative followup [3-71. In 1969, Kulbertus and his colleagues [8] described the electrocardiographic finding of right bundle branch block and left axis deviation after repair. They suggested that this might represent damage to the proximal right bundle and left anterior fascicle of the conduction system (bifascicular block) and, by progression to late complete heart block, be the causative agent in cases who died suddenly and unexpectedly. Despite a study by Wolfe et al. [9], which appeared to support this hypothesis, numerous follow-up studies

Correspondence to: J.E. Deanfield, The Hospital for Sick Children, Great Chmond Street, London WClN 3JH, U.K.

have failed to show increased mortality in patients with this electrophysiological substrate [7,10-121. In 1977, Gillette and his colleagues [13] reported 51 cases, nine of whom had ventricular extrasystoles on routine electrocardiograms. Three of the nine cases with ventricular extrasystoles died, one of intractable ventricular fibrillation and two suddenly. Gillette et al. [13], therefore, proposed that ventricular arrhythmia, rather than a conduction defect, was the likely basis for late sudden death. Widespread use of ambulatory electrocardiographic monitoring has greatly increased the detection of abnormal patterns of rhythm in survivors of surgery for congenital heart disease. With this have come a number of different clinical dilemmas for those managing this largely asymptomatic population of children and adolescents. Which, if any, arrhythmia indicates an increased risk and does treatment aimed at suppression of the disturbance reduce the subsequent risk? Current strategies for management differ widely between institutions. This review examines critically the available information on the prevalence of ventricular arrhythmia after repair of tetralogy of Fallot, the predisposing factors for disturbances of rhythm and their prognostic significance. Based on this information, the appropriate clinical response in terms of investigation and indications for anti-arrhythmic treatment is discussed.

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Prevalence of Arrhythmia In 1980, we [7] reported the first series of patients undergoing ambulatory electrocardiographic monitoring after repair of tetralogy of Fallot. Ventricular arrhythmia was classified according to frequency and morphology using a modification of the Lown system devised for adults with coronary arterial disease [14]. Significant ventricular arrhythmia was found during 48 hours of monitoring in 41% of 74 patients after a mean period of 10 years [l-20] subsequent to repair, the repair itself having been performed between 3 and 20 years of age, with a mean age of 11 (Fig. 1). The abnormalities observed included frequent uniform ventricular extrasystoles, complex forms (couplets and/or multiform) and asymptomatic non-sustained ventricular tachycardia. A very similar high incidence of disturbance of rhythm (42%) was subsequently found by Kavey et al. [6] in 72 post-operative survivors$ and the findings have since been confirmed by others [15-171. These data might imply that ventricular arrhythmia is a common and inevitable problem after repair of

Fig. 1. Ventricular arrhythmia during 48 hour ambulatory monitoring in 85 patients after repair of tetralogy of Fallot between 1959 and 1978. Group 0 = no VEs; group I = uniform VEs peak hourly count < 30; group II = < 30 uniform VEs in any hour; group III = couplets (2 consecutive VEs) or multiform VEs with peak hourly count of < 30; group IV = couplets (2 consecutive VEs) or multiform VEs with > 30 in any hour; group V = VT ( > 3 consecutive VEs with a mean rate of > 110 beats/mm).

tetralogy of Fallot. Care must be taken, however, before extrapolating from such findings to current surgical practice. A number of important differences exist, not least the relatively old age at repair which is accounted for by the selection of patients with long follow-up. These patients, -of necessity, underwent their procedures early in the era of corrective surgery. The influences of surgical era, age at repair and follow-up duration are difficult to separate. Less information is available for patients undergoing surgery in the last decade. Predisposing Factors The factors which predispose to the presence of ventricular arrhythmia during long term follow-up after tetralogy of Fallot repair have been controversial. Pre-operative, operative and post-operative influences may all be important in certain settings. Garson et al. [3], in 1979, were able to correlate the occurrence of ventricular arrhythmia with elevated right ventricular systolic pressure after repair. Kavey et al. [18], on the other hand, were unable to demonstrate a similar haemodynamic correlation but found more subtle functional abnormalities in the patients with ventricular arrhythmia using radionuclide angiography and cross-sectional echocardiography. Kobayashi et al. [16] in a study of 100 patients, found that ventricular arrhythmia was related to older age at operation, longer interval after surgery, increased right ventricular systolic pressure, decreased right ventricular ejection fraction and presence of a surgical scar in the right ventricle. In none of these reports, however, was the interaction of these various clinical, haemodynamic and electrophysiological factors examined in a critical fashion. Further analysis of our patients from the Hammersmith Hospital showed a significant increase in post-operative ventricular arrhythmia with increased age at repair when this was broken down into ages 2-7, 8-15 and 16 years or greater. This was independent of the era of surgery or the interval between surgery and monitoring (Fig. 2). We were unable to show [19] a relationship between any grade of ventricular arrhythmia and residual elevations of right ventricular systolic or diastolic pressure. Furthermore, there was no relation dem-

145 Age at repair

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16 23:

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4-10 Il.15

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Fig. 2. Relation between significant ventricular arrhythmia (grade 2 or greater), age at repair and duration of follow-up in 85 patients after repair of tetralogy of Fallot.

onstrated using radionuclide angiography between indices of right or left ventricular ejection and the presence of arrhythmia. This implies that pre-operative factors already present at the time of repair might be at least as important as the operation itself, or post-operative status, in the genesis of late arrhythmia. This hypothesis was subsequently tested [20] in a prospective study examining the incidence of ventricular arrhythmia before and after repair performed in both young and old patients (Fig. 3). In 32 patients, age.d from one to seven years at repair, the incidence of ventricular A

6

cl 0 NOVA q I VE 30/h

Fig. 3. Pre- and post-operative ECG monitoring in 35 patients repaired age 1.2-7.7 (median 4.3 years) - group A, and 20 patients age 13-43 (median 28 years) - group B. In group A, the frequency of VE was low before and after surgery. In contrast, in group B (older age at repair) there was a high incidence of frequent or complex ventricular arrhythmia before surgery, which persisted after repair.

Why does ventricular arrhythmia occur in patients with tetralogy of Fallot even before repair? The anatomic substrate for the electrophysiological disturbances may be progressive myocardial fibrosis occurring as part of the natural history of the disease. In older patients undergoing repair of tetralogy, pathological studies have demonstrated extensive right ventricular fibrosis which is not present in younger children [21]. We have noted similar extensive fibrosis in patients who died suddenly late after repair [22]. Hegerty and her colleagues [23] have performed a detailed histological evaluation of the development of fibrosis in right and left ventricles of patients with tetralogy of Fallot dying at surgery at different ages and compared the findings to age matched controls. In the hearts with tetralogy of Fallot, the degree of fibrosis in younger patients was normal, but there was an increased rate of fibrosis with age in the right ventricle, particularly in the outflow tract and sub-endocardium. Similar changes were not found in the left ventricle [23]. This implies that the hearts from patients with tetralogy of Fallot do not initially have an intrinsic abnormality of myocardial fibrosis, but that this can develop during the period of time prior to surgical correction. Electrophysiological studies using endocardial mapping [24] have demonstrated fractionated depolarisation at multiple sites in the right ventricle (but not the left ventricle) in patients after repair of tetralogy. This finding correlated with the presence of ventricular arrhythmia on electrocardiographic monitoring. This suggests a widespread abnormality of electrical activity, perhaps due to myocardial damage, rather than

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necessarily a local problem resulting directly from the surgical repair. Myocardial damage at operation, or during follow-up, certainly remains a potential basis for ventricular arrhythmia. In our patients [20], new post-operative ventricular arrhythmia occurred most frequently in those undergoing more extensive right ventricular surgery (for example, insertion of a conduit from the right ventricle to the pulmonary trunk) or those requiring re-operation, these findings being similar to those of an early report by Wessel and colleagues [25]. When surgical technique in patients with and without post-operative arrhythmia were compared by Kobyashi et al. [15], a new operative method without or with minimal right ventriculotomy had been performed more frequently in the patients without ventricular arrhythmia (49%) than in those with ventricular arrhythmia (15%). Sustained ventricular tachycardia originating from re-entry circuits localised to sites of local surgically-induced scarring in the right ventricle were mapped by Horowitz et al. [26] in the outflow tract, and by Kugler and his colleagues [27] in the inflow. The mechanism for sustained ventricular tachycardia and ventricular extrasystoles may be different, and the influences of surgery and post-operative haemodynamics on ventricular arrhythmia need more investigation. It is, as yet, impossible to refute the argument that an increase in incidence of ventricular arrhythmias, together with late clinical complications, may yet occur with longer follow-up in the more recently operated patients. Published series, however, do not support this hypothesis. They certainly show no accelerating pattern of late sudden death [28]. It is tempting to speculate that earlier surgical repair, which has become standard, may reduce the incidence of late electrophysiological problems. While it is too early yet to state categorically that this is the case, data from Walsh et al. [29], together with our own experience, is encouraging. Only 2 of 184 patients repaired at less than 18 months of age in Boston had ventricular extrasystoles on routine electrocardiograms, while 4 of 32 patients repaired at between the ages of one and seven years at the Hospital for Sick Children in London had ventricular arrhythmia on ambulatory monitoring up to 75 months after repair [20]. Thus, the high inci-

dence of ventricular arrhythmia currently seen in adolescents and young adult survivors of tetralogy of Fallot repair may be a feature of an earlier surgical era. Clinical significance The impact of ventricular arrhythmia for longterm survivors in terms of morbidity and mortality will determine the appropriate clinical response in terms of investigation and therapy. The aims of treatment are relief of symptoms and prevention of sudden death directly related to pre-existing arrhythmias. In our prospective follow-up of the clinical impact of late ventricular arrhythmia after repair, only 17% of patients had any symptoms which could be attributed to arrhythmia [30]. The majority of these were mild palpitations which were due to supraventricular arrhythmia. Dizziness or syncope were uncommon. There is little disagreement on the indication for anti-arrhythmic therapy in symptomatic patients. In contrast, since prophylactic therapy to suppress ventricular arrhythmia may involve lifelong administration of potentially toxic drugs to large numbers of asymptomatic patients, the evidence that it is beneficial needs very critical evaluation. We must examine whether, firstly, the presence of ventricular arrhythmia on ambulatory monitoring defines a group of patients at high risk of sudden death, and, secondly, that treatment with anti-arrhythmic which reduces the incidence of medication, arrhythmia, also reduces the risk of sudden death. A comparison of the incidence of ventricular arrhythmia considered significant in studies using ambulatory monitoring (up to 50%), and the incidence of late sudden death in similar groups of patients (approximately l-5% in studies with up to 25 years follow-up), implies that the association between all such ventricular arrhythmia and late complications cannot be strong. In early retrospective reports, many patients who died suddenly had ventricular arrhythmia [3,13]. The incidence of ventricular arrhythmia in patients who died, and in those who remained well, however, could not be compared. We have performed a prospective study of 86 patients who underwent repair of

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terralogy of FalIot between 1959 and 1976 [30]. Arrhythmic status was defined by 48 hour electrocardiographic monitoring 4-22 (mean 15) years after surgery and was related to symptoms, catheterisation data, and ventricular function by radionuclide angiography. Almost half the patients had ventricular arrhythmia, which consisted of frequent (greater than 30 per hour) uniform ventricular extrasystoles, complex extrasystoles or ventricular tachycardias. None of these patients with an asymptomatic arrhythmia received treatment. Despite this, all the patients remained alive and well over a follow-up of 48-82 months (mean 68 months). Within the large number of patients with post-operative arrhythmias observed on ambulatory monitoring, there may well be a small subgroup at higher risk. Several patients who have died suddenly have had both ventricular arrhythmia and significant haemodynamic abnormalities on retrospective review, suggesting that the combination of a “poor heart” and an arrhythmia may be a bad one. But neither the haemodynamic factors nor the specific characteristics of high risk arrhythmia have been investigated. Thus far, in our on-going prospective evaluation, all the patients in the categories previously suggested to be at “high risk” have remained alive and well, including patients with ventricular arrhythmia and elevated right ventricular systolic pressure (greater than 60 mm Hg), ventricular arrhythmia with reduced right or left ventricular ejection fractions, or ventricular arrhythmia with reduced ejection fractions and elevated systolic pressure. Our current knowledge, therefore, does not suggest a bad overall prognosis for the large numbers of patients with ventricular arrhythmia of various types on ambulatory electrocardiographic monitoring. Even if subgroups of patients with ventricular arrhythmia who are at high risk could be identified, it does not follow automatically that antiarrhythmic treatment to suppress the arrhythmia would lower this risk. The issue of whether ventricular arrhythmia is the pathophysiological basis (cause) for sudden death or merely a marker (association) of patients at high risk for other reasons (for example, poor myocardial function) has been controversial in adult cardiology for many years [31]. Policies of aggressive treatment

in survivors of repair for tetralogy of Fallot have been advocated on the basis of rather scanty data. Garson and colleagues [32] compared the incidence of sudden death in patients repaired before and after 1978, when they introduced prophylactic treatment with phenytoin for all ventricular arrhythmia discovered on routine electrocardiograms and greater than 10 ventricular extrasystoles per hour on 24 hour electrocardiographic monitoring. The incidence of sudden death since 1978 was significantly lower than it had been in the earlier era. It was concluded that this was the result of the treatment with phenytoin, despite the fact that many other aspects of medical and surgical management differing between the two study groups were not considered [32]. Furthermore, anti-arrhythmic drugs which have been shown to suppress ventricular arrhythmia have recognised side-effects [33,34]. While these have been reported to be less frequent in children, treatment, once started for prognostic reasons, will need to continue into adult life where side-effects are known to be significant. It has also become clear that anti-arrhythmic agents may themselves have pro-arrhythmic effects. This is, probably, one of the reasons why many drug studies in adults have failed to show improved prognosis [35]. Large prospective studies after repair of congenital cardiac malformations are necessary, but the available data do not yet support the concept of using ant&rhythmic treatment prophylactically in asymptomatic patients with all forms of ventricular arrhythmia after repair of tetralogy of Fallot. The high frequency, and low specificity, of ventricular arrhythmia , detected on ambulatory electrocardiographic monitoring has led to a search for better means of identifying those patients at risk of sustained ventricular arrhythmia and, presumably, subsequent sudden death. Invasive electrophysiological studies have been performed by a number of groups after repair of tetralogy of Fallot. Indices of conduction disturbance have been found to be of limited clinical value, and interest has centred on the ability to induce ventricular tachycardia by a variety of protocols of programmed stimulation. Garson et al. [15] found a relationship between the inducibility of

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ventricular tachycardia in the catheter laboratory and “spontaneous” ventricular arrhythmia on ambulatory monitoring [15], but this has not been seen by others [27]. It is important to distinguish the value of electrophysiologic studies in the management of patients who present with clinically sustained ventricular tachycardia from those with non-sustained episodes, with ventricular extrasystoles of different grades or those without arrhythmia. In adults with ischaemic heart disease, programmed ventricular stimulation, which reproduces the sustained monomorphic ventricular tachycardia experienced by the patient during daily life, has been shown to be of value in stratification of risks and selection of treatment [36]. It has resulted in decreased morbidity and mortality [37]. The value in lesser grades of non-sustained arrhythmia is much less apparent. Deal and colleagues [38] examined electrophysiological studies in symptomatic patients with both sustained and non-sustained ventricular arrhythmia after repair of tetralogy of Fallot. They were able to induce monomorphic ventricular tachycardia (sustained in 3, non-sustained in 1) in all 4 patients who presented with clinically sustained ventricular tachycardia by using up to 3 extra stimuli together with rapid ventricular pacing in the right ventricle. In contrast, in only 2 of 5 patients with symptomatic non-sustained ventricular arrhythmia was it possible to induce sustained monomorphic ventricular tachycardia with any protocol. The value of inducing ventricular tachycardia in symptomatic patients and, even more importantly, in asymptomatic patients, with and without ventricular arrhythmia on ambulatory electrocardiographic monitoring, therefore, is presently unknown. Before electrophysiological studies for prognostic stratification can be considered as anything other than a research investigation, prospective data using standardised protocols must demonstrate an increased incidence of clinically sustained ventricular tachycardia and increased mortality in patients with inducible arrhythmia compared to stratification of risk by non-invasive testing [19,39-411. It is hard to justify the recommendations of Macnamara and Gillette [42] for electrophysiologic study for the paediatric patient and adult with congenital heart disease. These

include as their strongest indications (“generally agreed”) any patient with residual right ventricular hypertension after an attempted repair of congenital heart disease, high grade ectopy in any late post-operative patients, palpitation in a late postoperative patient and, as an indication of second grade (some “difference of opinion”), follow-up after any ventriculotomy. Conclusions Ventricular arrhythmias have been widely recognised during the long term follow-up after repair of tetralogy of Fallot. They may be linked to the small number of late sudden unexpected deaths. Several factors are likely to influence the genesis of late ventricular arrhythmia, including pre-operative myocardial damage. As a result, the current practice of earlier repair may reduce the incidence of late complications. Widely differing approaches are being taken to the investigation and treatment of ventricular arrhythmia around the world. Currently, we believe that routine treatment of asymptomatic patients with nonsustained ventricular arrhythmia is not indicated. Further research is required to define those subsets of patients at high risk for potentially serious arrhythmia and to determine whether they will benefit from anti-arrhythmic therapy. References 1 Bertranou EG; Blackstone EH, Hazelrig JB, Turner ME, Kirklin JW. Life expectancy without surgery in tetralogy of Fallot. Am J Cardiol1978;42:458-466. 2 Katz NM, Blackstone EH, Kirklin JW, Pacific0 AD, Bargeron LM. Late survival and symptoms after repair of tetralogy of Fallot. Circulation 1982;65;403-410. 3 Garson A Jr, Nihill MB, McNamara DG, Cooley DA. Status of the adult and adolescent after repair of tetralogy of Fatlot. Circulation 1979;59:1232-1234. 4 Quattlebaum TG, Varghese PJ, Neil1 CA, Donaghoo JS. Sudden death among postoperative patients with tetralogy of Fallot. A follow-up study of 243 patients for an average of 12 years. Circulation 1976;54:289-293. 5 James FW, Kaplan S, Chou TC. Unexpected cardiac arrest in patients after surgical correction of tetralogy of Fallot. Circulation 1975;52:691-695. 6 Kavey BEW, Blackman MS, Sondheimer HM. Incidence and severity of chronic ventricular dysrhythrnias after repair of tetralogy of Fallot. Am Heart J 1982;102:342-350.

149 7 Deanfield JE, McKenna WJ, Ha&lie-Smith KA. Detection of late arrhythmia and conduction disturbance after correction of tetralogy of Fallot. Br Heart J 1980;44:248-253. 8 Kulbertus HE, Coyne JJ, Hallidie-Smith KA. Conduction disturbances before and after surgical closure of ventricular septal defect. Am Heart J 1969;77:123-131. 9 Wolff GS, Rowland TW, Ellison RC. Surgically induced right bundle branch block with left anterior hemiblock. An ominous sign in postoperative tetralogy of Fallot. Circulation 1972;46:587-595. 10 Cairns JA, Dobell ARC, Gibbons JE, Tessler I. Prognosis of right bundle branch block and left anterior hemiblock after intracardial repair of tetralogy of Fallot. Am Heart J 1975;90:549-554. 11 Downing JW Jr, Kaplan S, Bove KE. Postsurgical left anterior hemiblock and right bundle branch block. Br Heart J 1972;34:263-270. 12 Malm JR, Gersony WM. Postoperative left anterior hemiblock and right bundle branch block following repair of tetralogy of Fallot: clinical and etiologic consideration. Circulation 1975;51:1026-1029. 13 Gillette PC, Yeoman MA, Mullins CE, McNamara DG. Sudden death after repair of tetralogy of Fallot. Electrocardiographic and electrophysiologic abnormalities. Circulation 1977;56:566-571. 14 Ryan M, Lown B, Horn H. Comparison of ventricular ectopic activity during 24 hour monitoring and exercise testing in patients with coronary heart disease. N Engl J Med 1975;292:224-229. 15 Garson A Jr, Porter CJ, Gillette PC, McNamara D. Induction of ventricular tachycardia during electrophysiologic study after repair of tetralogy of Fallot. J Am Co11 Cardiol 1983;1:1493-1502. 16 Kobayashi J, Hirose H, Nakano S, Masuda H, Shirakura R, Kawashima Y. Ambulatory electrocardiographic study of the frequency and cause of ventricular arrhythmia after correction of tetralogy of Fallot. Am J Cardiol 1984;54: 1310-1313. 17 Bums RJ, Liu PP, Druck MN, Seawright SJ, Williams WG, McLaughlin PR. Analysis of adults with and without complex ventricular arrhythmias after repair of tetralogy of Fallot. J Am Co11 Cardiol 1984;4:226. 18 Kavey RW, Thomas FD, Byrum CJ, Blackman MS, Sondheimer HM, Bove EL. Ventricular arrhythmias and biventricular dysfunction after repair of tetralogy of Fallot. J Am Co11 Cardiol 1984;4:126-131. 19 Deanfield JE, McKenna WJ, Presbitero P, England D, Graham GR, Hallidie-Smith K. Ventricular arrhythmia in unrepaired and repaired tetralogy of Fallot. Relation to age, timing of repair and haemodynamic status. Br Heart J 1984;52:77-81. 20 Sullivan ID, Presbitero P, Gooch VM, Aruta E, Deanfield JE. Is ventricular arrhythmia in repaired tetralogy of Fallot an effect of operation or a consequence of the course of the disease? A prospective study. Br Heart J 1987;58:40-44. 21 Jones M, Ferrans VJ. Myocardial degeneration in con-

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genital heart disease. Comparison of morphologic findings in young and old patients with congenital heart disease associated with muscular obstruction to right ventricular outflow. Am J Cardiol 1977;39:1051-1063. Deanfield JE, Ho S, Anderson RH, McKemra WJ, Allwork SP, Hallidie-Smith KA. Late sudden death after repair of tetralogy of Fallot. A clinico-pathological study. Circulation 1983;67:626-631. Hegerty A, Anderson RH, Deanfield JE. Myocardial fibrosis in tetralogy of Fallot: effect of surgery or part of the natural history? (abstract). Br Heart J 1988;59:123. Deanfield JE, McKerma W, Rowland E. Local abnormalities of right ventricular depolarisation after repair of tetralogy of Fallot: a basis for ventricular arrhythmia. Am J Cardiol 1985;55:522-526. Wessel HU, Bastanier CK, Paul MH, Berry TE, Cole RB, Muster AJ. Prognostic significance of arrhythmia in tetralogy of Fallot after intracardiac repair. Am J Cardiol 1980;46:843-848. Horowitz LN, Vetter VL. Harken AH, Josephson ME. Electrophysiologic characteristics of sustained ventricular tachycardia occurring after repair of tetralogy of Fallot. Am J Cardiol 1980;46:446-452. Kugler JD, Pinsky WW, Cheatham JP, Hofschire PJ, Mooring PK, Fleming WH. Sustained ventricular tachycardia after repair of tetralogy of Fallot: new electrophysiologic findings. Am J Cardiol 1982;51:1137-1143. Fuster V, McGoon DC, Kennedy MA, Ritter DG, Kirklin JW. Long-term evaluation (12 to 22 years) of open heart surgery for tetralogy of Fallot. Am J Cardiol 1980;46:635642.

29 Walsh EP, Rockenmacher S, Keane JF, Hougen TJ, Lock JE, Castaneda AR. Late results in patients with tetralogy of Fallot repaired during infancy. Circulation 1988;77:10621067. 30 Deanfield JE, Franklin RF, McKenna WJ, Dickie S, Gersony W, Hallidie-Smith K. Prognostic significance of ventricular arrhythmia after repair of tetralogy of Fallot: A prospective study. In: Doyle EF, Engle MA, Gersony WM. Rashkind WJ, Talner NS, eds. Pediatric cardiology. Proceedings of the Second World Congress; Berlin: SpringerVerlag, 1986;467-468. 31 Surawicz B. Prognosis of ventricular arrhythmias in relation to sudden cardiac death: therapeutic implications. J Am Co11 Cardiol 1987;10:435-447. 32 Garson A Jr, Randall DC, et al. Prevention of sudden death after repair of tetralogy of Fallot: treatment of ventricular arrhythmias. J Am Coll Cardioll985;6:221-227. 33 Garson A Jr, Kugler JD, Gillette PC, Simonelli A, McNamara D. Control of late post-operative ventricular arrhythmias with phenytoin in young patients. Am J Cardiol 1980;46:290-294. 34 Moak JP, Smith RT, Garson A Jr. Mexiletine: an effective antiarrhythmic drug for treatment of ventricular arrhythmias in congenital heart disease. J Am Co11 Cardiol 1987; 10:824-829.

150 35 Hoffman BF, Dangman KH. The role of antiarrhythmic drugs in sudden cardiac death. J Am ColI Cardiol 1986;8: 104A-109A. 36 Wellens HJJ, Brugada P, Stevenson WG. Programmed electrical stimulation of the heart in patients with life-threatening ventricular arrhythmias: what is the significance of induced arrhythmias and what is the correct stimulation protocol? Circulation 1985;72:1-7. 37 Roy D, Waxman HL, Kienzle MG, Buxton AE, Marchlinski FE, Josephson ME. Clinical characteristics and long term follow-up in 119 survivors of cardiac arrest: relation to inducibihty at electrophysiologic testing. Am J Cardiol 1983;52:969-974. 38 Deal BJ, Scagliotti D, Miller SM, Gallastegui JS, Hariman RJ Levitsky S. Electrophysiologic drug testing in symptomatic ventricular arrhythmias after tetralogy of Fallot. Am J Cardiol 1987;59:1380-1385.

39 Garson A Jr, Gillette PC, Gutgesell HP, McNamara DG. Stress-induced ventricular arrhythmia after repair of tetralogy of FalIot. Am J Cardio11980;46:1006-1012. 40 Zimmerman M, Friedli B, Adamec R, Oberh8nsli I. Frequency of ventricular late potentials and fractionated right ventricular electrograms after operative repair of tetralogy of Fallot. Am J Cardiol 1987;59:448-453. 41 Breithardt G, Borggrefe M. Recent advances in the identification of patients at risk of ventricular tachyarrhythmias: role of ventricular late potentials. Circulation 1987;75: 1091-1096. 42 McNamara DG, Gillette PC. Indications for intracardiac electrophysiologic studies in pediatric patients and the adult with congenital heart disease. Circulation 1987;75(suppl 111):178-181.

Late ventricular arrhythmias occurring after repair of tetralogy of Fallot: do they matter?

International Journal of Cardiology, 30 (1991) 143-150 0 1991 Elsevier Science Publishers B.V. (Biomedical Division) 0167-5273/91/$03.50 ADONIS 016752...
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