(Circulation. 1995;92:231-237.)
© 1995 American Heart Association, Inc.
Articles |
Mechanoelectrical Interaction in Tetralogy of Fallot
QRS Prolongation Relates to Right Ventricular Size and Predicts Malignant Ventricular Arrhythmias and Sudden Death
From the Department of Paediatric Cardiology (M.A.G., J.A.T., A.N.R.), Grown-up Congenital Heart Unit (J.S.), Royal Brompton Hospital and National Heart and Lung Institute, London, England.
Correspondence to Dr Andrew N. Redington, Department of Paediatric Cardiology, Royal Brompton Hospital/National Heart and Lung Institute, Sydney St, London, UK, SW3 6NP.
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Abstract |
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Background Life-threatening ventricular arrhythmia and sudden death remain serious late complications after tetralogy of Fallot repair. Nevertheless, there remains no clear way of predicting which patients are at risk.
Methods and Results The study population included a total
of 178 adult survivors (mean follow-up, 21.4 years) of tetralogy of
Fallot repair who were currently attending our clinic.
Mechanoelectrical relations were sought in 41 of the patients (mean
follow-up, 23.6 years) who were operated on by one surgeon and who were
prospectively studied with a 12-lead ECG, chest radiography, and
two-dimensional and Doppler echocardiography. Nine patients (mean
follow-up, 17 years) from the total group of 178 were identified as
having had sustained ventricular tachycardia (8 with near-miss sudden
death), and their ECGs, Holter monitor readings, electrophysiological
studies, and chest radiographs were reviewed. The case notes of an
additional 4 patients with postoperative sudden cardiac death also were
available for review. QRS duration in the 41 patients in whom
mechanoelectrical interaction was sought ranged between 90 and 200
milliseconds and correlated with cardiothoracic ratio (CTR) on chest
radiography (r=.64, P<.001) and with right
ventricular size on echocardiography (r=.43,
P<.02). Twenty of the 41 patients had restrictive right
ventricular Doppler physiology (reduced ventricular compliance) with
mean QRS duration of 129.3±20 milliseconds and mean CTR of
0.51±0.03.
The remaining 21 patients with no evidence of right ventricular
restriction had prolonged QRS duration of 157.5±13.2 milliseconds
(P<.001) and CTR of 0.55±0.04 (P<.04) compared
with the restrictive. In the 9 patients with ventricular tachycardia,
the QRS duration ranged from 180 to 230 milliseconds (mean, 198.9±17.6
milliseconds), and the CTR ranged from 0.54 to 0.9 (mean, 0.67±0.12)
(P<.0001 and P<.01, respectively, compared with
patients without life-threatening arrhythmias). All patients with
documented sustained ventricular tachycardia and the 4 patients with
sudden death had a QRS duration of 
180 milliseconds (100%
sensitivity).
Conclusions Chronic right ventricular volume overload after
tetralogy of Fallot repair is related to diastolic function and
correlates with QRS prolongation. The risk of symptomatic arrhythmia is
high when marked right ventricular enlargement and QRS prolongation
develop. A QRS duration on the resting ECG of 180 milliseconds is the
most sensitive predictor of life-threatening ventricular arrhythmias
yet described.
Key Words: tetralogy of Fallot • arrhythmia • death • sudden • ventricles
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Arrhythmias remain a cause of morbidity and mortality after repair of tetralogy of Fallot.1 2 3 Sudden death, attributed to sustained ventricular arrhythmias, occurs in as many as 6% of patients after tetralogy of Fallot repair.1 4 Current management strategies for these patients vary widely, ranging from treatment for symptomatic patients only5 to active treatment of ventricular premature beats in asymptomatic patients.6 However, in a recent report, the presence of asymptomatic "complex ventricular arrhythmia" on Holter monitoring did not predict a worse outcome.7 There is some evidence that the chance of sudden death is increased in patients with residual right ventricular systolic and diastolic dysfunction.8 9 10 There are compelling data to suggest that left ventricular electrical instability may result from mechanical events (primarily ventricular dilatation and stretch),11 12 although such information in humans has been derived in the setting of ischemia. Tetralogy of Fallot represents a potentially important model for mechanolectricalal interactions because it is a nonischemic dilated model with both intrinsic myocardial and artificial scarring. A rational approach to this common clinical problem requires identification of patients who are clearly at risk of sudden death. The purpose of the present study was to address this problem by searching for any mechanolectricalal relation in adult survivors after tetralogy of Fallot repair that might relate to symptomatic ventricular arrhythmias and sudden death.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patients
We first performed a detailed study of 41 patients who underwent total repair of tetralogy of Fallot between 1958 and 1979, with a minimum follow-up of 15 years. This subgroup was chosen from the total number of 178 adult survivors who were followed in our clinic because they represent one of the earliest British cohorts of patients undergoing repair and they were operated on by one surgeon who used a uniform approach (otherwise, they were completely unselected, other than the fact that they had survived). Their age at the time of the study ranged from 16 to 46 years (mean, 28.8 years), and their age at complete repair ranged from 9 months to 18 years (mean, 5.2 years). Five patients (12.2%) had previously undergone palliative surgery (Blalock-Taussig shunts in 3 and the Brock procedure in 2). During repair, access in the majority was via a combined right atriotomy and ventriculotomy, although in 7 patients the transatrial/pulmonary approach was used. All patients had extensive infundibular resection, 7 patients had a patch to the infundibulum, and only 1 patient required a transannular patch. Eight patients (19.5%) required repeat operation (residual ventricular septal defect closure in 3, repeat operation on the right ventricular outflow tract because of severe pulmonary stenosis/regurgitation in 3 and bacterial endocarditis in 1, and balloon valvuloplasty for pulmonary stenosis in 1).
The
mechanoelectrical relation in these 41 patients was sought and then
tested and applied in our group of 178 adult survivors of tetralogy of
Fallot repair to establish whether this relation was sensitive,
specific, or both. Two additional groups derived from the 178 patients
currently attending our clinic were identified (Fig 1
):
a group of 9 patients with sustained ventricular tachycardia and a
group of 11 patients with atrial flutter. Data were also available from
hospital records on 4 cases of sudden death. Unfortunately, the case
records of 6 patients who died suddenly before 1989 had been destroyed.
These 178 patients represent a quaternary referral practice
from different primary and specialist hospitals and with different
surgeons; therefore, the observed incidence of hemodynamically
important arrhythmias or sudden death in our patients may not be
representative of an unselected cohort of patients after repair
of tetralogy of Fallot. However, this does not influence the
interpretation of our data.
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Techniques
Hemodynamic data were obtained for the 41 patients
with detailed
echocardiography as we have previously
described.13 14
Right and left ventricular long-axis lengths were measured from
two-dimensional echocardiograms in the four-chamber view at end
diastole. Patients had a 12-lead surface resting ECG performed with a
Hewlett-Packard PageWriter XLi (M1700A) at a speed of 25 mm/s and 1
mV/cm standardization and a posteroanterior chest radiograph. We
identified that QRS width in these patients correlated to right
ventricular size and related to both diastolic function and malignant
arrhythmias. ECGs were then reviewed in the 178 patients (before drug
therapy) and in the 4 cases of sudden death by two observers with no
knowledge of the clinical, radiographic, or echocardiographic findings.
Maximal QRS width in any lead was measured from the first to the last
sharp vector crossing the isoelectric line. Data from all 16 patients
who underwent electrophysiological study for symptoms (syncope or
palpitations) also were reviewed. Ventricular stimulation was performed
in all, as described by Wellens et al,15 including two
extrastimuli at two or three sites at two rates. Rapid pacing was not
performed. Standard conduction intervals were measured and AV
conduction was analyzed with incremental atrial pacing.
Statistical Analysis
Group data are expressed as
mean±SD. Student's t
tests were used to compare normally distributed variables; otherwise, a
Mann-Whitney U test was performed. Regression analysis
was performed using the method of least squares. The null hypothesis
was rejected when P<.05.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Mechanoelectrical Relation
Of the 41 patients studied in detail, 39 were in New York Heart Association functional class I (95.1%).
Biventricular Function
Twenty patients had evidence of right
ventricular restrictive
physiology (low right ventricular compliance), as demonstrated by the
presence of antegrade diastolic flow in the pulmonary artery coinciding
with atrial systole throughout the respiratory cycle. A detailed
analysis of the patients' right ventricular diastolic function has
been presented elsewhere.15 Biventricular systolic
function was well preserved in all (left ventricular shortening
fraction, 26% to 45%). Two patients had significant residual right
ventricular outflow tract obstruction (>40 mm Hg). No attempt was
made to measure the degree of pulmonary regurgitation because of the
inherent inaccuracy of clinical and Doppler echocardiography methods in
these patients.
ECG and Right Ventricular Size
All except 1 patient was in
sinus rhythm, and all of the patients
had a right bundle-branch block pattern on the surface ECG. It became
apparent during the initial investigations that there was a clinically
obvious difference in the QRS duration of the resting ECG of these
patients. Maximum QRS duration ranged from 90 to 200 milliseconds and
correlated with cardiothoracic ratio (CTR) on chest radiograph
(r=.64, P<.001; Fig 2) and with
right ventricular long-axis length when expressed as a ratio of
right-to-left ventricle (r=.43, P<.02; Fig
3). Those with restrictive right ventricular Doppler
physiology had a mean QRS duration of 129.3±20 milliseconds,
significantly shorter than those without, who had a prolonged QRS
duration (mean, 157.5±13 milliseconds; P<.001; Fig
4). The mean CTR was also smaller in those with
restrictive physiology (0.51±0.03) compared with those without
(0.55±0.04; P<.01). QRS duration was not particularly
prolonged in the 2 patients with significant right ventricular outflow
tract obstruction (150 ms/64 mm Hg and 130 ms/100 mm Hg,
respectively).
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Sustained Ventricular Tachycardia
Nine patients (5%) of the
178 were identified as having had
documented sustained ventricular tachycardia. Two of them were among
the 41 patients in whom a mechanoelectrical relation was sought, both
without evidence of restriction (QRS duration, 180 and 200
milliseconds, respectively). Eight of the 9 patients had syncopal
episodes requiring cardiopulmonary resuscitation (near-miss sudden
death). All 9 had undergone an electrophysiological study during which
ventricular tachycardia was easily inducible with one or two
extrastimuli and terminated, and a reentry mechanism was confirmed. The
maximum QRS duration on the resting ECG before onset of sustained
ventricular arrhythmia and before drug therapy ranged from 180 to 230
milliseconds (mean, 198.9±17.6 milliseconds), and CTR ranged from 0.54
to 0.9 (mean, 0.67±0.12), significantly longer (QRS,
P<.0001) and larger (CTR, P<.01) compared with
patients without life-threatening arrhythmias
(Table).
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Sudden Death
Four patients with sudden death after tetralogy
of Fallot
repair were identified from the available hospital records (age at
repair: range, 0.5 to 29 years; mean, 8.9 years; and time from repair
at death: range, 9 to 19 years; mean, 16 years). QRS duration on the
ECG before death ranged from 180 to 220 milliseconds (mean, 193.8±18.9
milliseconds), and CTR ranged from 0.59 to 0.67 (mean, 0.63±0.03). As
all patients were previously asymptomatic, they had not undergone
electrophysiological studies. Their QRS duration combined with that of
the syncopal arrhythmic patients from our complete group of 178
patients is compared with the QRS duration of the remainder of the
patients studied (Fig 5).
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Previous palliations, approach, age at repair or need for repeat operation, and age at follow-up were not significant factors in determining whether symptomatic ventricular tachycardia or sudden death occurred.
Atrial Flutter
Eleven patients (6.2%) with documented atrial
flutter were
identified from our total group of 178 survivors (age at repair: range,
6 to 21 years; mean, 10.4 years; and follow-up time: range, 16 to 30
years; mean, 23.3 years). The maximum QRS duration on the surface ECG
ranged from 160 to 200 milliseconds (mean, 177.8±13 milliseconds), and
CTR ranged from 0.57 to 0.78 (mean, 0.64±0.07). One patient, who had
severe tricuspid regurgitation (CTR, 0.78; QRS, 200 milliseconds), was
syncopal. The remaining 10 tolerated the arrhythmias well. There was no
overlap of patients between the group with atrial flutter and the group
with sustained ventricular tachycardia.
Seven additional patients of the 178 underwent electrophysiological studies (because of undiagnosed symptoms), during which no inducible sustained ventricular tachycardia was found. Four of the 7 patients were syncopal: 3 with neurogenic syncope and 1 with epilepsy. The other 3 were nonsyncopal patients with atrial flutter.
The mean age at repair
of patients with significant arrhythmias and
their mean follow-up time with maximum QRS width and CTR at onset of
arrhythmia are shown in the Table
.
Sensitivity and Specificity of QRS 180 Milliseconds as a Risk
Marker of Malignant Ventricular Arrhythmias
There was no patient with
sustained ventricular tachycardia or
sudden death with a QRS duration of <180 milliseconds (100%
sensitivity).
There are 9 additional patients, none of whom gave a
history of
life-threatening events, with a QRS duration of 180 milliseconds. Six
of them had atrial flutter, and 3 had no documented arrhythmia.
Therefore, the specificity of QRS duration of 180 milliseconds as a
single predictor of symptomatic ventricular tachycardia is 94.7%. The
negative predictive value for life-threatening ventricular arrhythmias
or sudden death with a QRS duration of <180 milliseconds was
100%.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The introduction of open heart repair of tetralogy of Fallot by Lillehei and colleagues in 195516 has transformed the outcome of a condition in which fewer than one fourth of patients could be expected to survive past the first decade17 to one in which early corrective surgery can be performed with a mortality rate of <5%. Although the late outcome of these patients is favorable in reported series,1 10 18 sudden death remains a complication. Sudden death has occurred in almost every large series with long postoperative follow-up,1 19 20 and death after tetralogy of Fallot repair is the most common cause of sudden death in childhood.21
Both atrial and ventricular arrhythmias are recognized after repair of tetralogy of Fallot, but there is no clear-cut relation between atrial arrhythmia and sudden death. There is no doubt, however, that patients who develop sustained ventricular tachycardia are at risk of syncope and sudden death. There is good evidence from electrophysiological studies that sustained ventricular tachycardia, in this setting, results from reentry,22 which requires areas of slow conduction. Right bundle-branch block is very common and may be central, "myocardial," or both.23 24 Furthermore, fragmented electrograms, indicative of localized areas of slowed conduction, have been recorded from both the inflow25 and the outflow tracts26 and throughout the right ventricle.27 Finally, the ventriculotomy scar,28 ventricular septal defect,25 and outflow patch26 have each been implicated as areas of potential block within the reentry circuit. Although patients with sustained ventricular tachycardia are relatively uncommon, nonsustained ventricular arrhythmia ranging from ventricular premature beats to nonsustained ventricular tachycardia is seen in as many as 42% of patients after repair of tetralogy on 24-hour tape.19 The great majority of such patients are asymptomatic. It has been suggested that ventricular electrical extra activity is a marker for patients at risk for sustained ventricular tachycardia and sudden death. This has led to asymptomatic patients with more than 30 ventricular premature beats per hour being treated with antiarrhythmic drugs.6 The wisdom of this has to be questioned.29 The relation between these nonsustained ventricular arrhythmias (which may result from a different mechanism) and sustained ventricular tachycardia is far from clear. Many studies have attempted to identify risk factors for sudden death by examining the relation between hemodynamic and electrophysiological variables and the frequent ventricular ectopy seen on 24-hour tape recordings; results have been unclear. Even if they are a reliable marker of patients susceptible to sustained ventricular tachycardia and therefore sudden death, the value of treatment to suppress a marker is a matter of debate.30 Cullen et al7 recently showed that even the so-called high-grade ventricular arrhythmias on Holter monitoring do not appear to be predictive for sudden death on long-term follow-up.7
Previous studies have emphasized the possible additional influence of persisting right ventricular hypertension8 and pulmonary regurgitation31 on late sudden death, and this suggests that a mechanoelectrical interaction may exist in these patients, but the basis of this phenomenon has not been explored. In the present study, we performed detailed studies of right ventricular diastolic function in one of the earliest cohorts of survivors of complete correction of tetralogy of Fallot. At a mean follow-up of 23.6 years, approximately half of the patients had evidence of restrictive right ventricular diastolic function. The presence of antegrade diastolic pulmonary arterial flow, which limits the degree of pulmonary regurgitation, is indicative of a limited end-diastolic volume.13 14 As a result, these patients have a significantly lower CTR, which in turn reflects lower right ventricular long-axis dimensions. The ultrastructural nature of the myocardial process that prevents progressive right ventricular dilatation, even in the presence of potentially free pulmonary regurgitation, is unknown but appears to be unrelated to surgical technique and other anthropometric details. Regardless of the cause, patients with restrictive right ventricular physiology have a significantly shorter QRS duration. Furthermore, we have shown a statistically significant correlation between right ventricular size and QRS duration for the group as a whole. Conversely, QRS width was not particularly prolonged in cases of significant residual right ventricular outflow obstruction alone, suggesting that the QRS prolongation reflects right ventricular dilation rather than an increase in right ventricular mass due to hypertrophy. That is, as the postoperative tetralogy right ventricle dilates, the QRS duration is prolonged, and this in turn creates the conditions required for reentry.
In the present study, all 9 patients with documented sustained
ventricular tachycardia had a reentry mechanism confirmed during
electrophysiological study. All had delayed conduction with a prolonged
QRS complex of 180 milliseconds (mean, 200 milliseconds;
P<.001 compared with nonarrhythmic patients) before the
onset of tachycardia. It has been suggested that in the presence of
large areas of delayed conduction, ventricular tachycardia is more
likely to break down to ventricular fibrillation,32 and 8
of the 9 patients had experienced near-miss sudden death. Not
surprisingly, the CTR was significantly larger in this subgroup
compared with the nonsymptomatic arrhythmia patients.
Eleven of the patients (5%) had documented atrial flutter. Only 1 was
syncopal, and this patient had a QRS width of 200 milliseconds at the
onset of symptomatic arrhythmia. This patient has severe tricuspid
regurgitation with gross cardiomegaly (CTR, 0.78). The mechanism of
syncope in this case is uncertain, and we cannot exclude ventricular
tachycardia even in the presence of atrial flutter. QRS duration and
CTR ratio were relatively increased in the atrial flutter group
compared with the nonarrhythmia patients (Table). Tricuspid
regurgitation on echocardiography was significant in 8 of these
patients, and this might be the cause of concomitant right atrial and
right ventricular enlargement. These patients are clearly susceptible
to atrial flutter and may, for the same reasons, also be predisposed to
ventricular arrhythmias. Even so, a resting QRS duration of 180
milliseconds is a highly sensitive predictor of hemodynamically
important arrhythmia in the group as a whole, with a negative
predictive value of 100%.
We believe that the mechanical and electrical properties of the right
ventricle after tetralogy of Fallot repair are interrelated, with a
potentially causative relation between right ventricular dilation and
life-threatening arrhythmias. Sustained ventricular tachycardias in
this group are more common. We speculate that there is a subgroup of
patients with both progressive dilatation of the right ventricle and a
predisposition to ventricular arrhythmias. When a certain threshold of
ventricular dilation and slowed conduction is reached (as demonstrated
by a QRS duration of 180 milliseconds), these patients, who may be
asymptomatic, are at risk of severe ventricular arrhythmia and sudden
death. Zhou et al33 showed stretch-induced ventricular
arrhythmias in experimental models, whereas Waxman et al34
showed that a decrease in right ventricular volume, caused by
Valsalva's maneuver, can lead to termination of ventricular
tachycardia in some patients. Exercise-induced sudden death in these
patients may be related to transient further right ventricular
dilatation secondary to increased stroke volume. Whether it follows
that restoration of a competent right ventricular outflow tract by
pulmonary valve replacement in cases of severe pulmonary incompetence
with resultant marked right ventricular dilatation could alter the
outcome remains speculative, however.
We have shown that the mechanical and electrical properties of the right ventricle after tetralogy of Fallot repair are interrelated. However, we recognize that our patients reflect the outcome of early surgery performed by many different surgeons, with different techniques. Furthermore, this is a retrospective, uncontrolled study with a potential for selection bias because of the nature of referrals. Nevertheless, it is reflective of these patients currently presenting in adult life.
It is not clear whether newer surgical strategies will influence outcome. The incidence of right bundle-branch block has been reduced by the transatrial approach to repair,24 for example. The timing and nature of surgery also may affect the mechanolectricalal relation. Nevertheless, in our group of patients, those with restrictive right ventricular Doppler physiology are protected from the effects of pulmonary incompetence15 35 and late sustained ventricular arrhythmias.
The immediate clinical implications of our data are obvious. We now
have a readily measurable, sensitive, and specific predictor for
patients at risk of life-threatening ventricular arrhythmias late after
repair of tetralogy of Fallot. Patients with a QRS duration of 180
milliseconds can be easily identified and evaluated. Their hemodynamic
status should be examined. The use of electrophysiological study in
this group may be able to further identify a subgroup of patients at
risk of clinical sustained reentry ventricular tachycardia. This group
may benefit from prophylactic antiarrhythmic therapy or more definitive
treatment in the form of catheter ablation or surgery.
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Acknowledgments |
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We thank Dr S.Y. Ho for her help with the figures and diagrams.
Received October 26, 1994; revision received December 29, 1994; accepted January 10, 1995.
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C. A. Warnes The Adult With Congenital Heart Disease: Born To Be Bad? J. Am. Coll. Cardiol., July 5, 2005; 46(1): 1 - 8. [Abstract] [Full Text] [PDF]
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C. Alexiou, H. Mahmoud, A. Al-Khaddour, J. Gnanapragasam, A. P. Salmon, B. R. Keeton, and J. L. Monro Outcome after repair of tetralogy of Fallot in the first year of life Ann. Thorac. Surg., February 1, 2001; 71(2): 494 - 500. [Abstract] [Full Text] [PDF]
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B. Discigil, J. A. Dearani, F. J. Puga, H. V. Schaff, D. J. Hagler, C. A. Warnes, and G. K. Danielson Late pulmonary valve replacement after repair of tetralogy of Fallot J. Thorac. Cardiovasc. Surg., February 1, 2001; 121(2): 0344 - 351. [Abstract] [Full Text] [PDF]
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S Brili, C Aggeli, K Gatzoulis, A Tzonou, C Hatzos, C Pitsavos, C Stefanadis, and P Toutouzas Echocardiographic and signal averaged ECG indices associated with non-sustained ventricular tachycardia after repair of tetralogy of Fallot Heart, January 1, 2001; 85(1): 57 - 60. [Abstract] [Full Text]
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J. Therrien, S. C. Siu, P. R. McLaughlin, P. P. Liu, W. G. Williams, and G. D. Webb Pulmonary valve replacement in adults late after repair of tetralogy of Fallot: are we operating too late? J. Am. Coll. Cardiol., November 1, 2000; 36(5): 1670 - 1675. [Abstract] [Full Text] [PDF]
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M A Gatzoulis, J Walters, P R McLaughlin, N Merchant, G D Webb, and P Liu Late arrhythmia in adults with the Mustard procedure for transposition of great arteries: a surrogate marker for right ventricular dysfunction? Heart, October 1, 2000; 84(4): 409 - 415. [Abstract] [Full Text]
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M Y A. El Rahman, H Abdul-Khaliq, M Vogel, V Alexi-Meskishvili, M Gutberlet, and P E Lange Relation between right ventricular enlargement, QRS duration, and right ventricular function in patients with tetralogy of Fallot and pulmonary regurgitation after surgical repair Heart, October 1, 2000; 84(4): 416 - 420. [Abstract] [Full Text]
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 M. E. Brickner, L. D. Hillis, and R. A. Lange Congenital Heart Disease in Adults- Second of Two Parts N. Engl. J. Med., February 3, 2000; 342(5): 334 - 342. [Full Text] [PDF]
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V. Rao, M. Kadletz, L. K. Hornberger, R. M. Freedom, and M. D. Black Preservation of the pulmonary valve complex in tetralogy of Fallot: how small is too small? Ann. Thorac. Surg., January 1, 2000; 69(1): 176 - 179. [Abstract] [Full Text] [PDF]
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R. R. Chaturvedi, D. F. Shore, C. Lincoln, S. Mumby, M. Kemp, J. Brierly, A. Petros, J. M.G. Gutteridge, J. Hooper, and A. N. Redington Acute Right Ventricular Restrictive Physiology After Repair of Tetralogy of Fallot : Association With Myocardial Injury and Oxidative Stress Circulation, October 5, 1999; 100(14): 1540 - 1547. [Abstract] [Full Text] [PDF]
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M. A. Norgaard, P. Lauridsen, M. Helvind, and G. Pettersson Twenty-to-thirty-seven-year follow-up after repair for Tetralogy of Fallot Eur. J. Cardiothorac. Surg., August 1, 1999; 16(2): 125 - 130. [Abstract] [Full Text] [PDF]
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E. N. Oechslin, D. A. Harrison, L. Harris, E. Downar, G. D. Webb, S. S. Siu, and W. G. Williams REOPERATION IN ADULTS WITH REPAIR OF TETRALOGY OF FALLOT: INDICATIONS AND OUTCOMES J. Thorac. Cardiovasc. Surg., August 1, 1999; 118(2): 245 - 251. [Abstract] [Full Text] [PDF]
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P. Schaffer, B. Pelzmann, E. Bernhart, P. Lang, H. Machler, B. Rigler, and B. Koidl Repolarizing currents in ventricular myocytes from young patients with tetralogy of Fallot Cardiovasc Res, August 1, 1999; 43(2): 332 - 343. [Abstract] [Full Text] [PDF]
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L Daliento, G Rizzoli, L Menti, M C Baratella, P Turrini, A Nava, and S Dalla Volta Accuracy of electrocardiographic and echocardiographic indices in predicting life threatening ventricular arrhythmias in patients operated for tetralogy of Fallot Heart, June 1, 1999; 81(6): 650 - 655. [Abstract] [Full Text]
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K A McLeod, W S Hillis, A B Houston, N Wilson, A Trainer, J Neilson, and W B Doig Reduced heart rate variability following repair of tetralogy of Fallot Heart, June 1, 1999; 81(6): 656 - 660. [Abstract] [Full Text]
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S. Conte, R. Jashari, B. Eyskens, M. Gewillig, M. Dumoulin, and W. Daenen Homograft valve insertion for pulmonary regurgitation late after valveless repair of right ventricular outflow tract obstruction Eur. J. Cardiothorac. Surg., February 1, 1999; 15(2): 143 - 149. [Abstract] [Full Text] [PDF]
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S. B. O'Blenes, D. B. Ross, M. A. Nanton, and D. A. Murphy Atrioventricular septal defect with tetralogy of fallot: results of surgical correction Ann. Thorac. Surg., December 1, 1998; 66(6): 2078 - 2082. [Abstract] [Full Text] [PDF]
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D. P. Zipes and H. J. J. Wellens Sudden Cardiac Death Circulation, November 24, 1998; 98(21): 2334 - 2351. [Full Text] [PDF]
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P. Munkhammar, S. Cullen, P. Jogi, M. de Leval, M. Elliott, and G. Norgard Early age at repair prevents restrictive right ventricular (RV) physiology after surgery for tetralogy of Fallot (TOF): Diastolic RV function after TOF repair in infancy J. Am. Coll. Cardiol., October 1, 1998; 32(4): 1083 - 1087. [Abstract] [Full Text] [PDF]
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G Norgård, M A Gatzoulis, M Josen, S Cullen, and A N Redington Does restrictive right ventricular physiology in the early postoperative period predict subsequent right ventricular restriction after repair of tetralogy of Fallot? Heart, May 1, 1998; 79(5): 481 - 484. [Abstract] [Full Text]
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I. M. Yemets, W. G. Williams, G. D. Webb, D. A. Harrison, P. R. McLaughlin, G. A. Trusler, J. G. Coles, I. M. Rebeyka, and R. M. Freedom Pulmonary Valve Replacement Late After Repair of Tetralogy of Fallot Ann. Thorac. Surg., August 1, 1997; 64(2): 526 - 530. [Abstract] [Full Text]
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R. R. Chaturvedi, P. J. Kilner, P. A. White, A. Bishop, R. Szwarc, and A. N. Redington Increased Airway Pressure and Simulated Branch Pulmonary Artery Stenosis Increase Pulmonary Regurgitation After Repair of Tetralogy of Fallot: Real-Time Analysis With a Conductance Catheter Technique Circulation, February 4, 1997; 95(3): 643 - 649. [Abstract] [Full Text]
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M. A. Gatzoulis, J. A. Till, and A. N. Redington Depolarization-Repolarization Inhomogeneity After Repair of Tetralogy of Fallot: The Substrate for Malignant Ventricular Tachycardia? Circulation, January 21, 1997; 95(2): 401 - 404. [Abstract] [Full Text]
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