(Circulation. 2001;103:3075.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Dispersion of Ventricular Depolarization-Repolarization
A Noninvasive Marker for Risk Stratification in Arrhythmogenic Right Ventricular Cardiomyopathy
From the Departments of Pathology (P.T., C.B., G.T.) and Cardiology (D.C., A.N., B.B.), University of Padua Medical School, Padua, Italy.
Correspondence to Gaetano Thiene, MD, FESC, Istituto di Anatomia Patologica, Via A. Gabelli, 61, 35121 Padua, Italy. E-mail cardpath{at}unipd.it
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Abstract |
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Background—We retrospectively investigated the value of clinical and ECG findings as well as QT-QRS dispersion in predicting the risk of sudden death in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC).
Methods and
Results—Duration and interlead variability of
the QT interval and QRS complex were measured manually from standard
ECGs in 20 sudden death victims with ARVC diagnosed at autopsy (group
I), in 20 living ARVC patients with sustained ventricular
tachycardia (group II), in 20 living ARVC patients with 
3
consecutive premature ventricular beats (group III), and in
20 control subjects (group IV). QT and QRS dispersions were greater in
group I (77.5±10.6 ms for QT and 45.7±8.1 ms for QRS) compared with
group II (64.5±13.9 ms for QT
[P=0.001] and 33.5±8.7 ms
for QRS [P=0.0004]) and in
group II compared with group III (48±8.9 ms for QT
[P<0.0001] and 28±5.2 ms
for QRS [P<0.0001]) and
group IV (33.5±4.8 ms for QT
[P<0.0001] and 18.5±3.6 ms
for QRS [P<0.0001]).
Negative T wave beyond V1 and syncope were
statistically more frequent in group I
(P=0.02 and
P=0.007, respectively). On
multivariate analysis, QRS dispersion remained
an independent predictor of sudden death
(P<0.0001), followed by
syncope (P=0.09). In assessing
risk of sudden death, QRS dispersion 
40 ms had a sensitivity and
specificity of 90% and 77%, respectively; QT dispersion >65 ms, 85%
and 75%, respectively; negative T wave beyond
V1, 85% and 42%, respectively; and syncope,
40% and 90%, respectively.
Conclusions—QRS
dispersion (40 ms) was the strongest independent predictor of sudden
death in ARVC. Syncope, QT dispersion >65 ms, and negative T wave
beyond V1 refined arrhythmic risk stratification
in these patients.
Key Words: cardiomyopathy • death, sudden • electrocardiography
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The natural history of arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) is a function of both the electrical instability of dystrophic myocardium, which can precipitate sudden death any time during the disease course, and the progressive myocardial loss that results in ventricular dysfunction and heart failure.1 2 3 4 5 Sudden death accounts for the majority of the fatal events, and it is more common in adolescents and young adults.6 Invasive markers for unfavorable outcome in ARVC include inducible ventricular tachycardia (VT), drug failure during serial electrophysiological studies, RV dilatation, and left ventricular involvement.7 8 In contrast, there is still limited clinical information on noninvasive risk stratification, especially when no sustained VT has been documented.9 Patients with a history of syncope,10 11 familial sudden death,12 and precordial T-wave inversion beyond V38 seem to have a worse prognosis.
Measurement of the interlead variability in QT-interval duration on the standard 12-lead ECG, known as QT dispersion, has been proposed as a simple noninvasive method for detecting regional differences in ventricular recovery times of excitability.13 In ARVC, body-surface QRST integral mapping revealed the presence of repolarization abnormalities,14 which might be correlated with vulnerability to malignant ventricular arrhythmias.15 Benn et al16 measured an increased QT dispersion in ARVC patients, without significant differences between individuals considered at low and high risk for life-threatening arrhythmias. Peters et al8 demonstrated that an increased dispersion of QRS complex in precordial leads was a noninvasive predictor of recurrent arrhythmic events. However, these ECG markers have never been evaluated in patients who died suddenly with ARVC proven at autopsy.
The present study was designed to investigate the value of clinical and ECG findings as well as QT-QRS dispersion in predicting the risk of sudden death in a large group of ARVC patients.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Population
We examined 12-lead ECGs in 4 different groups of patients, for whom Table 1
gives the main clinical and ECG data. Group I
included 20 consecutive patients with ARVC and available ECG who died
suddenly. The pathological diagnosis was proven at autopsy in all and
was based on the finding of gross and/or histological
evidence of transmural loss of myocardium with fibrofatty
replacement of the RV free wall myocardium, either regional
or diffuse, in the absence of valve, coronary, and pericardial
disease or other known cardiac or noncardiac causes of
death.1 3 6
Groups II and III included 20 age- and sex-matched living patients,
each with an overt form of ARVC. All the patients fulfilled the
diagnostic criteria of ARVC recommended by the Task Force
of the European Society of
Cardiology.17
According to these criteria, ARVC was defined to be diffuse when
imaging techniques such as echocardiography,
angiography, MRI, or radionuclide scintigraphy showed a
widespread RV involvement with a global RV dilatation and ejection
fraction reduction. Localized RV disease was diagnosed in the presence
of regional RV lesions, such as segmental RV wall motion abnormalities
(hypo-akinetic or dyskinetic areas), with mild or no ejection fraction
reduction. At postmortem examination, RV involvement was defined as
diffuse or regional when fibrofatty replacement of the RV was found to
be widespread or segmental, respectively. Left ventricular
involvement was diagnosed in the presence of either localized or
diffuse pathological lesions/wall motion abnormalities of the left
ventricular free wall, with or without septal involvement.
Endomyocardial biopsy was available for all
patients from group II and for 14 of 20 patients from group III. The
extent of RV disease and incidence of left ventricular
involvement were comparable in the 3 ARVC groups
(Table 1). Patients of group II experienced spontaneous
sustained (30-second) monomorphic VT (mean rate 210±37 bpm), whereas
patients of group III had 3 consecutive premature
ventricular beats at ECG and/or Holter monitoring. Group IV
consisted of 20 age- and sex-matched healthy control subjects with no
history of arrhythmia or syncope and normal ECG
patterns.
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ECG Features
Analysis of ECG focused on the following
parameters: 
waves, defined according to Fontaine et
al18 as distinct waves of
small amplitude that occupy the QT segment in the right precordial
leads; negative T wave beyond V1; ST-segment
elevation, defined as maximal displacement of ST segment with upward
convexity 0.5 mm from the isoelectric line; and complete right
bundle-branch block (RBBB), defined as a prolonged QRS complex 120
ms. Patients with a Brugada-like ECG pattern (Brugada and
Brugada19 ) characterized by
high take-off ST-segment elevation 1 mm of "coved" or
"saddle-back" type were excluded.
ECG Measurements
No patients were on antiarrhythmic drugs or other
drugs known to affect the QRS complex and/or the QT interval during or
before acquisition of the ECG tracings analyzed in the
present study. All patients were in sinus rhythm. The 12-lead ECGs
were obtained in the traditional lead position and recorded at
25 mm/s. To increase the accuracy of measurements, all the ECGs
were enlarged x2 to obtain for all a format comparable to 50
mm/s. The QT interval and QRS-complex duration were measured manually
at each lead by means of a method previously
described.20 21
The QT interval was measured from the onset of the QRS complex to the
end of the T wave, ie, return to the T-P baseline. When U waves
were present, the QT interval was measured to the nadir of the
curve between the T and U waves. The QRS-complex duration was measured
from the beginning of the QRS complex to its end. When the offset of
QRS complex was difficult to define because of a gradual slope toward a
plateau, it was measured at the intersection of the S wave with the
isoelectric baseline. The JT interval was calculated by subtracting QRS
duration from QT (means) interval in individual leads. Whenever
possible, 3 consecutive cycles were measured in each of 12 leads to
calculate a mean value of RR from these 3 values. When the end of the
QRS complex or T wave could not be identified, the lead was not
included. Three precordial leads at least and a minimum of 7 leads
were required for QT/QRS/JT dispersion. The QT, QRS, and JT dispersions
were defined as the difference between the maximum and minimum QT, QRS,
and JT values occurring in any of the 12 ECG leads,
respectively.
The percentage of missing leads for determination of QT dispersion and QRS dispersion was 8.7% and 4.2%, respectively, for group I; 9.2% and 5%, respectively, for group II; 7.9% and 4.6%, respectively, for group III; and 6.2% and 2%, respectively, for group IV.
Cutoff values and correlations between dispersions of QT, QRS, and JT intervals were assessed by using uncorrected values. In addition, we provide rate-corrected values of QT and JT intervals and dispersions with the use of Bazett’s formula.
Two independent observers, blinded as to the clinical data, tested the repeatability of these measurements in a random sample of 20 ECGs. For the same ECG tracings, the percentage differences in QT/QRS/JT dispersion measurements ranged from 2% to 6% for within-observer variability and 2% to 7% for between-observer variability.
Statistical Analysis
All analyses were performed with STATA,
version 6.0 (STATA Corp, 1999). All continuous variable values are
reported as mean±1 SD. Continuous variables were analyzed
by use of ANOVA with the Bonferroni correction for multiple comparisons
or by use of the Spearman correlation of ranks when appropriate.
Categorical variables were analyzed by use of contingency
tables and the Pearson 
2 method. The
independent correlation of clinico-ECG variables with sudden death
was determined by means of multivariate logistic
regression analysis, with sudden death as a dependent
variable. Variables with a value of
P0.1 in the
univariate analysis (maximum QT interval [both
uncorrected and rate-corrected] and QRS complex, QT/QRS/JT dispersion,
rate-corrected QT and JT dispersions, negative T wave beyond
V1, syncope, ST-segment elevation in right
precordial leads, and RBBB) were considered candidates for
multivariable analysis. We estimated the odds ratio and
95% CIs of the variables independently associated with sudden
death. A value P0.05 was
considered statistically
significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Clinical and ECG Findings
History of syncope was statistically more frequent in group I than in groups II and III (Table 1
). RR intervals were similar in the 4 groups. The
incidence of negative T wave beyond V1 was
higher in group I than in groups II and III.
There was no significant difference in waves as well as
ST-segment elevation among the ARVC groups. Isolated complete RBBB was
found in 3 patients each in groups I and II and in 1 patient in group
III. Only 1 patient of group I showed complete RBBB with
coexistent ST-segment elevation.
QT/QRS/JT Interval
Table 2 reports maximum and minimum QT, QRS, and JT
intervals in the 4 groups. QT and QRS intervals tended to be higher in
group I. Maximum values of QRS and QT intervals were measured in the
right precordial leads in all the patients of groups I, II, and
III. In group IV, maximum QT interval and QRS duration were found in
the right precordial leads in 10 and 8 subjects,
respectively.
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QT/QRS/JT Dispersion
QT and QRS dispersions
(Table 3) were greater in group I than in group II and
greater in group II than in groups III and IV. JT dispersion did not
differ significantly in the 3 ARVC groups. In group I, the subgroup of
4 patients with RBBB had similar values of QT, QRS, and JT dispersions
compared with values in the subgroup of patients without RBBB (with
RBBB versus without RBBB, respectively: 81.2±3 versus 76.8±11.9 ms
[P=NS] for QT, 50±8.1 versus
44.6±8 ms [P=NS] for QRS,
and 35±5.7 versus 32.8±4.4 ms
[P=NS] for JT). Also, in
group II, the subgroup of 3 patients with RBBB had similar values of
QT, QRS, and JT dispersions compared with the subgroup of patients
without RBBB (with RBBB versus without RBBB, respectively: 73.3±11.5
versus 62.9±14 ms [P=NS] for
QT, 43.3±11.5 versus 31.1±7.2 ms
[P=NS] for QRS, and 33.3±5.7
versus 32.3±8.3 ms [P=NS]
for JT).
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Figures 1 and 2 provide the individual values of QT and QRS
dispersions, respectively, in the 3 ARVC groups.
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Correlations Between Intervals and
Dispersions
There were significant correlations between QRS
duration or QT interval and the dispersions of QT/QRS/JT when all the
ARVC patients were considered as a single group
(Table 4). QT dispersion correlated strongly with QRS
dispersion and JT dispersion. There was a particularly close
correlation between QRS dispersion and maximal QRS duration. QT
dispersion had a significant relationship with maximum QT
interval.
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Accuracy of Clinico-ECG Variables in
Predicting the Risk of Sudden Death
A history of syncope had a sensitivity and specificity
in predicting the occurrence of sudden death of 40% and 90%,
respectively; a negative T wave beyond V1 had a
sensitivity and specificity in predicting the occurrence of sudden
death of 85% and 42%, respectively.
For QT, QRS, and JT dispersions, we considered as the upper
limit of low arrhythmic risk the 99% tolerance limits (mean±2 SD) of
the values of group III. The following cutoff values were indicative of
high risk: QT dispersion >65 ms, QRS dispersion 40 ms, and JT
dispersion 40 ms.
A QRS dispersion 40 ms showed a sensitivity and a
specificity in identifying patients at risk of sudden death of 90% and
77%, respectively
(Figure 2); a QT dispersion >65 ms, 85% and 75%,
respectively
(Figure 1); and a JT 40 ms, 30% and 72%, respectively.
When these parameters were used in combination, there was
an increased in specificity for QRS plus QT dispersion (82%) and for
QT plus QRS plus JT dispersions (85%) associated with a reduction of
sensitivity (85% and 30%, respectively).
Multivariate Analysis
of Risk Factors for Sudden Death
We performed a stepwise logistic regression
analysis incorporating all the clinical and ECG-derived
variables to determine independent predictors of sudden death. Only
QRS dispersion remained an independent predictor of sudden death (odds
ratio 1.22, CI 1.11 to 1.35;
P<0.0001), followed by history
of syncope (odds ratio 5.9, CI 0.71 to 49.44;
P=0.09).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The main findings of the present study were that QRS dispersion (
40 ms) was the strongest independent predictor of
sudden death in ARVC patients; increased QRS dispersion resulted mainly
from localized prolongation of the QRS complex in the right
precordial leads; syncope, QT dispersion >65 ms, and negative T
wave beyond V1 refined noninvasive risk
stratification for sudden death.
Pathophysiology of Ventricular
Arrhythmias in ARVC
VT and fibrillation are well-documented causes of
sudden death in
ARVC.1 2 4 8
The peculiar histopathology of the disease predisposes the patient to
malignant ventricular
arrhythmias.18 22
In ARVC, VT is generally believed to be
reentrant4 9 and is
usually accompanied by abnormalities of ventricular
activation.4 23
Localized prolongation of QRS duration in the right precordial
leads is a well-recognized feature of ARVC, and a duration of 110 ms
is considered a main diagnostic
criterion.17 A reentry
mechanism is suggested by the inducibility of VT by programmed
ventricular
stimulation,4 18 22
together with a high frequency of late
potentials,24 25
and by the finding of areas of slow conduction during endocardial
mapping of the
RV.4 26 27
Recently, it has been hypothesized that repolarization abnormalities in
ARVC may facilitate the occurrence of ventricular
arrhythmias15 with a
mechanism that can be modulated by autonomic nervous system
activity.24
QT Dispersion
Experimental studies have provided powerful evidence
that nonuniform recovery of ventricular excitability plays
an important role in the mechanism of ventricular
arrhythmias.28
Potentially arrhythmogenic nonuniform recovery of excitability is the
result of either dispersion of refractoriness or activation times
depending on the underlying pathophysiological
substrate.29 The interlead
variability in QT-interval duration on the standard 12-lead ECG, the
so-called QT dispersion, is a noninvasive method for detecting regional
differences in ventricular recovery
time.13 Experimental studies
confirmed that QT dispersion is significantly correlated with
dispersion of ventricular recovery time, measured directly
from
myocardium.30
The studies on QT dispersion have provided information about regional
variations in ventricular repolarization in many diseases
characterized by malignant ventricular arrhythmias,
such as myocardial
infarction,31
coronary artery
disease,32 long-QT
syndrome,13 hypertrophic
cardiomyopathy,33
chronic heart failure,34 and
repaired tetralogy of
Fallot.35
In our ARVC patient population, QT dispersion was significantly greater in the patients who died suddenly compared with living patients with different arrhythmic profiles. Our cutoff value for QT dispersion, >65 ms, is similar to that reported by Surawicz.36 Also, Benn et al16 measured an increased QT dispersion in ARVC patients, but they did not find significant differences between individuals considered at low and high risk for life-threatening arrhythmias. However, patients who died suddenly were only 5 of 11 high-risk patients (45%), and the mean QRS duration of the whole high-risk group was smaller than that of our victims of sudden death. Peeters et al,15 analyzing ARVC patients with sustained VT and overt forms of the disease, did not find an increased QT dispersion, although they demonstrated that repolarization abnormalities were present at body surface mapping and might have been related to the occurrence of ventricular arrhythmias. A smaller mean QRS duration and a lower number of patients could explain the discrepancy with the present findings.
It has been recently advanced that QT dispersion may be an index of general repolarization abnormalities instead of an expression of regional heterogeneity of myocardial refractoriness. Accordingly, T-wave loop dynamics and the variable projections of the loop into individual ECG leads has been proposed to be the true mechanistic background of QT dispersion.37 This concept was in keeping with our finding that in victims of sudden death, a negative T wave beyond V1, which is another marker of repolarization abnormalities, showed approximately the same sensitivity of QT dispersion but less specificity.
QRS Dispersion
Because QT dispersion has been taken to
represent regional inhomogeneity of repolarization times, QRS
dispersion is likely to represent regional inhomogeneity of
depolarization times, as a consequence of a ventricular
conduction defect. QRS dispersion was closely correlated with maximal
QRS duration in total patients with ARVC. This finding suggests the
major role of localized prolongation of QRS complex in determining the
increased QRS dispersion. Such an increased QRS dispersion has many
parallels with the revisited definition of waves, which are now
considered by Fontaine et
al38 as "any potential in
V1-V3 exceeding the QRS
duration in lead V6 by more than 25 ms" and
regarded as a diagnostic marker for ARVC. The present
study further demonstrated that an increased QRS dispersion is the
strongest independent predictor of sudden death. A cutoff value 40 ms
had a good sensitivity and specificity in predicting the occurrence of
sudden death. Also, Peters et
al8 demonstrated that
increased QRS dispersion 50 ms was a strong predictive factor of
recurrent malignant arrhythmic events.
Two mechanisms leading to sudden death in ARVC have been proposed by Fontaine et al,39 ie, depolarization abnormalities mediated by a sympathetic mechanism and repolarization abnormalities facilitated by parasympathetic drive. Our data confirm that both depolarization and repolarization abnormalities do exist in patients at risk for sudden death. However, depolarization abnormalities are most commonly associated with cardiac arrest.
Study Limitations
This is a retrospective study that was carried out in a
young population of ARVC patients with comparable clinical
characteristics. Therefore, the ability to transfer our results to ARVC
patients older or with different clinical picture remains to be
elucidated. The correlation between ECG parameters and the
risk of sudden death may change with age, extent, and progression of
ARVC and severity of left ventricular involvement, all
variables that may have a significant and independent influence on
the proposed ECG parameters and may affect the correlation
with sudden death risk.
The present study investigated the ECG features of ARVC patients, either living or experiencing sudden death, before starting antiarrhythmic drug therapy. The subsequent follow-up of these patients on antiarrhythmic drug treatment or after implantation of cardioverter defibrillator was not addressed. Whether pharmacological or nonpharmacological therapy modifies ARVC natural history by preventing sudden death cannot be derived from the present data and needs to be evaluated by prospective studies.40
Conclusions
This was the first study to address the prognostic
value of clinical and ECG variables in ARVC patients who died
suddenly compared with living patients with different degrees of
arrhythmic risk. Our data indicate that QRS dispersion (40 ms) is the
strongest independent predictive marker of sudden death in ARVC
patients and that syncope as well as QT dispersion (>65 ms) and
negative T wave beyond V1 refine noninvasive
arrhythmic risk stratification. Because maximum QRS complex and QT
interval were found in the right precordial leads, these leads
appear to be crucial in the diagnosis and risk stratification of
ARVC.
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Acknowledgments |
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This study was supported by Veneto Region, Venice; Fondazione Cassa di Risparmio, Padua; and Murst, Rome, Italy.
Received January 18, 2001; revision received April 6, 2001; accepted April 6, 2001.
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