Download Dispersion of QT interval in patients with and without

174
JACC Vol. 26, No. 1
July 1995:174-9
Dispersion of QT Interval in Patients With and Without Susceptibility
to Ventricular Tachyarrhythmias After Previous Myocardial Infarction
J U H A S. PERKIC)M,~KI, MD, M. J U H A N I K O I S T I N E N , MD, S I N I K K A Y L I - M A Y R Y , MD,
H E I K K I V. H U I K U R I , MD, F A C C
Oulu, Finland
Objectives. The aim of this study was to estimate the value of
QT dispersion measurement from the standard 12-1ead electrocardiogram (ECG) in identifying patients susceptible to reentrant
ventricular tachyarrhythmias after a previous myocardial infarction.
Background. Variability in QT interval duration on the different leads of the 12-lead ECG has been proposed as an indicator of
risk for ventricular arrhythmias in different clinical settings, but
the value of QT dispersion measurement in identifying patients at
risk for reentrant ventricular tachyarrhythmias after myocardial
infarction is not known.
Methods. The QT interval duration, QT dispersion and clinical
and angiographic variables were compared between 30 healthy
subjects; 40 patients with a previous myocardial infarction but no
history of arrhythmic events or inducible ventricular tachycardia
during programmed electrical stimulation; and 30 postinfarction
patients with a history of cardiac arrest (n = 12) or sustained
ventricular tachycardia (n = 18) and inducible, sustained monomorphic ventricular tachycardia by electrical stimulation.
Results. Dispersion of the corrected QT interval (QTc) differed
significantly between the study groups and was significantly
increased in patients with susceptibility to ventricular tachyarrhythmias ([mean -+ SD] 104 -+ 41 ms) compared with that in
both healthy subjects (38 _+ 14 ms, p < 0.001) and postinfarction
patients with no susceptibility to arrhythmias (65 + 31 ms, p <
0.001). Maximal QT interval duration was also prolonged in the
group with arrhythmias compared with that in the other groups
(p < 0.001). Multivariate analysis, including clinical and angiographic variables, QT dispersion and maximal QT interval,
showed that QT dispersion was the independent factor that most
effectively identified the patient groups with and without susceptibility to ventricular tachyarrhythmias (p < 0.001).
Conclusions. Increased QT dispersion is related to susceptibility to reentrant ventricular tachyarrhythmias, independent of
degree of left ventricular dysfunction or clinical characteristics of
the patient, suggesting that the simple, noninvasive measurement
of this interval from a standard 12-lead ECG makes a significant
contribution to identifying patients at risk for life-threatening
arrhythmias after a previous myocardial infarction.
(JAm 6bll Cardiol 1995;26:174-9)
Experimental studies have provided powerful evidence of the
significance of the dispersion of myocardial recovery times for
the occurrence of ventricular arrhythmias (1-4). However,
current methods of measuring recovery time dispersion (i.e.,
epicardial or endocardial monophasic action potentials) and
body surface mapping are not very practical for routine clinical
use. Recently, measurement of the variability in QT interval
duration among the different leads of the standard 12-lead
electrocardiogram (ECG) (i.e., QT dispersion) has been proposed as a noninvasive method for detecting the inhomogcneity of ventricular recovery times (5-9).
Previous clinical studies of QT dispersion have shown it to
be increased in patients after acute myocardial infarction (8),
in patients with the long QT syndrome (10) and in patients
with hypertrophic cardiomyopathy (11). In the two latter
patient groups, prolonged QT dispersion has also been shown
to be related to an increased risk for serious ventricular
arrhythmias (5,11). The mechanism of ventricular arrhythmias
in patients with an old myocardial infarction is probably
different from that in the other two patient groups, and, to our
knowledge, there is no information on the significance of QT
dispersion for susceptibility to arrhythmias in patients with a
previous myocardial infarction.
The present study was therefore designed to test the value
of QT dispersion measurement for identifying patients at risk
for life-threatening arrhythmias after a previous myocardial
infarction by comparing QT dispersion between healthy subjects and two patient groups with differing susceptibilities to
ventricular tachyarrhythmias.
From the Division of Cardiology, Department of Medicine, University of
Oulu, Oulu, Finland. ]"his study was supported by grants from the Orion
Corporation Research Foundation, the Finnish Foundation for Cardiovascular
Research and the Medical Council of the Academy of Finland, Helsinki, Finland.
Manuscript received October 19, 1994; revised manuscript received February.
1, 1995, accepted February,' 27, 1995.
Address fur correspondence: Dr. Juha S. PerkiOm~iki, Division of Cardiology, Department of Medicine, Oulu University Central Hospital, 90220, Oulu,
Finland.
351995 by the American ('o[lcgc ol ('ardiolog5
Methods
Patients. The study included 100 subjects: 30 healthy volunteers (control group) with no disease or medication and no
0735-1097/95/$9.50
0735-1097(95)00122-K
JACC Vol. 26. No. 1
July 1995:174-9
PERKIOMJkKI ET AL.
Q I DISPERSION FOR SUSCEPTIBILITY TO VT AFTER AM1
Table 1. Clinical Characteristics of the Study Patients
Age (yr)
Male/female
Time from previous MI (mo)
Medication
ACE inhibitor
Beta-blocker
Digitalis
Diuretic drugs
NYHA functional class I/H/Ill
Coronary angiographic CAD
1 vessel
2 vessel
3 vessel
LVEF (%)
Pts With MI
but No VT
(n 40)
Pts With MI
and VT
(n 30)
59 + 6
3t*/I
28 + 19
62 + 8*
27/3
16 + 18
5
32
II
It)
0/17/23
4
14"
9
9
1/15/12
I
17
22
47 + q
6
10
12*
43 - 11
*p < 0.05 between groups. Data presented are mean value + SD or numbcr
of patients (Pts). ACE
angiotensin-eonverting enzymc: CAD
coronary
artery disease; LVEF
left ventricular ejection fraction; MI
myocardial
infarction: NYHA - New York Heart Association: VT vcntricular tachyarrhythmia.
evidence of ischemic ST segment depression on exercise
electrocardiography (mean [_+SD] age 45 + 6 years, range 35
to 59; 28 men, 2 women); 40 patients with a history of
myocardial infarction but no history of nonsustained or sustained ventricular tachyarrhythmia and no inducible ventricular tachyarrhythmia during programmed electrical stimulation;
and 30 patients with a history of myocardial infarction and
sustained ventricular tachycardia (n = 18) or cardiac arrest
(n = 12) (>3 months after a previous myocardial infarction)
and inducible, sustained monomorphic ventricular tachyarrhythmia during programmed electrical stimulation. The patients without ventricular tachyarrhythmias were selected from
a consecutive series of patients referred to the Oulu University
Central Hospital for coronary angiography, and those with
ventricular tachyarrhythmias were selected from a consecutive
series of patients examined electrophysiologically because they
had experienced a documented sustained ventricular tachycardia or cardiac arrest. Patients without arrhythmic events but
with inducible nonsustained or sustained ventricular tachycardia were excluded from the consecutive series, as were those
with inducible ventricular fibrillation or polymorphic ventricular tachycardia.
All patients with a previous myocardial infarction were
examined by means of cardiac catheterization, coronary angiography and programmed electrical stimulation. A 12-lead
surface ECG at a paper speed of 50 rnm/s was recorded for
every healthy subject and postinfarction patient, and all were in
sinus rhythm. The clinical and angiographic characteristics of
the patients are presented in Table 1. Informed consent for the
electrophysiologic studies was obtained from the patients, and
the study protocol was approved by the hospital ethics committee.
Eleetrophysiologic testing. Electrophysiologic testing included programmed ventricular stimulation using up to three
175
extrastimuli and two basic drive cycle lengths (600 and 400 ms)
from the right ventricular apex and outflow tract. Ventricular
tachycardia was defined as 1) sustained when its duration was
>30 s or if defibrillation was required for its termination; and
2) as nonsustained if it lasted >5 beats but <30 s. The
electrophysiologic testing protocol and definitions of inducible
arrhythmias have been previously described (12).
Angiographic studies. Left-sided cardiac catheterization
was performed using the Judkins technique. Selective coronary
artery angiograms were obtained in multiple projections, including caudal and cranial views, and a lumen narrowing
>50% was considered significant stenosis.
Exercise test. The healthy subjects performed a symptomlimited, maximal, dynamic exercise test on an electrically
braked bicycle ergometer, starting at a work load of 30 to 50 W
that was increased by 10 to 15 W/min (13).
Measurement of QT interval and dispersion. The QT and
QT apex (QTa) intervals and QRS complex duration were
measured at each lead of the 12-lead surface ECG for two
consecutive cycles. The QT intervals were measured from the
onset of the QRS complex to the end of the T wave by means
of a tangential method. When U waves were present, the QT
interval was measured to the nadir of the curve between the T
and U waves, also with the aid of a tangential method. The
OTa intervals were measured from the onset of the QRS
complex to the apex of the T wave. The QRS complex duration
was measured from the beginning of the QRS complex to its
end. The T end-interval (Te) (from the apex of the T wave to
its end) was calculated from the equation Te = QT - QTa,
and the JT interval (from the J point to the end of the T wave)
from the equation JT = QT QRS. The measurements were
performed manually by two independent observers unaware of
the patient's clinical data. The QT, QTa, JT, Te and QRS
dispersions were defined as the differences between the maximal and minimal QT, QTa, JT, Te and QRS values, respectively, and the mean value of the two consecutive cycles was
calculated. Bazett's formula was used to obtain rate-corrected
values of the QT, QTa, JT and Te intervals and dispersions
(QTc, QTac, JTc and Tec, respectively). The intraobserver and
interobserver variation in the QT dispersion measurements
was calculated. The measurements of the more experienced
observer were used for statistical comparisons.
Statistics. Kruskal-Wallis one-way analysis of variance was
uscd to estimate differences in the QTc, QTac, JTc, Tec
intervals, QRS duration and QTc, QTac, JTc, Tec and QRS
dispersions between the three study groups. Thereafter, the
standard t test was performed to estimate the significance
levels between the groups. The Pearson correlation coelficient
was used to estimate univariate correlations between the
variables. Logistic multiple regression analysis (forward
method with Wald statistics) was used to evaluate the independent values of the different variables in differentiating the
patient groups with and without susceptibility to ventricular
tachyarrhythmias; p < 0.05 was considered significant.
176
PERKIOMJkKI ET At..
QT DISPERSION FOR SUSCEPTIBILITY TO VT A F T E R AMI
JACC Vol. 26, No. 1
July 1995:174-9
Table 2. RR Interval, QT Intervals and QT Dispersion
R R interval (ms)
QTc interval (ms)
Max
Min
QTac interval (ms)
Max
Min
250
Healthy Subjects
(n = 30)
Pts With MI
but No VT
(n = 40)
Pts With MI
and VT
(n = 30)
942 + 143
952 _+ 177
964 + 205
Min
Tec interval (ms)
412 +_ 25
448 + 39*
493 _+ 51*t
375 + 24
383 +_ 20
388 + 30
338 _+ 22
299 + 23
367 _+ 35*
305 -+ 29
383 + 38*
296 + 33
91 + 7
127 + 16"
137 + 25"
I
I
200
v
E
150
63 + 8
81 + 15"
89 + 20*
O3
L_
U]
97 + 17
104 _+ 22
Min
61 + 11
61 + 15
134 + 28'+
100
I
o
50
70 + 15:~§
O
0
334 _+ 21
341 + 35
378 + 4 9 ' t
289 + 23
269 + 275
269 _+ 30:~
QTc
38 +- 14
65 + 31"
104 _+ 4 l * t
QT
36 + 14
63 + 29*
101 +- 3 9 " t
QTac
QTa
QRS
39 +- 20
38 + 19
28 + II
f,2 + 325
60 _+ 30:~
46 + 13"
87 -+ 37'11
48 + 16"
Tec
Te
36 + 17
34 2 14
43 + 20
41 _+ 18
64 + 28"1'
62 +, 28"t
JTc
45 +- 14
72 + 33*
110 + 4(I*-
JT
44 +, 14
70 + 32*
106 + 39*-
s5 + 38"11
*p < 0.001, 5p < 0.01 between patients without ventricular tachycardia (VT)
and healthy subjects and between patients with ventricular tachycardia and
healthy subjects, t p < 0.001, §p < 0.05, lip < 0.01 between patients with and
without ventricular tachycardia. Data presented are mean value _+ SD. JTc,
QTac, QTc, Tec - rate-corrected JT. QTa, QT and Te intervals, respectively;
QTa - QT apex interval; Max - maximum; Min
minimum; Te = T
end-interval (from apex of T wave to its end); other abbreviations as in l~able 1.
Results
Clinical and angiographic data (Table 1). Patients with
arrhythmias were somewhat older than those without arrhythmias ([mean _+ SD] 62 _+ 8 vs. 59 _+ 6 years, p < 0.05), and
patients without tachyarrhythmias more frequently had multivessel coronary artery disease than those with arrhythmias.
There were no significant differences in time from the previous
myocardial infarction or in left ventricular ejection fraction
between the patient groups. Beta-adrenergic blocking agents
were more commonly used by patients without than with
tachyarrhythmias.
QT interval, QRS duration, RR interval. The maximal
QTc interval differed significantly between the three groups
(p < 0.001) and was longest in the ventricular tachyarrhythmia
group (Table 2). Both patient groups had a significantly longer
maximal QTac interval and maximal and minimal QRS duration (p < 0.001) and a shorter minimal JTc interval (p = 0.002)
than did the control group. Maximal and minimal Tec and
maximal JTc intervals were longer in the group with ventricular
tachyarrhythmia than in the other groups. Minimal QTc and
¥
J
JTc interval (ms)
Min
Dispersion (ms)
I
E
O
Max
Max
1
(2
QRS duration (ms)
Max
I
I
-p<O.O01-
-p<O.O01
0
healthy
' MI+, VT- ' MI+, VT+
subjects
Figure 1. QTc dispersion in the three study groups. Vertical bars
represent 95% confidence intervals of mean values. MI = myocardial
infarction; VT = ventricular tachyarrhythmia; + (-) = presence
(absence).
QTac intervals did not differ significantly, and average heart
rate was similar among the three study groups.
QT dispersions. QTc, JTc and QTac dispersions differed
significantly between the three groups and were broadest in the
group with ventricular tachyarrhythmia and narrowest in the
control group (p < 0.001) (Table 2, Fig. 1). Patients with
ventricular tachyarrhythmias had a longer Tec dispersion than
patients without arrhythmias and healthy subjects. QRS dispersion was broader in both patient groups than in the control
group (p < 0.001) but did not differ significantly between the
two patient groups.
Multiple regression analysis. Because the patient groups
differed with regard to age and use of beta-blockers as well as
severity of angiographic coronary artery disease, univariate
analyses were first performed to assess the possible effects of
these variables on QTc dispersion. Age had no significant
correlation with QTc dispersion in either the control group
(r -- 0.08, p = 0.7) or the patient groups (r = 0.19, p = 0.3), nor
did QTc dispersion differ between patients with (77 -+ 41 ms)
or without beta-blockers (82 _+ 31 ms, p = 0.5). QTc dispersion
was also unrelated to left ventricular ejection fraction (r =
-0.13, p = 0.3) or angiographic severity of the coronary artery
disease.
Logistic multiple regression analysis between patients with
and without tachyarrhythmias, including QTc dispersion, maximal QTc interval, age, left ventricular ejection fraction and
use of beta-blockers as covariates showed that QTc dispersion
was the most effective predictor of ventricular tachyarrhythmia
susceptibility (p < 0.001). Beta-blocker use also independently
(p < 0.05) differentiated between patient groups, but maximal
QTc interval, age and left ventricular ejection fraction were not
JACC Vol. 26, No. 1
July 1995:174-9
PERKIOMAK1 ET AL.
QT DISPERSION FOR SUSCEPTIBILITY TO VT AFTER AMI
Table 3. Intraobserver and Interobserver Variability of QT
Dispersion Measurement
Intraobserver variability between
two measurements
Mean difference (ms)
Relative difference (%)
Interobserver variability between
two observers
Mean difference (ms)
Relative difference (%)
Healthy
Subjects
Pts Without
VT
Pts With
VT
9
25
6
10
7
7
11
32
1l
18
13
13
Mean difference = mean of absolute values of measurement errors; Relative
difference = mean difference relative to mean value of QT dispersion in each
group. Abbreviations as in Table 1.
independently associated with susceptibility to ventricular
tachyarrhythmias.
Accuracy of QTc dispersion in predicting susceptibility to
ventricular tachyarrhythmias. When the 99% tolerance limits
of normal QTe dispersion were calculated for the control
group, 80 ms was obtained as the upper limit of normal QTc
dispersion. When this value was used as the upper limit, QTc
dispersion had a sensitivity of 70%, a specificity of 78% and a
positive predictive accuracy of 70% in differentiating the
postinfarction groups with and without susceptibility to ventrieular tachyarrhythmia. With the cutoff values of 70 or
100 ms, sensitivity was 77% and 53%, specificity 68% and 90%
and positive predictive accuracy 64% and 80%, respectively.
The absolute and relative values of intraobserver and interobserver variability of QT dispersion measurement are shown
in Table 3.
Discussion
QT dispersion in patients with and without susceptibility to
ventricular tachyarrhythmias. This cross-sectional study of
patients with different susceptibilities to ventricular tachyarrhythmias shows that QT dispersion is increased in patients
at risk for life-threatening arrhythmias after a previous myocardial infarction. Previous studies have shown that prolongation of the QT interval is a risk factor for ventricular arrhythmias and sudden death in patients with a previous myocardial
infarction (14-18), but there has been some controversy as to
the predictive accuracy of the prolonged QT interval (19-22).
In the present study, the maximal QT interval was also
observed to be prolonged in patients with an arrhythmic
susceptibility, but QT dispersion was a more powerful predictor of susceptibility to ventricular tachyarrhythmias, suggesting
that inhomogeneity of repolarization is more closely associated
with arrhythmic risk than is prolongation of repolarization
itself.
Previous studies on the relation between QT dispersion and
arrhythmic susceptibility were performed in patients with the
long QT syndrome (5,10,23), hypertrophic cardiomyopathy
(7,11) or congestive heart failure (24,25); in mixed patient
177
populations with ischemic heart disease (26); or in patients
with torsade de pointes induced by antiarrhythmic drugs (27).
In these clinical settings, the mechanisms of arrhythmogenesis
have been controversial. Triggered activity due to both early
afterdepolarizations and reentry have been proposed (28).
However, reentry has most commonly been shown to be a
mechanism of ventricular tachyarrhythmias in patients with
chronic myocardial infarction (29), where dispersion in the
regional recovery time may be a fundamental electrophysiologic substrate for the genesis of reentrant arrhythmias. In the
present series, reentry was indeed the most probable mechanism of arrhythmia because only patients with inducible,
sustained monomorphic ventricular tachycardias were included, which supports the postulation that QT interval dispersion is a sign of propensity to reentrant ventricular arrhythmias. The dispersion of QRS complex duration was similar in
the two patient groups, suggesting that there are no significant
differences in the dispersion of conduction in postinfarction
patients with different arrhythmic susceptibilities but that
changes in repolarization are most likely to be responsible for
the observed QT dispersion. The broad dispersion of the total
QT interval in the group with arrhythmias was mainly due to
the dispersion of the Te rather than the QTa interval. This
observation suggests that the regional slowing down of the
terminal phase of repolarization may be important for inhomogeneities in recovery time and arrhythmogenesis.
Comparison of QT dispersion between healthy subjects and
patients with a previous myocardial infarction. The QT dispersion values in our healthy subjects concur with those of
previous findings, demonstrating that dispersion of the QT
interval in a normal heart is usually <70 ms (8,30). The
patients with a previous myocardial infarction but with no
ventricular tachyarrhythmia showed a somewhat increased QT
dispersion compared with healthy subjects, but these dispersion values were clearly smaller than those of the patients with
ventricular tachyarrhythmias. These observations confirm the
assumption that chronic infarction itself creates inhomogeneities in ventricular recovery time. This inhomogeneity was not
related to ejection fraction, medication or other clinical variables, suggesting that measurement of QT dispersion may yield
information on the risk of ventricular tachyarrhythmias independent of degree of left ventricular dysfunction or clinical
characteristics of the patient.
Prediction of susceptibility to life-threatening arrhythmias.
Among postinfarction patients, the identification of those at
high risk for ventricular tachycardia is of great importance. The
old strategies, such as evaluation of left ventricular function,
ventricular ectopic activity and spontaneous arrhythmias cannot effectively identify subjects at high risk (31). The newer
noninvasive methods, such as signal-averaged electrocardiography, heart rate variability and baroreceptor reflex sensitivity, offer improved risk stratification (32). However, the positive predictive accuracy of each of these methods is still limited
with regard to identifying individual patients for therapeutic
interventions; it is possible that the combination of these
noninvasive methods may result in better accuracy (33).
178
PERKIOMAKIET At..
QT DISPERSION FOR SUSCEPTIBILITY TO VT AFTER AMI
In the present series, QT dispersion had a relatively good
accuracy compared with that of other noninvasive methods
used in previous studies for discriminating between patients
with different susceptibilities to ventricular tachyarrhythmias.
Measurement of Q T dispersion is easy and inexpensive and
should perhaps be included in the noninvasive evaluation of
arrhythmic risk. The relative accuracy of this method, compared with others, should also be tested. However, ours was a
cross-sectional study, and its results may not provide information as to the predictive accuracy of QT dispersion for future
arrhythmic events but may only demonstrate that Q T dispersion is increased in patients susceptible to life-threatening
arrhythmias. To estimate the predictive value of QT dispersion
for arrhythmic events, a longitudinal follow-up study should be
performed, but identifying tachyarrhythmic deaths or events in
epidemiologic studies can be problematic. The mechanism of
death attributed to ventricular arrhythmia may be bradyarrhythmia, recurrent myocardial infarction or a number of
other conditions that can develop rapidly. Therefore, a crosssectional study such as the present one can provide important
information on the power of different variables to predict risk
for specific life-threatening arrhythmias.
Study limitations. Measurements of Q T interval and its
dispersion are subject to intraobservcr and interobserver variability (30,34). Kautzner et al. (30) found a notable relative
interobserver error in QT dispcrsion measurements of healthy
subjects (>30%). This is in accordance with our findings of
interobserver variation in Q T dispersion measurements of
healthy subjects in terms of relative error, but more important
is the interobserver variability expressed in absolute values,
which is on the order of 10 ms. Furthermore, when QT
dispersion was increased, the relative interobserver and intraobserver errors became smaller. In the present study, where
measurements by the same experienced observer were used for
the statistical comparison of QT dispersion, the intraobserver
variation within the patient groups was found to be 6 to 7 ms,
which confirms that the differences in QT dispersion between
the patient groups cannot be explained by measurement
variability. Despite some shortcomings of Bazett's formula, it
has been shown to be applicable to correction of the QT
interval for heart rate in patients with myocardial infarction
(35). However, it has not been used in studies to correct QTa,
Te or JT intervals for heart rate. Despite that, to make these
subdivisions of the QT interval and dispersion more comparable to other studies, rate correction appears to be justified.
In our study, the patients with no susceptibility to ventricular tachyarrhythmia had no history, of malignant arrhythmia
and no inducible ventricular tachycardia. Such patients are
known to be at low risk for spontaneous ventricular tachyarrhythmias, but noninducibility during electrophysiologic testing may not provide complete predictive accuracy with regard
to arrhythmia-free survival. Indeed, some patients without
inducible ventricular tachycardia had a markedly increased Q T
dispersion. It will be important to follow up these patients for
the clinical occurrence of ventricular tachyarrhythmia.
JACC Vol. 26, No. 1
July 1995:174-9
Conclusions. QT dispersion is increased in patients with a
susceptibiliW for ventricular tachyarrhythmias. This indicates
that variability in the length of the QT interval between the
different leads of the standard 12-lead ECG is a marker for the
risk of reentrant ventricular arrhythmias in patients with a
previous myocardial infarction. The clinical utility of this
simple, noninvasive measure should be confirmed in prospective follow-up studies in postinfarction patients.
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