Majid Haghjoo, M.D., Arash Arya, M.D.,
Mohammad Ali Sadr-Ameli, M.D.
Department of Pacemaker and Electrophysiology, Rajaie
Cardiovascular Medical and Research Center, School of Medicine, Iran
University of Medical Sciences, Tehran, Iran
Address for
correspondence: Majid Haghjoo, M.D. Department of Pacemaker and
Electrophysiology, Rajaie Cardiovascular Medical and Research Center,
School of Medicine, Iran University of Medical Sciences, Vali-e-Asr
Avenue, Tehran 1996911151 Iran. E-mail: majid.haghjoo@gmail.com
Abstract
Background: By analyzing stored intracardiac electrograms
during spontaneous monomorphic ventricular tachycardia (VT), we
examined
the patterns of the VT initiation in a group of patients with
implantable
cardioverter defibrillators (ICDs).
Methods: Stored electrograms (EGMs) were monomorphic VTs and
at least 5 beats before the initiation and after the termination of VT
were analyzed. Cycle length, sinus rate, and the prematurity index for
each episode were noted.
Results: We studied 182 episodes of VT among 50 patients
with ICDs. VPC-induced (extrasystolic initiation) episode was the most
frequent pattern (106; 58%) followed by 76 episodes (42%) in
sudden-onset group.
Among the VPC-induced group, VPCs in 85 episodes (80%) were different
in
morphology from subsequent VT. Sudden-onset episodes had longer cycle
lengths
(377±30ms) in comparison with the VPC-induced ones
(349±29ms;
P= 0.001). Sinus rate before VT was faster in the sudden-onset compared
to that in VPC-induced one (599±227ms versus 664±213ms;
P=0.005).
Both of these episodes responded similarly to ICD tiered therapy.
There was no statistically significant difference in coupling interval,
prematurity index, underlying heart disease, ejection fraction, and
antiarrhythmic
drug usage between two groups (P=NS).
Conclusions: Dissimilarities between VT initiation patterns
could not be explained by differences in electrical (coupling interval,
and prematurity index) or clinical (heart disease, ejection fraction,
and
antiarrhythmic drug) variables among the patients. There is no
association
between pattern of VT initiation and the success rate of electrical
therapy.
Key words: ventricular tachycardia, implantable
defibrillator, intracardiac electrogram, initiation pattern
Introduction
Sustained
monomorphic ventricular tachycardia (VT) occurs as consequence of many
heart diseases affecting ventricles such as coronary artery disease
(CAD), congestive heart failure (CHF), myocardial infarction (MI), and
long QT syndrome and accounts for most cases of sudden cardiac death.
1 So emergent treatment of it is of
paramount importance in cardiology practice. Reentry, triggered
activity, or abnormal automaticity are mechanisms thought to be
responsible for the genesis of VT.
2,3 The contribution of each mechanism
depends on the presence of underlying arrhythmogenic substrate and
dynamic factors such as myocardial ischemia and autonomic influences.
4-6 In the setting of
CAD or previous MI, reentry is more common.
2,7-9 Recognition of
specific electrogram patterns occurring at time of VT initiation can
help to understand the electrophysiologic mechanism responsible for
arrhythmia initiation and may lead to better diagnostic and therapeutic
intervention.
Previous
studies analyzed the mechanism of VT based on retrospective evaluation
of 24-hour holter monitoring.
10-14 They are limited by the accidental
registration of arrhythmia episode, the small number of patients
included and the fact that each patient is only
registered once. An extended recording of electrical events surrounding
delivered
and aborted ICD therapy not only permits more accurate characterization
of
the rhythm leading to device intervention, but also provides
documentation
of electrical events immediately before index arrhythmia.
15-18
This study was
undertaken to evaluate the pattern of initiation of monomorphic VT by
analyzing stored intracardiac EGMs from patients with ICDs. We,
specially, tried to relate the initiation pattern of first episode with
subsequent VT. We also sought to correlate the presence of various
clinical factors and arrhythmia characteristics such as cycle length
with different patterns of VT initiation. Finally, we determined the
success rate of ICD therapy in two VT initiation groups.
Materials and Methods
Study population
All episodes
of VT in patients with ICD implanted at our center between January 1999
and
June 2001 were reviewed. Intracardiac stored EGMs with spontaneous
sustained
VT requiring therapy with antitachycardia pacing or direct-current
cardioversion were identified. Only events that were monomorphic and
had a minimum of
5 beats before the onset and after the termination of VT were selected
for
further analyses.
Study protocol
Monomorphic VT
was identified by a sudden increase in rate along with a change in
electrogram morphology from the baseline rhythm, a constant cycle
length that did not vary > 10% and uniform electrogram morphology
during the tachycardia.
A ventricular premature complex (VPC) was identified as any electrogram
preceding the VT with morphology different from that of the baseline
rhythm and coupling interval < 90% of the sinus cycle length. The
first beat of VT, when
morphologically different from subsequent tachycardia, was considered a
VPC. In cases in which the first beat of VT was morphologically similar
to
the subsequent tachycardia, the coupling interval between the first
beat
and the VT was evaluated. That beat was considered either (1) the first
beat
of VT when the coupling interval was <110% of VT cycle length, or
(2)
a VPC if the coupling interval was >110% of the VT cycle length. VT
episodes
were categorized into 2 groups depending on the type and morphology of
the
last 5 beats before the initiation of VT: (1) sudden onset without
preceding
VPC, (2) Extrasystolic onset (VPC-induced) with preceding VPCs.
Premature
depolarizations were recorded as similar or dissimilar to the
subsequent VT based qualitatively on electrogram morphology. The cycle
length of all beats during baseline
rhythm and VT was measured. Mean sinus rate was taken as the average of
all
sinus beats before VT.
Prematurity index was calculated by normalizing the
coupling interval to
the preceding RR interval. The coupling interval was defined
differently
depending on the initiation category. It was taken as the interval
between
the first beat of VT and the previous beat for sudden-onset initiation.
In
case of exatrasystolic initiation, it was defined as the interval
between
the first VPC and the previous beat.
Clinical information
Clinical data
for each patient including age, gender, underlying heart disease, left
ventricular ejection fraction, and antiarrhythmic drug usage at the
time of index arrhythmia was documented by review of clinical records.
Statistical analysis
Continuous
data are expressed as mean±SD. Means among different groups were
compared by the analysis of variance. In case of nominal or ordinal
data the groups were compared by using the chi-squire test. A P value
< 0.05 was considered statistically significant. A possible relation
between various clinical
variables and the different modes of initiation were evaluated by
logistic
linear regression. Data analysis was performed by SPSS 13.0 (SPSS Inc.,
Chicago, IL, USA).
Results
Baseline characteristics
A total of 92
patients had ICD devices implanted between January 1999 and June 2001
at
our institution. In this group of patients, 378 episodes of VT occurred
among 65 patients. Of these, 182 episodes among 50 patients met study
criteria;
of 196 disqualified episodes, 90 had < 5 beats before the initiation
of VT, 50 had no available EGM during VT for review, 19 had received no
therapy for VT, 16 were polymorphic in nature, 10 episodes were
pace-induced
and 11 episodes were result of VF treatment by ICD. The mean age of
patients
in our study was 43±19 years with a minimum of 11 years and a
maximum
of 78 years. There were 40 men and 10 women in the group. The
underlying
heart disease was coronary artery disease (20 of 50 patients),
arrhythmogenic
right ventricular dysphasia (ARVD) (10 patients), idiopathic dilated
cardiomyopathy
(14 patients), heart tumor (2 patients), congenital heart disease (2
patients),
and long QT syndrome (2 patients). The mean left ventricular ejection
fraction
for the group studied was 38±15%. All the patients were taking
antiarrhythmic
drug therapy at the time of index VT.
Table 1 shows baseline
characteristics
of the study population.
Arrhythmia characteristics
The most
frequent initiation pattern was VPC-induced (
figure 1), observed
in 106 episodes (58%), and followed by 76 episodes (42%) of VT with
sudden onset initiation (
figure 2). Among the VPC-induced group,
VPCs in 85 episodes (80%) were different in morphology from the
subsequent VT. In only 21 of 106 episodes (20%), the premature
depolarizations preceding the VT were of the same morphology.
Table
2 lists the arrhythmia characteristics and clinical variable of the
2 main initiation categories.
Figure 1: Initiation of VPC-induced sustained VT by a
single
VPC that is different in morphology from the VT.
Figure 2: Sudden-onset monomorphic VT preceded by a single
VPC that is similar in morphology to the VT.
Ten patients
had only one episode of VT, whereas 40 patients had ≥ 2 episodes. Among
the
40 patients with multiple episodes, 35(88%) had at least 2 events with
the
same initiation sequence, while 14 (34%) had the same single pattern of
initiation repeated during all subsequent episodes of VT.
The overall
mean prematurity index was 0.71± 0.56 for all episodes. The
sudden-onset group had a prematurity index of 0.71± 0.3, whereas
the VPC-induced group had a prematurity index of 0.67±0.15.
There was no statistically significant difference in prematurity index
among the 2 initiation groups before and after controlling for
underlying heart disease, antiarrhythmic drug usage, or degree of left
ventricular dysfunction.
The cycle
length of sudden onset VT was slower than that of VT following VPC (
figure
3). The mean cycle length for VT with a sudden-onset initiation
pattern was
377±30ms compared with 349±29 extrasystolic onset
(P=0.001).
The mean sinus rate was slower in the extrasystolic onset group (664
±213ms)
than the sudden-onset group (529±227ms) and the difference was
statistically significant at P= 0.005.
Figure 3: Relation of VT cycle length and
preceding sinus rate to different VT initiation sequences. VT episodes
following sudden-onset (black bars) initiation are slower than
extrasystolic (open bars) onset (upper
panel). Sinus rate is faster before sudden-onset than extrasystolic
onset
(lower panel).
Clinical
parameters from each patient were analyzed for any possible association
with modes
of initiation (
Table 2). There was no association of gender,
underlying heart disease, age, ejection fraction and use of various
types of antiarrhythmic drugs with an initiation sequence of
monomorphic VT. The mean age in sudden onset group of patients was
37±18 years whereas in the extrasystolic initiation group it was
44±17 years and the difference was not statistically significant
with P= 0.5. The mean ejection fraction was 37±16% in
the sudden-onset VT and 36 ±13% in the extrasystolic onset group
(P=
0.7)
ICD therapy
The mean
number of treatment applied by ICD to treat each episode of VT was
2.4±0.1 in the extrasystolic onset group and 2.3±0.2 in
the sudden-onset
group (P=0.5). The overall success rate was 93% for first therapy and
85%
for second to sixth therapy. The success rate was calculated in each
group
of VT initiation separately and there was no association between
different
patterns of VT initiation and the success rate in a particular level of
treatment.
(
Table 2)
Discussion
Our findings
demonstrate that most VT episodes were initiated by VPCs. These were
often different
in morphology from the subsequent VT. The coupling interval was
typically
long. These findings are in agreement with the data of Marchlinski et al
16,17,18
Roelke et al
19, and Saeed
et al
20 who studied mostly
patients with coronary artery disease and previous myocardial
infarction. They found a similar incidence and prematurity of VPCs
before VT in their patient population. Mayerfeldt et al
21 also investigated the mode of the
onset of VT in a group of patients with dilated cardiomyopathy and
coronary artery disease. In their study single premature beats or
couplets initiated three fourths of VT episodes.
A significant
percentage of VT episodes started suddenly without a preceding VPC.
Other
investigators have classified these as VT with single VPC of similar
morphology.
19 Like Saeed et
al, we chose to assign these episodes to the VPC-induced
(extrasystolic) category if VPC was loosely
coupled or to the sudden-onset category if it was tightly coupled to
the
subsequent VT. This classification was adopted because the presence of
tightly
coupled and morphologically similar VPC was thought to represent a
distinct
electrophysiologic mechanism.
Electrical and clinical differences between two VT initiation
groups
Our study
showed that the sudden-onset and extrasystolic initiation patterns tend
to have
different electrical characteristics. Sudden-onset VTs had longer cycle
lengths
and faster sinus rates before VT, where as VPC-initiated episodes had
shorter cycle lengths and a slower sinus rate. These finding did not
seem to be
due to differences in the electrical (eg, coupling interval,
prematurity
index) or clinical (eg, heart disease, ejection fraction, or
antiarrhythmic
drug usage) variables among patients.
Other studies
have shown that there is a high intraindividual reproducibility of VT
with
the same onset seen in up to 88% of patients with recurrent VT.
20,21,22
Our data are consistent with the observation of other investigators,
showing 88% reproducibility of the initiation sequence among our
patients. This
highlights patient-specific factors, namely, the presence of fixed or
functional
anatomic pathways are important in the genesis of recurrent monomorphic
VT.
Our study
showed no correlation between VT initiation pattern and left
ventricular systolic function. In contrast, other studies have revealed
that sudden-onset VT
is more common among patient with relatively preserved systolic
function
and VPC-initiated VT had poor left ventricular function (<35%).
20 This difference may be related to the
younger age of our patients and the inclusion of more cases of
non-coronary heart disease in our study (with better left ventricular
systolic function). Although we did not find any differences in
initiation among the various disease
categories, this could be related to the small sample size of the
patients
with coronary artery disease in our study. To the best of our
knowledge,
our study demonstrated for the first time that there is no association
between
pattern of VT initiation and the success rate of electrical therapy
(antitachycardia
pacing or direct-current cardioversion).
Electrophysiologic implications
Although our
study was an observational one and did not address the mechanism of VT
initiation directly, several inferences can be made. In our study, VPCs
that are often different in morphology and loosely coupled to
subsequent tachycardia likely initiated VT via setting up reentry. VT
may also start suddenly: (1) this may be due to a VPC arising from a
site very close to the reentrant circuit or concealed decremental
conduction of the sinus beat just before the VT
setting up a reentry
3; (2)
sudden-onset initiation could also be due to a focus of increased
automaticity or triggered activity. The first mechanism may be more
important in patients with coronary artery disease, whose sinus beat
may conduct slowly through diseased tissue to setup reentry, and the
first beat exiting the circuit is actually the
first beat of VT as evidenced by close coupling and similar morphology.
ICD tiered
therapy was successful similarly in two VT-initiation groups. Thus,
there is no
need for different programming of antitachycardia pacing and
direct-current
cardioversion in two modes of VT-initiation. In addition, large data
bases
of these events may be helpful in answering clinical questions
regarding
disease or gender specificity of ventricular arrhythmias.
Limitations
Visual
inspection of the intracardiac electrogram is subjective and carries
inherent limitations in interpreting morphologhy. Electrograms that
appear similar may not originate from the same ventricular site. Also,
all premature depolarizations were
assumed to be ventricular in origin and the fact that some of them
might
have been supraventricular premature depolarization cannot be excluded.
Conclusion
Dissimilarities between VT initiation patterns could not be explained
by differences in
electrical (coupling interval, and prematurity index) or clinical
(heart
disease, ejection fraction, and antiarrhythmic drug) variables among
the
patients. There is no association between pattern of VT initiation and
the
success rate of electrical therapy.
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