Circulation. 1998;98:671-677
(Circulation. 1998;98:671-677.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
First Postpacing Interval Variability During Right Ventricular Stimulation
A Single Algorithm for the Differential Diagnosis of Regular Tachycardias
Angel Arenal, MD;
Jesus Almendral, MD;
Julian Villacastin, MD;
Raimundo Morris, MD;
Eduardo Castellanos, MD;
; Juan Luis Delcan, MD
From the Department of Cardiology, Hospital General Universitario
Gregorio Marañon, Madrid, Spain.
Correspondence to Angel Arenal, MD, Laboratorio de Electrofisiologia, Departamento de Cardiologia, Hospital General Universitario Gregorio Marañon, C/Dr Esquerdo 46, 28007 Madrid, Spain.
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Abstract
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Background—Failure to differentiate
supraventricular from ventricular
arrhythmias is the most frequent cause of inappropriate
implantable cardioverter-defibrillator therapies. Although a
sudden-onset criterion is available to differentiate sustained
monomorphic ventricular tachycardias (SMVTs)
and sinus tachycardias (STs), SMVTs arising during ST and
SMVTs gradually accelerating above the cutoff rate can remain
undetected. Regular paroxysmal atrial tachycardias (ATs)
also can be undetected by onset and stability algorithms. We
hypothesized that the first postpacing interval (FPPI) variability
after overdrive right ventricular pacing may differentiate
SMVTs from STs and ATs.
Methods and Results—FPPI variability was measured in 23 SMVTs
(cycle length [CL] 366±50 ms [VT group]), 27
supraventricular tachycardias, 15 episodes of
induced or simulated ATs (CL 376±29 ms [AT group]), and 12
exercise-related STs (CL 381±24 [ST group]). Sequences of trains of
5, 10, and 15 beats were delivered with a CL 40 ms shorter than the
tachycardia CL. An FPPI absolute mean difference between
consecutive trains of 5 and 10 beats (
FPPI) 
25 ms identified all
VTs (mean difference 5±7 ms). In the AT group, the FPPI was >25 ms
in all sequences (mean difference 129±60 ms, P<0.01).
In the ST group, the FPPI was >50 ms in all STs (mean difference
118±47 ms, P<0.01).
Conclusions—FPPI variability may differentiate SMVT from AT and
ST. This criterion is potentially useful in implantable devices that
use a single ventricular lead.
Key Words: diagnosis • tachycardia • pacing
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Introduction
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The implantable
cardioverter-defibrillator is becoming one of the most powerful
therapeutic tools in the treatment of sustained ventricular
arrhythmias and for the prevention of sudden
death.1 2 3 4 The possibility of implanting
transvenous systems5 6 7 and the availability of
antitachycardia pacing therapies have undoubtedly increased
the use of these devices for the treatment of patients with frequent
episodes of SMVT, even if these tachycardias do not produce
loss of consciousness.8 9 10 Currently, slower
tachycardias are being treated by the new devices. The
recognition of these tachycardias implies a lower cutoff
rate and consequently an increasing risk for misdiagnosing atrial and
STs because of the overlapping in CLs.11 12 This
problem can be accentuated by the use of antiarrhythmic
drugs.13 Inappropriate therapy delivery for
supraventricular tachyarrhythmias has been
documented in up to 16% of patients, whereas only a minority of them
had the arrhythmia before the implant.11
Because aggressive antitachycardia pacing and low-voltage
cardioversion capabilities delivered during
supraventricular rhythms may induce VTs requiring
additional therapeutic intervention,14 the
recognition of supraventricular arrhythmias that
reach the cutoff cycle is essential for the adequate functioning of
this device. Detection enhancements have been incorporated in the new
devices to improve diagnostic accuracy. While the rate
stability criterion is useful in differentiating atrial
fibrillation,15 the sudden-onset algorithm may
help to discriminate ST.16 Nevertheless, the
onset criterion may provoke some discrimination errors: (1) VTs induced
by ST, (2) gradual acceleration of VTs above the cutoff rate, and (3)
ST and premature ventricular beats, simulating a sudden
rate change. The first 2 limitations are particularly worrisome because
they may leave VTs untreated. Finally, regular AT may have a sudden
onset and thus may be diagnosed as VT by use of this criterion.
This study aims to obtain a new algorithm to differentiate ST and AT
from SMVT independent of the type of onset. The purpose of our study is
to differentiate monomorphic VTs from regular ATs and STs, analyzing
the variability of the FPPI or return cycle after synchronized trains
of paced impulses with the same CL but with a different number of
beats, delivered at the RVA during tachycardia. Our
hypothesis is that the FPPI will remain constant in the setting of
SMVTs, whereas this interval will change if the tachycardia
originates in the atria. This hypothesis is based on the following: (1)
There is stability of the FPPI during entrainment of reentrant VTs,
provided the pacing CL is long enough to avoid the end of the shortest
relative refractory period of the circuit, so the tissue has recovered
full excitability. (2) The conduction time between a
ventricular pacing site and the tachycardia
origin is expected to be shorter in VTs than in ATs and STs (provided
there are no accessory AV connections), entrainment of SMVTs will
probably occur with ventricular trains of fewer beats.
Thus, in VTs the FPPI is expected to remain stable when short and long
trains are compared, whereas in ATs and STs if the short train does not
reach the circuit and a longer train does, the FPPI will be different.
(3) In cases of no 1:1 ventriculoatrial conduction at the
tachycardia rate, trains with different number of beats
might produce a different degree of retrograde AV nodal penetration,
modifying the anterograde conduction time of the first
postpacing beat.
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Methods
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Study Groups
VT Group
This group included 23 different SMVTs induced during the
electrophysiological study in 22 patients
(age 57±8 years) with chronic myocardial infarction and at least 1
episode of spontaneous monomorphic VT. All the induced VTs were
hemodynamically well tolerated, and the VT CL was
366±50 ms (range from 470 to 280 ms). The morphology of the VT was
similar to left bundle-branch block in 9 cases and similar to right
bundle-branch block in 14. The maximal range of RR variability before
ventricular pacing was 30 ms.
AT Group
This group included 15 ATs (11 of them were simulated by atrial
pacing) evaluated during the
electrophysiological study in 15 patients
(age 49±11 years). Four patients were included in the VT group; in the
remaining patients the clinical indication of
electrophysiological study was unexplained
syncope. None of these patients had an accessory pathway or AV nodal
reentrant tachycardia. The inclusion criterion for
simulated tachycardias was a Wenckebach CL <400 ms. The
shortest regular ventricular CL was 376±29 ms (range from
460 to 330 ms).
ST Group
This group included 12 STs (CL 381±24 ms) observed during
exercise testing in 12 patients (50±10 years) in whom a
third-generation implantable defibrillator with tiered therapies and
electrogram storing capabilities was implanted.
Electrophysiological Study
After written informed consent was obtained, the
electrophysiological study was performed in
the postabsorptive state. At least 3 quadripolar catheters were placed
at the right atrium, RVA, and right ventricular outflow
tract or His bundle area. The distal pair of electrodes was used for
pacing and the proximal pair for local electrogram recording.
Intracardiac recordings were filtered at 30 to 500 Hz and
displayed simultaneously with 
3 ECG leads (I, aVF,
V1) on a 12-channel photographic recorder
(VR-12, Honeywell), at a paper speed of 100 mm/s. Digitized
recordings from 6 patients were stored in a computer system
(Bard Electrophysiology) for further analysis. Stimulation was
performed with a programmable stimulator (UHS-20 Biotronik) set to
deliver rectangular pulses of 1-ms duration at twice
diastolic threshold. Programmed stimulation was performed
to eliminate the possibility of an atrioventricular
accessory pathway and to induce VT when indicated.
Ventricular Stimulation Protocol During
Tachycardia
Sequences of synchronized trains at a CL 40 ms shorter than the
tachycardia cycle, separated by 2-second intertrain pauses,
were delivered at the RVA during VT or AT. Each sequence consisted of 3
trains: the first train was 5 beats, the second train 10 beats, and the
third train 15 beats. The coupling interval of the first stimulated
beat was the CL of the train. SMVTs usually present some CL
variability, particularly soon after the
initiation.17 18 To study if the FPPI duration
was a function of the time after tachycardia initiation,
each sequence was delivered 3 times: during the first 20 seconds,
between 20 and 40 seconds, and between 40 and 60 seconds after
tachycardia initiation.
Specific Atrial Stimulation Protocol
In 11 patients atrial stimulation was used to simulate AT. In
these cases (1) The Wenckebach CL was determined during continuous
atrial pacing. If the Wenckebach cycle was >400 ms, the patient was
not included in the following part of the study. (2) AT was simulated
by continuous atrial pacing in AAI mode at a CL 20 ms longer than the
Wenckebach CL to avoid ventricular CL changes caused by
oscillations in the Wenckebach point. Only after the
ventricular rate was stable for 10 seconds was the
ventricular stimulation protocol started.
Exercise Test
The treadmill test, with modified Bruce protocol, was performed
in a postabsorptive state 4 days after the implantation procedure if
no contraindication was present. At least 2 therapy zones were
programmed. To calculate the FPPI variability, we programmed in the VT
zone 2 consecutive bursts of 5 and 10 beats at a CL of 91% of the
tachycardia CL as the first therapy. The VT zone
detection was activated at the peak of exercise if no angina,
hypotension, or intense dyspnea was present. The detection interval
was programmed 20 ms longer than the CL present at this particular
moment.
Measurements
FPPI was considered as the interval, in milliseconds, between
the last stimulus artifact of the pacing train and the first rapid
deflection crossing the baseline of the first nonstimulated
beat.
Train-dependent FPPI variability was defined as the difference between
the FPPI of consecutive trains. It was calculated between trains of 5
and 10 beats and between trains of 10 and 15 beats in VT and AT. In ST
it was calculated only between trains of 5 and 10 beats.
The parameter of time-dependent FPPI variability was
calculated only in tachycardia with sudden onset (AT and
VT). It was the SD of the FPPI measured after the pacing train with the
same number of beats but delivered at different intervals after VT and
AT initiation. For example, the time-dependent FPPI variability after
trains of 5 beats was the SD calculated with the FPPIs obtained during
the first 20 seconds, between 20 and 40 seconds, and between 40 and 60
seconds after VT initiation.
Data Analysis
Values are expressed as mean±SD. FPPIs were compared by ANOVA.
Post hoc comparisons between groups were made with the Tukey test.
Two-tailed probability values <0.05 were considered significant.
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Results
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Time-Dependent FPPI Variability
VT Group
The time-dependent FPPI variability was minimal after pacing
trains of 5, 10, and 15 beats (2±3, 3±4, and 3±3 ms, respectively).
Thus, it could be considered that the FPPI was time independent in
reference to VT onset when it was measured within the first
minute after VT initiation (Figure 1
, left).
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Figure 1. Time-dependent FPPI variability: changes in FPPI
duration in response to ventricular trains with the same
number of beats but delivered progressively later after
tachycardia induction. Var indicates variability.
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AT Group
FPPI variability after pacing trains of 5, 10, and 15 beats was
(24±28, 100±77, and 48±53 ms, respectively). Therefore, FPPI
variability in the setting of AT was greater than the variability
observed in VTs. The FPPI variability ranges from 5 to 98 ms, 0 to 230
ms, and 0 to 173 ms after 5-, 10-, and 15-beat trains (Figure 1
, right).
Train-Dependent FPPI Variability
VT Group
All the pacing sequences were considered for this
analysis. The FPPIs after 5, 10, and 15 beats were 477±90,
481±91, and 484±92 ms, respectively (Figure 2). When the FPPIs after 5 and 10 beats
were compared, the FPPI 5 to 10 was 5±7 ms (Figure 3). The FPPI 5 to 10 was 10, 20, and
25 ms in 88%, 98%, and 100% of the sequences, respectively (Figure 4). Comparing the FPPIs after 10 and 15
beats, the FPPI 10 to 15 was 4±6 ms. In 90% and in 100% of
sequences, the FPPI 10 to 15 was 10 and 20 ms, respectively
(Figure 4).
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Figure 2. Mean values of FPPI after pacing trains of 5, 10,
and 15 beats in VT group and AT group. VT group: FPPI is similar after
ventricular trains of 5, 10, and 15 beats when pacing CL
was 40 ms shorter than VT CL. AT group: FPPI increases notably from
578±68 ms after 5 beats to 639±152 ms after 10 beats and then remains
similar after 15 beats.
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Figure 3. Response to overdrive pacing trains with different
numbers of beats. Surface ECG leads I, aVF, aVR, V1, and
V6, as well as intracardiac electrograms from the His
bundle area; right ventricular outflow tract (RVOT), and
RVA are displayed during a right-bundle, superior-axis VT (300-ms CL).
A, Synchronized train of 5 beats at a CL of 260 ms (40 ms less than VT
cycle) is delivered at the RVA. FPPI is 340 ms. B, During the same VT
after a train of 10 beats, FPPI remains constant at 340 ms.
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AT Group
The FPPIs were significantly different after 5, 10, and 15 beats,
578±68, 639±152, and 618±83 ms (P<0.01, Welch ANOVA)
(Figure 2). The FPPI 5 to 10 was longer than in the VT group:
129±60 ms (Figure 5). In no sequence was
the difference 25 ms, in 87% it was >50 ms, and in only 13% of
sequences the difference was between 25 and 50 ms. Although the FPPI
10 to 15 was similar to the FPPI 5 to 10 (118±60 ms), in 7% and
17% of the sequences the difference was 25 and 50 ms, respectively.
In 83% of the sequences the difference was >50 ms (Figure 6).
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Figure 5. Differences in FPPI related to different duration
of ventricular trains during an example of AT. Four surface
ECG leads are recorded along with the intracavitary electrograms of
the His bundle (HB), right ventricular outflow tract
(RVOT), and RVA during ventricular pacing with trains of 5
(A) and 10 beats (B). FPPI is 125 ms shorter after a 10-beat
train.
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ST Group
The FPPIs were significantly different after 5 and 10 beats
(585±70 versus 663±132 ms, P<0.01)
(Table). In no sequence was the difference 50 ms
(Figure 7) despite the sinus CL being
identical before the first burst and after the last burst (380±25 and
381±25 ms).
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Figure 7. Intervals and electrograms stored during ST
observed during an exercise test. Two consecutive bursts of 5 and 10
beats at CL of 330 ms were delivered during ST at 370 ms. FPPI was 570
and 690 ms, even though the tachycardia CL remained stable
after both bursts. EG indicates electrogram; EGM, electrogram
mark.
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Discussion
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Our data suggest that a single comparison of the FPPI after 2
paced ventricular trains of 5 and 10 beats delivered during
tachycardia, even during the first 20 seconds, can
differentiate SMVTs from STs and ATs independent of the onset of the
tachycardia. A FPPI 5 to 10 shorter than 25 ms
identifies the regular rhythm as a VT, whereas if this difference is
longer, the rhythm should be supraventricular.
It is obvious that the rate criterion is insufficient to discriminate
between supraventricular and slow VTs. Although several
algorithms have been proposed for automatic differentiation between
ventricular and supraventricular
arrhythmias,19 only those that compare
the RR intervals are being widely used. The stability criterion that
measures the variability of the tachycardia CL is useful
for the differentiation of atrial fibrillation.15
For the diagnosis of ST, the sudden-onset
algorithm15 16 has recently been incorporated
into implantable devices. This algorithm measures the decrement in the
CL at the onset of the tachycardia in relation to previous
intervals. The decrement in CL during STs is expected to be gradual in
contrast to VTs, in which the shortening of the CL is usually abrupt.
Swerdlow et al20 prospectively evaluated the rate
stability and sudden-onset criteria in 100 patients. Although a
stability criterion of 40 ms allowed correct detection of all episodes
of spontaneous or induced VT, the sudden onset was less effective; it
failed to detect 0.5% episodes of spontaneous VTs. These VTs arose
during periods of ST or gradually accelerated above the cutoff rate.
Another limitation of the onset criterion is the impossibility to
differentiate paroxysmal ATs with sudden onset.
FPPI Variability in VT
Our data have shown that the FPPI during overdrive pacing in SMVTs
remains constant independent of the number of paced beats and the
pacing delay from the VT initiation. Most monomorphic VTs observed in
patients with chronic myocardial infarction are reentrant
arrhythmias based in an anatomic
circuit,21 in which it is possible to demonstrate
a fully excitable gap between the head and the tail of the wave
front.22 This fully excitable gap occurs when the
wavelength of the reentrant impulse is shorter than the path length; in
this situation a critical part of the circuit is fully excitable and
can be invaded by impulses initiated from outside the circuit. Hence
appropriately timed premature impulses can reset the
tachycardia when they enter the circuit and propagate
around it in the same way as the reentrant
impulse.23 24 Entrainment involves continuous
resetting of the tachycardia by overdrive
stimulation.25 26 In the presence of a fully
excitable gap, if the pacing CL is longer than the shortest functional
refractory period of the circuit, the head of the activation will never
impinge on the tail of refractoriness of the previous beat, therefore
each stimulus will conduct in a fully recovered circuit. Consequently,
the conduction velocity will be constant independent of the number of
beats of the train. In cases in which the stimulation CL is shorter
than the shortest functional refractory period, a stimulus will reach
the reentrant circuit when it is relatively refractory, resulting in
conduction delay. Because of this delay, subsequent stimuli will
encounter tissue that has had even less time to recover, resulting in
further conduction slowing and progressive increase in the return
cycle. In this circumstance the return cycle can increase in
relation to the number of beats.27 In our
protocol we used a pacing CL of only 40 ms less than the VT CL, in an
attempt to eliminate this possibility. Although resetting with single
or double extrastimuli demonstrated some duration of a flat response
curve compatible with a full excitable gap in only 70% of
VTs,23 the FPPI stability observed in our study
suggests that all included VTs presented a fully excitable gap;
this discrepancy can be explained first by the fact that these VTs were
relatively slow and second by the use of pacing train instead of
extrastimuli. The pacing trains may avoid the shortest intervals needed
by the extrastimuli technique; additionally the pacing trains may
modify and shorten the refractoriness inside and outside the
circuit.
Another important point is the supposed lack of effect in the FPPI
stability of the VT CL variability. This variability is more marked in
slower VTs and within the first 50 beats,17 18
the exact type of tachycardia and time in which this
protocol was analyzed. However, we did not observe significant
variability when the FPPI after trains with the same number of beats
were compared 20 seconds apart within the first minute of the VT
induction. The CL variability was not determined except for the period
preceding the first ventricular train, nevertheless it is
very improbable that we selected a group with such a low rate
variability, which might explain our results. It seems more possible
that the rapid pacing could stabilize the
electrophysiological properties of the
circuit and thus eliminate the spontaneous change in VT CL.
FPPI Variability in ST and AT
During pacing at the RVA, we observed important differences when
the FPPIs after consecutive trains were compared. But even more
important than these general differences was the fact that no sequence
was found in which the difference was 25 ms for AT and 50 ms for ST,
when FPPIs after 5 and 10 beats were compared, in contrast to the VT
group, in which in all the sequences the differences were 25 ms.
There are some possible explanations for these differences: (1) The
distance from the RVA to the atrial pacing site or sinus node is
greater than it is to any VT circuit, so whereas a 5-beat train is long
enough to reach the ventricular circuit, it is probably
insufficient to reach the atrial focus; in this case the FPPI is
usually shorter than the FPPI after a longer train in which the circuit
is reset, such as a 10-beat train. (2) Trains with a different duration
may produce different degrees of retrograde penetration in the AV node,
modifying in a different degree the AV nodal conduction of the first
postpacing sinus beat. We did not observe, even with 15-beat trains,
retrograde atrial capture during tachycardia, therefore the
second explanation seems to be the most reasonable. These results seem
to be independent of the AV nodal conduction state. In most simulated
AT, a very long PR interval was observed, reflecting a stressed
conduction status in the AV node, probably different from what is
present during ST in which the AV nodal conduction is improved by
catecholamines.
Limitations
Theoretically, in the following situations the FPPI algorithm may
lead to misdiagnosis: (1) VT acceleration or induction of a different
VT by the longest train can provoke substantial changes in the FPPI.
(2) Use-dependent effect of antiarrhythmic drugs, a prolongation of the
FPPI in response to longer pacing trains, might be observed in patients
with VT under antiarrhythmic drug treatment. (3)
Ventricular pacing trains, even during ST, may induce
reentrant ventricular beats with a similar coupling
interval simulating a VT. Nevertheless, we did not observe this
response with our stimulation protocol. (4) Although we were able to
entrain all tachycardias, even those with a morphology
similar to right bundle-branch block, we cannot exclude the
impossibility of achieving entertainment with a short train in a VT
located far from the RVA28 (laterobasal wall of
the left ventricle). (5) Most of the cases of the AT group were
"ATs" simulated by AAI pacing. This may be criticized as
artificial. However, because AAI pacing is completely regular and does
not present overdrive suppression, it will produce the most regular
FPPI at the atrial level. Thus, this AT simulation would have been the
most likely to behave against our hypothesis. (6) These data have been
obtained from induced VT and simulated tachycardias; we do
not have data about the applicability of this algorithm in spontaneous
VT, nor therefore in clinical practice. Further studies with implanted
devices should be conducted to validate the FPPI stability algorithms
with the use of electrogram morphology during
tachycardia.
Although we did not induce any VT by using ventricular
trains, this is a possibility to keep in mind. Nevertheless, an
electrophysiological study previous to
hospital discharge could easily identify these cases in which the
ventricular pacing could provoke some of the previously
mentioned undesirable effects.
Potential Clinical Implications
The FPPI variability algorithm could be incorporated in the
implantable cardioverter-defibrillator to enhance presently
available detection criteria in devices with a single
ventricular lead.
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Selected Abbreviations and Acronyms
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|---|
| AT |
= |
atrial tachycardia |
| CL |
= |
cycle length |
| FPPI |
= |
first postpacing interval |
| FPPI 5 to 10 |
= |
FPPI difference between pacing trains of 5 and 10 beats |
| FPPI 10 to 15 |
= |
FPPI difference between pacing trains of 10 and 15 beats |
| RVA |
= |
right ventricular apex |
| SMVT |
= |
sustained monomorphic ventricular tachycardia |
| ST |
= |
sinus tachycardia |
| VT |
= |
ventricular tachycardia |
|
Received November 10, 1997;
revision received March 23, 1998;
accepted April 20, 1998.
|
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Abstract
Introduction
