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An increasing number of trials is confirming the
implantable cardioverter defibrillator (ICD) in life threatening arrhythmias as clearly
superior to the best possible antiarrhythmic drug therapy regarding patient survival
improvement.
The treatment menu of modern ICDs, based on several possible programmable detection
and redetection algorithms, beside the basic cardioversion and defibrillation functions,
the programmable ventricular antibradycardia pacing possibility and the more recently
introduced dual chamber rate responsive pacing option, also has a variety of added
programmable antitachycardia pacing features.
Antitachycardia pacing, derived from the programmed electrical stimulation, long used
for the study and treatment of ventricular tachycardias in electrophysiology laboratories,
has a long tradition with both, completely automatic1
and patient activated radiofrequency commanded2
devices. Although a few of these had adequate tachycardia identification and
antitachycardia treatment features, the absence of a defibrillation backup greatly limited
their use.
Since a re-entry mechanism is a prerequisite for pacing induced termination of
tachycardias, the efficacy of antitachycardia pacing to interrupt a large percentage of
ventricular tachycardias is due to the assumption that a large majority of monomorphic
sustained ventricular tachycardias are due to a re-entry mechanism, based on the presence
of an area of slow conduction as its arrhythmogenic substrate3.
A conduction block terminating a re-entry tachycardia occurs when a stimulated
wavefront reaches the proximal zone of the slow conduction area, before distal
refractoriness expiry.
Three factors are called upon to determine if the stimulated wavefront reaches this
zone in time to cause conduction block: the cycle length of stimulation; the number of
stimulated beats and the site of stimulation4.
Tachycardia termination can be achieved if a stimulus is introduced in the excitable gap
constituted by the timing difference between a shorter refractory period respect to the
cycle length.
The newer generation of ICDs present a large number of antitachycardia ventricular
pacing modes. These include: the scanning of the diastole with pacing impulses; single
double or multiple pacing stimuli with fixed or adaptive coupling intervals; trains of
pacing impulses of programmable or automatically increasing length with fixed or adaptive
coupling intervals and: - fixed cycle length during stimulation (burst pacing); - burst
with final programmed electrical stimulation; - automatically decreasing cycle lengths
between the stimuli with fixed decrements (ramp) or adaptive decrements ("ramp
+"); - decreasing cycle lengths between impulse trains (scan); - decreasing and
increasing cycle lengths during the impulse trains (concertina). Among these the most
commonly adopted and tested modes appear to be the burst, the scan and the ramp algorithms5,6,7.
Several prospective randomised studies8-11,
undertaken to assess which of these is the most efficient in terminating induced
ventricular tachycardias, have shown that these pacing techniques have the same efficacy,
with a success rate of approximately 90% and no difference in the however low incidence of
tachycardia acceleration.
Slower tachycardias (cycle lengths above 300 ms) appear to be more prone to
termination by antitachycardia pacing and conversely faster tachycardias tend to be more
subject to acceleration by antitachycardia pacing5,11.
Acceleration seems also to be associated with longer trains of pacing impulses12, therefore it is usually suggested to work around
series of eight impulses and to pass on to cardioversion, or defibrillation if necessary,
after a limited number (usually three) of unsuccessful antitachycardia pacing attempts, to
prevent an excessive prolongation of an ongoing tachycardia with consequent cardiac
ischemia, which might increase the defibrillation threshold and hinder the final
termination of the arrhythmia6.
Spontaneous tachycardias appear to be slower than induced tachycardias13,8, therefore it can be speculated that they might
respond better to antitachycardia pacing, as demonstrated by studies comparing conversion
rates between spontaneous and induced tachycardias7,14
with a success rate of approximately 90%.
According to some studies antitachycardia pacing appears to be most often effective at
80-90% of the tachycardia cycle length and tends to accelerate the tachycardia at cycle
lengths inferior to 75%14,3, even though this last
finding could not be confirmed by Trappe et al7 in a
successive study.
Trappe et al believe pre- as well as post-ICD implant electrophysiologic studies are
mandatory in order to evaluate the most effective antitachycardia pacing mode, although
they demonstrated that electrophysiologic testing prior to ICD implantation is not a
reliable way to identify the most effective antitachycardia pacing mode. They believe
pre-discharge testing is extremely important to program the most likely effective
antitachycardia pacing mode and avoid frequent ICD discharges7.
The above illustrated features were used to satisfactorily treat a rather complicated
case of recurrent sustained ventricular tachycardia in the setting of arrhythmogenic right
ventricular dysplasia.
The patient, a 35 year old, active but very anxious woman, presented ventricular
tachycardia and syncope as her first clinical manifestation at the age of 26.
Subsequently, after the diagnosis of arrhythmogenic right ventricular dysplasia was
confirmed by echocardiography, cardiac angiography and nuclear magnetic resonance imaging
and an invasive electrophysiologic study demonstrated the possibility to induce sustained
ventricular tachycardias, the arrhythmia was satisfactorily treated with amiodarone
(electrophy-siologically tested). She did not experience the recurrence of ventricular
tachycardia until the drug had to be interrupted because of the appearance of amiodarone
related hyperthyroidism. She was therefore treated, under Holter control, with several
other drugs, among which metoprolol, atenolol, sotalol, flecainide and mexiletine, used
either alone or in association. She did not tolerate the adequate or higher dosages of
some of these and presented the recurrence of several, sporadic, hemodynamically
tolerated, episodes of sustained ventricular tachycardia, for which she was admitted to
hospital three times in the next six years, but without any more syncope or dizzy spells.
The documented episodes of spontaneous sustained ventricular tachycardia, of
apparently right ventricular origin, were of two different morphologies and of two cycle
lengths, respectively of 315 ms and 420 ms.
Without any apparent reason, about a year ago, she presented an abrupt increase of the
since then sporadic recurrences of the arrhythmic episodes, despite antiarrhythmic drug
therapy (which seemed capable only of reducing the number of episodes and of probably
increasing the tachycardia cycle length). On no occasion did the patient present atrial
fibrillation or sustained supraventricular tachyarrhythmias.
Due to the patient's, up to that moment, manifest reluctance to accept an ICD, she was
submitted to two radiofrequency ablative procedures, which acutely resolved, in both
occasions, both the earlier documented forms of monomorphic tachycardia, which originated
from different sites of the right ventricle, without re-inducibility at the end of the
procedures, but with the recurrence of the arrhythmia two to three weeks after these
therapeutic options. Although the tachycardias, induced during the pre-ablation
electrophysiologic studies, demonstrated the same morphologies as the spontaneous
episodes, their cycle lengths of approximately 340 ms did differ significantly and could
be terminated by several antitachycardia pacing modes.
Therefore an ICD using antitachycardia options as extensively as safety permits, but
with cardioversion and defibrillation backup, was proposed and finally accepted by the
patient. This choice was conditioned by: - the frequent recurrence (sometimes several a
day) and the, at least partial, refractoriness of the tachyarrhythmia to drugs; - the
impossibility of indefinitely administering amiodarone, which had also provoked
hyperthyroidism; - the complex arrhythmogenic substrate; - the possibility of
destabilisation of the arrhythmia as the already manifested sudden increase of the
ventricular tachycardia episodes; - the absence of syncope and/or dizzy spells; - the
hemodynamically tolerated tachycardia episodes; - the two morphology and the two
cycle-length ventricular tachycardias; - the patient's fear of ICD delivered shocks and
the possible life-style limitations due to it.
In this case, a Biotronik Phylax 06 active housing ICD, with a transvenous SPS
(shock/pacing/sensing) 75-UP/BP Biotronik lead, was implanted in a left subpectoral site,
approximately six months ago. This particular ICD, beside the possibility of non invasive
EPS studies, the recording of detected/treated/resolved episodes and storing the
electrocardiograms of these, has the possibility of subdividing a so-called ventricular
tachycardia detection zone in up to four different categories, using separately
programmable detection/redetection algorithms, beside a so-called ventricular fibrillation
detection zone with another possible independent detection/redetection algorithm. It can
then deliver an individually programmed tiered therapy for any, all, or none of the
detected episodes.
After the implant, the ICD was programmed in only the monitoring mode for tachycardias
with cycle lengths of up to 285 ms, with defibrillation backup for inferior cycle-lengths,
to test the accuracy of the detection and record the characteristics (cycle lengths and
frequency) of the spontaneous tachycardia episodes. After a few days of therapy washout,
during which time five tachycardia episodes were correctly recorded and classified (Tab. I), a non-invasive electrophysiologic study, using the implanted
ICD, was performed to test the therapy protocol in the hypothetically worst possible
arrhythmogenic condition for the patient.
After several antitachycardia protocols were tested, it was found that while the
shorter bursts of up to 7 impulses were partially successful on the induced episodes,
resolving 80% of them, a spontaneous tachycardia was not terminated by such a burst.
However, a 10 impulse burst at 81% of the tachycardia cycle length, could terminate all
the induced episodes and other three spontaneous ventricular tachycardias.
The ICD was consequently programmed to detect and (treat):
- events having cycle lengths between 480-403 ms, a sudden onset (defined as a 22%
cycle length decrement respect to the basic RR interval) and a duration superior to 50
cycles, defined VT1, only monitoring and storing the data, to document the frequency and
spontaneous outcome of the event in this still physiologic range;
- events having cycle lengths between 402-317 ms, a sudden onset and a duration
superior to 20 cycles, defined VT2, to be treated with up to five series of 10 impulse
cycles, with 8 ms decrements between bursts (scan) and a fixed minimum cycle length of 230
ms, without further treatment;
- events having cycle lengths between 316-278 ms, a sudden onset and a duration
superior to 13 cycles, defined VT3, to be treated with up to three series of 5 impulse
cycles, with 12 ms decrements between impulses (ramp) and a fixed minimum cycle length of
190 ms, followed by cardioversion in case of failure of tachycardia termination and/or its
acceleration, starting with a 15 J shock (the defibrillation threshold at implant was
inferior to 10 J), to be followed, if necessary, by up to eight 30 J DC biphasic shocks;
- events having cycle lengths inferior to 277 ms, to be considered in the ventricular
fibrillation zone, defined VF, to be treated by a first defibrillation biphasic shock of
18 J, to be followed by up to eight others of 30 J.
Drug therapy (sotalol and mexiletine) was reinstated before hospital discharge, during
which time a spontaneous episode was terminated at the first attempt.
At the successive follow-up after a month, the event recorder had stored four
episodes, classified as VT2, which were terminated by the first burst and a further
episode classified as VT1 which had, correctly, not been treated until its spontaneous
acceleration into the VT2 zone, when it had also been terminated at the first attempt.
At the follow-up after three months, during which the drug therapy had been partially
interrupted a week before the scheduled visit, because of the recurrence of chronic
gastro-intestinal problems, the patient had experienced an enormous increase of the
tachycardia episodes (up to 30 in a single day), without feeling the need to anticipate
the visit or notify these events.
The recorded events showed an overall satisfactory result with 100% ventricular
tachycardia termination. In particular, during the drug suspension period, beside an
enormous increase of the tachycardia episodes, all in the VT1 and VT2 categories, a cycle
length decrease, very near the limit of the faster VT3, was also noted. It can be
speculated that this could be due to the drug suspension, but the possibility that the
symptoms and factors correlated with her gastro-intestinal condition could have influenced
this cannot be excluded.
The event recorder showed respectively 21 and 75 initial episodes detected in the VT1
and VT2 categories. Of the 21 episodes classified as VT1, 13 accelerated into the VT2
category and were as such detected and consequently treated. Of the 88 VT2 episodes, 80
were terminated with the first burst, which resulted ineffective in the remaining 8. Seven
of these latter episodes were terminated at the second attempt and one was resolved at the
fourth attempt, without acceleration.
Considering the above observations, the antiarrhythmic drug therapy was re-established
(the gastrointestinal problems had in meantime been adequately medically treated) and the
ICD was reprogrammed with the intent to optimise the antitachycardia treatment algorithm
by:
- decreasing the upper frequency detection range of VT1, still to be only monitored
and stored without any treatment;
- dividing the previous VT2 category into:
1. a slower tachycardia, with a cycle length of 426-341, defined VT2, to anticipate
the detection of tachycardias in the previous VT1 cycle range (which then had to
accelerate before being treated), maintaining the same antitachycardia protocol assigned
to VT2, only increasing the total number of the scanning cycles up to 7;
2. a faster tachycardia, with a cycle length of 340-302 ms, now defined VT3, to be
treated with the same protocol, but after only 10 tachycardia cycles, instead of 20, to
avoid unnecessarily long bouts of tachycardia;
- redefining the previous VT3 as VT4, with a detection cycle length of 301-271 ms,
maintaining the same therapy (3 ramp sequences, eventually followed by cardioversion);
- reducing the cycle length of the so-called VF detection zone to less than 271 ms.
At the six month follow-up, the antitachycardia therapy efficacy appeared very
satisfactory, with a 100% termination rate, after a single burst, of all the 16 detected
tachycardia episodes, six of which were recorded in less than 30 m', during physical
exercise and a Holter recording.
All the stored and treated ventricular tachycardias up to this moment are summarised
and tabulated according to their cycle length, where possible, also in relation to the
drug therapy, in table I.
The apparent efficacy of the antitachycardia therapy in relation to the tachycardia
cycle length is illustrated in figure 1, showing a relationship between longer cycle
lengths and an "easier" termination of the tachycardia, as observed in several
studies5.
 
Fig. 1: Percentages of ventricular tachycardia terminations in relation to their cycle
lenghts.
In conclusion, the utilisation of the extended diagnostic and tiered therapeutic
options offered by a modern ICD, permitted appropriate identification and treatment of
monomorphic sustained ventricular tachycardias of different cycle lengths and morphologies
in the context of a complex arrhythmogenic substrate, with several complicating factors.
As intended, the use of the antitachycardia algorithms permitted the termination of all
the detected tachycardias, at the first attempt in 93% of these, at the second attempt in
6% and at the fourth attempt in less than 1%, avoiding unnecessary shocks, preventing both
physical and psychological trauma, particularly in the case of the necessity to intervene
so frequently and in the meantime also saving battery service life.
This case confirms the results of several studies asserting, the safety and efficacy
of the antitachycardia therapy options, the need of extensive investigation with pre- and
post-ICD implantation electrophysiologic testing, in order to evaluate the most effective
pacing mode7 and the necessity to reprogram the ICD
during the follow-ups, to tailor the therapeutic options to the patient's needs. Besides,
the results obtained in this case appear to be in line with previous observations of the
relation between a high tachycardia termination rate and slower tachycardias5.
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