David O’Donnell MD, Voltaire Nadurata
MD.
Electrophysiology Unit, Austin Hospital,
Heidelberg, Melbourne Australia.
Address for correspondence: David O’Donnell, Electrophysiology Unit,
Department of Cardiology,
Austin Hospital, Studley Road, Heidleberg 3084, Melbourne, Australia.
Email:
odonnell_research@hotmail.com
Abstract
Radiofrequency
ablation has an important role in the management of post infarction ventricular
tachycardia. The mapping and ablation of ventricular tachycardia (VT)
is complex and technically challenging. In the era of implantable
cardioverter defibrillators, the role of radiofrequency ablation is most
commonly reserved as an adjunctive treatment for patients with frequent,
symptomatic episodes of ventricular tachycardia. In this setting the procedure
has a success rate of around 70-80% and a low complication rate. With
improved ability to predict recurrent VT and improvements in mapping and
ablation techniques and technologies, the role of radiofrequency ablation
should expand further.
Introduction
Radiofrequency ablation
(RFA) is the treatment of choice in the management of symptomatic patients
with ventricular tachycardia (VT) in the absence of structural heart disease.
The role of RFA in-patients with VT in the setting of chronic ischemic
heart disease is less well defined. Ventricular tachycardia (VT) is a common
complication of ischemic heart disease, with significant associated morbidity
and mortality.
1,2 Traditionally,
anti-arrhythmic medications have formed the mainstay of treatment, despite
the low efficacy, the risk of pro-arrhythmia and long term adverse effects.
3 Anti-arrhythmic surgery is successful in abolishing
VT, however, the operative mortality in most series was unacceptably high.
4 Over the past 10 years, implantable cardioverter defibrillators
(ICDs) have become the treatment of choice for all but incessant VT. This
treatment is based on the evidence of a number of studies which have shown
that ICDs reduce overall mortality in certain subgroups of patients with
ischemic heart disease with documented VT
5, 6, or even in the absence of previously documented VT
7.
The development
of anti-tachycardia pacing algorithms has significantly reduced the need
for cardioversion
8 and resulted in much improved
patient acceptance of such devices. Whilst ICDs are associated with significant
mortality benefits in-patients with ischemic heart disease and VT, they
do not actually prevent the onset of arrhythmia and remain relatively contraindicated
in-patients with frequent arrhythmic episodes. In addition the implantation
and function of an ICD can contribute to pathological anxiety and depression
in some patients.
9 Furthermore, ICD therapy
is relatively expensive, when considered over the expected lifetime of particularly
younger patients. In-patients with ischemic heart disease RFA has developed
predominantly an adjunctive role in patients with incessant or highly symptomatic,
drug refractory VT.
Defining the Substrate for ventricular tachycardia in ischemic
heart disease
VT in the
setting of ischemic heart disease is predominantly manifest as monomorphic
VT, caused by stable reentrant circuits.
10,11 Whilst polymorphic VT and primary ventricular
fibrillation are seen in patients with ischemic heart disease these more
often relate to acute biochemical, ischemic or pharmacological insults;
whilst ablation has been proposed for these arrhythmias
12, correction of the underlying abnormalities form
the first line of treatment.
In simple
terms the mechanism of reentry in ischemic heart disease relates to zones
of heterogeneous conduction, typically at the edge of myocardial scars.
Residual functioning myocytes at the edge of, or interspersed within, myocardial
fibrous scar create zones of slow conduction and conduction block.
13 When appropriately located and with appropriate
electrophysiological properties, these slow conduction zones can take the
form of a discrete electrical channel or isthmus critical to the initiation
and continuation of VT.
The re-entrant
VT circuit utilizes the slow conduction properties of the critical isthmus.
(
Fig 1) The electrical activity propagates relatively slowly along
the isthmus during diastole and forms a silent zone on the surface ECG.
When electrical activity reaches the exit zone it rapidly propagates throughout
the ventricular myocardium, giving rise to mechanical systole and the
QRS complex on the surface ECG. The electrical wavefront courses a loop
through the myocardium before returning to the entrance zone and repeating
the isthmus passage.
14
Figure 1: Schematic representation of the re-entrant
circuit of ventricular tachycardia. The circuit has a central critical
isthmus located in a position intimately related to the scar border
zone. The isthmus can be formed between the scar zone and normal myocardium,
within or between two scar zones or between the scar zone and an anatomical
boundary such as the mitral valve.
The electrical
activation travels slowly through the isthmus before breaking out into normal
myocardium at the exit zones. The circuit courses a number of possible routes
(outer loops, inner loops or both) before returning to the critical isthmus
at the entrance zone.
The diagrammatic
representation of re-entry in
Fig 1 is a simplistic description
of a process, which can be highly complex. The reentry circuits can be
multiple with shared and separate components; the circuits can be located
in the endocardium, epicardium, transmuraly or throughout each of these
zones. The isthmuses can vary significantly in length and electrophysiological
properties. The regions of conduction block can be formed by scar tissue
or by anatomical boundaries (typically mitral annulus) and can manifest
absolute conduction block or functional conduction block developing only
during VT. A comprehensive knowledge of the anatomy and electrophysiology
is fundamental to approaching ablation of VT in ischemic heart disease.
Mapping techniques
Electrophysiological
mapping techniques are primarily focused to identify appropriate sites
for ablation. In the mapping of VT in the setting of ischemic heart
disease, the fundamental task is to identify and understand the critical
VT isthmus. A number of different techniques have been developed to guide
mapping.
Mapping During VT
Early systolic Activity
Traditional
mapping approaches during VT have focused on identification of earliest
systolic activation. The principle is that the electrical activation that
precedes the QRS complex represents the breakout point of the VT into relatively
normal myocardium. Fast moving discrete activity preceding the surface
QRS by at least 30 msec is regarded as early activation. As seen in
Figure
2, the activity preceding the surface ECG will be recorded at the exit
zone. Whilst identification of the exit zones is important, ablation here
alone is rarely sufficient to eliminate the re-entry circuit.
Figure 2: Intra-cardiac electrogram recordings from
a single patient with typical re-entrant ventricular tachycardia related
to a previous inferior infarction. The recordings were obtained sequentially
and superimposed.
The exit zone
is identified by a discrete electrogram, which occurred 33 msec before
the onset of the surface QRS. Pacing at this site in sinus rhythm produced
a QRS complex, which closely resembled that of the studied VT.
The common isthmus
is identified by a slow moving, complex, fractionated signal in late diastole.
This position was less than 1 cm from the exit site. Pacing at this site
during VT (with high local capture threshold) resulted in concealed entrainment,
with a post pacing interval of less than 20 msec different from the VT
cycle length. Pacing in sinus rhythm produced a complex similar to the VT
being studied and a long stimulus to QRS onset. A complex late potential
was seen at this site in sinus rhythm.
The entrance
zone and outer loop contained discrete local potentials, which were seen
early in diastole and mid QRS respectively.
Radiofrequency
ablation using an irrigated tip catheter applied at the site of the isthmus
recording terminated VT. The local lesion was consolidated with a linear
ablation encompassing the exit zone and extending to the mitral annulus. Following
this lesion this VT morphology was no longer inducible.
Diastolic potentials
Slow moving
activity during diastole can be identified in the critical isthmus during
VT.
11,15 The timing of this
activity will become progressively earlier as the mapping moves from the
exit to the entrance. Whilst this is often a useful finding, alone it is
inconsistent; blind loops and far field potentials can give rise to diastolic
activity that is unrelated to the critical isthmus. The diastolic potentials
which arise in the critical isthmus will remain associated with VT during
entrainment mapping (described below), whilst diastolic potentials arising
from bystander areas should be dissociated from the VT during entrainment.
15
The morphology of the diastolic activity has also been studied to predict
the location of the critical isthmus but has limited additional value.
Entrainment Mapping
Entrainment
refers to a specific response of an arrhythmia to a pacing stimulus at
rates greater than the tachycardia cycle length.
16
Whilst no one technique alone can fully identify the re-entrant circuit
in is entirety, entrainment mapping is perhaps of most use in localizing
the critical VT isthmus.
11,17
The principles of entrainment utilize the unique electrophysiological
properties, which lead to the establishment of a reentrant arrhythmia
with an excitable gap. Whilst a complete discussion of entrainment is
beyond the scope of this paper, the principles warrant discussion.
Pacing that
leads to classical entrainment will result in temporary QRS fusion. If
pacing is conducted from within the critical isthmus of the arrhythmia,
the resultant QRS morphology should match that of the VT being studied;
this is known as entrainment with concealed fusion or concealed entrainment.
During concealed entrainment, the duration from the pacing stimulus to
the surface QRS onset can localize the pacing site within the isthmus.
The shortest S-QRS will be recorded at the exit zone and this will progressively
lengthen as the site of pacing moves along the isthmus towards the entrance
zone.
When pacing
at a site within the re-entry circuit, the post pacing interval, from the
last pacing stimuli to the return electrogram seen at the pacing site
should be similar to the cycle length of the VT. (Post pacing interval
– VT cycle length less than 30 msec.) With the complexity of the reentry
circuits, neither concealed entrainment nor the post-pacing interval are
completely accurate in identifying the isthmus zone.
18
The utilization of entrainment mapping is further limited by a number of
factors including: the dependence upon haemodynamically tolerated rhythms
to enable mapping, the ability to capture the local myocardium, which can
be difficult in zones of scar with high capture threshold and the often complex
and fractionated signals within the scar border zone which complicate interpretation.
Mapping During Sinus Rhythm
Mapping during
VT can be limited by haemodynamic instability, difficulties in inducing
VT and uncertainties regarding the clinical significance of induced VTs.
Mapping during sinus rhythm is designed to delineate the anatomical and electrophysiological
substrate, which predispose to reentry and VT. Mapping in the area of previous
infarction can identify these potential areas of abnormal conduction.
Different
groups perform substrate mapping using a combination of different techniques.
Analysis of electrograms during sinus rhythm can identify regions of fractionated
electrograms and late potentials, which are markers of abnormal, slowed
conduction. Voltage mapping identifies scar zones and the scar border zones
in which most isthmuses are located. Pacing threshold maps add additional
information to the voltage map to identify electrically heterogeneous areas.
Pacemapping to produce a QRS morphology that is similar to that during VT
can roughly localize the site of the reentry circuit exit. The duration
from the pacing stimulus to the onset of QRS (S-QRS duration) can further
identify abnormal substrate that predisposes to reentry.
None of these
above techniques have adequate specificity to be used alone, but in combination
can successfully identify regions of abnormal conduction. Substrate mapping
does not identify a discrete point for ablation, but rather a zone or
region of abnormal myocardium with the potential to facilitate reentry.
Newer Mapping Tools
The newer
mapping tools utilized in electrophysiology all have the potential to
facilitate the mapping and ablation of VT. By providing reproducible anatomical
information the mapping tools each have the ability to simplify mapping
approaches and to guide the delivery of optimal radiofrequency ablation
lesions.
CARTO (Biosense-Webster,
Diamond Bar, USA) is the most studied mapping tool to aid ablation of
ventricular tachycardia. CARTO is most useful in providing accurate substrate
maps. The EnSite 3000 multielectrode array (Endocardial Solutions, St Pauls,
USA) uses non-contact virtual electrograms which can not only provide myocardial
substrate information, but can map ventricular activation with a little
as one recorded cardiac cycle.
As technology
improves, the mapping systems will become an integral part of the study
of ventricular tachycardia. In the foreseeable future, however, the mapping
tools will provide guidance and accuracy, but will not replace the need
for an operator with a full grasp of electrophysiology and anatomy.
Ablation Techniques
The ablation of VT in the setting
of ischemic heart disease has been performed according to two basic strategies.
The first strategy involves induction of ventricular tachycardia, mapping
and targeted ablation.
19,20,21,22,23,24,25,26,27 The second strategy involves substrate mapping in
sinus rhythm and linear ablation to eradicate regions of abnormal myocardium
with the potential to facilitate reentry.28 It is difficult to comment
on the relative success of the different approaches as most centers now
use a combination of these two approaches.
Targeted ablation
of a single morphology of haemodynamically stable VT can be successful
in over 80% of cases.
19,20,21,22,23,24,25,26,27
Unfortunately, acute procedural success does not always predict long term
recurrence of VT. Some studies have reported a recurrence of VT of close
to 50% if a single dominant morphology is successfully ablated.
25As
such the trend in ablation of VT has been to target all inducible morphologies
of monomorphic sustained VT. When multiple morphologies of VT are targeted
the acute success rate diminishes proportional to the number of different
morphologies and diminishes further when the VT is hemodynamically unstable.
26,29 However, even in-patients with more than
3 inducible morphologies of VT or with hemodynamically unstable VT procedural
success rates are approach 60%.
26
The linear approach pioneered
by Marchlinski
28 was acutely successful in
eradicating or modifying VT in 7 of 9 patients with a recurrence in less
than 20%. Using a combination approach large series report an acute success
rate of 60-80%, with a longer-term freedom from VT of 75-95% in those successfully
ablated. Recent developments in catheter technology have led to the use of
irrigated tip catheters, which enable deeper lesions to be formed. These
catheters have been shown to be more successful in the acute termination of
VT
30, long term data is not yet available. Alternative
approaches via the epicardium
31 and via the
coronary arteries
32 have also been used but
as yet are not applicable beyond a few expert centers.
Complications
In the larger
reported series, significant complications (cardiac tamponade, TIA, complete
heart block) occurred in 5 – 10% of patients and minor complications (access
site hematoma, nausea etc) in a further 5 – 10% of patients.
19,20,21,22,23,24,25,26,27,28,29
Defining success
Previous series
have reported the recurrence of VT following a successful procedure to
vary from15 - 40%
19,20,21,22,23,24,25,
depending upon the specific definitions used. The non-inducibility of
clinical VT is often regarded as a marker of success following RFA. However,
it has been shown that even following successful ablation of all clinical
VTs, the presence of inducible non-clinical VT is associated with an increased
incidence of recurrent VT
21.
Indeed, following ablation of all morphologies of clinical VT in one series,
further morphologies, which had not been documented clinically, were inducible
in 83% of patients
26.
Because of
the difficulties with recognizing and defining clinical VT, we prefer to
define success based on the level of stimulation required to induce VT rather
than the particular morphology of VT induced.
33
Prior to ablation, we conduct a stimulation protocol from the right ventricular
apex comprising an 8 beat drive followed by up to 5 extrastimuli introduced
at decreasing cycle lengths until refractoriness was reached. At the end
of the ablation procedure we repeat the stimulation protocol. Procedural
success was defined by comparing the results of the two stimulation protocols.
Acute success – No monomorphic VT induced at refractoriness
of 5 extra stimuli.
Modified Result –Monomorphic VT only inducible by 2 extra
stimuli more aggressive than at baseline.
Failed Procedure - Monomorphic VT inducible at similar
levels to baseline.
Using this
protocol we were able to accurately predict the patients who will remain
free of further VT following radiofrequency ablation. In patients with a
minimum follow up of 12 months the rate of recurrent VT with either a complete
success or a modified result was 4%, compared with 66% amongst patients with
a failed procedure
33.
Patient selection
At one end
of the spectrum, the patient with incessant or intractable ventricular tachycardia,
resistant to pharmacotherapy and overdrive pacing and requiring frequent
cardioversion is an obvious candidate for ablation of ventricular tachycardia.
At the other end of the spectrum there is presently no role for ablation
in the sense of primary prevention.
Patients with
frequent episodes of VT should be considered for ablation. The threshold
for deciding to undergo ablation should consider the local expertise,
the frequency of episodes, patient and economic factors. Comprehensive
data has shown a substantial mortality benefit supporting the use of ICDs
in-patients with post infarction VT. At present ablation should ideally
be considered to have a role as an adjunct to an ICD in-patients with
highly symptomatic VT.
As mapping
and ablation techniques develop and the accuracy of predicting the long-term
outcome improves, the role of RFA may expand, making it the therapy of first
choice in a growing proportion of patients. Perhaps with time ICDs may be
reserved as the treatment for failed ablation procedures or for prophylactic
indications, particularly in parts of the world where widespread implantation
of ICDs is financially impractical. Even if ICDs remain justified on the
basis of residual uncertainty, the quality of life is likely to be improved
by the reduction in discharges resulting from catheter ablation.
Conclusions
Radiofrequency
catheter ablation of patients with highly symptomatic, sustained, monomorphic
post infarction VT can be performed with high success rate and acceptable
procedural complication rate. The procedure can be successfully applied
to a wide spectrum of patients including those with multiple morphologies
of VT and hemodynamically unstable VT. The procedure at present requires
extensive understanding of anatomical and electrophysiological principles
and is prolonged and technically demanding. Its application beyond a few
expert centers is dependent upon electrophysiological and technological advances.
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