(Circulation. 1997;96:3499-3508.)
© 1997 American Heart Association, Inc.
Articles |
From Temple University School of Medicine, Philadelphia, Pa.
Correspondence to Steven A. Rothman, MD, Cardiology Section, Temple University School of Medicine, Parkinson Pavilion, Room 908, 3401 N Broad St, Philadelphia, PA 19140. E-mail sarcer{at}astro.ocis.temple.edu
| Abstract |
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Methods and Results RF ablation was attempted in 35 patients with a previous myocardial infarction and recurrent, hemodynamically tolerated VT. A mean of 3.9±2.7 VTs were induced per patient (range, 1 to 10). The clinically documented arrhythmia was successfully ablated in 30 of 35 patients (86%), and on follow-up electrophysiological testing, 11 patients had no inducible VT and were discharged without other therapy. Nineteen patients had inducible "nonclinical" arrhythmias on follow-up testing, and the majority underwent cardiac defibrillator implantation. Freedom from recurrent arrhythmias, including sudden death, was 91% in patients without inducible VT and 53% in patients with persistently inducible "nonclinical" arrhythmias (P<.05; mean follow-up, 17±12 and 12±11 months, respectively).
Conclusions In patients with well-tolerated VT, RF catheter ablation may be useful as a primary cure if no other ventricular arrhythmias are inducible on follow-up testing. Ablation of all hemodynamically tolerated arrhythmias should be attempted in patients with multiple inducible VT morphologies because of the high rate of recurrence of unablated VTs in these patients.
Key Words: tachyarrhythmias catheter ablation tachycardia coronary disease
| Introduction |
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| Methods |
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The mean age of patients undergoing attempted RF ablation was 62±13 years, and all except 2 patients were male. Seventeen of the patients had had a previous anterior wall myocardial infarction, 17 patients had had a previous inferior myocardial infarction, and 1 patient had multiple sites of infarction. The mean ejection fraction was 24±8%. VT first occurred 6.9±9.4 years after the myocardial infarction and had a frequency (mean±1 SD) of 4.2±8.4 episodes per month after its index occurrence (range, 1 episode per year to 40 episodes per month). Sixteen of the 35 patients had recurrent VT despite chronic treatment with antiarrhythmia agents. Of these patients, only 5 had been treated with amiodarone for their VT; in 1 patient, the amiodarone was discontinued 6 months before the electrophysiology study due to toxicity. An additional patient was being treated with a "low" dose of amiodarone (200 mg/d) for atrial fibrillation when the VT occurred
Electrophysiological Testing
The study protocol was approved by the Temple University
Institutional Review Board, and informed consent was obtained from all
patients. Patients were brought to the electrophysiology laboratory in
the fasting, drug-free state (except patients previously treated with
amiodarone). Three or four 6F quadripolar electrode catheters
were advanced from the femoral veins to the high right atrium (in
patients without atrial fibrillation), atrioventricular
junction (His-bundle recording), right ventricular
apex, and right ventricular outflow tract. Programmed
ventricular stimulation was performed at twice the
diastolic threshold with a 1-ms pulse width using a
programmable stimulator (Bloom Stimulator, Fischer Imaging Corp) with
one, two, and three extrastimuli from both RV sites at two drive CLs
(usually 600 and 400 ms). Left ventricular stimulation was
also performed in 1 patient; in 10 patients, programmed stimulation was
performed during three drive trains, including normal sinus rhythm. All
12 standard ECG leads were recorded continuously along with the
intracardiac ECGs through the use of a digital recording system
and optical storage (Arrhythmia Research Technologies). In 10
patients in whom the induced VT was only marginally tolerated
(hypotensive without syncope), intravenous
procainamide was infused with a maximum loading dose of 15
mg/kg at a rate of 50 mg/min followed by a continuous
infusion at a maximum rate of 0.11 mg · kg-1
· min-1; attempts at mapping and ablation were then
resumed.
Left ventricular mapping was performed with a 7F
deflectable quadripolar catheter advanced from a femoral artery and
retrogradely across the aortic valve to the left
ventricular cavity. The deflectable catheter had a 4-mm
distal tip electrode and 2- to 5-mm interelectrode spacing
(Mansfield-Webster, EPT Technologies, or Medtronic CardioRhythm). A
unipolar electrogram was recorded between the distal tip and a
large skin electrode, and bipolar electrograms (filtered 30 to 500 Hz)
were recorded between adjacent electrode pairs. The local
endocardial activation time was measured from the onset of the
diastolic electrogram in the distal bipolar
recording to the onset of the QRS during VT. Sites with a
diastolic local activation time were targeted for RF
ablation when participation of the electrogram in the VT circuit could
be inferred by one or more of the following criteria: (1) constant
electrogram morphology and timing relationship with the return cycle
onset after entrainment from a remote RV site with bipolar pacing at a
CL of 30 to 50 ms shorter than the VT CL,8,9 (2) concealed
entrainment by pacing from the target site at a CL of 30 to 50 ms
shorter than the VT CL and producing an exact morphological ECG match
to the VT (Fig 1
),2,10,11 and
(3) left ventricular pace mapping during normal sinus
rhythm that produced an exact morphologic ECG match to the
VT.12 Unipolar pace mapping, between the distal electrode
and a large skin electrode/grounding pad, was performed with an output
just above threshold. Bipolar pace mapping, between the two distal
electrodes, was performed in 6 patients when unipolar pacing with the
catheter ablation system was not technically feasible. A "perfect"
pace map was defined as an exact, superimposable morphological ECG
match to the VT QRS in all 12 standard ECG leads, and a "good" pace
map was defined as a nearly identical morphological match in all 12
standard ECG leads, when the ECGs of the induced VT and pacing were
compared on a side-by-side basis.
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Catheter Ablation
RF catheter ablation was attempted of all inducible and
hemodynamically tolerated VT morphologies. In 27
patients, RF energy was delivered as a continuous, unmodulated sine
wave at 500 kHz (Radionics model RFG-3C) with an average power delivery
of 30 to 50 W. In 8 patients, RF energy was applied using a
temperature-controlled system (Medtronic Atakr; EPT Technologies model
1000) with a temperature set point of 70°C. Power was generally
delivered during VT and continued for 60 to 90 seconds during
applications, which resulted in the termination of VT. A second RF
application was typically given at successful target sites if VT could
not immediately be reinitiated and the catheter had not moved
fluoroscopically. The complete protocol of programmed stimulation was
performed until all hemodynamically tolerated VTs were
successfully ablated. The full stimulation protocol was again repeated
after a 30-minute waiting period, and the study was concluded if no
hemodynamically tolerated VTs could be induced.
Follow-up
A predischarge electrophysiology study was performed a mean of
5±3 days after the ablative procedure. Programmed stimulation with
one, two, and three ventricular extrastimuli from the right
ventricular apex and right ventricular outflow
tract at two paced CLs was performed, along with burst
ventricular pacing, with patients in the drug-free state as
previously described. Patients with no inducible sustained
ventricular arrhythmias were discharged without
antiarrhythmic therapy. Patients with persistently inducible sustained,
rapid monomorphic ventricular arrhythmias were
advised to undergo implantation of an ICD despite the successful
ablation of their "clinical" VT. An ICD with electrogram storage
capabilities (Ventritex Cadence) was implanted, when possible, in these
patients. The induction of ventricular flutter with CL of
200 ms or ventricular fibrillation/polymorphic VT
with triple extrastimuli was considered a nonspecific finding and was
not treated in the absence of prior clinical episodes of a similar
arrhythmia.
A late follow-up electrophysiology study (3 to 4 months after ablation) was performed in 8 of 11 patients in whom no sustained VT could be induced at the time of their predischarge study. Programmed stimulation was performed as above to assess the long-term efficacy of the ablative procedure. A follow-up study was also performed in 7 of 12 patients who had successful RF catheter ablation of their clinical arrhythmia but persistent inducibility of a rapid monomorphic VT with no recurrent symptoms.
Patients were seen in follow-up by either their referring cardiologist or one of the authors every 3 to 4 months. In patients who underwent implantation of a cardiac defibrillator, the electrograms of all recurrent events were retrieved from the ICD and recorded on an ink-jet recording system (Mingograf 7, Siemens-Elema). The CLs of the recurrent ventricular arrhythmias were compared with the VT CL of the patient's spontaneous VT before catheter ablation. Recurrence of the patient's initial spontaneous VT was thought to occur if either (1) a 12-lead ECG demonstrated the same VT morphology as the initial VT or (2) the VT CL as recorded from the ICD was within 20 ms of the initial VT CL.
Definitions
The "clinical VT" was defined as an inducible VT that
matched the morphology of the patient's documented, spontaneously
occurring, monomorphic VT. "Nonclinical VTs" were defined as
inducible monomorphic VTs that were not previously known to have
occurred spontaneously. The induction of "polymorphic VT" was
considered a nonspecific finding. "Multiple VT morphologies" were
defined as two or more inducible VTs having contralateral bundle-branch
block patterns, frontal plane axis of
90° divergent, or marked
differences in individual ECG leads recorded from the same
electrode locations.
"Complete success" of the ablation procedure was defined as having no inducible, sustained monomorphic VT on predischarge follow-up testing. The patients in whom the "clinical" arrhythmia could no longer be induced at the predischarge follow-up study but had sustained, nonclinical VT induced with programmed stimulation were defined as having "partial success." "Failure" was defined as the inability to ablate the clinical VT, recurrence of the clinical VT before follow-up testing, or inducibility of the clinical VT at the time of the predischarge follow-up study. "Sudden cardiac death" was defined as a death from a presumed arrhythmic cause occurring within 1 hour of the onset of symptoms.
Statistical Analysis
All values are summarized as the mean±1 SD. Continuous
variables were compared using the Student's t test for
unpaired data, and categorical data were compared by
2
analysis. A Kaplan-Meier analysis and Mantel-Cox
log-rank test was used to compare the freedom from recurrent
arrhythmias between groups. Values of P<.05 were
considered significant.
| Results |
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Target sites for ablation were usually identified by activation mapping during the VT and confirmed, as described above, with entrainment techniques, pace mapping, or both. Approximately 62% of the successful target sites were confirmed by entrainment, and 77% had a "good" or "perfect" pace map; evidence of concealed entrainment was observed at 37% of the target sites. Of the 61 VTs not amenable to catheter ablation, 27 were not sufficiently well tolerated to allow adequate mapping and ablation, 19 could not be terminated with RF energy delivery despite extensive mapping, and during 15 VTs, no adequate target sites could be identified. A total of 324 applications of RF energy were delivered at potential target sites (9±8 RF applications per patient; range, 1 to 27).
Successful ablation of at least the clinical arrhythmia
was achieved in 31 of 35 patients (89%) (Fig 2
). In 4 patients in whom the clinical VT
could not be successfully ablated, the procedure was considered an
ablation failure. A follow-up electrophysiology study was performed
before discharge in 27 of the 31 patients with initial success. No
sustained monomorphic VT could be induced in 10 patients who were
subsequently considered complete successes. In 16 patients, only
nonclinical monomorphic VTs could be induced with programmed
stimulation, and they were considered partial successes. The ablation
procedure was considered a failure in 1 patient with persistent
inducibility of his clinical arrhythmia on follow-up testing.
The total procedure time was 311±164 minutes per patient, with a
fluoroscopy time of 67±49 minutes. Nine patients required two ablation
procedures (the second procedure performed 3 to 9 days after the first
procedure) to achieve clinical success.
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Of the 4 patients who did not undergo a predischarge electrophysiology study, two refused the follow-up study but had persistently inducible nonclinical VTs at the time of the initial procedure and were grouped as partial successes. A third patient underwent a follow-up study several weeks after ablation by his referring cardiologist and was found to have persistent inducibility of only nonclinical VTs, which were not ablated; this patient was also considered a partial success. One patient with frequently recurring (two or three times daily) but self-terminating sustained VT had a single inducible morphology of VT that was successfully ablated, and the procedure was considered a complete success. A follow-up study, however, was not performed because the patient remained hospitalized awaiting orthotopic heart transplantation while on intravenous inotropic agents for severe left ventricular dysfunction.
Complete Success
Complete success was achieved in 11 patients (31%). A mean of
2.3±1.2 VTs per patient were induced and ablated in this group (range,
1 to 4). The mean VT CL in this group was 385±63 ms. Before the
ablation procedure, 4 of these patients had recurrent VT despite
treatment with antiarrhythmic agents (none had received
amiodarone). On follow-up testing before discharge, no patient
had inducible sustained, monomorphic VT. Two patients did have
inducible ventricular flutter with closely coupled triple
extrastimuli, and 4 patients had inducible nonsustained VT (4 to 14
beats in duration). Ten of the 11 patients were discharged without
either antiarrhythmic therapy or implantation of a cardiac
defibrillator. One patient underwent implantation of a defibrillator at
the request of the referring physician due to the rapidity of his
presenting VT (CL of 260 ms, associated with marked
lightheadedness).
Long-term follow-up studies were performed in 8 of these 11 patients at 4.2±2.3 months after the initial ablative procedure. Of those not undergoing long-term follow-up stimulation, 1 patient had undergone his initial electrophysiology study before implementation of the long-term follow-up in our protocol, 1 patient refused a follow-up study, and the third patient underwent orthotopic heart transplantation 2 months after the ablative procedure. Six of the 8 patients had no inducible sustained arrhythmias at the time of the follow-up study, and 1 patient had inducible polymorphic VT with a CL of 150 ms. A monomorphic VT with a CL of 220 ms was induced with closely coupled triple extrastimuli in the eighth patient; this patient's clinical VT had a CL of 330 ms. Nonsustained ventricular arrhythmias of <18 beats in duration were induced in 4 of the remaining patients. There were no documented recurrences of VT in this group over a mean follow-up of 17±12 months (range, 2 to 34 months). One patient died suddenly 18 months after the ablative procedure; this patient had multiple recurrences of a well-tolerated VT before the ablative procedure and only rapid polymorphic VT induced at the time of his long-term follow-up study.
Partial Success
Nineteen patients had successful ablation of their clinical VT but
persistent inducibility of nonclinical VTs with programmed stimulation
before discharge. The mean number of inducible VTs per patient in this
group was 5.3±2.7, with a mean CL of 344±57 ms. There were 2.7±2.2
VTs per patient successfully ablated and not reinducible on the
predischarge follow-up study. These VTs had a mean CL of 376±51 ms and
included the clinical VT. Inducible VTs that could not be successfully
ablated had a mean CL of 300±64 ms; this was significantly shorter
than the ablated VTs (P<.0001). The number of inducible VTs
was significantly greater in the partial success group than in the
complete success group (P<.005).
Four of the 19 patients who had partial success were discharged without a cardiac defibrillator or antiarrhythmic therapy. Two of these patients had only rapid, sustained monomorphic VT (CL <230 ms) induced with programmed stimulation. The other 2 patients had persistently inducible VT with CLs ranging from 280 to 310 ms and refused implantation of a cardiac defibrillator. Thirteen patients underwent implantation or had a cardiac defibrillator previously implanted, and 2 of these patients also required antiarrhythmic medication for suppression of atrial fibrillation; 1 was continued on amiodarone, which he was receiving when he presented with VT, and a second was maintained on procainamide. Two of the 19 patients were placed on medical therapy alone for treatment of the inducible nonclinical arrhythmias; 1 received amiodarone empirically, and the second was placed on oral procainamide, which suppressed his nonclinical arrhythmias.
A late follow-up study at 2.5±0.5 months after the ablative procedure was performed in 7 of 12 patients who had no recurrent spontaneous episodes within 2 to 3 months of the ablative procedure. Three of these patients no longer had any inducible arrhythmias (rapid VTs, with CLs of <260 ms, were induced at the time of their predischarge follow-up study). The other 4 patients had persistently inducible sustained monomorphic VT, but none of the previously ablated VT morphologies were induced. One of these patients had previously received no concurrent treatment and was subsequently treated with empiric amiodarone after refusing to undergo implantation of cardiac defibrillator.
Nine of the 19 patients with successful ablation of their clinical VT
had a spontaneous VT recurrence during follow-up (Table 2
). Five of the 9 patients had
recurrence of a VT not previously seen clinically but
compatible with an inducible VT that was not ablated. The recurrent VTs
in these patients had a CL that was markedly shorter than their
clinical arrhythmia. A sixth patient had ICD electrogram
documentation of multiple VT CLs before ablation, and although the
recurrent VT was of a different CL than the ablated VTs, not all of his
clinical VTs could be definitively known. Two patients developed a
possible "new" arrhythmia during follow-up. One
presented with a bundle-branch reentrant VT 2 months after
ablation. This patient had been treated with amiodarone that
was discontinued at the time of ablation procedure; no bundle-branch
reentrant VT was induced at the ablative procedure or a follow-up study
performed 5 weeks later. The second patient died suddenly 3 months
after the ablation procedure; this patient had frequent
recurrences of a well-tolerated VT before ablation and only
rapid monomorphic VT, with a CL of 280 ms, induced at follow-up. His
clinical VTs had a CL of 420 and 520 ms, and the patient refused
implantation of a cardiac defibrillator. This patient also developed a
new anginal syndrome before his death. Documented recurrence of
the clinical, ablated VT occurred in 1 additional patient; this was the
only definitive recurrence of a "successfully" ablated VT
observed in our study.
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Patients with a VT recurrence during follow-up had a greater
number of VT morphologies that remained inducible after the ablative
procedure (3.7±2.4 versus 1.9±0.8, P=.05). There also was
a trend toward a longer CL of the persistently inducible VTs in
patients who had VT recurrence (326±79 ms in patients with
recurrent VT versus 275±33 ms in patients with no recurrent event,
P=.09). A comparison between patients with and without a
recurrent event is shown in Table 3
. One
of the 19 patients with partial success who did not undergo a complete
stimulation protocol was not included in this analysis. This
patient had heparin-induced thrombocytopenia, and the ablation
procedure was terminated after successful ablation of the clinical VT;
although no further tachyarrhythmias were induced, the
patient's follow-up study was performed via a previously implanted
cardiac defibrillator with up to triple extrastimuli from a single
site. The clinical VT occurred both spontaneously and in response to
single extrastimuli before ablation.
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Failure
In 4 of the initial 35 patients, the clinical VT could not be not
be successfully ablated. Reasons for unsuccessful ablation included
difficulty mapping secondary to marginal hemodynamic
tolerance and frequent, spontaneous terminations of the targeted VT in
2 patients, and the inability to ablate the targeted VT despite
apparently adequate mapping in a 1 patient. In a fourth patient, the
electrophysiology study was discontinued prematurely secondary to the
development of abdominal pain, which was thought to be caused by
peripheral embolization of an aortic atherosclerotic
plaque. Initial clinical success was achieved during the ablative
procedure in a fifth patient, but the clinical VT was again inducible
at the time of his follow-up study. Because of marginal
hemodynamic tolerance, the VT was not amenable to
repeat ablation.
The mean number of VTs induced in this group was 2.8±2.4 VTs per patient, with successful ablation of 0.6±0.5 nonclinical VT per patient. The mean VT CL in this group was 325±33 ms. Four of the patients in this group were treated with an implantable defibrillator3 in combination with an antiarrhythmic agent. The fifth patient underwent a subendocardial resection with no inducible arrhythmias at a follow-up study before discharge. Spontaneous recurrences occurred in 2 of the 5 patients; both had a recurrence of their clinical VT. The 1 patient with initial clinical success but persistent inducibility of the clinical VT on predischarge testing was treated with an ICD only and has had no spontaneous recurrences.
Overall, the clinical VT was ablated in 30 of 35 patients (86%), with
31% of all patients having no additional inducible
ventricular arrhythmias. The freedom from recurrent
arrhythmias and sudden death at 24 months was 91% in the
complete success group and 53% in the partial success group
(P<.05) (Fig 3
). The freedom
from recurrent arrhythmias at 24 months was 60% in the failure
group, with most of these patients being treated with antiarrhythmic
medications or surgical therapy. Six patients in the study group died
during the follow-up period. As previously noted, 2 patients died
suddenly1 in the partial success group and 1 in the complete success
group. Three other patients in the partial success group died of
congestive heart failure. One patient in the failure group died of
sepsis secondary to ischemic bowel disease.
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Complications
A total of 94 electrophysiology studies were performed in the 35
patients, not including cardiac defibrillator implants or their
follow-ups. Procedure-related complications occurred in 8 of the 35
patients. Three patients developed a hematoma at the
arterial access site. In 2 patients, the hematoma was
minor, and in the third patient, a blood transfusion was given because
of hypotension; surgical intervention was not required. Heart block
occurred in 4 patients and was catheter-induced in 3; 1 patient
developed transient right bundle-branch block, and 2 patients with a
preexisting right bundle-branch block developed complete heart block
during left ventricular mapping that remained permanent. A
third patient developed transient complete heart block after the
infusion of intravenous procainamide. As discussed
above, 1 patient developed severe abdominal pain during the procedure.
Although no definitive etiology was determined, the patient's symptoms
were thought to be best explained by a possible embolic event. In
addition to the above, in 1 patient in whom RF ablation was
unsuccessful, ICD implantation was undertaken and complicated by an
infection at the generator pocket. This required explantation of the
device and lead, intravenous antibiotic administration, and
subsequent reimplantation of the defibrillator and lead system.
| Discussion |
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Success of VT Ablation
The reported success rates of RF catheter ablation in the
postinfarction patient have varied widely, due, in part, to differing
definitions of "success." In our series, the spontaneously
occurring VT was successfully ablated in 86% of patients. More
importantly, however, almost one third of patients undergoing RF
ablation had all of their VTs rendered noninducible on follow-up study
and were discharged without further treatment. These results were
achieved despite an average of 2.3 VT morphologies induced per patient.
This group had no recurrence of a documented VT over a mean
follow-up of 17 months. In contrast, 9 of 19 patients with persistently
inducible nonclinical monomorphic VTs had a spontaneous VT
recurrence on follow-up. Most of these recurrences were
of a VT not previously observed to have occurred spontaneously.
Overall, a total of 140 distinct monomorphic VTs were induced in the 35
patients, 56% of which were rendered noninducible with RF catheter
ablation. Our study also demonstrates, for the first time, that once
monomorphic VTs are ablated, they remain noninducible on long-term
follow-up with programmed stimulation.
Previous reports of postinfarction VT ablation have demonstrated similar "clinical success" results. Morady et al1 reported successful RF ablation in 11 of 15 patients with postinfarction VT in whom ablation was performed as an adjunctive therapy. In this series, 16 of 20 spontaneously occurring VTs were successfully ablated. These 11 patients had no clinical recurrences of the ablated VT, although most were treated with some adjunctive therapy. The incidence of "nonclinical" VT recurrences in this series was not reported. Similar success rates were also reported in studies by Kim et al3 and Stevenson et al.2 In the study of Kim et al, 9 of 20 patients had recurrent VT, including all 4 patients with an initial unsuccessful result. Of the 16 patients with initial clinical success, 1 patient had a recurrence of their previous spontaneous VT and 4 patients had a recurrence of a VT morphology that was induced, but not ablated, at the initial electrophysiological study. In the study of Stevenson et al, ablation of all inducible VTs was attempted in 15 patients; on follow-up study, 6 patients had no inducible monomorphic VT, whereas 4 patients had only a "new" VT morphology induced. None of these patients had recurrent VT, but of the 5 patients with persistently inducible VT, 3 had recurrences. Compared with the present study, the lower incidence of "nonclinical" VT recurrences reported in these series might be explained by the use of adjunctive antiarrhythmic therapy. The majority of patients in the series of Kim et al who had persistently inducible VT were treated with antiarrhythmic agents, and in the study of Stevenson et al, most patients had been on amiodarone before the ablation procedure, with 4 patients continuing to receive antiarrhythmic therapy after ablation. In our study, most patients were initially treated with only an ICD, and the use of amiodarone before the ablation procedure was minimal.
Significance of Other Arrhythmias
Our study clearly demonstrates a risk of recurrent
ventricular arrhythmias in patients with
persistently inducible VTs even though these arrhythmias were
not previously documented clinically. These results are not surprising
in light of past experiences with surgical treatment of
ventricular arrhythmias. Several studies have shown
an excellent prognosis for patients without inducible VT on their
postsurgical follow-up study, with >90% remaining free from recurrent
arrhythmias and sudden death for up to 5 years, despite many
patients initially presenting with hemodynamically
unstable ventricular arrhythmias and sudden cardiac
death.6,2224 In contrast, up to 64% of patients with
postoperative inducible VT have had recurrent ventricular
arrhythmias on follow-up, despite concurrent antiarrhythmic
treatment,5,6,2527 and the recurrence rate was
even higher (77%) in patients with postoperative inducible VTs with a
CL equal to or longer than any clinically or preoperatively manifested
VT.28 In the present study, patients with recurrent
ventricular arrhythmias tended to have a greater
number of inducible nonclinical arrhythmias with a longer CL
after ablation compared with patients without clinical
recurrences. This is consistent with data in unselected
postmyocardial infarction patients where patients with rapid,
inducible ventricular arrhythmias (CL <230 ms) had
a lower risk of recurrent ventricular arrhythmias
than patients with a slower inducible VT.29
Role of VT Ablation
The role of RF catheter ablation in the management of
postinfarction VT continues to be refined. In patients with an ICD and
frequent recurrences of VT unresponsive to medical therapy,
catheter ablation can result in a marked decrease in the number of VT
recurrences.30 Few would argue with the use of RF
ablation in this patient population, but there has been little
experience in the use of this technique as a primary treatment of
postinfarction VT. Several factors have been given as contraindications
to attempting VT ablation,3,31 including (1) multiple
inducible VT morphologies, (2) inability to ablate large areas of scar,
and (3) inability to document the clinical VT.
The significance of multiple inducible ventricular arrhythmias cannot be underestimated, and many authors will not attempt catheter ablation on patients with more than one inducible morphology.32 In the present series, patients with persistently inducible arrhythmias did have a significantly higher number of inducible arrhythmias at the initial study. Complete success, however, was achieved in several patients with as many as four distinct VT morphologies induced. One reason for success in these patients may be the ablation of tissue essential for perpetuation of two or more VT morphologies. This phenomenon has been well characterized in previous studies,1,3335 and up to 20% of inducible morphologies may be terminated by the ablation of different VT morphologies.36
In postinfarction VT, a critical portion of the reentrant circuit has been shown to involve the peri-infarction subendocardium.37,38 This location lends itself to possible RF catheter ablation because RF energy can result in lesions of >5 mm in diameter and up to 3 mm in depth,39 although studies characterizing the morphology of such lesions in the postinfarction heart have been lacking. Our study demonstrates that the effects of such lesions tend to be stable over time, since previously ablated VTs could not be reinitiated on long-term follow-up, verifying the low rate of recurrence of ablated VTs seen in other studies.13 Not all inducible, hemodynamically tolerated VTs, however, can be successfully ablated despite extensive endocardial mapping. Possible reasons for unsuccessful ablation include relatively wide zones of critical conducting tissue, poor penetration of scar tissue with RF energy, and inadequate catheter contact. In addition, up to one third of inducible VTs may involve a reentrant circuit with a critical zone of conduction located in the deeper subepicardium.21
Study Limitations
Although this was one of the larger studies of RF catheter
ablation of postinfarction VT, the number of patients limits the
ability of the analysis to distinguish in detail factors
associated with both short- and long-term success. This study, however,
was designed to select a population with an increased frequency of
recurrences by excluding patients with only a single episode of
VT. The small study size is particularly limiting in determining any
characteristics that may predict subsequent events in patients with
successful ablation of only their clinical VT. The 1 patient in our
complete success group who died suddenly 18 months after ablation does
raise the concern of possible proarrhythmic effects of RF catheter
ablation as well as the significance of the patient's inducible
polymorphic VT on long-term follow-up. Larger studies will be
necessary to determine whether patients whose VTs are rendered
completely noninducible with RF ablation are at an increased risk of
subsequent cardiac events compared with other postinfarction patients.
The rate of sudden cardiac death that we observed, however (5.7% over
14±11 months of follow-up), is similar to that reported previously
with surgical and pharmacological treatment.40
Conclusions
RF catheter ablation of postinfarction VT can be performed
with a high degree of success when targeted against specific, inducible
VTs and is associated with a low likelihood of recurrence of
the successfully ablated VT. These VTs remain noninducible with chronic
programmed stimulation, demonstrating long-term stability of the RF
lesion. Therefore, in patients with well-tolerated VT, adjunctive
therapy may not be warranted if the patient has no inducible VTs on
follow-up study. The high rate of recurrent VT in patients with
persistently inducible "nonclinical"
tachyarrhythmias, however, suggests that all inducible
VTs should be treated with either antiarrhythmic drug therapy, ICD
implantation (ideally with antitachycardia pacing) or RF
catheter ablation of the nonclinical VTs. Ablation of all inducible,
hemodynamically tolerated ventricular
arrhythmias may help avoid the morbidity associated with
recurrent ICD discharges and antiarrhythmic therapy but can be expected
to result in long, arduous procedures requiring extensive fluoroscopy
time and operator expertise. In consideration of this and the
limitations of current technology, catheter ablation procedures for
postinfarction VT should probably be limited to centers willing to make
the necessary investments to afford the highest chances of success.
| Selected Abbreviations and Acronyms |
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| Footnotes |
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Received May 29, 1997; revision received July 18, 1997; accepted August 1, 1997.
| References |
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2. Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff HR, Natterson PD, Wiener I. Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation. 1993;88(pt 1):16471670.
3.
Kim YH, Sosa-Suarez G, Trouton TG, O'Nunain SS,
Osswald S, McGovern BA, Ruskin JN, Garan H. Treatment of
ventricular tachycardia by
transcatheter radiofrequency ablation in patients with
ischemic heart disease. Circulation. 1994;89:10941102.
4. Gonska BD, Cao K, Schaumann A, Dorszewski A, von zur Muhlen F, Kreuzer H. Catheter ablation of ventricular tachycardia in 136 patients with coronary artery disease: results and long-term follow-up. J Am Coll Cardiol. 1994;24:15061514.[Abstract]
5. Waspe LE, Brodman R, Kim SG, Matos JA, Johnston DR, Scavin GM, Fisher JD. Activation mapping in patients with coronary artery disease with multiple ventricular tachycardia configurations: occurrence and therapeutic implications of widely separate apparent sites of origin. J Am Coll Cardiol. 1985;5:10751086.[Abstract]
6.
Miller JM, Kienzle MG, Harken AH, Josephson ME.
Subendocardial resection for ventricular
tachycardia: predictors of surgical success.
Circulation. 1984;70:624631.
7. Wilber DJ, Davis MJ, Rosenbaum M, Ruskin JN, Garan H. Incidence and determinants of multiple morphologically distinct sustained ventricular tachycardias. J Am Coll Cardiol. 1987;10:583591.[Abstract]
8. EL-Sherif N, Gough WB, Restivo M. Reentrant ventricular arrhythmias in the late myocardial infarction period, 14: mechanisms of resetting, entrainment, acceleration, or termination of reentrant tachycardia by programmed electrical stimulation. PACE. 1987;10:341371.
9.
Almendral JM, Gottlieb CD, Rosenthal ME, Stamato NJ,
Buxton AE, Marchlinski FE, Miller JM, Josephson ME. Entrainment of
ventricular tachycardia: explanation for
surface electrocardiographic phenomena by analysis of
electrograms recorded within the tachycardia circuit.
Circulation. 1988;77:569580.
10. Morady F, Frank R, Kou WH, Tonet JL, Nelson SD, Kounde S, De Buitleir M, Fontaine G. Identification and catheter ablation of a zone of slow conduction in the reentrant circuit of ventricular tachycardia in humans. J Am Coll Cardiol. 1988;11:775782.[Abstract]
11. Morady F, Kadish A, Rosenheck S, Calkins H, Kou WH, De Buitleir M, Sousa J. Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction. J Am Coll Cardiol. 1991;17:678689.[Abstract]
12. Josephson ME, Waxman HL, Cain ME, Gardner MJ, Buxton AE. Ventricular activation during ventricular endocardial pacing, II: role of pace-mapping to localize origin of ventricular tachycardia. Am J Cardiol. 1982;50:1122.[Medline] [Order article via Infotrieve]
13.
Klein LS, Shih HT, Hackett FK, Zipes DP, Miles
WM. Radiofrequency catheter ablation of ventricular
tachycardia in patients without structural heart disease.
Circulation. 1992;85:16661674.
14. Calkins H, Kalbfleisch SJ, el-Atassi R, Langberg JJ, Morady F. Relation between efficacy of radiofrequency catheter ablation and site of origin of idiopathic ventricular tachycardia. Am J Cardiol. 1993;71:827833.[Medline] [Order article via Infotrieve]
15.
Wilber DJ, Baerman J, Olshansky B, Kall J, Kopp D.
Adenosine-sensitive ventricular
tachycardia: clinical characteristics and response to
catheter ablation. Circulation. 1993;87:126134.
16. Aizawa Y, Chinushi M, Naitoh N, Kusano Y, Kitazawa H, Takahashi K, Uchiyama H, Shibata A. Catheter ablation with radiofrequency current of ventricular tachycardia originating from the right ventricle. Am Heart J. 1993;125(pt 1):12691275.
17.
Wittkampf FHM, Hauer RNW, Robles de Medina EO. Control
of radiofrequency lesion size by power regulation.
Circulation. 1989;80:962968.
18. Simmers TA, Wittkampf FH, Hauer RN, Robles de Medina EO. In vivo ventricular lesion growth in radiofrequency catheter ablation. Pacing Clin Electrophysiol. 1994;17(pt 2):523531.
19. de Bakker JMT, van Capelle FJL, Janse MJ, van Hemel NM, Hauer RNW, Defauw JJAM, Vermeulen FEE, Bakker de Wekker PFA. Macroreentry in the infarcted human heart: the mechanism of ventricular tachycardias with a `focal' activation pattern. J Am Coll Cardiol. 1991;18:10051014.
20.
de Bakker JMT, van Capelle FJL, Janse MJ, Wilde AAM,
Coronel R, Becker AE, Dingemans KP, van Hemel NM, Hauer RNW. Reentry as
a cause of ventricular tachycardia in patients
with chronic ischemic heart disease: electrophysiologic and
anatomic correlation. Circulation. 1988;77:589606.
21.
Kaltenbrunner W, Cardinal R, Dubuc M, Shenasa M, Nadeau
R, Tremblay G, Vermeulen M, Savard P, Pagé PL. Epicardial and
endocardial mapping of ventricular tachycardia
in patients with myocardial infarction: is the origin of the
tachycardia always subendocardially localized?
Circulation. 1991;84:10581071.
22. Ostermeyer J, Borggrefe M, Breithardt G, Podczek A, Goldmann A, Schoenen JD, Kolvenbach R, Godehardt E, Kirklin JW, Blackstone EH. Direct operations for the management of life-threatening ischemic ventricular tachycardia. J Thorac Cardiovasc Surg. 1987;94:848865.[Abstract]
23. McGiffin DC, Kirklin JK, Plumb VJ, Blackstone EH, Waldo AL, Kirklin JW, Karp RB. Relief of life-threatening ventricular tachycardia and survival after direct operations. Circulation. 1987;76(suppl V):V-93V-103.
24. Cox JL. Patient selection criteria and results of surgery for refractory ischemic ventricular tachycardia. Circulation. 1989;79(suppl VI):VI-163VI-177.
25. Brandt BD, Martins JB, Kienzle MG. Predictors of failure after endocardial resection for sustained ventricular tachycardia. J Thorac Cardiovasc Surg. 1988;95:495500.[Abstract]
26. Page PL, Arciniegas JG, Plumb VJ, Henthorn RW, Karp RB, Waldo AL. Value of early postoperative epicardial programmed ventricular stimulation studies after surgery for ventricular tachyarrhythmias. J Am Coll Cardiol. 1983;2:10461052.[Abstract]
27. Platia EV, Griffith LS, Watkins LJ, Mower MM, Guarnieri T, Mirowski M, Reid PR. Treatment of malignant ventricular arrhythmias with endocardial resection and implantation of the automatic cardioverter-defibrillator. N Engl J Med. 1986;314:213216.[Abstract]
28. Miller JM, Hargrove WC, Josephson ME. Significance of `nonclinical' ventricular arrhythmias induced following surgery for ventricular tachyarrhythmias. In: Breithardt G, Borggrefe M, Zipes DP, eds. Nonpharmacological Therapy of Tachyarrhythmias. Mount Kisco, NY: Futura; 1987:133141.
29. Bourke JP, Richards DA, Ross DL, McGuire MA, Uther JB. Does the induction of ventricular flutter or fibrillation at electrophysiologic testing after myocardial infarction have any prognostic significance?. Am J Cardiol. 1995;75:431435.[Medline] [Order article via Infotrieve]
30. Willems S, Borggrefe M, Shenasa M, Chen X, Hindricks G, Haverkamp W, Wietholt D, Block M, Breithardt G. Radiofrequency catheter ablation of ventricular tachycardia following implantation of an automatic cardioverter defibrillator. Pacing Clin Electrophysiol. 1993;16:16841692.[Medline] [Order article via Infotrieve]
31. Blanchard SM, Walcott GP, Wharton JM, Ideker RE. Why is catheter ablation less successful than surgery for treating ventricular tachycardia that results from coronary artery disease?. Pacing Clin Electrophysiol. 1994;17(pt 1):23152335.
32. Gonska BD, Cao K, Schaumann A, Dorszewski A, von zur Muhlen F, Kreuzer H. Management of patients after catheter ablation of ventricular tachycardia. Pacing Clin Electrophysiol. 1994;17(pt 2):542549.
33. Hargrove WC, Miller JM, Vassallo JA, Josephson ME. Improved results in the operative management of ventricular tachycardia related to inferior wall infarction: importance of the annular isthmus. J Thor Cardiovascular Surg. 1986;92:726732.
34. Fitzgerald DM, Friday KJ, Yeung LWJ, Bowman AJ, Lazzara R, Jackman WM. Myocardial regions of slow conduction participating in the reentrant circuit of multiple ventricular tachycardias: report on ten patients. J Cardiovasc Electrophysiol. 1991;2:193206.
35.
Wilber DJ, Kopp DE, Glascock DN, Kinder CA, Kall JG.
Catheter ablation of the mitral isthmus for ventricular
tachycardia associated with inferior
infarction. Circulation. 1995;92:34813489.
36. Hsia HH, Rothman SA, Thome LM, Adelizzi NM, Whitely DM, Buxton AE, Miller JM. Multiple ventricular tachycardia morphologies: different look, same loop? Circulation. 1994;90(suppl IV):IV-557. Abstract.
37.
Horowitz LN, Josephson ME, Harken AH. Epicardial and
endocardial activation during sustained ventricular
tachycardia in man. Circulation. 1980;61:12271238.
38. Miller JM, Harken AH, Hargrove WC, Josephson ME. Pattern of endocardial activation during sustained ventricular tachycardia. J Am Coll Cardiol. 1985;6:12801287.[Abstract]
39. Bartlett TG, Mitchell R, Friedman PL, Stevenson WG. Histologic evolution of radiofrequency lesions in an old human myocardial infarct causing ventricular tachycardia. J Cardiovasc Electrophysiol. 1995;6:625629.[Medline] [Order article via Infotrieve]
40. Sarter BH, Finkle JK, Gerszten RE, Buxton AE. What is the risk of sudden cardiac death in patients presenting with hemodynamically stable sustained ventricular tachycardia after myocardial infarction? J Am Coll Cardiol. 1996;28:122129.[Abstract]
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