From the Cardiovascular Division, Department of Medicine, Brigham and
Women's Hospital, Harvard Medical School, Boston, Mass (W.G.S., P.L.F.,
L.A.S.); the Division of Cardiology, Department of Medicine, Wadsworth VA
Medical Center, UCLA School of Medicine, Los Angeles, Calif (P.T.S); and the
Division of Cardiology, Department of Medicine, Hospital of the University of
Pennsylvania, Philadelphia (D.K., B.P.). Dr Saxon is now at the Division of
Cardiology, Department of Medicine, University of California at San Francisco.
Correspondence to William G. Stevenson, MD, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail wgstevenso{at}bics.bwh.harvard.edu
Methods and Results—Radiofrequency catheter ablation targeting
all inducible monomorphic VTs that allowed mapping was performed in 52
patients with prior myocardial infarction. Antiarrhythmic drug therapy
had failed in 41 (79%) patients including amiodarone in 36
(69%) patients. An average of 3.6±2 morphologies of VT were induced
per patient. More than 1 ablation session was required in 16 (31%)
patients. Complications occurred in 5 (10%) patients, including 1
(2%) death caused by acute myocardial infarction. During follow-up
59% of patients continued to receive amiodarone; 23 (45%) had
implantable defibrillators. During a mean follow-up of 18±15 months
(range 0 to 51 months) 1 patient died suddenly, 2 died from
uncontrollable VT, and 5 died from heart failure. Three-year survival
rate was 70±10%, and rate for risk of VT recurrence was
33±7%.
Conclusions—Radiofrequency catheter ablation controls VT that is
sufficiently stable to allow mapping in 67% of patients despite
failure of antiarrhythmic drug therapy and multiple inducible VTs.
However, ablation was largely adjunctive to amiodarone and
defibrillators in this referral population.
Several investigators have reported series of patients selected for
having 1 predominant morphology of VT, who were treated with
radiofrequency (RF) catheter ablation.8 9 10 It is
likely that this represents <10% of the total population of
patients with VT.10 Ablation that focused on the
"clinical tachycardia" but did not target other
inducible VTs successfully abolished the "clinical" VT in 71% to
76% of cases. However, during follow-up, up to 31% of patients with
acutely successful ablation of the "clinical" VT had
arrhythmia recurrences, some of which were due to a VT
different from that initially targeted for ablation.
There are several difficulties with selecting a dominant,
"clinical" VT for ablation. Often it is not possible to determine
which VT is in fact the one that has occurred spontaneously. Only a
limited recording of 1 or a few ECG leads may be available. In
patients with implantable defibrillators VT is typically terminated by
the device before an ECG is obtained. Even if 1 VT is identified as
predominant, other VTs that are inducible may subsequently occur
spontaneously.
An alternative approach is not to consider the number of VT
morphologies in determining eligibility for catheter ablation but
rather to attempt ablation of all inducible VTs that are sufficiently
tolerated to allow mapping. The purpose of this report is to assess the
feasibility and summarize the initial experience with this
approach.
Mapping and Radiofrequency Ablation
Mapping data from the first 37 patients have been previously
reported.7 11 The general approach to mapping and
ablation is shown in Figure 1
RF current (250 or 500 Hz) was applied between the distal electrode on
the mapping catheter and a cutaneous adhesive electrode at 15 to 45 W
for 20 to 40 seconds during VT. In the first 29 patients power was
usually adjusted to produce a fall in impedance, which is an indication
of heating.14 In the subsequent patients,
temperature monitored from the electrode tip was adjusted to
Management After Ablation
If the patient remained free of VT for the following 3 to 7 days, a
follow-up electrophysiology study was recommended with additional
ablation attempts if VTs had been terminated at the previous session
and hemodynamically tolerated VT was again inducible.
This follow-up study was performed a mean of 7±14 days (range 3 to 57
days) after the last ablation in 41 of the 44 in whom VT did not recur
spontaneously in hospital. In the remaining 3 patients the last
electrophysiologic study was performed immediately after ablation.
Programmed stimulation included 1, 2, and 3 extrastimuli during pacing
at 100 and 150 bpm from the right ventricular apex and
right ventricular outflow tract. In 5 patients with VT that
had been repeatedly inducible from the right ventricular
apex, noninvasive programmed stimulation from an implanted
defibrillator was performed, with pacing at only 1 site. The end points
for stimulation were reproducible initiation of a tolerated VT,
initiation of VT producing syncope, or the third extrastimulus reaching
refractoriness. Effects of ablation were defined as (1) no inducible
VT: monomorphic VT with a duration of
If any sustained monomorphic VT remained inducible at the predischarge
study, therapy with amiodarone and/or an implantable
defibrillator was recommended. Prior amiodarone therapy was
continued regardless of the results of electrophysiologic testing
unless toxicity warranted stopping. If amiodarone was
discontinued, we recommended a repeat electrophysiologic study after 6
to 12 weeks.
Statistics
Catheter Mapping and Ablation
Procedure-related complications occurred in 5 (10%) patients. There
was 1 (2%) procedure-related death from acute inferior
wall myocardial infarction with cardiac rupture 12 hours after a second
ablation procedure performed for in-hospital VT recurrence that
has previously been reported in detail.15 This
patient is included as a death and arrhythmia
recurrence in the hospital for all follow-up analyses.
This patient also had transient atrioventricular (AV)
block observed during the first ablation procedure and developed
Staphylococcus epidermidis sepsis from a temporary pacing
catheter. One patient had a transient cerebral ischemic event
36 hours after ablation. This patient had a history of identical events
before ablation attributed to carotid artery disease. Two patients who
had chronic obstructive lung disease developed progressive
hypoventilation and required assisted ventilation during the procedure.
The remaining complication was a femoral artery pseudoaneurysm.
Implantable defibrillators, present in 16 patients, were programmed
off during the procedure, and all functioned normally afterward.
Early Effects of Ablation on Inducible and Spontaneous
Ventricular Tachycardias
Early after the final ablation procedure, 21 patients (40%) had no
spontaneous or inducible sustained monomorphic VT. These patients had a
total of 70 monomorphic VTs previously inducible. In 16 (31%) patients
VT was inducible but modified and did not recur spontaneously before
hospital discharge. The cycle length of the slowest inducible VT had
shortened by 97 ms, from 425±15 to 328±18 ms. A total of 60 VTs had
been previously inducible in these patients. Further ablation attempts
were not performed because VT was poorly tolerated in 11 patients and
because no endocardial target sites could be identified in 5
patients.
In 15 patients (29%), ablation was judged to be ineffective. In 8
patients (15%) VT recurred in the hospital; 5 of these had
persistently inducible VT at the end of the ablation procedure. In 7
patients (13%), VT did not recur in the hospital but a VT similar to
that initiated before ablation remained inducible at the last
electrophysiology study. Further ablation was not attempted in these 15
patients because inducible VTs were poorly tolerated in the
electrophysiology laboratory in 6 patients, no target sites could be
identified in 5 patients, previously frequent or incessant VT was now
controlled with drug therapy in 3 patients, and 1 patient died, as
noted above.
Survival and Ventricular Tachycardia
Recurrences
Ten patients died (19%): 1 was procedure related, 2 were in the
hospital from VT that was not controlled by ablation, 5 died of heart
failure, and 1 died of end-stage liver disease. One patient died
suddenly after 15 months. This patient had no VT inducible before
discharge; amiodarone (200 mg/d) had been started 6 months
later for atrial fibrillation. Three patients underwent cardiac
transplantation, all had severe ventricular dysfunction
before ablation (left ventricular ejection fractions of
0.15, 0.18, and 0.27, respectively) and unsuccessful ablations with
multiple VT recurrences afterward. Of the 5 patients who died
of congestive heart failure, all had symptomatic heart
failure before ablation. Left ventricular ejection fraction
was <0.20 in 3 patients, 2 of whom had class IV symptoms before
ablation. In the 2 patients with better left ventricular
ejection fractions (0.3 and 0.4, respectively), death occurred after
4.2 and 2.4 years of follow-up and followed coronary artery
bypass surgery and aneurysmectomy in 1 patient. Three-year
survival for all 52 patients was 70±10% (Figure 2A
Sustained VT that was not fatal recurred in 16 (31%) patients either
in the hospital before discharge (7 patients) or during follow-up (9
patients). For all 52 patients, the 3-year risk of recurrent
ventricular arrhythmia, including the 1 sudden
death, was 33±7% (Figure 2B
When ablation was not successful, it was evident soon after the
procedures. In 76% of patients with recurrences, the first VT
recurrence occurred within 4 weeks of ablation. For the
patients who did not recur spontaneously in the hospital after
ablation, predischarge electrophysiologic testing was predictive of
outcome (Table
Patients with spontaneous arrhythmia recurrences (VT or
sudden death) are compared with those remaining free of
recurrences in the Table
This study, although not randomized or controlled, provides useful
information regarding management of patients after ablation.
Modification of the reentry substrate was a common outcome of ablation.
Modification was defined as persistence of inducible VT that was
clearly different than the previously inducible
tachycardias. These VTs were usually faster and often not
tolerated sufficiently to allow mapping. On average, the VT cycle
length shortened by
Management of the patient who is receiving amiodarone at the
time of ablation is a particularly difficult issue. Even if VT is not
inducible after ablation, amiodarone may be suppressing other
VTs. Because of the long half-life of elimination of the drug,
withdrawal exposes the patient to a risk of arrhythmia
recurrence long after hospital discharge. Therefore we
continued amiodarone unless an implantable defibrillator was
present or amiodarone toxicity precluded continued therapy.
Our experience in 3 patients in whom amiodarone was
discontinued is instructive. All had inducible or spontaneous VT at
follow-up electrophysiologic studies 7 to 42 weeks later. However, all
had successful ablation of these VTs and remained free of VT during
subsequent follow-up. For patients who had not previously failed
antiarrhythmic drug therapy, catheter ablation was quite effective:
91% were free of arrhythmia recurrences during
follow-up. This was a select group of patients, however, who had
hemodynamically tolerated VT without cardiac arrest in
the absence of antiarrhythmic drug therapy.
In targeting multiple VTs, we probably applied ablation to larger
regions of the infarct, accounting for the greater number of RF
applications compared with previous series. In prior reports, surgical
ablation of VT removed 8 cm2 to >40
cm2 of subendocardial
tissue.17 Saksena and
coworkers18 observed that focal intraoperative
laser ablation of 2 to 25 cm2 was required for
interruption of VT. We performed ablation with conventional RF
catheters, which create lesions that are typically 5 to 10 mm in
diameter, and often substantially smaller because of vagaries of tissue
contact, electrode-tissue orientation, and cooling from the surrounding
blood pool.14 15 With present RF systems it
is likely that multiple RF applications are required to remotely
approach the effect achieved with surgery. This raises important safety
concerns because damage to contracting myocardium could
further depress ventricular function. We are careful to
confine RF applications to regions that have abnormal electrograms,
with the intention of avoiding damage to contractile muscle. In our
single patient who died of myocardial infarction after ablation, the RF
lesions were confined to the infarct region.15
Although we did not observe clinical exacerbations of heart failure
after ablation, mild alterations may have been difficult to appreciate
in patients with frequent episodes of VT. The 10% incidence of death
from heart failure during follow-up is not unexpected in this patient
population and is similar to that observed by Gonska and
coworkers,9 who targeted 1 VT for ablation.
Assessment of the impact of ablation on left ventricular
function will be important in future studies.
Limitations
We routinely used current strengths of up to 10 mA at 9 ms pulse width,
for pacing to entrain VT and to assess capture after ablation as an
indication that ablation had caused tissue damage. This current
strength was arbitrarily selected; it is possible that greater mapping
specificity would be observed by using lower stimulus strengths, but
this is not known.
Clinical Implications
Received December 19, 1997;
revision received March 20, 1998;
accepted March 26, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Radiofrequency Catheter Ablation of Ventricular Tachycardia After Myocardial Infarction
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Patients with
ventricular tachycardia (VT) after myocardial
infarction often have multiple morphologies of inducible VT, which
complicates mapping and is viewed by some as a relative
contraindication to ablation. Attempting to identify and target a
single "clinical" VT is often limited by inability to obtain
12-lead ECGs of VTs that are terminated emergently or by
defibrillators. This study assesses the feasibility of ablation in
patients selected without regard to the presence of multiple VTs by
targeting all VTs that allow mapping.
Key Words: catheter ablation • tachycardia • myocardial infarction
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Catheter ablation of
sustained monomorphic ventricular tachycardia
(VT) late after myocardial infarction has been challenging. These
arrhythmias arise from reentry circuits that can be large and
complex, with broad paths and narrow isthmuses, and that may traverse
subendocardial, intramural, and epicardial regions of the
myocardium.1 2 Mapping and ablation
are further complicated by the frequent presence of multiple reentry
circuits, giving rise to several morphologically different
VTs.2 3 4 5 6 7 In some cases different reentry circuits
form in the same abnormal region. In other cases reentry circuits form
at disparate sites in the infarct. The presence of multiple
morphologies of inducible or spontaneous VT has been associated with
antiarrhythmic drug inefficacy5 and failure of
surgical ablation.6
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
From February 1991 to December 1995 endocardial catheter mapping
and RF ablation were performed in 52 patients with sustained
monomorphic VT late after myocardial infarction referred to Brigham and
Women's Hospital, in Boston, Mass, UCLA Medical Center or Wadsworth VA
Medical Center in Los Angeles, Calif, and the Hospital of the
University of Pennsylvania, in Philadelphia. Catheter ablation was
offered to all patients who had sustained VT that was sufficiently
tolerated hemodynamically to allow catheter mapping,
provided that access to the left ventricle was possible and that there
was no left ventricular pedunculated thrombus present
on the transthoracic echocardiogram. Initially, catheter
ablation was offered only if spontaneous VT recurred despite
antiarrhythmic drug therapy. After the initial 21 patients, ablation
was also offered to patients with spontaneous VT without cardiac
arrest, who had not failed drug therapy (11 of the subsequent 21
patients). Patient characteristics are shown in the
Table
.
View this table:
[in a new window]
Table 1. Patient Characteristics and Comparison of Patients With and
Without Arrhythmia
Recurrences
Our methods have been described
previously.7 11 12 After obtaining informed
consent, mapping and RF catheter ablation were performed according to a
protocol approved by the human research committee of each respective
institution. Left ventricular mapping was performed with 6F
or 7F steerable catheters (EP Technologies or Webster Laboratories)
that had a 4 mm distal tip electrode and 2 to 2.5 mm spacing
between the distal 2 electrodes. Access to the left ventricle was
achieved retrogradely across the aortic valve or, in 6 procedures,
through transatrial septal puncture. Catheter position was assessed by
fluoroscopy and in 5 patients also by transesophageal
echocardiography.13 Systemic
anticoagulation was achieved with heparin, 5000 U
intravenously followed by 1000 U every hour or 2000 U every
2 hours. Sedation was achieved with intermittent doses of midazolam,
diazepam, meperidine HCl, and/or fentanyl. . If VT was
not incessant, fractionated electrograms were sought during sinus
rhythm and pace mapping was performed at these sites to locate regions
of slow conduction.12 VT was then initiated by
programmed stimulation from the right ventricular apex.
Unipolar pacing was performed at the mapping site during VT to reset or
entrain the VT, followed immediately by RF current application at
selected sites to determine whether or not heating would terminate VT.
In the first 15 patients RF current was applied if the site had low
amplitude, fractionated electrograms and if pacing from the site
entrained VT. On the basis of analysis of the data in these
initial 15 patients,7 priority for ablation sites
in subsequent patients was given to exit, central, or proximal sites as
defined by entrainment11 or if such sites could
not be found, sites with isolated potentials or entrainment features
suggesting an outer or inner loop,11 and finally
if none of these were present at sites with abnormal,
presystolic electrograms. If a previously tolerated VT did not
allow mapping because of hemodynamic compromise despite
adequate cardiac filling pressures, administration of dopamine for
hemodynamic support and/or intravenous
procainamide to slow the tachycardia was used.
View larger version (29K):
[in a new window]
Figure 1. Flow diagram of the general approach to mapping
and ablation of ventricular tachycardia (VT).
See text for discussion. RF indicates radiofrequency catheter
ablation. 
60°C
or a maximum RF current output of 45 to 50 W. If VT terminated, the
application was continued for a total of 60 to 120 seconds or until a
rise in impedance or boiling at the electrode tip on
transesophageal echocardiographic
imaging was observed.13 At sites where RF current
terminated VT, an attempt was made to enlarge the initial lesion by
applying RF current for 60 to 120 seconds during sinus rhythm to sites
within 5 mm of the initial lesion. RF ablation at this region
was considered adequate when unipolar pacing stimuli at the amplitude
that had captured before ablation (usually 10 mA, 2 to 9 ms pulse
width) failed to capture after ablation. If any
hemodynamically tolerated sustained monomorphic VT was
still inducible, the mapping procedure was continued. The procedure was
ended when either no hemodynamically tolerated VTs were
inducible or when no endocardial target sites critical to reentry, as
assessed from entrainment and interruption of VT by RF current, could
be found.
After ablation, patients were monitored on a cardiac step-down
unit or intensive care unit. If amiodarone had been
administered long term before the procedure, this medication was
continued unless toxicity necessitated stopping. Other antiarrhythmic
drugs were discontinued unless the ablation procedure had been clearly
unsuccessful; that is, the same VTs that had predominated at the
beginning of the procedure remained inducible at the end of the
procedure. Aspirin (325 mg) was administered daily. Patients treated
with warfarin before the procedure for known or presumed increased risk
of systemic emboli received a continuous intravenous
infusion of heparin until resumption of warfarin. If sustained VT
recurred spontaneously in the hospital after an apparently successful
ablation, a repeat ablation attempt was recommended. 
30 seconds or requiring earlier
termination due to hemodynamic compromise is not
inducible; (2) modified: a sustained monomorphic VT is inducible but is
different in QRS morphology (frontal plane axis by >30 degrees or
precordial transition zone 1 lead or a different dominant
deflection in >1 precordial lead) or cycle length (>100 ms for
VTs with a similar morphology) than the VTs for which ablation could be
attempted; and (3) inducible VT: a sustained monomorphic VT observed or
induced before attempted ablation remains inducible.
Continuous data are expressed as mean±1 SD. Groups were
compared with the Student's t test,
2 tests, or Fisher's exact test as
appropriate. Multivariable stepwise logistic regression was used to
assess predictors of arrhythmia recurrence.
Variables used were ejection fraction, failure of
amiodarone, failure of any drug, slowest cycle length of
induced VT, and number of inducible VTs. Variables with
P<0.1 were entered stepwise into the model. Continuous
variables were dichotomized at the median (BMDP statistical
software, 1992). Survival and arrhythmia recurrences
were determined from the date of last ablation with the Kaplan-Meier
method (BMDP statistical software, 1992). Arrhythmia
recurrences were spontaneous sustained VT or a VT termination
by an implanted defibrillator. Patients undergoing cardiac
transplantation were censored from the analysis on the day
of surgery.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
RF catheter ablation was attempted in 52 patients (Table
).
Antiarrhythmic drug therapy had failed to prevent spontaneous,
sustained VT in 41 (79%) patients. Long-term oral amiodarone
therapy had failed to suppress spontaneous VT in 33 (63%) patients and
had to be withdrawn because of toxicity in 3 (6%) patients. Two
patients had only 1 spontaneous episode of sustained monomorphic VT and
50 had had multiple episodes. VT was incessant in 7 (13%) patients. An
implantable defibrillator was present in 16 (31%) patients before
referral.
The 52 patients underwent 69 catheter mapping and ablation
sessions; 1 session in 36 patients, 2 sessions in 15 patients, and 3
sessions in 1 patient. At the initial session, 36 patients (69%) were
not receiving antiarrhythmic medications. During ablation an average of
3.6±2 different morphologies of monomorphic VT were observed per
patient (range 1 to 10). In 5 patients (10%) only 1 VT was induced
during the procedure. The average VT cycle length was 423±108 ms
(range 260 to 720 ms). Pacing was performed to attempt to entrain 132
VTs in the 52 patients. Reentry circuit exit, central, or proximal
regions were identified for 67 VTs in 40
patients.14 RF current was applied during 124 VTs
and acutely terminated 74 VTs in 48 patients. In 8 patients entrainment
mapping and RF application during VT were limited because pacing or
catheter manipulation in the target region terminated VT or
hemodynamic intolerance developed during VT. The
average number of RF applications per procedure, including those that
failed to terminate VT was 23±18 (range 1 to 98, median 19). For all
procedures, the average procedure time was 328±136 minutes (range 100
to 725 minutes) and the average fluoroscopy time was 60±32 minutes
(range 5 to 135 minutes, median 56 minutes).
In 10 patients, repeat ablation procedures were performed for VT
that recurred spontaneously in the hospital before follow-up study (5
patients) or that was inducible at the pre–hospital discharge study (5
patients). In addition, 5 patients had late repeat procedures. Two
patients had a repeat ablation attempt after VT recurred 21 and 18
days, respectively, after hospital discharge, despite no VT inducible
before hospital discharge. In 3 patients, amiodarone was
discontinued after initial ablation. In 2 of these patients, programmed
stimulation after 7 and 10 weeks, respectively, induced a new VT in 1
patient and a VT similar to 1 of 3 previously observed VTs in the other
patient. Both underwent an additional ablation procedure with no VT
inducible before discharge. The third patient who was seen with
incessant VT and had VT modified at the initial ablation session had a
new morphology of VT occur spontaneously 6 months after
amiodarone withdrawal. After repeat ablation, this VT was no
longer inducible, but other faster VTs that did not allow mapping
remained inducible.
After ablation, antiarrhythmic drugs continued to be administered
to 32 (63%) of 51 patients; amiodarone in 30 (59%) patients
and sotalol in 2 (4%) patients. Implantable defibrillators were
present in 23 (45%) patients, 7 of which were implanted after
ablation. Among the 23 patients with implantable defibrillators 14 also
continued to be treated with antiarrhythmic drugs for atrial
fibrillation (2 patients) or inducible VT after ablation. The mean
follow-up after the final ablation session was 18±15 months (range 0
to 59 months). ).
View larger version (12K):
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Figure 2. Survival after catheter ablation (A) and
cumulative arrhythmia recurrences (B), including 1
sudden death, are shown for all 52 patients. Number of patients at each
point in time is shown above the abscissa. VT indicates
ventricular tachycardia. ). Thus 67% of patients remained free of
VT during follow-up. ). Arrhythmia recurrences (including 1
sudden death) occurred in 3 of 19 (16%) patients without inducible VT,
2 of 16 (13%) patients in whom inducible arrhythmias were
modified, and 5 of 6 (83%) patients in whom inducible VT was not
changed (P=0.001). . Patients with recurrent
arrhythmias had worse ventricular function. The
number of morphologies of inducible VT was not significantly different
between the groups. Prior antiarrhythmic drug failure was associated
with a greater risk of arrhythmia recurrence (Table and
Figure 3). Of the 11 patients who had not
failed antiarrhythmic drugs, 10 (91%) were free of VT
recurrences during follow-up. However, 3 were treated with
amiodarone (2 patients) or sotalol (1 patient) for inducible
modified VT at follow-up study (1 patient) or at the referring
physician's request (2 patients). One of these patients received an
implanted defibrillator for modified but inducible VT. Patients with
recurrences had slower VTs inducible at initial study, probably
because of frequent amiodarone use before ablation in this
group. By multivariate logistic regression, failed
therapy with amiodarone (odds ratio 5.9, 95% confidence
interval 1.1 to 33) and a slowest VT cycle length >405 ms (odds ratio
4.0, 95% confidence intervals 0.97 to 16.5) were independent
predictors of arrhythmia recurrence. When failed
amiodarone therapy was excluded from the model, left
ventricular ejection fraction <0.34 was a predictor of
recurrences with borderline statistical significance (odds
ratio 3.3, 95% confidence interval 0.85 to 13) independent of VT cycle
length (odds ratio 5.14, 95% confidence interval 1.3 to 21).
View larger version (14K):
[in a new window]
Figure 3. Arrhythmia recurrences are shown
for the 41 patients who had previously failed antiarrhythmic therapy
(dashed line) and 11 patients who had not previously failed
antiarrhythmic drug therapy (solid line). Number of patients remaining
at each point in time is shown below the curves.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
Ablation of VT after myocardial infarction is often more difficult
than ablation of supraventricular tachycardia.
The presence of multiple morphologies of inducible monomorphic VT is a
frequent complicating factor. Recent studies of RF catheter ablation
for postinfarct VT have generally attempted to exclude patients with
more than 1 morphology of VT, offering the procedure to a small
minority of patients with sustained monomorphic
VT.8 9 10 Our study, as well as a recent study by
Rothman and coworkers16 suggests that RF catheter
ablation that targets any stable VT may be useful even if multiple VTs
are inducible. Initially all of our patients had failed antiarrhythmic
drug therapy because of spontaneous recurrences of VT. Later in
the study, for 11 patients, drug failure was not required. Despite the
predominance of patients with drug-refractory VT and multiple
morphologies of VT, two thirds were rendered free of recurrent VT
during follow-up with a low incidence of complications. When ablation
was not successful, 76% of patients had recurrent VT within 4 weeks.
However, these procedures are technically challenging, the procedure
times are relatively long, and many patients required multiple
procedures. 100 ms, which suggests that ablation damaged a
portion of the slowly conducting tissue in the reentry circuit, such
that the remaining circuits had faster revolution times. We cannot be
certain that these faster VTs were absent before ablation, however,
because slower tachycardias are usually induced more easily
and earlier in the stimulation protocol. In any case, modification was
associated with a favorable outcome and relatively low risk of
arrhythmia recurrence. However, these patients
generally continued to receive amiodarone or received an
implantable defibrillator. Defibrillator implantation is a reasonable
strategy, supported by the study of Rothman and coworkers, who observed
VT recurrences in 9 of 19 patients who had a "clinical" VT
ablated but other VTs still inducible.16
Antiarrhythmic drug management after ablation is a difficult
issue, and many of our patients continued to receive amiodarone
during follow-up. Continued amiodarone therapy is unlikely to
explain the long-term success after ablation because this drug
previously failed to prevent spontaneous VT. Our approach to mapping
limited our ability to characterize all of the potential
ventricular reentry circuits and to determine how
frequently multiple VTs originated from common or separate regions.
Ablation with enlargement of the initial lesion was performed at 1 of
the initial reentry circuit sites identified, regardless of whether
that VT had been previously identified as occurring spontaneously or
whether other VTs had been mapped. Ablation at 1 region often appeared
to abolish several VTs, as has been reported by
others.19 20 For example, 1 patient had several
episodes of VT with a right bundle-branch block configuration.
Programmed electrical stimulation repeatedly induced a VT with a left
bundle-branch block configuration. After ablation of this VT, only
rapid "ventricular flutter" was provokable. During
follow-up of 19 months there have been no arrhythmia
recurrences. Thus it is likely that ablation at 1 region
abolished more than 1 VT, as has been observed by
others.19 20
RF catheter ablation of VT after myocardial infarction abolishes
spontaneous episodes of VT in two thirds of patients regardless of the
presence of multiple morphologies of inducible VT. It provides
excellent palliation for many patients who have repeated episodes of
spontaneous VT. The procedure is, however, technically demanding.
Further studies are justified to determine how catheter ablation should
fit into the therapeutic strategy for patients with
hemodynamically tolerated VT.
Footnotes
Presented in part at the 69th Scientific Sessions of the American Heart Association, New Orleans, La, November 13–16, 1996, and previously published in abstract form (Circulation. 1994;94[suppl I]:I-22).
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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