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Original Article
Primary Radiofrequency Ablation of Ventricular
Tachycardia Early After Myocardial Infarction
Evaluation in an Ovine Model
Calvin H.C. Hsieh, MBBS(Hons), BSc(Med), FRACP;
Ee-May Chia, MBBS, BSc(Med), MPH, FRACP; Kaimin Huang, BSc; Juntang Lu, Dip(Vet);
Michael Barry, BE; Jim Pouliopoulos, BSc, PhD; David L. Ross, MBBS, FRACP;
Stuart P. Thomas, MBBS, FRACP, PhD; Pramesh Kovoor, MBBS, FRACP, PhD
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Background—Ventricular tachycardia (VT) is a significant complication of myocardial infarction. Radiofrequency ablation
for postinfarct VT is reserved for drug refractory VT or VT storms. Our hypothesis is that radiofrequency ablation in the
early postinfarct period could abolish or diminish late recurrences of VT.
Methods and Results—Myocardial infarct was induced by balloon occlusion of the left anterior descending artery in
35 sheep. The 25 survivors underwent programmed ventricular stimulation and electroanatomical mapping 8 days
postinfarct. Animals with inducible VT (12 out of 25 animals) underwent immediate radiofrequency ablation. Further VT
inductions were performed 100 and 200 days postinfarct. At day 8, 3.0±0.9 VT morphologies per animal were inducible.
All were successfully ablated with 24±6 applications of radiofrequency energy. All had ablations on the left ventricular
endocardium, and 67% had ablations on the right ventricular aspect of the interventricular septum. All targeted arrhythmias
were successfully ablated acutely. One animal was euthanized because of hypotension from a serious pericardial effusion.
The other 11 survived and remained arrhythmia free on subsequent inductions on the 100th and 200th days (P<0.001).
The 13 animals without inducible VT remained noninducible at the subsequent studies. A historical control arm of 9
animals with inducible VT at day 8 remained inducible at day 100.
Conclusions—Radiofrequency ablation on the eighth day after infarction abolished inducibility of VT at late induction studies
≤200 days in an ovine model. Early identification and ablation of VT after infarction may prevent or reduce late ventricular
arrhythmias but needs to be validated in clinical studies. (Circ Arrhythm Electrophysiol. 2013;6:1215-1221.)
Key Words: catheter ablation ◼ myocardial infarction
V
Methods
entricular arrhythmias are responsible for the majority
of cases of sudden cardiac death (SCD) after myocardial
infarction (MI), with the greatest risk within the first 30 days.1
Implantable cardioverter-defibrillators (ICDs) reduce the risk
of SCD in the postinfarct population at high risk.2,3
Study Design
This study was designed as an equivalence study in which the primary
outcome was the midterm noninducibility of VT. MIs were induced in
35 male cross-bred merino sheep (weight, 58±11 kg). In the 25 (71%)
survivors, programmed ventricular stimulation (PVS) was performed
8 days postinfarct. The animals that had inducible VT (VTrfa) underwent immediate catheter-based ablation and had subsequent PVS
100 and 200 days postinfarct. The control arm of animals without
inducible VT (VTneg) underwent the same PVS studies (Figure 1). A
transthoracic echocardiogram was acquired preinfarct and pre-PVS.
A secondary analysis of efficacy compared VTrfa animals with an historical control arm of animals with VT not ablated (VTpos) but followed up only to 100 days.
Clinical Perspective on p 1221
Catheter radiofrequency ablation (RFA) of ventricular
arrhythmias is indicated only in patients with a distant infarct
and an ICD with recurrent ventricular tachycardia (VT) or VT
storms refractory to medications. In this population, catheter
ablation has been shown to be effective.4 ICD implantation
combined with prophylactic catheter ablation remote from the
infarct (8–13 years) has been found to reduce the incidence of
ICD-delivered therapy.5,6
Our hypothesis is that RFA of inducible VT and its substrate early after an infarct would abolish or diminish late ventricular tachyarrhythmias.
Myocardial Infarction
Under general anesthesia and without class III antiarrhythmics, temporal occlusion by percutaneous angioplasty balloon (2.5–4.0×8–20
mm) of the midhomonymous artery (left anterior descending artery
equivalent) for 3 hours induced an MI.7
Received February 15, 2013; accepted October 1, 2013.
From the Westmead Hospital and the University of Sydney, Sydney, Australia.
The online-only Data Supplement is available at http://circep.ahajournals.org/lookup/suppl/doi:10.1161/CIRCEP.113.000447/-/DC1.
Correspondence to Pramesh Kovoor, MBBS, PhD, Westmead Hospital and University of Sydney, PO Box 531 Wentworthville, Sydney, NSW 2145,
Australia. E-mail [email protected]
© 2013 American Heart Association, Inc.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org
1215
DOI: 10.1161/CIRCEP.113.000447
1216 Circ Arrhythm Electrophysiol December 2013
Figure 1. Flowchart of experimental protocol. VT
indicates ventricular tachycardia.
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Electroanatomical Map
On the eighth postinfarct day, an electroanatomic map and simultaneous noncontact and contact data were collected via the Ensite
multielectrode array system (St Jude, St. Paul, MN) as previously
described.8 Mapping was performed before PVS on each day.
The dynamic substrate mapping (DSM) system was used to identify substrate on the noncontact system. Pacing from multiple sites and
sinus rhythm were recorded, and the local unipolar electrogram peak
negative voltage was used to create a global ratiometric map. Areas
of dense injury, borderline injury, and normal myocardium were defined by both contact bipolar electrograms (≤0.5, 0.5–1.5, and >1.5
mV, respectively) collected during sinus rhythm and noncontact DSM
(≤30%, 30%–50%, and >50% of the local unipolar electrogram peak
negative voltage).9,10
Electrograms were classified using standard criteria by 2 independent observers11–13:
1. Normal electrograms with ≤3 sharp intrinsic deflections, with
amplitude ≥3 mV and duration <70 ms, or amplitude/duration
>0.046.
2.Fractionated potentials with >3 deflections, with amplitude
≤0.5 mV and duration ≥133 ms, or amplitude/duration <0.005.
3.Isolated potentials with additional signals separated from the
local electrogram by >20 ms isoelectric interval.
4. Late potentials with additional signals occurring ≥100 ms after
the QRS.
PVS and VT Ablation
On the eighth, 100th, and 200th days, PVS was performed from the
right ventricular (pulse width 2 ms, drive train 8 beats, and ≤4 premature extrastimuli). The protocol was repeated twice each from
2 pacing sites (right ventricular apex and basal septum), and with
2 drive trains (400 and 450 ms). The end point of stimulation was
the final stimulus reaching refractoriness or initiation of a sustained
ventricular arrhythmia. An animal was considered VT inducible if
any induced arrhythmia was monomorphic, cycle length ≥200 ms,
sustained for ≥30 s if hemodynamically stable or ≥10 s if unstable,
and reproducible.14 All induced VTs were considered for ablation.
A 10- to 20-s segment of the induced arrhythmia was recorded before
termination.
Ablation Technique
Entrainment and contact activation mapping were not possible as
all VTs were not hemodynamically tolerated. Therefore, substrate
modification was performed during sinus rhythm within the region
identified to be critical for sustaining VT, with ≥1 of the following
criteria15–17:
1.Corresponding to early activation site determined by noncontact mapping (earliest onset of QS deflection with virtual electrograms during VT).18
2.Paced QRS morphology similar to target VT (match ≤11/12
ECG leads).19
3.Stimulus-QRS interval >40 ms pacing from the site in sinus
rhythm.
4. Anatomic continuity with other lesions.
Ablation was placed using a 3.5 mm, saline-irrigated tip 4-electrode deflectable ablation catheter (Navistar Thermocool; BiosenseWebster, Diamond Bar, CA). Radiofrequency energy was delivered
for 90 to 120 s in power control mode with 50 W maximum power,
and automatically terminated if the maximal temperature (48°C) or
impedance (300 Ω) was exceeded. Saline flow was maintained at 2
mL/min and increased to 30 mL/min during radiofrequency delivery.
Sequential point lesions created lines both parallel and perpendicular to the infarct border. The ablations were extended ≥1 cm into
the infarcted region. Parallel lesions were extended into distinctly
noninfarcted tissue (≥2 mV).16 All ablations that targeted the septum had corresponding ablations from the right ventricular to create
transmural lesions.7 Postablation, repeat PVS protocol was performed
to reinitiate VT. If another VT was induced, further ablations were
performed. The location of the new VT was determined by the same
Hsieh et al Primary Ablation of Postinfarct VT 1217
technique described above. The end point of the procedure was defined as noninducibility of any VT using the PVS protocol.
Data Analysis
Data were analyzed using Matlab version 2010a (Mathworks, Natick,
MA). Isochronal maps were created with local activations, defined as
the maximum negative deflection of the virtual electrogram.
Statistical analysis was performed using SPSS version 16 (SPSS
Inc, Chicago, IL). Two-tailed tests with 5% significance level were
used throughout. Continuous variables were summarized as mean±SD.
Association between categorical variables was tested using Fisher exact test. Repeated measures ANOVA was used to test for interaction
between the effects of VT inducibility and time on substrate area and
to test for changes over time separately within each group.
Animal Care
The care of the animals and study protocol were approved by the
Sydney West Area Health Service Animal Ethics Committee, and
complied with the ethical standards of the National Health and
Medical Research Council, Australia.
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End Points
The primary end point of the study was the long-term noninducibility
of VT. Acute success was defined as noninducibility of any VT≥200
ms at the end of the ablative procedure. Long-term success was defined as noninducibility at 2 subsequent PVSs on days 100 and 200.
A sample size of 12 per group (VTrfa and VTneg) has >90% power
to establish equivalence between VTrfa and VTneg groups to within
δ=12.5% (2-sided α 5%) if the rate of noninducibility of VT at day
200 is 99% in the VTneg group. The secondary analysis was an efficacy comparison between VTrfa animals and a historical control arm
of 9 animals with inducible VT at day 8 followed until day 100 under
identical conditions with the same research group. A sample size of
9 animals in each arm has 80% power to detect a statistically significant difference between an expected noninducibility rate at day 100
of 99% in VTrfa and a rate of ≤40% in the historical control arm (5%
significance level with 2-sided test).
Results
MI was induced in 35 healthy male sheep. Twenty-five (71%)
animals survived and underwent subsequent experiments.
Infarcts produced anterior and septal wall akinesis on echocardiography. The mean left ventricular ejection fraction was
36±6%, 37±8%, and 36±7% on the eighth, 100th, and 200th
days, respectively, without a statistical difference between
VTrfa and VTneg animals.
VT Characteristics
At the day 8 electrophysiological study, 12 out of 25 survivors (48%) had inducible sustained VT. A total of 37 VTs
were induced, with 3.0±0.9 distinct morphologies of VT per
animal, cycle length 251±27 ms, and requiring 3.5±0.7 extrastimuli for induction. There was a predominance of left bundle
branch pattern (23 out of 37 animals). Successful termination
of the induced VT by antitachycardia pacing occurred in 29
arrhythmias (78%). The remaining 8 required DC cardioversion because of either unsuccessful reversion with antitachycardia pacing or rapid hemodynamic compromise (Table I in
the online-only Data Supplement).
The earliest noncontact unipolar activation was 23±9 ms
earlier than the earliest surface ECG deflection. The most
common region with the earliest activation was the apicoseptum (17 out of 37 animals). Substrate mapping by DSM
located the earliest presystolic activation site as 2.0±3.0 mm
internal to the boundary between dense and borderline injury
(DSM 30th percentile).
VT Substrate
There were 516±181, 568±161, and 429±121 contact points
collected on days 8, 100, and 200, respectively. Before application of radiofrequency energy at day 8, there was no statistical
difference in the area of dense and borderline injury by contact
or noncontact measurements in VTrfa or VTneg animals (Table II
in the online-only Data Supplement). There was a larger area
of dense injury by contact measurements at day 100 in ablated
VTrfa animals compared with VTneg animals (10.2±6.2 versus
7.9±5.0; P=0.04), but this statistical difference was not detectable day 200. There was no change in the area of dense or
borderline injury in either group between days 100 and 200.
The contact electrogram characteristics were more marked,
with increased split, late, and fractionated potentials at all time
points in the VTrfa animals (Figure 2).
VT Ablation
A total of 37 VTs were targeted for catheter ablation. All ablations were performed from the left ventricular endocardial surface with 67% (8 out of 12 animals) requiring ablations on the
right ventricular side of the interventricular septum to create a
transmural lesion for arrhythmias arising from this location.7
Each animal required 24±6 applications of radiofrequency
energy and a total time of radiofrequency application of 49±23
minutes. The power delivered was 47W (range, 46W–48W)
with a temperature of 40°C (range, 38°C–42°C). Ablation
extended the total procedure time from 5.0±2.3 to 8.4±1.6
hours (P=0.001) and fluoroscopy time from 25.7±17.7 versus
38.9±26.8 minutes (P=0.162). There was no statistically significant difference in procedure or fluoroscopy times on other
experimental days.
A representative animal with 3 inducible VTs is shown in
Figure 3. VT−1: right bundle branch block, northwest axis
morphology, and cycle length 245 ms. The exit point, based
on the earliest virtual electrogram activation 37 ms before
onset of QRS on the surface EKG was the midanteroseptum.
VT−2: left bundle branch block, left anterior descending axis
morphology, and cycle length 205 ms. The exit point was the
apex, 15 ms earlier than the surface EKG. VT−3: right bundle
branch block, left anterior descending axis, and cycle length
290 ms. The earliest presystolic activation site was the apical anteroseptum. Each of these 3 VTs were targeted in turn
for ablation, with ablation lines drawn both perpendicular and
parallel to the scar border. The ablation line targeting VT−3
joined the former 2 ablation lines.
Procedural Success
Acute success, as defined as freedom from inducible sustained
VT at the end of the day-8 ablation, was 100% (12 out of 12
animals).
The 30-day mortality rate was 1/12 (8%). This animal had a
hemodynamically significant pericardial effusion secondary to
the MI found on day 8 before experimentation. Hemodynamics
did not improve after PVS, and the animal was euthanized
1218 Circ Arrhythm Electrophysiol December 2013
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Figure 2. A, Scar-related electrograms in a VTneg animal in the
top row and in a VTrfa animal in
the bottom row. Left to right,
Days 8, 100, and 200. Images
are orientated as labeled. Color
scale for dynamic substrate
mapping–based voltage substrate mapping. Electrograms
are annotated as fractionated
potentials (blue), split potentials
(white), late potentials (yellow).
Fractionated and split potentials found in borderzone, and
late potentials usually found
in lower voltage areas. B, The
higher percentage of split, late,
and fractionated potentials at
all time points in VTrfa animals.
Analysis by repeated measures
demonstrated a significant
effect of both time and ablation status in split (P=0.013),
late (P<0.001), and fractionated
(P=0.006) potentials. LAD indicates left anterior descending
artery; S, septum; and VT, ventricular tachycardia.
because of ethical concern about its condition. An immediate
autopsy of the animal confirmed a serious effusion, with no
perforation seen. All other animals survived and completed the
100th and 200th day procedures. Two animals required diuretics for 2 days postradiofrequency ablation, but there was no
long-term heart failure. No significant morbidity or mortality
in the VTneg group (13 out of 13 survived 200 days) was seen.
PVS and complex mapping was repeated on the 100th and
200th days. Monomorphic VT was not reinducible on either
day in any of the ablated animals (12 out of 12 VTrfa animals
Figure 3. Three separate activation patterns of ventricular
tachycardia (VT) induced in
this example, with subsequent
radiofrequency ablations.
Color scale of activation time
to left (ms). Left homonymous
artery and first diagonal branch
marked as a red line. Solid
white line dynamic substrate
mapping (DSM) 30% demarcation for dense injury, dotted
white line DSM 50% demarcation for borderline injury. For
each diagram, a representative
ECG (lead I) and 4 virtual electrograms with corresponding
green numbers on the diagram
to the bottom right. Yellow dots
demonstrating placement of
ablations. The first ablation set
(left) targeted the midseptal
earliest endocardial activation site, with ablations performed both perpendicular and parallel to the activation near the borderline and
dense injury areas. The second ablation set (middle) targeted an apical earliest endocardial activation site. The broader front required a
longer line of ablation. The third ablation set (right) targeted a VT originating in the apicolateral area. The line of ablation was joined to the
first ablation set. AL indicates anterolateral wall; Ao, aortic root; Ap, apex; and S, septal wall.
Hsieh et al Primary Ablation of Postinfarct VT 1219
day 8 before ablation compared with 11 out of 11 VTrfa animals day 100 and day 200; P<0.001). No inducible arrhythmia was seen in the VTneg control arm on subsequent studies
(13 out of 13 animals).
The historical VTpos arm of 9 animals with inducible VT
at day 8 remained inducible at day 100 and was compared
with the VTrfa group, which was rendered noninducible at day
100 with intervention at day 8 (9 out of 9 versus 11 out of 12
animals; P=1.0). Areas of deep and borderline injury did not
differ significantly between VTpos and VTrfa groups at day 8
before application of radiofrequency energy, or at day 100.
There was not a statistically significant difference in split
potentials between the 2 groups. However, there was a significant reduction in late and fractionated potentials with ablations (Table III in the online-only Data Supplement).
Discussion
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Main Findings
This longitudinal study demonstrates that noncontact-electroanatomical mapping-guided radiofrequency ablation of VT
induced at day-8 postinfarct abolished inducible VT or SCD
≤200 days without major adverse events. Conversely, early
noninducibility of VT postinfarct resulted in freedom from
inducible VT or SCD ≤200 days.
Early Postinfarct PVS
The role of PVS in risk stratification in the remote infarct setting has previously demonstrated benefit.2,20 Inducible VT at 9
to 21 days postinfarct was associated with an increased risk of
SCD or spontaneous VA, and noninducibility conversely was
associated with a lower mortality risk.21–23 Our recent work in
an ovine model has demonstrated inducibility and noninducibility of VT, the earliest presystolic activation site, and the
underlying voltage substrate remain stable from 8 to 100 days
postinfarct.8
Early Postinfarct RFA
In this study, acute ablation success of postinfarct VT in the
early period (day 8) demonstrated noninducibility at 2 subsequent studies spanning a further 192 days.
To the knowledge of the authors, there are no studies of
ablation of VT in this subacute period postinfarct, although
there have been several studies introducing the idea of earlier
ablations. The SMASH-VT study randomized patients with
a previous MI with unstable VT, VF, or syncope with inducible VT and an ICD-to-ICD therapy alone or ICD combined
with substrate-based prophylactic catheter ablation.5 The incidence of ICD therapy decreased from 33% to 12% (P=0.007)
>2 years with catheter ablation. The Ventricular Tachycardia
Before Defibrillator Implantation in Patients with Coronary
Heart Disease (VTACH) trial randomized postinfarct patients
with their first episode of stable VT to ICD therapy alone or
ICD and RFA. In an intention to treat analysis, patients in the
ablation arm had a longer time to first ICD therapy (18.6 versus 5.9 months) and greater freedom from VT/VF at 2 years
(47% versus 29%).6 These trials demonstrated a significant
benefit of earlier ablative therapy. However, they enrolled
patients years remote from their infarcts.
It is difficult to compare the success rate of this study
and the above-mentioned clinical studies given the different end points. Acute success in catheter ablation of VT in
remote MI is 73% to 86%.4,17 Long-term recurrence rates are
reported as 16% to 66%.16,24 Our acute success rate of radiofrequency ablation in the early postinfarct period was 100%,
which is unexpectedly high, possibly related to the ablations
being performed in the subacute period, before significant
left ventricular remodeling. Evolving substrate and fibrosis
over time may contribute to potentially multiple reentrant
circuits and make ablation more difficult. The midterm success, measured by reinducibility >200 days, is impressive
and may have important clinical implications. This cannot be
directly compared with clinical studies with ICD recordings
of spontaneous events. Further corroboration with clinical
trials is indicated.
Our technique of using combined substrate and noncontact
activation mapping proved to be effective in the early postinfarct
period, with faster and hemodynamically unstable VT. These
arrhythmias in the remote infarct setting have been treated with
radiofrequency ablation targeting substrate.15 We thought that
targeting substrate only, when scar tissue has not yet been fully
established, may not be as reliable in this early postinfarct period.
Noncontact mapping and ablation has been previously validated
in the setting of chronic postinfarct VT ablation.19,25 Pratola
et al19 achieved an acute success rate defined as VT noninducibility of 95%. Our study demonstrates similar acute success rates
and evidence of longer-term noninducibility with the noncontact
system. However, the relative merits of the 2 approaches can
only be established by further direct comparison.
VT Substrate
Noncontact mapping was used because of the rapid rate
(251±27 ms cycle length) and poor hemodynamic tolerability
of the early postinfarct induced VT. This is consistent with
clinical studies of VTs induced 1 week postinfarct (220 ms),23
and disparate from chronic postinfarct VT (428 ms).4
Similar to our previous animal8 and reported clinical studies,19 the earliest presystolic VT activation site was found
within the infarct borderzone (DSM<50%), usually in close
proximity to the boundary between borderline and dense
injury (DSM 30th percentile). This borderzone activation site
was confirmed on contact mapping by Verma et al.15
Our study demonstrated a no statistically significant difference between areas of dense and borderline injury between
day 8 and day 100 between the VTrfa and historical control
VTpos groups. However, this study was not powered to see a
difference in these comparisons made post hoc.
Our study found a significant increase in the quantity of
late and fractionated potentials in VTrfa animals compared
with VTneg animals at all time points, and in split potentials
at days 8 and 100. However, compared with the VTpos group,
VTrfa animals had a statistically significant reduction in late
and fractionated potentials, secondary to the day-8 ablations.
Our findings are consistent with Haqqani et al,11 who found
that in ischemic cardiomyopathy, spontaneous VT was associated with more split, late, and fractionated potentials compared with patients without spontaneous events. Haqqani
et al11 noted higher proportion of fractionated, split, and late
1220 Circ Arrhythm Electrophysiol December 2013
potentials compared with the present study; however, this is
likely related to variations in the clinical population with different infarct territories, revascularization, and in several previous infarcts. Haqqani et al11 also found larger areas of lower
voltage in the population with spontaneous VT.
Sources of Funding
This work was supported by a project grant awarded to Dr Kovoor
from the National Health and Medical Research Council, Australia
(project grant scheme 402669). Dr Hsieh was funded by scholarships
from the University Postgraduate Award (University of Sydney) and
the Westmead Millenium Institute.
RFA Versus ICD
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Current prophylaxis for postinfarct SCD is ICD implantation.
The benefit of ICDs however, is marred by several problems.
ICD therapy is not successful in preventing SCD in 3% to 7%
and is associated with a decline in psychosocial quality of
life.26 Multiple ICD shocks, whether appropriate or inappropriate, are associated with a 3.4- to 5.7-fold increase in relative risk for death.3,27 The current view is that ICD shocks are
a marker for increased mortality but may not be mechanistically related to death.28 However, ICD shocks are associated
with adverse cellular and mechanical responses temporarily
and permanently.28
Collectively, these results suggest that avoidance of ICDs
and shock delivery would improve patient outcomes. Our
study suggests that prophylactic ablative therapy delivered in
the subacute period may prevent or reduce the need for defibrillators. This needs further clinical corroboration.
Adverse Events
Subacute ablation of postinfarct VT needs to have a low
complication rate to be a viable option. In a meta-analysis
of chronic ischemic VT ablation, the adverse event rate was
6.3%.29 This included death, stroke or transient ischemic
attacks, perforation, and third-degree atrioventricular block.
In our animal study, there were no major procedural complications. Overall left ventricular function and the incidence of
heart failure were not impacted by the ablations likely because
of the ablations primarily targeting areas of dense and borderline injury. Again, this needs confirmation in further studies.
Study Limitations
This study used an animal model and had a moderate but not
prolonged follow-up period of 200 days. Clinical postinfarct
VT may seem for the first time years after the infarct. However, if VT is not inducible using a vigorous induction protocol such as in this study, clinical studies suggest a low chance
of late VT.30
Because of the hemodynamic instability of the induced VTs
in this study, we were unable to perform detailed contact activation or entrainment mapping. However, this reflects reality,
where only ≈30% of patients with postinfarction VT can tolerate their arrhythmia for contact activation mapping.4
Conclusions
Early ablation of inducible VT 8 days post-MI resulted in a
high acute and chronic success rate and seemed to be safe in
this animal model. This novel approach of RFA needs to be
validated in clinical studies.
Acknowledgments
We are grateful to the Westmead Animal Research Facility staff and
Karen Byth for their assistance.
Disclosures
None.
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CLINICAL PERSPECTIVE
Ventricular tachycardia (VT) is a potentially lethal complication of myocardial infarction. In an ovine model, we have
observed that VT that is inducible early after myocardial infarction remains inducible at late follow-up, suggesting a possible
role for early identification by programmed stimulation for potential treatment. This article tackles the question of whether
early intervention with radiofrequency ablation can abolish inducible VT early and prevent late inducible VT in this model.
Myocardial infarcts were induced in 35 animals, 12 of the 25 survivors had inducible VT on the eighth postinfarct day and
underwent radiofrequency ablation, rendering all noninducible at the end of the procedure. At repeat study, 100 and 200
days postinfarction, no VT was inducible. The findings in this animal model suggest that an early VT ablation approach for
patients with inducible VT early after myocardial infarction warrants consideration for further study.
Primary Radiofrequency Ablation of Ventricular Tachycardia Early After Myocardial
Infarction: Evaluation in an Ovine Model
Calvin H.C. Hsieh, Ee-May Chia, Kaimin Huang, Juntang Lu, Michael Barry, Jim Pouliopoulos,
David L. Ross, Stuart P. Thomas and Pramesh Kovoor
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Circ Arrhythm Electrophysiol. 2013;6:1215-1221; originally published online October 18, 2013;
doi: 10.1161/CIRCEP.113.000447
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