Integrative Physiology
Magnetic Resonance–Based Anatomical Analysis of
Scar-Related Ventricular Tachycardia
Implications for Catheter Ablation
Hiroshi Ashikaga, Tetsuo Sasano, Jun Dong, M. Muz Zviman, Robert Evers, Bruce Hopenfeld,
Valeria Castro, Robert H. Helm, Timm Dickfeld, Saman Nazarian, J. Kevin Donahue,
Ronald D. Berger, Hugh Calkins, M. Roselle Abraham, Eduardo Marbán,
Albert C. Lardo, Elliot R. McVeigh, Henry R. Halperin
Abstract—In catheter ablation of scar-related monomorphic ventricular tachycardia (VT), substrate voltage mapping is
used to electrically define the scar during sinus rhythm. However, the electrically defined scar may not accurately reflect
the anatomical scar. Magnetic resonance– based visualization of the scar may elucidate the 3D anatomical correlation
between the fine structural details of the scar and scar-related VT circuits. We registered VT activation sequence with
the 3D scar anatomy derived from high-resolution contrast-enhanced MRI in a swine model of chronic myocardial
infarction using epicardial sock electrodes (n⫽6, epicardial group), which have direct contact with the myocardium
where the electrical signal is recorded. In a separate group of animals (n⫽5, endocardial group), we also assessed the
incidence of endocardial reentry in this model using endocardial basket catheters. Ten to 12 weeks after myocardial
infarction, sustained monomorphic VT was reproducibly induced in all animals (n⫽11). In the epicardial group, 21 VT
morphologies were induced, of which 4 (19.0%) showed epicardial reentry. The reentry isthmus was characterized by
a relatively small volume of viable myocardium bound by the scar tissue at the infarct border zone or over the infarct.
In the endocardial group (n⫽5), 6 VT morphologies were induced, of which 4 (66.7%) showed endocardial reentry. In
conclusion, MRI revealed a scar with spatially complex structures, particularly at the isthmus, with substrate for multiple
VT morphologies after a single ischemic episode. Magnetic resonance– based visualization of scar morphology would
potentially contribute to preprocedural planning for catheter ablation of scar-related, unmappable VT. (Circ Res.
2007;101:939-947.)
Key Words: ventricular tachycardia 䡲 catheter ablation 䡲 MRI
C
atheter ablation of scar-related monomorphic ventricular
tachycardia (VT) is a promising therapy that may reduce
morbidity and mortality associated with this condition.1
Substrate voltage mapping allows ablation of scar-related VT
during sinus rhythm in patients with hemodynamically unstable VTs where conventional activation mapping is difficult.2
This electroanatomical mapping technique defines scar in the
endocardium or the epicardium during sinus rhythm, and the
infarct border zones are ablated.
However, scar detection using the voltage-based substrate
mapping has several limitations. First, it is essentially 2D
because it defines the extent of scar on the surface, either
endocardial or epicardial, and does not provide complex 3D
anatomy of the scar. Second, spatial resolution of the voltagebased scar definition is limited by the number of points
studied by the catheter operator. Lastly, electrically defined
scar may not necessarily be identical with anatomical scar.
For example, anatomically scarred myocardium with hypertrophy may be electrically defined normal.3
To elucidate the 3D anatomical correlation between the
fine structural details of the scar and scar-related VT circuits,
we registered VT activation sequence with the 3D scar
anatomy derived from high-resolution contrast-enhanced
MRI in a swine model of chronic myocardial infarction (MI).
To achieve precise registration between the electrode locations and the MRI-derived 3D scar anatomy, we used epicardial sock electrodes (n⫽6 animals), which have direct contact
with the myocardium where the electrical signal is recorded.
Because not all VTs were expected to show epicardial
reentry, we used endocardial basket catheters in a separate
Original received June 29, 2007; revision received September 11, 2007; accepted September 26, 2007.
From the Division of Cardiology (H.A., T.S., J.D., M.M.Z., R.E., V.C., R.H.H., S.N., R.D.B., H.C., M.R.A., E.M., A.C.L., H.R.H.), Johns Hopkins
University School of Medicine, Baltimore, Md; Laboratory of Cardiac Energetics (H.A., B.H., E.R.M.), National Heart, Lung, and Blood Institute, NIH,
Bethesda, Md; Division of Cardiology (T.D.), University of Maryland, Baltimore; and Heart and Vascular Research Center (J.K.D.), MetroHealth
Hospital, Case Western Reserve University, Cleveland, Ohio.
This manuscript was sent to James T. Willerson, Consulting Editor, for review by expert referees, editorial decision, and final disposition.
Correspondence to Hiroshi Ashikaga, MD, PhD, Division of Cardiology, Johns Hopkins University School of Medicine, 720 Rutland Ave, Traylor 903,
Baltimore, MD 20215. E-mail [email protected]
© 2007 American Heart Association, Inc.
Circulation Research is available at http://circres.ahajournals.org
DOI: 10.1161/CIRCRESAHA.107.158980
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Table 1.
October 26, 2007
Characteristics of VT Morphology in the Epicardial Group
Spatial Characteristics
Weeks
Post-MI
VT
Morph
CL
(ms)
Earliest
Activation
Latest
Activation
Overall Pattern
1
11.9
1
218
Ant MI border
Ant RV
Heterogeneous
2
10.4
2
241
Ant MI border
Posterior
Centrifugal
3
195
Posterior
Ant MI border
Centrifugal
4
242
Posterior
Ant RV
Centrifugal
5
199
Posteroapical
Posteroapical
Epicardial reentry
6
177
Ant MI border
Posterior
Centrifugal
7
178
Posterior
Ant MI border
Centrifugal
8
199
Lat RV
Lat LV
Heterogeneous
9
210
Lat LV
Lat LV
Heterogeneous
10
223
Lat LV
Ant RV
Heterogeneous
11
185
Lat LV
Ant MI border
Heterogeneous
12
242
Ant MI border
Ant MI border
Epicardial reentry
Animal
3
10.9
4
11.0
5
9.9
6
10.1
13
219
Posterior
Ant MI border
Centrifugal
14
199
Posterior
Posterior
Heterogeneous
15
175
Lat LV
Ant MI border
Centrifugal
16
168
Lat RV
Lat LV
Centrifugal
17
184
Lat LV
Lat RV
Centrifugal
18
175
Ant MI border
Ant MI border
Epicardial reentry
19
146
Ant MI border
Ant MI border
Epicardial reentry
20
205
Posterior
Lat LV
Heterogeneous
21
140
Ant LV
Ant MI border
Heterogeneous
In case of reentry, the time reference was arbitrarily determined at the time of electrical activation at the isthmus,
so that both the earliest and the latest activations were located at the isthmus. Morph indicates morphology; CL, cycle
length; Ant, anterior; Lat, lateral. n⫽6 animals.
group of animals (n⫽5 animals) to assess the incidence of
endocardial reentry in this infarct model. The electrical and
scar data in this group were not spatially registered because
the electrodes in the basket catheter are not in direct contact
with the myocardium.
approved by the Animal Care and Use Committee of the Johns
Hopkins University School of Medicine.
Experimental Protocol
In 11 domestic swine (27 to 31 kg), the mid–left anterior descending
coronary artery was occluded for 150 minutes using a balloon
angioplasty catheter (2.7 Fr) via a carotid artery to create MI under
general anesthesia.5 Ten to 12 weeks after MI, bipolar electrograms
were recorded from 300 to 380 sites over the ventricular epicardium
using a multielectrode epicardial sock placed via median sternotomy
Materials and Methods
All studies were performed according to the Position of the American Heart Association on Research Animal Use.4 All protocols were
Table 2.
Characteristics of VT Morphology in the Endocardial Group
Animal
Weeks
Post-MI
EF
(%)
VT
Morph
CL
(ms)
Configuration
Frontal Axis
Earliest Activation
Latest Activation
Overall Pattern
1
10.0
38
1
187
Neg Concord
RSAD
Anteroseptal
Anteroseptal
Endocardial reentry
2
11.4
26
2
316
RBBB
LAD
Anteroseptal
Anteroseptal
Endocardial reentry
3
11.6
32
3
164
LBBB
Normal
Anteroseptal
Anteroseptal
Endocardial reentry
4
9.9
26
4
198
Pos Concord
LAD
Anteroseptal
Anteroseptal
Endocardial reentry
5
12.0
32
5
218
Pos Concord
LAD
Anterior
Septal
Centrifugal
6
216
Neg Concord
LAD
Anteroseptal
Lateral
Centrifugal
ECG Characteristics
Spatial Characteristics
In case of reentry, the time reference was arbitrarily determined at the time of electrical activation at the isthmus, so that both the earliest and the latest activations
were located at the isthmus. EF indicates left ventricular ejection fraction; Neg Concord, negative concordance; RBBB, right bundle branch block, LBBB, left bundle
branch block; Pos Concord, positive concordance; RSAD, right superior axis deviation; LAD, left axis deviation. n⫽5 animals.
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A MR Image
B Basal view
Islands of infarct
within viable myocardium
Posterior
LV
RV
Branching
Anterior
C Anterior view
RV
D Posterior view
LV
RV involvement
Figure 1. A, High-resolution contrast-enhanced
MRI (spatial resolution, 0.39⫻0.39⫻0.39 mm).
The region of high intensity (indicated by white
arrows) is the infarct. The myocardium in the
infarct region is substantially thinner than the
remote myocardium, and a thin rim of the viable myocardium on both the septal and the
endocardial sides of the infarct was observed.
B through D, Basal (B), anterior (C), and posterior (D) views of the 3D infarct geometry reconstructed from MRI. The infarct regions are
represented by dark gray, and the normal ventricular myocardium (RV and LV) regions are
shown in pink. The scar exhibited variable wall
thickness, with occasional branching of the
infarct structure at the periphery. There are
islands of infarct within the viable myocardium
and also islands of viable myocardium within
the infarct. The scar involved the RV in the apical region.
RV
LV
Islands of viable myocardium
within infarct
(n⫽6 animals, epicardial group) at a minimum sampling rate of 1000
Hz for 10 seconds.6 A pair of bipolar stimulating electrodes were
attached to the ventricular myocardium to induce sustained monomorphic VT using a swine programmed electrical stimulation protocol.5 Sustained VT was defined as monomorphic VT lasting ⬎15
seconds confirmed in multiple leads. After each VT induction, the
stimulating electrodes were moved to another electrode location, and
the programmed electrical stimulation was repeated for a total of 10
to 20 arbitrary locations. Because epicardial sock data were obtained
in an open-chest setting, surface ECG was not recorded in the
epicrdial group. After completion of the programmed electrical
stimulation, ex vivo MRI7 was conducted to visualize infarct
geometry. Briefly, after intravenous administration of heparin 5000
IU and Gd-DTPA (gadolinium diethylene triamine pentaacetic acid
0.20 mmol/kg), the animals were euthanized, and the hearts were
removed and filled with vinyl polysiloxane.8 As markers for registering the MR and the epicardial sock data, eight to fifteen 10⫻1 mm
glass tubes filled with Gd-DTPA (5 mmol/L) were placed in the
myocardium, and the locations of the sock electrodes and the glass
tubes were digitized (Microscribe 3DLX, Immersion, San Jose,
Calif).8 The sock electrodes were then removed from the heart, and
the heart was scanned in a 1.5-T MR scanner with a 3D gradient echo
sequence to visualize the infarct and to locate the glass tube markers
(bandwidth, ⫾130 Hz/pixel; flip angle, 20°; echo time/repetition
time, 4.02/9.7 ms; field of view, 100⫻100 mm; image matrix,
256⫻256; spatial resolution, 0.39⫻0.39⫻0.39 mm).
The remaining 5 animals (endocardial group) underwent in vivo
MRI in a 1.5-T scanner for assessment of cardiac function, using an
ECG-gated, cine steady-state free precession sequence (bandwidth,
⫾977 Hz/pixel; echo time/repetition time, 1.9/3.9 ms; readout flip
angle, 45°; field of view, 300⫻300 mm; image matrix, 256⫻256;
spatial resolution, 1.2⫻1.2⫻8.0 mm). Subsequently, bipolar electrograms were recorded from 176 sites in the left ventricular cavity
using a multielectrode basket catheter placed via a carotid artery in
a closed-chest setup. The same swine programmed electrical stimulation protocol was conducted to induce VT using a pacing catheter
(7 Fr) advanced to the right ventricular apex through a femoral vein.
Data Analysis
Left ventricular volumes were calculated from in vivo MRI using
MIPAV (NIH).9 Custom programs in MATLAB (Mathworks Inc)
were used to visualize isochronal maps on the epicardial sock and the
endocardial basket during VT. For the epicardial group, the normal
ventricular myocardium and infarct were extracted from the ex vivo
MR images using a signal intensity threshold to visualize a volumetric image of infarct in the ventricles.10 Candidate hyperenhanced
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Figure 2. Epicardial sock data during reentry
VT. Left, An isochronal map. The black dots
indicate the location of electrodes. Right (A
through I), Signals from bipolar electrograms
at respective locations. This figure shows progression of electrical activation from point A
(blue, 1 ms) to point I (yellow, 147 ms) in alphabetical order.
areas were identified as infarct if hyperenhancement was seen in ⬎1
slice and the mean intensity of the hyperenhanced region was ⬎6 SD
above the mean intensity of the remote region.11 The locations of the
glass tube markers were determined from the ex vivo MR images,
and the electrodes were spatially referenced to the MR images using
rigid-body transformation.8
Electrical activation was defined as the first peak of the derivative
of QRS in the regional bipolar deflection.12,13 For the epicardial
group, epicardial reentry was defined as a visually confirmed
macroreentry circuit during VT where the activation pathway was
accounted for by sock recordings and the electrode locations of the
earliest and the latest activation were immediately adjacent to each
other. In case of reentry, the time reference was arbitrarily determined at the time of electrical activation of the isthmus, so both the
earliest and the latest activation were located at the isthmus. For the
endocardial group, the definition of endocardial reentry was the same
as that of epicardial reentry except that the activation was recorded
by the endocardial basket catheter.
Statistical Analysis
Values are means⫾SD. Parameters were compared between the
epicardial and endocardial groups using 1-way ANOVA. If a
statistically significant result was obtained, then individual locations
were compared by a 2-tailed t test. A value of P⬍0.05 was
considered statistically significant. Statistics were performed with
SigmaStat 3.0 (SPSS, Chicago, Ill).
was 61.2⫾14.9 mL, left ventricular end-systolic volume was
42.0⫾9.3 mL, and left ventricular ejection fraction was
30.8⫾5.1% (endocardial group; Table 2). Sustained monomorphic VT was reproducibly induced in all 11 animals. The
cycle length was 204⫾32 ms in the epicardial group (n⫽39
VTs) and 217⫾53 ms in the endocardial group (n⫽6 VTs),
and there was no significant difference between the 2 groups
(P⫽NS). All VTs were hemodynamically unstable.
Scar Geometry
High-resolution contrast-enhanced MRI revealed a 3D complex structure of the scar in this occlusion/reperfusion MI
model. The myocardium in the infarct region is substantially
thinner than the remote myocardium, and there was a thin rim
of the viable myocardium on both the septal and the endocardial sides of the infarct (Figure 1A). The scar exhibited
variable wall thickness with occasional branching of the
infarct structure at the periphery (Figure 1B through 1D).
There are islands of infarct within the viable myocardium,
and also islands of viable myocardium within the infarct. The
scar involved the right ventricle (RV) in the apical region.
Epicardial Reentry and Scar Geometry
Results
All animals survived the MI procedure, which resulted in
anteroseptal MI (n⫽11 animals). The animals underwent VT
induction 10.7⫾0.7 weeks after MI in the epicardial group
(n⫽6 animals) and 11.0⫾1.0 weeks after MI in the endocardial group (n⫽5 animals), and there was no significant difference between the two groups (P⫽NS; Tables 1 and 2). At the
time of VT induction, left ventricular end-diastolic volume
In the epicardial group (n⫽6 animals), a total of 76 sites were
stimulated (12.7⫾3.0 per animal), and 21 VT morphologies
(3.5⫾1.6 per animal) were induced at 39 sites (6.5⫾4.6 per
animal, Table 1). Four (19.0%) of 21 VT morphologies
induced at 7 sites were epicardial reentry (Figure 2 and Table
1). The epicardial reentry circuits were mostly of the classic
figure-of-8 type, and the central common pathway, or the
isthmus, was located at the infarct border zone or over the
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Figure 3. Epicardial reentry registered with
MR-derived scar. A possible electrical propagation at the infarct border zone is indicated by
dashed red arrows. A, VT no. 5. The isthmus
(circumscribed by a broken red line) was
located at the posteroapical segment of the
infarct border zone. The scar geometry at the
isthmus was characterized by scar tissue interspersed with multiple canals of viable myocardium. Electrical activation initially spread longitudinally toward the base, split into 2 opposite
lateral directions, and then returned longitudinally to the posteroapical region. B, VT no. 12.
The isthmus (circumscribed by a broken red
line) was located at the anterior irregular surface of the scar. This irregular surface consists
of thin interwinding layers of viable myocardium
(see the MR image on the right).
infarct in all 4 epicardial reentry morphologies. The scar
geometry at the isthmus often contained multiple threedimensionally intricate structures. In VT no. 5 (Table 1), the
isthmus was located at the posteroapical segment of the
infarct border zone. The scar geometry at the isthmus was
characterized by scar tissue interspersed with multiple canals
of viable myocardium (Figure 3A). Electrical activation
initially spread longitudinally toward the base, split into two
opposite lateral directions, then returned longitudinally and
apically to the posteroapical region. The isthmus of VT no. 12
was located at the anterior irregular surface of the scar (Figure
3B). This irregular surface consists of thin interwinding
layers of viable myocardium (see MR image in Figure 3B).
There were two distinct epicardial reentry circuits in the same
heart with different isthmus locations (VT nos. 18 and 19). In
VT no. 18, the isthmus was located at the anterior right
ventricular insertion where a small volume of viable myocardium bound by the infarct tissue is protruding into the RV
(Figure 4A). The isthmus of VT no. 19 was located at a small
volume of viable myocardium surrounded by the infarct
tissue at the anteroapical infarct border (Figure 4B).
The remaining 17 VT morphologies induced at 32 sites did
not show epicardial reentry, but mostly showed the centrifu-
gal pattern where unidirectional electrical propagation spread
from the breakthrough point to other regions of the heart
(Figures 5 and 6 and Table 1). In VT no. 2, the epicardial
breakthrough was located at the infarct border zone in the
anterior left ventricle (LV) and spread toward the RV and the
lateral LV, ending at the latest site in the posterior segment
(Figure 5A). The infarct geometry at the breakthrough regions was characterized by multiple islands and protrusions
of viable and scar myocardium, where electrical activation
exits from the endocardial side of the myocardium. In VT no.
4, the propagation pattern was centrifugal and similar to that
of VT no. 2 but spread in the opposite direction, from the
posterior segment to the anterior LV (Figure 5B). The latest
activation site was the normal myocardium at the infarct
border in the anterior LV. In VT no. 7, the breakthrough
points were located in the viable myocardium in the RV, and
the electrical wave propagated to the latest activation site in
the viable myocardium in the anterior LV (Figure 6A). In VT
no. 17, the breakthrough was located in the viable myocardium in the lateral LV, and the electrical wave propagated to
the latest activation site in the infarct border zone (Figure
6B). Some VT activation sequences showed a heterogeneous
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Figure 4. Epicardial reentry registered with
MR-derived scar (continued). A possible electrical propagation at the infarct border zone is
indicated by dashed red arrows. A, VT no. 18.
The isthmus (circumscribed by a broken red
line) was located at the anterior right ventricular
insertion, where a small volume of viable myocardium bound by the infarct tissue is protruding into the RV. B, VT no. 19. The isthmus (circumscribed by a broken red line) was located
at a relatively large volume of the viable myocardium surrounded by the infarct tissue at the
anteroapical infarct border. Note A and B are 2
distinct epicardial reentry circuits in the same
heart with different isthmus locations.
pattern where no clear propagation pattern was evident (data
not shown).
Endocardial Reentry
In the endocardial group (n⫽5 animals), a total of 7 sites were
stimulated (1.4⫾0.5 per animal), and 6 VT morphologies
(1.2⫾0.4 per animal) were induced at 6 sites (1.2⫾0.4 per
animal; Table 2). Four (66.7%) of 6 VT morphologies were
endocardial reentry (the Figure in the online data supplement
at http://circres.ahajournals.org), and the reentry circuits were
mostly of the classic figure-of-8 type. The isthmus of all 4 VT
morphologies was located at the anteroseptal aspect of the left
ventricular endocardium, where the scar was located. The 2
remaining VT morphologies did not show endocardial reentry; 1 showed the centrifugal pattern where unilateral electrical propagation spread from the anterior to the septal LV, and
the other morphology was of heterogeneous pattern without
global propagation pattern (data not shown).
Discussion
The present study combined electrical measurements and
contrast-enhanced MRI to examine the 3D anatomical correlation between the scar and VT reentry circuits in chronic MI.
To interpret the data accurately, we focused on studying only
macroreentry circuits visually confirmed on the epicardial
sock recordings. As anticipated, most VT activation sequences in the epicardial group did not show epicardial
reentry but the centrifugal or heterogeneous patterns (Table
1). This does not mean that those epicardial “nonreentry”
patterns arose from a triggered or automatic mechanism.
Rather, all of the VTs induced in the epicardial group were
most likely reentry because they were reproducibly induced
by programmed stimulation.14 It is possible that the electrical
activation propagated back to the site of origin by a pathway
undetectable by surface recordings.15 The relatively high
incidence of reentry in the endocardial group (66.7%)
strongly suggests that at least some of those epicardial
“nonreentry” patterns are accounted for by endocardial reentry. In addition, heterogeneous patterns in the epicardial
group likely represent both spatially and temporally heterogeneous arrival of propagation wavefront from endocardial or
intramural reentry.
Scar Geometry
Contrast-enhanced MRI with high spatial resolution
(0.39⫻0.39⫻0.39 mm) minimized the partial volume effect7
and visualized the fine details of the 3D infarct structure that
are not easy to grasp from the 3D tomographic images (Figure
1). Our results clearly demonstrate that the scar morphology
is not just transmural or nontransmural but much more
complex than previously thought. The occlusion/reperfusion
MI model in the present study reflects a clinical scenario in
which acute coronary artery occlusion is followed by early
revascularization, and our data indicate that only a single
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Figure 5. Epicardial centrifugal pattern of VT
registered with MR-derived scar. A possible
electrical propagation at the infarct border zone
is indicated by dashed red arrows. A, VT no. 2.
The epicardial breakthrough (circumscribed by
a broken red line) was located at the infarct
border zone in the anterior LV and spread
toward the RV and the lateral LV, ending at the
latest site in the posterior segment. The infarct
geometry at the breakthrough regions is characterized by multiple islands and protrusions of
viable and scar myocardium, where electrical
activation exits from the endocardial side of the
myocardium. B, VT no. 4. The propagation pattern was centrifugal and similar to that of VT
no. 2 but spread in the opposite direction, from
the posterior segment to the anterior LV. The
latest activation site (circumscribed by a broken
red line) was the normal myocardium at the
infarct border in the anterior LV.
ischemic episode without baseline atherosclerosis can create
3D intricate scar anatomy that could independently function
as a substrate for VT. This is consistent with the fact that
sustained VT can be induced in patients who receive
thrombolytic therapy after the first MI.16
myocardium.3 Furthermore, the same anatomical structure at
the infarct border was found to serve as the isthmus and a
centrifugal pathway in different VT morphologies (Figure 4B
and Figure 6B). Therefore, it appears valid to target the
complex anatomical structures in the peri-infarct region in
any VT circuits.
Electroanatomical Correlation During VT
Histologically, restoration of coronary blood flow by reperfusion within 2 to 3 hours rescues some of the ischemic cells
from cell death,17–19 resulting in heterogeneous necrosis in the
infarct region.20 –25 This creates multiple regions of nonuniform anisotropy26 where the electrical impulse conduction
can be significantly delayed.27 Contrast-enhanced MRI revealed that both the isthmus of the reentry circuits and the
epicardial breakthrough of the centrifugal circuits were characterized by 3D complex structures of the viable and scar
myocardium in the periinfarct region. Thus, MR-guided
morphological assessment of the scar may help narrow the
focus to the potential locations of ablation targets, rather than
targeting as much of the infarct border zone as possible.
However, there are no apparent anatomical characteristics
that distinguish between these 2 structures; thus it is not clear
whether all of such anatomical structures should be targeted
to successfully prevent recurrence of VT.
The epicardial breakthrough was mostly at the infarct
border (Figure 5A and 5B) but was often located at the viable
myocardium (Figure 6B). This indicates that the epicardial
breakthrough of the centrifugal circuits is not the site of
origin but simply a surface exit of a continuous circuit. This
is consistent with the clinical observation that a sizable
minority of the successful VT ablation sites are in the viable
Clinical Implications
It has been shown that MR-derived scar geometry can
noninvasively predict the presence of VT substrate in patients
in vivo.11,28 This study further advanced the concept and
presents a possibility to predict locations of potential VT
circuits and isthmus from scar geometry that could be
noninvasively obtained by MRI before ablation procedures.
Given the marked complexity of scar geometry, MR-based
scar analysis would potentially play a complementary role in
catheter ablation of unmappable VT, rather than replacing the
current approach of detailed mapping. This would be particularly important for preprocedural planning for some fraction
of scar-related VT circuits that are of epicardial origin3,29 or
involve both the epicardial and endocardial layers,29,30 where
successful ablation requires epicardial delivery of radiofrequency energy. Given the noninvasive nature of MRI, the
MR-based scar analysis could play a role not only in
preprocedural planning but also could be repeated after failed
procedures until successful ablation is accomplished. MRI
can visualize the spatial and temporal extent of ablation
lesions,31–33 which can also be incorporated in the MR-based
scar analysis. Detailed description of scar geometry would
facilitate electroanatomical mapping of VT substrate34 to
target all inducible and spontaneous monomorphic VTs to
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Figure 6. Epicardial centrifugal pattern of VT
registered with MR-derived scar (continued). A
possible electrical propagation is indicated by
dashed red arrows. A, VT no. 7. The breakthrough points were located in the viable myocardium in the RV, and the electrical wave
propagated to the latest activation site (circumscribed by a dashed red line) in the viable myocardium in the anterior LV. B, VT no. 17. The
breakthrough was located in the viable myocardium in the lateral LV, and the electrical wave
propagated to the latest activation site (circumscribed by a broken red line) in the infarct border zone.
reduce VT recurrences and implantable cardioverterdefibrillator firing.1,2,35 The spatial resolution of cardiac MRI
has improved dramatically over the past several years, and
high-resolution scar imaging used in the present study will
likely become available in vivo with high-speed imaging
techniques.
dural planning for catheter ablation of scar-related, unmappable VT.
Acknowledgments
We thank Edward J. Ciaccio, PhD, for valuable input on electrophysiological data analysis and Kenneth Rent for excellent
technical assistance.
Limitations
In the epicardial group, we were able to study anatomical
correlation between scar geometry and VT circuits for a
fraction of inducible VTs. In the endocardial group, the
electrical and scar data were not registered to characterize the
scar at the VT isthmus because the electrodes in the basket
catheter are not in direct contact with the myocardium and
precise registration cannot be conducted in vivo. Therefore,
scar characteristics of the isthmus described in this study
apply to only epicardial reentry circuits in this model.
Because we did not conduct simultaneous acquisition of
endocardial and epicardial signals, we could not study 3D
complex VT circuits that travel both the endocardium and the
epicardium with reference to the infarct geometry.29
Conclusions
MRI revealed a scar with spatially complex structures,
particularly at the isthmus, with substrate for multiple VT
morphologies after a single ischemic episode. The reentry
isthmus was characterized by a relatively small volume of
viable myocardium bound by the scar tissue at the infarct
border zone or over the infarct. MR-based visualization of
scar morphology would potentially contribute to preproce-
Sources of Funding
This work was supported by National Heart, Lung, and Blood
Institute grants R01-HL64795 (to H.R.H.), PO1-HL077180 (to D. A.
Kass and A.C.L.), and Z01-HL004609 (to E.R.M.) and the Donald
W. Reynolds Cardiovascular Research Foundation.
Disclosures
None.
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Online Supplement
Ashikaga et al., MR-based anatomical analysis of scar-related…
Supplemental Figure 1. Left panel (A-D): Endocardial reentry. Right panel (A-D):
Surface ECG of respective VT circuits. The endocardial reentry circuits were mostly of
the classic figure-of-eight type. The isthmus of all 4 VT morphologies was located at the
anteroseptal aspect of the LV endocardium, where the scar was located.
Septal
Anterior LV
CL = 187 ms
C
CL = 164 ms
Early
A
B
A
CL = 316 ms
D
CL = 198 ms
Late
Supplemental Figure
B
C
D