discordance in scar detection between electroanatomical

J A C C : C L I N I C A L E L E C T R O P H Y S I O L O G Y VO L . 6 , N O . 1 1 , 2 0 2 0

ª 2 0 2 0 B Y T H E A M E R I C A N C O L L E G E O F C A R D I O L O G Y F O U N D A T I O N

P U B L I S H E D B Y E L S E V I E R

Discordance in Scar Detection BetweenElectroanatomical Mapping and CardiacMRI in an Infarct Swine Model
Selcuk Kucukseymen, MD,a Hagai Yavin, MD,b Michael Barkagan, MD,a Jihye Jang, PHD,a
Ayelet Shapira-Daniels, MD,a Jennifer Rodriguez, BA,a David Shim, MD,a Farhad Pashakhanloo, PHD,a

Patrick Pierce, RT,a Lior Botzer,d Warren J. Manning, MD,a,c Elad Anter, MD,b Reza Nezafat, PHDa

ABSTRACT

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OBJECTIVES This study sought to investigate the sensitivity of electroanatomical mapping (EAM) to detect scar as

identified by late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR).

BACKGROUND Previous studies have shown correlation between low voltage electrogram amplitude and myocardial

scar. However, voltage amplitude is influenced by the distance between the scar and the mapping surface and its extent.

The aim of this study is to examine the reliability of low voltage EAM as a surrogate for myocardial scar using LGE-derived

scar as the reference.

METHODS Twelve swine underwent anterior wall infarction by occlusion of the left anterior descending artery (LAD)

(n ¼ 6) or inferior wall infarction by occlusion of the left circumflex artery (LCx) (n ¼ 6). Subsequently, animals un-

derwent CMR and EAM using a multielectrode mapping catheter. CMR characteristics, including wall thickness, LGE

location and extent, and EAM maps, were independently analyzed, and concordance between voltage maps and CMR

characteristics was assessed.

RESULTS LGE volume was similar between the LCx and LAD groups (8.5 � 2.2 ml vs. 8.3 � 2.5 ml, respectively;

p ¼ 0.852). LGE scarring in the LAD group was more subendocardial, affected a larger surface area, and resulted in

significant wall thinning (4.88 � 0.43 mm). LGE scarring in the LCx group extended from the endocardium to the

epicardium with minimal reduction in wall thickness (scarred: 5.4 � 0.67 mm vs. remote: 6.75 � 0.38 mm). In all the

animals in the LAD group, areas of low voltage corresponded with LGE and wall thinning, whereas only 2 of 6 animals in

the LCx group had low voltage areas on EAM. Bipolar and unipolar voltage amplitudes were higher in thick inferior walls

in the LCx group than in thin anterior walls in the LAD group, despite a similar LGE volume.

CONCLUSIONS Discordances between LGE-detected scar areas and low voltage areas by EAM highlighted the limi-

tations of the current EAM system to detect scar in thick myocardial wall regions. (J Am Coll Cardiol EP 2020;6:1452–64)

© 2020 by the American College of Cardiology Foundation.

N 2405-500X/$36.00 https://doi.org/10.1016/j.jacep.2020.08.033

m the aDepartment of Medicine (Cardiovascular Division), Beth Israel Deaconess Medical Center and Harvard Medical School,

ston, Massachusetts; bCardiac Electrophysiology Section, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland,

io; dDepartment of Radiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; and

iosense Webster, Yokneam, Israel. This study was supported by the National Institute of Health (1R01HL129185, 1R01HL129185-

, 1R01HL129157, and 1R01HL127015) and the American Heart Association (15EIA22710040) to Dr. Nezafat. Dr. Pashakhanloo was

pported by the American Heart Association (18POST33990040). Dr. Shapira-Daniels was supported by the National Institute of

alth T32 training grant. Dr. Anter has received research grants from Biosense Webster; and has received honoraria from Boston

entific. Dr. Nezafat has a research agreement with Siemens Healthineers, the manufacturer of the cardiac magnetic resonance

tem used in this study. All other authors have reported that they have no relationships relevant to the contents of this paper to

close.

e authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’

titutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information,

it the JACC: Clinical Electrophysiology author instructions page.

nuscript received June 23, 2020; revised manuscript received July 29, 2020, accepted August 11, 2020.

https://doi.org/10.1016/j.jacep.2020.08.033

http://www.electrophysiology.onlinejacc.org/content/instructions-authors

http://crossmark.crossref.org/dialog/?doi=10.1016/j.jacep.2020.08.033&domain=pdf

AB BR E V I A T I O N S

AND ACRONYM S

CMR = cardiac magnetic

resonance

CI = confidence interval

EAM = electroanatomical

mapping

EGM = electrogram

LAD = left anterior descending

LCx = left circumflex

LGE = late gadolinium

enhancement

LV = left ventricle

MI = myocardial infarction

RV = right ventricle

VT = ventricular tachycardia

J A C C : C L I N I C A L E L E C T R O P H Y S I O L O G Y V O L . 6 , N O . 1 1 , 2 0 2 0 Kucukseymen et al.O C T O B E R 2 6 , 2 0 2 0 : 1 4 5 2 – 6 4 Limitation of Voltage Mapping to Detect Scar

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V entricular tachycardia (VT) activation map-ping is the gold standard for mapping scar-related re-entry circuits, yet it is rarely

achieved due to long mapping times and/or hemody-namic intolerance (1). Substrate mapping during sinusrhythm has evolved as an alternative to activationand/or entrainment mapping to manage hemody-namically unstable VTs (2) by reducing the need formapping during prolonged periods of VT. However,substrate mapping techniques during sinus rhythmare often associated with substantial recurrence rates(3,4). Higher rates are partially due to assumptionsand misconceptions related to substrate mappingtechniques, such as the assumption that low voltageequals scar or the misconception that mapping ofthe ventricular surface provides accurate informationof the much larger unmapped intramural volume(5,6).

The relationship between low voltage amplitudeand the VT isthmus was initially established inarrhythmia surgeries of patients with large anteriorwall infarctions and aneurysms (1). Bipolar voltageamplitude <1.5 mV recorded with a quadripolar non-steerable woven catheter with a 2- mm tip, 1-mmring, and 5-mm interelectrode spacing was associ-ated with the location of the VT isthmus (7). Thisthreshold was later validated for a standard 4-mm tip,1-mm ring, and 2-mm interelectrode spacing mappingcatheter, and, more recently, for multielectrodemapping catheters in animal studies (8,9). Similar tothe original patients who underwent arrhythmiasurgery, these animal models had anterior infarctionsby left anterior descending artery (LAD) occlusion inwhich the anterior wall underwent remodeling withtransmural scarring, significant wall thinning, andpreservation of a thin endocardial layer (8–13). In-farctions at other territories, particularly at the leftcircumflex artery (LCx), often produced a more het-erogeneous scar without significant wall thinning(14,15). In humans, such infarctions often result inpatchy patterns of bipolar voltage abnormalities,which may suggest overall smaller infarct sizes, lowercollagen content relative to cardiomyocytes, largerareas of preserved sub-endocardium, and relativedifferences in scar-to-wall thickness ratios (16,17).

Cardiac magnetic resonance (CMR) imaging hasbecome an integral evaluation component in patientsundergoing VT ablation (18–20). Late gadoliniumenhancement (LGE) identifies scar regions associatedwith the ventricular substrate. In addition to the scar,wall thickness and strain can be accurately measuredvia cine images to better assess left ventricular (LV)remodeling and anatomical functional effects of thescar (10,21,22). Numerous studies have correlated scar

regions on LGE images to areas of low voltageon substrate mapping (6,9,21,23–28), and it iswell accepted that EAM can detect scarringobserved on LGE. However, voltage mapsonly represent tissue characteristics within afew millimeters of the catheter tip, limitingtheir sensitivity to detect mid-myocardialscar (29). In contrast, LGE is not capable ofidentifying scar within 1 to 2 mm (i.e., 1 to 2pixels) of the blood pool due toblood�myocardium partial voluming (30,31).These limitations have raised concernsregarding the sensitivity of current EAMtechnologies to detect myocardial scar.

We sought to investigate the concordancebetween myocardial scar detection by LGEand voltage amplitude in a swine model of
anterior and inferior healed myocardial infarction.
METHODS

EXPERIMENTAL STUDY DESIGN. This study included12 Yorkshire swine of either sex weighing 35 to 40 kg.The animals were divided into 2 groups and under-went infarction in either the LAD (n ¼ 6) or the LCx(n ¼ 6) using balloon occlusion as previouslydescribed (32). Differences between the proceduresincluded 1) balloon occlusion time (180 min for LAD,60 to 120 min for LCx); and 2) targeted coronary ar-teries (occlusion of the LAD was performed after thesecond diagonal branch and occlusion of the LCx wasperformed after the second obtuse marginal branch toreduce mortality and allow a similar territory ofischemia). Animals then lived for 8 to 10 weeks beforeCMR and electrophysiology studies. CMR and elec-trophysiology studies were performed under generalanesthesia with mechanical ventilation. The studywas conducted at Beth Israel Deaconess MedicalCenter and approved by the Institutional Animal Careand Use Committee.

CMR IMAGING. CMR was performed using a 3-T car-diac magnetic resonance scanner (Siemens Vida,Erlangen, Germany) with an 18-channel body receivercoil. Animals underwent in vivo CMR 1 week beforeterminal mapping and ex vivo CMR immediately afterbeing killed. The CMR protocol included evaluation offunction using short- and long-axis slices withbalanced steady-state free-precession imaging(TR¼ 3.2ms; TE¼ 1.4ms; flip angle¼40 degrees; voxelsize ¼ 0.9 � 0.9 � 8.0 mm3; field of view ¼ 360 �270 mm2). Ten to 15 min after administration of0.2 mmol/kg of intravenous gadobutrol (Gadavist,Bayer HealthCare, Berlin, Germany), 3-dimensionalLGE imaging was performed using an inversion-

TABLE 1 Cardiac Magnetic Resonance Imaging Parameters

LV FunctionsLAD

(n ¼ 6)LCx

(n ¼ 6) p Value

EDV, ml 209 � 17 172 � 21 0.009

ESV, ml 116 � 10 91 � 16 0.011

SV, ml 92 � 12 81 � 6 0.074

LVEF, % 44 � 3.7 47 � 3.0 0.160

CO, I/ml 7.9 � 0.9 6.9 � 0.8 0.081

CI, I/ml/m2 3.8 � 0.4 3.6 � 0.3 0.252

HR, min 85 � 10 84 � 5 0.788

Total mass, g 98 � 10 99 � 13 0.967

Tissue tracking (global systolic peak strain)

Radial, % 15 � 4.2 15 � 4.0 0.799

Circumferential, % 10 � 2.2 11 � 2.2 0.821

Longitudinal, % 12.0 � 3.1 12.5 � 2.5 0.783

LGE (in vivo)

Total volume, ml 8.6 � 2.2 8.3 � 2.5 0.852

Total mass, g 9.0 � 2.3 8.7 � 2.6 0.851

LGE burden, % 8.2 � 2 8.9 � 2 0.540

Area of subendocardial LGE bordering LV blood pool, cm2 12.5 � 3.1 4.1 � 1.2 <0.001

LGE (ex-vivo)

Total volume, ml 9.0 � 1.8 8.5 � 2.1 0.711

Total mass, g 9.5 � 1.9 9.1 � 2.2 0.688

LGE burden, % 7.9 � 1.6 8.3 � 1.8 0.802

Wall thickness

Mean wall thickness of remote myocardium, mm 6.6 � 0.4 6.7 � 0.4 0.703

Mean wall thickness of scarred segments, mm 1.8 � 0.3 5.4 � 0.7 <0.001

Wall thinning percentage on scarred segments, % 73 � 40 20 � 10 <0.001

Mean amount of thinning, mm 4.9 � 0.4 1.4 � 0.8 <0.001

Values are mean � SD.

CI ¼ cardiac index; CO ¼ cardiac output; EDV ¼ end-diastolic volume; ESV ¼ end-systolic volume; HR ¼ heartrate; LAD ¼ left anterior descending; LCx ¼ left circumflex; LGE ¼ late gadolinium enhanced; LGE burden ¼ LGEvolume to LV volume ratio; LV ¼ left ventricular; LVEF ¼ left ventricle ejection fraction; SV ¼ stroke volume;

Kucukseymen et al. J A C C : C L I N I C A L E L E C T R O P H Y S I O L O G Y V O L . 6 , N O . 1 1 , 2 0 2 0

Limitation of Voltage Mapping to Detect Scar O C T O B E R 2 6 , 2 0 2 0 : 1 4 5 2 – 6 4

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recovery sequence with gradient-echo imaging(TR ¼ 3.85 ms; TE ¼ 1.7 ms; flip angle ¼ 18 degrees;voxel size ¼ 1.5 � 1.5 � 1.5 mm3; field of view ¼ 385 �288 � 96 mm3).

For ex vivo CMR imaging, 0.2mmol/kg gadobutrol(Gadavist, Bayer HealthCare) was administeredintravenously 15min before the animals were killedduring the mapping procedure. Imaging commencedwithin 1 h of heart removal using an isotropic 3-dimensional T1-weighted spoiled gradient-echosequence with the following parameters:TR ¼ 27 ms; TE ¼ 4.9 ms; flip angle ¼ 25 degrees;voxel size ¼ 0.4 � 0.4 � 0.5 mm3.

Image analysis was performed using CVI42 appli-cation (version 5.11, Circle Cardiovascular ImagingInc., Calgary, Ontario, Canada). LV and right ven-tricular (RV) volumes were quantified by manuallytracing the end-diastolic and end-systolic endocardialcontours. For global strain measurement, LV endo-cardial and epicardial borders were manually tracedat end-diastole in electrocardiographically gatedbalanced steady-state free precession 4-, 3-, and 2-

chamber long-axis sequences using a point-and-clickapproach. The automatic border tracking algorithmwas applied to track image features throughout thecardiac cycle. Tracking was visually reviewed andmanually corrected. For LGE quantification, endo-cardial and epicardial borders were first manuallycontoured. LGE scar was defined as areas with signal>3 SDs above the healthy remote region. LGE volume,mass, and burden (i.e., percentage of LV scar to LVvolume) were calculated. The surface area of the LGEbordering the LV blood pool was measured by calcu-lating LGE scar length in contact with the LV bloodpool, multiplied by slice thickness (SupplementalFigure 1). The regional wall thickness was measuredby dividing the balanced steady-state free precessioncine short-axis images of the myocardium into 100equally distributed segments using CVI42 (CircleCardiovascular Imaging Inc.) (SupplementalFigure 2). Wall thinning was calculated as the per-centage—thinning rate of the scarred region versusthe healthy remote myocardium (SupplementalFigure 2). All analyses were performed by S.K. (with5 years of experience in CMR); an additional reviewer(F.P. with 10 years of experience) repeated the mea-surements of 4 variables to assess interobserverreproducibility: 1) remote wall thickness; 2) scarredwall thickness; 3) LGE volume; and 4) subendocardialLGE area.

EAM PROTOCOL. All animals underwent EAMfollowing a 10-week survival period and #1 week afterCMR by an experienced electrophysiologist with >15years of experience treating patients with ventriculararrhythmias and 7 years of experience with large an-imal models of arrhythmia. A 6-F pentapolar catheter(Bard EP, Lowell, Massachusetts) was placed in theRV apex for pacing and as an intracardiac activationreference. An intracardiac echocardiography catheterwas positioned in the right atrium or RV and routinelyused for each procedure. EAM was performed usingCarto3 (Biosense Webster Inc, Diamond Bar, Califor-nia) and a multielectrode bidirectional mappingcatheter (Octaray; Biosense Webster Inc,) thatincluding 8 splines and 48 electrodes (26,33). Theperformance of this catheter, including its bipolar andunipolar voltage cutoffs for scar tissue, were recentlyreported. Specifically, the fifth percentile of the bi-polar voltage amplitude recorded in healthy ventri-cles with this catheter was 1.34 mV, which was similarto the cutoff of other catheters (w1.5 mV). Similarly,its mean unipolar voltage amplitude in healthy ven-tricles was relatively similar to that of the PentaRaycatheter (Biosense Webster Inc; 5.2 � 1.9 mV [median:5.2 mV] vs. 5.6 � 2.1 mV [median: 5.5 mV]) (33).







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FIGURE 1 Tissue Characterization of Post-Infarct Scars Using 3D LGE

Reformatted 3-dimensional (3D) late gadolinium enhancement (LGE) images from 2 animals with (A and B) left anterior descending (LAD) and

(C and D) left circumflex (LCx) occlusion. Arrows show areas of scar in LGE images. Scar in LAD animals was mainly localized in the sub-

endocardial region in areas with significant wall thinning on cine images and in areas with low unipolar and bipolar voltages on electro-

anatomical mapping (EAM) as well, but scar extended from the endocardium to epicardium in LCx animals with preserved wall thickness and

showed normal unipolar and bipolar voltages on EAM.


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EAM of the LV was performed via a retrogradeaortic approach during RV pacing at a cycle length of450 to 550 ms using a fill threshold of <5 mm. Thehigh-pass filter was 0.5 Hz for unipolar and 30 Hz forbipolar electrograms (EGMs). The low-pass filter was500 Hz for both. Data acquisition was automated us-ing the following inclusion criteria: 1) QRSmorphology stability defined as $95% morphologystability compared with the paced QRS configuration;2) activation time stability of #5 ms between 2consecutive beats; and 3) maximal distance #3 mmfrom the pre-made anatomical shell. In 2 LAD and 4LCx cases, the epicardium was mapped by accessingthe pericardial space using the modified Sosa tech-nique (34).

EGM analysis was performed off-line at a sweepspeed of 200 to 400 mm/s on either Carto3 or theLabSystem Pro EP recording system (Bard, BostonScientific, Lowell, Massachusetts). The minimum bi-polar voltage amplitude of collected EGMs was30 mV, which is twice the voltage level in our labo-ratories. All EGMs were manually reviewed to excludeectopic beats and artifacts. Activation time was an-notated to the near-field potential as determined bypresence of high-frequency potentials exhibitingspatiotemporal propagation across multiple elec-trodes at a similar acquired beat (1).

Low voltage areas were measured using the stan-dard surface area measurement tool on the Carto3system. The border of the low voltage area on each

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FIGURE 2 Comparison of Myocardial Wall Thinning

Representative short-axis cine images and extracted left ventricular (LV) and right ventricular (RV) segmentation in diastole from base to apex in both groups show

differences in wall thinning on scar-related walls. Wall thickness is represented in millimeters.



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map was manually traced using Carto3 area mea-surement software. The low voltage burden wascalculated using the mesh feature on the Carto3software (endocardial low voltage area/total endo-cardial voltage area percentage). Low voltage cutoffswere set at 1.5 mV for bipolar amplitude.

HISTOLOGY DATA. In 1 animal from each group, theheart was harvested and placed in a 10% bufferedformalin solution for >1 week. After tissue fixation, 1heart from each group was serially sectioned parallelto the atrioventricular groove into 1-cm-thick slicesstarting from the apex. Tissue samples were paraffinembedded and sectioned at 5-mm thickness perpen-dicular to the epicardial surface so each sectionshowed the full thickness of the ventricular wall from

the epicardium to the endocardium. Slides werestained with Masson’s trichrome for collagen detec-tion and subsequently scanned and digitized. Thehistology technique was not systematically exam-ined; it was only used to validate the scar features.

STATISTICAL ANALYSIS. Continuous variables withnormal distribution are expressed as mean � SD.Categorical variables are expressed as percentages.The independent sample Student’s t-test and Pear-son’s chi-square test were used to compare normallydistributed continuous and dichotomous variables,respectively. For multiple group comparisons, 1-wayanalysis of variance was used with post hoc Bonfer-roni’s correction. The intraclass correlation coeffi-cient was used to assess intra- and interobserver

TABLE 2 EAM Bipolar Voltage Map Parameters Collected During RV Pacing

Scar-related LV Wall* LAD (n ¼ 6) LCx (n ¼ 6) p Value

Density of EGMs 1,533 � 543 618 � 192 0.010

Mean unipolar voltage, mV 3.8 � 0.9 9.3 � 2.1 <0.001

Mean bipolar voltage, mV 1.8 � 0.3 2.8 � 0.2 <0.001

EAM-derived scar

Mean unipolar voltage, mV 2.3 � 0.3 4.6 � 0.6 0.001

Mean bipolar voltage, mV 0.7 � 0.1 1.1 � 0.2 0.001

Endocardial low voltage area,† cm2 13.8 � 1.7 3.0 � 1.6 <0.001

Endocardial low voltage burden,‡ % 7.9 � 0.7 2.1 � 0.2 <0.001

Values are mean � SD. *Scar related wall: anterior for LAD group, inferior for LCx group. †Low voltage: bipolarvoltage <1.5 mV. ‡The Mesh feature on the Carto3 software was used to calculate.

EAM ¼ electroanatomical mapping; EGMs ¼ electrograms; other abbreviations as in Table 1.


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reliability. Analyses were performed using SPSSsoftware v.25.0 (IBM Corporation, Armonk, NewYork) and GraphPad Prism software v.8.0 (GraphPadSoftware, San Diego, California). p Values <0.05 wereconsidered statistically significant.

RESULTS

CMR ANALYSIS. All animals underwent in vivo CMRat a mean day of 60 � 3.6 following myocardialinfarction and at a mean day of 6 � 1.6 before the EAMprocedure.

Table 1 summarizes the comprehensive CMR data.LV end-diastolic and end-systolic volumes weregreater in the LAD group than those in the LCx group.LV mass and LV ejection fraction were similar in bothgroups. The global radial, circumferential, and lon-gitudinal systolic peak strain values were also similarin both of the LAD and LCx groups.

In LAD animals, LGE was present mostly in theanterior myocardial segments, extending from themid-ventricle to the apex (Figures 1A and 1B). In LCxanimals, LGE was observed on the inferior myocardialsegments, extending from the base to the apex(Figures 1C and 1D). LGE scar volume, mass, andburden in in vivo and ex vivo 3-dimensional LGEimages were similar for both groups (Table 1). Toavoid false-positive image results, we also analyzedex vivo images thoroughly and compared in vivo andex vivo images head-to-head (Supplemental Figure S3and Supplemental Table 1).

Areas of LGE scar bordering the blood pool were signif-icantly different between the LAD (12.5� 3.1 cm2) and LCx(4.1 � 1.2 cm2) groups (p < 0.0001) (Table 1 andSupplemental Figure 4). Although LGE scar was moresubendocardial in the LAD group, LCx animals had LGEscars that extended from the endocardium to the epicar-dium with a significant presence in the mid-myocardium(Supplemental Figure 5). There were significant changesinwall thickness between LCx and LAD animals (Figure 2).Although averagewall thickness in healthy remote regionswas similar between groups (LCx: 6.75� 0.38mmvs. LAD:6.66 � 0.42 mm; p ¼ 0.703), wall thickness in scarredsegments was significantly affected in the LAD group (1.78� 0.26 mm), but the scarred region was similar to healthyremote regions in the LCx animals (5.38 � 0.67 mm). Theextent of wall thinning was significant in the LAD group,whereas 73 � 40% of the wall had reduced thickness,consistent with our previous experience (10).

Intra- and interobserver reliability correlation co-efficients for each group were 0.97 (95% confidenceinterval: [CI]: 0.95 to 0.98) and 0.94 (95% CI: 0.8 to0.99) for remote wall thickness measurements, 0.97(95% CI: 0.95 to 0.98) and 0.87 (95% CI: 0.80 to 0.91)

for scarred wall thickness, 0.95 (95% CI: 0.91 to 0.97)and 0.86 (95% CI: 0.78 to 0.93) for LGE volume, and0.98 (95% CI: 0.97 to 0.99) and 0.95 (95% CI: 0.94 to0.99) for the subendocardial LGE area, respectively(Supplemental Table 2).

EAM ANALYSIS. Animals underwent EAM at a meanday of 59.5 (range 56 to 68 days) after infarct induc-tion, with the same survival period for LAD and LCxanimals. We analyzed EGMs on the scar-related walls:anterior wall for the LAD group and inferior wall forthe LCx group (1,533 � 543 vs. 618 � 192 EGMs,respectively; p ¼ 0.01) during RV pacing.

Table 2 shows EGM data for the anterior wall,inferior wall, and EAM-derived scar parameters. Forscar-related walls, the mean bipolar (1.77 � 0.3 mV vs.2.8 � 0.2 mV; p < 0.0001) and unipolar voltages (3.83� 0.9 mV vs. 9.25 � 2.1 mV; p < 0.0001) were lower inthe LAD group. The mean voltage within the EAM-derived scar was higher in the LCx group than thatin the LAD group: 1.12 � 0.2 mV versus 0.7 � 0.1 mV(p ¼ 0.001) for bipolar voltage; and 4.63 � 0.6 mVversus 2.3 � 0.3 mV (p ¼ 0.001) for unipolar voltage,respectively.

The low bipolar voltage (<1.5 mV) area and lowvoltage burden were 13.8 � 1.7 cm2 and 7 � 0.7% ofthe LV in LAD animals compared with 3.8 � 2.9 cm2

and 1.8 � 0.2% of the LV in LCx animals (p < 0.0001for both).

Epicardial EAM was performed in 6 of 12 animals (2in LAD and 4 in LCx). Small areas of low bipolarvoltage corresponding to LGE were seen in the LADgroup, indicating LGE presence on the endocardialanteroseptal location in both swine. However, therewere no areas of low bipolar or unipolar voltage in theLCx group corresponding to LGE scar (SupplementalFigure 6).

CONCORDANCE BETWEEN SCAR DETECTION USING

CMR AND EAM. In an all-swine analysis, wall








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FIGURE 3 Distribution of Bipolar and Unipolar Voltage Amplitudes

Bar plots show the (A) inverse association between mean bipolar (red bars) and unipolar (blue bars) voltage amplitudes and wall thinning

grade in all animals. (B) Comparison of mean bipolar (red bars) and unipolar (blue bars) voltage amplitudes between LV walls with LGE for both

groups. The LAD group with an anterior scar shows lower bipolar voltage amplitude than that in the LCx group with an inferior scar. Abbre-

viations as in Figures 1 and 2. * and " indicates p < 0.0001.



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thinning percentage (graded: <25% [mild], 25% to75% [moderate], >75% [severe]) was inversely asso-ciated with mean bipolar voltage (mild vs. moderate:2.70 � 1.4 mV vs. 2.26 � 1.4 mV; p < 0.0001; mild vs.severe: 2.70 � 1.4 mV vs. 1.14 � 1.2 mV; p < 0.0001;moderate vs. severe: 2.26 � 1.4 mV vs. 1.14 � 1.2 mV;p < 0.0001) (Figure 3A) and with mean unipolarvoltage (between mild and moderate: 7.14 � 2.9 mVvs. 6.23 � 3.5 mV; p < 0.0001; between mild and se-vere: 7.14 � 2.9 mV vs. 3.33 � 2.3 mV; p < 0.0001;between moderate and severe: 6.23 � 3.5 mV vs. 3.33� 2.3 mV; p < 0.0001) (Figure 3B). There were signif-icant differences in mean bipolar (0.63 � 0.69 mV vs.2.52 � 1.35 mV; p < 0.0001) (Figure 3A) and unipolarvoltages (2.28 � 0.84 mV vs. 7.23 � 2.94 mV;p < 0.0001) (Figure 3B) between scar-related LV wallsfor both groups (anterior wall for LAD, inferior wallfor LCx).

On EAM, all LAD animals had a large low bipolarvoltage area compatible with LGE-derived scar fea-tures. However, only 2 of 6 animals in the LCx grouphad low bipolar voltage areas, despite having asimilar large LGE scar on in vivo and ex vivo CMR,and histopathological gross as well (Figure 4,Supplemental Figure 6-8 and Supplemental Table 3).LGE scar in the LAD group corresponded with lowvoltage areas on EAM, whereas LGE scar in the LCx

group did not correspond with low voltage EAM areas(Central Illustration). Full dataset for each pig is alsoavailable in the Supplemental Tables 4 and 5.

HISTOPATHOLOGICAL ASSESSMENT. LGE-derivedscar was validated histologically in both groups. Inaddition, 1 swine from each group showed visualcorrelation between histology samples and CMR im-ages in both in vivo and ex vivo scans with respect toscar extension into the myocardial segment from 1swine for each group (Supplemental Figures 4 and 9).Preserved myocardial tissue was more notable in aslice from the LCx animal.

DISCUSSION

In this preclinical study, we demonstrated the limi-tations of EAM in identifying LGE scar. The discor-dance between low voltage EGMs on EAM and LGEscar highlighted the limitation of catheter mapping toidentify large scar extending from the endocardiumto epicardium within a normal wall thickness.

Despite similar LGE scar sizes between both animalgroups, there were differences in LGE scar charac-teristics. Infarction in the LAD group caused signifi-cant remodeling with greater wall thinning, whichresulted in better LGE scar detection by catheter





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FIGURE 4 Electroanatomic Characterization of Post-Infarct Scars

EAM bipolar and unipolar voltage maps for each animal (left column for LAD group and right column for LCx group) showing extensive low

voltage areas in the LAD group (anterior view) but limited low voltage areas in the LCx group (inferior view). Only 2 animals had EAM-derived

scar areas that were mostly mismatched with LGE-derived scar. Abbreviations as in Figure 1.


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CENTRAL ILLUSTRATION Mismatch in Scar Delineation Between Electroanatomical Bipolar/Unipolar Voltage Mapsand Late Gadolinium Enhancement

Kucukseymen, S. et al. J Am Coll Cardiol EP. 2020;6(11):1452–64.

Slices on electroanatomical mapping (EAM) bipolar and unipolar voltage maps (dotted lines) corresponding to short-axis 3-dimensional late gadolinium enhancement

(LGE) images showing low bipolar and unipolar voltage areas in the left anterior descending (LAD) group, but nearly normal voltage in the left circumflex (LCx) group

despite scar presence on LGE images. CMR ¼ cardiac magnetic resonance.



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mapping. However, wall thickness was considerablypreserved in the LCx group and in cases in which LGEscars extended from the subendocardial to epicar-dium regions. These differences contributed to thelimitations of catheter mapping in identifying LGEscar.

We and others have extensively used the anteriormyocardial infarction (MI) swine model for investi-gation of ventricular arrhythmia (25,35–38). However,

scars in this model were large and caused wall thin-ning and significant remodeling of the heart (10).With advances in acute MI guidelines and shorterdoor-to-balloon times (39), scars in patients with MIare often much smaller, with preserved wall thick-ness. Therefore, the LCx group might better representscar characteristics in our patients.

Scar identification mismatch between CMR andEAM mismatch might be more common than


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currently anticipated. Catheter mapping sensitivity toidentify scars is highly dependent on the location anddistance of the scar with respect to the epicardium(35). Wolf et al. (35) investigated the correlation be-tween the endocardial potential and infarct trans-murality in an anterior infarction dog model. Theydemonstrated that the extent of infarct transmuralitycould be accurately assessed in vivo using electricalparameters derived from the endocardial surface.Codreanu et al. (19) investigated the correlation ofLGE- and EAM-derived scar in 10 patients who un-derwent post-infarct VT ablation and reported amismatch in infarct surfaces between voltage mapsand LGE in one-third of infarcted areas. Takigawaet al. (40) used a previous version of the mappingcatheter we used to evaluate EGM amplitudes withinthe scar, including near- and far-field componentsbased on bipolar spacing in thin and thick myocardialwalls. They discovered that far-field voltages had apositive correlation with wall thickness; in contrast,near-field voltages had no correlation with wallthickness. This annotation issue was reported as animportant limitation of current EAM systems toexplain why an important number of EGMs showednormal voltages even in transmural scars on CMR(40). Desjardins et al. (41) correlated LGE with EAM inpost-infarct patients and demonstrated a somewhatsignificant correlation between unipolar voltage andscar depth (R ¼ �0.61) but a weak correlation withbipolar voltage (R ¼ �0.47). In post-MI patients,Wijnmaalen et al. (16) showed strong correlation be-tween transmural infarcts and low voltage areas onEAM. Despite this correlation, visual analysis,particularly in patients with inferior MI, showed amismatch between EAM- and LGE-derived scar areas.In these patients with inferior MI, they reportedlarger LGE-derived scar areas than low voltage areason EAM and several scar areas that were not detectedby EAM (16). Unlike the bipolar EGM, the usefulnessof the unipolar EGM to localize scar is not welldefined (42). Unipolar signals have been suggested tohave a larger field of view than bipolar signals, whichallows detection of subepicardial scars during endo-cardial EAM (35,42,43). Hutchinson et al. (42)described endocardial unipolar signal characteristicsin patients with epicardial scars. They identifiedabnormal epicardium using an endocardial unipolarvoltage of <8.3 mV in patients with nonischemiccardiomyopathy and normal LV endocardial bipolarvoltage. Compared with these previous studies(35,42,43), our unipolar voltage cutoff of 5.5 mV waslower. This difference in unipolar voltage cutoffmight be related to the smaller electrode size of themultielectrode catheter or differences in the scar-

related wall thicknesses between LAD and LCx ani-mals. However, the mean unipolar voltage ampli-tudes on scar-related walls in the LAD group were>8.3 mV in our study.

A novel mapping method technique for character-izing and targeting the intramural substrate using aretractable needle within an endocardial catheter isemerging as an effective approach for intra-myocardial mapping and ablation (44–46). Infusionneedle catheters were developed by modifying acatheter originally designed for intramyocardial drugdelivery (47). Unipolar EGMs can thus be recordedfrom the needle, and bipolar EGMs can be recordedbetween the needle and the tip of the catheter. Thisapproach also allows unipolar pacing and radio-frequency delivery (44–49). There are some studiesthat evaluated the safety and effectiveness of intra-mural needle ablation (45,46,49). A larger multi-center study of patients with treatment-refractoryventricular arrhythmias resulted in arrhythmia elim-ination in 48% of patients and improvement inarrhythmia burden (49). Although these novel tech-niques for targeting intramural sources of VT arepromising, their long-term effectiveness, safety, andcardiac complications warrant additional study.

Another mapping challenge with respect to inferiorinfarcts is the presence of scar tissue adjacent to orjust behind papillary muscles. EAM and ablationprocedures in patients in this region may be difficultdue to the lack of contact between the catheter tipand the tissue (50,51). However, this can be poten-tially overcome by flexible bidirectional catheters andadjunct imaging guidance (e.g., intracardiac echo-cardiography), which was used for each animal in thisstudy to avoid false-negative voltage mapping resultsand to improve success rates (50–52).

Several studies reported that advanced cardiacimaging integration techniques resulted in accuratecharacterization of the arrhythmogenic substrate andenhanced ablation procedure efficiency and safety(18,53–55). A total of 157 consecutive patients withventricular arrhythmias were prospectively enrolledby Hennig et al. (53). Diagnosis before performingCMR was based on standard diagnostic tests (echo-cardiography, stress test, and invasive angiography),yet the implementation of CMR determined a newdiagnosis or a diagnostic change in 48 patients. Njeimet al. (54) observed similar findings in 20 patientswith a history of failed ablation who underwent CMRfor substrate identification before a repeat ablationprocedure. In these patients, CMR identified bothepicardial and mid-myocardial scars, indicating thatepicardial mapping might not be effective in patientswith only a mid-myocardial substrate. Similarly, our

PERSPECTIVES

COMPETENCY IN MEDICAL KNOWLEDGE: Sub-

strate mapping using EAM systems during sinus

rhythm is a common approach for identifying the VT

substrate. A bipolar signal threshold of 1.5 mV is often

used to differentiate healthy and scarred regions.

Because there are multiple scar types with different

biophysical features, repeating this standard method

might not be applicable to most scars. In certain cases,

post-infarction remodeling could result in walls with

preserved thickness, thus presenting as a more com-

plex structure with unique electroanatomical proper-

ties. Operators should be vigilant to validate low

voltage areas on EAM even when using multielectrode

mapping catheters. CMR can provide detailed scar

characteristics that might not be readily available with

current state-of-the-art EAM systems.

TRANSLATIONAL OUTLOOK: This preclinical

study examined the sensitivity of EAM unipolar and

bipolar voltage maps to analyze the correlation be-

tween areas of low voltage on EAM- and LGE-derived

scar areas. Our results showed that voltage maps

could not identify all scarred regions and had limited

sensitivity at detecting scar in a thick LV wall.



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LCx swine had preserved epicardium with only mid-myocardial LGE scar, which suggested a lack of cor-relation between epicardial EAM and LGE scar.

STUDY LIMITATIONS. Our study had several limita-tions. The number of animals was small, althoughconsistent with larger preclinical studies. LGE imageswere often collected at mid-diastole, which did notcorrespond to the timing of EAM data collection. Thismight have resulted in spatial registration errors be-tween LGE and EAM. Therefore, we did not performspatial registration between the 2 modalities andinstead analyzed LGE and EAM data independently.The inability to obtain consistently good contact at allpoints when using the Octaray catheter might havecontributed to the reported discordance between lowvoltage area and CMR findings. This was especiallyrelevant for the endocardial surface of the infarctedLCx territory, which was less flat and had moreintracavitary structures than the anterior wall andapex. We used a Thermocool catheter with contactforce in only 2 swine, which showed large normalamplitudes. Further studies using catheters are war-ranted to verify our findings. Comprehensive analysisof epicardial mapping data was not performed,because epicardial mapping was not performed in allanimals. EGM characteristics were not described inthis study and warrant further investigation to betterunderstand the role of EGM morphology among LGE-and voltage-derived scars in thick and thin myocar-dium. Our study was not designed to investigate VTinducibility in our models; therefore, we did notsystematically collect and analyze VT inducibilitydata in all animals. Finally, histological analysis wasnot performed on all animals, which precluded in-depth investigation.

CONCLUSIONS

Our preclinical study demonstrated the limitations ofcurrent state-of-the-art catheter mapping systems toidentify scarred regions extending from sub-endocardial to epicardial regions because of discor-dances between low voltage areas in EAM and

scarring on CMR. Furthermore, voltage maps couldvary significantly between areas of reduced or pre-served wall thickness, regardless of the presence orthe extent of scar.

ACKNOWLEDGMENTS The authors acknowledgecontributions from Biosense Webster for providingassistance in performing the mapping and extractingthe electrogram data.

ADDRESS FOR CORRESPONDENCE: Dr. Reza Neza-fat, Department of Medicine, Cardiovascular Division,Beth Israel Deaconess Medical Center, 330 BrooklineAvenue, Boston, Massachusetts 02215. E-mail:[email protected].

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KEY WORDS cardiac cardiac magneticresonance, electroanatomical mapping,myocardial infarction model, wall thickness

APPENDIX For supplemental figures andtables, please see the online version of thispaper.





































discordance in scar detection between electroanatomical

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