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DOI: 10.1161/CIRCEP.113.000870

1

Reentrant Ventricular Tachycardia Originating from the Periaortic Region in

the Absence of Overt Structural Heart Disease

Running title: Nagashima et al.; Periaortic VT without structural heart disease

Koichi Nagashima, MD, PhD; Usha B. Tedrow, MD, MSc.; Bruce A. Koplan, MD; MPH;

Gregory F. Michaud, MD; Roy M. John, MD, PhD; Laurence M. Epstein, MD; Michifumi

Tokuda, MD, PhD; Keiichi Inada, MD, PhD; Tobias R. Reichlin, MD; Justin P. Ng, MD; Chirag

R. Barbhaiya, MD; Eyal Nof, MD; Thomas M. Tadros, MD; William G. Stevenson, MD

Arrhythmia Unit, Cardiovascular Division, Brigham and Women’s Hospital, Boston, MA

Correspondence:

William G. Stevenson, M.D.

Cardiovascular Division

Brigham and Women’s Hospital

75 Francis St.

Boston, MA, USA 02115

Tel: 1-857-307-1948

Fax: 1-857-307-1944

E-mail: [email protected]

Journal Subject Codes: [106] Electrophysiology, [171] Electrocardiology

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DOI: 10.1161/CIRCEP.113.000870

2

Abstract:

Background - In the absence of overt structural heart disease most left ventricular outflow tract

(LVOT) ventricular tachycardias (VTs) have a focal origin and are benign. We hypothesized that

multiple morphologies (MM) of inducible LVOT VT may indicate a scar-related VT that can

mimic idiopathic VT.

Methods and Results - Of 54 consecutive patients referred for ablation of sustained OT VT

without overt structural heart disease 24 had LVOT VT; 10 had MMVT and 14 had a single VT

(SM). The MM group were older (70.3±4.3 vs. 53.9±15.9 years p=0.004), had more

hypertension (100% vs. 29%, P=0.0006), had longer PR intervals and QRS durations than the

SM group. In contrast to the SM group, the MM group VTs had features consistent with

reentry including induction by programmed stimulation without isoproterenol, entrainment in

some and abnormal electrograms in the periaortic area. Periaortic region voltages suggested

scar in the MM group, but not the SM group. Magnetic resonance imaging in 2 MM patients

was consistent with scar, but not in 10 SM patients. Longer radiofrequency applications were

required in the MM group than the SM group. At a median follow-up of 9.7 (3.0, 32.0) months,

recurrences tended to be more frequent in the MM group than the SM group (70% vs. 22%,

P=0.07).

Conclusions - VTs from small regions of periaortic scar can mimic idiopathic VT but are

suggested by multiple VT morphologies and are more difficult to ablate. Whether these

patients are at greater risk, as feared for other scar-related VTs, warrants further study.

Key words: ventricular tachycardia, catheter ablation, reentry, periaortic region, structural normal heart

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MM group, but not the SM group. Magnetic resonance imaging in 2 MM patie

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DOI: 10.1161/CIRCEP.113.000870

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Introduction

Ventricular tachycardia (VT) originating from the periaortic region can occur in the absence of

structural heart disease.1, 2 These VTs are generally categorized as idiopathic and often have

features consistent with triggered activity due to delayed after depolarizations.3, 4 A single

morphology of VT originating from a focal site is typical, although exceptions having multiple

morphologies of VTs have been reported.5 Areas of ventricular scar can occur along the valve

annuli in cardiomyopathies and give rise to VT that often has characteristics consistent with

reentry. We have observed what appear to be scar-related VTs from the periaortic area in

patients with no other evidence of structural heart disease, but these have not been well described.

Some patients have multiple morphologies of VT that is more consistent with scar-related VT

than idiopathic focal VT. The aim of this study is to characterize the VTs and VT substrate that

gives rise to periaortic VT; and specifically to assess the presence of electrogram evidence of

scar in the region and the relation between VT characteristics, including multiple morphologies

of VT, and scar.

Methods

Patient characteristics

From a consecutive series of 54 patients (32 male; age 54.2±14.0 years) who underwent ablation

at our institution for sustained monomorphic VT (SMVT) originating from outflow tract (OT)

area in the absence of structural heart disease from January 2004 to April 2013, the 24 patients

who had SMVT originating from the periaortic region were included. Patients with a clinical

history of only nonsustained (NS) arrhythmias were excluded. All patients underwent an

assessment for the presence of overt structural heart disease with physical examination, 12-lead

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electrocardiography (ECG), chest x-ray, transthoracic echocardiography (TTE), exercise or

pharmacologic stress testing and/or coronary angiography. Magnetic resonance imaging (MRI)

was often limited by prior implantable cardioverter defibrillator (ICD) placement and was

performed in only 12 patients. Patients with structural heart disease defined as a history of

coronary artery disease, myocarditis, infiltrative heart disease, valvular heart disease,

hypertensive heart disease with depressed ventricular function [Left ventricular ejection fraction

(LVEF) <45%], congenital heart disease, dilated cardiomyopathy or with LVEF <45% on any

prior imaging study were excluded. All antiarrhythmic drugs except amiodarone were

discontinued for at least 5 half-lives before the procedure. A reference group for periaortic

bipolar voltage was obtained from 9 consecutive patients with no structural heart disease who

had idiopathic PVCs (without VT) originating from the periaortic area who were studied between

April 2012 and April 2013 (4 male; age, 55.2±12.2 years; LVEF, 57.3±7.4 %) as the reference of

voltage map.

Each patient gave written informed consent. Studies and data collection were performed

according to protocols approved by the Human Research Committee of Brigham and Women’s

Hospital.

Electrophysiological study

After local anesthesia femoral venous and/or arterial access was obtained and multipolar

electrode catheters were positioned in the right ventricular (RV) apex and the His bundle region.

Programmed ventricular stimulation for initiation of SMVT was performed with up to 3

extrastimuli scanned to refractoriness or a minimum coupling interval of 180 ms, applied

following a basic drive of 600 ms and then 400 ms from 2 RV sites and burst pacing. If SMVT

was not inducible, programmed stimulation was repeated during intravenous infusion of

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isoproterenol and/or epinephrine. The endpoint of ventricular stimulation was the induction of

SMVT lasting > 30 seconds or requiring termination because of hemodynamic intolerance or a

shortest interstimulus interval of 180 to 200 ms. At the end of the procedure, the same

stimulation protocol was repeated. Acute complete success was defined as the absence of any

inducible SMVT.

Electroanatomical mapping and quantitative assessment of low-voltage area

Electroanatomical mapping was performed (CARTO 3 or XP, Biosense Webster, Inc, Diamond

Bar, CA, USA) using a 3.5-mm-tip open irrigated catheter (NaviStar ThermoCool, Biosense

Webster) or with a 4-mm-tip nonirrigated catheter (NaviStar, Biosense Webster). In 10 patients

the LVOT and aortic root was defined with intracardiac ultrasound imaging (SoundStar,

64-element, 5.5–10.0 MHz, Biosense Webster). In the electroanatomic mapping system bipolar

electrograms were high pass filtered at 20 to 30 Hz and low pass filtered at 400 Hz. Bipolar

electrograms were also band pass filtered from 30 to 500 Hz and digitally recorded along with a

12-lead surface ECG utilizing the Cardiolab EP system (General Electric Healthcare,

Buckinghamshire, UK).

Voltage maps were created during sinus rhythm. Peak-to-peak bipolar electrogram

ampli 6

Low voltage areas >2 cm2 was measured using the standard surface area measurement tool on

the CARTO system (software version 9.0.34 in CARTO XP or 2.3 in CARTO 3).

Mapping protocol and ablation

Mapping of the RV endocardium and proximal pulmonary artery was performed in all patients,

followed by mapping of the great cardiac vein, then the LV endocardium and aortic root.

Epicardial mapping was done if endocardial mapping failed to identify the focus, either at the

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same or a subsequent session. Percutaneous subxiphoid epicardial access was obtained as

previously described.7 All inducible SMVTs were targeted for ablation. If SMVT was not

reliably inducible, NSVT or premature ventricular contractions (PVCs) felt likely to be

originating from the same site, were targeted. Pace-mapping was also used. If VT was

hemodynamically tolerated and reproducibly induced, mapping and ablation was performed

during VT. Sites were targeted for ablation if pacing entrained the SMVT with concealed

fusion and a post-pacing interval (PPI) within 30 ms of the VT cycle length (CL),8, 9 or an

isolated mid-diastolic potential or presystolic potential was present. If focal origin VT was

suspected the site of earliest presystolic electrical activity was targeted for ablation. If VTs

were “unmappable” because of hemodynamic intolerance or poor reproducibility, ablation was

guided by pace-mapping and limited VT electrogram assessment. If a bipolar low voltage area

was present, substrate modification was performed during sinus rhythm targeting presumptive

channels and exits within the low voltage area as identified from a paced QRS morphology

similar to the VT QRS morphology, abnormal fractionated potentials, double potentials or late

potentials during sinus or paced rhythm at sites where pacing captured, particularly if the

stimulus-QRS interval was >40 ms, consistent with abnormal conduction. Pace mapping and

entrainment mapping utilized unipolar stimuli with strength of 10 mA and pulse width of 2 ms.10

Radiofrequency (RF) energy was delivered at a power of 25 to 50 Watts targeting an

impedance drop of 10 ohms. At target areas below the aortic valve (AV) applications were

usually repeated until unipolar pacing at 10 mA at 2 ms stimulus strength failed to capture.11 At

target areas above the AV power exceeding 35 Watts was avoided.

Data collection and follow-up

Data were collected from a centralized system containing records of all patients treated and

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followed at Brigham and Women’s Hospital and all associated Partners Healthcare sites.

Referring cardiologists and primary care physicians were contacted for clinical follow-up of their

patients if necessary.

Statistical Analysis

Continuous variables were expressed as mean ± SD values or median and interquartile ranges are

shown in parentheses, as appropriate. Student’s t-test or Mann-Whitney’s U test was used to

compare continuous variables, depending on whether the values were normally distributed, and

the Fishers exact test was used to compare dichotomous variables. For age adjusted

comparisons we used analysis of covariance for continuous variables and the likelihood ratio test

with logistic regression for dichotomous variables. P <0.05 was considered to be statistically

significant. All statistical analyses were performed with JMP 9 software (SAS Institute, Cary,

NC, USA).

Results

Baseline characteristics

Periaortic SMVT was identified in 24 patients. In 10 patients, multiple morphologies (MM) of

SMVTs were induced (MM group), while only a single SMVT, NSVT or PVC morphology was

induced in 14 patients [single morphology (SM) group]. Characteristics of patients in the SM

and the MM groups are shown in Table 1. Older age (70.3±4.3 vs. 53.9±15.9 years, P=0.004)

and hypertension (100% vs. 29%, P=0.0006) were more frequent in the MM group. However,

there was no significant difference in gender, body mass index, the prevalence of hyperlipidemia

or history of prior ablation between the two groups. No patients had a history of cardiac arrest

in either group. A history of syncope was present in 2 (20%) MM and 5 (36%) SM patients

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(P=0.65). ICDs had been previously placed in 7 (70%) of the MM group, but only 1 patient

(7%) in the SM group.

The MM group had more evidence of mild cardiac impairment often associated with age

and hypertension (table 1). The sinus rhythm QRS duration was longer (115.8±19.3 vs.

94.1±12.6 ms, P=0.004) and left axis deviation was more frequent (-23.8±27.2 vs. 30.5±29.7 °,

P=0.0002) in the MM group compared to the SM group; the PR interval was longer but not

significantly so after age-adjustment. On echocardiography the E/A ratio was lower and the E/e’

ratio was greater in the MM group, consistent with impaired diastolic function,12 as compared to

the SM group. However, there were no significant differences between the two groups with

respect to heart rate, LVEF, interventricular septum thickness, and aortic root diameter. After

age-adjustment, precordial T-wave inversion in 2 or more leads was more frequent in the MM

group compared to the SM group. MRI was obtained in 10 SM group and only 2 MM group

patients, showed an area of late Gadolinium enhancement (LGE) in both MM compared to none

of the SM group, but with these small numbers these differences are not significant.

Electrophysiological characteristics

There were striking differences in VT findings between the MM and the SM groups. A mean of

3 (2, 4) different SMVTs were induced in the MM group. SMVT was more likely to be induced

during the procedure in the MM group (100%) compared to the SM group (36%, P=0.002).

Infusion of isoproterenol or epinephrine to induce SMVT was required in only 10% of the MM

group, but was needed in 71% of the SM group (P=0.005). SMVTs in the SM group were more

likely to occur spontaneously (60% vs. 0%, P=0.02) and less likely to be induced by extrastimli

(0% vs. 70%, p=0.03) as compared to the MM group (although these differences are not

significant after age-adjustment).

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In the SM group the induced VT was felt to be consistent with the clinical VT. This was less

certain for the MM group. In the MM group SMVTs exhibited either right bundle branch block

morphology or left bundle branch block morphology with relatively early precordial transition

and an inferior axis (Figure 1A and Supplemental figure 1). VTs did not differ between the two

groups with respect to QRS duration, bundle branch block configuration in V1, axis deviation

and precordial transition of VT. The MM group VTs tended to have a shorter VTCL than the

SM group (331.0±66.4 vs. 417.2±98.4 ms, P=0.07). Atrial-His bundle interval, His

bundle-ventricular (HV) interval and presence of ventriculo-atrial conduction were similar

between the two groups. The HV interval was prolonged >55 ms in 5 MM and 4 SM patients.

Detailed VT characteristics in the MM group are shown in the supplemental table.

Seven VTs in 3 patients exhibited spontaneous transition to a different VT morphology. Pacing

for entrainment was attempted during 17 VTs in 9 patients in the MM group; constant fusion was

observed in 15 VTs in 9 patients, and progressive fusion was also observed in 2 of these patients.

In 2 patients entrainment with concealed fusion and a PPI <30 ms of the VTCL occurred. In 3

patients attempted entrainment pacing during SMVT induced a different SMVT. Mid-diastolic

potentials were observed in 3 patients. In the SM group entrainment was attempted in 2

patients, and failed to produce constant fusion in either.

Voltage Maps and Electrograms

Bipolar electrogram voltage for the SM and MM groups were compared to those from a

reference group with idiopathic PVCs for maps in which the aortic annulus location was defined

by intracardiac ultrasound in 8 patients in the MM group and 2 patients in SM group (figure 2).

The bipolar voltages at both 1.0 and 1.5 cm from the AV annulus were <1.5 mV in all patients in

the MM group, but were >1.5 mV in all patients in the idiopathic PVC group and in both SM

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group patients. Periaortic region voltages at 1 and 1.5 cm from the aortic root were

significantly lower in the MM patients compared to the idiopathic PVC patients (1.0 cm,

0.55±0.17 vs. 2.46±0.85 mV, P<0.0001; 1.5cm, 0.88±0.32 vs. 3.26±1.19 mV, P<0.0001). In the

MM group the periaortic area of <1.5 mV was 18.5±8.9 cm2 in size.

Some abnormal appearing electrograms in the periaortic region with fractionation, late

potentials or double potentials were observed in all patients in the MM group (Figure 1B and

Supplemental figure 2). At sites with the best pace-map for VT, the S-QRS delay during

pace-mapping was longer (63.0±9.4 ms) in the MM group compared to the SM group (32.1±10.6

ms, P<0.0001; Table 2). At VT termination sites (see below), the local electrogram-to-QRS

interval during VT was longer in the MM group than the SM group [66 (46, 163) vs. 30 (22, 36)

ms; P=0.03].

Ablation

Ablation abolished all inducible VTs in 11 of 14 SM (79%) and 7 of 10 MM patients (70%,

P=0.67). In 5 SM patients ablation was performed during VT, and terminated VT in 4 patients.

In the other 9 SM patients PVCs (n=5) or NSVT (n=4) were targeted as a surrogate marker of VT,

and no arrhythmia was inducible after ablation in 7 patients. The ablation site that abolished

the arrhythmia was in a coronary cusp in 5 of 11 patients and in the great cardiac vein in 1

patient (table 3).

In the MM group ablation was performed during VT and terminated VT in 5 patients (at

the LVOT in 4, left coronary cusp in 1); but all had other morphologies of VT inducible, and

further ablation was performed during sinus rhythm or other induced VTs (table 3). In 5

patients ablation was performed only during sinus rhythm. Ablation at more than one region

was performed in 6 patients. Ablation was performed below the aortic valve in all; in the left

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11

coronary cusp in 2 patients with termination of a VT in one; in the right coronary cusp during

sinus rhythm in 1; and at the basal LV septum below the His bundle in 1. In 4 patients ablation

was also performed in the RVOT opposite the sites of the LV ablation. No RF energy was

delivered from within the pericardial space, although epicardial mapping was performed in 4

patients.

There was no difference in acute success between the 2 groups (Table 2). Total RF

application time was 784.2±243.3 sec in the MM and 427.4±322.4 s in the SM group.

Antiarrhythmic drug therapy was resumed after ablation in 8 (80%) of the MM group [4

amiodarone, 3 Sotalol and 1 dofetilide], and in 2 (14%) in the SM group [1 flecainide and 1

mexiletine]. Follow-up data were obtained in 9 of 14 SM patients and all MM patients. At a

median follow-up of 9.7 (3.0, 32.0) months [12.7 (2.6, 33.7) months in MM patients vs. 9.3 (1.7,

35.4) in SM patients; P=0.68], recurrence of any VT tended to be more frequent in the MM

group compared to the SM group (70% vs. 22%, P=0.07; Table 2).

Discussion

To our knowledge, this is the first study to define two groups of patients with periaortic sustained

VTs in the setting of normal ventricular function. One group has focal VT that is consistent

with idiopathic outflow tract VT. The second group has evidence of reentry in scar in the

periaortic region. Electrophysiological findings consistent with reentry in scar include: (1)

SMVTs induced by ventricular stimulation without isoproterenol or epinephrine infusion; (2)

more than one morphology of SMVT occurring either spontaneously or with repeated

programmed stimulation, pacing during VT, or ablation; (3) ablation in one region abolishing

more than one morphology of VT; (4) entrainment; (5) abnormal electrograms and voltage maps

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12

consistent with scar; and (6) pace-maps with S-QRS delays typically exceeding 40 ms.

The reliability of assessing scar from voltage maps in periannular locations is limited by

the smaller amount of myocardium adjacent to the valve annulus as compared to the body of the

ventricle. Hence studies that defined 1.5 mV as a useful indicator of scar, excluded the

periannular region.6 Similar concerns apply to the use of unipolar electrograms, which were not

evaluated in this study.13 However, lower voltages were present in the periaortic region in the

MM group than in a group of patients with idiopathic PVCs. The bipolar electrogram

amplitude 1 cm distant from the aortic annulus was <1 mV for all patients in the MM group, but

exceeded 1 mV for the reference group and the SM group, suggesting that this < 1 mV at 1 cm

criteria may be helpful in recognizing periaortic scar.

The etiology of scar in the MM group is not clear. Age related fibrosis or mild

cardiomyopathy is possible. Older age and hypertension were more frequent in the MM group

compared to the SM group, as were wider QRS duration and left axis deviation in sinus rhythm

that might reflect mild impairment of the LV conduction system or cardiac remodeling that can

be associated with aging, hypertension or cardiomyopathies.14-16 Echocardiographic evidence

of impaired LV diastolic function is also consistent with these processes and often precedes

development of LV systolic dysfunction.17-20

VTs in the MM group were more difficult to ablate, often require multiple RF

applications, sometimes at sites both below and above the aortic valve annulus, and recurrences

were common. The periaortic region can be thick and intramural reentry circuits are possible,

making ablation challenging. Furthermore, access to the periaortic region is often limited by

the overlying RVOT and pulmonary artery, and more leftward by epicardial fat and coronary

vessels.21, 22 Whether more aggressive ablation approaches could improve outcomes will need

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13

to be carefully evaluated in relation to the potential risk to adjacent structures, including the

aortic and mitral valves, coronary arteries, and the AV conduction system. Further novel

ablation strategies including transcoronary ethanol ablation or needle ablation likely warrant

investigation in these patients.

Whether these VTs are associated with a risk of sudden death, in contrast to the focal

idiopathic VTs that they can mimic, is not clear, but the poor hemodynamic tolerance for some of

these VTs do, raise this possibility. Several of our patients had ICDs implanted prior to referral

for ablation.

MRI with LGE can be useful to detect arrhythmogenic scar in structural heart diseases.23,

24 Although MRI data were available in only 2 patients in MM group, LGE was observed in the

periaortic region in both patients. MRI with LGE may be helpful in recognizing these patients.

Limitations

This is a retrospective descriptive case series, with a relatively small number of patients.

Characterization of the VTs is incomplete in several patients due to hemodynamic intolerance

and difficult reproducibility of sustained VT initiation. Electrophysiological maneuvers and

entrainment were not consistently performed in all patients. The mechanism of the apparent

focal VTs in the SM group is not proven. Although the methods of initiation are consistent with

triggered activity, other pharmacologic maneuvers were not performed and a small reentry circuit

can not be excluded.3, 4 Multiple morphologies of VT due to a focal origin with multiple exits

is also possible.25 The periaortic region can be thick and intramural reentry is possible, such

that the complete circuit was not defined. Our patients are referred for ablation and there are

likely selection biases that preclude an estimate of the frequency of these scar related VTs.

MRI analysis was limited because several patients had ICDs implanted prior to referral.

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Definition of the distance from the aortic annulus was accomplished by electroanatomic

mapping and intracardiac ultrasound which have some degree of measurement error.

Conclusions

There are two distinct groups of sustained monomorphic VTs that originate from the periaortic

area in people with normal ventricular function. The first are focal idiopathic VTs that have

been well documented previously. The second are VTs that are due to reentry in a small region

of periaortic scar, that often give rise to multiple morphologies of VT. We speculate that these

are due to aging or an early presentation of a cardiomyopathic process. The recognition of this

entity has clinical relevance as the VTs seem to be more difficult to ablate, often require multiple

RF applications below and above the valve annulus, and may have a higher risk of recurrence.

Funding Sources: Dr. Nagashima was supported in part by a Medtronic Japan Fellowship. Dr. Reichlin was supported by Swiss National Science Foundation, Prof. Max Cloetta Foundation and Uniscientia Vaduz Foundation.

Conflict of Interest Disclosures: William Stevenson is co-holder of a patent for needle ablationthat is consigned to Brigham and Women’s Hospital. Dr. John serves as a consultant of St. Jude Medical.

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WeWeWeWe sssspepepepecucucuculalalalatetetete tthahahaatt tttt

Thehehehe rrrrececececogogogogninininititititiononoon og g y p y p p g

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clilililininininical releeeevavavancncncnce asasas ttthehehehe VVVTsTsTsTs ssseeeeeem mm tototo bbbe momore ddddififififfififificucultltltlt tttto oo ababbablalll te,,,, ofofofofteteteten nn rerereququququiririreee e mu

tiiiononons ss below www anndd abbboove thththeee vavavalvlvlvlveee aana nununulllus,, aandddd mmmayayayy haavaveeee a aa hhighghhherererer riskkk k oofo reecurrrrrren

Sources: Dr. NaNaNagagg shima was supppppported in pppart byyby a Meddddtronnnicicic Japppan Fellloooowswswswshhhih p.ppas supportrtrtr edededed bbbyyy y SwSwSwSwisi s sss NaNNaN tititiononononalaaal SSSSciciccienenenencececece FFFFouououounddndndatatata ioioioon,n,n,n PPPProroror f.ff.f. MMMMaxaxaxax CCCClolooloetetetettatatata Foundati

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SSSSakakakakururururamamamamototototo o o o M,M,M,M, SSSSatatatatoooofocaaaallll scscscscarararar ddddetetetetececee teteteteddd d bbbb

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nssskikikiki FFFE, Calalala laanss DDDJ,, Gototottltltltliei b b b CDCDCDC ,,, Zaaadddod EE. Liinenennearrrr aablaatattioi n leesionononons s fooorrr r coccontntrolll ooof le venenenntriculllaraa taccchyhyhycardiaaa in patients wwwittth h isiischemmmicii and nonooo ischemmmmic cccardiomyopn. 20000000000;;1; 010101:1112828282 8-8-8-8 121212969696.



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--55555555....

Z Llooo dddd JoJoJoJ nenenesss DMDMDMDM, , g , , , , yn of qrs duration with left ventricular structure and function and risk of heart faile r2

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25. Yamada T, Platonov M, McElderry HT, Kay GN. Left ventricular outflow tract tachycardia with preferential conduction and multiple exits. Circ Arrhythm Electrophysiol. 2008;1:140-142.

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Table 1. Baseline characteristics of SMVT

Variable SM group (n=14)6

MM group(n=10)

P valueAge-adjusted

P valueAge (years) 53.9±15.9 70.3±4.3 0.004 -Male (%) 6(43%) 1(10%) 0.17 0.46Body mass index (kg/m2) 29.4±6.4 28.2±6.2 0.66 0.79Hypertension (%) 4(29%) 10(100%) 0.0006 0.004Hyperlipidemia (%) 6(43%) 8(80%) 0.10 0.85Diabetes mellitus (%) 3(21%) 0(0%) 0.24 0.04SymptomsSyncope 5(36%) 2(20%) 0.65 0.56Asymptomatic 1(7%) 3(30%) 0.27 0.50

Medication-blocker (%) 9(65%) 9(90%) 0.34 0.12

Calcium channel blocker (%) 3(21%) 0(0%) 0.24 0.03Antiarrhythmic drug therapy (%) 5(36%) 4(40%) 1.00 0.93Amiodarone (%) 1(14%) 2(20%) 0.55 0.81

ICD implantation (%) 1(7%) 7(70%) 0.002 0.17History of prior ablation (%) 7(50%) 4(40%) 0.70 0.6212-lead electrocardiogram in sinus rhythmHeart rate (bpm) 63.0±12.2 64.0±9.7 0.84 0.75PR interval (ms) 174.6±32.3 217.5±42.5 0.02 0.18QRS duration (ms) 94.1±12.6 115.8±19.3 0.004 0.03QRS axis (°) 30.5±29.7 -23.8±27.2 0.0002 0.0008Precordial T- 4/14(29%) 5/9(56%) 0.38 0.05

Transthoracic echocardiogramLeft ventricular ejection fraction (%) 57.8±3.9 60.2±10.0 0.43 0.79Interventricular septum thickness (mm) 10.3±2.0 11.0±2.5 0.60 0.93Posterior wall thickness (mm) 11.2±1.9 9.8±1.4 0.14 0.23Aortic root diameter (mm) 32.7±3.9 34.4±3.9 0.41 0.63Left atrial diameter (mm) 40.2±6.6 39.2±12.1 0.87 0.49E/A ratio 1.14±0.04 0.88±0.17 0.008 0.03E/e’ ratio 8.6±2.6 13.9±2.6 0.006 0.06

MRILGE in periaortic region 0/10(0%) 2/2(100%) 0.04 0.97

Values are the mean±SD, median (25th, 75th interquartile range) or n (%). SMVT, sustained monomorphic ventricular tachycardia; SM, single morphology; MM, multiple morphologies; ICD, implantable cardioverter defibrillator; MRI, magnetic resonance imaging; LGE, late gadolinium enhancement.

0.0 343444 0.0.00 1111220.244 0.0.0.0.03030303

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DOI: 10.1161/CIRCEP.113.000870

1

Table 2. Electrophysiological characteristics of SMVT

VariableSM group

(n=14)MM group

(n=10) P value Age-adjustedP value

Baseline measurementsAH interval (ms) 100.7±27.8 121.4±39.4 0.22 0.30HV interval (ms) 48.5±15.1 56.6±10.7 0.22 0.30VA conduction (%) 7(64%) 3(43%) 0.63 0.19

The longest arrhythmis induced during EPSSMVT (%) 5(36%) 10(100%) 0.002 <0.0001NSVT (%) 4(29%) 0(0%) 0.11 0.02PVC (%) 5(36%) 0(0%) 0.05 0.01

Isoproterenol or epinephrine required for VT induction (%) 10(71%) 1(10%) 0.005 0.0007Induced SMVT characteristicsOccurred spontaneously (%)* 3/5(60%) 0/10(0%) 0.02 0.10Induced by burst pacing (%)* 2/5(40%) 3/10(30%) 1.00 0.41Induced by extrastimuli (%)* 0/5(0%) 7/10(70%) 0.03 0.07Hemodynamically untolerated* 0/5(0%) 3/10(30%) 0.51 0.20Number of different VTs 1(0, 1) 3(2, 4) <0.0001 <0.0001

Induced arrhythmia morphologyMean VT cycle length (ms)* 417.2±98.4 331.0±66.4 0.07 0.95Mean QRS duration (ms) 153.7±20.5 158.1±12.0 0.60 0.87Axis (°) 89.4±14.1 81.7±20.9 0.35 0.32RBBB configuration in V1 (%) 7(50%) 7(70%) 0.42 0.78

MappingS-QRS interval at best pace-map site (ms) 32.1±10.6 63.0±9.4 <0.0001 0.0002Local EGM-QRS interval at VT termination site (ms) 30(22, 36) 66(46, 163) 0.03 0.22

AblationRF time (s) 427.4±322.4 784.2±243.3 0.008 0.10Acute complete success (%) 11(79%) 7(70%) 0.67 0.32Antiarrhythmic drug therapy after ablation (%) 2(14%) 8(80%) 0.003 0.20Recurrence (%) 2/9(22%) 7/10(70%) 0.07 0.03

Values are the mean±SD, median (25th, 75th interquartile range) or n (%). *The denominator is the number of patients with SMVT during the procedure. SMVT, sustained monomorphic ventricular tachycardia; SM, single morphology; MM, multiple morphologies; AH, atrial-His bundle; HV, His bundle-ventricular; VA, ventriculo-atrial; EPS, electrophysiological study; NSVT, non-sustained ventricular tachycardia; PVC, premature ventricular contraction; RBBB, right bundle branch block; S-QRS, stimulus to QRS; EGM-QRS, electrogram to QRS; RF, radiofrequency.

0(0%)0(0(0(0(0%0%0%0%))))1(1(1(1(10101010%)%)%)%)

417 2±98 4 331 0±66 4

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DOI: 10.1161/CIRCEP.113.000870

1

Table 3. Ablation Sites

Ablation sitesSM group*

(n=11) MM group**

(n=10)

Above the AV 5 (45%) 3 (30%)

RCC 4 (36%) 1 (10%)

LCC 1 (9%) 2 (20%)

Below the AV 6 (55%) 10 (100%)

LVOT 3 (27%) 10 (100%)

AMC 2 (18%) 3 (30%)

LV basal septum 0 (0%) 1 (10%)

GCV 1 (9%) 0 (0%)

Right ventricle 0 (0%) 4 (40%) SM Group* only acutely successful ablation sites are shownMM Group** each ablation region is counted once per patient SM, single VT morphology; MM, multiple VT morphologies; AV, aortic valve; RCC, right coronary cusp; LCC, left coronary cusp; LVOT, left ventricular outflow tract below the aortic annulus; AMC, Aorto-mitral continuity; GCV, Great cardiac vein.

Figure Legends:

Figure 1. (A) Twelve-lead electrocardiogram morphologies of sinus rhythm (SR) and 5 different

morphologies of VT recorded during electrophysiological study from one patient in the multiple

morphologies (MM) group. VTs exhibit a right or left bundle branch block morphology with

dominant R waves from V3 to V6 and an inferior axis. (B) Sinus rhythm recordings (left hand

panel) and bipolar voltage map of the left ventricle from the same patient as in panel A. At left

r

*VT morphology; MM, multiple VT morphologies; AV, aortic valve; RCC, right coronaryoal continuity; GCV Great cardiac vein

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DOI: 10.1161/CIRCEP.113.000870

2

are recording of 3 ECG leads and the bipolar electrograms from the distal and proximal electrode

pairs of the mapping catheter, illustrating examples of low voltage abnormal electrograms. At

right is the bipolar voltage map with the purple area indicating voltage area of >1.5 mV. The

area of <0.5 mV is colored red. Multicomponent (fractionated) electrograms are indicated by

light pink tags, late potentials by blue tags and double potentials by light blue tags. Ablation

sites are indicated by red tags. His-bundle electrograms are indicated by orange tags.

LV, left ventricle; RAO, right anterior oblique; LAO, left anterior oblique; ABL-d, ablation

catheter distal; ABL-p, ablation catheter proximal; AV, aortic valve; MV, mitral valve.

Figure 2. The relation of bipolar electrogram voltage versus distance from the aortic valve

annulus are plotted for the multiple morphologies group (MM group – dotted lines), idiopathic

premature ventricular contraction group (PVC group – solid lines) and single morphology group

(SM – dashed lines). The voltages at 1.0 and 1.5 cm caudal to the aortic valve annulus are <1.5

mV in all patients in the MM group, but are >1.5 mV in all patients in the SM and the PVC

group.

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hed lines).))) TTTThehehehe vvvvololololtatatat gegegeges sss ataata 111.0000 aandndndnd 111.5555 ccccm mmm cacacacaududududalalalal tttto ooo ththththe aoaoaoaortrtrtrticicicic vvvvalalalalveveveve aaaannnnnnnnuluu us are < by guest on May 25, 2018


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I

III

II

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

VT4VT3VT1SR

A

1000 ms

1 mV

VT5VT2



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I

II

V4

ABL-d

ABL-p

100ms

I

II

V4

ABL-d

ABL-p

I

II

V4

ABL-d

ABL-p

Multicomponent electrograms

Double potentials

Late potentials

B

RAO

LAO cranial

1 mV

AV

AV

MV



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0

1

2

3

4

0 0.5 1 1.5 2

PVC groupSM groupMM group

(mV)

(cm)

Bip

olar

vol

tage

Distance from the aortic annulus



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Eyal Nof, Thomas M. Tadros and William G. StevensonBarbhaiya,M. Epstein, Michifumi Tokuda, Keiichi Inada, Tobias R. Reichlin, Justin P. Ng, Chirag R.

Koichi Nagashima, Usha B. Tedrow, Bruce A. Koplan, Gregory F. Michaud, Roy M. John, LaurenceOvert Structural Heart Disease

Reentrant Ventricular Tachycardia Originating from the Periaortic Region in the Absence of

Print ISSN: 1941-3149. Online ISSN: 1941-3084 Copyright © 2013 American Heart Association, Inc. All rights reserved.

Dallas, TX 75231is published by the American Heart Association, 7272 Greenville Avenue,Circulation: Arrhythmia and Electrophysiology

published online December 20, 2013;Circ Arrhythm Electrophysiol.

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is online at: Circulation: Arrhythmia and Electrophysiology Information about subscribing to Subscriptions:

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document. Permissions and Rights Question and Answerinformation about this process is available in the

requested is located, click Request Permissions in the middle column of the Web page under Services. FurtherCenter, not the Editorial Office. Once the online version of the published article for which permission is being

can be obtained via RightsLink, a service of the Copyright ClearanceCirculation: Arrhythmia and Electrophysiology Requests for permissions to reproduce figures, tables, or portions of articles originally published inPermissions:



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SUPPLEMENTAL MATERIAL

Supplimental table. Mapping characteristics in the MM group

No. Age Sex

VT

No.

CL

(ms)

QRS

interval

(ms)

BBB

Configuration

in V1

Precordial

transition

(Vn)

Axis

(°)

Hemodynamic

tolerance

Ablation

site

Entrainment findings Other findings

S-QRS

interval

(ms)

1. 78 M VT1 266 161 Right <V1 98.6 Tolerated LVOT, LV

basal

septum, and

RVOT

Constant fusion

Entrainment pacing induced VT2

71

VT2 266 176 Left V1-2 2.4 Tolerated Constant fusion Spontaneous transition to VT2 60

VT3 431 161 Left V3 95.6 Tolerated Not done 63

VT4 277 161 Left V2-3 75.7 Tolerated Constant fusion and progressive fusion 59

VT5 311 187 Right <V1 108.4 Tolerated Not done 71

2. 71 M VT1 284 142 Left V1-2 69.3 Tolerated LVOT,

RCC and

RVOT

VT terminated 56

VT2 247 153 Right V1 74.7 Tolerated Not done 63

VT3 236 165 Right V1-2 56.3 Tolerated Constant fusion 71

3. 73 M VT1 337 134 Right <V1 61.7 Not tolerated LVOT,

LCC and

RVOT

Constant fusion Mid-diastolic potential 48

VT2 481 149 Right <V1 74.4 Not tolerated Constant fusion 69

VT3 288 165 Left V1-2 82.7 Not tolerated Not done Mid-diastolic potential 71

4. 74 M VT1 258 180 Right <V1 111.0 Not tolerated AMC and

LVOT

Constant fusion 67

VT2 285 168 Right <V1 115.9 Not tolerated Not done 48

5. 70 M VT1 419 146 Right <V1 76.6 Tolerated AMC and

LVOT

Constant fusion and progressive fusion Spontaneous transition to VT3

Mid-diastolic potential

75

VT2 330 161 Right <V1 105.4 Tolerated Constant fusion Spontaneous transition to VT1 63

VT3 322 161 Right <V1 110.3 Tolerated Constant fusion 89

VT4 442 172 Right V1 82.9 Tolerated Constant fusion


82

6. 67 M VT1 390 151 Right <V1 97.4 Tolerated AMC,

LVOT and

RVOT

Not done 56

VT2 408 168 Left V3 73.1 Tolerated Not done 56

7. 63 M VT1 284 161 Right V1 43.8 Not tolerated LVOT and Not done 48

VT2 288 168 Right <V1 116.0 Not tolerated LCC Constant fusion 78

8. 71 M VT1 390 159 Right V1 74.3 Tolerated LVOT

VT terminated Spontaneous transition to VT2, 3 and 4

Mid-diastolic potential

60

VT2 375 157 Right <V1 72.2 Tolerated Constant fusion


Spontaneous transition to VT1, 3 and 4 48

VT3 311 165 Right <V1 74.1 Tolerated Not done Spontaneous transition to VT1 and 2 N/A

VT4 292 138 Left V2 74.4 Tolerated Not done Spontaneous transition to VT1 N/A

9. 70 M VT1 400 N/A Right <V1 N/A Tolerated LVOT

Not done N/A

VT2 N/A N/A Right <V1 N/A Tolerated Not done N/A

VT3 218 N/A Right <V1 N/A Tolerated Concealed entrainment with PPI <30ms of VTCL N/A

10. 66 F VT1 N/A N/A Left N/A N/A Tolerated LVOT

Concealed entrainment with PPI <30ms of VTCL N/A

VT2 N/A N/A Right <V1 N/A Tolerated Not done N/A

MM, multiple morphologies; VT, ventricular tachycardia; CL, cycle length; BBB, bundle branch block; S-QRS, stimulus-QRS at the best pace-map site; LVOT, left ventricular outflow tract; RVOT, right ventricular outflow tract; RCC, right coronary cusp; LCC, left coronary cusp; AMC, Aorto-mitral continuity; PPI, post-pacing interval; N/A, not available.

Supplemental figures

I

III

II

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

VT3VT1SR

Supplemental figure 1

1000 ms

1 mV

VT2

III

V5

ABL-d

ABL-p

100ms

1 mV

Multicomponent electrograms with late potentials


RAO

AV

Supplemental figure legends


Twelve-lead electrocardiogram morphologies of sinus rhythm (SR) and 3 different

morphologies of VT recorded during electrophysiological study from a patient in the

multiple morphologies (MM) group. As in figure 1, panel A, VTs exhibit right or left

bundle branch block morphology with dominant R waves in the mid and lateral

precordial leads, and an inferiorly directed frontal plane axis.


Sinus rhythm recordings (left hand panel) and bipolar voltage map of the left ventricle

from the same patient as in panel A. At left are recording of 3 ECG leads and the

bipolar electrograms from the distal and proximal electrode pairs of the mapping

catheter, illustrating examples of low voltage abnormal electrograms. At right is the

bipolar voltage map with the purple area indicating voltage area of >1.5 mV. The

area of <0.5 mV is colored red. Multicomponent (fractionated) electrograms are

indicated by light pink tags and late potentials by blue tags. Ablation sites are

indicated by red tags. His-bundle electrograms are indicated by orange tags.

LV, left ventricle; RAO, right anterior oblique; ABL-d, ablation catheter distal; ABL-p,

ablation catheter proximal; AV, aortic valve; MV, mitral valve.

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