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\begin{document}

\title{Successful catheter ablation of postoperative atrial tachycardia with
conduction disturbances: assessment by late-gadolinium enhancement
magnetic resonance imaging and high-resolution electro-anatomical
mapping}



\author[1]{Kazutaka  Nakasone}%
\author[1]{kunihiko kiuchi}%
\author[1]{Mitsuru Takami}%
\author[1]{Yu Izawa}%
\author[1]{Koji Fukuzawa}%
\author[1]{Ken-ichi Hirata}%
\affil[1]{Kobe University Graduate School of Medicine}%


\vspace{-1em}



  
  \date{May 24, 2024}


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\selectlanguage{english}
\begin{abstract}
Atrial tachycardia (AT) in the right atrium often occurs following
open-heart surgery. Catheter ablation for these AT is challenging and
can lead to unintended conduction block. We performed late-gadolinium
enhancement magnetic resonance imaging prior to catheter ablation and
predicted wavefront propagation during SR as well as the slow conduction
zone%
\end{abstract}%



\sloppy


\textbf{Successful catheter ablation of postoperative atrial tachycardia
with conduction disturbances: assessment by late-gadolinium enhancement
magnetic resonance imaging and high-resolution electro-anatomical
mapping}

Kazutaka Nakasone, MD, Kunihiko Kiuchi, MD, PhD, FHRS, Mitsuru Takami,
MD, PhD, Yu Izawa, MD, Koji Fukuzawa, MD, PhD, Ken-ichi Hirata, MD, PhD

Section of Arrhythmia, Division of Cardiovascular Medicine, Department
of Internal Medicine, Kobe University Graduate School of Medicine,
Hyogo, Japan

\textbf{Corresponding author:}

Kunihiko Kiuchi, MD, FHRS

Division of Cardiovascular Medicine, Department of Internal Medicine,
Kobe University Hospital

\emph{7-5-2 Kusunoki-cho, Chuo-ku, Kobe city, Japan}

Fax: (81)-78-382-5859

Telephone: (81)-78-382-5846

E-mail:\emph{kunihikokiuchi@yahoo.co.jp}

\textbf{Financial support:}

The Section of Arrhythmia is supported by an endowment from Medtronic
Japan and Abbott Japan. KH chairs the Section, and KF and KK belong to
the Section. The authors report no relationships relevant to the
contents of this study.

\begin{CJK}{UTF8}{gbsn}\textbf{Conflict of interest:　} \end{CJK}\selectlanguage{english}All authors declare no conflicts of
interest for this article.

\begin{CJK}{UTF8}{gbsn}\textbf{Short title:　} \end{CJK}\selectlanguage{english}Catheter ablation of postoperative atrial
tachycardia

\begin{CJK}{UTF8}{gbsn}\textbf{Total word count:　} \end{CJK}\selectlanguage{english}2204 words

\textbf{Data Availability Statement} \textbf{:} The data underlying this
article will be shared upon reasonable request to the corresponding
author.

ABSTRACT

Atrial tachycardia (AT) in the right atrium often occurs following
open-heart surgery. Catheter ablation for these AT is challenging and
can lead to unintended conduction block. We performed late-gadolinium
enhancement magnetic resonance imaging (LGE-MRI) prior to catheter
ablation and predicted wavefront propagation during SR as well as the
slow conduction zone during tachycardia. LGE-MRI may assist predicting
the conduction disturbance and reducing the risk of unexpected sinus
exit block.

INTRODUCTION

Atrial tachycardia (AT) in the right atrium (RA) often occurs following
open-heart surgery and is difficult to treat. Although 3D mapping
systems have improved treatment rates of AT, catheter ablation (CA) can
lead to unintended conduction block.11\textsuperscript{1}Markowitz, S.
M., Choi, D.Y., Daian, F. et al. ''Regional isolation in the right
atrium with disruption of intra-atrial conduction after catheter
ablation of atrial tachycardia. Journal of Cardiovascular
Electrophysiology 2019;30(10): 1773-1785. Early detection of fibrosis in
RA is hence important. Recently, late-gadolinium enhancement magnetic
resonance imaging (LGE-MRI) has been proposed as a useful tool for
visualization of left atrial fibrosis. 22\textsuperscript{2}Oakes, R.
S., Badger, T.J., Kholmovski, E.G. et al. Detection and quantification
of left atrial structural remodeling using delayed enhancement MRI in
patients with atrial fibrillation.'' Circulation 2009;119(13):
1758-1767.

In this report we describe a successful ablation of postoperative AT in
the RA where LGE-MRI accurately predicted the conduction disturbance.

CASE REPORT

A 53-year-old male was referred to our hospital with dyspnea, and
12-lead electrocardiograms indicated AT. He had undergone surgery at the
age of 9 years for tetralogy of Fallot. At the age of 49 years, he
underwent tricuspid and mitral valvuloplasty, as well as pulmonary
artery replacement for severe tricuspid, mitral, and pulmonary valve
regurgitation, using a superior transseptal approach. On this occasion,
the patient was diagnosed with tachycardia-induced cardiomyopathy
because his heart function dramatically improved after electrical
cardioversion of the AT.

To prevent AT recurrence, CA was conducted. LGE-MRI was performed prior
to CA and showed linear or patchy late-gadolinium enhancements (LGEs) in
the RA (Figure 1 A and B). The long linear LGE reached from the RA free
wall to the septum, and an LGE gap was partly visible near the sinus
node (SN) (Figure 1 A and B, black arrows: long linear LGE, and white
arrows: visual LGE gap). Furthermore, five patchy LGEs were found around
the linear LGE: between the linear LGE and the inferior vena cava (Area
A), below the SN (Area B), and around the posterior septum (Areas C, D,
and E) (Figure 1 A and B). Based on the LGE-MRI, we speculated the wave
front propagation during sinus rhythm (SR) and tachycardia circuits
(Figure 2). The SN was surrounded by the long linear LGE and patchy LGEs
(Areas B and D), where radio frequency (RF) application potentially
risked isolation of the SN (Figure 2 A and D). On the other hand, the
atrioventricular node (AVN) was activated by two pathways through the
low lateral RA (Area A) and the posterior RA (Area C, E). Therefore, we
considered that RF application at the low lateral RA (Area A) could be
performed without compromising safety.

Concerning the possible AT circuit, in addition to cavotricuspid
isthmus-dependent atrial flutter, the following two macro re-entrant ATs
associated with the long linear LGE were considered: (1) incisional AT1,
which turns around at the visual LGE gaps (Figure 2 B and E) and (2)
incisional AT2, which turns around at the septum edge of the long linear
LGE (Figure 2 C and F). If the conduction velocity was decreased in Area
A, it was considered a possible ablation target, as both incisional AT 1
and 2.

An automated high-resolution mapping system (Rhythmia, Boston
Scientific, Marlborough, Massachusetts) clearly demonstrated wide double
potentials at the linear LGE reaching from the RA free wall to the
septum during SR. This indicated conduction block along the linear LGE
(Figure 3 A and C). The activation from the SN propagated posteriorly or
caudally behind the linear LGE. Subsequently, these two activations
turned around both edges of the linear LGE and collided at the tricuspid
valve site of the low lateral RA. Notably, a slightly fragmented atrial
voltage was found at the patchy LGE (Area A), and its conduction
velocity was extremely slow compared to the other patchy LGEs.
Therefore, the AVN was mainly activated by a posteriorly propagated
pathway rather than a caudally propagated pathway.

Clinical AT (Cycle length: 476ms) was easily induced by burst pacing,
and the rhythmic system demonstrated that the activation propagated
clockwise around the long linear LGE (Figure 3 B and D). The
fractionated potentials could be recorded at the patchy LGE (Area A),
where the single RF application could terminate the AT without
prolongation of the PR interval. At the end of the procedure, no AT was
induced. The patient has been free from AT recurrence for six months
after CA.

DISCUSSION

Our case report demonstrated the usefulness of LGE-MRI to assess
conduction delay or block during SR and tachycardia in postoperative
patients. To the best of our knowledge, there has been no previous
report of the relationship between LGE-MRI and conduction disturbances
in postoperative RA.

AT in the RA after open-heart surgery is difficult to diagnose and treat
because of the effects of scar tissue associated with surgery and
pre-existing functional conduction block specific to the RA. In
addition, CA has a potential risk of unintended localized conduction
block in the RA. Furthermore, in some cases, isolation of the lateral RA
may result in complete sinus exit block requiring pacemaker
implantation.\textsuperscript{1} Although this might be prevented if
wavefront propagation during SR was assessed in advance, in many cases
the RF application is performed during tachycardia. Therefore, it is
beneficial to assess fibrosis distribution of the RA prior to the
procedure.

Recently, LGE-MRI has been proposed as a method to assess atrial
fibrosis.\textsuperscript{2} Cardiac fibrosis leads to conduction delay
and local conduction block, which promote functional
re-entry.33\textsuperscript{3}Spach, M. S. and P. C. Dolber. ''Relating
extracellular potentials and their derivatives to anisotropic
propagation at a microscopic level in human cardiac muscle. Evidence for
electrical uncoupling of side-to-side fiber connections with increasing
age.'' Circulation Research 1986;58(3): 356-371. It has been reported
that increased left atrial LGE is associated with lower local conduction
velocity.44\textsuperscript{4} Fukumoto, K., Habibi, M., Ipek, E.G. et
al. Association of left atrial local conduction velocity with late
gadolinium enhancement on cardiac magnetic resonance in patients with
atrial fibrillation. Circulation: Arrhythmia and Electrophysiology
2016;9(3): e002897. In the our case, LGE-MRI was performed in the RA.
This showed a correlation between the LGE sites and conduction delay or
block in high-resolution mapping. Comparing the LGE-MRI and
electro-anatomical mapping, the conduction velocities were slower in
Areas A and D than in Area B, despite similar patchy LGE sites. This
discrepancy may be caused by the direction of wavefront propagation.
Animal studies have shown that longitudinal conduction velocities are 2
to 10 times faster than transversal velocities in the RA, owing to a
uniform longitudinal arrangement of muscle fibers and non-uniform
distribution of connexins to the interstitial
collagen.55\textsuperscript{5} Gonzalez, M. D., Erga, K.S., Rivera, J.
et al. Rate-dependent block in the sinus venosa of the swine heart
during transverse right atrial activation: Correlation between
electrophysiologic and anatomic findings. Journal of Cardiovascular
Electrophysiology 2005;16(2): 193-200. This suggests that, although
fibrosis causes conduction delay, transversal fibrosis causes a more
pronounced conduction delay and may form the basis of the re-entry
circuit.

Linear LGE appeared to have a visual gap in the superior right appendage
on LGE-MRI; however, no conduction across the line during both SR and AT
could be detected. A previous report showed that the visual gap length
in the PV ablation line on LGE-MRI was associated with AF recurrence
after PV isolation, and the threshold for the highest specificity was a
gap length of 4.3 mm.66\textsuperscript{6} Linhart, M., Alarcon, F.,
Borras, R. et al. Delayed gadolinium enhancement magnetic resonance
imaging detected anatomic gap length in wide circumferential pulmonary
vein ablation lesions is associated with recurrence of atrial
fibrillation. Circulation: Arrhythmia and Electrophysiology 2018;11(12):
e006659. In our case, the gap length on LGE-MRI was 2.7 mm. Therefore,
we should have speculated that these small visual gaps might demonstrate
a conduction block.

CONCLUSIONS

By using the LGE-MRI prior to CA, wavefront propagation during SR as
well as the slow conduction zone during tachycardia could be assessed.
After CA of postoperative AT, this may assist in reducing the risk of
unexpected sinus exit block and it may negate the need for pacemaker
implantation.

ACKNOWLEDGMENTS

We would like to thank Editage (\emph{www.editage.com}) for English
language editing.

FIGURE LEGEND\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1: 3D LGE-MRI}

3D LGE-MRI of the RA in the right anterior oblique (RAO) (A) and
posterior-anterior (PA) (B) views. The green areas indicate LGE. The
black arrows show the long linear LGE and the yellow dotted circles show
the patchy one. The white arrows indicate the visual gap of the LGE.

LGE-MRI = late-gadolinium enhancement magnetic resonance imaging; RA =
right atrial; RAO = right anterior oblique; PA = posterior-anterior\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 2: The possible propagation during SR and AT}

The left panel shows the possible SR propagation in the RAO (A) and PA
(D) views. The wavefront propagation from the SN was assumed in three
directions. The first one was to propagate to the upper edge of the
incision line, the second one was to propagate downward from the SN and
bifurcated posteriorly and laterally, and the last one was to propagate
through the gap of the incision line.

The middle one shows one of the possible AT circuits in RAO (B) and PA
(E). The wavefront propagates the RA free wall around the incision line
through the gap.

The right one shows one more possible AT circuit in RAO (C) and PA (F).
The wavefront turns from the free wall to the septum around the linear
LGE.

LGE-MRI = late-gadolinium enhancement magnetic resonance imaging; SR =
sinus rhythm; AT = atrial tachycardia; RA = right atrial; SN = sinus
node; RAA = right atrial appendage; TA = tricuspid annulus; IVC =
inferior vena cava; RAO = right anterior oblique; PA =
posterior-anterior.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{Figure 3 Activation map during SR and AT}

The left panels show the activation map during SR of the RA in the RAO
(A) and PA (C) views. The total activation window was divided into 15
isochronal zones, from red to purple. The wavefront propagation extended
from the SN in three directions. Pathway 1 propagates superiorly with
conduction delay at the superior edge of the incision line. Pathway 2
also propagates posteriorly from the SN. Subsequently, Pathway 1 and 2
collided at the RA posterior wall and propagated to the anteroseptal
wall after the turn at the septal end of the linear LGE. Pathway 3
propagates caudally along the linear LGE and slowly turns around the
edge of the linear LGE. Pathways 2 and 3 collided with the low lateral
RA. The conduction velocities at each site during SR were 136 mm/s in
Area A, 467 mm/s in Area B, 398 mm/s in Area D, and 527 mm/s at the site
without LGE.

The right panels show the activation map during AT of the RA in the RAO
(B) and PA (D) views. The activation map demonstrated that the
activation propagated clockwise around the long linear LGE. The total
activation window was also divided into 15 isochronal zones. Pathway 1
showed slow conduction at the upper edge of the incision line during AT,
conducted superiorly, and then collided with Pathway 2. Pathway 2 was
the main circuit during AT, which was conducted posteriorly through the
sinus venosa. Subsequently, it propagated to the anteroseptal wall after
the turn at the septal end of the LGE. The conduction velocities at each
site during AT were 116 mm/s in Area A, 985 mm/s in Area B, and 520 mm/s
in Area D, and 1257 mm/s at the site without LGE.

SR = sinus rhythm; AT = atrial tachycardia; RA = right atrial; RAO =
right anterior oblique; PA = posterior-anterior; SN = sinus node; LGE =
late-gadolinium enhancement

REFERENCES\selectlanguage{english}
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