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\begin{document}

\title{Left Bundle Pacing in a Patient with Atrio-Ventricular Canal Defect
Presenting with Atrial Standstill and Junctional Bradycardia}



\author[1]{Kostantinos Aronis}%
\author[1]{Eunice Yang}%
\author[2]{Benjamin T. Barnes}%
\author[1]{Ari Cedars}%
\author[1]{Caridad de la Uz}%
\author[1]{Andreas Barth}%
\affil[1]{Johns Hopkins Medicine Division of Cardiology}%
\affil[2]{Johns Hopkins Children's Center}%


\vspace{-1em}



  
  \date{June 14, 2024}


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\selectlanguage{english}
\begin{abstract}
A 37-year-old woman with a history of incomplete atrioventricular canal
and an extensive history of corrective cardiac surgeries presented with
recurrent episodes of acute decompensated heart failure in the presence
of junctional bradycardia with chronotropic incompetence. The initial
plan was to proceed with implantation of a dual chamber pacemaker but
given high index of suspicion for the presence of atrial standstill in
the context of her extensive cardiac surgical history, we performed
electroanatomical mapping and echocardiography at the time of pacemaker
implantation that confirmed atrial standstill. Islands of electrically
functional atrial myocardium were detected. Pacing from these locations
resulted in local atrial capture, but failed to result in global atrial
electrical capture, mechanical atrial contraction, or atrioventricular
conduction. In light of the dismal outcomes of right ventricular pacing
in patients with atrial standstill, we implanted a left bundle branch
pacing lead that resulted in improvement of patient's cardiac output and
prevented future admissions for decompensated heart failure in one year
follow up.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Patients with atrioventricular canal defects that undergo corrective
surgery can experience disturbance of sinus node and atrioventricular
node function with rates up to 19 and 25\%,
respectively.\textsuperscript{1,2} Atrial standstill was first
documented in a case report by Chavez et al. in 1946, and constitutes a
rare clinical condition defined by the absence of atrial electrical and
mechanical activity.\textsuperscript{3} Atrial standstill is
characterized by fibroelastosis and fatty infiltration in the
atrium,\textsuperscript{4} and is a barrier in successful implantation
of atrial leads.\textsuperscript{5} Right ventricular pacing has been
traditionally the only method of pacing in patients presenting with
symptomatic bradycardia in the setting of atrial standstill, but in
limited case series, this commonly results in deterioration of
ventricular function and poor outcomes.\textsuperscript{6}

In this case report, we present a patient with atrioventricular canal
defect and an extensive cardiac surgical history who developed recurrent
episodes of acute decompensated heart failure in the presence of
junctional bradycardia with chronotropic incompetence. Our initial plans
were to proceed with implantation of a dual chamber pacemaker, but we
had high index of suspicion for the presence of atrial standstill in the
setting of her extensive cardiac surgical history. Our aim in reporting
these findings is twofold: (1) to demonstrate how electroanatomic
mapping can be used intra-operatively to evaluate for the feasibility of
atrial lead implantation in patients with atrial standstill and, (2) how
left bundle branch pacing may be a viable alternative for individuals
with complex congenital heart disease and atrial standstill.

\textbf{Case Report}

\emph{Patient History}

Our patient is a 37-year-old woman who was born with incomplete AV canal
defect with complete absence of the interatrial septum, cleft mitral
valve, and a persistent left SVC anomalously connected to the left
atrium. She underwent primum atrial septal defect closure and rerouting
of the left SVC to the right atrium at the age of 1 year old. She had
repeat atrial septal defect patch closure one year later. At the age of
20 years, she developed severe mitral valve regurgitation and underwent
mitral valve cleft repair, annuloplasty, and surgical closure of a
residual atrial septal defect. Two years later she developed atrial
flutter and underwent ablation of typical cavo-tricuspid isthmus atrial
flutter. At the age of 35 years, she developed mitral valve stenosis and
atrial fibrillation for which she underwent mitral valve replacement
with a 25 mm bioprosthetic Mosaic valve (Medtronic) and bi-atrial Maze
procedure. Her post-surgical course was further complicated by
development of constrictive pericarditis for which she underwent
pericardial stripping 7 months following mitral valve replacement. Her
medical history is also notable for morbid obesity with a body mass
index of 38 kg/m\textsuperscript{2}, heart failure with preserved
ejection fraction, asthma, chronic pain with opioid use disorder and
bipolar disorder. A year prior to her current presentation, she had
recurrent episodes of acute decompensated heart failure that were
attributed to medication non-adherence. Review of her electrocardiograms
revealed episodes of sinus rhythm with marked first degree
atrioventricular conduction delay and junctional bradycardia.

At the age of 37 she was admitted to the cardiac intensive care unit of
the Johns Hopkins Hospital with acute decompensated heart failure and
hypotension requiring norepinephrine support. Her echocardiogram showed
normal left ventricular size and function with an ejection fraction of
65-70\%, moderate pulmonary hypertension (estimated right ventricular
systolic pressure of 54 mmHg) and mild bioprosthetic mitral valve
stenosis with a mean gradient of 8 mmHg and estimated mitral valve
orifice of 1.5 cm\textsuperscript{2} by the pressure half-time method.
Despite her normal left ventricular ejection fraction, her stroke volume
indexed to her body surface area was 38 mL/m\textsuperscript{2} and at a
heart rate of 69 bpm her cardiac index was 2.6
L/min/m\textsuperscript{2} which is borderline low. Her ECG showed a
junctional rhythm with rates between 50-60 bpm (Figure 1). She was not
on any atrioventricular nodal blocking agents and thus her heart rate,
in the setting of decompensated heart failure, was thought to represent
chronotropic incompetence. No evidence of atrial activity or
atrioventricular block was noted for the period that patient was on
electrocardiographic monitoring. She was diuresed using IV furosemide
and norepinephrine was weaned off 24 hours after her admission. A right
heart catheterization was performed when patient was felt to be
clinically euvolemic and showed a pulmonary capillary wedge pressure of
19 mmHg, cardiac index of 2.74 L/m/m2, and systemic vascular resistance
index of 1821 dyn*sec*cm\textsuperscript{-5}/m\textsuperscript{2}. In
view of her recurrent hospitalizations for acute decompensated heart
failure in the setting of borderline cardiac indices and junctional
rhythm/bradycardia with chronotropic incompetence a multi-disciplinary
meeting between adult congenital heart disease teams (AC), pediatric
cardiology/electrophysiology (CU) and adult electrophysiology (KA, AB)
was held. The prevailing hypothesis was that her junctional rhythm and
chronotropic incompetence contribute to her recurrent episodes of acute
decompensated heart failure.

A decision was made to proceed with implantation of a dual chamber
pacemaker with physiologic pacing. The patient was anticipated to have a
very high percentage of ventricular pacing given the previously
documented significant prolongation of the PR interval and thus the
rationale behind pursuing physiologic pacing was the desire to avoid
right ventricular apical pacing that has the potential to result in a
decline in LV systolic function and worsen heart failure. Furthermore,
given the extensive surgical and ablation history involving the
patient's atria, it was anticipated that her right atrium would be
severely fibrosed and intra-atrial conduction block might be present.
Peri-procedural electroanatomic mapping was therefore arranged to guide
placement of the right atrial lead.

\emph{Electroanatomic Mapping of the Right Atrium and Implantation of
Permanent Pacemaker at the Left Bundle Branch Procedure}

The patient was brought to the electrophysiology laboratory and two
venous vascular sheaths (8.5Fr SR-0 and 9F) were inserted in the right
femoral vein. Next, a multielectrode electrophysiology mapping catheter
(Penta-Ray, Biosense Webster) was advanced under fluoroscopic guidance
to the right atrium via the SR-0 sheath. An intracardiac
echocardiography catheter was advanced into the right atrium via the
long 9F sheath and assisted with delineation of critical anatomic
structures such as the interatrial septum, the tricuspid valve annulus,
and the aortic valve cusps. Using an electroanatomic mapping system
(CARTO, Biosense Webster) a detailed map of the right atrium extending
up to the right and left superior vena cava was made (Figure 2A). The
entire right atrium was severely fibrosed. There were 3 isolated islands
of surviving atrial tissue. The first was in the anterolateral right
atrium/right atrial appendage, the second was located in the superior
septal aspect of the right atrium, close to the junction with the left
superior vena cava, and the third was located distal in the left
superior vena cava, that likely constituted the posterior wall of the
left atrium. Pacing from all 3 locations confirmed local atrial capture
by the electrograms of the adjacent Penta-Ray electrodes (Figure 2B).
However, there was no evidence of global atrial capture (no P-wave on
surface ECG) and simultaneous transthoracic echocardiogram performed by
the pediatric cardiology team during atrial pacing demonstrated no
mechanical atrial contraction during atrial pacing. Furthermore, the
local atrial capture did not result in ventricular activation, likely
due to intra-atrial conduction block from the prior surgeries.
Therefore, the decision was made to abandon atrial lead placement (to
minimize lead burden) and proceed with single-chamber physiologic
pacing. A 5 French multipurpose diagnostic angiography catheter was
introduced from the SR 0 sheath into the right subclavian vein and
contrast venography was performed showing normal right-sided vein
anatomy and patent veins. The sheaths were removed from the body and
hemostasis was achieved with a figure-of-eight hemostatic suture.

Following infiltration with 1\% lidocaine, a right infraclavicular
prepectoral pocket was created. Under direct fluoroscopic guidance, the
axillary vein was entered once. A 9Fr sheath was inserted into the vein
using the modified Seldinger technique. A deflectable sheath (Medtronic
SelectSite C304-His) was inserted over a guidewire to the right
ventricular apex. Using orthogonal fluoroscopic views this sheath was
withdrawn back approximately to a distance one third from the tricuspid
valve plane and was rotated septally. A fixed helix lumenless lead
(Medtronic 3830) was then deployed in the septum. The initial pacing QRS
morphology had the ``W sign'' on lead V1. The lead continued to be
rotated with periodic assessment of the QRS morphology during pacing and
the pacing impedance, until there was a slight decrease in the pacing
impedance. At the final lead position, the pacing QRS morphology had a
qR morphology and time from pacing stimulus to peak R-wave in lead V5
was 80 ms, consistent with left bundle branch capture (Figure 3A).
Intra-operative echocardiographic assessment showed that during
junctional rhythm her stroke volume index was 43.8
mL/m\textsuperscript{2} and with a heart rate of 57 bpm corresponded to
a cardiac index of 2.5 L/min/m\textsuperscript{2}, when patient was
paced VVI at 75 bpm her stroke volume index remained 45.2
mL/m\textsuperscript{2} and her cardiac index increased to 3.4
L/m2/m\textsuperscript{2}. Stimulation and sensing thresholds were found
to be satisfactory. The lead was then checked at 10V output, and no
diaphragm stimulation was noted. After the lead was placed into the
connector, the generator was inserted into the pocket and the pocket was
then closed in multiple layers of absorbable suture. The final lead
parameters were impendence 532 ohms, R-wave 7.3 mV, capture threshold
0.5 V at 0.4 msec. The device was programmed as VVIR 60 to 120 bpm.
Patient was discharged home the following days (Figure 3B).

\emph{Patient Follow-up}

The patient has not had any additional admissions for acute
decompensated heart failure in the one year following implantation of
conduction system pacing. She had one admission 6 months after
implantation for community acquired pneumonia (treated with antibiotics)
and a second admission one month later for COVID-19 pneumonia. Her
baseline functional status is improved. Her lead parameters have been
stable with capture 0.75V@ 0.4ms, sensing at 11.4 mV and impedance of
418 ohms.

\textbf{Discussion}

Atrial standstill is a rare condition defined by the lack of atrial
electrical and mechanical function, and it may be intermittent or
permanent, partial or total, and congenital or acquired (myocardial
disease or metabolic/toxic).\textsuperscript{1-3,6} Myocardial causes of
acquired atrial standstill include surgical myocardial
injury,\textsuperscript{7,8} acute
myocarditis,\textsuperscript{9,10}myocardial
infarction,\textsuperscript{11} cardiac sarcoidosis,\textsuperscript{12}
mitral valve stenosis,\textsuperscript{13} rheumatic heart
disease,\textsuperscript{14} and muscular
dystrophy.\textsuperscript{15}Histologically, atrial standstill is
characterized by fibroelastosis and fatty infiltration in the
atrium.\textsuperscript{4,6,16} In limited studies it is suggested that
the disease starts at the high lateral right atrium and progresses
towards the lower right atrium to finally involve the tricuspid valve
annulus.\textsuperscript{4,6,16} Clinically, atrial standstill manifests
as symptomatic bradycardia with dizziness, syncope, dyspnea, heart
failure, and stroke or systemic embolism.\textsuperscript{1-3,6} In the
case that we present here, atrial standstill was likely caused by her
extensive prior cardiac surgery and biatrial maze procedure and likely
contributed to recurrent admissions for acute decompensated heart
failure.

Given the rarity of this condition, currently there are no guidelines or
consensus statements to guide treatment of patients with atrial
standstill. It is generally accepted that systemic oral anticoagulation
is warranted to minimize the risk of thromboembolic complications. In
cases of symptomatic bradycardia, implantation of a permanent pacemaker
is indicated. In limited case reports of patients with partial atrial
standstill identification of a site that allows atrial capture and
atrioventricular conduction has been helpful to guide atrial lead
placement.\textsuperscript{16-18} In these patients a dual chamber
pacemaker was implanted. However, given the potentially progressive
nature of the disease, frequent evaluation of atrial capture and
atrioventricular conduction is warranted. In the case that we present
here, although our patient had some islands of electrically active
myocardium, local capture of this myocardium did not result in
atrioventricular conduction, due to inter-atrial conduction block, and
thus implantation of an atrial lead was not pursued.

Right ventricular pacing has been used in patients with atrial
standstill and inability to place an atrial lead. However, in limited
studies, right ventricular pacing in patients with atrial standstill has
resulted in deterioration of ventricular function and poor
outcomes.\textsuperscript{6} Thus, physiologic left bundle pacing has
the potential to preserve LV systolic function in cases of adult
congenital heart disease where the underlying anatomy precludes or
complicates placement of a coronary sinus lead (e.g. persistent left
superior vena cava). Single chamber left bundle branch pacing has been
used in a case report of a 46 year-old man who presented with syncope
from atrial standstill and bradycardia-induced torsades de pointes, in
the setting of a giant right atrium.\textsuperscript{19} In this case,
the operators macroscopically mapped the right atrium during the
permanent pacemaker implantation procedure and did not identify any
viable atrial tissue. Contrary to our case, an electroanatomic mapping
system or a multi-electrode mapping catheter was not used. Prospective
follow up of the patient was not reported in the previous case report.
Our patient did not have any readmissions for acute decompensated heart
failure, following implantation, which represents a marked improvement
of her heart failure status, considering that the year prior to the
implant she had multiple admissions for acute decompensated heart
failure.

To summarize, we present a case report of left bundle branch pacemaker
implantation in a 37-year-old woman with atrial standstill, likely as a
sequalae to an extensive cardiac surgery history, and recurrent
admissions for acute decompensated heart failure in the setting of
junctional bradycardia. By implanting a left bundle branch pacemaker and
increasing her heart rate without introducing inter-ventricular
dyssynchrony, we were able to acutely improve her hemodynamics and
cardiac output both in the short term, as well as in long-term
follow-up, with no additional admissions for acute heart failure
decompensation following device placement.

\textbf{Key Teaching Points}

\begin{itemize}
\tightlist
\item
  Atrial standstill is a rare clinical entity characterized by the
  absence of atrial electrical and mechanical activity and can occur in
  patients with extensive cardiac surgical history.
\item
  In patients with suspicion of atrial standstill, electro-anatomical
  mapping and echocardiography can be used at the time of pacemaker
  implantation to assess for the presence of any electrically functional
  atrial tissue.
\item
  In patients with atrial standstill, even in the presence of islands of
  electrically functional atrial tissue, interatrial conduction block
  may result in the absence of atrial mechanical function and
  atrioventricular conduction.
\item
  Left bundle pacing is feasible in patients with atrial standstill and
  bradycardia; it can result in improvement of cardiac output by
  correction of bradycardia without the potential deleterious effects of
  right ventricular apical pacing.
\end{itemize}

\textbf{References}

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2. Haneda K, Togo T, Sato N, Ogata H, Mohri H. Late results after repair
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4. Rosen KM, Rahimtoola SH, Gunnar RM, Lev M. Transient and persistent
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5. Bellmann B, Roser M, Muntean B, Tscholl V, Nagel P, Schmid M,
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11. Koshimizu TA, Komori S, Ishihara T, Kohno I, Umetani K, Sawanobori
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14. Yoneda S, Murata M, Ueda A, Sato M, Takahashi M, Ito T, Sada T,
Matsumoto S, Ito Y, Furuta S, et al. Persistent atrial standstill
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15. Boriani G, Gallina M, Merlini L, Bonne G, Toniolo D, Amati S, Biffi
M, Martignani C, Frabetti L, Bonvicini M, et al. Clinical relevance of
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17. Suzuki Y, Takei A, Takahara H, Taniguchi Y, Ozawa T, Inoue N. A case
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19. \textless{}fcvm-09-836964.pdf\textgreater{}. doi:
10.3389/fcvm.2022.836964

\textbf{Figures}

\textbf{Figure 1.} Patient's ECG upon her admission. Junctional
bradycardia at a rate of 60 bpm. Incomplete right bundle branch bock
with left axis deviation and poor precordial R-wave progression
suggesting left anterior fascicular block.

\textbf{Figure 2.} \textbf{2A} Electro anatomical mapping of the right
atrium and superior vena cava. The left superior vena cava has been
surgically connected to the right atrium. There were 3 ``islands'' of
electrically active atrial myocardium at the (a) anterolateral right
atrium/right atrial appendage, (b) superior septal aspect of the right
atrium, close to the junction with the left superior vena cava, and (c)
distal in the left superior vena cava (likely constituting the posterior
wall of the left atrium). \textbf{2B} Example of pacing from the
multi-electrode mapping catheter in location (a). There is local atrial
capture as demonstrated by the atrial electrograms in the neighboring
electrodes. However, there is no global atrial capture as demonstrated
by the lack of P-wave on ECG, lack of mechanical capture demonstrated by
doppler echocardiography (not shown) and lack of atrioventricular
conduction due to inter-atrial block. Local capture without global
capture, mechanical atrial contraction, and atrioventricular conduction
was demonstrated in all three locations (a) through (c).

\textbf{Figure 3.} \textbf{3A} Patient's ECG post implantation of the
left bundle branch pacing lead. Ventricularly paced rhythm with narrow
QRS complex, qR complex in lead V1 and lead aVR/aVL discordance. Time
from pacing stimulus to peak of QRS complex in lead V5 is 80
ms.\textbf{3B} Anterior-posterior chest X-ray showing the final position
of the left bundle branch pacing lead in the proximal interventricular
septum.\selectlanguage{english}
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