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\begin{document}

\title{Title : Recurrent syncope late after permanent pacemaker implantation -
What is the mechanism?}



\author[1]{Debabrata Bera}%
\author[1]{Radhey Shyam Joshi}%
\author[1]{Mrityunjay Bauri}%
\author[2]{Anunay Gupta}%
\affil[1]{Rabindranath Tagore International Institute of Cardiac Sciences}%
\affil[2]{Vardhman Mahavir Medical College and Safdarjung Hospital}%


\vspace{-1em}



  
  \date{May 27, 2024}


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\selectlanguage{english}
\begin{abstract}
A 68-yr-old lady underwent a VVI pacemaker implantation 10 years back
for infra-hisian complete heart block. Now she presents with 3 episodes
of syncope within the last 2 months. Detailed neurological evaluation
and pacemaker checkup was initially unremarkable. Real time electrograms
during device interrogation were suspicious of lead noise resulting in
oversensing. She became alright when the pacing mode was made VOO
immediately. After discussion with patient relatives she underwent
ventricular lead replacement and upgradation to a dual chamber
pacemaker. However, in the immediate post-operative period she became
unresponsive requiring immediate resuscitation. Monitor suggested short
runs of polymorphic VT which was reproducibly suppressed with higher
rate obligatory pacing @ 110 bpm. The runs of VT resurfaced immediately
as the rate was lower than 90. She was managed by overdrive pacing at a
lower rate of 110 bpm. Over the next 2 months the lower rate was brought
down to 70 bpm in a stepwise manner. A retrospective analysis of her
initial stored device electrogram suggested that it was all PMVT and no
noise at all. The cause of her polymorphic VT is not clear. Relative
hypomagnesemia, late presenting long QT syndrome and long term VVI
pacing in isolation or combination remain the probable offender. She is
presently doing well on oral propranolol.%
\end{abstract}%



\sloppy


\textbf{Title page}

\textbf{Title~} : Recurrent syncope late after permanent pacemaker
implantation - What is the mechanism?

\textbf{Short title:} Syncope long after VVI pacemaker- lead noise or
VT?



\textbf{Authors~}

Debabrata Bera, DM, Dept Cardiology, RTIICS, Kolkata. India.

Radhey Shyam Joshi, MD, Dept of Cardiology, RTIICS, Kolkata. India.

Mrityunjay Bauri, PGDCC, Dept of Cardiology, RTIICS, Kolkata. India.

Anunay Gupta, VMMC and Safdarjung Hospital, New Delhi, India.



\textbf{Corresponding author:}

Debabrata Bera. Rabindranath Tagore International Institute of Cardiac
Sciences (RTIICS), 124 Mukundapur, Kolkata. West Bengal, India. PIN-
700099.

Ph: +91-8013894181, Fax: +91-33 2426 4204.Email- debu2000pgi@gmail.com

\textbf{Keywords:} Ventricular tachycardia; Polymorphic VT; VVI
pacemaker.

Funding: None

\textbf{Conflict of interest:} None.

\textbf{Acknowledgements: None.}

\textbf{Word Count: 995.}







\textbf{Abstract~}

A 68-yr-old lady underwent a VVI pacemaker implantation 10 years back
for infra-hisian complete heart block. Now she presents with 3 episodes
of syncope within the last 2 months. Detailed neurological evaluation
and pacemaker checkup was initially unremarkable. Real time electrograms
during device interrogation were suspicious of lead noise resulting in
oversensing. She became alright when the pacing mode was made VOO
immediately. After discussion with patient relatives she underwent
ventricular lead replacement and upgradation to a dual chamber
pacemaker. However, in the immediate post-operative period she became
unresponsive requiring immediate resuscitation. Monitor suggested short
runs of polymorphic VT which was reproducibly suppressed with higher
rate obligatory pacing @ 110 bpm. The runs of VT resurfaced immediately
as the rate was lower than 90. She was managed by overdrive pacing at a
lower rate of 110 bpm. Over the next 2 months the lower rate was brought
down to 70 bpm in a stepwise manner. A retrospective analysis of her
initial stored device electrogram suggested that it was all PMVT and no
noise at all. The cause of her polymorphic VT is not clear. Relative
hypomagnesemia, late presenting long QT syndrome and long term VVI
pacing in isolation or combination remain the probable offender. She is
presently doing well on oral propranolol.

\textbf{Case~}

A 68-yr-old lady underwent a VVI pacemaker {[}Verity ADx XL SR{]}
implantation 10 years back for baseline bifascicular block with
intermittent complete heart block. She was doing well with annual follow
up. Now, she presents with 3 episodes of syncope within the last 2
months. Detailed evaluation of pacemaker and extensive neurological work
was unremarkable during one of the prior hospital admissions. Device did
not show any alert. It neither detected any high ventricular rate (HVR)
episode.~ Her blood biochemistry (K, Mg, Ionised Calcium levels) was
normal. Echocardiography revealed good biventricular systolic function.
A coronary angiogram done in last admission was also normal. After
another recent recurrence she visited the outpatient department. ECG
showed adequate VVI pacing (Fig 1A). This time, during a repeat device
interrogation, as soon as her lower rate was made 45 bpm, she developed
a presyncope in front of us. The real time electrograms are shown in Fig
1B. What could be the mechanism of syncope and how to troubleshoot?

\textbf{Commentary:}

The electrograms in Fig 1B suggested a possible lead noise (Fig 1B)
resulting in oversensing. She was promptly managed by making the device
into VOO mode temporarily and she regained consciousness immediately.
Based on the above findings, lead malfunction was suspected in spite of
normal lead impedance and threshold trends. It is well known that lead
noise is the earliest to manifest during lead failure even when
impedance is normal. Therefore, after a discussion with patient
relatives she underwent ventricular lead replacement. The device was
also upgraded to a dual chamber pacemaker {[}DDDR Assurity MRI{]}.
Unexpectedly, in the immediate post-operative period she became
unresponsive requiring prompt resuscitation when she was being
transferred from the Cath lab to recovery area. Monitor suggested
frequent short runs of polymorphic VT which correlated with the recorded
and real time HVR episode in the pacemaker (Fig 2). There was a drop in
invasive BP during the PMVT runs. The PMVT got suppressed with high rate
obligatory pacing (DDDR 110 bpm -Ap-Vp). Similar runs of VT resurfaced
immediately as the rate was lowered below 90 and became very frequent at
lower rate below 80. All these indicated some triggered activity related
to PMVT. The lower rate was kept at 110 bpm for next 48 hours. She was
started on intravenous lignocaine and propranolol. Her blood
biochemistry revealed K of 4.3 and Mg of 2.2 . Her ionized Ca was
normal. As she recovered well without any further recurrence, the lower
rate was brought down gradually. She was discharged home with a lower
rate of 90 bpm. Over the next 2 months the LRL was brought down to 70 in
a stepwise manner every 15 days. Her cardiac PET-CT done on follow up
did not reveal any cardiac uptake.

A retrospective analysis of her initial electrogram suggested that it
was PMVT and there was \emph{no lead noise at all} (Fig 3). Neither they
were reflected in the marker channel. All `VS' in the marker channel
were true QRS complexes from the run of PMVT (Fig 3). Being a unipolar
lead, those noise-mimicker were possibly some external artefacts.
Retrospectively, it also appears that she has some underlying pathology
to produce PMVT and we should have implanted an ICD instead of dual PPI.
However, she is doing well for the last one and half years on oral
propranolol. Mexiletine stopped 6 months ago. Oral Mg supplementation
was given empirically targeting Mg level above 2.5. It also stopped 6
months ago. Since her discharge, there are no more episodes of NSVT on
device and Holter monitoring despite lowering the rate to 70 bpm. She
was offered an ICD upgrade but the patient is not willing as she is
doing well and does not want to undergo another invasive procedure. She
also did not want to undergo any genetic testing for channelopathies. In
essence, this patient developed a PMVT late after a VVI pacemaker
implant. The artefacts during device checkup were misdiagnosed as lead
noises. The reason for her syncope was PMVT which is relative
bradycardia dependent. The cause for her PMVT is although unclear. The
QTc does not seem to be prolonged in old and recent ECGs (Appendix).~
The relative hypomagnesemia could be contributory but additional
underlying long QTc is a strong possibility.

We wondered whether the PMVT was related to long term VVI pacing. There
are studies suggesting the same {[}1{]}. VDD pacemakers have a higher
tendency for PMVT due to \emph{intermittent} bradycardia associated with
atrial undersensing {[}2,3{]}. Dual chamber upgradation can reduce the
arrhythmogenicity in them {[}3{]}. Similar finding was observed in our
case too as she can tolerate a rate \textless{} 80-90 after a few days
of her dual chamber upgradation. The immediate postoperative episode
(PMVT) might suggest residual arrhythmogenicity which abated over time.
There is another case reported by our group where symptomatic VT
happened late after a VVI pacemaker and the stored EGM revealed VT
{[}4{]}. However, in that case, a long-short sequence was noted at the
onset of VT. The long cycles probably resulted from hysteresis {[}4{]}.
In this index case, the episodes happened without any active hysteresis.
However, the immediate appearance of VT in device clinic (when the LR
was set to 45 bpm) points to a preponderance of the VT linked to a
relative bradycardia. The same was noted in the postoperative period.
Putting these together, it appears that long term VVI pacing itself
might be arrhythmogenic with an aggravation during long cycles.

To summarize, this case highlights one of the rarer causes of arrhythmic
syncope in pacemaker patients despite a normally functioning pacemaker
circuit. It also highlights the importance for careful interpretation of
stored / real time electrograms to preclude any inappropriate
intervention. The exact cause for her polymorphic VT is still not clear.
Relative hypomagnesemia, late presenting long QT syndrome and
arrhythmogenicity of VVI pacing in isolation or combination remain the
probable offenders.

\textbf{Figure legends}

Fig 1: A: ECG during the presentation in outpatient clinic (VVI @ 80
bpm). The lower rate was increased from 60 to 80 bpm empirically during
the last device checkup; B: The device interrogation after the ECG. The
lower rate was made 6545 to see whether any episode or symptom is
experienced. Lot of artefacts were noted. As the patient became dizzy a
diagnosis of oversensing was made.

Fig 2: The stored electrogram showing induction of VT by PVCs.

Fig 3: The reanalyzed and annotated Fig 1B showing that the artefacts
were not lead noise. All the `VS' was related to QRS complex of the
PMVT. The induction was facilitated by the relative bradycardia (lower
rate @ 45 bpm).

\textbf{References:}

\begin{enumerate}
\tightlist
\item
  Himmrich E, Przibille O, Zellerhoff C, Liebrich A, Rosocha S, Andreas
  K, Nebeling D, Omogbehin B, Meyer J. Proarrhythmic effect of pacemaker
  stimulation in patients with implanted cardioverter-defibrillators.
  Circulation. 2003 Jul 15;108(2):192-7.
\item
  Elsokkari I, Abdelwahab A, Parkash R. Polymorphic ventricular
  tachycardia due to change in pacemaker programming.~\emph{HeartRhythm
  Case Rep} . 2017;3(5):243-247. Published 2017 Feb 20.
  doi:10.1016/j.hrcr.2017.02.003
\item
  Palanca V., Navarro A., Jim\selectlanguage{ngerman}énez J., Quesada A., Morell S., Roda J.
  Intermittent atrial undersensing in single-lead VDD pacemakers in
  patients with bradycardia-sensitive repolarization: a possible
  mechanism for ventricular arrhythmia.~\emph{Rev Est Cardiol.~}
  2010;63:229--232.
\item
  Bera D, Joshi RS, Mukherjee SS, Majumder S. Ventricular
  tachyarrhythmia after single chamber pacemaker programming - what is
  the mechanism? J Electrocardiol. 2021 Sep-Oct;68:114-116. doi:
  10.1016/j.jelectrocard.2021.07.020.
\end{enumerate}\selectlanguage{english}
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