\documentclass[10pt]{article}

\usepackage{fullpage}
\usepackage{setspace}
\usepackage{parskip}
\usepackage{titlesec}
\usepackage[section]{placeins}
\usepackage{xcolor}
\usepackage{breakcites}
\usepackage{lineno}
\usepackage{hyphenat}





\PassOptionsToPackage{hyphens}{url}
\usepackage[colorlinks = true,
            linkcolor = blue,
            urlcolor  = blue,
            citecolor = blue,
            anchorcolor = blue]{hyperref}
\usepackage{etoolbox}
\makeatletter
\patchcmd\@combinedblfloats{\box\@outputbox}{\unvbox\@outputbox}{}{%
  \errmessage{\noexpand\@combinedblfloats could not be patched}%
}%
\makeatother


\usepackage{natbib}




\renewenvironment{abstract}
  {{\bfseries\noindent{\abstractname}\par\nobreak}\footnotesize}
  {\bigskip}

\titlespacing{\section}{0pt}{*3}{*1}
\titlespacing{\subsection}{0pt}{*2}{*0.5}
\titlespacing{\subsubsection}{0pt}{*1.5}{0pt}


\usepackage{authblk}


\usepackage{graphicx}
\usepackage[space]{grffile}
\usepackage{latexsym}
\usepackage{textcomp}
\usepackage{longtable}
\usepackage{tabulary}
\usepackage{booktabs,array,multirow}
\usepackage{amsfonts,amsmath,amssymb}
\providecommand\citet{\cite}
\providecommand\citep{\cite}
\providecommand\citealt{\cite}
% You can conditionalize code for latexml or normal latex using this.
\newif\iflatexml\latexmlfalse
\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}}%

\AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}}

\usepackage[utf8]{inputenc}
\usepackage[english]{babel}



\usepackage{float}








\begin{document}

\title{Preventive algorithm ending up being the `Cause'!}



\author[1]{Anindya Ghosh}%
\author[2]{Deep  Raja}%
\affil[1]{Madras Medical Mission Institute of Cardio Vascular Diseases}%
\affil[2]{Kauvery Hospital}%


\vspace{-1em}



  
  \date{June 17, 2024}


\begingroup
\let\center\flushleft
\let\endcenter\endflushleft
\maketitle
\endgroup








\sloppy


\textbf{Preventive algorithm ending up being the `Cause'!}

Anindya Ghosh, MD\textsuperscript{1} | Deep Chandh Raja,
MD\textsuperscript{2}

\textsuperscript{1}Department of Cardiac Electrophysiology and Pacing,
Arrhythmia Heart Failure Academy, The Madras Medical Mission, Chennai,
Tamil Nadu, India

\textsuperscript{2}Department of Cardiac Electrophysiology and Pacing,
Kauvery Hospital, Chennai, India

\textbf{Correspondence}

Dr Deep Chandh Raja MD, DM

Consultant Cardiologist \& Clinical lead of Cardiac Electrophysiology

Kauvery Hospital, Chennai, Tamil Nadu India

Phone: 9936572236;~Extension:~044 40006000

Email:~deepchandh@gmail.com

Abstract

N/A

1| Case Presentation

A 75 year-old male, who is a known case of chronic renal insufficiency
and on twice weekly renal replacement therapy, presented with sudden
onset and rapidly progressive dyspnoea of 3 days duration associated
with palpitations. He had previously undergone a dual chamber automatic
implantable cardioverter defibrillator (AICD) implantation (Abbott,
Ellipse\textsuperscript{TM} DR MRI) for degenerative intermittent
complete heart block (CHB) and non-ischemic cardiomyopathy with a left
ventricular ejection fraction of 35\%. An electrocardiogram (ECG) in the
emergency department demonstrated a regular wide QRS tachycardia at 110
beats per minute (bpm) with left bundle branch block (LBBB) morphology a
pacing spike preceding each QRS complex. His device was programmed to a
lower rate of 40 bpm and a maximum track rate of 110 bpm. The pacemaker
mediated tachycardia (PMT) response was turned `ON'. The device was
interrogated and the ongoing electrogram (EGM) is shown in Figure 1. It
shows a tachycardia annotated by the device as PMT and the tachycardia
continues despite PMT intervention by the device. What is the probable
mechanism of initiation and perpetuation of the tachycardia?

2|Discussion

The differential diagnoses of a regular wide QRS tachycardia with
morphology identical to the paced QRS morphology at the maximal tracking
rate in a patient with a dual chamber pacemaker includes PMT, sinus
tachycardia/ atrial tachycardia tracked by the ventricular lead and
ventricular tachycardia (VT) with exit site close to the ventricular
lead implant site. Ventricular tachycardia is ruled out here as the
ventricular complexes follow pacing stimulus throughout the trace. An
onset of tachycardia which is sudden and heralded by a premature
ventricular contraction argues against sinus tachycardia or atrial
tachycardia.

The device EGM in Figure 1 shows three channels- atrial near-field EGM
(AEGM), ventricular near-field EGM (VEGM) and the device marker
annotations. The trace begins with a sinus atrial signal being tracked
by the ventricular lead at the programmed AV delay. Next comes a
premature ventricular complex (PVC) with retrograde ventriculoatrial
(VA) conduction (VA- 120 ms) to the atrium (note the difference in
atrial EGM near-field characteristics from the sinus node origin atrial
EGM). This is followed by atrial pacing approximately 330 ms after the
atrial event which fails to capture the atrium (Note the atrial EGM
corresponding to Ap doesn't have an evoked potential).

This Ap at 330 ms after an atrial event following a PVC is the
characteristic `PVC response' seen in Abbott's newer generation of
pacemakers. Ventricular pacing then follows at the programmed AV delay.
Loss of atrial capture allows the paced ventricular complex to conduct
retrogradely to the atrium (note the near- field atrial EGM morphology
matches that of retrograde atrial EGM) which is in turn is tracked by
the ventricular lead and starts a cycle of PMT at the upper tracking
rate. After confirming the stability of the Vp- As intervals on the
2\textsuperscript{nd} attempt (each attempt includes a count of 8 Vp-As
intervals) which includes an extension of the AV delay by 50 ms, the
device extends the post- ventricular atrial refractory period (PVARP)
followed by an atrial pacing event at 330 ms similar to the PVC
response. However, as seen earlier in the trace, this Ap fails to
capture again and allows the subsequently ventricular paced QRS complex
to conduct retrogradely to the atrium and start another cycle of PMT.
Thus, a vicious cycle is perpetuated leading to heart failure symptoms.

The current generation of Abbott pacemakers have PMT prevention
(\emph{PVC response} ) and termination (\emph{Auto- detect} ) algorithms
with operation settings similar to other device manufacturers, that is,
extension of the post ventricular atrial refractory period (PVARP).
Their algorithms, in addition, involve atrial pacing after the
retrograde atrial event followed by ventricular pacing at the programmed
paced AVD.\textsuperscript{1}

The PVC response algorithm detects and responds to PVCs when the device
is in DDD(R) mode. It detects a PVC if: 1) an R-wave is not preceded by
an atrial event; or 2) a P-wave is detected in the relative refractory
portion of the PVARP period but is not followed by an R-wave within 280
ms of the atrial event.

The Atrial Pace setting is a response to a PVC confirmation. The
response consists of a continuous extension of the PVARP setting to 475
ms, followed by an atrial alert period of 330 ms until a P-wave is
tracked outside the extended PVARP period, followed by an atrial pace.

The PMT termination algorithm (Auto- detect) also behaves in a similar
fashion confirming Vp- As interval stability and ultimately manifesting
itself as PVARP extension followed by an atrial pace.

The probable reason for loss of capture with the Atrial Pace setting of
the PVC response algorithm (even 330ms after the last atrial
depolarisation) in this was the long refractory period of atrial
myocardial tissue due to the metabolic milieu of chronic renal
insufficiency.

Also noted was a VA interval which was longer for paced QRS morphology
than for the PVC which could be explained by the closer location of the
PVC origin to the His- Purkinje conduction system. This long intrinsic
VA was responsible for the perpetuation of the PMT, the retrograde A
falling outside the PVARP each time.

Although any event causing AV dissociation can start a PMT, PVCs are the
most common triggers and hence the need of a specific algorithm directed
towards it. But the same proved to be arrhythmogenic as has also been
reported previously in literature but with respect to ventricular and
atrial tachyarrhythmias.\textsuperscript{2}

This case represents a unique hitherto unheard-of clinical scenario,
where an algorithm (PVC response) meant for a specific purpose (prevent
PMT initiation) not only fails but starts the very phenomenon it was
meant to prevent. In fact, the PMT would not have been initiated if it
were not for the algorithm. The PVC response was eventually switched
off, as was Atrial Pace setting after PVARP extension resulting
resolution of symptoms.

References

St. Jude Medical Inc.: MerlinTM Patient Care System Help Manual, St.
Jude Medical. Bradycardia and tachycardia devices, bradycardia
parameters, 61--84

Konishi H, Fukuzawa K, Mori S, Kiuchi K, Hirata K. The limitations and
potential adverse effects of the premature ventricular contraction
response. \emph{J Arrhythmia} . 2018;34:572--575.
https://doi.org/10.1002/ joa3.12082

Figure Legends

Figure 1- Three channel Device EGM showing initiation of tachycardia
with Vp-As sequences and device label of Pacemaker Mediated Tachycardia
(PMT)

Figure 2- Explanation-

(A) The first intrinsic atrial event is tracked by the ventricle (Vp) at
the programmed atrioventricular delay (AVD). This is followed by a
premature ventricular contraction (PVC) with retrograde atrial
activation with ventriculoatrial interval (VA) of 120 ms. The PVC
triggers the `PVC response' which include a Post Ventricular Atrial
Refractory Period (PVARP) extension followed by atrial pacing (Ap) at
330ms from the retrograde atrial event. However, the Ap fails to capture
atrial myocardium because of longer refractory period which allows the
next Vp to have retrograde conduction to the atrium. This starts the
Pacemaker Mediated tachycardia (PMT) which is detected by the device
(B\textbf{)} after one failed attempt (as 8 consecutive Vp-As interval
average was more than 16 ms longer than the first Vp-As). However, the
PMT response from the device fails to terminate the tachycardia in the
same way as the PVC response and again starts the PMT (C).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1/Figure-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2A/Figure-2A}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2B/Figure-2B}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2C/Figure-2C}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

