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\begin{document}

\title{Sudden QRS widening while ablating a concealed left accessory pathway
during left ventricular pacing}



\author[1]{Anunay Gupta}%
\author[2]{Raghav Bansal}%
\author[3]{Deep  Raja}%
\author[4]{Yash Lokhandawala}%
\affil[1]{Vardhman Mahavir Medical College and Safdarjung Hospital}%
\affil[2]{All India Institute of Medical Sciences Cardio-Thoracic Sciences Centre}%
\affil[3]{Madras Medical Mission Institute of Cardio Vascular Diseases}%
\affil[4]{Arrhythmia Associates}%


\vspace{-1em}



  
  \date{May 21, 2024}


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\textbf{Title: Sudden QRS widening while ablating a concealed left
accessory pathway during left ventricular pacing}

\textbf{Anunay Gupta, MD, DM\textsuperscript{1}; Raghav Bansal, MD,
DM\textsuperscript{2}; Deep Chand Raja, MD, DM\textsuperscript{3}; Yash
Lokhandwala, MD, DM\textsuperscript{4}}

\textsuperscript{1} Department of Cardiology, Vardhaman Mahavir Medical
College and Safdarjung Hospital, New Delhi

\textsuperscript{2} Department of Cardiology, All India Institute of
Medical Sciences, New Delhi

\textsuperscript{3} Department of Cardiology, The Canberra Hospital and
Health Services, Canberra,

Australia

\textsuperscript{4} Department of Cardiology, Holy Family Hospital and
Medical Research Centre, Bandra West, Mumbai

\textbf{Corresponding author: Raghav Bansal}

Department of Cardiology

All India Institute of Medical Sciences

New Delhi - 110029, India

Email: raghav.mamc@gmail.com

\textbf{Keywords:} Ventricular fusion, Fusion QRS, Left ventricular
pacing, Orthodromic re-entrant tachycardia, Left free wall accessory
pathway

\textbf{Word count:} 594 (excluding references and figure legends)

\emph{There are no conflicts of interest to declare}

\textbf{Case Presentation}

A 26-year-old man presented to emergency department with acute onset
palpitations with a history of such episodes since two months. The
electrocardiogram revealed a regular short RP narrow QRS tachycardia at
the rate of 145 beats per minute. The echocardiogram showed a left
ventricular ejection fraction of 0.25 during tachycardia but was normal
during sinus rhythm. He underwent an electrophysiology study which
revealed eccentric activation in the coronary sinus during right
ventricular pacing and during tachycardia \textbf{(Figure 1)} ,
suggestive of a retrograde conducting concealed left free wall accessory
pathway (AP). The mitral annulus was mapped via the transseptal route
and the AP was localized to the left anterolateral mitral annulus.
Radiofrequency energy was delivered during entrainment of the
orthodromic tachycardia by left ventricular (LV) lateral wall
pacing\textbf{(Figure 2 left panel)} . A sudden change in QRS morphology
was seen during energy \textbf{(Figure 2 right panel)} , coincident with
elimination of accessory pathway conduction \textbf{(Figure 3 left
panel)} . What is the mechanism?

\textbf{Commentary}

The intracardiac electrograms (EGMs) during delivery of radiofrequency
energy reveal initially a RBBB-like morphology in lead V1, suggesting
ventricular pacing from the left ventricle. The QRS duration is 130 ms,
which is unusually short for left ventricular lateral wall pacing. Fused
ventricular and atrial EGMs can be appreciated in the bipolar signal
from the tip of the ablation catheter (RFD, \textbf{Figure 3 left panel}
). Retrograde AP conduction is seen until the fifth QRS complex,
followed by ventriculo-atrial (VA) block; later there is variable VA
conduction via the AV node. Immediately after the VA block, there is an
abrupt vivid change in the QRS morphology with an increase in the QRS
width to 187ms.

In trying to understand the rationale behind the change in QRS
morphology, it is important to consider yet another important
observation in the intracardiac electrograms. The clue lies in the EGMs
on the His channel (HISD, \textbf{Figure 3 left panel} ). Clear sharp
His signals (H) are seen to precede the ventricular EGMs during LV
pacing until the retrograde VA block and change in QRS morphology. This
suggests antegrade activation of the His bundle, which can happen only
if LV pacing was being performed concomitant with the orthodromic
atrioventricular reentrant tachycardia. The relatively narrow QRS
complex is the result of fusion of ventricular activation from LV pacing
and the tachycardia wavefronts. This is further suggested by the short
HV interval of 20 ms \textbf{(Figure 3 right panel)} . This was actually
the case here, as the LV was being overdrive paced at 30 ms shorter than
the tachycardia cycle length, so as to maintain stability of the
ablation catheter during ablation, in case of termination of
tachycardia.

For a fusion to perpetuate between the orthodromic AVRT and ventricular
pacing, the following conditions are necessary: pacing close to the
insertion of the AP, pacing just shorter than the TCL, rapid AP
conduction, brisk antegrade AV nodal conduction and sluggish retrograde
AV nodal conduction. Basal pacing site near the pathway insertion leads
to more ventricular muscle activation by the orthodromic tachycardia
wavefront (1). Fusion can be identified by the presence of an
orthodromically captured His or right bundle potential.

In conclusion, a relatively narrow QRS during LV lateral wall pacing
along with evidence of antegrade activation of His bundle suggests
fusion between ventricular pacing and the ongoing orthodromic
tachycardia; here one would expect the QRS to change in morphology as
soon as the tachycardia terminates during the energy delivery. While one
concentrates on the atrial activation while ablating concealed accessory
pathways during ventricular pacing, the QRS complex can display valuable
evidence too!

\textbf{References:}

Veenhuyzen GD, Coverett K, Quinn FR, Sapp JL, Gillis AM, Sheldon R,
Exner DV, Mitchell LB. Single diagnostic pacing maneuver for
supraventricular tachycardia. Heart Rhythm. 2008 Aug;5(8):1152-8.

\textbf{Figure Legends:}

\textbf{Figure 1.} Surface electrocardiogram (I, aVF, V1, V6) and
intracardiac electrograms - His bundle electrogram distal and proximal
(HISD, HISP), coronary sinus (CS) 9,10 dipoles at CS ostium, \& CS 1,2
dipoles at distal CS. Pacing is being done from HBD and is followed by
tachycardia; both show identical eccentric atrial activation patterns
(marked by arrows) with earliest activation at CS 3,4 channel.

\textbf{Figure 2. Left panel.} Fluoroscopic image showing location of
left ventricle pacing site and ablation catheter positioned at the
mitral annulus transeptally in RAO 30 (left upper panel) and LAO 40
(left lower panel). \textbf{Right panel.} 12-lead surface
electrocardiogram at the initiation of radiofrequency energy delivery
depicting sudden change in QRS morphology after the
6\textsuperscript{th} beat.

\textbf{Figure 3. Left panel.} Surface electrocardiogram (I, aVF, V1,
V6) and intracardiac electrograms recorded from catheters as depicted in
figure 2 left panel. The arrow after the 2\textsuperscript{nd} beat
denotes the artefact at the initiation of radiofrequency energy
delivery. The orthodromically captured His bundle potentials on the HISD
channel and the ventricular/atrial potentials on the RFD channel are
marked with H, V and A respectively. Note the sudden change in QRS
morphology and width with loss of ventriculo-atrial conduction after the
6\textsuperscript{th} beat. \textbf{Right panel.} The shaded beat on the
left panel at a higher speed of 300 mm/sec to demonstrate a short HV
interval of 20 ms suggesting fusion between wavefronts originating from
the ongoing othrodromic re-entrant tachycardia and the LV pacing.\selectlanguage{english}
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