AbstractA 76 y/o women presented with 2 different types of premature ventricular contractions (VPCs 1 and 2) arising from the right ventricular outflow tract (RVOT). Catheter ablation (CA) eliminated PVC1 at the earliest activation site (EAS), but thereafter another PVC morphology (PVC3) appeared. Small potentials preceding the local potential were broadly exhibited from the RVOT’s supero-anterior region to the EAS during PVC3. Point CA targeting such prepotentials failed. Transverse-linear CA with a line connecting sites with such pre-potentials eliminated both PVCs 3 and 2. In cases with broadly spreading preferential pathways, extensive CA might be needed to eliminate the PVCs

Akira, Ueno

Iida, Takayuki

Kobayashi, Yoshinori

Morita, Norishige

Elsevier - Publisher Connector 

Extensive Preferential Pathway Ablation for the Elimination of Premature Ventricular Contractions Arising from the Right Ventricular Outflow Tract 

www.ipej.org 88
Case Report
Extensive  Preferential  Pathway  Ablation  for  the 
Elimination  of  Premature  Ventricular  Contractions 
Arising from the Right Ventricular Outflow Tract
Norishige Morita, MD, PhD1,2 Takayuki Iida, MD1  Ueno Akira, MD1,2 Yoshinori 
Kobayashi, MD1,2
1Division of Cardiology, Department of Medicine, Tokai University Hachioji Hospital, Tokyo 
2Division of Cardiology, Department of Medicine, Nippon Medical School, Tokyo, Japan
Address for Correspondence: Norihsige Morita, MD, PhD, 1838 Ishikawa-machi Hachioji-shi, 
Tokyo, 1920032, Japan. E-mail: morita@nms.ac.jp
Abstract
A 76 y/o women presented with 2 different types of premature ventricular contractions (VPCs 
1 and 2)  arising  from the  right  ventricular  outflow tract  (RVOT).  Catheter  ablation  (CA) 
eliminated PVC1 at the earliest activation site (EAS), but thereafter another PVC morphology 
(PVC3) appeared. Small potentials preceding the local potential were broadly exhibited from 
the RVOT's supero-anterior region to the EAS during PVC3. Point CA targeting such pre-
potentials failed. Transverse-linear CA with a line connecting sites with such pre-potentials 
eliminated  both  PVCs  3  and  2.  In  cases  with  broadly  spreading  preferential  pathways, 
extensive CA might be needed to eliminate the PVCs.                                      
            
Key words: Preferential pathway, Pre-potential,  Right Ventricular outflow tract, Premature 
ventricular  contraction,  Ablation                                   
Introduction
Most premature ventricular  contractions  (PVCs) arising from the right ventricular  outflow 
tract  (RVOT)  can  be  cured  by the  radiofrequency  catheter  ablation  (RFCA).  The  earliest 
activation site (EAS) during the PVCs has been known to be the best target site for RFCA 
eliminating those PVCs . Although such an approach targeting the EAS with RFCA has been 
known to eliminate the PVCs, there have been some cases in which the RFCA of the EAS 
during the PVCs could not result in the elimination of the PVCs even though pace mapping 
from the EAS exhibited an excellent match to the QRS morphology during the spontaneous 
PVCs. In general RFCA applications for the EAS are appropriate for curing the PVCs when 
the PVCs arise from an identical site as the EAS. If the PVC arises from a site away from the 
EAS,  whether  the  origin  is  located  in  the  end/mid,  or  epicardial  myocardium,  such  an 
approach targeting the EAS might fail to eliminate the PVC since it is possible that the EAS 
reflects the activation of an endocardial exit site to which the excitation from the PVC origin 
might preferentially propagate [1,2]. Here we present a case with RVOT-PVCs which could 
not be eliminated by point RFCA applications at the EAS, but could be eliminated by a linear 
RFCA with a line intersecting the area where small potentials were recorded preceding the 
local  ventricular  activation.                                                
Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 13 (2): 88-93 (2013)
This is an open access article under the CC BY-NC-ND license.
Morita N et al, “Extensive Preferential Pathway Ablation of the PVC”                               89
Case  Report                                                       
A 76 y/o women experienced frequent episodes of palpitations and consulted our hospital. The 
12-lead ECG exhibited normal sinus rhythm with a PQ interval and QRS width of 100 and 66 
ms, respectively. The QT and QTc intervals were 520 and 425ms, respectively. Two types of 
PVCs  were  documented  on  the  12-lead  ECG,  and  the  morphology  of  one  PVC (PVC1) 
exhibited a left bundle branch block with an inferior axis, and the other (PVC2) was similar to  
PVC1 but its QRS morphology was slight different (PVC2) (Figure 1). 
Figure  1. 12-lead  ECGs  demonstrating  two  types  of  premature  ventricular  contractions  (PVCs).  (A)  The 
morphology of PVC1, which was the main morphology documented, was a left bundle branch block pattern with 
a superior axis (left panel). The 12-lead ECGs during pace mapping from the earliest activation site (EAS) during 
PVC1 (right panel). (B) The 12-lead ECGs of PVC2 were similar to those of PVC1, but the amplitude of the R 
wave in the inferior leads was greater than that of PVC1 and the transitional zone of the R/S wave differed. (C)  
Newly appearing PVC (PVC3) after the RFCA of PVC1 (left panel). The 12-lead ECGs during pace mapping at  
the EAS during PVC3 (right panel).
Routine  check-ups  including  a  transthoracic  echocardiogram  revealed  no  structural 
abnormalities. Her Holter monitoring revealed 21,564 PVC beats over 24 hrs which coincided 
in  time  with  her  palpitations.  She  was  admitted  to  our  hospital  and  underwent  an 
electrophysiologic  study (EPS).  In  the  baseline  study,  the  atrio-His  and His-to-ventricular 
intervals  during  sinus  rhythm  were  135  ms  and  42ms,  respectively.  Based  on  the 
morphologies of those two types of PVCs, the sites from which the PVCs arose were thought 
to be located in the right ventricular outflow tract (RVOT) [3]. The earliest activation site 
(EAS) during the PVCs was determined using an electroanatomical mapping system (CARTO 
XP, Biosense Webster,  Diamond Bar, CA). Since PVC1 was more frequently documented 
than PVC2 during the EPS, mapping of PVC1 was performed first to try and cure PVC1. The 
EAS during PVC1 was located in the anteroseptal region of the RVOT (Figure 2A), where the 
local excitation preceded the QRS onset by 32ms and a QS complex was recorded by the 
mapping  catheter  in  the  unipolar  electrogram  (Figure  3).  The  pace  map  from  the  EAS 
exhibited an excellent match to the QRS morphology during spontaneous PVC1 (Figure 1A). 
RFCA was applied at the EAS and to sites within close proximity to the EAS determined by 
CARTO during PVC1, and are indicated by red tags in Figure 2A. Those RFCA applications 
eliminated PVC1, but another type of PVC (PVC3) with a different morphology from that of 
PVCs 1 and 2 appeared with a similar frequency to PVC1 (Figure 1C).  Therefore a new 
electro-anatomical map was created to define the EAS during PVC3 after the initial RFCA 
applications targeting PVC1. The mapping revealed that the EAS during PVC3, where the 
Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 13 (2): 88-93 (2013)
Morita N et al, “Extensive Preferential Pathway Ablation of the PVC”                               90
local excitation preceded the QRS onset by 24ms, was located in the septal  region of the 
RVOT and around 15mm more posterior than the EAS during PVC1 (Figure 2B). The pace 
map performed from the EAS during PVC3 also revealed a good match (Figure 1C). Again 
the RFCA applications to the EAS and the area around the EAS during PVC3 as indicated by 
the asterisks in Figure 2B however, could not eliminate PVC3. 
Figure 2. (A) Activation map during PVC1 (upper panels) and the ablation catheter position in the fluoroscopic  
views (lower panels). The earliest activation site (EAS) is shown in red and the latest in purple. (B) Activation 
map during PVC3 (upper panels) and the ablation catheter position in the fluoroscopic views (lower panels). The 
ablation  catheter  was  positioned  at  Point  A corresponding  to  the  site  indicated  on  Fig.  4.  The  presumable 
borderline between the right ventricular outflow tract and pulmonic artery is indicated by the arrowhead. The 
asterisks indicate the initial  ablation points targeting the sites exhibiting the pre-potential  during PVC3. The 
light-blue circles indicate the sites where the pre-potentials were recorded and the red ones the sites where the  
ablation  was  performed.  Abl=ablation  catheter,  CS=recording  catheter  for  coronary  sinus  electrograms, 
HBE=recording catheter for His-bundle electrograms, LAO=left anterior oblique projection RAO=right anterior 
oblique projection. Refer to the text for the details.
Careful mapping around the EAS during PVC3 revealed a small potential preceding the local 
ventricular potential when PVC3 appeared, and is indicated by the arrows in  Figure 4. The 
region where such potentials could be recorded is indicated by the light blue tags in  Figure 
2B. Such potentials could be seen during the late phase of the QRS complex and might be 
superimposed  by  the  local  ventricular  potential  during  sinus  rhythm,  as  indicated  by  the 
arrowheads in  Figure 4.  The sites where such pre-potentials  could be recorded covered a 
relatively large area of the RVOT, and were observed mainly in the superior region, both 
anteriorly  and  posteriorly,  to  the  EAS,  and  in  particular  beneath  the  pulmonic  valve  as 
indicated  by  the  arrowheads  in  Figure  2B.  Although  this  was  not  determined  with 
ventriculography,  the  position  of  the  pulmonic  valve  could  be  assumed  from the  cardiac 
silhouette. The spatio-temporal relationship between the antecedent timing of the pre-potential 
and the emergence of the onset of the QRS, and the location where the pre-potentials could be 
recorded is shown in  Figure 2B and  4. The pre-potentials appeared earlier in timing to the 
QRS  onset  as  the  recording  site  became  further  away  from  the  EAS.  To  assess  the 
electrophysiologic  relationship  between  such  pre-potentials  and  the  emergence  of  PVC3, 
pacing from the sites demonstrating such potentials was performed. The selective capture of 
such pre-potentials without local ventricular capture by pacing however, was impossible. A 
few applications of RFCA targeting the sites exhibiting such potentials, as indicated by the 
asterisks in  Figure 2B, were delivered to see if they had any influence on suppressing the 
Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 13 (2): 88-93 (2013)
Morita N et al, “Extensive Preferential Pathway Ablation of the PVC”                               91
incidence of PVC3, but the RFCA did not have any influence on either  the frequency or 
morphology of PVC3. Based on the results of the failure to eliminate PVC3 by RFCA at a few 
points, we presumed that the origin of PVC3 was located at a site some distance away from 
the  EAS  and  that  the  excitation  was  propagating  from  the  PVC  origin  through  several 
preferential  pathways,  resulting  in  a  single  phenotypic  presentation  of  the  PVC3  QRS 
morphology even though the course of the conduction differed. The strategy for the RFCA 
applications was changed to create RFCA regions that intersected an arbitrary line connecting 
points between the sites where the pre-potentials could be recorded. The linear but actually 
stepped linear RFCA applications between the posterior and anterior septum in the RVOT, as 
indicated by the red tags in Figure 2B, resulted in the complete elimination of PVC3. In the 
process of delivering those RFCA applications for PVC3, the frequency of the occurrence of 
PVC2 decreased. Since PVC2 never appeared again after the final RFCA application targeting 
PVC3, the session was completed. During 6 months of follow-up, no further occurrences of 
PVCs 1-3 have been documented. 
Figure 3.  The intracardiac electrograms during PVC1. The local potential recorded from the ablation catheter 
which was located at the EAS preceded the QRS onset by 32ms. Shown from the top to bottom are the body 
surface ECG leads I, aVF, and V1 and the intracardiac signals from the right atrium (RA), proximal, mid-, and 
distal  His-bundle electrogram recording  sites  (HBEp,  HBEm, and HBEd, respectively),  proximal,  mid-,  and 
distal  coronary  sinus  (CSd,  CSm,  and  CSp,  respectively),  right  ventricular  outflow tract  (RVOT),  unipolar  
electrogram recorded from the distal electrode of the ablation catheter (Abl uni), and the distal and proximal pair 
of electrodes of the ablation catheter located at the EAS in the right ventricular outflow tract (Abl d and Abl p,  
respectively). Refer to the text for the details.
Discussion
To eliminate RVOT-PVCs with RFCA, the precise localization of their origin reflected as the 
EAS during the PVC has been thought to lead to a successful RFCA. In addition,  a pace 
mapping procedure is usually performed to ensure whether pacing from the EAS can elicit the 
same  QRS  morphologies  in  the  12-lead  ECG  as  those  during  spontaneous  PVCs,  thus 
confirming that the EAS is  a proper site for  RFCA.  An estimation based on the results 
Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 13 (2): 88-93 (2013)
Morita N et al, “Extensive Preferential Pathway Ablation of the PVC”                               92
obtained from pace mapping however, has been known to be limited because of the capture of 
a  large  area  of  the  myocardium  around  the  EAS  or  a  rate-dependent  alternation  in  the 
conduction during pacing. Another complementary procedure for searching for the appropriate 
site for RFCA is known to be searching for a site exhibiting a QS complex pattern recorded in 
the local unipolar electrogram. This method also has the limitation of the surrounding area of 
the EAS exhibiting a QS morphology pattern in an area. Because of these limitations on the 
determination of the proper RFCA site, the complete elimination of the PVCs often requires 
several RFCA applications not only at the EAS, but also in the surrounding area in close 
proximity to the EAS. Therefore it seems that the EAS sometimes might move to a site close 
to the EAS which was initially identified,  when VPCs still  emerge after the initial  RFCA 
applications. Further, when the EAS moves to a site >10mm away from the initially identified 
EAS and the PVC morphology changes after several RFCA applications to the EAS and the 
area within close proximity to the EAS, this may imply that the substrate of the PVC origin 
involves a relatively large area with a few exist sites located in the area neighboring the EAS 
or another PVC becomes unmasked from a different origin. In our case, although the distance 
between the EAS during PVCs 1 and 3 was more than 10mm, the frequency of the incidence 
of PVC3 was almost same as that of PVC1. Therefore it could be possible that the origin of 
PVCs 1 and 3 was a common substrate containing a relatively large area and the direction of 
the conduction from the PVC origin became altered after the initial  RFCA application for 
PVC1, resulting in the change in the QRS morphology from PVC 1 to 3. Even if the origin of 
both PVCs 1 and 3 were composed of such a substrate, the failure to eliminate PVC3 by a 
further RFCA application to the EAS as well as the area in close proximity to the EAS during 
PVC3, led us to consider that the PVC origin might be located distant from the EAS since 
pace mapping from the EAS during PVC3 exhibited a good match. Careful mapping around 
the endocardial EAS during PVC3 exhibited small potentials preceding the local ventricular 
activation. Cases in which the PVC was expected to arise from the RVOT or pulmonic artery 
(PA) have been reported to exhibit small pre-potentials preceding the local excitation in the 
PA during the PVC, as was the case in our current report [1,2,4]. In addition, an alteration in 
the QRS morphology of the PVC and increased amplitude of the R wave in the inferior leads 
was seen after the RFCA applications at the EAS during the PVC in cases with PVCs arising 
from the PA, and that was a similar finding to that in our case [5]. In such cases, the RFCA 
application to the EAS failed to eliminate the PVC, but that to the site where the pre-potentials 
were recorded lead to the elimination of the PVC. The EAS during PVC3 in our case was 
thought to be located in the RVOT based on the catheter position on fluoroscopy, but this was 
not actually determined with ventriculography. A part of the RFCA sites superior to the EAS 
during PVC3 exhibiting small pre-potentials might have been located in the PA (Figure 2B). 
The sites that exhibited pre-potentials, were spread out over a relatively large area, anterior 
and posterior to the EAS located in the RVOT septal region. When the RFCA application at  
the EAS and its vicinity during the RVOT-PVCs fails to eliminate the PVCs or changes the 
morphology of the PVC, careful mapping in the neighboring area of the RVOT should be 
made to search for small potentials preceding the local excitation during PVCs. Further, when 
some point RFCA applications to sites where pre-potentials are recorded can not eliminate the 
PVCs, a linear RFCA to intersect a line connecting the sites exhibiting pre-potentials may be a 
useful  procedure.  In  our  case,  PVC2 disappeared  after  this  procedure  to  cure PVC3.  The 
reason why PVC2 disappeared could not actually be addressed, but one consideration might 
be that the RFCA of some preferential pathways arising from the origin of PVC3, which might 
also have been connected to the exit site during PVC2, resulted in the elimination of PVC2. It  
may be concluded that  the careful  mapping of the neighborhood of the EAS to find pre-
potentials during RVOT-PVCs might aid in leading to the successful elimination of the PVCs 
when PVCs still appear after several RFCA applications to the EAS and its vicinity.
Acknowledgement
The Authors wish to thank Yumi Abe, M.E., Goichi Nagata, M.E., and Ayumu Miura, M.E., 
for their technical assistance, and Mr. John Martin for his linguistic assistance.
Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 13 (2): 88-93 (2013)
Morita N et al, “Extensive Preferential Pathway Ablation of the PVC”                               93
Figure 4. The intracardiac electrograms recorded from Points A to D during PVC3, which correspond to each 
site shown in Fig 2B. The numerical numbers shown on each figure indicate the difference in time between the  
emergence  of  the  pre-potentials  recorded  on  the  local  electrograms  and  QRS  onset  during  PVC3.The 
abbreviations are the same as in Fig. 3. Refer to the text for the details.
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Extensive Preferential Pathway Ablation for the Elimination of Premature Ventricular Contractions Arising from the Right Ventricular Outflow Tract

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