Europace Advance Access originally published online on May 10, 2006
Europace 2006 8(6):434-437; doi:10.1093/europace/eul032
© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
ACCESSORY PATHWAYS
Evidence for an incomplete mitral isthmus block after failed ablation of a left postero-inferior concealed accessory pathway
Agustín Bortone1,*,
François Brigadeau2,
Jean Luc Pasquié1 and
Dominique Lacroix2
1 Service de Cardiologie A, Centre Hospitalo-Universitaire de Montpellier, Hôpital Arnaud de Villeneuve, 371, avenue du Doyen Gaston Giraud, 34295 Montpellier Cedex 5, France;
2 Service de Cardiologie A, Hôpital Cardiologique, Centre Hospitalier Régional Universitaire de Lille, Lille, France
Manuscript submitted 13 August 2005. Accepted after revision 26 February 2006.
* Corresponding author. Tel: +33 467 33 62 15; fax: +33 467 33 62 18. E-mail address: a-bortone{at}chu-montpellier.fr
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Abstract
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We report the case of a young woman in whom previous ablation
of a concealed left-sided accessory pathway (AP) created an
iatrogenic mitral block. The mitral block was responsible for
a split retrograde atrial activation pattern during orthodromic
atrioventricular re-entrant tachycardia (AVRT). The differential
diagnoses are discussed. The AP was ablated at the site with
the shortest interval between the ventricular signal and the
earliest component of the retrograde atrial activation. Meticulous
mapping is paramount during AVRT with an unusual retrograde
atrial activation pattern.
Key Words: Concealed accessory pathway, Split retrograde atrial activation, Mitral isthmus block.
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Introduction
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Concealed accessory pathways (APs) are one of the underlying
mechanisms of supraventricular tachycardia with an incidence
ranging from 15 to 50%. The most common concealed APs have retrograde
AV conduction without decremental properties and usually
participate in paroxysmal arrhythmias, which are atrioventricular
re-entrant tachycardias (AVRT).
1
We report the case of a young woman in whom previous ablation of a left postero-inferior concealed AP created an incomplete iatrogenic mitral block. This mitral block was responsible for a split retrograde atrial activation during orthodromic AVRT.
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Case report
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A young woman suffering from palpitations was admitted for electrophysiological
study in 2002 in a cardiac electrophysiology laboratory. A concealed
accessory pathway (AP) without decremental conduction properties,
located at the postero-inferior aspect of the mitral annulus,
was diagnosed. This AP was the source of orthodromic atrioventricular
re-entrant tachycardia (AVRT). A first ablation procedure was
attempted by a transseptal approach and failed. The patient
was referred to our institution 2 years later for a second catheter
ablation procedure because of recurrent paroxysmal AVRT episodes.
The patient had a normal baseline ECG and no structural heart
disease. After written informed consent, the second procedure
was performed in October 2004. Antiarrhythmic drug therapy had
been discontinued for >5 half-lives. Under sedation with
nalbuphine and midazolam, two 6-French quadripolar catheters
were introduced through the right femoral vein and placed in
the coronary sinus (CS) and the His bundle positions. A 7-French
CELSIUS
TM ablation catheter (Biosense Webster
®, Diamond
Bar, USA) was introduced retrogradely through the right femoral
artery. Twelve-surface ECG leads and multiple intracardiac bipolar
electrograms filtered at 30500 Hz were recorded
using a computerized EP recording system (Cardiolab
® II
Plus, GE Marquette Medical Systems, Milwaukee, USA). Orthodromic
AVRT (cycle length 400 ms) was easily induced by a train
of electrical stimuli from the CS at a cycle length of 375 ms
(
Figure 1). This tachycardia had a short and fixed RP
interval. The retrograde atrial activation was eccentric either
during ventricular pacing in sinus rhythm or during the tachycardia
at comparable cycle lengths. There were no changes in the atrial
eccentric activation neither spontaneously nor during ventricular
pacing, suggesting the presence of only one bypass tract. Two
reasons allowed us to rule out a focal atrial tachycardia. First,
the tachycardia could be reset by delivering a ventricular premature
complex during the His refractory period. Second, right ventricular
pacing during tachycardia, at a cycle length just shorter than
that of the tachycardia, changed the atrial cycle length. Mapping
of the postero-inferior aspect of the mitral annulus during
tachycardia showed a split fragmented retrograde atrial electrogram
(A1 and A2). A1 was the earliest component of the retrograde
atrial activation and A2 was the later component. The A1A2
interval was 114 ms. The atrial activation time in the
CS was recorded between A1 and A2. The mapping catheter was
moved through the double potential (DP) line from a site near
the mitral annulus (Site 1) to a site near the left inferior
pulmonary vein (Site 3) via Site 2, in between the two. Site
1 had the shortest VA1, A1A2, and VA2 intervals,
thus suggesting a conduction gap within the DP line. When the
mapping catheter was moved from Site 1 to Site 3 through Site
2, we observed a progressive increase in the VA1, A1A2,
and VA2 intervals, indicating a greater conduction delay
at Site 2 with the greatest at Site 3. The shortest VA1
interval (30 ms) was recorded at Site 1 and was targeted
for ablation (
Figures 2 and
3). One RF current application
with a target temperature of 50°C and a maximum power output
of 65 W terminated the tachycardia (procedure time: 39 min;
fluoroscopy time: 23 min). The procedure was deemed successful.
We failed to re-induce the tachycardia by pacing from the CS,
and incremental RV apical pacing was associated with concentric
activation of the atria and retrograde Wenckebach block (
Figure 4).

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Figure 1 (A) Twelve-lead ECG during orthodromic AVRT. Sweep speed 100 mm/s. (B) Orthodromic AVRT. Shown are three surface leads and intracardiac recordings from distal (d), medial (m), and proximal (p) His bundle (HBE) and from distal (d), medial (m), and proximal (p) coronary sinus (CS). For technical reasons, the CS catheter could not be advanced deeper into the CS. Consequently, a shorter VA interval was not recorded in the CS catheter. Sweep speed 100 mm/s.
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Figure 2 Evidence of an incomplete mitral block by mapping a DP line, separated by a non-isoelectric baseline, e.g. a fragmented baseline, within the postero-inferior aspect of the mitral annulus during orthodromic AVRT. Site 1: VA1=30 ms, A1A2=123 ms, VA2=150 ms; Site 2: VA1=32 ms, A1A2=126 ms, VA2=161 ms; Site 3: VA1=41 ms, A1A2=134 ms, VA2=175 ms. Shown are three surface leads and intracardiac recordings from distal (d), medial (m), and proximal (p) His bundle (HBE), from distal (d), medial (m), and proximal (p) coronary sinus (CS), and from the ablation catheter (ABL). Sweep speed 200 mm/s.
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Figure 3 Diagram of the mitral annulus and the left atrium: 45° left anterior oblique (LAO) view. The left superior, left inferior, right superior, and right inferior pulmonary veins (LSPV, LIPV, RSPV, and RIPV), the His bundle (HBE), the coronary sinus (CS), and the concealed AP are represented. Mapped Sites 1 (1), 2 (2), and 3 (3) are shown. The mitral isthmus lies medial to the AP and is delimited by two discontinuous lines. Sites 1, 2, and 3 are located within the mitral isthmus. The solid black arrow represents a partial activation pathway of the mid-inferior aspect of the LA.
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Figure 4 Concentric activation of the atria and retrograde Wenckebach block during 500 ms right ventricle (RV) apical pacing after AP ablation at Site 1. Sweep speed 100 mm.
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Discussion
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During orthodromic AVRT, the recording of a retrograde split
atrial potential, separated by a non-isoelectric baseline, e.g.
a fragmented baseline, at the postero-inferior aspect of the
mitral annulus (
Figures 2 and
3) led us to consider the
presence of an incomplete mitral isthmus block. The incomplete
mitral isthmus block, located between the left inferior pulmonary
vein orifice and mitral annulus, was probably created during
the first ablation procedure targeting the atrial AP insertion
using a transseptal approach.
2
In this situation, the atrial
insertion of the AP lies lateral to the mitral isthmus.
2
Indeed,
the earliest A signal and the merged VA interval (Site
1) were recorded lateral to the distal CS; furthermore, CS activation
showed an activation pattern from distal to proximal, via medial,
thus indicating a concealed AP lateral to the CS-tip catheter.
Alternatively, we also considered the possibility of a wide
AP with the exit of which was divided into two by the previous
ablation.
3
The changing relationships of A1A2, VA1,
and VA2 intervals as the mapping catheter was moved from
Sites 1 to 3, the activation in the CS after A1 and before A2
and the constant non-isoelectric line between A1 and A2 along
the whole mitral isthmus line (i) validated the presence of
an incomplete mitral isthmus block responsible for partial clockwise
activation of the mid-inferior LA and (ii) eliminated the possibility
of a wide AP with a double atrial exit iatrogenically created
during the first ablation procedure. The possibility of two
APs co-existing in the postero-inferior aspect of the mitral
annulus was eliminated, as after successful RF current application
at Site 1 (with successful ablation of the lateral AP), (i)
a change in the activation sequence in the CS would be expected,
(ii) retrograde Wenckebach block during incremental RV pacing
would be highly improbable, and (iii) another orthodromic AVRT
(involving the intact AP) is likely to be initiated by pacing
in the CS or the RV apex. Furthermore, the possibility of a
concealed epicardial AP associated with multiple connections
between the CS and the LA is also improbable for three main
reasons. First, in this case, a single dominant atrial signal
is expected during tachycardia, whereas a wide split LA activation,
as found in our case, is unlikely. Indeed, fragmented and concomitant
multiple retrograde atrial signals during tachycardia are uncommon.
Second, after successful RF application, a shift in the retrograde
atrial activation is expected. Third, endocardial RF application,
as performed at Site 1, would not ablate the AP as easily as
described. The presence of a mitral isthmus after a failed prior
left-sided pathway ablation causing unusual patterns of retrograde
atrial activation during orthodromic AVRT and RV pacing has
been previously suggested in an elegant study by Luria
et al.
2
and in a case report by de Vasconcelos
et al.
3
These authors
demonstrated the mitral block by analysing the CS activation
sequence during orthodromic AVRT and by pacing either the LA
or the RV apex in sinus rhythm. Nonetheless, to our knowledge,
proving the presence of an incomplete mitral isthmus block by
mapping, in the same fashion as that performed for the cavotricuspid
isthmus,
4
has not been reported. However, it may be that our
case points out the potential pro-arrhythmic risk and the difficulty
of signal interpretation related to RF lesions after unsuccessful
RF ablation procedures, as do the studies from Luria
et al.
2
and de Vasconcelos
et al.
3
We were unable, for technical
reasons, to advance the CS catheter deeper into the CS. Therefore,
the tip of our CS catheter was at all times medial to the mitral
block. Thus, the low infero-lateral LA activation could not
be recorded by the CS catheter. Had the catheter been advanced
further into the CS, delayed lateral atrial activation vis-à-vis
A1 and the distal CS would probably have been recorded as seen
by Luria
et al.
2
and by de Vasconcelos
et al.
3
In
addition, pacing from the low infero-septal LA was not performed.
Thus, the mitral block was only studied in a unidirectional
manner.
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Conclusion
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When a split retrograde atrial activation is recorded during
orthodromic AVRT, due to a concealed AP, several diagnoses should
be considered. In the absence of LA lesions, which may be responsible
for functional or anatomic block, multiple APs and multiple
connections between the CS and the LA must be eliminated. Conversely,
if an atrial lesion is present, e.g. RF ablation lines previously
created, one should consider a wide AP with an iatrogenic Y-shaped
exit or a LA block line, e.g. mitral isthmus, responsible for
a double atrial signal. In the latter case, after meticulous
mapping of the circuit, the shorter VA1 interval must
be targeted for RF ablation.
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References
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[1] Josephson ME. Supraventricular tachycardias. Clinical Cardiac Electrophysiology: Techniques and Interpretations 2002; 3rd ed. Philadelphia, PA Lippincott Williams & Wilkins pp. 219227.
[2] Luria DM, Nemec J, Etheridge SP, Compton SJ, Klein RC, Chugh SS, Munger TM, Shen WK, Packer DL, Jahangir A, Rea RF, Hammil SC, Friedman PA. Intra-atrial conduction block along mitral valve annulus during accessory pathway ablation: evidence for a left atrial isthmus. J Cardiovasc Electrophysiol 2001; 12: 7449.[CrossRef][Medline]
[3] De Vasconcelos JT, Rodrigues Bento Costa E, dos Santos Galvão Filho S, Monteiro Boya Barcellos C, Arnez Maldonado JG. Block of the mitral-pulmonary isthmus during ablation of a single left-sided accessory pathway causing different patterns of retrograde atrial activation. Arq Bras Cardiol 2002; 78: 497509.[Medline]
[4] Cosío FG, Awamleh P, Pastor A, Núñez A. Determining vena cava-tricuspid isthmus block after typical flutter ablation. Heart Rhythm 2005; 2: 32832.[Medline]

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