Europace (2012) 14, ii3–ii6
doi:10.1093/europace/eus212
Changes in the propagation pattern within the
conduction channel during sinus rhythm and
ventricular tachycardia demonstrated by noncontact mapping: role of late potential activity
Pasquale Vergara1, Nicola Trevisi1, Annarita Bisceglie 2, and Paolo Della Bella 1*
1
Arrhythmia Unit and Electrophysiology Laboratories, San Raffaele Hospital, Milano, Italy; and 2St Jude Medical, Agrate Brianza, Italy
Sustained monomorphic ventricular tachycardia (VT) in patients with a previous myocardial infarction is due to re-entry mechanism in areas
of slow conduction. The recognition of the pathogenic mechanism and the characterization of the activation pathway are usually obtained by
indirect measures with entrainment mapping and pacing manoeuvres. We studied a 61-years-old patient with a history of previous inferior
myocardial infarction and we provided the in vivo direct visualization of the critical components of re-entry circuit by non-contact mapping.
VT circuit entrance, central pathway, and exit were characterized during the same beat by virtual electrodes and visualized on a three-dimensional map both during sinus rhythm, ongoing VT, and pacemapping. The analysis demonstrated an activation of the conductive channel
in opposite directions during the sinus rhythm and ventricular tachycardia. Late potentials during sinus rhythm turned into mid-diastolic activity during VT; non-contact mapping allowed the ablation procedure to be performed in sinus rhythm, targeting the central pathway of the
conducting channel and the abolition of VT inducibility.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Non-contact mapping † Late potentials † Ventricular tachycardia ablation † Substrate mapping
A 61-year-old male with a history of inferior myocardial infarction
leading to severe left ventricular systolic dysfunction (ejection fraction 32%) had an implantable cardioverter defibrillator (ICD)
implantation for haemodynamically untolerated ventricular tachycardias (VTs); he was referred for ablation of recurrent VT
episodes treated by ICD shocks despite amiodarone therapy.
Programmed ventricular stimulation induced a monomorphic
VT, with a cycle length of 390 ms, reproducing the clinically documented VT. Because of poor haemodynamical tolerance, classical
VT mapping during ongoing arrhythmia was not feasible and the
tachycardia had to be interrupted by overdrive pacing.
During sinus rhythm, the arrhythmia substrate was characterized
by Dynamic Substrate Mapping using the EnSite System (St Jude
MedicalTM Inc., Milwaukee, WI, USA) with a multielectrode array
inserted via the left femoral artery and advanced retrogradely
into the left ventricle. Peak negative voltage values of all local
virtual unipolar electrograms of the left ventricle were plotted
on the previously acquired chamber geometry, to provide a
static isopotential voltage map during sinus rhythm (Figure 1A).
The criteria of peak negative voltage ,34% of unipolar noncontact electrograms was used to define scar tissue1; a wide scar
*
area was thus identified in the basal portion of the inferior was
of the left ventricle. Sinus rhythm propagation in the left ventricle
was then analysed. The impulse emerging from the bundle
branches in the posterior septum reached the left ventricular
apex and then the lateral wall, travelling around a region of functional block in the mid portion of the inferolateral wall; subsequently, the portion of the inferior wall between the area of scar
and the area of functional block was slowly activated in
postero-anterior direction (Figure 1B, Supplementary Video S1).
Virtual electrograms registered a slow continuous diastolic activity
in that area spanning to 200 ms after the surface QRS onset; the
distal bipolar electrode of the ablation catheter (Biosense-Webster
Thermocool) placed in the area corresponding to the virtual electrode 13 in Figure 1B confirmed the presence of a late potential occurring a 200 ms after the surface QRS onset and 105 ms after the
surface QRS end.
Ventricular tachycardia was then induced by programmed
ventricular stimulation and interrupted by overdrive pacing; left
ventricular activation during tachycardia was then analysed by
non-contact mapping (Figure 2 and Supplementary Video S2).
The impulse travelled in an antero-posterior direction from
Corresponding author. Paolo Della Bella. Tel: +39 02 26433689; fax: +39 02 26437326, Email: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2012. For permissions please email: [email protected].
ii4
P. Vergara et al.
Figure 1 (A) Dynamic substrate mapping was analysed by a non-contact EnSite system. The wide yellow circumference encircles the area with
peak negative voltage ,34% of unipolar non-contact electrograms; a wide scar area was thus identified in the basal portion of the inferior was
of the left ventricle. (B) Sinus rhythm propagation in the left ventricle. The yellow arrows describe the impulse propagation pattern identified by
non-contact mapping. The impulse, travelling around a region of functional block in the mid portion of the inferolateral wall, activated the area
between the scar tissue and the zone of functional block in postero-anterior direction. The yellow zig-zag line highlights an area of slow conduction in correspondence of virtual electrograms 11 – 13, evident as slowing of sinus rhythm impulse progression at video propagation analysis;
those electrograms registered a slow continuous diastolic activity spanning to 200 ms after the surface QRS onset; the distal bipolar electrode of
the ablation catheter placed in the area corresponding to the virtual electrode 13 recorded a late potential occurring a 200 ms after the surface
QRS onset.
Figure 2 Left ventricular activation during tachycardia analysed by non-contact mapping. The yellow arrows describe the direction of conducting channel activation during VT (antero-posterior direction). The yellow zig-zag line highlights an area of slow conduction in correspondence of virtual electrograms 10 –11, evident as slowing of sinus rhythm impulse progression at video propagation analysis; virtual electrode 10,
placed in the central portion of the conducting channel, registrated a small mid diastolic activity 70 ms before the surface QRS onset.
the site of virtual electrode 8 (entrance site), which registered a
small early diastolic activity, to the site of virtual electrode 10
(central portion); in that area a slowing down of the conduction
was evident and the virtual electrode registered a small mid
diastolic activity 70 ms before the surface QRS onset; finally
the impulse emerged at the site of virtual electrode 12 (exit),
synchronous to the surface QRS onset, to activate the left
ventricular mass.
Non-contact mapping of channel activation
ii5
Figure 3 Characterization of impulse propagation during pacemapping. The stimulus-to-QRS interval is long (130 ms), consistent with slow
conduction. Virtual electrograms in the area of supposed VT re-entry circuit registered a slow continuous activity between the pacing artefact
and the surface QRS onset; when the impulse reached the site of virtual electrode 12, it spread out from the conducting channel to activate the
left ventricle.
Figure 4 Left ventricular endocardial activation during sinus rhythm after radiofrequency ablation. The impulse reached the inferior wall following the same pathway used before radiofrequency ablation and it blocked at the virtual electrode 11; no late potential activity could be
recorded after the QRS end (the red vertical caliper was placed at 200 m after the QRS onset).
ii6
P. Vergara et al.
The paced QRS from the site of late activity during sinus rhythm
matched the VT morphology with a long stimulus-to-QRS interval
(130 ms); virtual electrograms in the area of supposed VT re-entry
circuit registered a slow continuous activity between the pacing
artefact and the surface QRS onset; when the impulse reached
the site of virtual electrode 12, it spread out from the conducting
channel to activate the left ventricle (Figure 3 and Supplementary
Video S3).
Radiofrequency ablation was performed by repeated pulses
(35 W, 43 8C) to intersect the conductive channel. Programmed
stimulation after the ablation was not able to induce any VT. Left
ventricular endocardial activation during sinus rhythm was then
analysed by non-contact mapping (Figure 4 and Supplementary
Video S4). The impulse emerging from the bundle branches in
the posterior septum reached the inferior wall following the
same pathway used before radiofrequency ablation, but propagation failed to penetrate the conductive channel with block at the
virtual electrode 11; no late potential activity could be recorded
after the QRS end (the red vertical caliper highlight the time
frame of 200 ms after the QRS onset, where previously a late potential was found).
an activation of the conductive channel in opposite directions
during the sinus rhythm and ventricular tachycardia. In previous
studies, entrainment mapping showed that late potentials were frequently recorded in sites classified as central or proximal in the
re-entry circuit.2,3 Late potentials during sinus rhythm turned
into mid-diastolic activity during VT; non-contact mapping
allowed the ablation procedure to be performed in sinus
rhythm, targeting the central pathway of the conducting channel;
successful ablation was associated with disappearance of late
potentials on contact mapping and to the disappearance of conduction within the channel, as assessed by non-contact mapping.
This appears to be the first in vivo demonstration during sinus
rhythm of arrhythmia substrate modification by radiofrequency
ablation.
Discussion
Supplementary material
Sustained monomorphic VT in patients with a previous myocardial
infarction is due to re-entry mechanism in areas of slow conduction; however, the recognition of the pathogenic mechanism and
the characterization of the activation pathway are usually obtained
by indirect measures with entrainment mapping and pacing manoeuvres. The present is, to our knowledge, the first published in
vivo direct visualization of the critical components of re-entry by
non-contact mapping; VT circuit entrance, central pathway, and
exit were characterized during the same beat by virtual electrodes
and visualized on a three-dimensional map both during sinus
rhythm, ongoing VT, and pacemapping. The analysis demonstrated
Supplementary videos for each figure are available at Europace
online.
Disclosures
Dr Paolo Della Bella PDB is consultant for St Jude Medical and has
received honoraria for lectures form Biosence Webster, St Jude
Medical and Biotronik.
References
1. Voss F, Steen H, Bauer A, Giannitsis E, Katus HA, Becker R. Determination of myocardial infarct size by noncontact mapping. Heart Rhythm 2008;5:308 –14.
2. Hsia HH, Lin D, Sauer WH, Callans DJ, Marchlinski FE. Relationship of late potentials to the ventricular tachycardia circuit defined by entrainment. J Interv Card Electrophysiol 2009;26:21 –9.
3. Harada T, Stevenson WG, Kocovic DZ, Friedman PL. Catheter ablation of ventricular tachycardia after myocardial infarction: relation of endocardial sinus
rhythm late potentials to the reentry circuit. J Am Coll Cardiol 1997;30:1015 –23.