(Circulation. 1995;91:2002-2009.)
© 1995 American Heart Association, Inc.
Articles |
Body Surface Potential Distributions During Idiopathic Ventricular Tachycardia
From the Research Center, Hôpital du Sacré-Coeur de Montréal and the Departments of Medicine and Pharmacology, Institut de Génie Biomédical and Ecole Polytechnique, Université de Montréal, Québec, Canada.
Correspondence to Dr Réginald Nadeau, Research Center, Hôpital du Sacré-Coeur de Montréal, 5400 Gouin Blvd W, Montreal, Québec, Canada H4J1C5.
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Abstract |
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Background The purpose of this report is to describe the body surface potential maps (BSPMs) during idiopathic ventricular tachycardia (VT) and to determine what differences exist between different idiopathic VT morphologies.
Methods and Results We performed BSPMs during VT on 12 consecutive patients (3 women and 9 men; mean age, 42±13 years) presenting symptomatic idiopathic VT referred to our institution for electrophysiological study. Basal ECG, chest radiograph, and echocardiogram were normal in all patients. Clinical tachycardia showed left bundle branch block pattern (LBBB) in 9 patients, with sustained VT in 5 and nonsustained VT in 4, and right bundle branch block pattern (RBBB) in 3 with sustained VT. We found a unique pattern of BSPMs in each of the 9 patients during idiopathic LBBB VT configuration, whether sustained or nonsustained VT. This pattern appeared at the onset of the QRS and remained stable during the whole QRS complex. The area of minimal potential located in the upper anterior part of the torso was compatible with an origin of VT in the right ventricular outflow tract, as confirmed in 5 patients by successful radiofrequency ablation. We found an evolving pattern with two phases in each of the three RBBB VTs. The electrical axis during the initial part of the QRS could correspond to an endocardial-epicardial vector. The second phase, with a high voltage and area of minimal potential located in the inferior and anterior part of the torso, was compatible with a left ventricular apical origin that was confirmed by epicardial and endocardial mapping during cryosurgery in 1 patient. For all the VTs, the QRS isoarea maps showed the same pattern as the second phase of the QRS.
Conclusions Two different BSPM patterns were found. All LBBB VTs had the same stable pattern corresponding to an infundibular origin. All RBBB VTs had an evolving pattern that stabilized in the second part of the QRS complex corresponding to an apical origin.
Key Words: tachycardia • potentials • mapping
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Idiopathic ventricular tachycardias (VTs) occur in patients without structural heart disease. Two groups have already been described1 2 3 4 5 : one with a left bundle branch block configuration on the ECG (LBBB VT) and the other with a right bundle branch block configuration (RBBB VT). However, these two groups do not seem to be homogeneous.1 6 Clinical presentations range from repetitive trains of monomorphic nonsustained VT to infrequent episodes of sustained VT. Exercise may either suppress or facilitate VT initiation.7 8 9 The responses to programmed stimulation and different pharmacological manipulations are variable and suggest diverse mechanisms, including reentry, triggered activity, and automaticity.10 11 12 13 14 15 16 Moreover, idiopathic VT, with a usually excellent prognosis, can be the first sign of an evolving cardiomyopathy.2 3 17 The purpose of this report is to describe the body surface maps of patients with idiopathic VT. Such analysis in these subgroups may help in our understanding of idiopathic VT and may be useful in guiding future ablative techniques.18 19 20
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Methods |
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From October 1986 through January 1993, 12 patients (3 women, 9 men; mean age, 42±13 years) were referred to our center for recurrent monomorphic VT without clinical evidence of heart disease. The absence of organic heart disease was diagnosed by (1) normal cardiac examination, (2) normal resting ECG, (3) normal chest radiograph, (4) absence of coronary artery disease evidenced by a submaximal treadmill exercise test or by coronary arteriography, and (5) normal echocardiogram. The absence of organic heart disease was confirmed in all the patients. Late potentials according to standard criteria13 were found in 2 of 9 patients (22%), both having sustained VT.
Definitions
Nonsustained VT was defined as VT of more than
three beats and
terminating spontaneously before 30 seconds. Sustained VT was defined
as VT for >30 seconds. Trains of nonsustained VT were defined as
successions of nonsustained VT separated by a few sinus complexes.
Body Surface Potential Mapping
The body surface potentials
were measured with 63 unipolar leads
referenced to the Wilson central terminal. The electrodes, which
consisted of plastic disks containing Ag-AgCl particles, were mounted
on 12 vertical adhesive strips with an interelectrode distance of 6 cm,
with 43 electrodes on the front and sides of the torso and 20
electrodes on the back.21 The first strip was applied over
the sternum, with the top electrode over the suprasternal notch. The
first electrode of each of the 11 other strips was applied at the same
level. The setup time for the body surface potential mapping (BSPM)
leads was about 5 to 10 minutes. The 63 ECGs were amplified, filtered
with a bandwidth of 0.05 to 200 Hz, multiplexed, sampled at 500 Hz,
digitized with a 10-bit analog-to-digital converter, and stored in a
circular memory buffer.22
During data acquisition, a reference signal from 1 of the 63 leads was constantly displayed on a terminal to allow the selection of any particular beat for the BSPM analysis, which was carried out on a MicroVAX II computer (Digital Equipment Corp).
The first step of the
BSPM analysis consisted of displaying all the
63 ECGs of the selected beat to visually identify faulty leads. Any
faulty signal was then replaced by interpolating the signals from
neighboring leads. Baseline shift was corrected by subtracting from
each ECG a straight line joining two isoelectric points that were
manually selected during the intervals that preceded and followed the
beat. This preprocessing phase could be performed in <2 minutes. Two
different types of maps were used in this study (Fig 1
). First,
to characterize the spatial
distribution of the body surface potentials at any specific instant,
isopotential maps were drawn. On these maps, the torso surface is
represented in a rectangular format. The left side of the
map corresponds to the anterior torso, and the right side corresponds
to the posterior torso. The isopotential lines that join points with
the same potential value at a specific instant are obtained by cubic
spline interpolation. The zero potential line is identified by a
heavier line, and the plus and minus signs identify the locations of
the maximum and minimum. The successive maps, drawn every 2 ms,
demonstrate the position and the evolution of the surface potentials
during the whole QRS.
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Second, QRS isoarea maps, which have been demonstrated to represent an index of global depolarization,23 were computed for the same beats. The onset and offset of the QRS complex were visually identified, and the net area under the QRS complex was computed. Contour lines joining points having the same net area were then plotted to obtain QRS isoarea maps.
Electrophysiological Study
All patients underwent an
electrophysiological study after
discontinuation of all cardioactive drugs for more than 5 half-lives.
Three quadripolar 6F catheters were introduced percutaneously into a
femoral vein and were positioned in the high right atrium,
atrioventricular junction, right ventricular apex, and outflow tract.
Four surface leads (I, II, III, and V1) were recorded
simultaneously with intracardiac electrograms (filtered at 30 to 500
Hz) on a multichannel oscilloscope (Electronics for Medicine VR-16,
Honeywell Inc) and recorded on a thermal printer (MT-9600, Astro-Med
Inc) at a paper speed of 100 mm/s and on a Kyowa videocassette
recorder. Pacing was performed with a programmable stimulator (Bloom
Associates) with stimuli of 2-ms duration and a current strength twice
the late diastolic threshold. Programmed right ventricular stimulation
was performed at two ventricular sites with one, two, and three
ventricular extrastimuli introduced after pacing for eight beats at
cycle lengths of 600, 500, and 400 ms. The end of the stimulation
protocol was refractoriness or induction of a sustained VT. If it was
impossible to induce sustained VT, a second stimulation series with up
to three extrastimuli was performed under a perfusion of isoproterenol
(dose to increase sinus rhythm by 20%).
Radiofrequency Ablation
Therapy with radiofrequency (RF)
catheter ablation was attempted
in 6 patients. A 7F quadripolar catheter with a 4-mm electrode tip and
a deflectable curve (Mansfield-Webster) was positioned in the right
ventricle through the femoral vein in LBBB VT and in the left ventricle
through the femoral artery in RBBB VT. RF current was delivered between
the ablation catheter and a backplate by use of a 500-kHz RF generator
(HAT 200, Dr Osypka GmbH). The goal of RF
application19 20
was the elimination of all spontaneous ventricular ectopy and inducible
VT (nonsustained or sustained VT). The localization of the putative
site of tachycardia origin was identified by a pace mapping performed
during sinus rhythm at a rate similar to the induced tachycardia or
during tachycardia at a rate slightly faster than the tachycardia rate.
Early depolarization during VT was not used on a regular basis but only
as a screening tool when VT was incessant: If endocardial electrograms
recorded by the ablation catheter were not earlier than surface ECG
ventriculograms, pace mapping was not performed. Abnormal electrograms
were not found during the RF ablation procedures. The QRS morphology in
each of 12 leads was compared with the morphology during VT. Optimal
pace maps were defined as those with the closest possible match between
QRS morphologies in each of the 12 leads.
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Results |
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Ventricular Tachycardia
We found two distinct morphologies of VT: an LBBB configuration with an inferior axis and an RBBB configuration with a superior axis.
LBBB morphology was found in 9 patients (3 women, 6 men; mean age, 45±14.5 years). Three patients had sustained VT without trains of nonsustained VT. Six patients had trains of nonsustained VT, unceasing in 2 and associated with episodes of sustained VT in 2 others. Treadmill tests were performed in all patients. Treadmill tests increased the frequency or the length of VT runs in 5 patients and induced sustained VT in 2. Programmed ventricular stimulation in the basal state failed to induce VT in 7 of 7 patients who were not in unceasing runs of VT. Isoproterenol infusion induced VT in 6 of these 7 patients. Verapamil was used for termination of VT in 4 patients but was always ineffective. RF ablation was performed in 5 patients. In each case, catheter mapping localized the origin of the VT in the right ventricle outflow tract, and ablation was successful in eliminating VT.
RBBB morphology was found in 3 patients (3 men; mean age,
35±7.5
years). The 3 patients had sustained VT without trains of nonsustained
VT. The results of treadmill testing were variable
(Table). An isoproterenol infusion was required in 2
patients to induce sustained VT. Verapamil terminated VT in the 3
patients. RF ablation was attempted in only 1 patient (patient 11) and
was unsuccessful; however, cryoablation during open-heart surgery was
carried out successfully in this patient. Pace mapping localized the
origin of the VT in the apical and paraseptal-posterior area of the
left ventricle.
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Body Surface Potential Mapping
LBBB Morphology
A unique pattern of BSPM common to all the patients appeared at
the onset of the QRS and remained stable thereafter (Fig 2).
The area of minimal potential was located on the
upper anterior torso, indicating a basal right ventricular
breakthrough, with a trend to progressively shift to the middle
anterior torso. The axis was inferior, with a maximal potential located
on the left inferior anterior torso in the region of the apex, which
remained stable. Fig 3 shows the maps of the 9 LBBB VTs
at the onset and at the time of maximal voltage; each patient had a
similar pattern that was stable with the time.
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RBBB
Morphology
In each of the 3 patients, we found the same evolving
pattern as
illustrated in Fig 2B
from patient 11. In the first part of the
QRS,
the voltages were low (0.02 to 0.1 mV) and the axis was inferior, with
an area of minimal potential located on the upper torso and the maximal
potential located on the inferior and anterior part of the torso. In
the second part of the QRS, the voltage was higher (0.2 mV), and the
pattern was more stable and was the opposite of the first. The axis was
superior, with an area of minimal potential located on the inferior and
anterior part of the torso and the maximal area on the upper torso,
indicating an apical breakthrough. The second phase began at 24 ms in 2
patients, with a QRS duration of 122 ms (at 20% of the QRS complex)
and at 30 ms in the third patient, with QRS duration of 160 ms (at 25%
of the QRS complex). The BSPM of patient 11 (Fig 2B) was
correlated
with intraoperative mapping data (Fig 4) as a regional
cryoablation guided by computerized epicardial and endocardial mapping
was performed24 after failure of the RF ablation.
Epicardial breakthrough occurred 12 ms after the apical endocardial
origin; apical depolarization occurred during the first 20 ms, with
ventricular depolarization proceeding from the apex to the base. The
endocardial breakthrough was widespread, and the total duration of
depolarization was 50 ms on the endocardium and 104 ms on the
epicardium. Cryolesions that eliminated VT were produced in the left
ventricle on the apex of the septum, and several small RF lesions were
observed in this area.
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Body Surface Isoarea QRS Mapping
In the 9 patients with LBBB
VT, a common pattern (Fig 5A) occurred, with the area of
minimal potential located
on the upper anterior torso, indicating a basal right ventricular
breakthrough.
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In the 3 patients with RBBB VT, a common pattern (Fig
5B) was also
found, with the area of minimal potential located on the inferior and
anterior part of the torso and the maximal area on the upper torso,
indicating an apical breakthrough.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Population
All the patients fulfilled the diagnostic criteria for idiopathic VT. One patient with each VT configuration had late potentials without other abnormality. The 22% incidence of late potentials in our population is comparable to the 18% found by Mehta et al.25 In 30 patients with LBBB VT configuration (23 nonsustained VT), Buxton et al4 detected no late potentials. In accordance with Mehta et al,25 who found a higher incidence of late potentials in patients with sustained VT than in patients with nonsustained VT (33% versus 9%), in our study late potentials were present only in patients with sustained VT.
Ventricular Tachycardia
As previously described, we found two
groups of idiopathic VT,
with LBBB and RBBB morphologies. The clinical heterogeneity within
these two groups is shown in the Table. Presentations ranged
from
unceasing trains of monomorphic nonsustained VT to infrequent episodes
of sustained VT. Exercise could either suppress or facilitate VT
initiation. The responses to programmed stimulation and to different
pharmacological manipulations were variable. Unfortunately, not all the
useful pharmacological manipulations were attempted, since this study
was retrospective and was begun in 1986. Verapamil was administered in
each patient with an RBBB configuration of verapamil-sensitive
VT5 and in 4 of 9 patients with an LBBB
configuration. Isoproterenol was infused only when ventricular
stimulation failed to induce sustained VT. Adenosine was not used.
Body Surface Maps
This study is the first, to the best of our
knowledge, to report
surface maps of VT in a set of patients without structural heart
disease, although isoarea maps in two patients with LBBB VT morphology
who underwent later surgery have been described.26 Despite
the clinical heterogeneity, the results of body surface mapping were
homogeneous.
LBBB Morphology
In each case of LBBB VT, the
BSPM showed the same pattern from the
onset to the end of the QRS complex. The minimal potential area was
located on the upper anterior torso, indicating a basal right
ventricular breakthrough. This VT origin was confirmed in 5 of 5
patients by pace mapping with successful RF ablation. This result is in
agreement with several studies4 19 20
that located the VT
origin in the right ventricular outflow tract. The isoarea maps of the
QRS showed a pattern similar to that of the BSPM. In the two cases
described by SippensGroenewegen et al26 and also
originating from the right outflow tract, isoarea maps were very
similar to the pattern we found in this study.
RBBB
Morphology
The 3 sustained VTs (without trains of nonsustained VT)
were
verapamil sensitive and showed the same evolving BSPM pattern, with 3
phases. The second phase, with a higher voltage, was very stable. The
area of minimal potential, located on the inferior and anterior part of
the torso, evoked an apical breakthrough. Several facts confirmed this
hypothesis. In one patient, pace mapping during an unsuccessful RF
ablation found an apical and paraseptal-posterior origin. Subsequently,
endocardial mapping during a successful cryosurgery confirmed this
localization, and some RF lesions were seen at the breakthrough area.
Endocardial breakthrough preceded epicardial breakthrough, confirming
an endocardial origin. A broad endocardial breakthrough and a short
activation time (50 ms) were also in favor of an origin in rapidly
conducting tissue.27 These results agree with several
previous studies that suggest a left posterior fascicular origin for
this morphology.
Further, this case can provide an explanation for the
evolution of the
BSPM in two phases. We know that the BSPM is correlated with the
epicardial map.28 This patient had an epicardial
breakthrough 12 ms after the endocardial breakthrough, and
depolarization of the apex occurred at around 20 ms. The axis and the
duration of this sequence of depolarization were compatible with the
first phase of the BSPM, with a low voltage, a duration of 
20 ms,
and an inferior axis. The epicardial depolarization from the apex to
the base of the heart was responsible for the last phase of the BSPM,
with a higher voltage and a superior axis. The isoarea maps of the QRS
showed a pattern similar to the second phase of the BSPM. The higher
voltage and better stability of this last phase explain this result.
The absence of structural heart disease such as myocardial infarction
and aneurysm simplifies BSPM interpretation and possibly accounts for
the close correlation that was found between BSPM and the site of
origin as determined by intraoperative mapping.
Potential Clinical Value of the Findings
The descriptive
results of this study must be understood in the
decade of catheter ablation. All the tools that can precisely localize
the origin of an arrhythmia have to be studied. Like the standard ECG,
BSPM can serve as a quick localization tool to identify a myocardial
area, but with a greater spatial resolution than the 12-lead
ECG.26 Moreover, it is probable that pace mapping with 63
leads is more accurate than with 12 leads,21 and this
possibility has to be studied in patients without structural disease
first. BSPM could detect the onset of endocardial activation before
epicardial activation in patient 11, and this finding opens the field
of the identification of the VT that could be accessible to endocardial
ablation.
Conclusions
A common pattern of BSPM occurs in idiopathic VT
of LBBB
configuration with inferior axis, regardless of clinical
presentation. This pattern is compatible with a VT origin in the
right ventricular outflow tract and was confirmed in 5 of 9 patients by
pace mapping with successful RF ablation.
A common evolving pattern in two phases occurs in idiopathic VT with an RBBB configuration. The second, high-voltage, phase is compatible with a left ventricular apical origin. This was confirmed by epicardial and endocardial mapping during cryosurgery in one patient. The isoarea maps showed the same pattern as the second, high-voltage, phase of the BSPM.
Received July 21, 1994; revision received October 24, 1994; accepted November 6, 1994.
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