(Circulation. 1997;96:3904-3912.)
© 1997 American Heart Association, Inc.
Articles |
Three-dimensional Mapping of the Common Atrial Flutter Circuit in the Right Atrium
From Service d'Electrophysiologie Cardiaque, Hôspital Cardiologique du Haut-Lévêque, Bordeaux-Pessac, France.
Correspondence to Docteur Dipen C. Shah, Service d'Electrophysiologie Cardiaque, Hôpital Cardiologique du Haut-Lévêque, Avenue de Magellan, 33604 Bordeaux-Pessac, France.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background The full circuit of common atrial flutter using conventional methods of sequential or multielectrode activation mapping is not completely understood.
Methods and Results We performed three-dimensional right atrial endocardial activation mapping during common counterclockwise atrial flutter in 17 patients (16 men, 1 woman; mean age, 53±11 years) by using the Cordis-Biosense EP Navigation system and assessed the distribution of estimated conduction velocities and double and fractionated potentials. ECG flutter wave morphologies were compared with activation patterns. Points (91±29) were sequentially acquired covering 88±11% of the flutter cycle length of 239±22 ms. A wide and variable posterior zone of double and fractionated potentials coincided with blocking and colliding wave fronts and formed the posterior limit of the circuit. A progressively widening septal (sep) wave front ascending from just beyond the coronary sinus ostium, passed cranially as a broad front anterior to the superior vena cava (SVC) in 14 patients, whereas fusion around the SVC formed the superior (sup) limb of the circuit in 3. Bounded anteriorly by the tricuspid valve, the wave front descended down the lateral (lat) aspect of the right atrium before completing the circuit in all cases through the inferior vena cava–tricuspid annulus isthmus. The estimated conduction velocity in the medial isthmus (0.6±0.3 m/s) was lower than in the other limbs of the circuit (sup=1±0.5 m/s, lat=1±0.5 m/s, sep=0.9±0.4 m/s, P=.05). Double and fractionated potentials were constant and more prevalent in the posterior right atrium. ECG flutter wave morphology did not correlate with three-dimensional activation maps.
Conclusions Interindividual variations occur in the right atrial circuit of common atrial flutter, with constant activation through the cavotricuspid isthmus. A variable zone of block forms the posterior limit. Fusion around the SVC can occur, and ascending medial septal activation does not follow a consistent pattern.
Key Words: atrial flutter • mapping • electrocardiography
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Activation mapping has been a mainstay for understanding many cardiac arrhythmias, particularly supraventricular and reentrant tachycardias.1 The limitations of conventional techniques involving single bipolar/unipolar sequential mapping or multielectrode/multicatheter mapping based on fluoroscopic correlations are, however, particularly obvious when attempting to relate to a three dimensional structure.
Previous studies2–8 have shown that typical atrial flutter is a stable macroreentrant tachyarrhythmia with a counterclockwise circuit revolving around anatomic and functional blocks in the right atrium. A common isthmus between the inferior vena cava and the tricuspid annulus critical to this arrhythmia has been identified by ablation techniques.6,9–12 Both conventional activation as well as entrainment mapping have been used to infer the participation of parts of the atria,13 but the full circuit remains relatively ill defined. In this study we describe the three-dimensional (3D) activation pattern in the right atrium (RA) during typical atrial flutter by using a new technique of correlative 3D mapping with particular emphasis on superior and septal-medial right atrial activation.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
Seventeen patients referred for radiofrequency (RF) catheter ablation of symptomatic typical atrial flutter were included in this study after informed consent was obtained. The study was approved by our institutional review board. All antiarrhythmic drugs were stopped at least 4 half-lives before the study except for amiodarone in 8. Sixteen of these patients were men; their mean age was 53±11 years (range, 41 to 74). Two patients had structural heart disease, including 1 with dilated cardiomyopathy and 1 with mitral regurgitation. All patients were required to have a typical surface ECG flutter wave morphology, which included sawtooth flutter waves negative in leads II, III, and aVF. Patients with nonsustained atrial flutter, surface ECGs not suggestive of typical atrial flutter, or exhibiting frequent degeneration into atrial fibrillation were excluded. None of the patients had undergone previous catheter ablation or cardiac surgery.
Electrophysiological Study
Introducer sheaths (8F and 9F) were placed in the right (and if
required, left) femoral veins to allow introduction of mapping and
reference catheters. The examination was performed on fasting patients.
Light sedation was administered with intravenous midazolam
and/or buprenorphine as necessary. Two patients who were in sinus
rhythm before the procedure underwent rapid burst pacing from the
proximal coronary sinus or low right atrium to induce typical
atrial flutter. The preliminary part of the study protocol required
confirmation of caudocranial septal and craniocaudal lateral right
atrial activation with a duodecapolar Halo catheter (Cordis-Webster) in
16- and a 14-pole custom-designed woven dacron catheter (Bard Inc) in
one patient.
Three-dimensional Mapping
The EP Navigation System includes a location pad, the Carto
processor, a monitor, and workstation (Silicon Graphics Inc) as well as
sensor-equipped mapping catheters (Cordis EP Navigation catheters). The
location pad with its three pods mounted on a triangular frame is
attached to the underside of the fluoroscopy table and emits a weak
electromagnetic field allowing a passive sensor incorporated in the
catheter tip of an 8F EP Navigation catheter to sense and transmit
these signals back to the processor unit. A triangulation algorithm is
used to precisely determine the position of the catheter tip in this
electromagnetically coded space. One such catheter is placed in a
suitable reference position, in this protocol within the proximal
coronary sinus so as to record a large and stable atrial
electrogram and a minimal ventricular electrogram. A second
such catheter is used as a roving map catheter in the right atrium. The
real-time spatial coordinates of the reference catheter (which, like
the map catheter, vary phasically both with respiration and cardiac
motion) are used to provide a dynamic corrective reference for the
spatial location of the map catheter tip. This allows correct location
and relocation of the position of the map catheter tip despite absolute
intrathoracic positional changes (due to respiration and cardiac
motion). The tip of the map catheter is depicted as a 3D icon on the
screen of the monitor, and its position and orientation in space can be
ascertained both by changes in the orientation or position of the icon
as well as by manipulating the background 3D grid (with the workstation
mouse) to alter the viewing perspective. With a rapid update rate, such
a capability can allow a certain amount of nonfluoroscopic manipulation
inside the reconstructed cardiac chamber.
A 3D map of the right atrium during atrial flutter is constructed by sequential mapping, ie, incorporating electrogram-derived activation times as well as spatial coordinates from each of multiple sites over the right atrial endocardium. At a given location, 2 to 3 seconds of electrograms are retained in memory and if variations in successive cycles of local activation times as well as spatial coordinates are within specified limits indicating both catheter and rhythm stability, this data point is incorporated in the map. The software uses a STAR algorithm to construct a polyhedral 3D structure using triangular panels from the spatial coordinates obtained at different locations. This algorithm incorporates a programmable distance threshold for interpolation that was progressively decremented during data acquisition to achieve a greater uniformity of point distribution for this study. The panels are color coded by assigning the colors of the rainbow to relative local activation timings (relative to a reference electrogram fiducial point). Activation times as well as the reference electrogram fiducial point are automatically detected according to programmable criteria. The accuracy of this system has been tested both in vitro and in vivo and found to be reproducible and accurate.14
For the first two patients the peak of the surface ECG (lead II) R wave
was used as the reference fiducial point after verification of stable
and fixed 2:1 atrioventricular conduction. The minimum
electrogram slope (ie, maximum negative dv/dt) of the proximal
coronary sinus atrial electrogram was selected in the next 15
patients. Bipolar (in 15) and unipolar tip electrograms (in the initial
2 cases) were acquired for mapping purposes with bandpass filter
settings of 30 to 400 Hz and 0 to 400 Hz, respectively. In some
patients both unipolar and bipolar signals were
simultaneously stored in the memory with unipolar signals
used to edit/assign local activation times in the presence of double
potentials. A double potential was defined as a double spike (bipolar)
or double deflection (unipolar) electrogram with an interval of at
least 20 ms measured between the points with the minimum dv/dt in each
spike or deflection. This interval for each double potential complex
was measured in milliseconds with an on screen caliper. Bipolar
electrograms with a duration longer than 50 ms and consisting of
continuous fractionated electrical activity or with multiple (>3)
deflections were also identified.4 The positions
of points recording stable, consistent (
3 consecutive
cycles) double potentials or fractionated potentials fulfilling the
above definition were marked graphically on the 3D maps by prominent
separately colored roundels. The distribution of double potentials and
fractionated potentials was assessed during atrial flutter in the
context of their role as markers of local conduction block or delay.
Analysis of acquired data therefore included the following
steps:
(1) All the acquired map data points were manually scrutinized for fulfillment of local activation time and location stability criteria. Screening requirements were a variation <5 ms and a tip location variability of <3 mm on successive beats. Points not fulfilling these criteria were excluded from the database and the reconstructed 3D map.
(2) Reference electrogram fiducial points were manually checked; if incorrectly annotated these data points were excluded from the map database.
(3) Map electrogram local activation times were also verified manually and corrected if necessary.
(4) Double potentials and fractionated potentials were marked by
differently colored roundels on the 3D map. They were assigned to the
following areas of the RA: (1) posterior RA, (2) superior vena cava
(SVC), (3) pericoronary sinus ostium region, (4) septal RA, (5)
inferior anterolateral RA, (6) superior anterolateral RA
and (Fig 1
). These areas were determined
on the reconstructed 3D map by correlation with fluoroscopic landmarks,
electrogram markers (eg, the His bundle electrogram, A-V electrograms
at the tricuspid valve annulus) and the reconstructed map itself (see
later). Two points closer than approximately 4 mm in any dimension
were considered as one for quantitative analysis.
|
(5) The volume of the reconstructed 3D map was automatically calculated.
(6) Software-generated animated propagation maps were superimposed on the reconstructed anatomic contours. The animation maps were qualitatively analyzed for macro activation patterns as well as colliding activation wave fronts, particularly in relation to anatomic landmarks/obstacles such as the orifices of the vena cava and the tricuspid annulus. Activation fronts were considered to be within the reentrant circuit when they were part of the spatially shortest route encompassing the full range of mapped activation times and returned adjacent to or within close proximity of the site with the earliest activation. Wave fronts colliding with each other (either traveling in opposite directions or with an angle between them of more than 90° in two dimensions) with significantly disparate activation times (>20 ms) were considered presumptive of local block at the site of collision. Each limb of divergent wave fronts was evaluated contextually and on the basis of its destination. Wave fronts converging at an angle of less than 90° and without significantly disparate activation times were considered to fuse. Activation times were also compared anterior and posterior to the SVC on a line perpendicular to the advancing wave front using the means of activation times of three points relatively equally spaced around this line.
Activation fronts as well as double and fractionated potentials were
assigned to specific anatomic locii on the basis of the reconstructed
3D map of the RA. In all cases the orifice of the tricuspid valve and
the SVC were easily recognizable-the former by an appropriately placed
defect in the map contour and the latter by a crownlike extension
(representing electrical activity in this proximal great
vessel segment) of the cranial aspect. Similarly the
inferior, posterior, and leftward extremity of the
reconstruction represented the proximal coronary
sinus and its ostium (Fig 1
). Because we used a proximal
coronary sinus atrial electrogram as a time reference, our
mapped and demarcated activation cycle commenced at the
coronary os and terminated in or around the coronary
ostium–tricuspid isthmus, thus locating the "frameshift" region of
the map there and precluding detailed analysis of activation in
this region. We could thus demarcate posterior as well as septal-medial
regions of the RA beyond the ostium of the coronary sinus. The
septum was further subdivided into roughly equal vertical thirds:
anterior (ventral), central, and posterior (dorsal), as judged from a
superior (cranial) perspective for analyzing the sequence of activation
in this area.
(7) An estimate of regional conduction velocity was calculated from the ratio of distances between points located in the mainstream of well-defined activation wave fronts and differences in activation times. Thus four points forming a quadrilateral within such a wave front were selected. The difference of the means of the activation times of the two points forming each side of the quadrilateral parallel to the advancing flutter wave front was divided by the estimated distance between the midpoints of these sides (23±8 mm). This distance varied because of the method of data acquisition utilized but points too close together or too far apart were excluded. Points were also selected to minimize marked intervening curvatures. For double potentials, the activation time of the potential corresponding to the orthodromically proximal wave front was used; in case of fractionated potentials the maximum negative dv/dt activation time was used for estimating conduction velocity. Conduction velocities were assessed in this manner in the medial part of IVC–tricuspid isthmus, the mid septum, the superior RA (anterior to the SVC), and the lateral RA. Because of the heterogeneous and complex activation observed in the posterior RA, conduction velocity could not be estimated.
Relation to Surface ECG Morphology
Interindividual variations in the surface ECG morphology were
compared with activation mapping data. For 16 of 17 patients, 12-lead
recordings with 3:1 or higher AV ratios were available. Two
independent observers, blinded to the results of the animated
propagation maps compared the following ECG features in lead III: (1)
amplitude of the summed negative and positive components of the F wave,
(2) the slopes of the flutter wave sharp component, and (3) of the
plateau phase as well as (4) the ratio of the duration of the plateau
(Tpl) to the duration of the F wave (Tf) (Fig 2). These were then related to the
results of 3D mapping.
|
Ablation Procedure
All patients subsequently underwent catheter ablation of the
inferior vena cava–tricuspid annulus (IVC-TA) isthmus,
with the use of methods described in earlier
reports.6,12 During ablation, isthmus
electrograms were in all cases confirmed to be centered on the surface
F-wave plateau. Standard quadripolar 4-mm, deflectable-tip electrode
catheters were used in conjunction with a Cordis-Stockert RF generator.
Closed loop temperature controlled and sequential point by point RF
applications were performed in a linear fashion.
Statistical Methods.
Each continuous variable was expressed as a mean±SD, and
comparisons were made using the Kruskall-Wallis
nonparametric test, the Fisher's exact test, the W-paired
Wilcoxon test, Student's t test ,and ANOVA as
considered appropriate. A value of P<.05 was considered
significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Three-dimensional Activation During Common Atrial Flutter
Three-dimensional maps of the RA during typical atrial flutter were successfully generated for all 17 patients, and a mean of 91±29 points were acquired per map covering 88±11% of the flutter cycle length in terms of the range of local activation times mapped. The mean reconstructed RA volume was 77±36 mL (range, 36 to 188) and the mean atrial flutter cycle length was 239±22 ms (range, 200 to 268). There were no significant differences in cycle lengths (234±28 ms on and 243±15 ms off; P=NS) and RA volume (62±26 mL on versus 91±40 mL off; P=NS) between patients on and off amiodarone. All patients underwent successful RF catheter ablation after completion of the mapping procedure with a mean of 10±7 pulses (range, 2 to 29; median, 8). There were no significant side effects.
In all cases, counterclockwise activation of the right
atrium was limited anteriorly by the boundary of the tricuspid valve.
However, there was no similar discrete posterior boundary (Fig 3). A posterior area of double potentials
was noted in each map consistent with the presumed anatomic
location of the crista terminalis, forming the posterior limit of the
circuit as previously described.13 However, this
posterior area was ragged and covered a zone that reached a maximum
width of 1.7±0.8 cm (Fig 4). Cranial
activation during flutter consisted of a broad limb extending uniformly
between the SVC and the superior tricuspid annulus in 14 cases before
continuing caudocranially down the lateral RA wall (Fig 5a). In three patients, the activation
wave front was noted to spread both anteriorly and posteriorly to the
SVC then fuse around the SVC before activating the lateral RA
craniocaudally. In these patients there were gaps in the distribution
of double potentials in the posterior RA behind the SVC (as also in
other patients) and the region posterior to the SVC was
activated just a little earlier (5 to 25 ms) than the anterior
(Fig 5b). The flutter cycle lengths were not different from the rest
(233±25 versus 240±22 ms, P=NS). There were no significant
differences in conduction velocities, and only one of them was
receiving amiodarone.
|
|
|
In the septum there was caudocranial activation in all cases, without a
constant pattern: In 6 cases a symmetrical wave front swept upwards
(Fig 6), in 4 the central septum was
activated early and followed by centrifugal spread; in another
4 the anterior (ventral) septum was activated earlier with
subsequent spread; whereas in 1 patient the posterior (dorsal) septum
was activated before the anterior septum. There was random and
patchy activation in 2.
|
In all cases, however, the flutter circuit was completed by activation through the IVC-TA isthmus and correspondingly activation was noted to occur to varying extents in the opposite direction posterior to the IVC before blocking. On the animated propagation map, one or more major activation wave front collisions with disparate activation times were observed in all cases in the posterior RA coinciding in some cases very well with locations where double potentials were recorded. The posterior RA region was consistently noted to be activated by diverging relatively horizontal and asynchronous activation wave fronts in contrast to activation in the vertical plane in the lateral and septal regions as previously described.
Regional Conduction Velocity Estimates
Table 1 summarizes the data.
Conduction velocity was significantly lower in the medial IVC-TA
isthmus (0.6±0.3 m/s) when compared with that in the other regions.
While this was slowest in 13/17 (76%) it was not so in 4 cases (2 of
these 4 patients-50%-and 6 of the previous 13% to 46%-were
receiving amiodarone). Though the velocities were lower in
patients who were still under the effect of oral amiodarone,
this was not statistically significant.
|
Regional Distribution of Double Potentials and Fractionated
Potentials During Atrial Flutter
Double potentials and fractionated potentials were found at
22±8% and at 16±11% of points, respectively, in the RA (Figs 3 and 4); their incidence, extent, and characteristics are summarized in
Table 2. In some instances, "double
potentials" with a Wenckebach-type relationship or frank dissociation
were noted in the proximal SVC.24 A general
pattern of posterior right atrial as well as septal and
pericoronary ostial double potential clustering was noted (Fig 3). The incidence, extent, and interspike DP intervals in the posterior
RA were significantly greater than in the lateral RA and the anterior
RA regions. There were also no significant differences between patients
receiving and those not receiving amiodarone.
|
Comparison of Surface ECG Flutter Waves With Three-dimensional
RA Maps
Morphologies of individual patients' flutter waves varied (Table 3), but there was no evident correlation
between the RA maps of patients and the surface ECG variables.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Three-dimensional Mapping of Common Atrial Flutter
Recent anatomic studies and those derived from activation and entrainment data have improved our understanding of the circuit of common atrial flutter, particularly in the low septal region.6,7,15-24 The present study using a new technique of reconstructive 3D mapping of the right atrium in humans completes previous data by providing panoramic and comprehensive (360°) mapping during common type I right atrial flutter.
A mean of 91 points were used to reconstruct the RA and delineate the 3D activation patterns of the right atrium during flutter, which is similar to the mapping density in most experimental studies. Anteriorly RA activation is obviously limited by the tricuspid valve annulus. However unlike some previous descriptions in animal models,17 the activation front covers not just a peritricuspid band but in fact a wide area bordered by the annulus. This may explain why attempts in such models to terminate the flutter by limited ligatures in the lateral right atrial region were unsuccessful.17 In contrast, the posterior limit is more uneven as inferred from the constantly present but ragged distribution of double potentials in this area. Such double potentials have been demonstrated to be indicative of conduction block by entrainment techniques.13,18 19,23 Moreover, analysis of animated activation maps indicates diverging asynchronously traversing oblique and horizontal wave fronts in the posterior RA, suggesting a nonuniform and nonlinear zone of block as the posterior limit. This area corresponds broadly to the expected position of the crista terminalis,13 although the irregular outline and scattered distribution suggest a functional area of block beyond this discrete anatomic structure.
The precise delineation of the cranial limb of the flutter
circuit has not been previously reported. This study shows that
activation in this region consists of a broad front extending between
two boundaries-the SVC posteriorly and the tricuspid annulus
anteriorly in 14 of 17 cases. However, in 3 cases, activation proceeded
almost simultaneously anterior and posterior to the SVC,
fused around it, and then proceeded to activate the
anterolateral RA wall craniocaudally. This suggests that the superior
RA between the SVC and the tricuspid annulus is not necessarily an
obligatory isthmus for type I atrial flutter. Activation of the
medial-septal aspect of the RA (above the coronary sinus
ostium) is altogether much more variable, since no
consistent pattern (except for caudocranial activation) could
be discerned. Although we could not corroborate previous data that the
region between the coronary sinus ostium and the tricuspid
valve annulus confined the circuit,17,24 our data
indicate that the activation wave front widens considerably as it
ascends upward in the septum. Also, the fossa ovalis is probably not
associated with activation, skirting it or proceeding around what might
be considered a potential endocardial obstacle. The
inconsistent and somewhat irregular activation patterns in the
septum could represent local "blind alleys" that may
underlie previous findings of a long post pacing interval after
entrainment from a fluoroscopically demarcated fossa
ovalis.18 Anatomic studies showing prominent
circumferential bundles encircling the anterior, lateral, and posterior
aspects of the tricuspid valve with narrowing and
heterogeneity of fiber arrangement in the medial and
low septal regions support these activation
patterns.20,21 Last, a consistently
obligatory activation was observed in all cases through the IVC-TA,
confirming that this structure still remains the target of choice for
interrupting typical atrial flutter by transcatheter RF
energy application. However this isthmus may be bypassed in some types
of atypical atrial flutter circuits. Estimated conduction velocity was
significantly slower (0.6 m/s) in the medial IVC-TA isthmus compared
with other limbs of the circuit, where it was 
1 m/s. There was no
statistically significant difference in conduction velocity caused by
amiodarone effect.
Regional Disparities of Complex Atrial Potentials During
Flutter
Unlike previous studies using conventional catheter
mapping4,19,22,23 the incidence and distribution
of double potentials was quantitatively estimated in our study at 22%
of mapped points. They were constantly present in the posterior
right atrium and less frequently in the septum as well as near the
coronary sinus (which includes the region corresponding to the
eustachian ridge). Such potentials may be associated with the take-off
site of diverging posterior right atrial wave fronts. We did sometimes
find double potentials in the lateral RA wall and in the superior
anterior RA but significantly less frequently and they were not
associated with major changes in activation patterns probably because
the changes were too circumscribed. Longer interspike double potential
intervals were found in the posterior RA as compared with the double
potentials in other regions in the RA. Similarly, during
atrial flutter fractionated potentials were most extensive as well as
invariably present in the posterior right atrium, and sometimes in
a wide area. They were less frequent in the area around the tricuspid
annulus probably correlating with smooth and even impulse propagation
here. Although the interspike intervals would obviously vary according
to the location of the recording electrode relative to the
line/area of block, and the direction of propagating wave fronts, they
support the role of the pericristal posterior RA as the preferential
zone of conduction slowing around which the flutter circuit appears to
be formed.4,13,19
The surface ECG flutter waves of patients with variant patterns on 3D EA mapping were not specifically distinctive. The lack of correlation with any distinctive surface ECG features is evidence that most of these differences in activation patterns are too subtle to be evident on the surface. Conversely the variations noted in the surface ECG flutter wave patterns may reflect differences in individual volume conductor properties and/or differences in activation in unmapped areas ie, the left atrium.
Limitations
Although common atrial flutter is generally a stable
arrhythmia with a stable cycle length, the software
parameters used here do not allow data acquisition if
consecutive local activation times vary beyond preset limits and thus
provides an averaging mechanism. Although double spike electrograms are
commonly considered to represent two activation fronts on
either side, we selected one spike in the context of surrounding
activation (to mark the local activation time). Sequential mapping
resulted in a less even distribution of mapped points compared to
multielectrode mapping data but when compared to the range of atrial
volumes encountered, the mean density of mapping in our series was
quite high. Qualitative analysis of 3D propagation was
performed on software generated animation sequences with attendant
limitations of interpolation, as with the analysis of
traditional isochronal maps.25,26 An
activation pattern indicating fusion/collision also cannot be
differentiated from an underlying block between two wave fronts, which
in fact may arrive locally simultaneously or nearly so,
thus precluding the recording of double potentials. The
assessment of regional conduction velocities was limited by the
estimate of intervening curved endocardial distances.
However, the estimates do provide a guide to regional differences as
well as a possible index of similar drug effect. The phasic effects of
respiration on the absolute intrathoracic position of the catheter tip
did not contribute to the relatively wide zone of posterior double
potentials in view of the corrective input from the sensor equipped and
similarly positioned reference catheter. This was confirmed by the lack
of artifactually wide 3D reconstructions, the precise capability of
relocating known landmarks, such as the His bundle and supported by
evidence from recent experimental
studies.25,27
Conclusions
By performing panoramic mapping of the RA and using unique
reconstructive software, we derived 3D activation maps during typical
counterclockwise atrial flutter in humans. The circuit as revealed by
high density 3D mapping indicates significant variations between
individuals. The posterior limit of the circuit is marked by a ragged
and wide zone of slow conduction surmounted by the orifice of the SVC
in the majority. Fusion of activation wave fronts around the SVC can
occur. Medial-septal RA activation though caudocranial in all does not
follow a consistent pattern. However, in contrast to these
variations, there is a constant obligatory activation wave front
proceeding with a slower estimated conduction velocity through the
narrow cavotricuspid isthmus.
|
Acknowledgments |
|---|
We are greatly indebted to Joëlle Bassibey for helping prepare the manuscript.
Received May 12, 1997; revision received August 22, 1997; accepted August 28, 1997.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. DeBakker JMT, Hauer RNW, Simmers TA. Activation mapping: unipolar versus bipolar recording. In: Zipes D, Jalife J, ed. Cardiac Electrophysiology: From Cell to Bedside. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1995:1068.
2. Puech P, Latour H, Grolleau R. Le flutter et ses limites. Arch Mal Coeur. 1970;63:116–144.
3. Chauvin M, Brechenmacher C, Voegtlin JR. Application de la cartographie endocavitaire à l'étude du flutter auriculaire. Arch Mal Coeur. 1983;76:1020–1030.
4. Olshansky B, Okumura K, Hess PG, Waldo AL. Demonstration of an area of slow conduction in humans atrial flutter. J Am Coll Cardiol. 1990;16:1639–1648.[Abstract]
5.
Feld GK, Fleck RP, Chen PS, Boyce K, Bahuson TD, Stein
JB, Calisi CM, Ibassa M. Radiofrequency catheter ablation for the
treatment of human type I atrial flutter: identification of a critical
zone in the reentrant circuit by endocardial mapping techniques.
Circulation. 1992;86:1233–1240.
6. Cosio FG, Lopez-Gil M, Giocolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol. 1993;71:705–709.[Medline] [Order article via Infotrieve]
7. Waldo AL. Atrial flutter: mechanisms, clinical features and management. In: Zipes, Jalife, eds. Cardiac Electrophysiology: From Cell to Bedside. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1995:666.
8.
Saoudi N, Atallah G; Kirkorian G, Touboul P. Catheter
ablation of the atrial myocardium in human type I atrial
flutter. Circulation. 1990;81:762–771.
9. Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of macroreentry and feasibility of operative therapy in the common type of atrial flutter. Am J Cardiol. 1986;57:587–591.[Medline] [Order article via Infotrieve]
10.
Poty H, Saoudi N, Aziz AA, Nari M, Letac B.
Radiofrequency catheter ablation of type I atrial flutter: prediction
of late success by electrophysiological
criteria. Circulation. 1995;92:1389–1392.
11.
Cauchemez B, Haïssaguerre M, Fischer B,
Thomas O, Clémenty J, Coumel P.
Electrophysiological effects of catheter ablation
of inferior vena cava-tricuspid annulus isthmus in common
atrial flutter. Circulation. 1996;93:284–294.
12. Fischer B, Haïssaguerre M, Garrigues S, Poquet F, Gencel L, Clémenty J, Marcus FI. Catheter ablation of common atrial flutter in 80 patients. J Am Coll Cardiol. 1995;25:1365–1372.[Abstract]
13.
Olgin J, Kalman J, Fitzpatrick A, Lesh MD. Role of
right atrial structures as barriers to conduction during human type I
atrial flutter: activation and entrainment mapping guided by
intracardiac echocardiography.
Circulation. 1995;92:1839–1848.
14. Shah DC, Haïssaguerre M, Jaïs P, Gencel L, Chouairi S, Clémenty J. Disparate electrical SVC activity during atrial fibrillation. Eur J Cardiac Pacing Electrophysiol. 1996;6:70. Abstract.
15. Cosio FG, Arribas F, Lopez-Gil M, Palacios J. Atrial flutter mapping and ablation, I: studying atrial flutter mechanisms by mapping and entrainment. PACE. 1996;19:841–853.
16.
VanHare GF, Waldo AL. The atrial flutter reentrant
circuit. Additional pieces of the puzzle. Circulation. 1996;94:244–246. Editorial.
17.
Frame LH, Page RL, Hoffman BF. Atrial reentry around an
anatomic barrier with a partially refractory excitable gap: a canine
model of atrial flutter. Circ Res. 1986;58:495–511.
18.
Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh
MD. Activation and entrainment mapping defines the tricuspid annulus as
the anterior barrier in typical atrial flutter. Circulation. 1996;94:398–406.
19. Cosio FG, Arribas F, Barbero JM, Kallmeyer C, Giocolea A. Validation of double-spike electrograms as markers of conduction block or delay in atrial flutter. Am J Cardiol. 1988;61:775–780.[Medline] [Order article via Infotrieve]
20.
Wang K, Ho SY, Gibson DG, Anderson RH. Architecture of
atrial musculature in humans. Br Heart J. 1995;73:559–565.
21. Racker DK. Transmission and reentrant activity in the sinoventricular conducting system and in the circumferential lamina of the tricuspid valve. J Cardiovasc Electrophysiol. 1993;4:513–525.[Medline] [Order article via Infotrieve]
22. Cosio FG, Arribas F, Palacios J, Tascon J, Lopez-Gil M. Fragmented electrograms and continuous electrical activity in atrial flutter. Am J Cardiol. 1986;57:1309–1314.[Medline] [Order article via Infotrieve]
23. Olshansky B, Okumura K, Henthorn RW, Waldo AL. Characterization of double potentials in human atrial flutter: studies during transient entrainment. J Am Coll Cardiol. 1990;15:833–841.[Abstract]
24.
Nakagawa H, Lazzara R, Khastgir T, Beckman JK,
McClelland JH, Imai S, Pitha JV, Becker AE, Arruda M, Gonzalez MD,
Widman LE, Rome M, Neuhauser J, Wang X, Calame JD, Goudeau MD, Jackman
WM. Role of the tricuspid annulus and the Eustachian valve/ridge on
atrial flutter: relevance to catheter ablation of the septum isthmus
and a new technique for rapid identification of ablation success.
Circulation. 1996;94:407–424.
25.
Gepstein L, Hayam G, Benttaim SA. A novel method for
non fluoroscopic catheter-based electroanatomical mapping of the heart:
in vitro and in vivo accuracy results. Circulation. 1997;95:1611–1622.
26.
Kaltenbrunner W, Cardinal R, Dubuc M, Shenasa M, Nadeau
R, Tremblay G, Vermeulen M, Savard P, Pagé PL. Epicardial and
endocardial mapping of ventricular tachycardia
in patients with myocardial infarction: is the origin of the
tachycardia always subendocardially localized?
Circulation. 1991;84:1058–1071.
27. Shpun S, Gepstein L Hayam G, Ben-Haim SA. High accuracy of radiofrequency catheter ablations guided by non-fluoroscopic mapping system in the swine atrium. J Am Coll Cardiol. 1997;29:331-A. Abstract.
This article has been cited by other articles:
 |
|
 |
|
  B. F. McBride The Emerging Role of Antiarrhythmic Compounds With Atrial Selectivity in the Management of Atrial Fibrillation J. Clin. Pharmacol., March 1, 2009; 49(3): 258 - 267. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Maury, A. Duparc, A. Hebrard, M. El Bayomy, and M. Delay Prevalence of typical atrial flutter with reentry circuit posterior to the superior vena cava: Use of entrainment at the atrial roof Europace, February 1, 2008; 10(2): 190 - 196. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Da Costa, E. Faure, J. Thevenin, M. Messier, S. Bernard, K. Abdel, C. Robin, C. Romeyer, and K. Isaaz Effect of Isthmus Anatomy and Ablation Catheter on Radiofrequency Catheter Ablation of the Cavotricuspid Isthmus Circulation, August 31, 2004; 110(9): 1030 - 1035. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-J. Lin, C.-T. Tai, J.-L. Huang, T.-Y. Liu, P.-C. Lee, C.-T. Ting, and S.-A. Chen Characteristics of virtual unipolar electrograms for detecting isthmus block during radiofrequency ablation of typical atrial flutter J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2300 - 2304. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T.-Y. Liu, C.-T. Tai, B.-H. Huang, S. Higa, Y.-J. Lin, J.-L. Huang, Y. Yuniadi, P.-C. Lee, Y.-A. Ding, and S.-A. Chen Functional characterization of the crista terminalis in patients with atrial flutter: implications for radiofrequency ablation J. Am. Coll. Cardiol., May 5, 2004; 43(9): 1639 - 1645. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Scaglione, D. Caponi, P. Di Donna, R. Riccardi, M. Bocchiardo, G. Azzaro, S. Leuzzi, and F. Gaita Typical atrial flutter ablation outcome: correlation with isthmus anatomy using intracardiac echo 3D reconstruction Europace, January 1, 2004; 6(5): 407 - 417. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. M.S. de Groot, M. J. Schalij, K. Zeppenfeld, N. A. Blom, E. T. Van der Velde, and E. E. Van der Wall Voltage and Activation Mapping: How the Recording Technique Affects the Outcome of Catheter Ablation Procedures in Patients With Congenital Heart Disease Circulation, October 28, 2003; 108(17): 2099 - 2106. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Kornowski Left ventricular electromechanical mapping for determination of myocardial function and viability J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1075 - 1078. [Full Text] [PDF]
|
|
|
|
|
|
N. F. Marrouche, A. SippensGroenewegen, Y. Yang, S. Dibs, and M. M. Scheinman Clinical and electrophysiologic characteristics of left septal atrial tachycardia J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1133 - 1139. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-T. Tai, J.-L. Huang, Y.-K. Lin, M.-H. Hsieh, P.-C. Lee, Y.-A. Ding, M.-S. Chang, and S.-A. Chen Noncontact three-dimensional mapping and ablation of upper loop re-entry originating in the right atrium J. Am. Coll. Cardiol., August 21, 2002; 40(4): 746 - 753. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. J.J. Wellens Contemporary Management of Atrial Flutter Circulation, August 6, 2002; 106(6): 649 - 652. [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Waldo Mechanisms of atrial flutter and atrial fibrillation: distinct entities or two sides of a coin? Cardiovasc Res, May 1, 2002; 54(2): 217 - 229. [Full Text] [PDF]
|
|
|
|
|
|
J. B. Morton, P. Sanders, V. Deen, J. K. Vohra, and J. M. Kalman Sensitivity and specificity of concealed entrainment for the identification of a critical isthmus in the atrium: relationship to rate, anatomic location and antidromic penetration J. Am. Coll. Cardiol., March 6, 2002; 39(5): 896 - 906. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Da Costa, C Romeyer, S Mourot, M Messier, A Cerisier, E Faure, and K Isaaz Factors associated with early atrial fibrillation after ablation of common atrial flutter. A single centre prospective study Eur. Heart J., March 2, 2002; 23(6): 498 - 506. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. J Schilling Which patient should be referred to an electrophysiologist: supraventricular tachycardia Heart, March 1, 2002; 87(3): 299 - 304. [Full Text] [PDF]
|
|
|
|
|
|
P. Ricard, M. Imianitoff, K. Yaici, J. M. Coutelour, M. Bergonzi, J. P. Rinaldi, and N. Saoudi Atypical atrial flutters Europace, January 1, 2002; 4(3): 229 - 239. [Abstract] [PDF]
|
|
|
|
|
|
P. D. Bella, A. Fraticelli, C. Tondo, S. Riva, G. Fassini, and C. Carbucicchio Atypical atrial flutter: clinical features, electrophysiological characteristics and response to radiofrequency catheter ablation Europace, January 1, 2002; 4(3): 241 - 253. [Abstract] [PDF]
|
|
|
|
|
|
L.-M. Rodriguez, C. Timmermans, A. Nabar, L. Hofstra, and H. J.J. Wellens Biatrial Activation in Isthmus-Dependent Atrial Flutter Circulation, November 20, 2001; 104(21): 2545 - 2550. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Schilling, N. S. Peters, J. Goldberger, A. H. Kadish, and D. W. Davies Characterization of the anatomy and conduction velocities of the human right atrial flutter circuit determined by noncontact mapping J. Am. Coll. Cardiol., August 1, 2001; 38(2): 385 - 393. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N Saoudi, F Cosio, A Waldo, S.A Chen, Y Iesaka, M Lesh, S Saksena, J Salerno, and W Schoels A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. A Statement from a Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology Eur. Heart J., July 2, 2001; 22(14): 1162 - 1182. [PDF]
|
|
|
|
|
|
Y. Yang, J. Cheng, A. Bochoeyer, M. H. Hamdan, R. C. Kowal, R. Page, R. J. Lee, P. R. Steiner, L. A. Saxon, M. D. Lesh, et al. Atypical Right Atrial Flutter Patterns Circulation, June 26, 2001; 103(25): 3092 - 3098. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Delacretaz, L. I. Ganz, K. Soejima, P. L. Friedman, E. P. Walsh, J. K. Triedman, L. J. Sloss, M. J. Landzberg, and W. G. Stevenson Multiple atrial macro-re-entry circuits in adults with repaired congenital heart disease: entrainment mapping combined with three-dimensional electroanatomic mapping J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1665 - 1676. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Matsuo, K. Uno, C. M. Khrestian, and A. L. Waldo Conduction left-to-right and right-to-left across the crista terminalis Am J Physiol Heart Circ Physiol, April 1, 2001; 280(4): H1683 - H1691. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Reithmann, E. Hoffmann, U. Dorwarth, T. Remp, and G. Steinbeck Electroanatomical mapping for visualization of atrial activation in patients with incisional atrial tachycardias Eur. Heart J., February 1, 2001; 22(3): 237 - 246. [Abstract] [PDF]
|
|
|
|
 |
|
 David M. Harrild, Craig S. Henriquez ; A Computer Model of Normal Conduction in the Human Atria Circ. Res., September 29, 2000; 87 (7): e25 - e36. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. P. Chan, G. F. Van Hare, J. A. Mackall, M. M. D. Carlson, and A. L. Waldo Importance of Atrial Flutter Isthmus in Postoperative Intra-Atrial Reentrant Tachycardia Circulation, September 12, 2000; 102(11): 1283 - 1289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Jais, D. C. Shah, M. Haissaguerre, M. Hocini, J. T. Peng, A. Takahashi, S. Garrigue, P. Le Metayer, and J. Clementy Mapping and Ablation of Left Atrial Flutters Circulation, June 27, 2000; 101(25): 2928 - 2934. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Friedman, D. Luria, A. M. Fenton, T. M. Munger, A. Jahangir, W. K. Shen, R. F. Rea, M. S. Stanton, S. C. Hammill, and D. L. Packer Global Right Atrial Mapping of Human Atrial Flutter: The Presence of Posteromedial (Sinus Venosa Region) Functional Block and Double Potentials : A Study in Biplane Fluoroscopy and Intracardiac Echocardiography Circulation, April 4, 2000; 101(13): 1568 - 1577. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C Reithmann, E Hoffmann, G Spitzlberger, U Dorwarth, A Gerth, T Remp, and G Steinbeck Catheter ablation of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation Eur. Heart J., April 1, 2000; 21(7): 565 - 572. [Abstract] [PDF]
|
|
|
|
|
|
P. Jais, D. C. Shah, M. Haissaguerre, M. Hocini, S. Garrigue, P. Le Metayer, and J. Clementy Prospective Randomized Comparison of Irrigated-Tip Versus Conventional-Tip Catheters for Ablation of Common Flutter Circulation, February 22, 2000; 101(7): 772 - 776. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Shah, P. Jais, A. Takahashi, M. Hocini, J. T. Peng, J. Clementy, and M. Haissaguerre Dual-Loop Intra-Atrial Reentry in Humans Circulation, February 15, 2000; 101(6): 631 - 639. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Bhargava and R. Kornowski Biosense Left Ventricular Electromechanical Mapping Asian Cardiovasc Thorac Ann, December 1, 1999; 7(4): 345 - 348. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Sun, E. O. Velipasaoglu, D. E. Wu, H. A. Kopelen, W. A. Zoghbi, W. H. Spencer III, and D. S. Khoury Simultaneous Multisite Mapping of the Right and the Left Atrial Septum in the Canine Intact Beating Heart Circulation, July 20, 1999; 100(3): 312 - 319. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Cabrera, D. Sanchez-Quintana, S. Y. Ho, A. Medina, F. Wanguemert, E. Gross, J. Grillo, E. Hernandez, and R. H. Anderson Angiographic Anatomy of the Inferior Right Atrial Isthmus in Patients With and Without History of Common Atrial Flutter Circulation, June 15, 1999; 99(23): 3017 - 3023. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Takahashi, D. C. Shah, P. Jais, M. Hocini, J. Clementy, and M. Haissaguerre Partial cavotricuspid isthmus block before ablation in patients with typical atrial flutter J. Am. Coll. Cardiol., June 1, 1999; 33(7): 1996 - 2002. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Cheng, W. R. Cabeen Jr, and M. M. Scheinman Right Atrial Flutter Due to Lower Loop Reentry : Mechanism and Anatomic Substrates Circulation, April 6, 1999; 99(13): 1700 - 1705. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Shah, M. Haissaguerre, P. Jais, A. Takahashi, M. Hocini, and J. Clementy High-Density Mapping of Activation Through an Incomplete Isthmus Ablation Line Circulation, January 19, 1999; 99(2): 211 - 215. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J-L Lin, L-P Lai, L-J Lin, Y-Z Tseng, W-P Lien, and S K S Huang Electrophysiological determinant for induction of isthmus dependent counterclockwise and clockwise atrial flutter in humans Heart, January 1, 1999; 81(1): 73 - 81. [Abstract] [Full Text]
|
|
|
|
|
|
P. Jais, M. Haissaguerre, D. C. Shah, A. Takahashi, M. Hocini, T. Lavergne, S. Lafitte, A. Le Mouroux, B. Fischer, and J. Clementy Successful Irrigated-Tip Catheter Ablation of Atrial Flutter Resistant to Conventional Radiofrequency Ablation Circulation, September 1, 1998; 98(9): 835 - 838. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||