(Circulation. 1995;92:1839-1848.)
© 1995 American Heart Association, Inc.
Articles |
Role of Right Atrial Endocardial Structures as Barriers to Conduction During Human Type I Atrial Flutter
Activation and Entrainment Mapping Guided by Intracardiac Echocardiography
From the Section of Cardiac Electrophysiology, Department of Medicine and Cardiovascular Research Institute, University of California San Francisco.
Correspondence to Michael D. Lesh, MD, Section of Cardiac Electrophysiology, Department of Medicine and the Cardiovascular Research Institute, University of California, San Francisco, 500 Parnasus Ave, Room MU 428, Box 1354, San Francisco, CA 94143-1354. E-mail lesh@ep4.ucsf.edu.
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background The importance of barriers in atrial flutter has been demonstrated in animals. We used activation and entrainment mapping, guided by intracardiac echocardiography (ICE), to determine whether the crista terminalis (CT) and eustachian ridge (ER) are barriers to conduction during typical atrial flutter in humans.
Methods and Results In eight patients, ICE was used to guide the placement of 20-pole and octapolar catheters along the CT and interatrial septum and a roving catheter to nine sites: just posterior (1) and anterior (2) to the CT along the lateral right atrium, at the fossa ovalis (3), and just posterior and anterior to the ER at the low posterolateral (4 and 5), low posterior (6 and 7), and low posteromedial (8 and 9) right atrium. Entrainment was performed, and each site was considered within the flutter circuit if the postpacing interval–flutter cycle length (PPI-FCL) and the stimulus time–activation time (stim time-act time) were <10 msec. Split potentials were recorded along the CT with components activated in a low-to-high pattern and a high-to-low pattern. Conduction times, as percentage of FCL, were significantly different at sites on either side of the CT and ER: site 1 (33±13%) and site 2 (43±12%) (P=.02), site 4 (48±24%) and site 5 (75±8.9%) (P=.02), and site 6 (22±10%) and site 7 (82±5.3%) (P=.0009). During entrainment, no surface fusion was observed at sites 5, 7, or 9. The PPI-FCL and stim time-act time were not significantly different than 0 at sites 2, 7, 5, or 9, indicating that they were within the flutter circuit, whereas sites 1, 3, 4, and 6 were not.
Conclusions ICE enabled the correlation of functional electrophysiological properties with specific anatomic landmarks, identifying the CT and ER as barriers to conduction during human atrial flutter.
Key Words: conduction • echocardiography • mapping
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
As early as 1947, when Rosenblueth developed a canine atrial flutter model by crushing endocardium between the venae cavae, it was realized that atrial flutter likely involved the propagation of a wave front around anatomically defined obstacles.1 More recently, canine models of atrial flutter have demonstrated the importance of anatomic obstacles in the reentry circuit.2 3 4 5 It is now well established that human type I atrial flutter is a reentrant rhythm localized to the right atrium.6 7 8 A protected, narrow isthmus of conduction has been identified in the low right atrium between the inferior vena cava and the tricuspid annulus.6 9 10 11 More recent evidence suggests that this area extends across the floor of the right atrium to the os of the CS.12 13 14 15 16 A line of block has also been observed in the lateral right atrium, extending superior from the orifice of the inferior vena cava.6 17 However, the extent to which these areas of conduction block are related to anatomic architecture has not been established.
Transient entrainment of atrial flutter was first described in 1977.18 Since then, activation and entrainment (or pace resetting) mapping have been used to localize regions of myocardium critical to the maintenance of reentrant circuits.9 19 20 21 22 However, because current imaging modalities, such as fluoroscopy, that are used to guide catheter placement do not allow direct visualization of anatomic structures, such mapping techniques are unable to directly relate functional properties of the circuit to specific anatomic features in the intact human heart. Intracardiac echocardiography is a technique that can be used to visualize various intra-atrial structures that are not visualized on fluoroscopy (eg, the fossa ovalis, CT, eustachian ridge, CS, venae cavae) and allow precise localization of intracardiac catheters relative to these anatomic structures.23 24 25 26
The present study was performed to define the role of right atrial endocardial structures that may serve as barriers to conduction during type I atrial flutter. Specifically, we used activation and entrainment mapping with anatomically determined catheter positioning guided by intracardiac echocardiography to test the hypothesis that the CT and eustachian ridge are anatomic barriers to conduction during typical flutter.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patients
The study included 8 patients (2 women and 6 men), age 52 to 72 years (mean, 66 years), with type I atrial flutter who were referred to the University of California, San Francisco, between August 1994 and December 1994 for curative atrial flutter ablation. All patients had characteristic flutter waves with a superior axis (negative complexes in leads II, III, and aVF). The range of atrial rates was 210 to 270 bpm (cycle length, 220 to 290 msec) with a mean of 234±24 bpm (cycle length, 258±26 msec). All antiarrhythmic drugs, with the exception of digoxin, were stopped at least 24 hours before the study. Six of 8 patients were in typical flutter at the onset of the study. The remaining 2 patients had type I atrial flutter documented clinically before the study and had type I atrial flutter reproducibly induced with atrial burst pacing and atrial extrastimulation. Informed consent was obtained from all patients before the study according to the protocol approved by the Committee on Human Research.
Intracardiac Echocardiography
A 10F, 10-MHz ICE catheter
(Cardiovascular
Imaging Systems, Inc) was inserted through a femoral vein sheath and
advanced into the right atrium. Images were obtained with an Insight 3
(Cardiovascular Imaging Systems, Inc) intravascular
ultrasound machine and recorded on videotape. The technique of ICE
to guide electrophysiology procedures has been previously
described.23 24 25 26 ICE was
used to identify the endocardial
structures of the right atrium, including the orifices of the venae
cavae, fossa ovalis, CT, eustachian ridge, CS, and tricuspid annulus
and, along with fluoroscopy, to guide the placement of all catheters as
well as to manipulate the roving catheter to specific anatomic
positions as described.
Catheters
A custom 8F, 20-pole steerable catheter (Mansfield)
with 2-mm
interelectrode distance was placed through an 8F long vascular sheath
(SRO, Daig) in the femoral vein and positioned along the CT. ICE was
used to ensure continuous catheter position firmly against the CT along
its entire extent from the superomedial right atrium (junction of the
right atrium and superior vena cava) to the inferior right
atrium (junction of the right atrium and inferior vena
cava) (Figs 1
and 2A). A 7F, octapolar
steerable catheter (EP Technologies) (2.5-mm distance between bipole
electrodes and 10-mm distance between bipole pairs) was positioned
under ICE guidance along the interatrial septum (Figs 1 and
2). An 8F,
open-lumen, decapolar catheter (Elecath) (2-mm interelectrode
distance and 5-mm intraelectrode distance) was placed via the internal
jugular vein into the CS. Positioning of the proximal electrode pair at
the os of the CS was confirmed with contrast injection viewed with
fluoroscopy. An 8F, quadipolar catheter (EP Technologies) (4-mm
electrode tip; other electrodes, 2 mm with 2-mm interelectrode spacing)
was used as a roving mapping, pacing, and ablation catheter.
|
|
The roving
catheter tip was guided precisely to the following nine
sites under ICE guidance based on the characteristic fan-shaped
artifact cast by the large distal electrode (Figs 1
and
2): (1)
approximately 0.5 cm posterior to the CT, on the smooth right atrium;
(2) approximately 0.5 cm anterior to the CT, on the
trabeculated right atrium; (3) at the fossa ovalis; (4)
posterior to the eustachian ridge, far lateral from the CS os, where
the CT joins the eustachian ridge; (5) anterior to the eustachian ridge
(opposite site 4), between it and the tricuspid annulus, far lateral
from the CS os, where the CT joins the eustachian ridge; (6) posterior
to the eustachian ridge, midway between the CS os and site 4; (7)
anterior to the eustachian ridge (opposite site 6), between it and the
tricuspid annulus, midway between the CS os and site 5; (8) posterior
to the eustachian ridge at the CS os (posterior to the CS os); and (9)
anterior to site 8, between the CS os (anterior to the CS os) and the
tricuspid annulus.
Electrogram Recordings
Bipolar intracardiac electrograms
filtered between 30 and 500 Hz
were recorded and stored digitally on a Cardiolab system (Prucka
Engineering) simultaneously with 12-lead surface ECGs. All
measurements were performed with the Cardiolab system at screen speeds
of 400 to 1600 mm/s using on-screen digital calipers.
Entrainment
During atrial flutter, unipolar pacing was
performed at each
site from the distal electrode of the roving catheter. A large patch
skin electrode was used as the indifferent electrode. A custom-made
Y-splitter that attached to the lead from the distal
electrode allowed simultaneous recording of the
distal bipole pair during unipolar pacing. Pacing was performed at 10,
20, and 40 msec less than the spontaneous FCL for at least 10 beats at
the lowest capturing current with a 2-msec pulse width. In those
patients who were in sinus rhythm at the onset of the study, pacing at
the previously documented FCL was performed during sinus rhythm.
Definitions
"Split potentials" were defined as
distinct early and late
potentials separated by an isoelectric phase.10 When split
potentials were present, separate measurements were made for each
component. Fragmented potentials were not considered split, and
measurements were made at the onset of the fragmented potentials.
During entrainment, "fusion" was defined as being present,
and thus manifest, when a different morphology of the surface flutter
wave and/or change in activation sequence of the intracardiac
recordings occurred during pacing compared with spontaneous
flutter. Entrainment with "concealed fusion" was defined as
entrainment with identical flutter wave morphology as during
spontaneous flutter. The interval between the last paced beat
entraining the tachycardia and the first beat after pacing was
carefully measured. This "PPI" was defined as the time necessary
to conduct from the pacing site to the reentrant circuit, through the
circuit and back to the pacing site (Fig 3). It was
measured from the last pacing artifact to the onset of the first atrial
signal on the distal electrode pair of the roving catheter (pacing
catheter) (Fig 4). The "FCL" was determined from
the average of three beats after the first postpacing beat.
|
|
Because the
onset of the flutter wave is often difficult to discern on
the surface ECG—either because of rapid
atrioventricular conduction or lack of a true
isoelectric point on the surface flutter wave—the electrogram from
the coronary sinus os was used as a surrogate marker for the
onset of the flutter wave, as previously
described.9 10 12 21 27
"Stim Time" was defined as
the orthodromic time of conduction from the pacing site to the exit
site from the protected isthmus (CS os) during entrainment (Fig
3). The
last entrained beat is, by definition, not fused and therefore
activated orthodromically.18 Because it is the
orthodromic Stim Time that is relevant, the interval from the last
pacing artifact to the onset of the last CS os electrogram that is
entrained at the pacing rate was used for this measurement (Fig
5).19 21 "Act Time" was
defined as
the time between the onset of the local electrogram of the roving
catheter and activation of the CS os during spontaneous flutter (Fig
3). To distinguish it from Act Time, "conduction
time" was
defined as the time between the onset of the local electrogram from the
electrode pair positioned at the CS os and activation of electrode
pairs at each recording site during spontaneous flutter (Fig
3). Conduction times were expressed as the percentage of the
FCL to
compare values from patients with differing flutter rates.
|
Sites were
considered to be within the reentrant circuit if both the
PPI was within 10 msec of the FCL (PPI-FCL
10 msec) and the Stim Time
was within 10 msec of the Act Time (Stim Time-Act Time10 msec) (Fig
3). Ten milliseconds was chosen because it is the estimated
precision
of measurement using the digital calipers (determined by 10 repeated
measures of 20 different intervals). Sites were considered to be in a
relatively protected isthmus if concealed fusion resulted during
entrainment.
All intervals during entrainment were measured three times at each site at the three different pacing rates for each patient. PPI-FCL and Stim Time-Act Time were calculated at each site for each patient as an average of values for each pacing rate at each site.
Ablation
Ablation was performed between the distal electrode
of the
roving catheter and a large surface area skin electrode with 550 kHz
unmodulated radiofrequency current from a generator with temperature
monitoring (EP Technologies). During ablation, radiofrequency power was
adjusted to obtain a catheter tip temperature of between 65° and
90°C. Sites for ablation were selected if entrainment demonstrated
concealed fusion, a PPI within 10 msec of the FCL, and a Stim Time
within 10 msec of the Act Time, indicating the site is within the
circuit and in a protected isthmus. If tachycardia terminated
with ablation, reinduction of flutter was attempted using atrial burst
pacing down to a cycle length at which 2:1 capture occurred and
with triple atrial extrastimuli at pacing cycle lengths of 400 and 300
msec. Successful ablation was defined as termination of flutter with
the inability to reinduce atrial flutter.
Statistical Analysis
Values are expressed as mean±SD.
Statistical comparisons were
performed using the Student's t test, paired and unpaired
when appropriate. A value of P<.02 was considered
statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Patients
Four of the eight patients had no structural heart disease with normal left ventricular function and atrial size. Three patients had coronary artery disease and previous myocardial infarctions. One patient had a prior aortic valve replacement for aortic insufficiency. The mean left ventricular ejection fraction, determined by transthoracic echocardiography, was 53±9%, with two patients having ejection fractions of less than 45%. Left atrial enlargement (>4 cm) was present in only four patients, and right atrial dimensions were normal (<3 cm) in all patients, as determined by surface echocardiography. All patients failed at least three antiarrhythmic drugs, and at least one had DC cardioversion attempted before the procedure.
Intracardiac Echocardiography
The eustachian ridge, the
entire extent of the CT, the fossa
ovalis, and the tricuspid annulus were identified by ICE in all
patients. The catheters placed along the CT and the interatrial septum
were identified along their entire intracardiac length by ICE in all
patients. Successful localization of the tip of the roving mapping
catheter in relation to each of the endocardial structures at sites
shown in Fig 1 was achieved in all patients.
Activation Maps
Conduction times from the CS os to each
recording site are
shown in Tables 1 through 3.
Split
potentials—composed of distinct early and late potentials
separated by an isoelectric phase—were recorded along the
length of the CT in seven of eight patients (Table 1). Fig
6A shows typical split potentials recorded from the
CT catheter in one patient. The conduction time from the CS os,
expressed as a percentage of the FCL, was significantly longer for the
late deflections compared with the early deflections for each of the
bipoles from which they were recorded (Table 1). The early
component had a low-to-high activation sequence, whereas the
late component had a high-to-low activation sequence. The
septal catheter was activated in a low-to-high sequence
in every patient (Table 2). Fig 6B shows a
typical activation sequence
in the septal catheter from one patient. Split or fragmented potentials
were not recorded from the septal catheter in any patient.
|
|
|
|
Conduction
times from the CS os to each of the nine ICE-determined,
anatomically defined mapping sites are shown in Table 3.
Conduction
times were significantly longer at site 2, just anterior to the CT on
the trabeculated right atrium, compared with site 1, just
posterior to the CT on the smooth right atrium. Site 3, at the fossa
ovalis, was activated on time with the septal catheter poles
and sites 1, 4, 6, and 8. Conduction times from the CS os to sites 4,
6, and 8, confirmed by ICE to be just posterior to the eustachian
ridge, were not statistically different from each other or from the
septal catheter poles. Sites 5, 7, and 9, confirmed by ICE to be just
anterior to the eustachian ridge, were activated in sequence
significantly later than any other site (P<.005). In
addition, split potentials were recorded in three patients at site
7 (Fig 7).
|
Activation of the trabeculated right atrium—separated from the smooth right atrium by the CT—occurred significantly later than the smooth right atrium (site 2 versus sites 1 and 3). Activation of sites just posterior to the eustachian ridge occurred significantly earlier than sites directly opposite (sites 4 versus 5 and 6 versus 7) and just anterior to the eustachian ridge.
Entrainment Maps
Criteria for entrainment, as defined in
previous reports, were
established for each patient from one or more of the nine mapping
sites.28 29 Results of entrainment mapping are shown
in
Table 4 and Fig 8. At site 1, manifest
fusion was observed, the PPI was significantly longer than the FCL and
the Stim Time was significantly longer than the Act Time in all
patients. In no patient were these values less than 15 msec at this
site. When entrainment from site 2 was performed, fusion was observed
in all patients, but the PPI was not significantly different from the
FCL and the Stim Time was not different from the Act Time. In no
patient were these values >3 msec at this site. Thus, although site 1
(confirmed by ICE to be just posterior to the CT) was not a part of the
flutter circuit, site 2 (confirmed by ICE to be just anterior to the
CT) was. Manifest fusion was observed during entrainment at site 3 (at
the fossa ovalis) in all patients. In addition, the PPI was
significantly longer than the FCL and the Stim Time was significantly
greater than the Act Time, indicating that the fossa ovalis was not a
part of the flutter circuit.
|
|
, maximum; 
, minimum). Values that are within
10 msec of 0 are indicative of being a part of the reentrant circuit,
whereas values greater than 10 msec are indicative of being outside of
the reentrant circuit. Sites 2, 5, 7, and 9 have values that are
statistically not different than 0, whereas sites 1, 3, 4, and 6 have
values that are significantly greater than 0. Site 8 has a large SD
because two patients had values that were near 0, whereas the other
patients had values significantly greater than 0 (see text). B, Plot of
difference between the Stim Time and the Act Time for each entrained
mapping site. Values are mean±SD (error bars). Values that are within
10 msec of 0 are indicative of being a part of the reentrant circuit,
whereas values greater than 10 msec are indicative of being outside of
the reentrant circuit. Sites 2, 5, 7, and 9 have values that are
statistically not different than 0, whereas sites 1, 3, 4, and 6 have
values that are significantly greater than 0. Site 8 has a large SD
because two patients had values that were near 0, whereas the other
patients had values significantly greater than 0 (see text).At sites 4 and 6, confirmed by ICE to be just posterior to the eustachian ridge, fusion was observed, the PPI was significantly longer than the FCL, and the Stim Time was significantly longer than the Act Time in all patients. In no patient were these values <15 msec. Conversely, at sites 5, 7, and 9, confirmed by ICE to be just anterior to the eustachian ridge, no fusion was seen in any patient, the PPI was not different from the FCL, and the Stim Time was not different from the Act Time. In no patient were these values >7 msec at these sites. Thus, sites 4 and 6 were not within the flutter circuit, whereas sites 5, 7, and 9 were within the circuit and in a protected isthmus since no fusion occurred.
At site 8, fusion was not observed in two patients during entrainment. In these two patients, the PPI was not different from the FCL (PPI-FCL=0±0), and the Stim Time was not different from the Act Time (Stim Time-Act Time=5±2 msec). In the other patients, fusion was observed during entrainment, the PPI trended toward being longer than the FCL (PPI-FCL=41±23 msec), and the Stim Time trended toward being longer than the Act Time (Stim Time-Act Time=116±45 msec). Thus, in two patients site 8 was in the flutter circuit, whereas in the others it was not.
Ablation
All patients underwent successful ablation of their
atrial
flutter. Seven patients had successful ablation at sites far lateral to
the CS os, between the tricuspid annulus and the orifice of the
inferior vena cava (site 5 or 7). Only one patient had a
successful ablation near the CS os (site 9), despite attempts at this
site in five patients. As confirmed by ICE, all patients required a
pullback of the ablation catheter tip to the eustachian ridge at the
anterior rim of the inferior vena cava during
radiofrequency application—in effect, ablating in a line from the
tricuspid annulus to the orifice of the inferior vena
cava.
Atrial overdrive pacing with and without extrastimuli induced no arrhythmia in five patients after initial termination of atrial flutter by ablation. In three patients, atypical flutter (one nonsustained and two sustained) was induced. These arrhythmias had the opposite activation pattern of typical flutter, with a low-to-high activation pattern in the CT and a high-to-low activation pattern in the septum. In addition, the cycle lengths of these atypical flutters were from 50 to 100 msec longer than each patient's typical flutter. A single repeat radiofrequency application at the previously successful site rendered these arrhythmias no longer inducible.
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
In the present study, activation and entrainment mapping guided by ICE were used to identify the CT and eustachian ridge as lines of block during type I (typical) atrial flutter in humans. Three sets of results are provided that demonstrate that the CT and eustachian ridge are barriers to conduction during flutter. First, split potentials were recorded along the length of the CT—with opposite activation sequences of each component—and across the eustachian ridge. Second, activation mapping demonstrated that sites determined by ICE to be just anterior to the CT (site 2) and the eustachian ridge (site 5, 7, and 9) were activated significantly later than sites determined by ICE to be just posterior to these structures (sites 1 and 3 and sites 4, 6, and 8, respectively). Third, entrainment mapping identified sites determined by ICE to be just anterior to the CT and the eustachian ridge as within the reentrant circuit, whereas sites determined to be just posterior to these structures were identified as not being within the circuit. These data indicate that the flutter wave front is directed inferiorly along the trabeculated right atrium anterior to the CT into a narrow isthmus between the eustachian ridge and the tricuspid annulus and then medially between these two structures to exit near the CS os (Fig 9
).
|
ICE reliably identified key right atrial endocardial structures not visible with fluoroscopy, including the CT, eustachian ridge, tricuspid annulus, interatrial septum, fossa ovalis, and CS. Because the tip of the roving mapping catheter casts a characteristic fan-shaped artifact on ICE images, the catheter tip could be precisely guided to these anatomic positions for mapping and entrainment.23 24 25 26 Fluoroscopy provides only a rough estimate of anatomic location and is inadequate for mapping in relation to specific endocardial structures. With ICE, in this study we were able to correlate the findings of activation mapping and entrainment with specific endocardial anatomic structures by confirming the spatial relationship of the catheters to these structures.
Entrainment
Entrainment with concealed fusion has been
previously demonstrated
in protected isthmuses of conduction for ventricular
tachycardia and atrial
flutter.9 10 19 27 During
entrainment (either manifest or concealed), local fusion occurs at some
point. Fusion will be observed on the surface ECG if and only if the
area of myocardium activated antidromically is
large enough to affect the surface ECG. Concealed fusion occurs when
pacing is delivered to areas where functional or fixed barriers prevent
capture of a significant area of the chamber (ie, enough to affect the
surface ECG) in any direction other than from the normal exit of a
protected isthmus.
In the present study, we used ICE to demonstrate that this zone (containing sites 5, 7, and 9), from which concealed fusion is demonstrated during entrainment, is constrained anatomically by the eustachian valve and the tricuspid annulus. The pacing impulse propagates only orthodromically, and the flutter wave is not inscribed until the wave exits this isthmus. Antidromic fusion occurs within the protected isthmus in an area too small to affect the surface electrogram. Pacing anterior to the CT (site 2), however, produces manifest entrainment, even though it is within the flutter circuit. This occurs because it is not in a protected isthmus, allowing activation of a large enough area of atrium to inscribe a flutter/P wave immediately after the pacing impulse is delivered, and manifest fusion occurs.
In addition to evaluating whether entrainment produces
fusion, the Act
Times from the pacing stimulus (Stim Time) during entrainment and the
PPI for the first beat after cessation of entrainment have been
previously demonstrated to be useful in evaluating a reentrant circuit
(Fig 3).10 19 30 Inoue et
al30 observed that
the PPI varied depending on where the pacing and recording
sites were in relation to the reentrant circuit. Stevenson et
al19 demonstrated in both a computer model and in human
ventricular tachycardia that the PPI at the pacing
site is a useful indication of whether that site is inside or outside
of the reentrant circuit. In our study, entrainment from sites just
anterior to the CT (site 2) and just anterior to the eustachian ridge
(sites 5, 7, and 9) produced PPIs equal to the FCL and were thus
determined to be within the circuit (Fig 8A). Entrainment from
sites
just posterior to the CT (sites 1 and 3) and to the eustachian ridge
(sites 4, 6, and 8) produced PPIs longer than the FCL and thus were not
within the circuit (Fig 8A).
The Stim Time (Act Time
from the stimulus) can also be used to
determine sites that are within the reentrant circuit during
entrainment.19 31 If ventricular
tachycardia is entrained without fusion, the Act Time (local
electrogram to QRS) and the Stim Time (stimulus to QRS) both reflect
the time necessary for conduction from the pacing site to the QRS-onset
site—which is defined as the exit site from a critical isthmus
(Fig 3).19 31 However, if local
electrograms are
recorded from a known exit site from a protected isthmus (or any
site known to be in the reentrant circuit), then neither concealed
entrainment nor surface electrograms are necessary for analysis
of these times of conduction. Several reports have demonstrated that
the exit of the narrow isthmus of conduction in type I flutter is the
CS os, which correlates with the onset of the flutter
wave.9 10 12 21 27
In our study, the first nonpaced cycle
length in the CS os electrogram after entrainment from any site in all
patients was always that of the FCL, confirming that the CS os is
within the reentrant circuit. Therefore, the CS os is valid as the exit
site from the protected isthmus and a surrogate for the flutter
wave–onset site.30
The use of the stimulus to CS os
electrogram (Stim Time) and the
activation time from the pacing site to the CS os electrogram (Act
Time) as determinates of whether a site is in the reentrant circuit
assumes that local conduction velocities are not significantly affected
by pacing rates slightly faster than tachycardia
rates.19 31 In our study, there were no significant
changes in the FCL after pacing, and there were no significant
differences in Stim Times at different pacing rates, suggesting that
conduction velocities were indeed not affected. Sites anterior to the
CT (site 2) and eustachian ridge (sites 5, 7, and 9) had Stim Times
equal to Act Times and thus were a part of the circuit, whereas sites
posterior to the CT (sites 1 and 3) and eustachian ridge (sites 4 and
6) had Stim Times greater than Act Times and thus were not a part of
the circuit (Fig 8B). These findings are consistent with the
results from the analysis of the PPIs.
Anatomic Barriers
The CT has been previously implicated as a
barrier in animal
models of atrial flutter.32 33 34
Observations in humans have
demonstrated an area of block in the lateral right atrium, but to date
the exact anatomic correlate of this
electrophysiological event had been
unresolved.6 35 36 Cosio et
al6 20 35 37 have
demonstrated that activation of the septum is in a low-to-high
(caudocranial) pattern, whereas activation of the anterior wall is in a
high-to-low (craniocaudal) pattern. He and
others6 20 35 38 have also
reported double potentials
recorded along the lateral right atrium similar to those observed
in our study. However, the present study demonstrates conclusively,
based on ICE, that the CT is the anatomic structure that acts as the
barrier to conduction.
Our study also demonstrates that the eustachian ridge forms a barrier to conduction during atrial flutter in the low right atrium; it, along with the tricuspid annulus, forms the borders of a narrow isthmus of conduction. The area of the low right atrium between the tricuspid annulus and the inferior vena cava has been previously demonstrated to be a critical area in atrial flutter.6 9 10 13 16 27 35 With entrainment techniques, Nakagawa et al12 recently reported that a line of block existed between the inferior vena cava and the CS os in two patients. This is consistent with the findings reported in the present study. However, until the present study, the anatomic features that delineate this region, and in particular the role of the eustachian ridge, were not completely known. ICE was used in the present study to identify the eustachian ridge as the anatomic correlate of this line of block extending from the inferior vena cava to the CS os.
The exit of this narrow isthmus between the
eustachian ridge and
tricuspid annulus is believed to be near the CS os, since electrograms
recorded from this site correspond to the onset of the flutter
wave.9 10 12 21 27
However, it was not known whether the
wave propagates anterior to the CS os (between it and the tricuspid
annulus), posterior to the CS os, or both (Fig 9). In the
present
study, six of eight patients were demonstrated to have an exit site
only on the anterior aspect of the CS os (site 9), whereas in two
patients the exit was on both sides of the os (sites 8 and 9) (Fig
9).
This may have some implications for ablation, since it may be difficult
to determine which patients have these "dual" exit sites.
Therefore, ablation at the medial aspect of this isthmus, near the CS
os, may not be successful in some patients. In fact, in these eight
patients, seven were ablated successfully from the lateral approach
(including the two with "dual" exits), whereas only one had
successful ablation medially.
Although this study has demonstrated that the CT and eustachian ridge are anatomic barriers to conduction during atrial flutter, they may be either fixed or functionally determined. Our study demonstrates that such lines of block, whether fixed or functional, occur along anatomically defined regions. Observations in a few of these patients allow some inference as to whether the block is fixed or functional. During sinus rhythm, in two patients, the CT catheter was activated in a high-to-low sequence, and the split potentials were no longer present. This is not unexpected because the sinus impulse originates superiorly in the CT itself and activates both the anterior wall and septum in a high-to-low pattern. However, pacing from the low right atrium demonstrated late activation of the CT electrodes, after the septal electrodes, and with the reappearance of split potentials along the CT. In addition, pacing from site 4 demonstrated a relatively short time from stimulus to the CS os, whereas pacing from site 5 (just on the anterior side of the eustachian ridge to site 4) demonstrated a much longer Stim Time to the CS os, similar to that during atrial flutter. Although not conclusive, this suggests that the lines of block established by the CT and the eustachian ridge are both fixed, at least in some patients. This is consistent with the findings of Saffitz et al,39 who demonstrated that longitudinal conduction in the CT is 10 times greater than in the transverse direction. This is likely related to the type and distribution of gap junctions in crista myocytes. It is also intriguing to speculate that structural abnormalities of the CT and eustachian ridge, on a microscopic level, are the primary abnormalities in patients with atrial flutter and may explain the occurrence of atrial flutter even in patients with grossly normal atria. This may be analogous to the dog described by Boineau et al33 with congenital thinning in the floor of the right atrium and spontaneous atrial flutter.
Flutter Circuit
From the activation maps obtained in the
present study,
typical atrial flutter occurs in a counterclockwise rotation (Fig
9).
From the CS os, the flutter wave passively activates the
interatrial septum and left atrium. After this, the
trabeculated right atrium anterior to the CT is
activated, directing the impulse into the narrow isthmus of
slow conduction between the eustachian ridge and tricuspid annulus.
Arribas et al40 have shown that the superior aspect of the
circuit is activated along the anterior right atrium, and not
along the smooth right atrium below the superior vena cava orifice.
With data from their study and data from the present study, the
flutter circuit would appear as in Fig 9. How the impulse
travels from
the exit of the protected isthmus in the low right atrium to the
anterior, trabeculated right atrium is not known, but
because the septum is not within the reentrant circuit, the impulse
must continue around the tricuspid valve. Double potentials have been
reported in the area of the triangle of Koch.6 38 In
addition, there are reports of an association between
atrioventricular nodal reentry tachycardia and
inducible atrial flutter, suggesting the possibility of a shared
pathway around the tricuspid annulus to the anterior right
atrium.15 41 The tendon of Todaro may act as a
continued
line of block, or the impulse may be more rapidly conducted toward the
apex of the triangle of Koch over specialized fibers. Further studies
are needed to elucidate this last link in the flutter circuit.
Clinical Implications
Our data suggest that for successful
ablation, a lesion must be
applied between the tricuspid annulus and the eustachian ridge. Perhaps
the shortest such lesion is a perpendicular one between the tricuspid
annulus and the eustachian ridge. However, such a lesion may be
difficult to create with current technology because the eustachian
ridge is not seen with fluoroscopy. Alternatively, as was done in all
patients in this study, a slanted linear lesion can be applied between
the tricuspid annulus and the orifice of the inferior vena
cava, in a similar anatomic location to that reported by Cosio et
al.35 The distance between the tricuspid annulus and the
eustachian ridge is variable and can be quite large in some
patients. Long pullbacks with a 4-mm-tipped catheter are often
required for successful ablation. Catheters with longer tips may be
able to produce the necessary lesion with a single radiofrequency
application.
Study Limitations
Although this study conclusively
demonstrated that the CT and
eustachian ridge are barriers to conduction, the exact mechanism of
block was not identified. Pacing was not performed from all sites in
all patients during sinus rhythm. Moreover, pacing was performed only
at the FCL during sinus rhythm and not at rates slightly faster than
sinus rate. Therefore, the conduction block may be due to disparate
refractory periods or use-dependent conduction failure along these
anatomic structures rather than being fixed lines of block.
Although this study suggests that ablation directed laterally in the protected isthmus in the low right atrium should be more successful than that directed medially near the CS os, this has not been conclusively shown. The patients were not randomized, and only a small number of patients were included. Moreover, there is no long-term follow-up available on this cohort of patients.
Conclusion
ICE was useful in identifying anatomic features of
the right
atrial endocardium. With ICE, functional
electrophysiological properties were
correlated with specific anatomic landmarks. With activation mapping
and entrainment guided by ICE, we identified the CT and eustachian
ridge as anatomic barriers to conduction during type I atrial flutter.
Further study is needed to determine the role of other septal
structures, such as the tendon of Todaro and the entire tricuspid
annulus in typical atrial flutter and to determine whether the block
along the CT and eustachian ridge is fixed or functional.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
Dr Olgin is supported by the North American Society of Pacing and Electrophysiology and is the recipient of the Albert S. Hyman NASPE Postdoctoral Fellowship. Dr Kalman is supported by the Ralph Reader Overseas Research Fellowship of the National Heart Foundation of Australia and the Telectronics Traveling Fellowship of the Royal Australian College of Physicians. Dr Lesh is supported in part by National Institutes of Health grant HL-45664.
Received January 31, 1995; revision received April 26, 1995; accepted May 3, 1995.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Rosenblueth A, Garcia-Ramos J. The influence of artificial obstacles on experimental auricular flutter. Am Heart J. 1947;33:677-684.
2.
Frame LH, Page RL, Boyden PA, Fenoglio JJ, Hoffman B.
Circus movement in the canine atrium around the tricuspid ring
during experimental atrial flutter and during reentry in vitro.
Circulation. 1987;76:1155-1175.
3.
Boyden PA, Frame LH, Hoffman BF. Activation
mapping of reentry around an anatomic barrier in the canine atrium:
observations during entrainment and termination.
Circulation. 1989;79:406-416.
4. Schoels W, Kuebler W, Yang H, Gough WB, El Sherif N. A unified functional/anatomic substrate for circus movement atrial flutter: activation and refractory patterns in the canine right atrial enlargement model. J Am Coll Cardiol. 1993;21:73-84. [Abstract]
5. Feld GK, Shahandeh RF. Activation patterns in experimental canine atrial flutter produced by right atrial crush injury. J Am Coll Cardiol. 1992;20:441-451. [Abstract]
6. Cosio FG, Lopez GM, Goicolea A, Arribas F. Electrophysiologic studies in atrial flutter. Clin Cardiol. 1992;15:667-673. [Medline] [Order article via Infotrieve]
7. Olshansky B, Wilber DJ, Hariman RJ. Atrial flutter: update on the mechanism and treatment. PACE Pacing Clin Electrophysiol. 1992;15:2308-2335. [Medline] [Order article via Infotrieve]
8.
Waldo AL. Atrial flutter: new directions in
management and mechanism. Circulation. 1990;81:1142-1143.
9.
Feld GK, Fleck RP, Chen PS, Boyce K, Bahnson TD, Stein
JB, Calisi CM, Ibarra M. Radiofrequency catheter ablation for
the treatment of human type 1 atrial flutter: identification of a
critical zone in the reentrant circuit by endocardial mapping
techniques. Circulation. 1992;86:1233-1240.
10. Olshansky B, Okumura K, Hess PG, Waldo AL. Demonstration of an area of slow conduction in human atrial flutter. J Am Coll Cardiol. 1990;16:1639-1648. [Abstract]
11. Touboul P, Saoudi N, Atallah G, Kirkorian G. Electrophysiologic basis of catheter ablation in atrial flutter. Am J Cardiol. 1989;64:795-825.
12. Nakagawa H, Wang X, McClelland J, Beckman K, Lazzara R, Hazlitt A, Arruda M, Santoro I, Abdalla I, Singh A, Sweidan R, Gossinger H, Hirao K. Line of conduction block extends from inferior vena cava to coronary sinus ostium in common atrial flutter. PACE Pacing Clin Electrophysiol. 1993;16:881. Abstract.
13.
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.
14. Calkins H, Leon AR, Deam AG, Kalbfleisch SJ, Langberg JJ, Morady F. Catheter ablation of atrial flutter using radiofrequency energy. Am J Cardiol. 1994;73:353-356. [Medline] [Order article via Infotrieve]
15. Interian AJ, Cox MM, Jimenez RA, Duran A, Levin E, Garcia O, Cooper DK, Castellanos A, Myerburg RJ. A shared pathway in atrioventricular nodal reentrant tachycardia and atrial flutter: implications for pathophysiology and therapy. Am J Cardiol. 1993;71:297-303. [Medline] [Order article via Infotrieve]
16. Lesh MD, Van Hare GF, Fitzpatrick AP, Griffin JC, Chu E. Curing reentrant atrial arrhythmias: targeting protected zones of slow conduction by catheter ablation. J Electrocardiol. 1993;26:194-203.
17. Yamauchi S, Schuessler RB, Kawamoto T, Shuman TA, Boineau JP, Cox JL. Use of intraoperative mapping to optimize surgical ablation of atrial flutter. Ann Thorac Surg. 1993;56:337-342. [Abstract]
18.
Waldo AL, McLean WAH, Karp RB, Kouchoukos NT, James TN.
Entrainment and interruption of atrial flutter with atrial
pacing: studies in man following open heart surgery.
Circulation. 1977;56:737-745.
19.
Stevenson WG, Khan H, Sager P, Saxon LA, Middlekauff
HR, Natterson PD, Wiener I. Identification of reentry circuit
sites during catheter mapping and radiofrequency ablation of
ventricular tachycardia late after myocardial
infarction. Circulation. 1993;88:1647-1670.
20.
Cosio FG, Lopez GM, Arribas F, Palacios J, Goicolea A,
Nunez A. Mechanisms of entrainment of human common flutter
studied with multiple endocardial recordings.
Circulation. 1994;89:2117-2125.
21. Arenal A, Almendral J, San Roman D, Delcan JL, Josephson ME. Frequency and implications of resetting and entrainment with right atrial stimulation in atrial flutter. Am J Cardiol. 1992;70:1292-1298. [Medline] [Order article via Infotrieve]
22. Della BP, Marenzi G, Tondo C, Cardinale D, Giraldi F, Lauri G, Guazzi M. Usefulness of excitable gap and pattern of resetting in atrial flutter for determining reentry circuit location. Am J Cardiol. 1991;68:492-497.[Medline] [Order article via Infotrieve]
23.
Chu E, Fitzpatrick AP, Chin MC, Sudhir K, Yock PG, Lesh
MD. Radiofrequency catheter ablation guided by intracardiac
echocardiography.
Circulation. 1994;89:1301-1305.
24. Chu E, Kalman JM, Kwasman MA, Jue JCY, Fitzgerald PJ, Epstein LM, Schiller NB, Yock PG, Lesh MD. Intracardiac echocardiography during radiofrequency catheter ablation of cardiac arrhythmias in man. J Am Coll Cardiol. 1994;24:1351-1357. [Abstract]
25. Kalman JM, Lee RJ, Fisher WG, Chin MC, Lesh MD, Scheinman MM. Radiofrequency catheter modification of sinus node function guided by intracardiac echocardiography. Circulation. 1994;90(suppl I):I-41. Abstract.
26. Kalman JM, Fitzpatrick AP, Chin MC, Lee RJ, Scheinman MM, Lesh MD. Efficiency of heating with radiofrequency energy is related to stability of tissue contact: evaluation by intracardiac echocardiography. Circulation. 1994;90(suppl I):I-270. Abstract.
27. Fujimoto T, Inoue T, Fukuzaki H. Characterization of slow conduction in the common type of atrial flutter—using transient entrainment. Jpn Circ J. 1990;54:21-31. [Medline] [Order article via Infotrieve]
28. Waldo A, Carlson M, Biblo L, Henthorn R. In: Waldo, ed. Atrial Arrhythmias. 1993;210-228.
29.
Okumura K, Henthorn RW, Epstein AE, Plumb VJ, Waldo AL.
Further observations on transient entrainment: importance of
pacing site and properties of the components of the reentry
circuit. Circulation. 1985;72:1293-1307.
30. Inoue H, Toda I, Saihara S, Sugimoto T. Further observations on entrainment of atrial flutter in the dog. Am Heart J. 1989;118:467-474. [Medline] [Order article via Infotrieve]
31. Fontaine G, Frank R, Tonet JL, Grosgogeat Y. Identification of a zone of slow conduction appropriate for ventricular tachycardia ablation: theoretical considerations. PACE Pacing Clin Electrophysiol. 1989;12:262-267. [Medline] [Order article via Infotrieve]
32.
Pastelin G, Mendez R, Moe GK. Participation of
atrial specialized conduction pathways in atrial flutter.
Circ Res. 1978;42:386-393.
33. Boineau JP, Schuessler RB, Mooney CR, Miller CB, Wylds AC, Hudson RD, Borremans JM, Brockus CW. Natural and evoked atrial flutter due to circus movement in dogs: role of abnormal atrial pathways, slow conduction, nonuniform refractory period distribution and premature beats. Am J Cardiol. 1980;45:1167-1181. [Medline] [Order article via Infotrieve]
34. Yamashita T, Inoue H, Nozaki A, Sugimoto T. Role of anatomic architecture in sustained atrial reentry and double potentials. Am Heart J. 1992;124:938-946. [Medline] [Order article via Infotrieve]
35. Cosio FG, Lopez GM, Goicolea 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]
36. Ferguson TJ, Schuessler RB, Hand DE, Boineau JP, Cox JL. Lessons learned from computerized mapping of the atrium: surgery for atrial fibrillation and atrial flutter. J Electrocardiol. 1993;26:210-219.
37. Cosio FG, Goicolea A, Lopez GM, Arribas F. Catheter ablation of atrial flutter circuits. PACE Pacing Clin Electrophysiol. 1993;16:637-642. [Medline] [Order article via Infotrieve]
38. 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]
39.
Saffitz JE, Kanter HL, Green KG, Tolley TK, Beyer EC.
Tissue-specific determinants of anisotropic conduction
velocity in canine atrial and ventricular
myocardium. Circ Res. 1994;74:1065-1070.
40. Arribas F, Lopex-Gil M, Nunez A, Puigdueta B, Goicolea A, Cosio F. The upper link of the common atrial flutter circuit. Circulation. 1994;90(suppl I):I-376. Abstract.
41. Kalbfleisch SJ, El Atassi R, Calkins H, Langberg JJ, Morady F. Association between atrioventricular node reentrant tachycardia and inducible atrial flutter. J Am Coll Cardiol. 1993;22:80-84.[Abstract]
This article has been cited by other articles:
 |
|
 |
|
  G. Barbato, V. Carinci, C. Tomasi, V. Frassineti, M. Margheri, and G. Di Pasquale Is electrocardiography a reliable tool for identifying patients with isthmus-dependent atrial flutter? Europace, August 1, 2009; 11(8): 1071 - 1076. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.#x.;n. Farré, H. J.J. Wellens, J.#x. M. Rubio, and J. Benezet CHAPTER 28 Supraventricular Tachycardias ESC Textbook of Cardiovascular Medicine, January 1, 2009; 2(1): med-9780199566990-chapter - med-9780199566990-chapter. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Saremi, L. Pourzand, S. Krishnan, O. Ashikyan, S. V. Gurudevan, J. Narula, K. Kaushal, and A. Raney Right Atrial Cavotricuspid Isthmus: Anatomic Characterization with Multi-Detector Row CT Radiology, June 1, 2008; 247(3): 658 - 668. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. C. Roberts-Thomson, I. H. Stevenson, P. M. Kistler, H. M. Haqqani, J. C. Goldblatt, P. Sanders, and J. M. Kalman Anatomically Determined Functional Conduction Delay in the Posterior Left Atrium: Relationship to Structural Heart Disease J. Am. Coll. Cardiol., February 26, 2008; 51(8): 856 - 862. [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]
|
|
|
|
 |
|
 J. E. Marine Catheter Ablation Therapy for Supraventricular Arrhythmias JAMA, December 19, 2007; 298(23): 2768 - 2778. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Moreira, C. Timmermans, H. J.J. Wellens, Y. Mizusawa, S. Philippens, D. Perez, and L.-M. Rodriguez Can Common-Type Atrial Flutter Be a Sign of an Arrhythmogenic Substrate in Paroxysmal Atrial Fibrillation?: Clinical and Ablative Consequences in Patients With Coexistent Paroxysmal Atrial Fibrillation/Atrial Flutter Circulation, December 11, 2007; 116(24): 2786 - 2792. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Dong, H. Calkins, S. B. Solomon, S. Lai, D. Dalal, A. Lardo, E. Brem, A. Preiss, R. D. Berger, H. Halperin, et al. Integrated Electroanatomic Mapping With Three-Dimensional Computed Tomographic Images for Real-Time Guided Ablations Circulation, January 17, 2006; 113(2): 186 - 194. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M R M Jongbloed, M J Schalij, K Zeppenfeld, P V Oemrawsingh, E E van der Wall, and J J Bax Clinical applications of intracardiac echocardiography in interventional procedures Heart, July 1, 2005; 91(7): 981 - 990. [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]
|
|
|
|
|
|
N. F. Marrouche, A. Natale, O. M. Wazni, J. Cheng, Y. Yang, H. Pollack, A. Verma, P. Ursell, and M. M. Scheinman Left Septal Atrial Flutter: Electrophysiology, Anatomy, and Results of Ablation Circulation, May 25, 2004; 109(20): 2440 - 2447. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Wong, P. A. Davlouros, W. Li, C. Millington-Sanders, D. P. Francis, and M. A. Gatzoulis Mechano-Electrical Interaction Late After Fontan Operation: Relation Between P-Wave Duration and Dispersion, Right Atrial Size, and Atrial Arrhythmias Circulation, May 18, 2004; 109(19): 2319 - 2325. [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]
|
|
|
|
|
|
T.-a. Matsuyama, S. Inoue, Y. Kobayashi, T. Sakai, T. Saito, T. Katagiri, and H. Ota Anatomical diversity and age-related histological changes in the human right atrial posterolateral wall Europace, January 1, 2004; 6(4): 307 - 315. [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]
|
|
|
|
|
|
P. Sanders, J. B. Morton, N. C. Davidson, S. J. Spence, J. K. Vohra, P. B. Sparks, and J. M. Kalman Electrical Remodeling of the Atria in Congestive Heart Failure: Electrophysiological and Electroanatomic Mapping in Humans Circulation, September 23, 2003; 108(12): 1461 - 1468. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A Doi, M Takagi, I Toda, M Teragaki, M Yoshiyama, K Takeuchi, and J Yoshikawa Real time quantification of low temperature radiofrequency ablation lesion size using phased array intracardiac echocardiography in the canine model: comparison of two dimensional images with pathological lesion characteristics Heart, August 1, 2003; 89(8): 923 - 927. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Schmieder, G. Ndrepepa, J. Dong, B. Zrenner, J. Schreieck, M. A.E. Schneider, M. R. Karch, and C. Schmitt Acute and long-term results of radiofrequency ablation of common atrial flutter and the influence of the right atrial isthmus ablation on the occurrence of atrial fibrillation Eur. Heart J., May 2, 2003; 24(10): 956 - 962. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Morton, P. Sanders, J. K. Vohra, P. B. Sparks, J. G. Morgan, S. J. Spence, L. E. Grigg, and J. M. Kalman Effect of Chronic Right Atrial Stretch on Atrial Electrical Remodeling in Patients With an Atrial Septal Defect Circulation, April 8, 2003; 107(13): 1775 - 1782. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Yamada, K. Tsukada, T. Miyashita, K. Kuga, and I. Yamaguchi Noninvasive, direct visualization of macro-reentrant circuits by using magnetocardiograms: initiation and persistence of atrial flutter Europace, January 1, 2003; 5(4): 343 - 350. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F G Cosio The right atrium as an anatomic set-up for re-entry: electrophysiology goes back to anatomy Heart, October 1, 2002; 88(4): 325 - 327. [Full Text] [PDF]
|
|
|
|
|
|
D Sanchez-Quintana, R H Anderson, J A Cabrera, V Climent, R Martin, J Farre, and S Y Ho The terminal crest: morphological features relevant to electrophysiology Heart, October 1, 2002; 88(4): 406 - 411. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Milliez, A. W. Richardson, O. Obioha-Ngwu, P. J. Zimetbaum, P. Papageorgiou, and M. E. Josephson Variable electrocardiographic characteristics of isthmus-dependent atrial flutter J. Am. Coll. Cardiol., September 18, 2002; 40(6): 1125 - 1132. [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]
|
|
|
|
 |
|
 O. Berenfeld, A. V. Zaitsev, S. F. Mironov, A. M. Pertsov, and J. Jalife Frequency-Dependent Breakdown of Wave Propagation Into Fibrillatory Conduction Across the Pectinate Muscle Network in the Isolated Sheep Right Atrium Circ. Res., June 14, 2002; 90(11): 1173 - 1180. [Abstract] [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]
|
|
|
|
|
|
D. L. Packer, C. L. Stevens, M. G. Curley, C. J. Bruce, F. A. Miller, B. K. Khandheria, J. K. Oh, L. J. Sinak, and J. B. Seward Intracardiac phased-array imaging: methods and initial clinical experience with high resolution, under blood visualization: Initial experience with intracardiac phased-array ultrasound J. Am. Coll. Cardiol., February 6, 2002; 39(3): 509 - 516. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Morton, M. J. Byrne, J. M. Power, J. Raman, and J. M. Kalman Electrical Remodeling of the Atrium in an Anatomic Model of Atrial Flutter: Relationship Between Substrate and Triggers for Conversion to Atrial Fibrillation Circulation, January 15, 2002; 105(2): 258 - 264. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Tritto, R. de Ponti, M. Zardini, G. Spadacini, and J. A. Salerno-Uriarte Bystander cavo-tricuspid isthmus activation during post-incisional intra-atrial reentrant tachycardia Europace, January 1, 2002; 4(1): 91 - 97. [Abstract] [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]
|
|
|
|
|
|
J. Chen, C. de Chillou, O-J. Ohm, P. I. Hoff, O. Rossvoll, M. Andronache, N. Sadoul, I. Magnin-Poull, K. S. Erga, and E. Aliot Acute resumption of conduction in the cavotricuspid isthmus after catheter ablation in patients with common atrial flutter: Real-time evaluation and long-term follow-up Europace, January 1, 2002; 4(3): 255 - 263. [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]
|
|
|
|
|
|
T Szili-Torok, G. Kimman, D Theuns, J Res, J R T C Roelandt, and L J Jordaens Transseptal left heart catheterisation guided by intracardiac echocardiography Heart, November 1, 2001; 86(5): e11 - 11. [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]
|
|
|
|
|
|
R. Becker, A. Bauer, S. Metz, R. Kinscherf, J. C. Senges, K. D. Schreiner, F. Voss, W. Kuebler, and W. Schoels Intercaval Block in Normal Canine Hearts : Role of the Terminal Crest Circulation, May 22, 2001; 103(20): 2521 - 2526. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Stabile, A. De Simone, P. Turco, V. La Rocca, P. Nocerino, C. Astarita, F. Maresca, C. De Matteis, T. Di Napoli, E. Stabile, et al. Response to flecainide infusion predicts long-term success of hybrid pharmacologic and ablation therapy in patients with atrial fibrillation J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1639 - 1644. [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]
|
|
|
|
|
|
F. Anselme, A. Savoure, A. Cribier, and N. Saoudi Catheter Ablation of Typical Atrial Flutter : A Randomized Comparison of 2 Methods for Determining Complete Bidirectional Isthmus Block Circulation, March 13, 2001; 103(10): 1434 - 1439. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Fragakis, A. Kotsakis, N. Patel, J. Bostock, E. Rosenthal, P. Holt, C. Bucknall, and J. Gill Atrial flutter ablation: Efficacy and cost-effectiveness of a single decapolar electrode to demonstrate bidirectional isthmus block Europace, January 1, 2001; 3(4): 304 - 310. [Abstract] [PDF]
|
|
|
|
|
|
J. M. Pastore and D. S. Rosenbaum Role of Structural Barriers in the Mechanism of Alternans-Induced Reentry Circ. Res., December 8, 2000; 87(12): 1157 - 1163. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y.-G. Wang, M. B. Wagner, R. Kumar, W. N. Goolsby, and R. W. Joyner Fast pacing facilitates discontinuous action potential propagation between rabbit atrial cells Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2095 - H2103. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Kottkamp, B. Hugl, B. Krauss, U. Wetzel, A. Fleck, G. Schuler, and G. Hindricks Electromagnetic Versus Fluoroscopic Mapping of the Inferior Isthmus for Ablation of Typical Atrial Flutter : A Prospective Randomized Study Circulation, October 24, 2000; 102(17): 2082 - 2086. [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]
|
|
|
|
|
|
H. J. Sih, D. P. Zipes, E. J. Berbari, D. E. Adams, and J. E. Olgin Differences in organization between acute and chronic atrial fibrillation in dogs J. Am. Coll. Cardiol., September 1, 2000; 36(3): 924 - 931. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. L Waldo ELECTROPHYSIOLOGY: Treatment of atrial flutter Heart, August 1, 2000; 84(2): 227 - 227. [Full Text] [PDF]
|
|
|
|
|
|
A. Natale, K. H. Newby, E. Pisano, F. Leonelli, R. Fanelli, D. Potenza, S. Beheiry, and G. Tomassoni Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter J. Am. Coll. Cardiol., June 1, 2000; 35(7): 1898 - 1904. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Becker, R. Klinkott, A. Bauer, J. C. Senges, K. D. Schreiner, F. Voss, W. Kuebler, and W. Schoels Multisite pacing for prevention of atrial tachyarrhythmias: potential mechanisms J. Am. Coll. Cardiol., June 1, 2000; 35(7): 1939 - 1946. [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]
|
|
|
|
|
|
A. SippensGroenewegen, M. D. Lesh, F. X. Roithinger, W. S. Ellis, P. R. Steiner, L. A. Saxon, R. J. Lee, and M. M. Scheinman Body surface mapping of counterclockwise and clockwise typical atrial flutter: a comparative analysis with endocardial activation sequence mapping J. Am. Coll. Cardiol., April 1, 2000; 35(5): 1276 - 1287. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Iesaka, T. Yamane, M. Goya, A. Takahashi, H. Fujiwara, Y. Okamoto, Y. Soejima, J. Nitta, A. Nogami, K. Aonuma, et al. A jump in cycle length of orthodromic common atrial flutter during catheter ablation at the isthmus between the inferior vena cava and tricuspid annulus: Evidence of dual isthmus conduction directed to dual septal exits Europace, January 1, 2000; 2(2): 163 - 171. [Abstract] [PDF]
|
|
|
|
|
|
J. Chen, Christian de Chillou, T. Basiouny, N. Sadoul, J. D. S. Filho, I. Magnin-Poull, M. Messier, and E. Aliot Cavotricuspid Isthmus Mapping to Assess Bidirectional Block During Common Atrial Flutter Radiofrequency Ablation Circulation, December 21, 1999; 100(25): 2507 - 2513. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Zrenner, G. Ndrepepa, M. Schneider, M. Karch, F. Hofmann, A. Schomig, and C. Schmitt Computer-assisted animation of atrial tachyarrhythmias recorded with a 64-electrode basket catheter J. Am. Coll. Cardiol., December 1, 1999; 34(7): 2051 - 2060. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Yamabe, I. Misumi, H. Fukushima, K. Ueno, Y. Kimura, and Y. Hokamura Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia Circulation, August 10, 1999; 100(6): 621 - 627. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Schumacher, W. Jung, H. Schmidt, C. Fischenbeck, T. Lewalter, A. Hagendorff, H. Omran, C. Wolpert, and B. Luderitz Transverse conduction capabilities of the crista terminalis in patients with atrial flutter and atrial fibrillation J. Am. Coll. Cardiol., August 1, 1999; 34(2): 363 - 373. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Gepstein, G. Hayam, S. Shpun, D. Cohen, and S. A. Ben-Haim Atrial Linear Ablations in Pigs : Chronic Effects on Atrial Electrophysiology and Pathology Circulation, July 27, 1999; 100(4): 419 - 426. [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]
|
|
|
|
|
|
A. Arenal, J. Almendral, J. M. Alday, J. Villacastin, J. M. Ormaetxe, J. L. M. Sande, N. Perez-Castellano, S. Gonzalez, M. Ortiz, and J. L. Delcan Rate-Dependent Conduction Block of the Crista Terminalis in Patients With Typical Atrial Flutter : Influence on Evaluation of Cavotricuspid Isthmus Conduction Block Circulation, June 1, 1999; 99(21): 2771 - 2778. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J. Callans, J.-F. Ren, D. Schwartzman, C. D. Gottlieb, F. A. Chaudhry, and F. E. Marchlinski Narrowing of the superior vena cava-right atrium junction during radiofrequency catheter ablation for inappropriate sinus tachycardia: analysis with intracardiac echocardiography J. Am. Coll. Cardiol., May 1, 1999; 33(6): 1667 - 1670. [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]
|
|
|
|
|
|
H. Paydak, J. G. Kall, M. C. Burke, D. Rubenstein, D. E. Kopp, R. J. Verdino, and D. J. Wilber Atrial Fibrillation After Radiofrequency Ablation of Type I Atrial Flutter : Time to Onset, Determinants, and Clinical Course Circulation, July 28, 1998; 98(4): 315 - 322. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C.-T. Tai, S.-A. Chen, A.-N. Feng, W.-C. Yu, Y.-J. Chen, and M.-S. Chang Electropharmacologic Effects of Class I and Class III Antiarrhythmia Drugs on Typical Atrial Flutter : Insights Into the Mechanism of Termination Circulation, May 19, 1998; 97(19): 1935 - 1945. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Shah, P. Jais, M. Haissaguerre, S. Chouairi, A. Takahashi, M. Hocini, S. Garrigue, and J. Clementy Three-dimensional Mapping of the Common Atrial Flutter Circuit in the Right Atrium Circulation, December 2, 1997; 96(11): 3904 - 3912. [Abstract] [Full Text]
|
|
|
|
|
|
F. X. Roithinger, M. R. Karch, P. R. Steiner, A. SippensGroenewegen, and M. D. Lesh Relationship Between Atrial Fibrillation and Typical Atrial Flutter in Humans : Activation Sequence Changes During Spontaneous Conversion Circulation, November 18, 1997; 96(10): 3484 - 3491. [Abstract] [Full Text]
|
|
|
|
|
|
W. G. Fisher, M. A. Pelini, and M. E. Bacon Adjunctive Intracardiac Echocardiography to Guide Slow Pathway Ablation in Human Atrioventricular Nodal Reentrant Tachycardia : Anatomic Insights Circulation, November 4, 1997; 96(9): 3021 - 3029. [Abstract] [Full Text]
|
|
|
|
|
|
D. C. Shah, M. Haissaguerre, P. Jais, B. Fischer, A. Takahashi, M. Hocini, and J. Clementy Simplified Electrophysiologically Directed Catheter Ablation of Recurrent Common Atrial Flutter Circulation, October 21, 1997; 96(8): 2505 - 2508. [Abstract] [Full Text]
|
|
|
|
|
|
C.-T. Tai, S.-A. Chen, C.-E. Chiang, S.-H. Lee, K.-C. Ueng, Z.-C. Wen, J.-L. Huang, Y.-J. Chen, W.-C. Yu, A.-N. Feng, et al. Characterization of Low Right Atrial Isthmus as the Slow Conduction Zone and Pharmacological Target in Typical Atrial Flutter Circulation, October 21, 1997; 96(8): 2601 - 2611. [Abstract] [Full Text]
|
|
|
|
|
|
C. Pandozi, L. Bianconi, M. Villani, A. Castro, G. Altamura, S. Toscano, A. P. Jesi, G. Gentilucci, F. Ammirati, F. L. Bianco, et al. Local Capture by Atrial Pacing in Spontaneous Chronic Atrial Fibrillation Circulation, May 20, 1997; 95(10): 2416 - 2422. [Abstract] [Full Text]
|
|
|
|
|
|
T. Yamashita, Y. Murakawa, K. Ajiki, and M. Omata Incidence of Induced Atrial Fibrillation/Flutter in Complete Atrioventricular Block: A Concept of `Atrial-Malfunctioning' Atrio-Hisian Block Circulation, February 4, 1997; 95(3): 650 - 654. [Abstract] [Full Text]
|
|
|
|
|
|
H. Poty, N. Saoudi, M. Nair, F. Anselme, and B. Letac Radiofrequency Catheter Ablation of Atrial Flutter: Further Insights Into the Various Types of Isthmus Block: Application to Ablation During Sinus Rhythm Circulation, December 15, 1996; 94(12): 3204 - 3213. [Abstract] [Full Text]
|
|
|
|
|
|
G. F. Van Hare and A. L. Waldo The Atrial Flutter Reentrant Circuit: Additional Pieces of the Puzzle Circulation, August 1, 1996; 94(3): 244 - 246. [Full Text]
|
|
|
|
|
|
P. Papageorgiou, K. Monahan, N. G. Boyle, M. J. Seifert, P. Beswick, J. Zebede, L. M. Epstein, and M. E. Josephson Site-Dependent Intra-Atrial Conduction Delay: Relationship to Initiation of Atrial Fibrillation Circulation, August 1, 1996; 94(3): 384 - 389. [Abstract] [Full Text]
|
|
|
|
|
|
J. M. Kalman, J. E. Olgin, L. A. Saxon, W. G. Fisher, R. J. Lee, and M. D. Lesh Activation and Entrainment Mapping Defines the Tricuspid Annulus as the Anterior Barrier in Typical Atrial Flutter Circulation, August 1, 1996; 94(3): 398 - 406. [Abstract] [Full Text]
|
|
|
|
|
|
H. Nakagawa, R. Lazzara, T. Khastgir, K. J. Beckman, J. H. McClelland, S. Imai, J. V. Pitha, A. E. Becker, M. Arruda, M. D. Gonzalez, et al. Role of the Tricuspid Annulus and the Eustachian Valve/Ridge on Atrial Flutter: Relevance to Catheter Ablation of the Septal Isthmus and a New Technique for Rapid Identification of Ablation Success Circulation, August 1, 1996; 94(3): 407 - 424. [Abstract] [Full Text]
|
|
|
|
 |
|
 S. K. Gandhi, B. I. Bromberg, and C. B. Huddleston Surgical technique and atrial arrhythmias after total cavopulmonary connection J. Thorac. Cardiovasc. Surg., June 1, 1996; 111(6): 1291 - 1292. [Full Text]
|
|
|
|
 |
|
 S. K. Gandhi, B. I. Bromberg, M. D. Rodefeld, R. B. Schuessler, J. P. Boineau, J. L. Cox, and C. B. Huddleston Lateral Tunnel Suture Line Variation Reduces Atrial Flutter After the Modified Fontan Operation Ann. Thorac. Surg., May 1, 1996; 61(5): 1299 - 1309. [Abstract] [Full Text]
|
|
|
|
|
|
M. D. Rodefeld, B. I. Bromberg, R. B. Schuessler, J. P. Boineau, J. L. Cox, and C. B. Huddleston ATRIAL FLUTTER AFTER LATERAL TUNNEL CONSTRUCTION IN THE MODIFIED FONTAN OPERATION: A CANINE MODEL J. Thorac. Cardiovasc. Surg., March 1, 1996; 111(3): 514 - 526. [Abstract] [Full Text]
|
|
|
|
|
|
J. M. Kalman, G. F. VanHare, J. E. Olgin, L. A. Saxon, S. I. Stark, and M. D. Lesh Ablation of `Incisional' Reentrant Atrial Tachycardia Complicating Surgery for Congenital Heart Disease : Use of Entrainment to Define a Critical Isthmus of Conduction Circulation, February 1, 1996; 93(3): 502 - 512. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||