(Circulation. 1999;99:1700-1705.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Right Atrial Flutter Due to Lower Loop Reentry
Mechanism and Anatomic Substrates
From the Section of Cardiac Electrophysiology, University of California San Francisco, and the Pacific Heart Institute, Santa Monica, Calif (W.R.C.). Dr Cheng is now at SUNY Health Science Center at Syracuse, Syracuse, NY.
Correspondence to Melvin M. Scheinman, MD, Cardiac Electrophysiology, University of California San Francisco, 500 Parnassus Ave, MU East 4S Box 1354, San Francisco, CA 94143-1354. E-mail scheinman{at}ep4.ucsf.edu
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Abstract |
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Background—The mechanisms of an atrial flutter (AFL) that is more rapid and at times more irregular than typical AFL are unknown.
Methods and Results—Twenty-nine patients with AFL were studied. Atrial electrograms were recorded from a 20-pole catheter placed against the tricuspid annulus (TA), with its distal electrodes lateral to the isthmus between the TA and the eustachian ridge (ER), and from the His bundle and coronary sinus catheters. Atrial extrastimuli were delivered in the TA-ER isthmus during typical AFL. Episodes of a right atrial flutter rhythm that was different from typical AFL were induced in 3 patients and occurred spontaneously in 3 patients. This sustained AFL, designated as lower-loop reentry (LLR), involved the lower right atrium (RA), as manifested by early breakthrough in the lower RA, wave-front collision in the high lateral RA or septum, and conduction through the TA-ER isthmus. Linear ablation resulting in bidirectional conduction block in the TA-ER isthmus terminated spontaneous LLR in 3 patients and rendered LLR noninducible in all patients. The cycle length of LLR was shorter than that of typical AFL (217±32 versus 272±40 ms, P<0.01). Alternating LLR and typical AFL in 1 patient resulted in cycle length oscillation.
Conclusions—LLR is a subtype of right atrial flutter and depends on conduction through the TA-ER isthmus.
Key Words: atrial flutter • ablation • electrical stimulation
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The mechanism of typical atrial flutter (AFL) has been well studied.1 2 3 4 5 6 7 8 The isthmus between the tricuspid annulus (TA) and eustachian ridge (ER) has been recognized as a critical portion of the typical AFL circuit and the target site for ablative therapy.5 9 10 11 12 13 14 15 16 17 Studies by Cosio et al14 elegantly demonstrated that the same reentrant circuit can support both clockwise and counterclockwise circus movement. However, the mechanisms of more rapid and irregular flutter rhythms are unknown. We recently described a subtype of AFL, designated as double-wave reentry (DWR), that is due to the presence of 2 activation wave fronts circulating simultaneously in the original reentrant circuit of typical AFL.18 We showed that DWR is transient and more rapid, with an irregular rate compared with typical AFL. The purpose of the present study is to describe the mechanism of a sustained subtype of right atrial flutter, which we have designated as lower-loop reentry (LLR), that also depends on conduction through the TA-ER isthmus but involves only the lower portion of the right atrium (RA).
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Selection
Twenty-nine patients with AFL were included in the study. There were 27 men, averaging 61.6±14.6 years old (range, 23 to 79 years). Eleven patients had coronary artery disease, but none had clinical evidence of myocardial ischemia at the time of study. Five had cardiomyopathy, with left ventricular ejection fractions ranging from 25% to 45%. Eleven had hypertension. One patient had moderate to severe mitral regurgitation. The remaining patients had no structural heart disease. All had normal thyroid function. Twelve patients were also included in our previous report on DRW.18 None were taking antiarrhythmic medications or digitalis except 4 who were taking amiodarone for a history of atrial fibrillation. These 4 patients were excluded from data analysis.
All patients had typical AFL. Twenty-seven had chronic AFL (>1 month), and 2 had recurrent paroxysmal AFL. Three patients also had episodes of spontaneous flutter, with flutter wave morphology similar to that of typical counterclockwise AFL but with more rapid and, at times, variable atrial rates.
Electrophysiology Study
After having given informed consent, all patients were brought
to the Electrophysiology Laboratory in a postabsorptive state. A
coronary sinus catheter was inserted via the right internal
jugular vein access with its proximal electrodes placed at the
coronary sinus ostium. A 20-pole electrode was inserted via the
right femoral vein and placed against the TA (Figure 1
). A catheter was placed across the
tricuspid valve to record the right anterior septal atrial and His
bundle electrograms. All catheters were deployed under fluoroscopy.
Pulse oximetry and vital signs were monitored throughout the study.
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Twelve-lead surface ECGs and intracardiac electrographic signals were recorded with a computerized data acquisition system (CardioLab by Prucka Engineering Inc). All signals were filtered with a low cutoff frequency of 30 Hz and a high cutoff frequency of 500 Hz. The sampling rate was 1000 Hz. The delivery of programmed electrical stimulation (PES) was controlled through a programmable stimulator (Bloom Associates, Ltd).
Induction of Typical AFL
All but 1 patient presented with AFL at the beginning of
the study. In the remaining patient, atrial overdrive was used to
induce AFL.
Determination of Atrial Effective Refractory Period during
Typical AFL
The atrial effective refractory period (ERP) in the TA-ER
isthmus was defined as the longest coupling interval that failed to
result in local capture. It was determined during typical AFL with
single extrastimuli, at 2 to 3 times the pacing threshold, delivered in
the TA-ER isthmus at 5- to 10-ms decrements to scan the entire AFL
cycle.
Twenty-two patients with typical AFL alone underwent the PES protocol during AFL to determine the electrophysiological properties of the TA-ER isthmus. Atrial ERP was not determined in the remaining 3 patients with spontaneous LLR and typical AFL because of variable cycle lengths. To investigate the effect of atrial ERP on the inducibility of LLR, 12 patients with typical AFL received 2 mg ibutilide IV given over 15 minutes. In 7 of these 12 patients, ibutilide did not terminate AFL immediately, and the same PES protocol was repeated 10 to 15 minutes after the ibutilide infusion.
After the study protocol, patients underwent radiofrequency (RF) ablation of AFL with bidirectional TA-ER isthmus block as the end point. Programmed stimulation with up to 2 extrastimuli and aggressive overdrive atrial pacing was performed after ablation. The study protocol was approved by the Institutional Review Board of the University of California San Francisco Medical Center.
Statistical Analysis
Statistical analyses were performed with commercial
software (Excel 4.0, Microsoft Corp). Results are reported as mean±SD.
A 2-tailed t test was used to compare means. A value of
P<0.05 was considered statistically significant.
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Results |
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In 28 patients who presented with AFL, the surface ECG showed negative flutter waves in the inferior leads (II, III, and aVF) associated with counterclockwise endocardial activation around the TA. Among these 28 patients, 3 had both counterclockwise typical AFL and a spontaneous but different flutter rhythm evidenced by a more rapid atrial rate and, at times, cycle length variation. Clockwise typical AFL was induced by atrial overdrive pacing at 200 ms in 1 patient with paroxysmal AFL. The diagnosis of typical AFL was confirmed by intra-atrial recordings from multiple electrodes and by concealed entrainment from the TA-ER isthmus during typical AFL. The baseline cycle length during typical AFL was 272±40 ms. In the 22 patients who had only typical AFL and were not taking amiodarone, the ERP determined from the TA-ER isthmus during typical AFL was 161±19 ms.
Induction of LLR
In 3 of the 26 patients with typical AFL, another type (LLR) of
AFL that was distinctively different from and more sustained than DWR
was induced.
These episodes of LLR shared a common, distinctive activation pattern
characterized by an early breakthrough at the lower lateral RA that
generated 2 activation wave fronts in the trabeculated
lateral RA, 1 propagating in a caudocranial or clockwise direction
along the lateral RA and the other propagating in a counterclockwise
direction through the TA-ER isthmus (Figure 2). Consequently, there was collision of
the counterclockwise and clockwise wave fronts in the high lateral RA.
This finding excluded the upper portions of the RA from the
tachycardia circuit. The activation sequence in the left
atrium, as reflected in the coronary sinus recordings,
remained the same as during typical AFL. The reentrant circuit of LLR
appears to involve only the base of the RA, ie, the TA-ER isthmus, the
portions of the smooth or posterior RA, and across the lower segment of
the crista terminalis. Therefore, we designated this type of AFL as
LLR.
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Two sustained episodes (>30 seconds) of induced LLR were recorded
after block of 1 of the double wave fronts of DWR in the TA-ER isthmus
(Figure 2
). These findings were reproducible in that multiple
nonsustained episodes of LLR were induced after termination of DWR in
these 3 patients.
Spontaneous LLR
Multiple spontaneous episodes of LLR were observed in 3 patients.
The duration of these episodes ranged from a single beat, as in
alternating LLR and typical AFL (see below), to more than several
minutes. All 3 also had spontaneous episodes of sustained
counterclockwise typical AFL. Examples of sustained episodes of typical
AFL and LLR in the same patient are shown in Figure 3. In all 3 patients, there were similar
flutter wave morphologies but at 2 different cycle lengths, with the
longer cycle length associated with the counterclockwise typical AFL
and the shorter cycle length associated with LLR. In 1 patient,
alternating LLR and typical counterclockwise AFL resulted in
oscillation in the cycle length that coincided with changes
in the RA activation sequence (Figure 4).
However, the isthmus conduction time, measured from TA 1 to proximal
CS, remained unchanged during the alternans. This finding is
consistent with alternation between a large circuit (typical
AFL) and a small circuit (LLR) that shared a common isthmus. However,
in 1 patient, the difference in local activation time between TA 1 and
proximal CS was shorter during LLR than during typical AFL (Figure 5). We postulate that in this particular
case, the early breakthrough occurred more distal to TA 1 and generated
2 activation wave fronts, 1 counterclockwise to the CS and the other
clockwise to TA 1, resulting in simultaneous activation of
the proximal CS and lower lateral RA. In all 3 patients, changes in
flutter cycle length coincided with corresponding transitions between
typical AFL and LLR.
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Electrophysiological Characteristics of Induced
and Spontaneous LLR
In all episodes of induced LLR, the breakthrough of activation at
the lower lateral RA was preceded by a short-long sequence resulting
from block of 1 of the 2 wave fronts during DWR in the TA-ER isthmus
(Figure 2). In contrast to DWR, induced LLR was a more stable
rhythm that persisted for as long as 4 minutes, compared with DWR,
which lasts only for 2 to 12 beats.18 The duration of
spontaneous LLR also varied from 1 beat to sustained episodes (>30
seconds).
The cycle length of LLR ranged from 170 to 250 ms, which was
significantly shorter than that of typical AFL (217±32 versus 272±40
ms, P<0.01). During sustained episodes of induced LLR (>30
seconds), there was little if any change in flutter cycle length (<10
ms) except, before termination of sustained LLR, a significant cycle
length variation was seen as a result of conduction variation in the
posterior limb of the circuit (Figure 5).
Patients with inducible LLR had a shorter atrial ERP determined in the TA-ER isthmus than those without LLR (138.8±13.4 versus 168.5±13.9 ms, P<0.005). Intravenous ibutilide (2 mg over 15 minutes) was administered before RF ablation in 2 of the 3 patients with inducible LLR, and the ERP increased (from 132 to 180 ms and from 144 to 247 ms, respectively). No further episodes of LLR were inducible after ibutilide infusion. In all 6 patients with either inducible or spontaneous LLR before RA ablation, neither typical AFL, DWR, or LLR could be induced, despite aggressive pacing protocol after bidirectional conduction block in the TA-ER isthmus.
Termination of LLR
Most episodes of the induced LLR reverted spontaneously to typical
counterclockwise AFL (Figures 4 and 5). Such reversion
occurred with the loss of the early breakthrough, which suggested block
of the activation wave front from the posterobasal RA at the lower
segment of the crista terminalis and allowed for resumption of
counterclockwise typical AFL. One episode persisted for >4 minutes and
deteriorated into atrial fibrillation. In all 3 patients with
spontaneous LLR, RF energy applied to the TA-ER isthmus during LLR led
to termination of LLR with bidirectional block (Figure 6).
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Surface Flutter Wave Morphology of LLR
In all patients with LLR, either induced or spontaneous, the
surface ECG showed negative flutter waves in the inferior
leads and a positive deflection in V1, similar to
that of typical counterclockwise flutter (Figures 3 and 4). However, the terminal portion of the flutter wave lost its
positive deflection in the inferior leads during LLR in
association with wave-front collision along the lateral
trabeculated RA wall during LLR. In 1 patient, multiple
breakthroughs occurred along the crista terminalis in association with
a blocked premature atrial depolarization in the TA-ER isthmus that led
to nearly simultaneous cristal activation and allowed for
reversal of both the sequence of septal activation and surface flutter
wave (Figure 7).
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) was
seen in TA-ER isthmus. Premature depolarization itself may have
resulted from a breakthrough between TA 1 and Isthmus and was blocked
between isthmus and CS os, as indicated in middle inset. This allowed
clockwise wave front in upper lateral RA to propagate further toward
septum and resulted in a reversal of septal activation sequence (top).
Simultaneous surface ECG (bottom) shows reversal of flutter
wave polarity associated with reversal in septal activation sequence.
Initial complexes (
) were recorded during LLR when collision
occurred over lateral RA. Subsequent complexes (
) were recorded
with reversal of septal activation sequence. Although the exact
mechanism of the arrhythmia is unclear, presence of multiple
breakthroughs along the crista terminalis is proposed as depicted in
the inset on right. Abbreviations as in previous figures. |
Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Our most important observation was to define the mechanism and probable substrate of a subtype of more rapid right atrial flutter, which we designate as LLR. Our data suggest that during LLR, the activation wave front traverses the TA-ER isthmus, activates the posterior RA, and then skirts the IVC with breakthrough along the low RA. The latter generates 2 wave fronts, which collide and are extinguished in the high lateral or septal RA while the tachycardia is driven by the circuit at the base of the RA. Termination of LLR by linear RF lesions delivered in the TA-ER isthmus provides definitive proof for the involvement of the TA-ER isthmus and the strongest evidence against a focal mechanism. Moreover, an aggressive pacing protocol after ablation failed to provoke the tachycardia, providing evidence against alternative mechanisms such as abnormal automaticity or triggered activity or of a reentrant circuit that does not involve the TA-ER isthmus.
Anatomic Considerations of the LLR Circuit
Compelling evidence indicates that typical flutter circuits in
humans depend on the crista terminalis and ER as its posterior barrier,
whereas the TA forms the anterior barrier. The TA-ER isthmus forms the
critical component of the AFL circuit. The same isthmus must also be
involved in the LLR. We have shown that the interruption of conduction
through the TA-ER isthmus terminated LLR (Figure 6). In
addition, the isthmus conduction time remained identical with
alternating LLR and typical AFL, consistent with switching
between a larger reentrant circuit (typical AFL) and a shorter one
(LLR) that share a common pathway in the TA-ER isthmus (Figure 4).
Recently, the septal isthmus of typical flutter was shown to be fixed
and present during sinus rhythm,13 but controversy
exists regarding the nature of conduction barrier along the lateral
portions of the crista terminalis. A recent elegant study by Shah et
al19 in patients with typical AFL demonstrated that during
pacing from the coronary sinus, there appears to be relatively
rapid and homogeneous activation with wave fronts from the
posterobasal RA and IVC–TA isthmus fusing (at the lower crista) and
ascending upward. The latter observation is in accord with our
hypothesis that the crista terminalis, at least distally, is a
functional rather than fixed conduction barrier during typical AFL.
During 1 episode of LLR, the RA activation became much more complex
(Figure 7), which we speculate was a result of conduction
breakthrough at multiple sites along the crista terminalis. This
episode eventuated in atrial fibrillation soon after the multiple
breakthroughs occurred. This raises an interesting possibility that
piecemeal breakdown of the conduction barrier along the crista
terminalis may form the substrate for multiple smaller reentrant
circuits and thereby herald atrial fibrillation.
Physiological Considerations of the LLR
Circuit
The chief paradox relating to our hypothesis is that all patients
with LLR also had typical AFL. If a short circuit between the exit
point from the TA-ER isthmus to the low lateral RA exists, why is it
not manifest all the time? The answer to this question is not clear
from our data, but certain points may help explain the paradox. Frame
et al20 showed that monophasic action potential
recordings obtained from atrial tissue in an isolated tricuspid
ring model of AFL showed marked oscillation of action
potential duration at more rapid tachycardia rates. Perhaps
this oscillation allows impulse breakthrough to the lower
segments of the crista terminalis that had a shorter refractoriness.
Another observation relates to the finding of DWR termination
introducing LLR. Termination of 1 of the DWR wave fronts produces a
pause after a period of rapid rate, which may facilitate conduction
through the lower lateral cristal region. Previous studies by Pinto et
al21 and Boyden et al22 also suggested that
premature activation of a site in the flutter circuit could be due to
the breakdown of lateral boundaries. Regardless of the precise
mechanism of the lower cristal breakthrough, LLR appears to be
perpetuated by a linking phenomenon in which the upper portions of the
RA are excluded from the circuit by repetitive collision.
We also found that patients with induced LLR had a significantly shorter ERP than those without. In addition, in the patients with induced LLR, this arrhythmia could not be initiated after intravenous ibutilide. The effects of ibutilide during AFL were to increase atrial refractoriness and to decrease the excitable gap in the TA-ER isthmus.23 24 We hypothesize that the lengthening of the refractory period in the TA-ER isthmus precluded initiation of this rapid reentrant tachycardia.
Determination of Flutter Wave Morphology During Right Atrial
Flutter
Our data support the observation by Okumura et al25
from canine experiments that the flutter wave morphology is largely
determined by the activation sequence of the septum and left atrium
(Figures 3, 4, and 7). Although the activation
sequences in the RA are significantly different during LLR and typical
AFL, the flutter wave morphology is similar to the counterclockwise
typical AFL when the collision of wave fronts occurs along the lateral
RA, with the activation of the interatrial septum remaining in a
caudal-to-cranial direction. However, there was a subtle difference in
the terminal portion of the flutter wave, ie, the loss of the terminal
positive deflection of the flutter wave in the inferior
leads (Figures 3 and 4). This temporally coincided with
and could be accounted for by the wave-front collision along the
lateral trabeculated RA wall. Furthermore, the flutter wave
polarity changed to that of clockwise typical AFL when the interatrial
septum was activated in a cranial-to-caudal direction
(Figure 7).
Limitations
The chief limitation of our study is lack of sufficient
intracardiac recording sites, especially in the posterior RA,
to define the course of the entire LLR circuit. Entrainment during LLR
to prove that the TA-ER isthmus was an integral part of the
tachycardia circuit was not successful because of frequent
conversion of LLR to typical AFL. However, TA-ER isthmus conduction
block always terminated LLR.
Clinical Significance
Existing data in the literature suggest that only typical AFL,
either counterclockwise or clockwise, is amenable to ablation in the
TA-ER isthmus. The important practical significance of our observations
relates to the findings of a rapid and, at times, irregular flutter
rhythm (LLR) that may be TA-ER isthmus–dependent and curable by RF
ablation. Close scrutiny of the surface ECG may yield clues to
the presence of LLR.
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Acknowledgments |
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Dr Cheng was supported in part by a Mark C. Lidwill Traveling Fellowship from the North American Society of Pacing and Electrophysiology.
Received July 16, 1998; revision received December 11, 1998; accepted December 30, 1998.
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C. Blomstrom-Lundqvist, M. M. Scheinman, E. M. Aliot, J. S. Alpert, H. Calkins, A. J. Camm, W. B. Campbell, D. E. Haines, K. H. Kuck, B. B. Lerman, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias*--Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias) Circulation, October 14, 2003; 108(15): 1871 - 1909. [Full Text] [PDF]
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 Committee Members, C. Blomstrom-Lundqvist, M. M Scheinman, E. M Aliot, J. S Alpert, H. Calkins, A.J. Camm, W.B. Campbell, D. E Haines, K. H Kuck, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: A Report of the American College of Cardiology/American HeartAssociation Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines(Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias)Developed in collaboration with NASPE-Heart Rhythm Society Eur. Heart J., October 2, 2003; 24(20): 1857 - 1897. [Full Text] [PDF]
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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]
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A. Bochoeyer, Y. Yang, J. Cheng, R. J. Lee, E. C. Keung, N. F. Marrouche, A. Natale, and M. M. Scheinman Surface Electrocardiographic Characteristics of Right and Left Atrial Flutter Circulation, July 8, 2003; 108(1): 60 - 66. [Abstract] [Full Text] [PDF]
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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]
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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]
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 Y. A. Louagie, D. Blommaert, and L. De Roy Radiofrequency ablation of atrial flutter combined with closure of atrial septal defect Interactive CardioVascular and Thoracic Surgery, September 1, 2002; 1(1): 38 - 40. [Abstract] [Full Text] [PDF]
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J. Cheng, K. Glatter, Y. Yang, S. Zhang, R. Lee, and M. M. Scheinman Electrophysiological Response of the Right Atrium to Ibutilide During Typical Atrial Flutter Circulation, August 13, 2002; 106(7): 814 - 819. [Abstract] [Full Text] [PDF]
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H. J.J. Wellens Contemporary Management of Atrial Flutter Circulation, August 6, 2002; 106(6): 649 - 652. [Full Text] [PDF]
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 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]
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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]
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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]
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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]
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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]
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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]
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J. K. Triedman, M. E. Alexander, C. I. Berul, L. M. Bevilacqua, and E. P. Walsh Electroanatomic Mapping of Entrained and Exit Zones in Patients With Repaired Congenital Heart Disease and Intra-Atrial Reentrant Tachycardia Circulation, April 24, 2001; 103(16): 2060 - 2065. [Abstract] [Full Text] [PDF]
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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]
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P. B. Sparks, S. Jayaprakash, J. K. Vohra, and J. M. Kalman Electrical Remodeling of the Atria Associated With Paroxysmal and Chronic Atrial Flutter Circulation, October 10, 2000; 102(15): 1807 - 1813. [Abstract] [Full Text] [PDF]
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M. M. Scheinman Mechanisms of atrial fibrillation: is a cure at hand? J. Am. Coll. Cardiol., May 1, 2000; 35(6): 1687 - 1692. [Abstract] [Full Text] [PDF]
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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]
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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]
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