(Circulation. 2000;101:2928.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Mapping and Ablation of Left Atrial Flutters
Presented in part at the 19th Annual Meeting of the North American Society of Pacing and Electrophysiology, San Diego, Calif, May 6–9, 1998.
From the Hôpital Cardiologique du Haut-Lévêque, Bordeaux-Pessac, France.
Correspondence to Docteur Pierre Jaïs, Hôpital Cardiologique du Haut-Lévêque, Avenue de Magellan, 33604 Bordeaux-Pessac, France.
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Abstract |
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Background—Typical right atrial isthmus–dependent flutters have been described in detail, but very little is known about left atrial (LA) flutters.
Methods and Results—We performed conventional and 3D mapping of the LA for 22 patients with atypical flutters. Complete maps in 17 patients demonstrated macroreentrant circuits (n=15) with 1 to 3 loops rotating around the mitral annulus, the pulmonary veins, and a zone of block or a silent area. In 2 patients, a small reentry circuit with a zone of markedly slow conduction was identified. Linear ablation performed across the most accessible part of the circuit cured 16 patients (73%) with a follow-up of 15±7 months.
Conclusions—LA reentrant tachycardias are related to individually varying circuits and are amenable to mapping guided radiofrequency ablation.
Key Words: atrial flutter • mapping • ablation
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Macroreentrant arrhythmias designated as flutters are divided into typical flutter (with counterclockwise or clockwise peritricuspidian rotation) and atypical flutters. Peritricuspid flutters have been studied extensively with conventional or 3D computerized mapping, and their ablation in the cavotricuspid isthmus is remarkably effective and safe.1 A few cases of atypical flutters have been reported, usually after surgical incisions of the right atrium (RA).2 Few data are available about left atrial (LA) flutters.3 This study describes the electrophysiological characteristics and results of ablation in a series of 22 patients presenting with spontaneous LA flutter.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients
Between March 1997 and March 1999, 22 patients (7 women, 15 men, 60±14 years old) were studied. They had been suffering from persistent atrial flutter for 5±7 years despite the use of 4±1 ineffective antiarrhythmic drugs. Amiodarone failed in 18 and was interrupted because of side effects in 2. Seventeen of the 22 (77%) had structural heart disease, including 3 who had undergone mitral valve replacement or repair (Table 1
). Two patients had common
flutter ablation before being included in this study. In all patients,
the surface ECG showed a regular monomorphic persistent atrial
arrhythmia with a P wave predominantly positive in lead
V1 and distinct in the limb leads from the
pattern described for peritricuspidian flutters (Figure 1). In 4 patients, however, the surface
ECG morphology was compatible with a common counterclockwise RA
flutter.
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Oral informed consent was obtained in all cases after discussion of the
risks and benefits of the procedure. Patients had been under effective
oral anticoagulants for 
1 month before the ablation, and
transthoracic and transesophageal
echocardiography were performed to rule out LA
thrombi. Oral anticoagulants were stopped at admission and replaced by
subcutaneous heparin to maintain a partial thromboplastin time of 2 to
3 times the control value. This was stopped 6 to 8 hours before
ablation for possible transseptal catheterization.
Electrophysiological Study
All antiarrhythmic drugs except amiodarone were
discontinued 3 to 4 days before the study. After 6 hours of fasting,
2 to 3 multipolar catheters (Cordis-Webster and Bard or ELA Medical)
were used to record bipolar electrograms filtered at 30 to 500 Hz
and amplified at 0.1 mV/cm on a PPG Midas polygraph with a paper speed
of 100 mm/s. An LA flutter was defined as an atrial
arrhythmia with a regular and monomorphic ECG pattern
demonstrated by intracardiac mapping to be due to a reentrant circuit
in the LA.
The first step was to exclude an RA atypical flutter circuit based on
1 of the following 3 RA mapping criteria: (1) RA activation time as
determined by sequential conventional mapping (with 8 evenly
distributed points) accounting for <50% of the arrhythmia
cycle length; (2) postpacing interval (PPI) in the RA longer than the
cycle length by 40 ms in 3 different points in the RA, including
the cavotricuspid isthmus and RA free wall but excluding the septum and
coronary sinus; and (3) spontaneous variations of >100 ms in
the RA with concomitant variations of <20 ms in the LA.
The second step was direct LA mapping to demonstrate the reentrant circuit during tachycardia with a 3D electroanatomic mapping system (Biosense Cordis-Webster). A transseptal puncture (Brockenbrough needle and Daig sheath) was required in 20 cases, whereas 2 patients had a patent foramen ovale. The mapping system has been described previously.1 Briefly, it includes a location pad, a processor (Carto), and a monitor and workstation (Silicon graphics), as well as 2 sensor-equipped catheters. One of these sensor-equipped catheters was used as a reference and placed in a stable position (RA appendage or coronary sinus in the event of spontaneous RA variations) to record a stable high-amplitude atrial signal. For the last 4 patients, an external reference was placed on the patient’s back, with a diagnostic quadripolar catheter used as the electrophysiological reference. A sensor-equipped rove catheter was used for mapping and identification of anatomic landmarks. Local activation time was automatically determined by the computer, according to the maximum negative slope dV/dt of bipolar electrograms filtered at 30 to 400 Hz. After sequential construction of the map, all points were manually checked and corrected if necessary. Bipolar voltage maps were analyzed in relation to activation maps. Mapping was complete when a sufficient density (>80 points) was achieved to allow understanding of the LA circuit. Some maps could not be completed because of premature termination of tachycardia, irregular varying cycle length (despite a monomorphic ECG aspect of the flutter), or change to another morphology and/or cycle length and/or atrial fibrillation (AF) or technical dysfunction. In these patients, conventional mapping, including entrainment maneuvers and PPI analysis, was performed after reinduction of the clinical tachycardia. Pacing sites with a PPI not exceeding the cycle length by >20 ms were considered to be part of the circuit. Pacing for entrainment resulted in transformation to another morphology or to AF in 3 of 6 initial patients. Subsequently, it was not performed systematically.
Definitions
Electrically silent areas were defined as no recordable
activity or amplitude <0.05 mV (which is the baseline noise in the
Biosense system), accompanied by inability to capture the atria from
these areas at 20 mA. Such areas were tagged as "scar" and
therefore appear in gray on the 3D maps (Figures 2, 3, and 4). With conventional mapping, slow
conduction was arbitrarily defined as complex and fractionated activity
of long duration (>50 ms). A zone of block was defined by double
potentials separated by an isoelectric interval of 50 ms. With the
Biosense system, isochronal crowding indicating a conduction
velocity of <0.033 cm/ms (slower than 0.05 cm/ms)4 was
considered a zone of slow conduction, whereas a collision of 2 wave
fronts traveling in different directions separated temporally by 50 ms
was defined as a region of local block1 (Figures 2, 3, and 4).
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A macroreentrant circuit was defined as a circuit propagating in a
large part of the cavity with a minimum diameter of >3 cm. Conversely,
small reentrant circuits were defined as circuits with a diameter of
<3 cm along with activation covering the entire cycle length and
centrifugal activation of the remaining LA (Figure 5).
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Ablation
After each successful mapping procedure, radiofrequency (RF)
ablation was performed by targeting either the narrowest and/or the
most accessible part of the circuit (allowing the best electrode-tissue
contact along the desired line). The ablation line was chosen to
transect an area critical for the circuit and connected 2 anatomic
areas of block or an electrically silent area to an anatomic zone of
block (pulmonary vein [PV], mitral annulus). In patients with
incomplete maps, the ablation was guided by conventional mapping
targeting a critical isthmus and/or a zone of slow conduction shown to
be part of the circuit by pacing maneuvers. After ablation, the
catheter was used to retrace the same line (during sinus rhythm),
showing either the absence of electrograms or a complete line of block
demonstrated by parallel double potentials recorded all along the
line. Finally, high-rate pacing with a stimulus strength of 20 mA was
performed on the RA and/or the LA after successful termination to
assess flutter or fibrillation inducibility. Any arrhythmia
lasting 3 minutes was considered sustained. The procedural end point
was defined as interruption and noninducibility of the targeted
flutter morphology.
A Stockert Cordis generator was used to deliver RF for 60 seconds at each site with a target temperature of 50°C to 55°C and a power limit of 70 W, except when there was an impedance rise. The catheter was progressively pulled back during RF delivery to produce coalescent lesions from one part to the other of the predetermined line.
An irrigated-tip catheter was used for the initial cases in which the flutter was not interrupted because of resistant gaps in the ablation line and systematically for the last 15 patients with a protocol previously shown to be safe.5 Heparin was administered after transseptal puncture to maintain a partial thromboplastin time of 2 to 3 times the control value.
Postablation Management
Patients were maintained on anticoagulation and monitored by
telemetry and ambulatory ECG recordings.
Transthoracic echocardiography was
performed 1 to 3 days after the ablation. A previously ineffective
antiarrhythmic drug was used in case of AF during days 6 to 10 of
in-hospital telemetry surveillance after ablation. Patients were then
discharged under oral anticoagulation for 6 months to 1 year. Late
follow-up consisted of visits to the hospital or the referring
physician and ambulatory recordings. The outcome of the
procedure was considered a success in case of persistent sinus rhythm
or success with drug if previously ineffective antiarrhythmic drugs
were required for persistent flutter or associated AF. A second
procedure was performed in case of a recurrence of organized
atrial arrhythmia.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Mapping Results
The results of mapping in the RA are shown in Table 2
. The RA activation time accounted for
<50% of the cycle length in all but 3 patients in whom spontaneous
local variations or local PPI interval ruled out an RA
arrhythmia.
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In 17 patients, complete maps were obtained for 18 LA flutter
morphologies. Varying macroreentrant circuits were identified in 15
patients and a small reentry circuit in 2 (Figure 6). The mean LA volume was 134±33 mL
(median, 127 mL) versus 34±10 mL in normal LA in our laboratory. A
mean of 112±28 points covering 95±3% of the arrhythmia cycle
length were recorded. In 9 patients, LA pacing showed a PPI not
exceeding the cycle length by >20 ms. In 5 patients, a complete map
could not be achieved.
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Electrically Silent Areas and/or Zone of Block
Eleven electrically silent areas were noted in 8 patients with
complete maps (Figure 6
). They were located in the posterior LA
(n=5) and were associated with an anterior silent area in 2 patients.
The posterior silent area was of varying dimensions, extending to the
roof in 3 or to the septum in 1. An isolated silent area in the roof
was observed in 2 patients and associated with an anterior area in 1.
Three patients had 2 different silent areas: roof and anterior LA (n=1)
and anterior and posterior LA (n=2). In 3 patients with incomplete
maps, 2 posterior and 1 anterior silent areas were noted.
Thirty-two zones of block (1 per patient) were identified in various
locations, as shown in Figure 7. These
zones of block were anchored at the ostium of the left PV (35%), right
PV (15%), or base of the appendage (22%). They coincided with regions
of significant voltage gradient (0.1±0.7 versus 1±0.6 mV) in 11 of 17
patients (65%) (Figure 5).
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Characteristics of Circuits
The complete map results are summarized in Table 1.
Single-Loop Reentrant Circuits
A single-loop reentrant circuit was identified in 13 patients
(Figure 2). It was rotating around the mitral annulus in 7
(counterclockwise rotation [left lateral view] in 1, clockwise in 5,
both in 1) and was bounded by a silent area in 4 (posterior, n=1;
anterior plus posterior, n=2; roof, n=1).
In 2 patients (patients 12 and 16), the core center of the circuit was a posterior or a roof silent area bounded by a zone of block anchored in the left PV ostium (n=1) or at the left appendage base (n=1).
A vertical zone of block anchored in the right (n=3) or left (n=1) PVs was the center of the circuit in 4 patients.
Multiple-Loop Circuits
One patient had a figure-8 reentrant circuit with 2 loops rotating
in opposite directions: one around a posterior silent area and the
other around a vertical zone of block anchored in the right PVs (Figure 3). The common channel was in the posterior LA, with the
activation proceeding upward, dividing itself into 2 waves in the LA
roof, one going downward in the anterior LA around the right PVs and
the other proceeding posteriorly around the silent area. In another
patient, 3 loops were coexisting during the same flutter (Figure 4). One was rotating around an anterior silent area, with
another one around a posterior silent area. The third loop was
ascending in the anterior LA, propagating downward in the lateral LA
through a channel common for the 3 circuits between the base of the
appendage and the left PVs.
Small Reentry
Patient 5 had a wide vertical zone of block extending from the
lower part of the lateral LA to the roof through the left PVs
and then to the LA appendage base (Figure 5). A gap at
the base of this line of block constituted a critical zone of slow
conduction which permitted the maintenance of a small reentrant circuit
in the lateral LA. The entire cycle length was recorded in this
small area, with the (successful) ablation site displaying a continuous
activity of 206 ms for a cycle length of 286 ms. The rest of the LA was
passively activated, as well as the RA. Another small reentrant
circuit was identified in patient 22 in the left septum, rotating
around the right superior PV and fossa ovalis, with a
slow-conduction area at the junction between right superior PV and LA
roof.
Ablation Results
One, 2, or 3 sessions were required in 14, 7, and 1 patients,
respectively (mean, 1.4±0.5; median, 1). The mean cumulative procedure
and fluoroscopy durations were 339±113 and 95±42 minutes per
patient.
Macroreentrant Circuits
A total of 39±33 minutes of RF application resulted in the
interruption of the 18 mapped flutter morphologies in 17 patients. The
7 perimitral flutter circuits were ablated by a line connecting the
mitral annulus to the left superior PV (n=2), the right superior PV
(n=2), or a silent area located anteriorly (n=2) or in the LA roof
(n=1). The circuits propagating around a silent area were interrupted
when the silent area was connected to either the right or left superior
PV. The peri-PV circuits were ablated by joining of the PV to the
mitral annulus (n=3) or to the contralateral superior PV across the LA
roof (n=1).
The double-loop figure-8 circuit (patient 7) was ablated by connection
of the posterior silent area to the right inferior PV
(Figure 3). The 3-loop reentrant circuit (patient 13) was
ablated targeting the common channel in the roof from the left superior
to the right superior PV ostium (Figure 4).
For patient 11, with a perimitral circuit, the right superior PV mitral line could not be completed. As a result, cycle length increased from 280 to 450 ms without interruption. Another line joining the mitral annulus to the left PV was again incomplete and did not modify the arrhythmia. For patient 15, the ablation line joining the mitral annulus to the left PV resulted in interruption of the clinical arrhythmia, which, however, remained inducible despite multiple attempts to complete the line of block.
Small Reentrant Circuits
Both small reentrant circuits were successfully ablated by local
discrete lesions delivered on the slow conduction area, with flutter
interruption obtained within 1 minute of RF delivery.
Incomplete Maps
In the 5 patients without complete Biosense maps, the ablation was
guided by conventional mapping data for 2 patients. In patient 10, 2
different morphologies of flutter were ablated, the first one by
connection of a zone of double potentials present in the roof to
the right superior PV and the second by connection of the right
superior PV to an area of complex and fractionated electrograms of the
fossa ovalis. In patient 4, flutter was interrupted with an ablation
line joining the right superior PV to the mitral annulus. In 3 other
patients (patients 2, 3, and 17), multiple flutter morphologies were
observed, and we therefore performed the 3 LA ablation lines used for
AF ablation with a successful outcome in 1, an increase of the cycle
length without conversion to sinus rhythm in a second (patient 17), and
no change in the third.
Postablation Flutters
Another flutter morphology not previously documented occurred
after the initial ablation of a perimitral circuit in 4 patients.
Mapping showed that the initial ablation line between PV and mitral
annulus was complete and that the new circuit was rotating around the
opposite PV. They were successfully ablated by a line connecting the
left superior to the right superior PV (across the roof of the LA).
Safety
The first patient had a reversible ischemic neurological
deficit at the end of the procedure. No other significant side effects
were observed.
Outcome
Acute
Twenty patients were in sinus rhythm after ablation, but the
clinical arrhythmia persisted in 2. Despite high-rate pacing,
10 of them were noninducible; atypical sustained flutter was inducible
in 5, atypical nonsustained in 3, and AF in 2.
Midterm Follow-Up
With a mean follow-up of 15±7 months, 16 patients (73%) were
successfully treated, with no antiarrhythmic drugs in 15; 1 was taking
amiodarone for paroxysmal AF. LA flutter persisted in 2 and
reoccurred in 3 patients 1 day to 2 months after the last ablation. One
woman had chronic AF.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates the varying characteristics of reentrant tachycardia in the human LA (LA flutter), occurring mainly in patients with underlying structural heart disease and the feasibility and safety of curative catheter ablation.
Diagnosis of LA Flutters
The diagnosis of LA flutter was established by comprehensive
mapping, including in 17 patients with a 3D electroanatomic system, and
was confirmed by the results of catheter ablation achieving sinus
rhythm for 20 patients or prolonging the tachycardia cycle
length in 2.
Various circuits were demonstrated. In most cases, the arrhythmia rotated around the mitral annulus, a zone of block including the PVs, or a silent area. Lines of block and silent areas also acted as lateral barriers, probably allowing the stabilization of the circuit and preventing short circuiting. In a few patients, the circuits were more complex, with 2 or 3 loops rotating concomitantly. There was no marked area of slow conduction in these macroreentrant circuits, in contrast to the 2 cases of small reentrant circuit, in which a zone of very slow conduction was found, accounting for >2/3 of the cycle length. Slow-conduction areas were frequently reported in animal models, usually being the center of the circuit, either alone or in association with anatomic obstacles.4
In contrast, a silent area has not previously been reported clinically. It seems to be a distinctive and relatively common feature of human LA flutter, present in 50% of the patients in this series. This is probably related to severe atrial fibrosis (and atrial myocardial cell modification/disappearance), a common phenomenon in patients with structural heart disease.6 It may also be possible that in those patients who had suffered from atrial arrhythmias for many years, histological changes have occurred as a result of atrial arrhythmia.7
Review of the Literature
Various studies have described atypical RA reentrant
arrhythmias, frequently related to surgical
incisions.2 A flutter circuit involving the
coronary sinus has also been reported with conventional
mapping.8 However, there is no previous study on LA
arrhythmia circuits and on their mechanisms in humans. Schoels
et al4 and Uno et al9 demonstrated some right
atypical circuits with single- or double-loop reentry in the canine
sterile pericarditis model. The LA was rarely involved.
Surgical lines of block placed in the LA (to simulate unilateral or bilateral lung transplantation) provided an electrophysiological substrate for LA flutter in a dog model.10 Again, the circuit was large enough to sustain reentry in the absence of marked slow conduction.
In a dog model, Schuessler et al11 also demonstrated atrial flutters, usually rotating around anatomic and functional zones of block. However, in dogs with enlarged and/or hypertrophied LA, most of the circuits were located in the RA. Pure LA circuits were rarely found, usually rotating around the PV (4 dogs in Schuessler’s experience). Therefore, both human and animal data suggest that the RA is more frequently involved in flutters than the LA. However, the exact incidence of LA flutters in humans is currently unknown.
Catheter Ablation
The ablation procedure duration and x-ray exposure involving the
mapping part were relatively long, but the long-term results clearly
indicate the feasibility of successful ablation. There was a 73%
short-term success rate for patients resistant to
antiarrhythmic drugs, and in 70%, sinus rhythm persisted with a
follow-up of >1 year without drug. This success rate is smaller than
the one achieved for common flutter ablation but can probably be
improved. This is likely to be due to the greater thickness of the LA
and to the longer ablation line required.
It is also interesting to note that there was a limited incidence of AF after ablation despite the underlying structural heart disease. This may be related to the presence of silent areas and lines of block (spontaneous and created by RF), which could reduce the electrically active atrial mass below a critical threshold for fibrillation.
Limitations
Several limitations in this study were inherent to the mapping
system used.
The arrhythmia must be perfectly stable, with cycle length variations of <10% to provide exploitable maps.
It is impossible to differentiate very slow conduction from complete block in the present clinical conditions. Isochronal mapping is limited by interpolation and by the selection of local activation time. Moreover, the absence of systematic pacing and entrainment because of the risk of inducing AF is a limitation in this study.
Conclusions
LA flutters sustained by highly variable macroreentrant or
small-reentrant circuits can occur in humans, usually with structural
heart disease affecting the LA, mainly mitral disease. These
arrhythmias require detailed mapping to guide successful
ablation.
Received September 7, 1999; revision received December 31, 1999; accepted January 31, 2000.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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1. Shah DC, Jaïs P, Haïssaguerre M, et al. Three-dimensional mapping of the common atrial flutter circuit in the right atrium. Circulation. 1997;96:3904–3912.
2.
Kalman JM, VanHare GF, Olgin JE, et al. Ablation of
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critical isthmus of conduction. Circulation. 1996;93:502–512.
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4. Schoels W, Offner B, Brachmann J, et al. Circus movement atrial flutter in the canine sterile pericarditis model: relation of characteristics of the surface electrocardiogram and conduction properties of the reentrant pathway. J Am Coll Cardiol. 1994;23:799–808.[Abstract]
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Jaïs P, Haïssaguerre M, Shah DC, et
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A. Chugh, R. Latchamsetty, H. Oral, D. Elmouchi, D. Tschopp, S. Reich, P. Igic, T. Lemerand, E. Good, F. Bogun, et al. Characteristics of Cavotricuspid Isthmus-Dependent Atrial Flutter After Left Atrial Ablation of Atrial Fibrillation Circulation, February 7, 2006; 113(5): 609 - 615. [Abstract] [Full Text] [PDF]
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P. Sanders, M. Hocini, P. Jais, L.-F. Hsu, Y. Takahashi, M. Rotter, C. Scavee, J.-L. Pasquie, F. Sacher, T. Rostock, et al. Characterization of Focal Atrial Tachycardia Using High-Density Mapping J. Am. Coll. Cardiol., December 6, 2005; 46(11): 2088 - 2099. [Abstract] [Full Text] [PDF]
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P. M. Kistler, S. P. Fynn, H. Haqqani, I. H. Stevenson, J. K. Vohra, J. B. Morton, P. B. Sparks, and J. M. Kalman Focal Atrial Tachycardia From the Ostium of the Coronary Sinus: Electrocardiographic and Electrophysiological Characterization and Radiofrequency Ablation J. Am. Coll. Cardiol., May 3, 2005; 45(9): 1488 - 1493. [Abstract] [Full Text] [PDF]
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S. M. Narayan, A. Hassankhani, G. K. Feld, and V. Bhargava Separating non-isthmus- from isthmus-dependent atrial flutter using wavefront variability J. Am. Coll. Cardiol., April 19, 2005; 45(8): 1269 - 1279. [Abstract] [Full Text] [PDF]
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F. H.M. Wittkampf, M. F. van Oosterhout, P. Loh, R. Derksen, E.-j. Vonken, P. J. Slootweg, and S. Y. Ho Where to draw the mitral isthmus line in catheter ablation of atrial fibrillation: histological analysis Eur. Heart J., April 1, 2005; 26(7): 689 - 695. [Abstract] [Full Text] [PDF]
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R. Cappato, H. Calkins, S.-A. Chen, W. Davies, Y. Iesaka, J. Kalman, Y.-H. Kim, G. Klein, D. Packer, and A. Skanes Worldwide Survey on the Methods, Efficacy, and Safety of Catheter Ablation for Human Atrial Fibrillation Circulation, March 8, 2005; 111(9): 1100 - 1105. [Abstract] [Full Text] [PDF]
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F. Kilicaslan, A. Verma, H. Yamaji, N. F. Marrouche, O. Wazni, J. E. Cummings, S. Hao, M. W. Andrews, S. Beheiry, A. Abdul-Karim, et al. The need for atrial flutter ablation following pulmonary vein antrum isolation in patients with and without previous cardiac surgery J. Am. Coll. Cardiol., March 1, 2005; 45(5): 690 - 696. [Abstract] [Full Text] [PDF]
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C. Pappone, F. Manguso, G. Vicedomini, F. Gugliotta, O. Santinelli, A. Ferro, S. Gulletta, S. Sala, N. Sora, G. Paglino, et al. Prevention of Iatrogenic Atrial Tachycardia After Ablation of Atrial Fibrillation: A Prospective Randomized Study Comparing Circumferential Pulmonary Vein Ablation With a Modified Approach Circulation, November 9, 2004; 110(19): 3036 - 3042. [Abstract] [Full Text] [PDF]
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P. Jais, M. Hocini, L.-F. Hsu, P. Sanders, C. Scavee, R. Weerasooriya, L. Macle, F. Raybaud, S. Garrigue, D. C. Shah, et al. Technique and Results of Linear Ablation at the Mitral Isthmus Circulation, November 9, 2004; 110(19): 2996 - 3002. [Abstract] [Full Text] [PDF]
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P. Sanders, P. M. Kistler, J. B. Morton, S. J. Spence, and J. M. Kalman Remodeling of Sinus Node Function in Patients With Congestive Heart Failure: Reduction in Sinus Node Reserve Circulation, August 24, 2004; 110(8): 897 - 903. [Abstract] [Full Text] [PDF]
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P. M. Kistler, P. Sanders, S. P. Fynn, I. H. Stevenson, S. J. Spence, J. K. Vohra, P. B. Sparks, and J. M. Kalman Electrophysiologic and electroanatomic changes in the human atrium associated with age J. Am. Coll. Cardiol., July 7, 2004; 44(1): 109 - 116. [Abstract] [Full Text] [PDF]
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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]
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P. Sanders, J. B. Morton, P. M. Kistler, S. J. Spence, N. C. Davidson, A. Hussin, J. K. Vohra, P. B. Sparks, and J. M. Kalman Electrophysiological and Electroanatomic Characterization of the Atria in Sinus Node Disease: Evidence of Diffuse Atrial Remodeling Circulation, March 30, 2004; 109(12): 1514 - 1522. [Abstract] [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 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) Developed in Collaboration with NASPE-Heart Rhythm Society J. Am. Coll. Cardiol., October 15, 2003; 42(8): 1493 - 1531. [Full Text] [PDF]
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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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I. A. Fuller and M. A. Wood Intramural Coronary Vasculature Prevents Transmural Radiofrequency Lesion Formation: Implications for Linear Ablation Circulation, April 8, 2003; 107(13): 1797 - 1803. [Abstract] [Full Text] [PDF]
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W. Anne, H. van Rensburg, J. Adams, H. Ector, F. Van de Werf, and H. Heidbuchel Ablation of post-surgical intra-atrial reentrant tachycardia. Predilection target sites and mapping approach Eur. Heart J., October 2, 2002; 23(20): 1609 - 1616. [Abstract] [Full Text] [PDF]
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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]
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S. M. Markowitz, R. F. Brodman, K. M. Stein, S. Mittal, D. J. Slotwiner, S. Iwai, M. K. Das, and B. B. Lerman Lesional tachycardias related to mitral valve surgery J. Am. Coll. Cardiol., June 19, 2002; 39(12): 1973 - 1983. [Abstract] [Full Text] [PDF]
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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]
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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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K. Tanaka, S. Satake, S. Saito, S. Takahashi, Y. Hiroe, Y. Miyashita, S. Tanaka, M. Tanaka, and Y. Watanabe A new radiofrequency thermal balloon catheter for pulmonary vein isolation J. Am. Coll. Cardiol., December 1, 2001; 38(7): 2079 - 2086. [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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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. Ouyang, S. Ernst, T. Vogtmann, M. Goya, M. Volkmer, A. Schaumann, D. Bansch, M. Antz, and K.-H. Kuck Characterization of Reentrant Circuits in Left Atrial Macroreentrant Tachycardia: Critical Isthmus Block Can Prevent Atrial Tachycardia Recurrence Circulation, April 23, 2002; 105(16): 1934 - 1942. [Abstract] [Full Text] [PDF]
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