(Circulation. 2000;101:1568.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Division of Cardiovascular and Internal Medicine, Mayo Clinic, Rochester, Minn.
Correspondence to Paul A. Friedman, MD, Division of Cardiovascular and Internal Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail pfriedman{at}mayo.edu
| Abstract |
|---|
|
|
|---|
Methods and ResultsPatients with counterclockwise flutter (n=20), clockwise flutter (n=3), or both (n=5) were studied using two 20-pole catheters. Biplane fluoroscopy determined catheter positions. During counterclockwise flutter, craniocaudal activation occurred along the entire lateral and posterior right atrial walls. Septal activation proceeded caudocranially. In all patients, a line of block was seen in the posteromedial (sinus venosa) right atrium; this was manifested by the presence of double potentials where the upward and downward activations collided. Anatomic location was confirmed by intracardiac echocardiography in 9 patients. In patients with clockwise flutter, the line of block and double potentials were seen in the same location during counterclockwise flutter, but the activation sequence around the line of block was reversed. Pacing near the site of double potentials during sinus rhythm excluded a fixed line of block, and premature atrial complexes demonstrated functional block with manifest double potentials. In 2 patients, posterior ectopy organized to subsequently initiate isthmus-dependent atrial flutter.
Conclusions(1) A functional line of block is seen at the posteromedial (sinus venosa region) right atrium during counterclockwise and clockwise atrial flutter. (2) All lateral wall right atrial activation can be uniform during flutter, without linear block or double potentials in the region of the crista terminalis. (3) Activation at the site of posteromedial right atrial functional block can organize to subsequently initiate isthmus-dependent atrial flutter.
Key Words: atrial flutter catheter ablation intracardiac echocardiography crista terminalis
| Introduction |
|---|
|
|
|---|
|
Several recent observations, however, have suggested that the crista
terminalis may not be a barrier to conduction in isthmus-dependent
atrial flutter, and thus may not be critical in arrhythmia
mechanism. First, a variant of atrial flutter, lower loop reentry, has
been described by Cheng et al.10 Lower loop reentry uses
the sub-Eustachian isthmus, but the circuit encircles the
inferior vena cava, penetrates the crista terminalis, and
subsequently "splits" to both return across the isthmus and
ascend the anterolateral right atrium (Figure 1
, B and C). This
is a stable rhythm, occurs spontaneously, is isthmus dependent, and has
crista penetration at various atrial sites within the same
patient.10 The occurrence of lower loop reentry
demonstrates the absence of crista terminalis conduction block during
atrial flutter, indicating that conduction block at the crista
terminalis is not necessary for arrhythmia
maintenance.
Additional evidence has also suggested that the crista terminalis may not always function as the posterior boundary during human atrial flutter. In preliminary mapping studies of atrial flutter using multipolar catheters, biplane fluoroscopy, and ICE, we found double potentials (a sign of linear block)1 2 in the posteromedial (sinus venosa) right atrium, the smooth-walled region posterior to the crista terminalis. The purpose of the present study, therefore, was to define the posterior boundary of typical isthmus-dependent atrial flutter and to determine whether this posterior boundary is associated with specific anatomical barriers. Additionally, this study sought to determine whether the boundary is fixed or functional.
| Methods |
|---|
|
|
|---|
40% (range, 35% to 40%); and 7 had
structurally normal hearts. The mean ejection fraction of all patients
was 54±11% (range, 35% to 79%).
Electrophysiological Study and Global Right
Atrial Mapping
Patients were brought to the electrophysiology laboratory in the
postabsorptive state and were lightly sedated with fentanyl, diazepam,
and midazolam. All antiarrhythmic drugs had been discontinued for
5
half-lives, except in 2 patients who discontinued amiodarone 5
and 14 days before the procedure. Oxygen saturation and blood pressure
were continuously monitored. A 7-French orthogonal catheter was
advanced into the coronary sinus via the right internal jugular
vein. Via the femoral veins, a 5-French quadripolar catheter was placed
in the right ventricle, a 6-French octapolar catheter was placed near
the His bundle, and two 7-French 20-pole deflectable mapping catheters
were positioned in the right atrium. These 20-pole catheters had 10
electrode pairs with 1 mm of distance within pairs and 4 mm
of spacing between pairs. All intracardiac electrograms were displayed
at 5 to 20 mV/cm after filtering from 30 to 500 Hz.
Global Right Atrial Mapping
One of the 20-pole mapping catheters (the isthmus
catheter) was positioned via a long guiding sheath (SR0, Daig, Inc)
across the sub-Eustachian isthmus; it was kept there throughout the
study. The second 20-pole catheter (the roving catheter) was initially
placed at the anterolateral tricuspid valve annulus, and subsequently
repositioned around the atrium to record 5-mm lengths of right
atrial activation, resulting in a global map (Figure 2
).
Standardized recordings were obtained at the anterolateral,
lateral, posterolateral (in the region of the crista terminalis),
posterior, posteromedial (sinus venosa region), septal (vicinity of the
fossa ovalis), and anteroseptal right atrium. Catheter positions were
recorded via biplane cine fluoroscopy (right and left anterior
oblique positions), and electrograms were stored on an
electrophysiology workstation (Prucka, Inc).
|
Only patients with isthmus-dependent atrial flutter, as determined by surface ECG tracings, isthmus conduction during arrhythmia, and arrhythmia termination during isthmus ablation, were included. In 11 patients, entrainment studies were performed to confirm the arrhythmia mechanism; in another 17 patients, a global right atrial map consistent with isthmus-dependent flutter was thought to be sufficient with confirmation by arrhythmia termination during isthmus ablation. Patients with previous surgery who had scar reentry were excluded from this study.
Localizing Posterior Block in Atrial Flutter
While continuously recording electrograms, the roving
catheter was swept from the anterolateral to posterolateral and then
posteromedial right atrium. The site at which double potentials were
recorded and a change in activation sequence from craniocaudal to
caudocranial occurred (during CCW flutter) was taken as the posterior
line of block. In CW flutter, the transition occurred in the opposite
direction. Biplane fluoroscopy determined catheter position in all
patients. In the left anterior oblique view, catheter positions medial
to the SVC (as determined by the coronary sinus catheter
in the SVC) were defined as septal; those lateral to the SVC were
defined as lateral (Figure 2
). Anterior and true posterior (ie,
trabeculated versus sinus venosa region) positions were
defined by the right anterior oblique image.
ICE
In 9 patients, ICE was used to determine catheter position
relative to intracardiac structures (5 patients had coronary
artery disease and 2 had an atrial septal defect). In the first
4 patients, a 6.2-French 12.5-MHz catheter (Boston Scientific) was
used; in all subsequent patients, a 9-French 9-MHz catheter was
employed (Boston Scientific). With the roving catheter positioned at
the posterior line of block during atrial flutter, the ICE catheter was
advanced to the SVC and gradually withdrawn. The position of the roving
catheter (continuously recording double potentials to confirm
catheter stability at line of block) relative to intracardiac
structures and fluoroscopic location were noted. The position of the
crista terminalis (clearly seen at the junction of the smooth and
pectinated right atrium) and the relationship of the intracardiac
catheters to the crista terminalis were noted throughout the ICE
study.
| Results |
|---|
|
|
|---|
Figure 2
is an image-based table of the global right atrial map
in a patient who had both CCW and CW atrial flutter during the course
of the electrophysiological study. In that
patient, activation propagated in a craniocaudal direction along the
entire lateral wall and the true posterior wall; caudocranial
activation was not apparent until the roving catheter was placed in a
posteromedial position, indicating that propagation occurred
caudocranially in parallel along both sides of the crista terminalis
during typical atrial flutter. During CW flutter, double potentials
were seen at the same location, and activation spread caudocranially
along the entire lateral wall and craniocaudally along the septum
(Figure 3
). Additionally, the
double potentials formed an upside-down "V" configuration (Figure 2
, C4 and C5), demonstrating a superior boundary to the line of
block, around which wavefront propagation occurred.
|
ICE demonstrated that the posterior line of block occurred in the
posteromedial right atrium in the sinus venosa region. Figure 4
shows the fluoroscopic, ICE, and
electrographic data in a patient during typical CCW flutter. As seen in
Figure 4
, the double potentials occurred approximately midway
between the fossa ovalis and the crista terminalis. Quantitative
measurements were available in 7 of 9 patients who had ICE. With
measurements taken at the midfossa level, the distance from the crista
terminalis to the site of double potentials was 2.7±0.7 cm; the
distance from the double potentials to the posterior rim of the fossa
ovalis was 1.8±0.6 cm.
|
In 6 patients (3 with only CCW flutter, 3 with CCW and CW flutter), the
arrhythmia terminated at a time when the roving catheter was
positioned at the line of block. In all 6 patients, a separate pacing
catheter was placed adjacent to the roving catheter, and extrastimuli
were delivered to assess local conduction. In all patients, no double
potentials were recorded on the roving catheter during normal sinus
rhythm or with pacing at long cycle lengths; thus, conduction proceeded
from the pacing catheter across the sinus venosa region of the right
atrium at which the roving catheter was located without interruption
(ie, no line of block). With the placement of premature atrial
complexes and with spontaneous premature atrial complexes, double
potentials appeared, demonstrating functional block (Figure 5
). In 2 patients, sinus venosa atrial
extrastimuli initiated atrial flutter. Interestingly, a reentrant
arrhythmia with double potentials appeared in the sinus venosa
region before the occurrence of organized reentry at the isthmus,
demonstrating that at times, sinus venosa functional block with
premature complexes may lead to local reentry, which is subsequently
followed by stable isthmus-dependent atrial flutter (Figure 6
).
|
|
| Discussion |
|---|
|
|
|---|
Although many investigators have noted double potentials during atrial flutter and their association with a line of block,1 2 ICE permits the correlation of the electrical phenomenon with intracardiac structures.6 7 In a series of elegant studies using ICE, Olgin et al6 7 8 9 and Kalman et al11 found the crista terminalis was the posterolateral boundary in human flutter, in contrast to the present finding of sinus venosa block. It is unclear why our results differed from theirs. There is likely heterogeneity in right atrial activation outside of the sub-Eustachian isthmus in patients with atrial flutter.12 This might explain why lower loop reentry, which clearly proves crista terminalis permeability to transverse wavefront propagation, was seen in some (6 of 20), but not all, patients in the study by Cheng et al10 Similarly, in a study assessing crista conduction in patients with and without atrial flutter, nearly half of flutter patients demonstrated crista terminalis permeability.13 This again suggests variability in crista terminalis conduction in patients with atrial flutter. Because all of our patients had sinus venosa linear block, we were unable to determine whether any structural or patient characteristics predicted which patients might have crista impermeability.
The posterior line of block we found formed an inverted V pattern,
suggesting an upper limit or terminus to the line of block. In the
present study, we were unable to determine the exact relationship
of this line of block to the SVC; however, in a study using
electroanatomical mapping,12 the flutter circuit was
constrained by a superior isthmus (between the tricuspid annulus and
SVC) in some patients but not others, demonstrating that at least in a
subpopulation of flutter patients, the posterior line of block does not
extend superiorly to the SVC. Interestingly, in that report, double
potentials were seen in the posterior right atrium in a position
corresponding to the location of double potentials in the present
report (Figure 4
in Reference 1212 ). That study, like ours, showed
variability in the flutter circuit outside of the sub-Eustachian
isthmus.
Given the known occurrence of lower loop reentry in some patients, it
can be postulated that flutter macro reentry is composed of 2 broad and
competing pathways with a figure-of-eight type anatomyone
circuit follows the tricuspid annulus (as shown in Figure 3
),
and the other flows around the inferior vena cava (the
lower loop reentry circuit, Figure 1B
). The degree of posterior
functional block and crista terminalis permeability would determine
which circuit dominates. The combination of crista permeability and a
short line of block at the sinus venosa region may make available a
shorter (and hence dominant) circuit around the inferior
vena cava rather than the "usual" circum-tricuspid circuit, which
would favor lower loop reentry atrial flutter. Conversely, crista
terminalis impermeability and/or a long posterior line of block
increase the circuit time of the lower loop and favor the tricuspid
annulus flutter circuit. Because the sub-Eustachian isthmus is critical
to both circuits, successful isthmus ablation would not distinguish
between the 2 variants of isthmus-dependent flutter. Because the
flutter wave is predominantly determined by left atrial activation and
both variants have similar surface lead appearances,10
surface electrocardiography cannot readily
distinguish the forms either. The concept of variability of the flutter
circuit outside of the sub-Eustachian isthmusand the inability to
observe this variability by isthmus ablation or by surface
electrocardiographyhas been supported by
electroanatomical 3D mapping.12
There has been great interest in determining which anatomic boundaries
may be critical for or predispose a patient to the development of
intra-atrial arrhythmias.2 6 7 8 9 This study found
that outside of the isthmus region, functional properties may be as
important as anatomic boundaries in human atrial flutter. This is
consistent with other reports in which a site-dependent atrial
conduction delay in patients prone to intra-atrial arrhythmias
has been described14 and in which an alteration of
functional characteristics by dual-site atrial pacing may account for
the possible benefit of that technique.15 Posteromedial
functional block may occur because embryologically right and left
atrial myocytes with differences in
electrophysiological properties join in
this region. Interestingly, in 2 patients, extrastimuli led to sinus
venosa linear block and double potentials that were followed by
organized isthmus-dependent flutter only after several posterior
reentrant cycles (Figure 6
). This suggests that posterior
functional block may support rotors of reentry that initiate atrial
flutter, in addition to its required presence for preventing the
posterior "collapse" of the flutter circuit. Other investigators
have observed that atrial flutter often begins with a brief episode of
atrial fibrillation, the development of functional posterior block, and
subsequent stable flutter.16 These observations are
consistent with our finding of functional posterior block
during atrial flutter, which at least in some cases precedes the
establishment of stable flutter.
Conclusions
We found that a functional line of block is present at the
posteromedial (sinus venosa) right atrium during counterclockwise and
clockwise atrial flutter. The absence of double potentials in the
region of the crista terminalis suggested that crista terminalis block
was not required for the maintenance of atrial flutter in these
patients. Outside of the sub-Eustachian isthmus, functional
characteristics may be important for atrial flutter initiation and for
the determination of whether flutter preferentially occurs around the
tricuspid annulus or the inferior vena cava (lower loop
reentry).
Received June 9, 1999; revision received October 25, 1999; accepted November 5, 1999.
| References |
|---|
|
|
|---|
2. Nakagawa H, Lazzara R, Khastgir T, Beckman KJ,
McClelland JH, Imai S, Pitha JV, Becker AE, Arruda M, Gonzalez MD,
Widman LE, Rome M, Neuhauser J, Wang X, Calame JD, Goudeau MD, Jackman
WM. Role of the tricuspid annulus and the eustachian valve/ridge on
atrial flutter: relevance to catheter ablation of the septal isthmus
and a new technique for rapid identification of ablation success.
Circulation. 1996;94:407424.
3. Poty H, Saoudi N, Nair M, Anselme F, Letac B.
Radiofrequency catheter ablation of atrial flutter: further insights
into the various types of isthmus block: application to ablation during
sinus rhythm. Circulation. 1996;94:32043213.
4. Schwartzman D, Callans DJ, Gottlieb CD, Dillon SM, Movsowitz C, Marchlinski FE. Conduction block in the inferior vena cavaltricuspid valve isthmus: association with outcome of radiofrequency ablation of type I atrial flutter. J Am Coll Cardiol. 1996;28:15191531.[Abstract]
5. Kalman JM, Olgin JE, Saxon LA, Lee RJ, Scheinman MM, Lesh MD. Electrocardiographic and electrophysiologic characterization of atypical atrial flutter in man: use of activation and entrainment mapping and implications for catheter ablation. J Cardiovasc Electrophysiol. 1997;8:121144.[Medline] [Order article via Infotrieve]
6. Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of
right atrial endocardial structures as barriers to conduction during
human type I atrial flutter: activation and entrainment mapping guided
by intracardiac echocardiography.
Circulation. 1995;92:18391848.
7. Olgin JE, Kalman JM, Lesh MD. Conduction barriers in human atrial flutter: correlation of electrophysiology and anatomy. J Cardiovasc Electrophysiol. 1996;7:11121126.[Medline] [Order article via Infotrieve]
8. Olgin JE, Lesh MD. The laboratory evaluation and role of catheter ablation for patients with atrial flutter. Cardiol Clin. 1997;15:677688.[Medline] [Order article via Infotrieve]
9. Olgin JE, Lesh M, Kalman J. Electrical mapping in combination with intracardiac ultrasound for electrical-anatomic correlation. J Electrocardiol. 1998;30(suppl):610.
10. Cheng J, Cabeen WR, Scheinman M. Right atrial flutter
due to lower loop reentry: mechanism and anatomic substrate.
Circulation. 1999;99:17001705.
11. Kalman JM, Olgin JE, Saxon LA, Fisher WG, Lee RJ, Lesh
MD. Activation and entrainment mapping defines the tricuspid annulus as
the anterior barrier in typical atrial flutter. Circulation. 1996;94:398406.
12. Shah DC, Jais P, Haissaguerre M, Chouairi S, Takahashi
A, Hocini M, Garrigue S, Clementy J. Three-dimensional mapping of the
common atrial flutter circuit in the right atrium.
Circulation. 1997;96:39043912.
13. Natale A, Richey M, Tomassoni GF, Beheiry S, Rajkovich K, Wides B, Nickel D, Leonelli FB. Three-dimensional non-fluoroscopic electroanatomical mapping of the right atrium during coronary sinus pacing: comparison of patients with and without atrial flutter. J Am Coll Cardiol. 1999;33:123A.
14. Papageorgiou P, Monahan K, Boyle NG, Seifert MJ,
Beswick P, Zebede J, Epstein LM, Josephson ME. Site-dependent
intra-atrial conduction delay: relationship to initiation of atrial
fibrillation. Circulation. 1996;94:384389.
15. Friedman PA, Hill MRS, Hammill SC, Hayes DL, Stanton MS. Randomized prospective pilot study of long-term dual site atrial pacing for prevention of atrial fibrillation. Mayo Clin Proc. 1998;73:139144.[Abstract]
16. Waldo AL. Pathogenesis of atrial flutter. J Cardiovasc Electrophysiol. 1998;9(suppl 8):S18S25.
This article has been cited by other articles:
![]() |
D. L. Packer, S. B. Johnson, M. W. Kolasa, T. J. Bunch, B. D. Henz, and Y. Okumura New generation of electro-anatomic mapping: full intracardiac ultrasound image integration Europace, November 1, 2008; 10(suppl_3): iii35 - iii41. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. P. Gerstenfeld Functional Block in the Posterior Left Atrium: Another Piece in the Puzzle of Atrial Fibrillation Initiation J. Am. Coll. Cardiol., February 26, 2008; 51(8): 863 - 864. [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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
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] |
||||
![]() |
P. A. Friedman, B. Dijkman, E. N. Warman, H. A. Xia, R. Mehra, M. S. Stanton, and S. C. Hammill Atrial Therapies Reduce Atrial Arrhythmia Burden in Defibrillator Patients Circulation, August 28, 2001; 104(9): 1023 - 1028. [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] |
||||
![]() |
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] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |