(Circulation. 2001;103:1025.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Role of Functional Block Extension in Lesion-Related Atrial Flutter
From the Department of Medicine, Division of Cardiology, Case Western Reserve University/University Hospitals of Cleveland, Cleveland, Ohio.
Correspondence to Albert L. Waldo, MD, Division of Cardiology, University Hospitals of Cleveland, 11100 Euclid Ave, Cleveland, OH 44106-5038. E-mail alw2{at}po.cwru.edu
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Abstract |
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Background—A line of block in the right atrium (RA) between the venae cavae is necessary to obtain classic atrial flutter (AFL). We tested the hypothesis that the location of that line of block would determine whether the AFL reentrant circuit would be due to single-loop reentry or figure-of-8 reentry.
Methods and Results—Simultaneous mapping from 392 sites (both atria and the atrial septum) was performed in 13 normal dogs before and after creating a linear lesion on the RA free wall. The lesion was 1 to 1.5 cm anterior and parallel to the crista terminalis (7 dogs) or posterior and close to the crista terminalis region (6 dogs). Sustained AFL (>2 minutes) was then induced. In 4 dogs with an anterior lesion, the AFL reentrant circuit traveled around the lesion (lesion reentry). In 9 dogs (3 with anterior lesions and 6 with posterior lesions), the AFL reentrant circuit included the anterior RA free wall, the atrial septum, and Bachmann’s bundle (single-loop reentry). In these 9 dogs, the fixed line of block was extended to the superior and/or inferior vena cava by a functional line of block, thereby preventing lesion reentry. No figure-of-8 reentry was induced.
Conclusions—In this model, the location of a fixed line of block and its functional extension determine the type of AFL reentry. These data provide an explanation for the chronic AFL that occurs in some patients after surgical repair of congenital heart lesions.
Key Words: atrial flutter • electrophysiology • lesion • mapping • reentry
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Aline of block, functional or fixed anatomic, in the right atrial free wall between the venae cavae is recognized as being necessary to obtain stable classic atrial flutter (AFL).1 This was first shown by Rosenblueth and Garcia Ramos,2 who created a crush injury between the venae cavae in the canine heart and then were able to induce stable AFL. Since that time, others3 4 5 have studied the same or a similar model to investigate AFL in an otherwise normal heart. When this model was modified by Frame et al6 to form a Y-shaped lesion in the right atrial free wall, the AFL reentrant circuit was confined to the tricuspid ring. When a crush lesion was made to form a line of block in the anterior right atrial free wall by Feld and Shahandeh-Rad,7 AFL limited to reentry around the line of fixed block was induced. The model of Feld and Shahandeh-Rad can be likened to AFL due to incisional reentry, ie, reentry around a fixed anatomic obstacle, which is sometimes seen after surgical repair of a congenital lesion in which at least 1 incision was made in the right atrial free wall.8 9 10 11
Nevertheless, in a series of 21 episodes of AFL that occurred chronically in 19 patients after surgical repair of congenital heart disease, we have shown that most often (in 15 of the 21 episodes), the AFL was due to a classic AFL reentrant circuit rather than incisional reentry.12 Also, we have shown in the canine sterile pericarditis AFL model that when the line of functional block between the venae cavae is posterior in the right atrial free wall, generally parallel to and close to the crista terminalis, it is associated with the presence of classic single-loop reentry AFL.13 However, when the line of functional block between the venae cavae is more anterior in the right atrial free wall, it is associated with figure-of-8 reentry AFL. We designed a study in normal canine atria to help clarify these relationships and to test the hypothesis that a posterior location of the line of block in the right atrial free wall would result in induced single-loop reentrant AFL, whereas an anterior location would result in figure-of-8 reentrant AFL.
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Methods |
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All studies were performed in accordance with guidelines of our Institutional Animal Care and Use Committee, the American Heart Association Policy on Research Animal Use, and the US Public Health Service Policy on Use of Laboratory Animals. In 13 normal adult mongrel dogs weighing 17 to 24.5 kg, the heart was exposed under general anesthesia and mechanical ventilation as previously described.13 14 Stainless-steel wire electrodes for pacing, recording, or monitoring were sutured on the right ventricle, right atrial appendage, and posterior-inferior left atrium. Radiofrequency catheter ablation of the His bundle was then performed to create complete atrioventricular block,13 14 followed by ventricular pacing at a rate of 60 to 100 bpm.
Creation of Right Atrial Free Wall
Lesion
In each dog, an attempt to induce AFL was made before
the creation of any lesion. A linear lesion in the right atrial free
wall was then created by epicardial cryoablation (10 dogs), crush (1
dog), or surgical incision with suture repair (2 dogs). The lesion was
1 to 1.5 cm anterior and parallel to the crista terminalis (anterior
lesion group) in 7 dogs and in the crista terminalis region (posterior
lesion group) in 6 dogs
(Figure 1
). Before cryoablation was performed, two 4-0
Prolene stay sutures were placed 2 to 2.5 cm apart both to mark the
location and the length of the lesion to be created and to lift the
atrial free wall to permit placement of a DeBakey-Satinsky vena cava
clamp. To create a cryolesion in the beating heart, an 
5-mm width of
atrial tissue was first gently clamped over the extent (length 3 cm) of
the clamp. After the tissue was clamped in all 11 dogs, induction of
AFL was attempted. In 1 dog (No. 9,
Table),
because sustained AFL was induced after the tissue was clamped, no
cryoablation was performed, and this was considered a crush lesion. In
the other 10 dogs, a series of cryoablation lesions were performed with
the use of a 5-mm-diameter cryoprobe and cryosurgical system at a
temperature of -80°C for 5 minutes each. The first cryoablation
application was placed at the site of one of the stay sutures. After 3
side-by-side applications of the cryoprobe (cryolesion 1.5 cm long),
an attempt was made to induce AFL. If unsuccessful, the length of the
lesion was extended by the diameter (5 mm) of the cryoprobe from the
initial length until either sustained AFL was induced or at least 6
applications with the cryoprobe were made and completed. To create a
surgical lesion with the heart beating, an 5-mm width of atrial
tissue was gently clamped by using the vena cava clamp
(DeBakey-Satinsky). A surgical incision was made on the clamped tissue,
which then was repaired with continuous suture (4-0 Prolene). This was
extended in 1 dog until AFL could be induced.
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Data Acquisition
Simultaneous mapping from 392 sites in both atria was
performed. An epicardial electrode array containing 372 unipolar
electrodes arranged in 186 bipolar pairs (95 for the right atrium, 77
for the left atrium, and 14 for Bachmann’s bundle) was used as
previously
described13 14
(Figure 1
). The interatrial septum was also mapped
simultaneously with the epicardial sites by using a single 24-polar
electrode catheter (Bard) with an interelectrode distance of 1 mm,
placed as previously
described13 14
(Figure 1). We recorded from the proximal 20 electrodes of
the 24-polar electrode catheter during septal recording.
Data were recorded and processed by our cardiac mapping system.14 15 16 Atrial electrograms from both atria and the interatrial septum along with ECG lead II were recorded during sinus rhythm and induced sustained AFL after creating the right atrial free wall lesion. AFL was induced by rapid atrial pacing from one of the atrial stainless-steel electrode sites at a rate of 400 to 600 bpm for at least 2 seconds.13 The length of fixed block was measured during a paced or spontaneous atrial rhythm first by mapping the sequence of atrial activation, then by identifying the line of block,14 and then by establishing its length by using the known distances between the electrode recording sites.17 Then the shortest distance between the superior and inferior ends of the line of block and the superior vena cava (SVC) and inferior vena cava (IVC), respectively, were measured.
Data were expressed as the mean±SD (range). Statistical analysis was performed with an unpaired t test for comparison of means. A value of P<0.05 was considered statistically significant.
Definitions
Definitions are as follows: (1) line of fixed block,
a line of block created by cryoablation, clamping, or a surgical
incision and present during sinus rhythm or atrial pacing; (2) line of
functional block, a line of block not caused by a lesion or another
anatomic obstacle and not present during a sinus or paced atrial
rhythm; (3) sustained AFL, AFL lasting 
2 minutes; (4) single-loop
reentry AFL, AFL due to a reentrant circuit consisting of the anterior
right atrial free wall, atrial septum, and Bachmann’s bundle; (5)
lesion reentry AFL, AFL due to a reentrant circuit consisting of
activation around a right atrial free wall lesion; and (6) figure-of-8
reentry AFL, AFL in which 2 reentrant circuits (single-loop reentry and
lesion reentry) are present and share the anterior right atrial free
wall as a common pathway.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Before creating a lesion, no sustained AFL was induced. After a lesion of sufficient length was made, sustained AFL was induced in all dogs.
Effects of a Posterior Lesion
Figure 2A shows a representative example of an activation
map and selected atrial electrograms during sinus rhythm after a
posterior right atrial lesion was created by cryoablation (dog 12,
Table).
The earliest atrial activation began in the sinus node region close to
the SVC. Wave fronts traveled from the earliest activation site toward
the right atrial appendage and toward the IVC. The later wave front
turned around the inferior aspect of the lesion, advanced upward, and
merged with the wave front crossing the superior aspect of the lesion.
Electrograms a through d, recorded from recording sites a through d
shown on the activation map, show conduction across the inferior aspect
of the lesion, no double potentials, and a low amplitude potential at a
site (site b) very close to the cryolesion.
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Figure 2B shows the activation map and atrial electrograms
recorded from the same sites from the same dog as shown in
Figure 2A during induced AFL due to single-loop reentry. The
AFL reentrant circuit travels up the anterior right atrial free wall
and down the atrial septum, with breakthrough to the epicardium in the
peri-IVC region and reentry into the septum at Bachmann’s bundle.
Double potentials were recorded at sites b and c, indicating the
presence of a line of block. Note also that each potential of the
double potential corresponds to activation on either side of the area
of block (sites a and d). The line of block that extended from the
inferior end of the fixed anatomic lesion to the IVC was functional,
inasmuch as there was no line of block there during sinus rhythm
(Figure 2A). In this example
(Figure 2B), a similar line of functional block extended from
the superior end of the fixed anatomic lesion to the SVC. Thus, during
induced AFL, each end of the line of fixed anatomic block became
extended to the IVC and SVC by a line of functional block.
In all the posterior lesions, the induced AFL reentrant
circuit consisted of single-loop reentry. In 2 dogs, the reentrant
impulse traveled around the reentrant circuit in either direction
during induced AFL episodes
(Table,
bidirectional). In all, the fixed line of block was extended to the SVC
and/or IVC by a line of functional block
(Table).
In 4 of 6 dogs, the line of functional block extended from each end of
the lesion to the SVC and IVC, respectively; in 1 of 6, it extended
from the superior end of the lesion to the SVC; and in 1 of 6, it
extended from the inferior end of the lesion to the IVC
(Table).
Effects of an Anterior Lesion
Figure 3 shows a representative example of an activation map
and selected atrial electrograms during AFL due to a reentrant circuit
that traveled around an anterior lesion. Another potential reentrant
circuit (denoted by a dashed line with arrows) consisted of activation
from the right atrial free wall, entry to the atrial septum in the
peri-IVC region (black asterisk), inferior-to-superior septal
activation, and epicardial breakthrough at Bachmann’s bundle
(Figure 3, white asterisk). This potential figure-of-8
reentry did not develop, because the activation wave front that
traveled around the inferior aspect of the lesion (solid black line)
arrived at the superior pivot point relatively early compared with
activation from the atrial septum via Bachmann’s bundle. Also shown
are atrial electrograms from selected sites recorded during AFL: a
through g from epicardial sites around the lesion, h through j from
sites in the atrial septum, and k and l from sites in Bachmann’s
bundle. Activation arrives at site e before it arrives at site k,
preventing figure-of-8 reentry.
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In 4 of 7 dogs in the anterior group
(Table),
only lesion reentry AFL was induced, with another potential reentrant
circuit present as just described. However, in 3 of 7 dogs in this
group
(Table),
single-loop reentry AFL was induced just as in the posterior group.
This occurred because a line of functional block extended from each end
of the lesion to the SVC and IVC, respectively, in 1 dog and from the
superior end of the anatomic lesion to the SVC in the other 2 dogs. In
sum, in the anterior group, the AFL was due to lesion reentry in 4 dogs
and single-loop reentry in 3 dogs. In the 3 latter dogs, a line of
functional block extending from the lesion to one or both venae cavae
was present, preventing lesion reentry.
Comparison of Selected Characteristics of
Induced AFL
The
Table
shows the characteristics of the lesions and the induced AFL in each
group. There was no significant difference in the length of the lesions
or AFL cycle lengths between groups. However, the mean cycle length of
AFL due to single-loop reentry was significantly longer than that of
AFL due to lesion reentry (152±16 versus 128±7 ms, respectively;
P<0.05). The mean length of
the line of functional block (9 dogs with single-loop reentry) between
the lesion and the closest vena cava was 1.2±0.3 cm (range 0.4 to 1.6
cm). In the dogs with lesion reentry AFL, the mean gap between the end
of the lesion and the closest vena cava was 1.6±0.3 cm (range 1.2 to
2.2 cm). Although there was overlap in the range between these
measurements (lines of functional block length in single-loop reentry
AFL versus gap length in lesion reentry AFL), the mean of 1.6±0.3 cm
for lesion reentry was significantly longer than the mean of 1.2±0.3
cm for single-loop reentry
(P<0.05).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Critical Role of Functional Block
The present study demonstrates once again that a line of block between the venae cavae is critical for the development of classical AFL. However, the present study also provides important new and clinically useful insights into the nature of that block in the presence of a lesion. First, single-loop reentrant AFL occurred when the line of fixed block was extended to either or both venae cavae by a line or lines of functional block. This occurred regardless of whether the fixed block was anterior or posterior in the right atrial free wall and prevented an activation wave from turning around the fixed lesion, thereby preventing either figure-of-8 reentry or lesion reentry.
Second, although figure-of-8 reentry did not develop in the
presence of an anterior right atrial free wall lesion in this model,
the potential for figure-of-8 reentry was there
(Figure 3). However, the lesion reentry circuit had a cycle
length sufficiently shorter than the activation time of the wave front
of the potential reentrant circuit using the atrial septum, so that
daughter wave fronts from the lesion reentry circuit collided with the
former wave front, which traveled via the atrial septum. Therefore, no
figure-of-8 AFL was present. This is clearly different from that
described for the sterile pericarditis
model.13 The reason for this
difference is suggested from comparisons with the data from previous
studies of induced AFL in the latter model. In those studies, the mean
AFL cycle length in figure-of-8 AFL was 157 and 159 ms,
respectively.13 18
However, in the present study, the mean cycle length of AFL due to
lesion reentry was 128 ms. This difference between models may be
explained by differences in the length of the line of block, conduction
velocity around the line of block, or both. Review of the data suggests
that it is primarily, if not entirely, explained by differences in
conduction velocity as a result of the pericarditis. Thus, this
difference between the results in the canine sterile pericarditis model
and the lesion model in normal atria serves to emphasize the importance
of substrate in the pathophysiology of
arrhythmias.
Mechanism of Development of Functional
Block Extension
The mechanism of functional extension of the line of
fixed block is not explained in the present study. It is known from
experimental and simulation studies that many factors may play a role,
including anisotropic conduction, the rapid atrial rate during
induction of the arrhythmia, and curvature of the activation wave front
around the ends of the fixed line of
block.19 20 21
We know that conduction across the isthmus between either end of the
lesion and its respective vena cava was possible because it occurred
during sinus rhythm or atrial pacing at rates in the range of sinus
rhythm. However, when a wave front has to turn around the end of a line
of block, the arc of curvature determines the nature of conduction at
this pivot
point.19 20 21
We suggest that it is likely, if not probable, that at the high rate of
pacing used to induce AFL in the present study, the arc of curvature
around the end or ends of the line of block was so severe that
conduction around it could not be sustained. In any event, a definitive
explanation requires further study.
Implications for AFL Associated With Surgical
Repair of Congenital Lesions
We believe that these observations have important
clinical and theoretical implications. For a long time, it has been
recognized that several open-heart surgical procedures to repair
congenital heart lesions, including the complex (Mustard, Senning,
Fontan) and the simple (ASD repair), are associated with an important
incidence of chronic postoperative
AFL.22 23 24
AFL in these instances sometimes may be due to incisional
reentry.8 9 10 11
However, as we have recently
shown,12 in these
circumstances, AFL is probably more often due to reentry involving the
classic AFL isthmus. The present study provides insight into why the
latter often happens. Surgical incisions and/or suture lines placed as
part of the surgical repair in the right atrial free wall in the region
between the venae cavae may not, of themselves, be long enough to
create the critical line of block between the cavae, which leads to the
development of AFL. However, when a line of functional block between
one or both ends of the lesion and one or both of the venae cavae
develops, eg, as the result of activation from 1 premature atrial
beats or a run of atrial fibrillation, the substrate to support stable
AFL may then be realized.
There are still further clinical implications that logically follow the insights from the present study. One is to modify the nature of incisions and suture lines placed as part of the surgical repair so that a functional line of block from the "surgical lesion" to one or both of the venae cavae will not develop. For example, this could include modifying the atriotomy (length, direction, or both). A second implication is that perhaps a prophylactic ablation of the AFL isthmus between the inferior venae cavae and the tricuspid ring should be performed to avoid the subsequent development of classic AFL.12 Another implication is that in the presence of incisional reentry, simply extending the atriotomy lesion to one or both venae cavae may eliminate incisional reentry only to promote classic AFL using the flutter isthmus.
Finally, there is the implication for ablative treatment of incisional reentry AFL. Although an option may be to prevent lesion reentry by extending the line of fixed block with a radiofrequency line of block to one of the venae cavae, one may thereby simply change lesion reentry to single-loop reentry AFL.
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Acknowledgments |
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This study was supported in a part by grant RO1-HL-38408 from the US Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Md.
Received February 18, 2000; revision received August 25, 2000; accepted August 31, 2000.
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