Ching- Tai Tai, M.D., Shin-Ann Chen, MD
Division of Cardiology, Department of Medicine, National Yang-Ming
University School of Medicine, Taipei Veterans General Hospital,
Taiwan, R.O.C.
Supported
in part by grants from National Science Council (NSC 94-2314-B-075-093).
Address for
correspondence: Ching-Tai Tai, M.D., Division of Cardiology,
Department of Medicine, Taipei Veterans General Hospital
201 Sec 2. Shih-Pai Road, Taipei, Taiwan Email: ct.tai@msa.hinet.net
Abstract
Atrial flutter
(AFL) is a common arrhythmia in clinical practice. Several
experimental models such as tricuspid regurgitation model, tricuspid
ring model, sterile pericarditis model and atrial crush injury model
have provided important information about reentrant circuit and can
test the effect of antiarrhythmic drugs. Human atrial flutter has
typical and atypical forms. Typical atrial flutter rotates around
tricuspid annulus and uses the crista terminalis and sometimes sinus
venosa as the boundary. The IVC-tricuspid isthmus is a slow
conduction zone and the target of radiofrequency ablation.
Atypical atrial flutter may arise from the right or left atrium.
Right atrial flutter includes upper loop reentry, free wall reentry and
figure of eight reentry. Left atrial flutter includes mitral
annular atrial flutter, pulmonary vein-related atrial flutter and left
septal atrial flutter. Radiofrequency ablation of the isthmus
between the boundaries can eliminate these arrhythmias.
Key Words: Antiarrhythmic
drugs; Atrial flutter
Introduction
Atrial flutter (AFL) is a frequent arrhythmia second only to atrial
fibrillation in clinical practice. Since Jolly and Ritchie first
recorded AFL in 1910, over the next several decades there was
surprisingly little progress in understanding its mechanisms
1. In 1921, Sir Thomas Lewis and his
colleagues were the first to investigate the mechanism of this
arrhythmia
2. Using a
combination of epicardial maps and ECG recordings from a canine model
of AFL induced by rapid atrial pacing, they showed that the activation
circulated in either a cranial-caudo or a caudo-cranial direction in
the right atrium. They concluded that AFL was due to intraatrial circus
movement around the vena cava. Subsequent works that supported
the notion that AFL was due to reentry included those of Rosenbleuth
and Garcia-Ramos who created a crush injury model of this arrhythmia by
making a lesion between the vena cava in 1947
3.
Based on the epicardial maps, the authors inferred that the reentry
loop circled around the atrial crush lesion. In 1947 and 1948, Scherf
et al injected aconitine into the atrial subepicardium and found a
uniformly discharging ectopic focus to provide an evidence that AFL was
due to a focal activation mechanism
4.
However, it was not until the last three decades that numerous studies
in animal models and human AFL developed and advanced in understanding
the mechanism of AFL. The purposes of this review article are to review
the recent progress in the experimental models of AFL and clinical
studies of human AFL and to improve the ablative therapy of AFL.
Experimental Models of AFL
Tricuspid
Regurgitation Model
Boyden et al
cut the chorda tendineae of the anterior and septal leaflets of the
tricuspid valve using a knife and produced some degree of tricuspid
insufficiency and volume overload induced enlargement of the right
atrium
5. From their
endocardial mapping, they found a progressive delay and inhomogeneity
in conduction with successive stimuli. After a critical number of
stimuli, a fixed area of functional block occurred at one site. With
subsequent stimuli, the line of block was maintained by continuous
collision of a wavefront from the previous beat with the current
stimulated beat. When the stimulation is terminated, the paced wave
front from the last paced beat begins to propagate across the right
atrial free wall and produces reentry by circling around the line of
functional block. In all episodes of sustained AFL, the rhythm was due
to reentrant excitation in tissues of the right atrium. Impulse
propagation was either clockwise or counterclockwise and functional
block provided an important boundary of AFL.
Tricuspid Ring
Model
Frame et al
made an intercaval incision connected with a second incision in the
right atrial free wall to create a Y-shaped lesion
6. The atrial flutter can be easily and
reliably induced by programmed electrical stimulation. The range of
cycle length was 140 to 170 ms. The duration of the excitable gap was
60 to 80 ms , which represented 40% to 50% of the atrial flutter cycle
length. High density mapping using a computer multiplexing system
demonstrated that the reentrant impulse circulated around the tricuspid
annulus in a clockwise or counterclockwise direction. In this model,
reentry occurred entirely in normal fast response tissue, with no
single area of markedly slower conduction. Sodium channel
blocking drugs slow conduction in all parts of the reentrant pathway.
The Y-shaped lesion and tricuspid annulus were two fixed barriers of
this atrial flutter.
Sterile
Pericarditis Model
After
pericardiotomy, the atrial surfaces were then generously dusted with
sterile talcum powder, a single layer of gauze is then put on the right
and left atrial free walls, and the pericardiotomy is repaired
7. The atrial flutter could be induced by
rapid atrial pacing in the first 4 postoperative days. During the
onset of atrial flutter, there is a transional rhythm like atrial
fibrillation. A period of atrial fibrillation activated the right
atrium through wave fronts which produced a relatively large localized
area of slow conduction. Then, unidirectional conduction block of the
wave front occurred for one beat in the area of slow conduction and
this permitted the unblocked wave front to turn around an area of
functional block, thereby initiating the reentry. Sequential site
atrial mapping using a hand-held probe during atrial flutter in the
open-chest state demonstrated either clockwise or counterclockwise
reentrant excitation in the right atrial free wall. The mean sustained
atrial flutter cycle length was 131 ± 20 ms, with a range of 100
to 170 ms. Double potentials were recorded in the center of the
reentrant circuit during atrial flutter and denoted a line of
functional conduction block with each deflection representing
activation on either side of the area of functional block. Fractionated
electrograms were recorded from areas of slow conduction, principally
the pivot points of the reentrant wave front.
Atrial Crush
Injury Model
Atrial crush
injury was created with a surgical clamp placed on the right atrial
free wall, producing a lesion parallel to and 1.5 cm above the
atrioventricular ring, extending from the base of the right atrial
appendage 1.5 to 2.5 cm posteriorly toward the intercaval zone and 3 to
4 cm wide
8. Atrial
flutter was induced by programmed atrial stimulation or rapid atrial
pacing. The atrial flutter cycle length was 140 to 150 ms.
During atrial flutter the earliest atrial activation relative to F wave
onset was noted in the right atrium and the reentrant wave front
revolved around the crush injury. Inverted F wave atrial flutter
was typically associated with a counterclockwise activation pattern
around the crush injury, with initial activation of the left atrium
posteriorly. In contrast, upright F wave atrial flutter was
typically associated with a clockwise activation pattern around the
crush injury, with initial activation of the left atrium
anteriorly. Direct induction of atrial flutter was associated
with the development of progressive conduction delay in the isthmus
between the crush injury and the tricuspid annulus, eventually
culminating in unidirectional block and initiation of reentry. In
many instances, however, the onset of atrial flutter followed a brief
period of atrial fibrillation. The conduction velocity was
generally slower in the isthmus between the crush injury and tricuspid
annulus.
Human AFL
Typical AFL
Human AFL is
defined by the undulating P wave in the ECG with saw-tooth
appearance. Typical AFL has positive P waves in lead V1, negative
P waves in lead V6, and negative P waves in lead II, III, and
aVF. Activation mapping using the Halo catheter and 3-D mapping
system showed the activation wave front goes downward in the free wall
, travels through the cavotricuspid isthmus, spread upward in the
septal wall, and crosses the crista terminalis to complete the
reentrant circuit. Reverse typical FL has negative P waves in
lead V1, positive P wave in lead V6, and positive P waves in lead II,
III, and aVF. The action sequence was the reverse of typical AFL.
Slow Conduction Zone of the
Typical AFL Circuit
In this
laboratory, we have studied the electrophysiologic properties of
typical AFL circuit. It was consistent with previous findings
that the low right atrial isthmus, defined as a path bounded by the
orifice of inferior vena cava, eustachian valve/ridge, coronary sinus
ostium, and tricuspid annulus, is a zone of slow conduction during AFL
9-11. Furthermore,
this laboratory demonstrated that during sinus rhythm incremental
pacing from the low lateral right atrium and coronary sinus ostium
could produce rate-dependent conduction delays
10,
culminating in unidirectional block in the low right atrial isthmus,
and induction of counterclockwise or clockwise AFL in patients with or
without clinical AFL (
Figure 1).
These findings were confirmed by Feld et al and suggested that slow
conduction in the low right atrial isthmus may be mechanistically
important for the development of human typical AFL
11. In contrast, decremental conduction
properties or rate-dependent conduction delays were not found in the
right atrial free wall. The mechanism of slow conduction in the
isthmus was not clear. Spach et al. have shown that conduction velocity
of atrial impulses is faster parallel to the long axis of myocyte
fibers and slower along the plane transverse to myocyte fiber
orientation
12. This
phenomenon was explained by higher axial resistance due to scant
cell-to-cell coupling encountered when impulses propagated
perpendicular to the long axis of muscle fibers
12,13. With aging or atrial dilatation,
intercellular fibrosis can change the density of gap junctions and
produce nonuniform anisotropic conduction through the trabeculations of
the low right atrial isthmus
13.
This hypothesis is supported by a recent anatomic study of the low
right atrial isthmus in humans
14.
Furthermore, observations in dogs with natural and evoked atrial
flutter suggest that thinning of atrial myocardium with intervening
spaces may predispose to both slow and nonuniform conduction
15.
Figure 1. A. Incremental pacing from the low
lateral right atrium (near H6 and H7) using a cycle length of 210 ms
produced gradual conduction delays and block in the isthmus (between H4
and H2) of the counterclockwise wave front and initiated clockwise
atrial flutter. B.
Incremental pacing from the coronary sinus ostium (OCS) using a cycle
length of 180 ms produced gradual conduction delays and block in the
isthmus (between H1 and H2) of the clockwise wave front and initiated
counterclockwise atrial flutter. HBE indicates recordings at the
His bundle area; PCS indicates recordings at the proximal coronay
sinus. (Reproduced from Tai CT, Chen SA, Chiang CE, et al.
Characterization of low right atrial isthmus as the slow conduction
zone and pharmacological target in typical atrial flutter. Circulation
1997;96:2601-2611.)
Using
activation and entrainment mapping from closely spaced sites around the
tricuspid annulus during typical AFL, Kalman et al confirmed that all
sites around the circumference of the tricuspid annulus were a part of
the flutter reentrant circuit, since the postpacing interval was equal
to the flutter cycle length
16.
Thus, the tricuspid annulus is the anterior and fixed barrier in
typical AFL. Using intracardiac echocardiography to place a multipolar
catheter along the length of the crista terminalis and eustachian
ridge, split potentials could be recorded along these structures with
disparate activation sequences of each component by Olgin et al
17. Moreover, entrainment could be used
to demonstrate that one component of the split potential is within the
reentrant circuit while the other is not. These findings are strong
evidence of these structures forming the posterior barrier in typical
AFL. In this laboratory, we have studied the conduction properties of
the crista terminalis in patients with and without clinical AFL
18. We found that split potentials could
be recorded along the length of the crista terminalis during pacing
from the low posterior right atrium at a long cycle length in patients
with clinical AFL (
Figure 2),
suggesting that poor transverse conduction property in the crista
terminalis may be the requisite substrate for clinical occurrence of
typical AFL
18,19.
However, Friedman et al found that a functional line of block was
present at the posteromedial (sinus venosa region) right atrium during
counterclockwise and clockwise AFL, suggesting that crista terminalis
block was not required for the maintenance of typical AFL
20. These different results may be due to
heterogeneity in the right atrial activation outside of the low right
atrial isthmus in patients with typical AFL
21.
Figure 2. Case with clinical atrial
flutter. (A) Double
potentials with opposite activation sequences were recorded along the
crista terminalis (CrT) during counterclockwise atrial flutter (cycle
length 205ms). The early component is activated low to high
(indicating the smooth right atrial side of the CrT) and the late
component is activated high to low ((indicating the trabeculated right
atrial side of the CrT). The maximal interdeflection interval
(80ms) was measured in the recordings from the most proximal electrode
dipole located in the lower CrT. (B)
Double potentials with the same activation sequences and maximal
interdeflection interval as those in panel A were recorded during
pacing from the low posterior right atrium (POST RA) at a cycle length
of 600msec. (C) After infusion
of propranolol, double potentials with the same activation sequences
and maximal interdeflection interval as those in panel A were recorded
during pacing from the posterior right atrium (POST RA) at a cycle
length of 900 ms. CS OS=recordings at the coronary sinus ostium ;
S= stimulus artifact. (Reproduced with permission from Tai CT,
Chen SA, Chen YJ, et al. Conduction properties of the crista terminalis
in patients with typical atrial flutter: basis for a line of
block in the reentrant circuit. J Cardiovasc Electrophysiol
1998;9:811-819, Blackwell Publishing)
A flat
resetting response was observed in most cases of typical AFL,
signifying a fully excitable gap
22,23. The total duration of excitable gap
is relatively wide and occupies about 13 to 20 % of the flutter cycle
length depending on the pacing site.
Variant Circuit
Using the
noncontact mapping system, we could demonstrate that some patients had
a single incomplete line of block in the crista terminalis during
typical atrial flutter. This resulted in double loop reentry during
typical atrial flutter, one circulating around the tricuspid annulus,
and the other rotating around a part of crista terminalis through the
conduction gap (
Figure 3). RF
ablation of the cavotricuspid isthmus and crista gap could eliminate
this atrial flutter.
Figure 3. A: Isochronal map showing the
reentrant circuit of double loop reentry, indicating CW typical atrial
flutter and CW upper loop reentry, in the right posterior oblique view
(black arrows). Note slow conduction through the CT gap with
fractionated unipolar electrogram (virtual 12). Virtual 10 to 14 were
located along the a conduction gal in the CT and virtuals 15 to 19 were
located in the inferior right atrium involving the isthmus. B: Isochronal map showing the
reentrant circuits of double loop reentry, including CW typical atrial
flutter and lower loop reentry, in the right posterior oblique view
(black arrows). Note slow conduction through the CT gap with
fractionated unipolar electrogram (virtual 18). Virtual 10 to 14 were
located in the superior lateral right atrium and virtual 15 to 19 were
located along a conduction gap in the CT. CT = crista terminalis;
CW = clockwise; IVC = inferior vena cava; SVC = superior vena
cava. (Reproduced with permission from Tai CT, Huang JL, Lee PC,
et al. High resolution mapping around the crista terminalis during
typical atrial flutter: new insights into mechanisms. J
Cardiovasc Electrophysiol 2004;15:406-414, Blackwell
Publishing)
Atypical AFL may arise from the right or left atrium. There are no
consistent ECG characteristics. However, using three criteria (positive
P waves in lead V6, negative P wave in lead aVL, and low amplitude of
the P waves in inferior leads) can differentiate left from right AFL
24.
Right Atrial Upper Loop Reentry
Using a
noncontact, 3D mapping technique, we have demonstrated a macroreentrant
circuit localized to the upper portion of the right atrium
25. The wave front had
counterclockwise activation (descending activation sequence in the free
wall anterior to the crista) or clockwise activation (ascending
activation sequence in the free wall anterior to the crista) around the
central obstacle, which was composed of the crista terminalis, the area
of functional block and superior vena cava (
Figure 4). The lower
turn-around points were located at the conduction gap in the crista
terminalis. RF linear ablation of the conduction gap in the
crista terminalis eliminated atrial flutter.
Figure
4: (A) Isopotential
maps showing the activation sequence (frame 1 to 6) of counterclockwise
upper loop reentry in the right posterior oblique view. Color
scale for each isopotential map has been set so that white indicates
most negative potential and blue indicates least negative
potential. The activation wave front propagates down the
anterolateral right atrium (RA) near the superior vena cava (SVC)
(frame 1) to the middle and inferior anterolateral RA (frame 2), then
splits into two wavefronts (frame 3); one passes around the area of
functional block, and the other passes through the cavotricuspid
isthmus. The wavefront in the lateral RA continue through the gap
in the crista terminalis (CT) (frame 4) to the superior posterior RA
(frame 5) and activates the atrial wall surrounding the SVC before
reactivation of anterolateral RA once again. (B) The virtual electrograms from the
area of functional block (virtual 11 to 15) and the CT (virtual 16 to
20) including the conduction gap (virtual 16 to 18) demonstrate double
potentials. The numbers 1 to 6 represent the time points at which
the isopotential maps have been displayed in A. IVC = inferior
vena cava. (Reproduced from Tai CT, Huang JL, Lin YK,
et al. Noncontact three-dimensional mapping and ablation of upper loop
reentry originating in the right atrium. J Am Coll Cardiol
2002;40:746-753, with permission from the American College of
Cardiology Foundation.)
Right Atrial Free wall Reentry (
Figure 5)
Usually there
is a low voltage zone in the anterior free wall, which may be due to
spontaneous scar formation. The activation wave front circulates
around this low voltage zone and the electrograms at this zone show
double potentials
26. RF
ablation of the channel between the Inferior vena cava or tricuspid
annulus and the central obstacle can eliminate this atrial flutter.
Figure 5. Isopotential maps showing
the activation sequence (frame 1 to 6) of single loop reentry in the
right lateral view. Color scale for each isopotential map has
been set so that white indicates most negative potential and blue
indicates least negative potential. The activation wave front
proceeds through the channel between the CT and the central obstacle
(frame 1), activates the low anterior wall (frame 2), and turn around
the line of block (frame 3), then the wave front propagates upward to
the roof in front of the right atrial appendage (frame 4), turns around
the superior vena cava (SVC) to activate the posterior wall (frame 5),
and spreads over the top of the crista terminalis (CT) to complete the
reentrant circuit (frame 6). The virtual electrograms (virtual 10
to 14) on the line of block showed double potentials (Reproduced from
Tai CT, Liu TY, Lee PC, Lin YJ, Chang MS, Chen SA. Noncontact
mapping to guide radiofrequency ablation of atypical right atrial
flutter. J Am Coll Cardiol 2004;44:1080-1086, with permission from the
American College of Cardiology Foundation.) HIS = his bundle
region; IVC = inferior vena cava; RAA = right atrial appendage; TV =
tricuspid valve.
The type I
figure-of-eight reentry (n = 4) demonstrated simultaneous upper and
lower loop reentry sharing a common pathway through conduction gap in
the crista terminalis
26.
The two separate central obstacles were the superior vena cava (SVC)
combined with upper crista and the inferior vena cava combined with
lower crista (
Figure 6).
The type II figure-of-eight reentry (n = 8) demonstrated simultaneous
upper loop reentry and free wall reentry
26.
The channel between the crista terminalis and the low voltage zone was
a common pathway. The two separate central obstacles were the SVC
with upper crista and a part of the low voltage zone. RF ablation
of the conduction gap in the crista terminalis (for type I reentry) and
the channel between the crista terminalis and low voltage zone (for
type II reentry) was effective in eliminating atrial flutter.
Figure 6. Isopotential map showing
type I figure of eight reentry in the right posterior oblique
view. The activation wave front propagated through the conduction
gap in the crista terminalis (CT) and separated into two wave
fronts. The counterclockwise wave front (virtual 8 to 13) rotate
around the superior vena cava (SVC) and upper CT, and the clockwise
wave front (virtual 14 to 18) rotate around the inferior vena cava
(IVC) and lower CT. The virtual elecetrogram 9 at the CT gap
showed low amplitude potential between double potentials, representing
slow conduction (Reproduced from Tai CT, Liu TY, Lee PC, Lin YJ, Chang
MS, Chen SA. Noncontact mapping to guide radiofrequency ablation
of atypical right atrial flutter. J Am Coll Cardiol 2004;44:1080-10866,
with permission from the American College of Cardiology
Foundation.)
RAA = right atrial appendage.
(
Figure 7)
This
macroreentrant circuit rotates around the mitral annulus, either
counterclockwise or clockwise
27.
The boundaries of the critical isthmus include the mitral annulus
anteriorly, and low voltage zone or scars in the posterior wall of the
left atrium posteriorly. RF ablation of the isthmus between the left
inferior pulmonary vein and the mitral annulus can eliminate this
atrial flutter.
Figure 7 Isochronal map in the
left anterior oblique view demonstrates a left atrial macroreentrant
circuit around the mitral annulus , denoted by the black arrow.
(
Figure 8)
Macroreentrant
circuits can rotate around one or more pulmonary veins and a scar in
the posterior wall or roof of the left atrium
28.
These circuits may have multiple loops. The peri-pulmonary vein
circuits can be cured with ablation by creating a lesion from a
pulmonary vein to the mitral annulus or to the contralateral pulmonary
vein.
Figure
8 Isochronal map in the right anterior oblique view
demonstrates a left atrial macroreentrant circuit around the right
superior pulmonary vein , denoted by the black arrow.
Left Septal Atrial Flutter
The
macroreentrant circuit rotates around the left septum primum, either
counterclockwise or clockwise
29,30. The characteristics of the ECG
showed
dominant positive P waves in lead V1 and low amplitude waves in the
other leads. The critical isthmus is located between the septum primum
and the pulmonary veins or between the septum primum and the mitral
annulus ring. RF ablation of this isthmus can eliminate this atrial
flutter.
Conclusion
AFL is a
reentrant arrhythmia and needs anatomic or functional barriers to
maintain its activation. Typical AFL rotates around the tricuspid
annulus with the crista terminalis and tricuspid annulus as barriers.
Atypical AFL may originate from the right or left atrium without
involving the cavotricuspid isthmus. The barriers may be scars, crista
terminalis, mitral annulus, pulmonary veins, or septum primum. RF
ablation of the isthmus between the boundaries can cure this
arrhythmia.
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