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Surface Electrocardiographic Characteristics of Right and

Left Atrial Flutter


Andres Bochoeyer, MD*; Yanfei Yang, MD*; Jie Cheng, MD, PhD; Randall J. Lee, MD, PhD;
Edmund C. Keung, MD; Nassir F. Marrouche, MD; Andrea Natale, MD; Melvin M. Scheinman, MD

BackgroundThere is little information about the surface expression of non cavotricuspid isthmus (CTI) dependent
right atrial (RA) or left atrial (LA) flutter circuits.
Methods and ResultsWe retrospectively evaluated 32 episodes (in 26 patients) of atypical RA and 22 episodes (in 21
patients) of LA flutter. The surface ECG of 13 patients with lower-loop reentry was similar to that of their pattern during
counterclockwise (CCW) CTI atrial flutter (AFL), except for decreased amplitude of the terminal forces in the inferior
leads. In 11 of 24 episodes characterized by high or multiple breaks over the crista, the ECG showed changes that
depended on the initial activation sequence of the LA. In 7 of 8 episodes of upper-loop reentry, the ECG pattern
completely mimicked that for clockwise (CW) CTI AFL. All 11 patients with an LA septal circuit showed a typical ECG
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pattern characterized by prominent forces in lead V1 with flat deflections in the other surface leads. Eleven patients with
other LA circuits had a more variable pattern but showed decreased voltage in the inferior leads compared with that of
a group with CCW-CTI AFL (1.61 vs 2.680.7 mV, respectively; P0.05).
ConclusionsThe RA surface-ECG patterns different from those of CCW or CW-CTI could still be CTI dependent. In
contrast, a typical CW-CTI surface pattern was always seen in patients with upper-loop reentry, which was nonCTI
dependent. LA AFL circuits had either flat or low-amplitude forces in the inferior leads. (Circulation. 2003;108:60-66.)
Key Words: electrophysiology atrial flutter mapping catheter ablation

A lthough a large variety of atrial flutter (AFL) circuits


have been defined,1 8 there are few data that correlate
known AFL circuits with surface ECG patterns. The purpose
flutters were generally sustained (30 seconds) and allowed for
mapping and ablation.

Left Atrial AFL


of this study was to define the ECG patterns of flutter circuits We included only those patients with left atrial (LA)-AFL circuits
in an effort to help localize the flutter pathway. without atriotomy in whom a complete electroanatomic map
(CARTO) was available. Eight were excluded because of an incom-
Methods plete map. A total of 21 consecutive patients with 22 episodes of LA
macroreentrant circuit were analyzed; 17 of 21 were studied at the
Study Population Cleveland Clinic. All patients with LA-AFL were studied during
their sustained, clinically manifest arrhythmias.
Right Atrial AFL
This study retrospectively analyzed consecutive patients referred for
catheter ablation of AFL. The patients (n372) were recruited from Analysis of the ECG
the University of California at San Francisco from January 1996 to We compared simultaneous surface and intracardiac recordings
August 2000. and/or CARTO maps with the surface recordings. We also compared
Patients with clockwise (CW) or counterclockwise (CCW) surface recordings from our study patients with 38 consecutive
cavotricuspid isthmus (CTI) dependent flutter (CTI-AFL; n328 patients with CCW CTI-AFL who underwent successful CTI abla-
patients) and 18 patients with prior cardiac surgery were excluded tion. Surface flutter waves were usually analyzed during higher
from study. We studied 26 patients who had experienced 32 episodes (2:1) grades of atrioventricular block to avoid superimposition of
of atypical right atrial (RA)-AFL. In 20 of 26 cases, the patients also the flutter on T waves. In 3 instances, recordings of 2:1 block were
had CCW or CW CTI-AFL. Among these 32 episodes of atypical used because the P or flutter waves that preceded the QRS complexes
flutter, 20 (63%) were spontaneous and 12 were pacing induced. The were free of T waves.

Received December 31, 2002; revision received April 1, 2003; accepted April 9, 2003.
From the Cardiovascular Research Institute and Section of Cardiac Electrophysiology (A.B., Y.Y., R.J.L., M.M.S.), University of California, San
Francisco; Texas Heart Institute, St Lukes Episcopal Hospital, Houston, Tex (J.C.); the Veterans Affairs Medical Center (E.C.K.), San Francisco, Calif;
and the Section of Cardiac Electrophysiology (N.F.M., A.N.), Cleveland Clinic Foundation, Cleveland, Ohio.
*Drs Bochoeyer and Yang are cofirst authors.
Guest editor for this article was Hein J.J. Wellens, MD, Cardiovascular Research Institute, the Netherlands.
Presented in abstract form at the 22nd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology Boston, Mass, May
25, 2001.
Correspondence to Melvin M. Scheinman, MD, Cardiac Electrophysiology, University of California, San Francisco, 500 Parnassus Ave, MU E 4S, Box
1354, San Francisco, CA 94143-1354. E-mail scheinman@medicine.ucsf.edu
2003 American Heart Association, Inc.
Circulation is available at http://www.circulationaha.org DOI: 10.1161/01.CIR.0000079140.35025.1E

60
Bochoeyer et al ECG Characteristics of Atypical Flutter 61

TABLE 1. Clinical and Electrophysiological Characteristics of


Patients With Atypical Flutter
RA LA
(n26) (n21) P
Age, y, meanSD 5913 678.6 0.03
Male sex, % (n) 92 (24) 71.5 (15) 0.11
History of atrial fibrillation, % (n) 61 (16) 71.5 (15) 0.48
Structural heart disease, % (n) 19 (5) 62 (13) 0.002
CL, ms 25240 297.564 0.005
LA size, mm 414 464 0.001

Electrophysiology Study
The study was approved by the University of California at San
Francisco and Cleveland Clinic institutional review boards. Antiar-
rhythmic drugs were discontinued for at least 5 half-lives before the
study, except for 11 patients who were treated with amiodarone. Figure 1. Sustained, spontaneous AFLs with 2 different CLs
The study was performed as previously described by using from same patient. Tracings on left show 12-lead ECG in a
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recordings from a 20-pole halo, His bundle, and coronary sinus (CS) patient with CCW-AFL with CL of 285 ms. Adjacent 12-lead
catheters.7 The distal pole of the halo catheter was positioned at 7 ECG was recorded during LLR. Arrows (left-hand panel) point to
oclock on the tricuspid annulus (TA) in the left anterior oblique decrease in inferior forces with LLR and slight changes in V1
(arrow). Tracings on right show intracardiac recordings during
projection. Twelve-lead ECGs and intracardiac recordings were
both CCW and LLR. Schema below shows LLR with early break
obtained and displayed simultaneously. Entrainment mapping was (marked by asterisk) in the region of low lateral RA (TA1). Con-
attempted in all patients at a cycle length (CL) of 10 to 30 ms less version of CCW to LLR is associated with increase in transisth-
than the flutter CL. Concealed entrainment was present when the mus conduction time (TA1-CSPX). Shortening of tachycardia CL
difference between the tachycardia CL and postpacing interval was with LLR is responsible for increase in isthmus conduction time.
25 ms with identical intracardiac activation sequence and surface Arrows (right-hand panel) point to activation wavefront, and
flutter wave morphology (when possible). Electroanatomic mapping refers to areas of collision. SVC indicates superior vena cava;
with the CARTO system (Biosense, Cordis-Webster Inc) was avail- IVC, inferior vena cava; CSds, distal CS; CSpx, proximal CS; and
able for 2 patients with atypical RA-AFL and for 21 patients with CT, crista terminalis.
LA-AFL. Low voltage was defined as a voltage amplitude 0.1 mV
and scar that showed no recordable activity. Entrainment mapping
was attempted from various sites in those with lower-loop reentry lateral RA (Figure 1). This circuit was found in 13 of 24
(LLR) and upper-loop reentry (ULR). In all patients with LLR,
concealed entrainment was present in the CTI but was absent from episodes and was usually associated with a slight decrease in
the CTI in those with ULR. CTI ablation was successful in the amplitude of the late positive deflection in the inferior
arrhythmia termination and resulted in a lack of arrhythmia induc- leads. It was thought that the decrease in the late inferior
ibility for all patients with LLR. forces was caused by an impulse collision over the lateral
portion of the RA, which served to cancel the forces caused
Statistics by late craniocaudal lateral RA activation. Because activation
All numeric variables are expressed as meanSD. A value of of the septum and LA remains the same as with CCW
P0.05 was considered statistically significant. Mean voltage com- CTI-AFL, the AFL wave patterns remain very similar.
parisons were made with use of a t test for a 2-tailed distribution with
2 samples of unequal variance. Sensitivity and specificity were The second ECG pattern involved a total of 11 of 24
calculated by using Fishers exact probability test. episodes that showed wavefront breaks over more superior
portions of the TA. An illustrative example of a high break
is shown in Figure 2A and is characterized by advancement of
Results
the atrial electrogram from the His bundle region compared
RA Flutter with the CS recordings during CCW-AFL. Of note was the
This group consisted of 24 men and 2 women with an average finding that the surface recordings were identical during
age of 5913 years. The demographic data for patients with CCW CTI-AFL when compared with the LLR pattern. We
RA-AFL is detailed in Table 1. In both patients who changed interpreted this finding as being due to capture of the LA from
from CCW to LLR or from CW to ULR, the CL decreased the CS connection. The wavefront collision occurred high
from 266 to 253 ms (P0.02) and from 259 to 250 ms over the septum, and hence, most of lateral wall was still
(P0.03), respectively. activated in a craniocaudal direction.
Figure 2B shows another example of LLR with a high
Counterclockwise LLR break over the TA6. In this patient, the change to a higher
A total of 19 patients with 24 episodes showed a pattern of break site (TA8) was associated with a marked change in the
LLR, which involves a breakthrough over the crista with the surface ECG morphology. Note that the surface ECG during
circuit around the inferior vena cava; hence, LLR is a LLR1 (with the break at TA6) showed a pattern that mimicked
CTI-AFL. We found 3 different ECG patterns for patients CCW-AFL. With conversion to the higher break (TA8), the
with LLR. The first pattern was previously described by surface ECG pattern was now more consistent with that seen
Cheng et al9 and involved a wavefront break over the low in CW-AFL. We explain this finding by assuming earlier
62 Circulation July 8, 2003

Figure 3. Left-hand panel shows 12-lead ECGs in patient with


CCW-AFL and LLR with multiple cristal breaks. Right-hand pan-
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els show corresponding intracardiac recordings. CCW pattern is


characterized by caudocranial activation of LA and is associated
with typical surface morphology. During LLR (right), early breaks
(asterisks) over TA1, TA6/7, and TA10 are manifested. Note that
during LLR (right), atrial electrogram from His bundle region is
advanced relative to that from CSos, compared with sequence
during CCW-AFL. In addition, changes in atrial activation
sequence and morphology are observed in atrial electrogram
from His bundle recording site between CCW and LLR patterns
(see change in arrow orientation over His recording site). We
explain both early TA10 activation relative to TA8/9 as well as
changes in His atrial electrogram to more superior cristal break
(see schema). Schema shows early breaks over crista in regions
corresponding to TA1, TA6/7, and TA10. We suggest that surface
patterns observed for LLR and multiple breaks (characterized by
diminished inferior flutter wave and negative flutter wave in V1)
results from competition in activation of LA from both CS as
well as from right-to-left connections from Bachmanns bundle
Figure 2. A, Left-hand panels show 12-lead ECGs of spontaneous Isth indicates cavotricuspid isthmus.
episodes of CCW and LLR. Right-hand panels show intracardiac
recordings during CCW and LLR. Note that during LLR, patient
developed high cristal break over TA9 (see schema). High break
explains early activation over RA roof as well as advancement of the flutter circuit changed from CCW to LLR with multiple
atrial deflection on His bundle electrogram relative to CS record- breaks (Figure 3). The flutter wave in V1 changed from
ings. TA8TA10 electrograms are probably out of plane relative to positive to negative and was associated with diminished late
His atrial recordings, because they show small changes relative to
forces in the inferior leads. The latter is explained by a
that from His. Direction of both LLR and CCW wavefronts are
identical (caudocranial) and explain why 12-lead ECGs (left-hand collision of wavefronts over the lateral wall, with cancellation
panels) are identical for both circuits. Isth indicates cavotricuspid of the late craniocaudal forces. The change in polarity of V1
isthmus. B, Serial recordings from patient with CCW-AFL (not might result from slightly earlier activation of the LA from
shown) who developed 2 patterns of LLR. Left-hand panel shows
Bachmanns bundle (Figure 3).
surface ECGs of both, and right-hand panel shows corresponding
intracardiac recordings. In 1 pattern (LLR-1), 12-lead ECG (extreme
left) shows flat flutter waves in inferior leads and positive flutter
waves in V1 (see arrows). In endocardial recordings shown on right,
Clockwise ULR
LLR-1 is characterized by cristal break over TA6 (marked by aster- Another flutter pattern was characterized by a circuit con-
isk), whereas LLR-2 shows higher break (TA8), as shown in schema fined to the upper portion of the RA that was nonCTI
at bottom. Note that higher cristal break in LLR-2 again results in dependent. There were 8 episodes of CW-ULR in 7 patients:
earlier activation of His bundle atrial electrogram relative to CS
(compare LLR-2 with LLR-1). Larger circuit (LLR-2) is associated
5 were spontaneous and 3 were induced by pacing. Seven of
with shorter transisthmus conduction time, whereas shorter circuit the 8 episodes showed breakthrough over the low crista
(LLR-1) shows opposite trend, suggesting that circuit size deter- terminalis, with wavefront collision over the midlateral TA.
mines isthmus conduction time. Surface ECG leads for LLR-2 (left) An example is shown in Figure 4. Note that there is no change
shows positive flutter waves in inferior leads and negative flutter
waves in V1 and are explained by craniocaudal activation of sep-
in the surface ECG pattern despite clear-cut evidence of
tum and LA. CSos indicates the ostium of CS. change from a typical CW circuit to 1 with a wavefront
collision in the CTI, which was associated with an early break
activation of the septum and anterior LA over Bachmanns over the low lateral TA. This pattern is explained by the
bundle, with the wavefront akin to that observed in CW-AFL. identical craniocaudal activation sequence of the septum and
The third type of flutter circuit was observed in 9 patients LA for both flutter circuits. One patient had a persistent 2:1
and was characterized by LLR, with multiple, early breaks atrioventricular conduction, which impaired our ability to
over the lateral TA. A very unusual ECG pattern evolved as compare the surface pattern with CW CTI-AFL.
Bochoeyer et al ECG Characteristics of Atypical Flutter 63

Mitral Annulus AFL


Three patients had a reentrant CCW circuit around the mitral
annulus. All had concealed entrainment from both the CS and
mitral annulus. Two had a surface ECG pattern that showed
prominent, positive P waves in V1/V2, with inferior leads that
showed 1-mV positive or multiphasic waves (Figure 6). The
third case had an ECG pattern that mimicked a typical CCW
pattern, except for a negative P wave of 1 mV in lead I. In
these patients, the mitral annulus was the anterior boundary,
and low-voltage areas in the posterior wall served as the
posterior boundary; successful ablation was achieved in 2 of
the 3 patients.

Posterior Wall Scar Circuits


There were 8 patients who had low-voltage or scarred areas
Figure 4. Right-hand panel records episode of CW flutter, which over the LA posterior wall and posterior scar circuit. The
spontaneously evolved into a pattern of ULR) with early break- surface ECG of 4 of them mimicked typical CCW CTI-AFL
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through at TA3. Two surface ECGs (left-hand panel) are, how-


ever, identical, because 2 wavefronts during ULR (see endocar- patterns in terms of P-wave orientation, except for 1 patient,
dial recordings at right) collide at isthmus (Isth) and do not whose ECG showed a negative deflection in V1 without the
result in any change in activation sequence of LA, septum, or classic sawtooth pattern in the inferior leads. One patient
caudocranial activation of lateral RA.
had a surface ECG with a low-voltage CW pattern, and
another 2 cases showed the characteristic LA septal circuit
LA Flutter pattern previously described (Figure 7). One patient had a
The demographic pattern for these patients is detailed in fixed 2:1 atrioventricular block, which precluded definition of
Table 1. The LA-AFL patients were separated into 3 groups. the surface wave morphology. Ablation was successful in
terminating these circuits in all 8 patients.
LA Septal Circuit
We observed 11 episodes of LA-AFL around the left fossa
ovalis. All patients showed an ECG pattern characterized by Surface ECG Comparison
a dominant positive or multiphasic flutter wave in V1 with flat Comparison of the 12-lead ECG between those with LA-AFL
or isoelectric flutter waves in the others leads (Figure 5A). and those with CCW CTI-AFL is detailed in Table 2. Inferior
CARTO mapping in these patients showed either CCW or leads in all patients with the LA septal circuit pattern had
CW revolution around the left side of the septum primum almost flat-line recordings. The maximal amplitude in any of
(Figure 5B). Concealed entrainment was found in the isthmus the 3 inferior leads (II, III, aVF) was significantly smaller for
between the right pulmonary veins and the left septum those with mitral annulus or posterior wall scar circuits
primum. We failed to terminate the flutter circuit by radio- compared with those with CCW CTI-AFL (1.61 vs
frequency ablation in 1 patient. 2.680.7 mV, P0.05).

Figure 5. Representative example from


patient with LA septal circuit. A, ECG
with a pattern characterized by domi-
nant, positive P wave in V1 with near-
isoelectric P waves in other leads. B,
CARTO map illustrates LA septal circuit
in left anterior oblique projection. The
circuit involves LA septum, with func-
tional barriers between septum primum
(SP), right superior and inferior pulmo-
nary veins (RSPV-RIPV), and mitral annu-
lus (MA).
64 Circulation July 8, 2003

Figure 6. Surface and endocardial re-


cordings from patient with CCW mitral
annulus circuit, with CL of 310 ms. Sur-
face ECG (A) shows low-amplitude flutter
waves in inferior leads and prominent,
positive waves in V1/V2. B shows CARTO
maps in both anteroposterior (AP) and
caudal left anterior oblique (LAO) proj-
ection. Low-voltage areas and scar are
identified near ostuim of left superior pul-
monary vein (LSPV). Dark red points
denote sites of concealed entrainment.
Ablation line connecting LSPV with mitral
annulus resulted in tachycardia
termination.
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Discussion Lower-Loop Reentry


The surface ECG pattern was very similar for those with LLR and
Major Findings CCW CTI-AFL. For some, the changes were manifested by a
We found that surface flutter recording for those with decreased amplitude of the late positive waves in the inferior leads,
LA-AFL might often be an inadequate indication of CTI- probably as a result of wavefront collision over the lateral RA wall.
AFL, whereas LA-AFL shows even more inhomogeneous Of interest was the finding that high cristal breaks could be
patterns. Previous elegant animal studies showed that flutter associated with a CW pattern (Figure 2B). Even more interesting
wave polarity was dependent on the activation sequence of surface patterns were recorded with LLR circuits and multiple
the LA,10 13 and this principle has been confirmed in human cristal breaks (Figure 3). These surface patterns were typical for
studies.14 16 More recently, studies with 62-lead body-surface neither CCW nor CW-AFL and emphasize the need for careful
mapping in humans with CCW-AFL showed evidence that entrainment mapping of the CTI to document its involvement.
the terminal positive deflections in the inferior leads could be
caused by late craniocaudal activation of the lateral RA Upper-Loop Reentry
wall.17 We used these principles to explain the relation ULR is a circuit with CW orientation in the upper RA with
between surface and endocardial recordings. wavefront collision in the CTI. In our series of 7 patients with

Figure 7. Surface ECG in A and


3-dimensional map of patient with poste-
rior wall macroreentry (B). Cranial right
anterior oblique (RAO) view shows that
circuit goes around scar (gray area)
located at roof of LA, with CL of 330 ms.
Another scar is also seen in anterior
mitral annulus (MA), and arrhythmia was
terminated with radiofrequency applica-
tion, sealing channel between these 2
scars. There is third scar close to left
superior pulmonary vein (LSPV), which
provides potential for another circuit.
Bochoeyer et al ECG Characteristics of Atypical Flutter 65

TABLE 2. Surface ECG Features: Comparison of Mean Voltage (in mV)


LA

RA LA Septal Mitral Posterior Wall


CCW Circuit Annulus Macroreentry
(n38) (n11) (n3) (n8)
Inferior leads* 2.620.7 0.080.1 1.20.35 1.61
Lead I 0.0050.4 0 0.30.57 0.91
V1 1.970.35 2.30.4 1.60.35 1.61.2
*MeanSD of maximal amplitude in lead II, III, or aVF.
P0.05 by t test compared with CCW.
Only 1 patient had negative flutter wave in lead I.
PNS compared with CCW.

8 ULR circuits, we could not detect any clear-cut changes mation by more detailed studies. The data derived from this
between ULR and CW-AFL patterns. This finding is consis- study might not be an accurate indication of the incidence of
tent with a report of Lai et al18 and shows that a typical CW LA-AFL circuits. This is because some LA circuits could not
pattern is not always associated with CTI-AFL. In a recent
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be completely mapped and thus, were not included in this


important study by Tai et al,19 the ECG morphology appeared study.
to be dependent on the CS/LA activation sequence.

Clinical Implications
LA Atrial Flutter
Our studies for those with RA-AFL highlight the impor-
Those with LA-AFL had a significantly higher incidence of
LA enlargement, atrial fibrillation, and longer tachycardia CL tance of entrainment mapping. We found instances of
compared with those with RA-AFL. Jais et al8 first reported atypical surface patterns that were CTI dependent and vice
LA-AFL maps and pointed out a rather variegated pattern of versa. LA-AFL showed more inhomogeneous patterns. A
surface expression for the LA-AFL population. large-amplitude flutter (or P) wave in V1 associated with
flat, inferior P waves was pathognomonic of LA septal
LA Septal Circuit circuit but was observed in other LA circuits. In addition,
Patients with LA septal circuit typically showed large, those with LA-AFL had a tendency for a greater isoelectric
usually positive waves in V1 with almost flat waves in interval, which might reflect wide areas of slow
other leads. We suggest that this pattern might be caused conduction.20
by a septal circuit with anterior-posterior forces projecting
on V1 and the cancellation of caudocranial forces. This
pattern was 100% sensitive for an LA septal circuit, but the References
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Surface Electrocardiographic Characteristics of Right and Left Atrial Flutter
Andres Bochoeyer, Yanfei Yang, Jie Cheng, Randall J. Lee, Edmund C. Keung, Nassir F.
Marrouche, Andrea Natale and Melvin M. Scheinman

Circulation. 2003;108:60-66; originally published online June 30, 2003;


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doi: 10.1161/01.CIR.0000079140.35025.1E
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