relationship between the spectral characteristics of atrial

8/3/2019 Relationship Between the Spectral Characteristics of Atrial

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Relationship between the spectral characteristics of atrial

fibrillation and atrial tachycardias that occur after catheter

ablation of atrial fibrillation

Kentaro Yoshida, MD, Aman Chugh, MD, Magnus Ulfarsson, PhD,* Eric Good, DO, Michael Kuhne, MD,Thomas Crawford, MD, Jean F. Sarrazin, MD, Nagib Chalfoun, MD, Darryl Wells, MD,Warangkna Boonyapisit, MD, Srikar Veerareddy, MD, Sreedhar Billakanty, MD, Wai S. Wong, MD,Krit Jongnarangsin, MD, Frank Pelosi, Jr., MD, Frank Bogun, MD, Fred Morady, MD, Hakan Oral, MD

From the Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, Michigan, and *Department of

Electrical and Computer Engineering, University of Iceland, Reykjavik, Iceland.

BACKGROUND During catheter ablation of complex fractionated

atrial electrograms, persistent atrial fibrillation (AF) may convert

to an atrial tachycardia (AT).

OBJECTIVE The purpose of this study was to investigate the

possible mechanisms of AT by examining the spectral and electro-

physiologic characteristics of AF and ATs that occur after catheter

ablation of AF.

METHODS The subjects of this study were 33 consecutive pa-

tients with persistent AF who had conversion of AF to AT during

ablation of AF (group I) and 20 consecutive patients who

underwent ablation of persistent AT that developed more than

1 month after AF ablation (group II). Spectral analysis of the

coronary sinus (CS) electrograms and lead V1

was performed

during AF at baseline, before conversion, and during AT. The

spatial relationship between the AT mechanism and ablation

sites was examined.

RESULTS A spectral component with a frequency that matched

the frequency of AT was present in the baseline periodogram of AF

more often in group I (52%) than in group II (20%, P .02).

Ablation resulted in a decrease in the dominant frequency of AF

but not in the frequency of the spectral component that matched

the AT. There was a significant direct relationship between thebaseline dominant frequency of AF and the frequency of AT in the

CS in group I (r 0.76, P.0001) but not in group II (r 0.38,

P .09). ATs were macroreentrant in 64% and 60% of patients in

groups I and II, respectively (P .8). The AT site was more likely

to be distant (1 cm) from AF ablation sites in group I (70%) than

in group II (35%, P .007).

CONCLUSION The findings of this study suggest that ATs ob-

served during ablation of AF often may be drivers of AF that

become manifest after elimination of higher-frequency sources

and fibrillatory conduction.

KEYWORDS Atrial fibrillation; Atrial tachycardia; Catheter abla-

tion; Spectral analysis

(Heart Rhythm 2009;6:1117) 2009 Heart Rhythm Society. Pub-

lished by Elsevier Inc. All rights reserved.

Persistent atrial fibrillation (AF) often involves drivers

outside the pulmonary veins (PVs).14 Complex fraction-

ated atrial electrograms are targeted in an attempt to ablate

these drivers.37 When AF converts during ablation of com-

plex fractionated atrial electrograms, it converts much more

often to an atrial tachycardia (AT) than to sinus rhythm.1,4,8

The mechanistic implication of ATs that become manifest

during ablation of complex fractionated atrial electrogramsis unclear.

The hypothesis underlying this study was that ATs to

which AF converts during ablation represent drivers of

persistent AF that were obscured by fibrillatory conduction

and by higher-frequency drivers. To test this hypothesis, we

examined the spectral and electrophysiologic characteristics

of AF and the ATs that the AF converted to during an

ablation procedure.

Methods

Study subjects

The subjects of this study consisted of two groups of pa-

tients who underwent radiofrequency catheter ablation of

persistent or long-lasting persistent AF. Group I consisted of

33 consecutive patients in whom AF converted to AT at the

time of the catheter ablation procedure. Group II consisted

of a control group of 20 consecutive patients who under-

went a repeat ablation procedure for persistent AT at a mean

of 7 5 months after catheter ablation of AF. In each of

these 20 patients, AF had been converted to sinus rhythm by

direct-current countershock during the index procedure. The

Supported in part by a grant from St. Jude Medical, Inc. Drs. Oral and

Morady are founders and equity owners of Ablation Frontiers, Inc. Address

reprint requests and correspondence: Dr. Hakan Oral, Cardiovascular

Center, SPC 5853, 1500 East Medical Center Drive, Ann Arbor, Michigan

48109-5853. E-mail address: [email protected]. (Received June 17, 2008;

accepted September 25, 2008.)

1547-5271/$ -see front matter 2009 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved. doi:10.1016/j.hrthm.2008.09.031
mailto:[email protected]:[email protected]:[email protected]


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clinical characteristics of the study subjects are given in

Table 1.

Electrophysiologic study and catheter ablationThe study protocol was approved by the Institutional Re-

view Board, and all patients provided informed written

consent. Electrophysiologic studies were performed in the

fasting state. Antiarrhythmic drug therapy was discontinued

four to five half-lives before the procedure, except for ami-

odarone, which was discontinued 8 to 12 weeks before the

procedure. Vascular access was obtained through a femoral

vein. A steerable quadripolar catheter with 2.5-mm inter-

electrode spacing (EP Technologies, Sunnyvale, CA, USA)

was positioned in the coronary sinus (CS). The CS catheter

was positioned in the posterolateral CS throughout the pro-

cedure. After the transseptal puncture, systemic anticoagu-

lation was achieved with intravenous heparin to maintain an

activated clotting time of 300 to 350 seconds. The PVs were

mapped with a decapolar ring catheter (Lasso, Biosense

Webster, Diamond Bar, CA, USA). An open-irrigation,

3.5-mm-tip deflectable catheter (ThermoCool, Biosense

Webster) was used for mapping and ablation. Bipolar elec-

trograms were displayed and recorded at filter settings of 30

to 500 Hz during the procedure (EPMed Systems, West

Berlin, NJ); they also were recorded at 0.5 to 200 Hz for

offline spectral analysis.

Left atrial and PV geometry was reconstructed with an

electroanatomic mapping system (CARTO, Biosense Web-

ster). Conscious sedation was achieved with fentanyl and

midazolam after barium swallow for visualization of the

esophagus.

Radiofrequency energy was delivered at a power of 25 to

35 W, maximum flow rate of 30 mL/min, and maximum

temperature of 45C. The ablation strategy consisted of

antral ablation to isolate all of the PVs, followed by ablation

of complex fractionated atrial electrograms in the left

atrium, CS, and right atrium aimed at conversion of AF to

AT or sinus rhythm.

Mapping and ablation of AT

AT was defined by three criteria: (1) discrete and mono-morphic P waves on the ECG; (2) regularity of the electro-

grams recorded in the left atrium and CS with 20 ms

variability in cycle length; and (3) stable activation se-

quence.

As described previously, the mechanism of AT was con-

sidered to be macroreentry if activation mapping accounted

for 90% of the tachycardia cycle length and if the diam-

eter of the reentrant circuit was 3 cm.9 The mechanism of

the tachycardia was considered to be due to microreentry ifthe diameter of the circuit was 3 cm. Sites where the

postpacing interval was within 20 ms of the tachycardia

cycle length were considered to be within the reentrant

circuit. A focal mechanism was confirmed if mapping

showed centrifugal activation from a point source. Among

the 20 patients with AT in group II, 7 received an antiar-

rhythmic drug after the index ablation procedure for recur-

rent atrial arrhythmia: amiodarone in 4, sotalol in 1, and

propafenone in 2. Therapy with propafenone and sotalol

was discontinued four half-lives before the ablation proce-

dure for AT, and therapy with amiodarone was discontinued

4 weeks before the procedure.

Digital signal processing and data analysisAll patients in group I presented to the laboratory in AF. CS

electrograms and 12-lead ECG were acquired for 60 sec-

onds at baseline, at 3 minutes before conversion of AF to

AT, and during sustained AT 2 minutes after conversion of

AF to AT. Spectral analysis of only the first AT to which AF

converted was performed in this study.

In group II, 12 of 20 patients were in AT upon presen-

tation to the electrophysiology laboratory, and sustained AT

was induced by rapid atrial pacing in the remaining 8

patients. CS electrograms were acquired during sustainedAT for 60 seconds before radiofrequency ablation. In addi-

tion, electrograms of baseline AF were acquired from the

index procedure. The sites at which ATs were ablated were

annotated on the electroanatomic maps.

Electrograms recorded for 60 seconds in the CS and lead

V1 were processed offline in the MatLab environment

(MathWorks, Inc., Natick, MA, USA) using custom soft-

ware. As described previously, the QRS or QRST com-

plexes (in lead V1) were subtracted.10 First, digitized bipolar

electrograms, sampled for 60 seconds at 1,000 Hz (60,000

points), underwent the following preprocessing steps of

band-pass filtering at 40 to 250 Hz, rectification, and low-pass filtering at 20 Hz. Then the discrete Fourier transform

of the preprocessed signal was computed using the fast

Fourier transformation algorithm to analyze the 0.5- to

80-Hz spectral band. An estimate of the signal spectrum was

obtained by computing the periodogram, which is the mod-

ulus squared of the discrete Fourier transform. The fre-

quency resolution was 0.017 Hz. The dominant frequency

(DF) was defined as the frequency of the highest peak of the

smoothed periodogram in the interval from 0.5 to 20 Hz.11

AF has significant periodic elements with varying de-

grees of regularity. The Fourier transform takes advantage

of the fact that continuous signals can be decomposed to asum of weighted sinusoidal functions.12 Although the DF is

Table 1 Clinical characteristics of the study patients

Group I

(N 33)

Group II

(N 20) P value

Age (years) 61 8 63 9 .3Gender (male/female) 27/6 12/8 .1Duration of atrial fibrillation

(months)

32 24 57 52 .02

Left atrial size (mm) 45 6 46 4 .8Left ventricular ejection

fraction%

53 8 56 8 .3

Structural heart disease 13 9 .7Ischemic heart disease 5 5Nonischemic cardiomyopathy 4 1Hypertensive heart disease 8 7

Values are given as mean SD.

12 Heart Rhythm, Vol 6, No 1, January 2009


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the frequency of the sinusoidal waveform with the highest

power, the Fourier transform also shows neighboring peri-

odic and stable waves with less power as other peaks in the

periodogram. The periodogram during AF was systemati-

cally analyzed to identify spectral components other than

the DF (and its harmonics) that matched the frequency of

the AT (within 5%). All spectral components with a peak

frequency power 20% of the DF were compared with the

frequency of the AT.

Statistical analysisContinuous variables are expressed as mean 1 SD and

were compared by Students t-test or paired t-test, as appro-

priate. Categorical variables were compared by Chi-square

analysis or with Fishers exact test, as appropriate. P.05 was

considered significant.

ResultsDF of AF and frequency of AT

The baseline DF of AF in the CS was similar in groups I andII (5.64 0.69 Hz vs 5.73 0.58 Hz, P .66). The mean

cycle length of AT was 225 20 ms (4.48 0.40 Hz) in

group I and 229 33 ms (4.46 0.65 Hz) in group II

(P .62). Among patients in group II, there was no sig-

nificant difference in the mean cycle length of induced and

spontaneous ATs (218 27 ms vs 236 36 ms, P .25).

The baseline DF of AF in lead V1 also was similar between

groups I and II (5.69 0.72 Hz and 5.87 0.68 Hz,

respectively, P .38).

AT frequency and spectral components of AF inthe CSA spectral component of AF with a frequency similar to the

AT frequency was identified in the baseline AF perio-

dogram in 17 (52%) of 33 patients in group I (Figure 1) and

in 4 (20%) of 20 patients in group II (P .02). A similar

spectral component was identified in the periodogram of the

AF shortly before conversion to AT in 26 (79%) of 33

patients in group I and before transthoracic cardioversion of

AF to sinus rhythm in 10 (50%) of 20 patients in group II

(P .03).A matching spectral component was identified in 7

(78%) of 9 patients in group I with an AT involving the

mitral isthmus or the CS and in none of the 8 patients with

a microreentry localized to the roof or the anterior wall

(P .001). A matching spectral component was identified

in 10 (63%) of 16 of the remaining ATs (Table 2).

AT frequency and spectral components of AF inlead V

1

A spectral component with a frequency similar to the AT

frequency was identified in the baseline periodogram of

AF in lead V1 in 10 (30%) of 33 patients in group I andin 3 (15%) of 20 patients in group II ( P .21). A similar

spectral component was identified in the periodogram of

AF in lead V1 shortly before conversion to AT in 14

(42%) of 33 patients in group I and before cardioversion

of AF to sinus rhythm in 3 (15%) of 20 patients in group

II (P .04).

A matching spectral component was identified in 7

(78%) of 9 patients in group I who had a cavotricuspid

4.96 Hz

.

(202 ms)

B

.

4.85 Hz(206 ms)

4.84 HzC

(207 ms)

Figure 1 Periodogram of atrial fibrillation (AF) recorded in the coronary

sinus at baseline (A), 3 minutes prior to conversion (B), and the frequency

of atrial tachycardia (AT; C). At baseline, the dominant frequency (DF) of

AF is 6.60 Hz (A). There is a spectral component with a frequency of 4.96

Hz (arrow). Ablation of complex fractionated atrial electrograms results in

a decrease in DF of AF; however, there is no change in the frequency of

the spectral component (B, arrow). After termination of AF to AT, thefrequency of AT (4.84 Hz) is similar to the frequency of the spectral

component identified in the periodogram of AF (C). The mechanism of AT

was mitral isthmusdependent flutter in this example. Cycle length is given

in parentheses.

Table 2 Mechanisms of atrial tachycardia

Group I

(N 33)

Group II

(N 20) P value

Macroreentry 21 12 .8Cavotricuspid isthmus flutter 9 0 .008Mitral isthmus flutter 6 10 .003Interatrial septum 3 1 .4Roof 2 0 .1Right-sided PV antrum 1 1 .3

Microreentry 10 7 .7Anterior wall 6 1 .06Coronary sinus 3 3 .8Left-sided PV antrum 1 3 .1

Focal 2 1 .9Left atrial septum 1 0 .4

Right-sided PV antrum 1 1 .4PV pulmonary vein.

13Yoshida et al Atrial Tachycardia and Atrial Fibrillation


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isthmus-dependent atrial flutter. In the other two patients,the mechanism of AT was macroreentry around the right-

sided PVs in one and a focal tachycardia originating close to

the right-sided antrum in the other patient. In group I, the

prevalence of a matching spectral component in lead V1 was

higher when AT was cavotricuspid isthmus dependent than

when it was not (78% vs 13%, P .001).

Duration and effect of ablation and DF of AFand ATThe mean duration of RF for conversion of AF to AT was

75 18 minutes in group I (Figure 2). The mean duration

of radiofrequency energy application was 62 13 minutesin group II. There was a significant correlation between the

DF of AF in the CS at baseline and the duration of RF

required for conversion to AT (r 0.54, P .002).

The DF of AF was significantly lower shortly before

conversion to AT (5.10 0.51 Hz) than at baseline (5.64

0.69 Hz) in group I (P .0001, Figure 3). However, there

was no significant change in the frequency of the spectral

component of AF that matched the frequency of the AT

(4.52 0.46 Hz and 4.54 0.46 Hz, P .8, Figure 3). In

group II, the DF of AF shortly before cardioversion to sinus

rhythm was significantly lower than at baseline (5.13

0.62 Hz vs 5.73 0.58 Hz, P .0004).The analysis of DF of AF in lead V1 yielded similar

results to those of DF of AF in CS as described earlier

(Figure 3).

Relationship between the DF of AF and frequencyof ATThere was a direct correlation between the baseline DF of

AF in the CS and the frequency of AT in group I (r

0.76, P .0001, Figure 4) but not in group II (r 0.38,

P .09, Figure 5). There also was a significant correla-

tion between the DF of AF shortly before conversion to

AT and the frequency of AT in group I (r 0.66,P .0001, Figure 4) but not in group II (r 0.29, P .21,

Figure 5). A similar significant correlation also existedbetween the baseline DF of AF in lead V1 and the frequency

of AT in group I (r 0.58, P .0005) but not in group II

(r 0.03, P .92).

Mechanisms of AT in group IIn group I, all ATs were targeted for ablation during the

index procedure. AT converted to sinus rhythm during

ablation in 22 (67%) of 33 patients. The remaining 11

patients underwent transthoracic cardioversion to termi-

nate AT because of a long procedure duration (5

hours). The mechanism of the 33 ATs was macroreentry

in 21 (64%), microreentry in 10 (30%), and focal AT in2 (6%) patients (Table 2). The macroreentrant circuit

involved the cavotricuspid isthmus in 9 patients, the

Figure 2 Conversion of atrial fibrilla-

tion (AF) to atrial tachycardia (AT).

Shown are ECG leads I, II, III, aVF, and

V1 intracardiac electrograms recorded

from the distal bipole of an ablation cath-

eter positioned in the left atrium (Abl) and

distal bipole of a quadripolar catheter po-

sitioned in the coronary sinus (CS). Elec-trograms were recorded at baseline (A), 3

minutes before conversion to AT (B), dur-

ing conversion of AF to AT (C) and during

AT (D). During transition from AF to AT,

the AF became more organized before

converting to AT. At times during the ab-

lation procedure, the degree of organiza-

tion varied, suggesting a gradual effect of

ablation on fibrillatory conduction.

Figure 3 Effect of ablation on dominant frequency (DF) of atrial fibril-

lation (AF). Shown are the DF of AF recorded in the coronary sinus (CS;

hatched bars) and lead V1 (gray bars) at baseline and before conversion of

AF to atrial tachycardia (AT) among patients in group I. The DF recorded

from the CS and lead V1 were similar in all groups. Ablation resulted in a

significant decrease in the DF of AF. However, the frequency of the

spectral component in the periodogram of AF that matched AT and fre-

quency of AT after conversion was similar.



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mitral isthmus in 6, interatrial septum in 3, and left atrial

roof in 2, and there was macroreentry around the right-

sided PVs in 1 patient. The 10 microreentrant circuits

were localized to the left atrial anterior wall in 6 patients,

the CS in 3, and the left-sided PV antrum in 1. In another2 patients, the sites of AT were the left atrial septum and

the right-sided PV antrum.

Mechanisms of AT in group IIThe mechanisms of AT in group II were macroreentry in 12

(60%) patients, microreentry in 7 (35%), and a focal AT in

1 (5%, Table 2). The macroreentrant circuits involved the

mitral isthmus in 10 patients, the left atrial septum in 1, and

right-sided PV antrum in 1. The sites of 7 microreentrant

ATs were the left-sided PV antrum in 3 patients, the CS in

3, and the left atrial anterior wall in 1 ( Table 2).

Spatial relationship between AF ablation sitesand ATATs that used a reentrant circuit or had a site of origin

within 1 cm of a prior ablation site were considered to be

secondary to radiofrequency ablation. In group I, 23 (70%)

of 33 ATs were not adjacent to an AF ablation site, and 10

(30%) were considered secondary to ablation. In group II, 7

(35%) of 20 ATs were not adjacent to an AF ablation site,

and 13 (65%) were secondary to ablation (P .01).

Discussion

Main findingsThe main findings of this study were as follows. (1) There

often was a spectral component in the periodogram of AF

that matched the frequency of the AT to which AF con-verted. (2) Although ablation of AF resulted in a decrease in

the DF of AF, it did not eliminate the frequency in the

periodogram that matched the frequency of the subsequent

AT. (3) There was a direct relationship between the duration

of ablation necessary for conversion of AF to AT and the

baseline DF of AF. (4) The baseline DF of AF strongly

correlated with the frequency of AT to which the

AF converted during ablation of AF but not with the frequency

of ATs that developed late after ablation. (5) ATs to which AF

converted during ablation usually were not adjacent to AF

ablation sites, whereas ATs that developed late after AF abla-

tion usually were adjacent to prior ablation sites.These findings suggest that the majority of ATs that

occur during ablation of AF coexist with higher-frequency

sources during AF and may represent drivers of AF that

become manifest only after elimination of higher-frequency

drivers and fibrillatory conduction. On the other hand, as

previously reported, ATs that develop late after AF ablation

usually are a manifestation of proarrhythmia caused by

ablation-induced conduction slowing or a gap in an ablation

line.13

Figure 4 Relationship between atrial fi-

brillation (AF) and atrial tachycardia (AT)

recorded in the coronary sinus among pa-

tients in group I. There was a significant

direct correlation between the dominant

frequency (DF) of AF and the frequency ofAT at baseline (A) and shortly before con-

version to AT (B).

Figure 5 Relationship between atrial fibrillation (AF) and atrial tachycardia (AT) recorded in the coronary sinus among patients in group II. There wasno significant relationship at baseline (A) or shortly before cardioversion to sinus rhythm (B). DF dominant frequency.



6/7

Conversion of AF during catheter ablationATs that occur acutely during an AF ablation procedure

could be due to either proarrhythmia or emergence of an

underlying AF driver. ATs that occur late after AF ablation

have been demonstrated to usually be related to a gap in a

prior ablation line, consistent with proarrhythmia.13 The

match between a frequency in the AF periodogram and the

AT frequency strongly suggests that acutely occurring ATsare a manifestation of preexisting drivers that are uncovered

by the ablation process. It seems likely that ablation elimi-

nated higher-frequency drivers that created fibrillatory con-

duction in the atria. This presumably allowed an AT with a

lower frequency to become manifest.

Frequency of AF and ATIn a stable and electroanatomically homogeneous substrate,

tachycardias with different frequencies would not coexist.

However, during AF, anatomic and functional heterogene-

ities in conduction, refractoriness, and propagation exist in

the atria. Fixed and functional barriers14,15 may explain howtachycardias with a lower frequency than the DF were

identified in the AF periodograms in this study.

In this study, there was a direct correlation between the

frequency of the AF and the AT to which AF converted

during ablation. The DF of AF is a function of the refractory

period, and the atrial effective refractory period also is one

of the determinants of AT cycle length. Different degrees of

remodeling during persistent AF will influence atrial refrac-

toriness to different degrees. Therefore, the direct relation-

ship between the DF of AF and the frequency of the ATs to

which AF converted during ablation may be explained by

the extent to which atrial remodeling affected atrial refrac-toriness among the patients in this study.

Role of macroreentry in AFThe ATs in group I were mostly due to macroreentry, not

localized microreentry or focal sources. This does not nec-

essarily imply that the underlying drivers of AF are more

often macroreentrant as opposed to microreentrant or focal.

As evident from the baseline AF periodogram, the AT

frequency always was lower than the DF of AF. It is pos-

sible that the higher-frequency components of the perio-

dogram were caused by high-frequency rotors or focal dis-

charges.In this study, cavotricuspid isthmus-dependent atrial flut-

ter accounted for approximately 40% of the macroreentrant

ATs in group I. In none of the 9 cases ablation was per-

formed in the right atrium before emergence of these right

atrial flutters. Therefore, proarrhythmia was an unlikely

cause of these cavotricuspid isthmus-dependent atrial flut-

ters. In a prior study, the AF recurrence rate after PV

isolation tended to be lower when cavotricuspid isthmus

ablation was also performed than when it was not.16 In a

more recent study, a history of atrial flutter was associated

with a higher AF recurrence rate after PV isolation, sug-

gesting that non-PV drivers may be more likely in patientswith atrial flutter.17 It is possible that cavotricuspid isthmus-

dependent atrial flutter is one of the lower-frequency drivers

in some patients with AF, possibly explaining the long-

recognized association between the two arrhythmias.18

Of note, microreentrant and focal ATs arising in the left

atrium, because of their smaller size, would be more likely

than macroreentrant ATs to be undetected in a CS electro-

gram. Therefore, the proportion of ATs caused by macro-

reentry may have been overestimated in this study.

DF of AF and duration of ablation necessary toconvert AF to ATThere was a significant direct relationship between the DF

of AF at baseline and the duration of ablation necessary to

convert AF to AT in this study. This observation suggests

that drivers with a higher frequency may be more likely to

result in fibrillatory conduction and a higher prevalence of

complex fractionated atrial electrograms. It also is possible

that, in a remodeled atrium where the DF of AF is often

higher, multiple drivers may develop and subsequently ne-

cessitate more extensive ablation.

Periodogram of AF in the CS versus lead V1

CS electrograms reflect both local CS and adjacent left atrial

depolarizations, but they do not reflect global spatiotempo-

ral dynamics in the left and right atria. As would be ex-

pected, ATs closer to the CS (e.g., mitral isthmus flutters)

were more readily identified in the periodogram of the AF

than the ATs remote from the CS (e.g., left atrial roof

flutters). Therefore, it is likely that spectral analysis of

global atrial activation would have enabled identification of

a higher proportion of ATs in the periodogram of AF than

identified in this study.

To better represent global atrial activation, lead V1 was

also analyzed in this study. Although lead V1 often has a

more favorable signal-to-noise ratio compared with the

other leads, it may be more representative of right than left

atrial depolarizations.19 Right atrial ATs, in fact, were easily

identified in lead V1 in this study. Precise assessment of

global left atrial depolarization may require simultaneous

high-density multisite mapping, which often is not feasible

during the course of an ablation procedure in human sub-

jects.

Study limitations

The majority of ATs in group II occurred in proximity toprior ablation sites and therefore appeared to be gap related.

However, the possibility that some of these ATs in group II

were primary ATs that coexisted with AF during the index

procedure and persisted after ablation cannot be excluded

because AF did not terminate during ablation in any of the

patients in group II. These residual ATs may have resur-

faced during follow-up with a different frequency because

of changes in the electrophysiologic properties of the atrium

as a result of radiofrequency ablation.

Conclusion

The genesis of AF is multifactorial. The PVs and their antraplay a critical role in the initiation and perpetuation of AF.



7/7

However, drivers beyond the PVs also are important in

persistent AF. The findings of this study suggest that mac-

roreentrant ATs often coexist with persistent AF, becoming

manifest only after ablation of higher-frequency drivers

and/or fibrillatory conduction. It is possible that these mac-

roreentrant ATs also serve as drivers of AF. The most

efficient way to identify and ablate AF drivers without

having to perform extensive ablation at sites of passivefibrillatory conduction remains to be determined in future

studies.

References1. Haissaguerre M, Hocini M, Sanders P, et al. Catheter ablation of long-lasting

persistent atrial fibrillation: clinical outcome and mechanisms of subsequent

arrhythmias. J Cardiovasc Electrophysiol 2005;16:11381147.

2. Haissaguerre M, Hocini M, Sanders P, et al. Localized sources maintaining atrial

fibrillation organized by prior ablation. Circulation 2006;113:616625.

3. Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation

of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll

Cardiol 2004;43:20442053.

4. Oral H, Chugh A, Good E, et al. Radiofrequency catheter ablation of chronic

atrial fibrillation guided by complex electrograms. Circulation 2007;115:2606

2612.5. Jalife J, Berenfeld O, Mansour M. Mother rotors and fibrillatory conduction: a

mechanism of atrial fibrillation. Cardiovasc Res 2002;54:204216.

6. Kalifa J, Tanaka K, Zaitsev AV, et al. Mechanisms of wave fractionation at

boundaries of high-frequency excitation in the posterior left atrium of the

isolated sheep heart during atrial fibrillation. Circulation 2006;113:626633.

7. Konings KT, Smeets JL, Penn OC, et al. Configuration of unipolar atrial

electrograms during electrically induced atrial fibrillation in humans. Circulation

1997;95:12311241.

8. Haissaguerre M, Sanders P, Hocini M, et al. Catheter ablation of long-lasting

persistent atrial fibrillation: critical structures for termination. J Cardiovasc

Electrophysiol 2005;16:11251137.

9. Chae S, Oral H, Good E, et al. Atrial tachycardia after circumferential pulmo-

nary vein ablation of atrial fibrillation: mechanistic insights, results of catheter

ablation, and risk factors for recurrence. J Am Coll Cardiol 2007;50:17811787.

10. Lemola K, Ting M, Gupta P, et al. Effects of two different catheter ablation

techniques on spectral characteristics of atrial fibrillation. J Am Coll Cardiol

2006;48:340348.

11. Yoshida K, Ulfarsson M, Tada H, et al. Complex electrograms within the

coronary sinus: time- and frequency-domain characteristics, effects of antral

pulmonary vein isolation and relationship to clinical outcome in patients with

paroxysmal and persistent atrial fibrillation. J Cardiovasc Electrophysiol 2008;19:10171023.

12. Ng J, Goldberger JJ. Understanding and interpreting dominant frequency anal-

ysis of AF electrograms. J Cardiovasc Electrophysiol 2007;18:680685.

13. Chugh A, Oral H, Lemola K, et al. Prevalence, mechanisms, and clinical

significance of macroreentrant atrial tachycardia during and following left atrial

ablation for atrial fibrillation. Heart Rhythm 2005;2:464471.

14. Berenfeld O, Zaitsev AV, Mironov SF, et al. Frequency-dependent breakdown

of wave propagation into fibrillatory conduction across the pectinate muscle

network in the isolated sheep right atrium. Circ Res 2002;90:11731180.

15. Klos M, Calvo D, Yamazaki M, et al. The atrial septopulmonary bundle of the

posterior left atrium provides a substrate for AF initiation in a model of vagally

mediated pulmonary vein tachycardia of the structurally normal heart. Circ

Arrhythmia Electrophysiol 2008;1:175183.

16. Scharf C, Veerareddy S, Ozaydin M, et al. Clinical significance of inducible

atrial flutter during pulmonary vein isolation in patients with atrial fibrillation.

J Am Coll Cardiol 2004;43:20572062.17. Moreira W, Timmermans C, Wellens HJ, et al. Can common-type atrial flutter

be a sign of an arrhythmogenic substrate in paroxysmal atrial fibrillation?

Clinical and ablative consequences in patients with coexistent paroxysmal atrial

fibrillation/atrial flutter. Circulation 2007;116:27862792.

18. Waldo AL, Feld GK. Inter-relationships of atrial fibrillation and atrial flut-

ter mechanisms and clinical implications. J Am Coll Cardiol 2008;51:

779786.

19. Dibs SR, Ng J, Arora R, et al. Spatiotemporal characterization of atrial

activation in persistent human atrial fibrillation: multisite electrogram anal-

ysis and surface electrocardiographic correlationsa pilot study. Heart

Rhythm 2008;5:686693.


relationship between the spectral characteristics of atrial

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