From the Clinical Electrophysiology Laboratories, Section of Cardiology,
University of Chicago, Chicago, Ill.
Correspondence to David J. Wilber, Section of Cardiology, MC 9024, University of Chicago Hospitals, 5758 South Maryland Ave, Chicago, IL 60637. E-mail dwilber{at}medicine.bsd.uchicago.edu
Methods and Results—Of 110 consecutive patients with ablation of
type I atrial flutter, atrial fibrillation was documented in 28 (25%)
during a mean follow-up of 20.1±9.2 months (cumulative probability of
12% at 1 month, 23% at 1 year, and 30% at 2 years). Among 17
clinical and procedural variables, only a history of spontaneous
atrial fibrillation (relative risk 3.9, 95% confidence intervals 1.8
to 8.8, P=0.001) and left ventricular
ejection fraction <50% (relative risk 3.8, 95% confidence intervals
1.7 to 8.5, P=0.001) were significant and independent
predictors of subsequent atrial fibrillation. The presence of both
these characteristics identified a high-risk group with a 74%
occurrence of atrial fibrillation. Patients with only 1 of these
characteristics were at intermediate risk (20%), and those with
neither characteristic were at lowest risk (10%). The determinants and
clinical course of atrial fibrillation did not differ between an early
(
Conclusions—Atrial fibrillation after type I flutter ablation is
primarily determined by the presence of a preexisting structural and
electrophysiological substrate. These data
should be considered in planning postablation management. The
persistent risk of atrial fibrillation in this population also suggests
a potentially important role for atrial fibrillation as a trigger
rather than a consequence of type I atrial flutter.
Despite technical refinements and improved long-term efficacy of the
ablation procedure, the subsequent occurrence of atrial fibrillation
remains a significant clinical problem. It is reported to follow 18%
to 30% of ablation procedures,4 5 8 10 13 14
often within the first month, and may be an important cause of
recurrent symptoms and renewed or continued antiarrhythmic therapy.
However, detailed information regarding the frequency, duration, and
therapy of atrial fibrillation in individual patients is limited. A
contributing role by the procedure remains a concern, although
preliminary data indicate that atrial fibrillation is more common in
patients with a history of this
arrhythmia.5 8 13 14
Improved identification of patients at high risk for subsequent atrial
fibrillation may facilitate optimal patient selection for flutter
ablation and permit more effective use of additional or adjunctive
therapies after ablation. In addition, this population provides the
opportunity to examine the pathophysiologic links between these 2
arrhythmias. The purpose of this study was to characterize the
onset, determinants, and clinical course of postablation atrial
fibrillation. In addition, we examined potential differences in the
clinical significance and determinants of atrial fibrillation as a
function of time after the procedure.
Two-dimensional and M-mode echocardiographic assessment
was obtained within 1 month of the ablation procedure in all patients.
Echocardiograms were analyzed by independent observers without
knowledge of the clinical outcome. Left ventricular
hypertrophy was defined as left ventricular
wall thickness exceeding that predicted for body surface area. Left
ventricular dysfunction was considered present if the
left ventricular ejection fraction was <50%. Left atrial
enlargement was considered present if the dimensions exceeded that
predicted for body surface area (2.4 cm/m2).
Right atrial enlargement was assessed qualitatively.
Electrophysiological Study
Simultaneous surface 12-lead ECGs and bipolar intracardiac
ECGs were continuously acquired with a filter bandwidth of 30 to 500
Hz, digitized (1000 samples/s), and displayed on a high-resolution
video monitor at 200 mm/s for inspection and subsequent review
(Prucka Engineering). Data were stored on optical disk for retrieval
and off-line analysis.
For patients in atrial flutter at the onset of the procedure, mapping
and pacing during atrial flutter was performed before pace termination
and reinduction. Burst pacing was performed in sinus rhythm at 2 atrial
sites (proximal coronary sinus and inferolateral tricuspid
annulus). Burst pacing was performed at cycle lengths of 600, 500, and
400 ms, then progressively shortened by 10 ms/burst until 2:1 atrial
capture or the induction of atrial flutter or atrial fibrillation. If
type I atrial flutter was not induced, programmed atrial stimulation
with up to 2 extrastimuli was also performed, including additional
right atrial sites. During spontaneous or induced flutter, pacing was
performed at multiple sites within the annular–eustachian ridge
isthmus to verify participation of the isthmus in the flutter
circuit.
Type I atrial flutter was induced in 108 of 110 patients,
counterclockwise only in 52, clockwise only in 6, and both in 50. The
mean cycle length of counterclockwise flutter was 245±32 ms, and the
mean cycle length of clockwise flutter was 242±35. Atrial fibrillation
lasting >30 seconds was induced in 31 patients. Atypical atrial
flutter (see "Definitions") lasting >30 seconds was induced in 24
patients.
Ablation
Follow-up
Definitions
Bidirectional isthmus conduction block was considered present when
the following conditions were met7,8,10–12: (1)
pacing during sinus rhythm from inferolateral tricuspid annulus
posterior and lateral to the ablation line resulted in sequential
clockwise activation of the tricuspid annulus, with late activation of
the atrium in the His bundle recording and latest activation in
the proximal coronary sinus, and (2) pacing in sinus rhythm
from the proximal coronary sinus resulted in sequential
counterclockwise activation of the tricuspid annulus, with early
activation of the atrium in the His bundle recording and latest
activation at the inferolateral tricuspid annulus site. In all
instances, activation around the annulus was assessed by
recordings from multiple sites.
Statistical Analysis
Spontaneous atrial fibrillation was documented in 44 patients (40%)
before the ablation procedure. In 23 patients only a single episode was
documented. In 15 patients, more than 1 prior episode of atrial
fibrillation was documented; in each of these patients, episodes of
documented flutter exceeded fibrillation by a ratio of at least 3:1. In
6 patients (5%), recurrent atrial fibrillation was the initial
presenting arrhythmia that was subsequently suppressed by
amiodarone. In each of these 6 patients, only atrial flutter
was observed in the 3 months preceding the ablation procedure. Overall,
20 of 44 patients (45%) with a history of atrial fibrillation had
received prior treatment with class I or III antiarrhythmic drug
therapy.
Atrial Flutter Ablation
Atrial Flutter Recurrence
Four patients with recurrent type I flutter underwent a second
procedure. Each had bidirectional conduction through the isthmus. Two
patients in whom prior success was judged by noninduction alone had
relatively large areas (>1 cm) of sharply defined single electrograms
during atrial flutter adjacent to the prior site of ablation. Two
patients in whom prior success was judged by the presence of
bidirectional isthmus conduction block had either no potentials or
double potentials recorded during flutter along most of the
previous ablation line. However, each had a relatively discrete area of
single electrograms located in the mid or posterior isthmus. Additional
radiofrequency energy applications produced bidirectional conduction
block in all 4 patients, and none have had further recurrences
during follow-up. One patient who declined a second procedure has had
infrequent recurrences on a class I antiarrhythmic drug. Only 1
patient with recurrent type I flutter also had atrial fibrillation
documented during follow-up.
Three patients had spontaneous atypical atrial flutter during
follow-up. Each of these patients also had postablation atrial
fibrillation. The diagnosis of atypical flutter was confirmed by
follow-up electrophysiological study in all
3 patients, and each had persistent bidirectional isthmus conduction
bock. Only 1 of these patients had atypical flutter documented during
the initial electrophysiological study.
Postablation Atrial Fibrillation
Predictors of postablation atrial fibrillation were further evaluated
by multivariate Cox regression. Two variables were
significantly and independently associated with the onset of
postablation atrial fibrillation, a history of spontaneous atrial
fibrillation (relative risk 3.9, 95% confidence intervals 1.8 to 8.8,
P=0.001), and left ventricular ejection fraction
<50% (relative risk 3.8, 95% confidence intervals 1.7 to 8.5,
P=0.001). The additive risk associated with these 2
variables is illustrated in Figure 2
Early Versus Late Atrial Fibrillation
There was no difference in the clinical course of patients with early
compared with a late onset of postablation atrial fibrillation. Of the
13 patients with early-onset atrial fibrillation, 8 had episodes that
were persistent and recurrent beyond the initial month, requiring 1 or
more cardioversions. Of these 8 patients, 6 were ultimately placed on
amiodarone treatment and have subsequently remained in sinus
rhythm, and 2 underwent AV nodal ablation and permanent pacing. One
patient had a single episode of persistent atrial fibrillation and was
placed on a class I antiarrhythmic after cardioversion. The drug was
stopped after 1 month, and no further symptomatic episodes
have occurred. Four patients had infrequent self-terminating episodes
of atrial fibrillation (<24-hour duration) and were never cardioverted
or placed on antiarrhythmic drugs therapy. In 2 of these 4 patients,
occasional brief episodes persisted beyond 3 months.
The clinical course of the 15 patients with late-onset atrial
fibrillation was similar. Ten patients had episodes that were
persistent and recurrent beyond 1 month of initial onset, requiring 1
or more cardioversions. Of these 10 patients, sinus rhythm was
ultimately maintained with amiodarone in 7, sotalol in 1, a
class I antiarrhythmic in 1, and 1 patient underwent AV node ablation
and placement of a permanent pacemaker. Two patients were cardioverted
for a single episode of persistent atrial fibrillation, and after brief
antiarrhythmic therapy, remained in sinus rhythm without antiarrhythmic
drugs. The 3 other patients had only infrequent self-terminating
episodes of atrial fibrillation (<24-hour duration), and did not
receive antiarrhythmic drug therapy. In 1 of the 3 patients, occasional
brief episodes persisted more than 3 months after the initial
onset.
Overall, at the end of follow-up, 18 patients required long-term
therapy for control of symptomatic postablation atrial
fibrillation: antiarrhythmic therapy in 15 patients and ablation and
pacing in 3 patients. Twelve of 19 patients (63%) with left
ventricular dysfunction and a history of atrial
fibrillation required long-term therapy for postablation atrial
fibrillation. In contrast, only 6 of 91 (7%) with only 1 or neither of
these preprocedure risk factors required additional long-term therapy
(P<0.001).
Determinants of Atrial Fibrillation
Despite the relative infrequency of preablation episodes of atrial
fibrillation in individual patients, documentation of at least 1
spontaneous episode was one of the strongest predictors of postablation
atrial fibrillation. The importance of this risk factor has been noted
by other investigators in smaller series of
patients.5 8 13 14 Atrial fibrillation during
follow-up occurred in 45% of patients with previously documented
atrial fibrillation, and in only 12% of patients without a prior
history. Chen et al9 and Fischer et
al24 reported a 7% incidence of postablation
atrial fibrillation in patients without a history of this
arrhythmia. We also observed a relation between the laboratory
induction of atrial fibrillation at the time of ablation and the
subsequent occurrence of spontaneous atrial fibrillation, similar to
that of Philippon et al.5 However, this
variable was not predictive of outcome in the
multivariate analysis.
Collectively, these observations suggest that the occurrence of atrial
fibrillation after type I flutter ablation is primarily determined by
the presence of a preexisting structural and
electrophysiological substrate for this
arrhythmia.
Role of the Ablation Procedure
Large-tip catheters may produce more extensive lesions, which
potentially could be proarrhythmic. The use of these catheters for
ablation of type I flutter is
increasing.7 8 10 12 We used 8-mm-tip catheters
in 80% of study patients, but their use did not influence the
subsequent risk of atrial fibrillation. The presence or absence of
bidirectional isthmus conduction block at the end of the procedure also
had no influence on subsequent atrial fibrillation. Finally, we found
no significant differences in the determinants and clinical course of
atrial fibrillation occurring early after the procedure compared with a
later onset. Overall, the data from this study do not support a direct
proarrhythmic effect of radiofrequency energy applied in the annular
isthmus, compatible with the findings of Chiang and
coworkers.25
Indirect effects related to the procedure could play a role in the
early onset of atrial fibrillation in some patients.
Disturbances of autonomic function are common in the initial
weeks after radiofrequency ablation of the posterior
septum,26 most commonly loss of parasympathetic
tone. However, parasympathetic denervation associated with ablation may
potentially reduce the risk of atrial fibrillation, as recently
reported in an animal model autonomically mediated atrial
fibrillation.27 Diminished antagonism of
adrenergic tone associated with parasympathetic denervation could
facilitate atrial fibrillation, particularly those with an underlying
structural and electrophysiological
substrate.
Discontinuation of suppressive class I or III antiarrhythmic drugs may
play a potential role in the early appearance of atrial fibrillation in
some patients. However, this effect is unlikely to have been a major
influence in the study population. Only 41% of patients were treated
with class I or III antiarrhythmic drugs before ablation, and a history
of treatment with these drugs did not predict either early or late
atrial fibrillation. Only 6 patients required class I or III therapy
for suppression of recurrent atrial fibrillation before the ablation
procedure, and in each the drug was continued after procedure.
Relation of Type I Flutter to Atrial Fibrillation
The mechanistic relation between these 2 rhythms is incompletely
defined. Waldo and Cooper32 identified atrial
fibrillation as a common transitional rhythm before the onset of
spontaneous type I flutter after surgical coronary
revascularization. Similarly, Watson and
Josephson33 reported atrial fibrillation as a
frequent transitional rhythm during the induction of type I flutter by
high right atrial extrastimulus testing. Roithinger et
al34 examined the spontaneous conversion of
atrial fibrillation to type I flutter in humans. They identified a
transitional period of organized activation "streaming" in either
clockwise or counterclockwise direction along the lateral and
inferior annulus, which reliably predicted the onset and
rotational direction of type I flutter. Atrial fibrillation was also
identified as a common precursor to induced atrial flutter associated
with canine sterile pericarditis.35 The
transition from fibrillation to flutter was heralded by lengthening
lines of functional block, permitting the emergence of a large stable
reentrant circuit. These observations suggest a potentially important
role for atrial fibrillation in the genesis of type I atrial flutter.
In many patients, interruption of conduction through the
annular–eustachian ridge isthmus may prevent the organization of
atrial fibrillation into flutter. Depending on the extent of underlying
structural and electrophysiological
abnormalities, fibrillation may then self-terminate or persist.
In some patients, the converse relation may also exist. Atrial flutter
is occasionally observed to spontaneously disorganize into atrial
fibrillation in the electrophysiology laboratory. The right atrial
flutter circuit is postulated to play a critical role in the initiation
and maintenance of atrial fibrillation in some
patients.36 These observations may explain the
absence of recurrent fibrillation in some patients with previous
documentation of this rhythm. The absence of left
ventricular dysfunction and atrial enlargement may identify
those patients with infrequent prior atrial fibrillation who are least
likely to have symptomatic fibrillation during follow-up.
However, the conclusion that such patients are no longer at risk of
late atrial fibrillation may be premature until additional follow-up
has accrued.
The frequent coexistence of atrial fibrillation and flutter in the
study population, and the persistent risk of atrial fibrillation in a
substantial number of these patients despite long-term elimination of
flutter, suggest that atrial fibrillation as a trigger, rather than a
consequence, of type I flutter, may be more important than previously
recognized.
Limitations
Clinical Implications
However, these data have important implications for management.
Patients with both left ventricular dysfunction and a
history of atrial fibrillation should be advised of the risk of
recurrent symptoms and late atrial fibrillation. Continuation or
initiation of systemic anticoagulation may be appropriate, as well as
continuation of suppressive antiarrhythmic drug therapy. Some of these
patients may be considered for additional ablation procedures that
directly modify the substrate for further atrial
fibrillation.37 38 In patients without both risk
factors, a policy of observation without additional treatment appears
warranted.
Received December 8, 1997;
revision received March 4, 1998;
accepted March 17, 1998.
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© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Atrial Fibrillation After Radiofrequency Ablation of Type I Atrial Flutter
Time to Onset, Determinants, and Clinical Course
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The occurrence of atrial
fibrillation after ablation of type I atrial flutter remains an
important clinical problem. To gain further insight into the
pathogenesis and significance of postablation atrial fibrillation, we
examined the time to onset, determinants, and clinical course of atrial
fibrillation after ablation of type I flutter in a large patient
cohort. 
1 month) compared with a later onset. Atrial fibrillation was
persistent and recurrent, requiring long-term therapy in 18 patients,
including 12 of 19 (63%) with prior atrial fibrillation and left
ventricular dysfunction.
Key Words: atrial fibrillation • atrial flutter • catheter ablation
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Catheter ablation of
type I atrial flutter directed at a protected isthmus of atrial tissue
between the tricuspid valve annulus and the eustachian ridge, which
constitutes an obligate portion of the flutter circuit, has emerged as
an effective therapeutic option.1 2 3 4 5 6 7 8 9 10 11 12 During the
evolution of this procedure, diverse approaches have been taken to the
identification, location, and extent of target sites within the
annular–eustachian ridge isthmus. Initial experience with the end
points of flutter termination during radiofrequency energy application
and subsequent noninduction of type I atrial flutter were associated
with a variable risk of recurrence (10% to
30%).1 2 3 4 5 6 9 More recent reports indicate that
the production and demonstration of bidirectional conduction
block through the annular–eustachian ridge isthmus may lower this risk
considerably.7 8 10 11 12
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Study Population
The study population consisted of 110 consecutive patients who
underwent radiofrequency catheter ablation for recurrent type I atrial
flutter from July 1994 to June 1997. Each patient had recurrent flutter
or unacceptable side effects during 1 to 3 previous antiarrhythmic drug
trials. Previous episodes of atrial fibrillation were not considered a
contraindication to atrial flutter ablation if it they were infrequent
and not the predominant clinical arrhythmia (see
"Results"). Vigorous attempts were made to obtain documentation of
all prior atrial arrhythmias.
Written informed consent was obtained before
electrophysiological study and
radiofrequency catheter ablation in all patients.
Electrophysiological study was performed after
discontinuation of all antiarrhythmic drugs for at least 5 half-lives
except in patients treated with amiodarone at the time of the
procedure. Five multipolar catheters were inserted from the right and
left femoral veins and the right internal jugular vein. One quadripolar
catheter was positioned in the right atrial appendage (and repositioned
to the right ventricular outflow tract during ablation). An
octapolar catheter (Cordis-Webster) was positioned at the His bundle
and a decapolar catheter (Bard-USCI, 2–5-2 mm intervals) was
positioned in the coronary sinus, with the proximal electrode
pair located at the ostium. A deflectable quadripolar catheter (Cordis
Webster, 2–5-2 mm spacing) was positioned at the inferolateral
tricuspid annulus for pacing and recording from the lateral
isthmus.15 Annular activation during atrial
flutter or atrial pacing was assessed by either a second roving
deflectable quadripolar catheter, or a 20-electrode Halo catheter
(Cordis Webster, 2–7-2 mm intervals). Patients were studied in
the fasting state and sedated with intravenous midazolam
and fentanyl. An initial bolus of heparin (2000 U) was administered
after the insertion of catheters, followed by 1000 U/h until completion
of the study. Noninvasive blood pressure and oxygen saturation were
monitored continuously.
The method of ablation was anatomic, with the primary goal to
produce a line of conduction block between the tricuspid annulus and
the eustachian ridge/inferior vena cava. The ablation
catheters had distal electrodes of 4 mm (19 patients), 5 mm
(3 patients), or 8 mm (88 patients). The output of a
radiofrequency generator (Radionics) was delivered to the distal pole
of the ablation catheter and 1 or 2 posteriorly positioned adhesive
electrosurgical dispersive pads. Radiofrequency energy was applied with
an initial power of 30 W and was progressively increased to a maximum
of 45 W (4 to 5 mm tip) or 60 W (8 mm tip) during continuous
impedance monitoring. Energy application was continued for 30 to 60 ms
or until an impedance rise was observed. A line of sequential
overlapping lesions was given beginning at the tricuspid valve annulus,
with stepwise withdrawal of the catheter until the last lesion was
delivered at the eustachian ridge/inferior vena cava.
Radiofrequency energy was applied during flutter in 108 patients and
during sinus rhythm in the 2 patients without inducible or spontaneous
flutter at the time of the procedure.10 In the
initial 16 patients, only termination of flutter during radiofrequency
application and subsequent noninduction of type I flutter was used as
the procedural end point. In the subsequent 94 patients, including the
2 patients without inducible or spontaneous flutter at the time of the
procedure, an additional goal of ablation was to produce bidirectional
conduction block through the annular–eustachian ridge isthmus
(see below).
After catheter ablation, all patients underwent continuous ECG
monitoring for at least 24 hours before hospital discharge. Class I or
III antiarrhythmic drugs were not prescribed in 104 patients. In 6
patients, amiodarone had been initiated before the procedure
for control of atrial fibrillation and was continued. Outpatient
follow-up and electrocardiograms were performed at 1
month and at 4- to 6-month intervals thereafter. Patients were
encouraged to contact 1 of the investigators at any time for recurrent
symptoms or palpitations. Patients with palpitations underwent
additional Holter or transtelephonic ambulatory ECG monitoring.
Records from hospital and clinic visits at other institutions were
periodically reviewed for evidence of recurrent atrial
arrhythmias. Transtelephonic monitoring in
asymptomatic patients was not routinely performed. Patients
received aspirin 325 mg daily unless there existed an indication for
systemic anticoagulation with warfarin.
Counterclockwise type I atrial flutter was considered
present if counterclockwise activation around the tricuspid annulus
was demonstrated (as viewed in the left anterior oblique
projection) and concealed entrainment could be demonstrated from
annular pacing sites within the tricuspid valve-eustachian ridge
isthmus, with a postpacing interval similar to the flutter cycle
length.15 16 17 The surface ECG generally
demonstrated negative flutter waves in leads II, III, and aVF, and
isoelectric or positive flutter waves in lead V1.
Clockwise type I atrial flutter was considered present if clockwise
activation around the tricuspid annulus was demonstrated and concealed
entrainment could be demonstrated from annular pacing sites within the
tricuspid valve–eustachian ridge isthmus, with a postpacing interval
similar to the flutter cycle length. Flutter waves were generally
positive or biphasic in leads II, III, and aVF, with varying morphology
in V1. Atypical atrial flutter was defined as all
other flutters with a stable activation sequence and atrial intervals
in which participation of the isthmus in the circuit was excluded by
the above criteria.
Descriptive data are presented as mean±SD or as
frequencies. Univariate comparisons between variables
were made by Fisher's exact test for categorical variables and
unpaired t test for continuous variables. The actuarial
probability of freedom from atrial fibrillation after ablation was
calculated with the method of Kaplan and Meier.18
Baseline clinical and procedural variables were subsequently
subjected to multivariate analysis with a Cox
proportional hazards model and stepwise backward selection to identify
significant and independent predictors of time to onset of postablation
atrial fibrillation.19 Variables in the
initial model included age, sex, symptom duration, functional class,
history of atrial fibrillation, preablation treatment with class I or
III antiarrhythmic drugs, presence of structural heart disease, left
ventricular ejection fraction, presence of left
ventricular dysfunction, left ventricular
hypertrophy, atrial enlargement, presence of bidirectional
isthmus conduction block at the end of the procedure, number of
radiofrequency energy applications, catheter tip size, induced atrial
fibrillation and induced atypical flutter during
electrophysiological study, and
antiarrhythmic drug treatment at discharge. Survival analysis
and Cox regression were performed with Systat 7.0 statistical software
(SPSS Inc) A value of P<0.05 was considered
significant.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Study Population
Baseline patient characteristics are summarized in Table 1
. There were 86 men and 24 women with a
mean age of 62±14 years. Structural heart disease was present in
71 patients (65%). Coronary artery disease was present in
33 patients (including 15 with remote surgical
revascularization), nonischemic
cardiomyopathy in 16 patients, valvular
heart disease in 13 patients, congenital heart disease in 5 patients,
right ventricular cardiomyopathy in 2
patients, and hypertrophic cardiomyopathy in 2
patients. The mean left ventricular ejection fraction was
50±14%, and left ventricular dysfunction was present
in 44 patients (40%). Atrial enlargement was present in 54
patients (49%): left atrial only in 26, right atrial only in 13, and
biatrial in 15. The mean duration of symptoms before flutter ablation
was 25±36 months (range 1 to 161 months). Forty-five patients (41%)
had received at least 1 class I or III antiarrhythmic drug before the
ablation procedure, including amiodarone in 15 patients. The
remaining patients received 1 or more trials of ß-blockers,
Ca2+ channel blockers, and/or digoxin.
View this table:
[in a new window]
Table 1. Patient
Characteristics
Type I atrial flutter could not be induced at the end of the
procedure in 108 of 110 patients. In 18 of 108 patients, termination of
atrial flutter during radiofrequency application and noninduction of
atrial flutter at the end of the procedure were the only criteria for
success, including 4 patients in whom bidirectional isthmus conduction
block could not be achieved. In the remaining 90 of 108 patients,
including the 2 in whom atrial flutter could not be induced at
baseline, both bidirectional isthmus conduction block and noninduction
of type I atrial flutter were demonstrated at the end of the procedure.
The mean number of radiofrequency applications was 14±8 (median 12).
More radiofrequency energy applications were required for patients with
right atrial enlargement (19±7 versus 12±7, P=0.027).
All patients were followed for a minimum of 4 months, with a mean
follow-up duration of 20.1±9.2 months. One of the 2 patients with
persistently inducible flutter continued to have frequent spontaneous
episodes and underwent AV nodal ablation and implantation of a
permanent pacemaker. Type I atrial flutter recurred in 5 of 108
patients with successful ablation, at 1, 2, 4, 18, and 22 months,
respectively. Type I flutter recurred in 3 of 18 patients (17%) with a
procedure judged to be successful by noninduction alone, and in 2 of 90
patients (2.2%, P=0.03) with bidirectional isthmus
conduction block demonstrated at the end of the procedure.
Spontaneous atrial fibrillation occurred in 28 of 110 patients
(25%) during follow-up. In 13 of these patients (46%), atrial
fibrillation occurred within the first month after ablation (early
atrial fibrillation), and the remainder occurred from 2 to 22 months
after the procedure (late atrial fibrillation). The cumulative
probability of postablation atrial fibrillation was 12% at 1 month,
23% at 1 year, and 30% at 2 years (Figure 1). By univariate
analysis, several preablation clinical variables known to
be associated with atrial fibrillation in other populations
significantly influenced the probability of atrial fibrillation during
follow-up. Patients with postablation atrial fibrillation were
significantly older and had a greater frequency of preablation atrial
fibrillation, left ventricular dysfunction, and atrial
elargement (Table 2). The risk of atrial
fibrillation was similar whether atrial enlargement was left atrial
alone, right atrial alone, or biatrial. For the purpose of subsequent
analysis, atrial enlargement was considered as a single
variable. Of procedural variables, only the induction of atrial
fibrillation during electrophysiological
testing significantly influenced the likelihood of subsequent
spontaneous atrial fibrillation.
View larger version (15K):
[in a new window]
Figure 1. Kaplan-Meier cumulative probability of survival
free of atrial fibrillation during follow-up. Numbers in italics
indicate the number of patients at risk at various points during
follow-up.
View this table:
[in a new window]
Table 2. Univariate Predictors of Postablation Atrial
Fibrillation .
In patients with normal ventricular function and no history
of atrial fibrillation, postablation atrial fibrillation was uncommon
(4 of 41 patients [10%]). Patients with only 1 of the 2
variables (left ventricular dysfunction alone or
previous atrial fibrillation alone) were at intermediate risk of
postablation atrial fibrillation (20%). Patients with both findings
had a high likelihood of developing postablation atrial fibrillation
(14 of 19 patients [74%]).
View larger version (39K):
[in a new window]
Figure 2. Risk of atrial fibrillation during follow-up as a
function of a prior history of atrial fibrillation and left
ventricular dysfunction. Bars indicate the proportion of
each of 4 patient subgroups that developed atrial fibrillation.
Numerical proportions are in italics within each bar. AF indicates
atrial fibrillation; LVEF, left ventricular ejection
fraction.
We also evaluated potential differences in the determinants and
clinical course of atrial fibrillation occurring early (within 1 month
of ablation) compared with onset later during follow-up. None of the
clinical, procedural, or follow-up characteristics differed between the
2 groups of patients (Table 3). Patients
with early atrial fibrillation had a slight excess of structural heart
disease, preablation atrial fibrillation, and left
ventricular hypertrophy. These trends were not
statistically significant.
View this table:
[in a new window]
Table 3. Comparison of Early vs Late Atrial
Fibrillation
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
Major Findings
This study confirms previous observations of a moderately high
incidence of symptomatic postablation atrial fibrillation
(30% probability at 2 years) despite a low recurrence of type
I atrial flutter (5% overall, 2.2% in patients with bidirectional
isthmus conduction block). Although episodes of atrial fibrillation
were often transient, in two thirds of patients the episodes were
persistent and recurrent, ultimately requiring long-term therapy. Risk
could be stratified by the presence or absence of 2 independent and
significant predictors, prior atrial fibrillation (3.9-fold increased
risk), and left ventricular dysfunction (3.8-fold increased
risk). The presence of both these clinical characteristics identified a
high-risk group of which 74% developed atrial fibrillation during
follow-up. Patients with only 1 of these characteristics were at
intermediate risk (20%), and those without prior atrial fibrillation
and with normal ventricular function were at lowest risk
(10%) for subsequent atrial fibrillation. Further, patients in the
high-risk group accounted for the majority of patients requiring
long-term therapy for control of recurrent fibrillation. Although the
initial onset of atrial fibrillation was greatest in the first month
after ablation, neither the clinical course nor risk factors differed
by time of onset.
Age,20 21 left ventricular
dysfunction,21 22 23 and atrial
enlargement21 22 23 have each been related to the
spontaneous occurrence of atrial fibrillation in epidemiologic studies;
thus their significance as univariate predictors of
postablation atrial fibrillation in this study is not surprising.
Structural heart disease alone, identified by others as a
univariate predictor of atrial
fibrillation,5 8 14 did not influence the risk of
atrial fibrillation in this study. However, left
ventricular dysfunction and atrial enlargement may
represent more advanced structural disease and were significant
predictors. Atrial enlargement was also identified as a risk factor in
the study of Nakagawa and colleagues.8
The frequent onset of atrial fibrillation early after type I
flutter ablation raises concerns about a potential proarrhythmic effect
of the procedure itself. The number of radiofrequency applications in
this study was similar to that reported by others using similar
techniques.5 10 11 24 We found a trend, not
statistically significant, for more radiofrequency applications in
patients with subsequent atrial fibrillation, similar to the findings
of Philippon et al.5 In contrast, Nakagawa and
colleagues8 reported that significantly more
radiofrequency applications were given in patients who subsequently
developed atrial fibrillation. In our patients, only right atrial
enlargement was significantly associated with a greater number of
radiofrequency energy applications, reflecting both greater technical
difficulties and a larger area required for ablation in dilated atria.
The trend toward more radiofrequency applications in patients who
subsequently develop atrial fibrillation may reflect the influence of
this substrate.
Ambulatory monitoring in patients with atrial flutter frequently
documents the coexistence of atrial
fibrillation.28 29 Precise epidemiologic data
regarding the prevalence of this finding are not yet available. In
addition, atrial flutter may become more frequent, stable, or appear
for the first time during antiarrhythmic drug therapy of atrial
fibrillation.28 30 Thus the high frequency of
atrial fibrillation in patients referred for type I flutter ablation
(40% in the present series, and 20% to 56% of previous
series5,8,10,13,24) is not unexpected. It is
possible that the actual prevalence of atrial fibrillation in patients
with type I flutter may be even higher, as symptomatic
episodes are more likely to be documented. Page and
coworkers31 reported a high ratio of
asymptomatic to symptomatic episodes in these
patients.
Although extensive electrocardiographic documentation of
symptomatic arrhythmias was available before
ablation and was routinely obtained after ablation, the frequency of
atrial fibrillation both before and after the procedure may be
underestimated. Asymptomatic atrial arrhythmias are
frequent in this population31 and no attempt was
made to prospectively identify asymptomatic
arrhythmias either before or after the procedure by systematic
Holter or transtelephonic monitoring. While the study population was
heterogeneous and relatively large, the total number of
early and late occurrences of postablation atrial fibrillation was
relatively small; it is possible that in even larger groups of patients
or with longer follow-up, variables predictive of early versus late
atrial fibrillation may be identified. Patients with atrial flutter who
had a history of frequent atrial fibrillation were excluded from this
study, and patients in whom flutter occurred while taking
antiarrhythmic drugs to suppress atrial fibrillation comprised only a
small minority (5%). The incidence and predictors of postablation
atrial fibrillation may differ in populations with more frequent
episodes of preablation atrial fibrillation.
In this study, a small group of patients with both left
ventricular dysfunction and a history of atrial
fibrillation (17% of the study population) were responsible for 67%
of all postablation atrial fibrillation requiring long-term treatment.
These findings do not necessarily imply that such patients are
inappropriate candidates for catheter ablation of type I flutter. In
many, atrial fibrillation was suppressed by antiarrhythmic therapy that
had previously been ineffective in suppressing atrial flutter;
elimination of flutter resulted in symptomatic improvement
and facilitated pharmacologic control of the ventricular
rate. In addition, a small number of these high-risk patients remain
without atrial fibrillation and on no antiarrhythmic therapy during
initial follow-up.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
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Stein JB, Calisi CM, Ibarra M. Radiofrequency catheter ablation for the
treatment of human type 1 atrial flutter. Circulation. 1992;86:1233–1240.
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