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(Circulation. 2000;101:995.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Identification of the Substrate of Atrial Vulnerability in Patients With Idiopathic Atrial Fibrillation
From the Heart-Lung Institute (H.R., R.N.W.H., F.H.M.W., A.E., E.O.R.d.M.), University Medical Center Utrecht, Utrecht, the Netherlands; Interuniversity Cardiology Institute of the Netherlands (J.M.T.d.B.), Utrecht, the Netherlands; and St Antonius Hospital (E.F.D.W.), Nieuwegein, the Netherlands.
Correspondence to Hemanth Ramanna, MD, Heart-Lung Institute, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands.
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Abstract |
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Background—Experimental studies have shown that atrial fibrillation (AF) causes remodeling, which facilitates AF perpetuation. AF may also, however, occur in patients without remodeling and underlying structural cardiac disease. The substrate for enhanced vulnerability in these patients is unknown.
Methods and Results—We studied 43 patients without structural heart disease: 18 patients with documented sporadic paroxysmal AF and 25 control patients without AF. In each patient, a decapolar catheter was positioned against the right atrial free wall, and a quadripolar catheter was positioned in the right atrial appendage. Unipolar electrograms were recorded. Atrial vulnerability was assessed according to an increasingly aggressive stimulation protocol. Mean local fibrillatory interval (FI) was used as an index of local refractoriness. Spatial dispersion of refractoriness was assessed through the calculation of the coefficient of dispersion (CD), which was defined as the SD of mean local FI expressed as a percentage of the mean FI. In the AF group, AF was induced with a single extrastimulus in 16 of 18 patients; the CD was 5.4±2.6, and the mean FI was 164±29 ms. In the control group, AF could be induced only with more aggressive pacing in 23 of the 25 patients; the CD was 1.4±0.7 (P<0.0001), and the mean FI was 175±26 ms (NS).
Conclusions—Patients with idiopathic AF showed increased dispersion of refractoriness, which may be the substrate for the observed enhanced inducibility and spontaneous occurrence of AF.
Key Words: atrium • fibrillation • electrophysiology
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Atrial fibrillation (AF) may occur in patients without structural cardiac disease. In animal models, sustained AF causes remodeling of the atria, which facilitates AF perpetuation.1 2 In patients, however, AF may also occur without previous remodeling. The initiation of AF requires a trigger, which often is atrial tachycardia or atrial premature depolarizations.3 4 Not all patients with atrial arrhythmias, however, will develop AF; therefore, the presence of a trigger alone may not lead to AF. A substrate for atrial propensity to fibrillation (ie, atrial vulnerability) may also be required for AF initiation.
Atrial vulnerability may be increased in the presence of the dispersion of electrophysiological properties, as suggested on the basis of experimental data.5 6 With the use of epicardial multielectrode recordings during cardiac surgery, Ramdat Misier et al7 found increased dispersion of refractoriness and shortened refractory periods in patients with idiopathic AF compared with control patients. However, these patients had frequent AF episodes, so it is unclear whether the observed electrophysiological changes in dispersion were the cause or the result of AF.
The aim of the present study was to assess whether patients with idiopathic paroxysmal AF without electrophysiological remodeling have specific atrial electrophysiological properties that might increase the propensity to AF in comparison with control subjects.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients
A total of 245 patients (age <60 years) undergoing an electrophysiological study at the Heart-Lung Institute for supraventricular tachycardia were screened for inclusion on the basis of the criteria listed in Table 1
.
Informed consent was obtained from the patients, and the study was
approved by the hospital review board. All patients had a physical
examination and underwent ECG, echocardiography,
and biochemical and hematological testing to exclude structural heart
disease and conditions with potential effects on cardiac
hemodynamic or
electrophysiological functions. Telemetry
was performed for 
24 hours before the
electrophysiological study. Of these 245
patients, 23 had prior documented AF, 4 were excluded due to an
abnormal echocardiogram, and 1 was excluded due to alcoholism. Thus, 18
patients with AF remained, and they were assigned to the AF group. Of
the patients without AF, 25 were randomly selected and assigned to the
control group. The study was carried out during the routine
electrophysiological investigation before
catheter ablation of the tachycardia.
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AF Group
The 18 patients in the AF group (15 men and 3 women, mean age
33.1±9.2 years, maximum age 46 years) had prior paroxysmal AF
episodes. ECG documentation of 1 episode was required for inclusion
in the study, and each patient was specifically questioned about the
duration and onset of previous episodes. All patients were able to
distinguish AF episodes from their regular supraventricular
tachycardia. A rapid irregular heartbeat was interpreted as
an AF episode. These patients had experienced a median of 1 (mean 1.8,
SD 2.5, range 1 to 12) episode of AF with a median duration of 1 hour
(range 0.25 to 4 hours). The last spontaneous symptomatic
episode of AF preceded the
electrophysiological study by a median of
162 days (range 6 to 529 days). None of the patients had AF episodes
during the telemetric observation period. In this group, all patients
had an accessory atrioventricular pathway, of which 2
were concealed (pathway location: 12 left free wall, 2 left
posteroseptal, 2 right posteroseptal, 1 right
anteroseptal, and 1 parahisian).
Control Group
The 25 control patients (17 men and 8 women, mean age 33.5±11.0
years, maximum age 52 years) did not have a history of AF or episodes
of irregular heartbeat. There were 18 patients with accessory pathways,
of which 2 were concealed (accessory pathway location: 14 left free
wall, 1 left posteroseptal, 2 right free wall, and 1
parahisian), and 7 patients with atrioventricular nodal
reentrant tachycardia (AVNRT). Telemetry did not reveal any
AF episodes.
Study Protocol
All patients were studied in the fasting, nonsedated state.
After right femoral venous access was obtained, 2 electrode catheters
(electrode spacing 5 mm) were positioned in the right atrium, a
decapolar catheter (Bard USCI) was positioned at the lateral free wall,
and a quadripolar catheter (Bard USCI) was positioned in the appendage
as shown (Figure 1). The position of the
decapolar catheter was selected to maximize the number of electrodes
with good tissue contact and to minimize the effects of far-field
interference from ventricular activity on the unipolar
electrogram. The catheters were repositioned until a stable position
with 8 unipolar electrograms of >0.5 mV was obtained during sinus
rhythm. Twelve unipolar electrograms were recorded (gain 2 mV/cm,
filter 0.05 to 500 Hz) (10 from the decapolar and 2 from the proximal
pair of the quadripolar catheter) with the use of an
electrophysiological recording
system (Cardiolab; Prucka Engineering).
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The inducibility of AF was assessed through programmed stimulation with
the use of unipolar cathodal pacing (pulse width 2 ms). Pacing
consisted of a 4-stage, progressively aggressive stimulation protocol
to achieve AF with a duration of 1 minute. Stage 1 consisted of
pacing at twice diastolic threshold current with an 8-pulse
drive train and 1 extrastimulus starting at the tip electrode of the
decapolar catheter. The extrastimulus interval
S1S2 of 100 ms was
incremented in steps of 5 ms until atrial capture occurred. If AF with
duration of >1 minute was not obtained in this manner, stage 1 was
successively repeated at all of the other electrodes. If AF was not
induced, the next stage was performed. Stage 2 consisted of pacing at 4
times diastolic threshold current with an 8-pulse drive
train and 1 extrastimulus from the tip electrode of the quadripolar
catheter. Stage 3 was the same as stage 2 but with 2 extrastimuli.
Stage 4 consisted of multiple 5-second ramp bursts at a cycle length of
100 to 50 ms at 4 times diastolic threshold current from
the tip electrode of the quadripolar catheter. Other induced types of
tachycardia were pace terminated immediately, and the
pacing protocol was interrupted for 1 minute after these episodes as
well as after AF episodes that lasted for <1 minute. For this study,
AF with a duration of >1 minute was considered sustained AF. If AF
persisted beyond 5 minutes, electrical cardioversion was performed.
Data Analysis
The segment between 15 and 30 seconds after AF onset was used
for electrogram analysis. Fibrillation intervals were measured
through the detection of the intrinsic negative deflections with
negative slopes of >0.5 mV/s.7 For each recording
site, histograms of fibrillatory intervals were plotted. Undersensing
of intrinsic deflections, resulting in multiples of fibrillatory
intervals, was detected through the observation of secondary peaks in
the histogram. Such intervals were discarded, as described by Opthof et
al.8 For each recording site, the sum of all
discarded intervals was calculated. If this sum exceeded 4 seconds, the
electrogram recording site was excluded from further
analysis.
The mean fibrillatory intervals were calculated for each site to serve as an index for the local refractory period.9 The average and SD values of these indices were calculated. Spatial dispersion was defined as the coefficient of dispersion (CD) and calculated as the SD of the mean fibrillatory intervals expressed as a percentage of the mean fibrillatory interval: [(SDx100)/mean fibrillatory interval].7
Statistical Analysis
The AF group was compared with the control group. Categorical
variables were compared with the use of the
2 test, and mean values were compared with the
use of Student’s t test. A probability value of 0.05 was
considered statistically significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The measurement of fibrillatory intervals resulted in histograms such as that shown in Figure 2
. The mean
fibrillatory intervals detected at all recording sites were
displayed as shown in Figure 3. The range
of local mean fibrillatory intervals indicates the spatial dispersion
measured in 1 patient. It is readily observed that in the patient with
prior AF, there is more spatial dispersion of mean fibrillatory
intervals than in the control patient without AF (Figure 3).
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AF Group
Baseline data are given in Table 2.
AF was induced with a single extrastimulus at twice
diastolic threshold current in 16 of 18 patients. In the
other 2 patients, only nonsustained AF episodes (2 per patient) could
be induced, with a mean duration of 28±4.5 seconds; more aggressive
pacing was required to obtain sustained AF. Adequate recordings
with a <4-second dropout were obtained from an average of 9 (range 7
to 11) electrodes per patient. Of these 15-second recordings, a
mean of 1.16 (range 0.15 to 2.70) seconds were excluded due to
inadequate dV/dt.
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The mean number of measured fibrillatory intervals per
recording site was 85±20. The overall mean CD value for the AF
group was 5.4±2.6, and the overall mean fibrillatory interval was
164±29 ms. In 3 patients, the mean fibrillatory interval was between
200 and 225 ms. However, the irregularity and polymorphic character
of the electrograms, with cycle length variations of 20% of the mean
cycle length, were compatible with AF.
Control Group
The baseline and electrophysiological
parameters of the control patients are given in Table 3. Sustained AF was induced with a single
extrastimulus at twice diastolic threshold current in only
2 of 25 patients. Nonsustained AF could be induced in an additional 2
patients (2 and 3 episodes, mean duration 17±5.2 seconds). In these 2
and the remaining 21 patients, more aggressive pacing was required to
obtain sustained AF, with 17 patients requiring burst pacing at 4 times
diastolic threshold. Adequate recordings with
<4-second dropout were obtained from an average of 9 (range 8 to 12)
electrodes per patient. Of these 15-second recordings, a mean
of 1.62 (range 0.14 to 2.91) seconds were excluded due to inadequate
dV/dt.
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The mean number of measured fibrillatory intervals per
recording site was 80±24. The overall mean CD value for the
control group was 1.4±0.7, and the overall mean fibrillatory interval
was 175±26 ms. In 4 patients, the mean fibrillatory interval was
between 200 and 225 ms. However, the irregularity and polymorphic
character of the electrograms, with cycle length variations of 20%
of the mean cycle length, were compatible with AF.
In the control group, the patients with Wolff-Parkinson-White (WPW) syndrome had a mean CD value of 1.4±0.6 and an overall mean fibrillatory interval of 173±27 ms. In the patients with AVNRT, these values were 1.5±1.0 and 182±27 ms, respectively. These subgroups did not differ significantly.
Comparison Between AF and Control Groups
The electrophysiological
parameters are given in Table 4. There were no significant differences
in left atrial dimensions, baseline heart rate, and pacing thresholds.
AF was induced more easily, with 1 extrastimulus, in the AF group than
in the control group (P<0.0001), as shown in Figure 4. The average CD value was significantly
higher in the AF group than in the control group with only minimal
overlap (P<0.0001), as shown in Figure 5A.
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Mean fibrillatory intervals did not differ significantly between the
groups (P=0.17), as shown in Figure 5B
. The shortest
preexcited RR interval (ie, refractoriness of accessory pathway) and
the average heart rate during AF did not differ between the groups.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the present study, patients without demonstrable structural heart disease and with short-lasting and infrequent symptomatic episodes of AF had increased spatial dispersion of refractoriness. This increased dispersion could not be attributed to electrical remodeling because most patients had experienced only a single, short symptomatic episode of AF that occurred a long time (median 162 days, minimum 6 days) before the electrophysiological study. Telemetric monitoring also did not reveal any asymptomatic episodes for
24 hours before the study. In addition, in the AF group, the mean
fibrillatory intervals were not significantly shorter than those in the
control group. The increased dispersion of refractoriness was
associated with enhanced atrial inducibility of AF, as would be
expected on the basis of experimental findings.5 10
Increased dispersion of refractoriness thus may be a major predisposing
factor for the initiation of AF.
Dispersion and Remodeling
Several recent experimental studies in animals have shown that AF
causes shortening of refractoriness,1 2 10 11 an increase
in atrial inducibility of AF,1 10 and an increase in
dispersion of refractoriness.10 11 With the use of
intraoperative epicardial recordings, Ramdat Misier et
al7 found increased spatial dispersion of refractoriness
in patients undergoing surgery for AF. These patients had frequent
symptomatic AF episodes for which they were undergoing
surgery, and the time from the last AF episode to the measurements was
not known. It is conceivable that these patients had long-standing AF
that caused atrial remodeling, as suggested by their significantly
shorter average fibrillatory intervals.1 2 Thus, on the
basis of their study, it was unclear whether the increased dispersion
was the cause or the result of AF. These mentioned findings in
experimental models1 2 10 11 and in patients7
underlie the importance of the exclusion of the effects of remodeling
when studying the propensity for AF at an early stage of idiopathic
AF.
Substrate for Increased Dispersion
The pathophysiology of the increased dispersion of refractoriness
is not known. Atrial fibrosis, as found in structural heart disease and
in the elderly,12 may give rise to electrical
inhomogeneity. Our patients did not have identifiable structural heart
disease, and their mean age was 33 years. Atrial dilatation may be
another causative factor,13 but
echocardiography did not demonstrate atrial
enlargement in our patients and Doppler-derived measurements did
not show increased atrial pressure. Inhomogeneity of autonomic
innervation may be another mechanism for increased dispersion of
refractoriness as shown by Olgin et al14 in a canine model
of sympathetic denervation.
AF and WPW Syndrome
Most of the patients in the present study had WPW syndrome.
Branched accessory pathways causing microreentry have been suggested as
causative factors for AF. Fujimura et al15 found that in
patients with WPW syndrome, AF usually was initiated in the right
atrium regardless of accessory pathway location. In addition, Wathen et
al16 did not find any changes in atrial
electrophysiological properties after
accessory pathway ablation. In our study, the measurements and
induction of AF were performed in the right atrium, whereas the
accessory pathway was left-sided in most patients (AF group: 14 of 18,
control group: 15 of 18). Moreover, the control group included a large
number of patients who also had WPW syndrome. These patients had low
dispersion and low inducibility despite their accessory pathway. The
anterograde refractory period of the accessory pathway did not
differ significantly between these patients and those in the AF group,
and the average heart rate during AF was comparable. Therefore, a
hemodynamic cause for the difference in dispersion
between these patients seems unlikely. In addition, we studied control
patients with AVNRT (ie, without an atrioventricular
bypass tract). Dispersion in these patients did not differ from that in
control patients with WPW syndrome. The results of our study suggest
that in patients with prior paroxysmal AF, the atria had abnormal
electrophysiological properties that could
not be directly attributed to the accessory pathway.
Study Limitations
In the AF group, the incidence of AF episodes was quantified
through questioning of patients about symptoms of irregular heartbeat.
Asymptomatic AF episodes therefore could not be entirely
excluded. In the AF group, however, 16 of 18 patients also had
preexcitation and rapid ventricular rates during AF.
Therefore, in this subset of patients, AF episodes would be more likely
to cause symptoms than they would in the general population. In
addition, AF (symptomatic or asymptomatic)
during the 24-hour period before the study was excluded through the use
of telemetric monitoring.
One may question the use of mean fibrillatory intervals as the most appropriate method to estimate local refractoriness. Previous experimental studies by Allessie et al17 have demonstrated an excitable gap during AF. Nevertheless, several studies have demonstrated a strong correlation between local refractory period as measured with extrastimuli and the local mean fibrillatory interval.7 9 18 19
Data were obtained from a small portion of the right atrium with a
relatively limited number of electrodes. The septum and left atrium
were not investigated. In 3 AF patients, the CD value was within the
normal range (
3.0). This may be due to catheter positioning;
dispersion may have been increased at other positions.
Conclusions
Patients with idiopathic AF had increased spatial dispersion of
refractoriness unrelated to electrical remodeling. This increased
dispersion appeared to be the substrate for the enhanced atrial
vulnerability.
Received July 12, 1999; revision received September 21, 1999; accepted October 7, 1999.
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B. J.J.M Brundel, J. Ausma, I. C van Gelder, J. J.L Van Der Want, W. H van Gilst, H. J.G.M Crijns, and R. H Henning Activation of proteolysis by calpains and structural changes in human paroxysmal and persistent atrial fibrillation Cardiovasc Res, May 1, 2002; 54(2): 380 - 389. [Abstract] [Full Text] [PDF]
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 S.P Fynn, D.M Todd, W.J.C Hobbs, K.L Armstrong, and C.J Garratt Role of dispersion of atrial refractoriness in the recurrence of clinical atrial fibrillation. A manifestation of atrial electrical remodelling in humans? Eur. Heart J., October 1, 2001; 22(19): 1822 - 1834. [Abstract] [PDF]
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H. Ramanna, A. Elvan, F. H. M. Wittkampf, J. M. T. de Bakker, R. N. W. Hauer, and E. O. Robles de Medina Increased dispersion and shortened refractoriness caused by verapamil in chronic atrial fibrillation J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1403 - 1407. [Abstract] [Full Text] [PDF]
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Z. Li, E. Hertervig, S. Yuan, Y. Yang, Z. Lin, and S. B. Olsson Dispersion of atrial repolarization in patients with paroxysmal atrial fibrillation Europace, January 1, 2001; 3(4): 285 - 291. [Abstract] [PDF]
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