(Circulation. 2000;102:1807.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Electrical Remodeling of the Atria Associated With Paroxysmal and Chronic Atrial Flutter
Presented in part at NASPE 20th Annual Scientific Sessions, Toronto, Canada, May 1999.
From Royal Melbourne Hospital Department of Cardiology and the University of Melbourne, Department of Medicine (P.B.S., J.M.K.), Melbourne, Australia.
Correspondence to Dr Jonathan Kalman, Department of Cardiology, Royal Melbourne Hospital, Grattan St, Parkville, Melbourne, Victoria 3050 Australia. E-mail jon.kalman{at}nwhcn.org.au
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Abstract |
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Background—Atrial electrical remodeling may be important for the initiation and perpetuation of atrial arrhythmias. Whether paroxysmal atrial flutter (AFL) and chronic AFL cause electrical remodeling of the atria has not been conclusively determined.
Methods and Results—Before radiofrequency ablation of paroxysmal
AFL, 15 patients in sinus rhythm were evaluated under autonomic
blockade. Lateral right atrial (LRA) effective refractory periods
(ERPs) at 600 and 450 ms were measured before and at 1-minute intervals
for 10 minutes after spontaneous or pace termination of a 5- to
10-minute period of induced AFL. In 10 patients with chronic AFL, LRA,
septal, and coronary sinus (CS) ERPs and corrected sinus node
recovery times (cSNRTs) at 600 and 450 ms were measured under autonomic
blockade 15 minutes, 30 minutes, and 3 weeks after termination of
chronic AFL by ablation. In the paroxysmal AFL group, LRA ERPs
decreased by 18% at 600 ms and 12% at 450 ms (P<0.01)
after induced AFL and recovered to baseline over 
5 minutes. Atrial
fibrillation developed during AFL in 3 patients and during ERP testing
in 3 patients when refractoriness was at its nadir. In the chronic AFL
group, LRA, septal, and CS ERPs at 3 weeks were significantly greater
than at 15 and 30 minutes after termination of chronic AFL at both
cycle lengths (P<0.01). Three weeks after ablation,
cSNRT decreased 35% at 600 ms (P<0.05) and decreased
44% at 450 ms (P<0.05). Both ERPs and cSNRTs measured
15 and 30 minutes after ablation of chronic AFL were not significantly
different.
Conclusions—Both paroxysmal AFL and chronic AFL cause reversible electrical remodeling of the atria but demonstrate different time courses of recovery.
Key Words: ablation • fibrillation • atrial flutter • remodeling
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Electrical remodeling of the atrium has been clearly demonstrated both in animal models and in humans.1 2 3 4 Experimental studies have shown that atrial fibrillation (AF) begets AF predominantly because of a fall in atrial effective refractory periods (ERPs), suggesting that this may contribute to the development of the chronic form of the arrhythmia.1 2 Several minutes of pacing-induced AF in humans is sufficient to abbreviate atrial refractoriness for up to 8 minutes, facilitating the subsequent induction and perpetuation of AF.3 4 However, these studies have been performed mostly in patients without clinical AF, and there is a relative lack of data demonstrating the phenomenon of electrical remodeling in humans with paroxysmal or chronic atrial arrhythmias.
Atrial flutter (AFL) accounts for 15% of
supraventricular arrhythmias and frequently
coexists with or precedes AF.5 6 7 8 9 10 Recent data suggest
that chronic AFL may also produce electrical remodeling in a fashion
similar to that observed with AF, but whether this is a reversible
phenomenon and whether paroxysmal AFL is also associated with
electrical remodeling are unknown.11 This is of importance
because it raises the hypothesis that AFL might contribute to the
development and/or maintenance of AF by way of electrical
remodeling.
We prospectively evaluated the effects of both paroxysmal and chronic AFL on atrial electrophysiological properties to determine whether this arrhythmia produces electrical remodeling. Studies were performed in patients undergoing radiofrequency ablation (RFA) of AFL.
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Methods |
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Paroxysmal AFL Group
The study population comprised 15 patients undergoing RFA of paroxysmal AFL (Figure 1
). Demographic
details are presented in Table 1. Antiarrhythmic drugs, including
calcium blockers, were ceased >5 half-lives before ablation, and no
patients received amiodarone in the 6 months before study.
Patients gave written informed consent to the study, which was approved
by the Board of Medical Research of Royal Melbourne Hospital.
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Paroxysmal AFL Definition
Paroxysmal AFL was defined by a history of 
3 episodes of
typical AFL confirmed by its characteristic ECG
appearance.6 12 13 Patients in this group had reverted
spontaneously or were overdrive paced or electrically cardioverted >1
month before RFA. All patients were in sinus rhythm immediately before
ablation, and no patient described symptoms referable to paroxysmal AFL
in the 4 weeks before ablation. Paroxysmal AFL duration was defined as
the time between the initial diagnosis and the time of ablation.
Electrophysiological Study
Intracardiac electrodes were placed in the lateral right
atrium (LRA), coronary sinus (CS), His bundle, and tricuspid
annulus positions as previously described.12 13 An 8F
ablation catheter was positioned in the subeustachian isthmus for
entrainment mapping and RFA. Pharmacological autonomic blockade was
administered (atropine 0.04 mg/kg IV and propranolol 0.2
mg/kg IV) over 10 minutes.14 The doses of atropine and
propranolol were 2.4±0.6 and 12.5±3.0 mg,
respectively.
Ten minutes after autonomic blockade, ERPs were evaluated from the LRA and distal CS at twice the diastolic threshold (for a pacing threshold of <2 mA) at cycle lengths (CLs) of 600 and 450 ms.1 3 Baseline ERPs were measured 3 times and averaged. The ERP was determined by use of an 8-beat S1 drive and an incremental technique starting with an S2 coupling interval of 160 ms and increasing by 5 ms. This technique was used to minimize the possibility of inducing AF or AFL. ERP was defined as the longest S1S2 coupling interval failing to propagate to the atrium. Archived digital images were used to ensure stable catheter positioning during the study.
AFL Induction
After baseline ERP measurement, typical AFL was induced by
pacing from the CS.13 Incremental pacing was performed
until unidirectional block in the isthmus was demonstrated by a change
in activation sequence on the tricuspid annulus catheter (Figure 2). Pacing was discontinued immediately
when this was observed. AFL was induced without the development of
transitional AF so that the effects of AFL on refractoriness could be
evaluated in isolation.5 6 15 Patients in whom AFL could
not be induced (n=4) or in whom AF developed during the induction
protocol (n=2) were excluded. The flutter mechanism was confirmed on
the basis of counterclockwise activation sequence in the RA in the
frontal plane, manifest entrainment from the high right atrium, and
concealed entrainment from the isthmus.6 12 13
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CSp
indicates CS distal to proximal; H1–2 , halo catheter in low LRA,
through H19–20, halo catheter in high RA.
AFL Termination and ERP Assessment
After 10 minutes of AFL, the arrhythmia was pace
terminated with a 1- to 8-beat train delivered from the isthmus at a CL
40 to 60 ms below the flutter CL. Because pace termination of AFL may
be associated with intra-atrial reentry lasting 1 second (considered
unlikely to have a significant effect on refractoriness), a
transitional atrial rhythm lasting <1 second before termination of AFL
did not exclude patients from subsequent evaluation (Figure 3). Patients developing longer-lasting AF
during pace termination were excluded from further assessment because
of the known effects of AF on atrial refractoriness
(n=2).3 4 If AFL terminated spontaneously 5 to 10 minutes
after its initiation, ERP measurements were made at that time.
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On reversion to sinus rhythm, ERPs from the LRA were evaluated at
alternating drive CLs of 600 and 450 ms. Measurement of ERP was made at
each CL immediately on reversion and at 1-minute intervals for 10
assessments after termination of AFL. These measurements are designated
ERP1 through ERP10. To estimate the temporal change in ERP, the time
from reversion of AFL to each ERP was measured to the nearest
second.3 Development of AF during AFL or induction of AF
during ERP determinations precluded subsequent measurements.
Chronic AFL Group
The study population comprised 10 patients undergoing RFA of
chronic AFL (Figure 1
). The patients had documented AFL for
17±18 months (range, 2 to 60 months) and had failed a mean of 2.1±0.4
antiarrhythmic drugs before ablation (Table 2). Antiarrhythmic drugs, including
calcium blockers, were stopped >5 half-lives before ablation. No
patients were taking amiodarone.
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Chronic AFL Definition
Typical AFL was defined by its characteristic 12-lead
ECG.6 12 13 Chronicity was defined by the presence of AFL
on ECG on 2 separate occasions separated by 1 month >1 month
before ablation. All patients were in AFL at the time of the study and
at the time of ablation. Duration of chronic AFL was defined as the
time from initial diagnosis to the time of ablation.
Mechanism and Ablation of AFL
Intracardiac electrodes were placed in the LRA, CS, His, and
tricuspid annulus positions as described above. An ablation catheter
positioned in the subeustachian isthmus was used for entrainment
mapping and delivery of radiofrequency energy.6 12 13
Digital images were archived to help replicate catheter locations for a
follow-up study performed 3 weeks after ablation. After confirmation of
the flutter mechanism, an anatomic approach was used to create a line
of conduction block between the tricuspid annulus and the eustachian
ridge.12 In all patients, ablation was performed during
AFL. On termination of AFL, atrial
electrophysiological properties were
evaluated as described below.
Atrial Electrophysiology After AFL Ablation
On termination of AFL, pharmacological autonomic blockade was
administered over 10 minutes as described above.14 The
doses of atropine and propranolol were 2.3±0.7 and
12.2±4.5 mg, respectively.
Fifteen and 30 minutes after termination of AFL, ERPs were evaluated from the LRA, CS, and right atrial septum (RAS) via repositioning of the radiofrequency catheter at CLs of 600 and 450 ms. To estimate the variability of ERP assessments associated with catheter repositioning, the following was performed in 6 patients. After the 30-minute ERP measurements were completed, the LRA electrode was withdrawn into the inferior vena cava and then repositioned at the original LRA site as determined by archived digital images. The intrastudy variability was 4.8% for ERPs at 600 ms and 4.2% for ERPs at 450 ms.
The corrected sinus node recovery time (cSNRT) was assessed at CLs of 600 and 450 ms after a 30-second S1 pacing train 15 and 30 minutes after ablation. Pacing was performed twice from the LRA site and averaged.
AFL ablation end point was bidirectional isthmus block.12 Attempted AFL reinduction was not attempted, and all antiarrhythmic drugs were ceased after ablation.
Three-Week Follow-Up Study
All patients returned for a second
electrophysiological evaluation 3 weeks
after RFA of AFL. Three intracardiac electrodes (LRA, CS, and RAS) were
introduced as described above to assess atrial refractoriness and sinus
node function.
Statistical Analysis
All variables are reported as mean±SD. A repeated-measures
ANOVA was used to compare continuous variables. Scheffé’s F
test was used for multiple comparisons. Intrastudy ERP variability was
calculated using the following equation: 
(observation 1-observation
2/observation 1)/total observations. Two-tailed paired or unpaired
Student’s t tests were performed when appropriate.
Statistical significance was established at P<0.05.
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Results |
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Paroxysmal AFL Group
Induction, Duration, and Termination of AFL
Sustained AFL of
5 minutes was achieved in 15 patients. The
duration of induced AFL was 8.6±2.4 minutes, excluding the time
required to induce AFL (0.5±0.3 minutes). The mean CL of induced AFL
was 241±14 ms. Spontaneous termination of AFL occurred in 8 patients
(53%) after a period of AFL ranging from 5.2 to 9.0 minutes. Pace
termination of AFL was required in 4 patients (27%) after a total AFL
duration of 10 minutes. AFL degenerated into AF in 3 patients (20%)
after a mean AFL duration of 7.7±1.5 minutes (Figure 4). These patients required electrical
cardioversion after 15 minutes of AF and were excluded from subsequent
evaluation because of the known effects of AF on atrial
refractoriness.3 4
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Atrial ERPs
Data are summarized in Tables 3 and 4 and
illustrated in Figures 5 and 6. In the 12 patients in whom sinus
rhythm was established after induced AFL, the LRA ERP at 600 ms
decreased from 243±34 ms before AFL to 200±33 ms immediately after
AFL (P<0.01). The LRA ERP at 450 ms decreased from 225±33
ms before AFL to 198±32 ms immediately after AFL (P<0.01).
In 2 patients, the first captured extrastimulus after a 600-ms drive
(at 180 and 185 ms, respectively) induced AF, and subsequent ERP
determinations were not performed. In 1 patient, sustained AF was
induced with the fifth ERP determination (ERP4) after a 450-ms drive
(at 175 ms), and subsequent ERP testing was not performed.
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) depicting
recovery of 600-ms LRA ERPs after termination of paroxysmal AFL. ERPs
plotted vs time. Intervals at which ERPs were determined are indicated
in Table 3
, development of AF.
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Serial ERPs were measured in the remaining 9 patients,
permitting estimation of the temporal recovery of atrial refractoriness
(Figures 5 and 6). At 600 ms, post-AFL ERPs were lower
than pre-AFL ERPs for up to 260±55 seconds (ERP4) after AFL
termination (P<0.01). At 450 ms, post-AFL ERPs were lower
than pre-AFL ERPs for up to 304±53 seconds (ERP4) after AFL
termination (P<0.05). In 4 patients, ERPs at drive CLs of
600 and 450 ms did not return to within 10 ms of pre-AFL values after
the final ERP determination.
The AFL CL did not change significantly between immediately after induction and immediately before termination of AFL (241±14 versus 239±16 ms, P=0.83).
Development of AF
Six patients developed AF during AFL or during atrial ERP
determination. Of these 6, 3 patients had a history of paroxysmal AF, 2
developed AF during AFL, and 1 developed AF during ERP testing. There
were no significant differences between patients who developed AF and
those who did not in terms of age (61.2±10.0 versus 59.8±11.1 years,
P=0.84) or left atrial size (4.2±0.5 versus 4.1±0.5 cm,
P=0.72).
Chronic AFL Group
ERPs and Adaptation to Rate After Termination of Chronic
AFL
The mean AFL CL of the population was 257±25 ms. RFA was
successful in terminating AFL, and bidirectional isthmus block was
achieved in all patients.
Complete data were available for all patients at the LRA and CS
sites. ERP data at the RAS were available for 6 patients at 15 and 30
minutes and 4 patients at 3 weeks after ablation. ERPs measured 15 and
30 minutes after AFL termination were not significantly different.
Results were consistent at LRA, RAS, and distal CS sites at
both measured CLs (Table 5 and Figures 7 and 8).
Atrial refractoriness increased significantly 3 weeks after ablation
compared with ERPs measured 15 and 30 minutes after ablation. At LRA,
RAS, and CS sites, ERPs were consistently less at a drive CL of
450 ms compared with 600 ms. This relationship was maintained at 15 and
30 minutes and 3 weeks after termination of AFL, suggesting rate
adaptation of refractoriness at the CLs measured.
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SNRT After Chronic AFL Ablation
No patients were excluded from analysis on the basis of
SNRTs >1500 ms at baseline. cSNRTs 15 and 30 minutes after termination
of chronic AFL were comparable (Table 5). However, a significant
decrease in cSNRT 3 weeks after termination of chronic AFL at 450 and
600 ms drive CLs was demonstrated.
Chronic Versus Paroxysmal AFL
LRA ERPs at 600 and 450 ms 30 minutes after termination of chronic
AFL were not significantly different from those measured immediately
after termination of induced AFL in the paroxysmal AFL group (600 ms:
215±20 versus 200±33 ms, P=0.22; 450 ms: 205±16 versus
198±32 ms, P=0.65).
LRA ERPs at 600 and 450 ms 3 weeks after RFA of chronic AFL were not significantly different from LRA ERPs measured in the paroxysmal AFL group before induction of AFL (600 ms: 235±23 versus 243±34 ms, P=0.54; 450 ms: 229±20 versus 225±33 ms, P=0.77). Similarly, CS ERPs at 600 and 450 ms 3 weeks after RFA of chronic AFL were not significantly different from those measured in the paroxysmal AFL group before AFL induction (600 ms: 250±16 versus 254±32 ms, P=0.75; 450 ms: 241±20 versus 242±20 ms, P=0.93).
A trend toward a longer flutter CL was observed in patients with chronic AFL (257±25 ms) compared with that immediately before flutter termination in the paroxysmal group (239±16 ms, P=0.069).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study of patients with paroxysmal and chronic AFL presents new information regarding electrophysiological remodeling of the atria in humans. The processes of acute and chronic atrial electrical remodeling were examined in patients with clinical atrial arrhythmias under standardized levels of autonomic tone in the absence of antiarrhythmic agents and cardioverting DC energy.
In patients with paroxysmal AFL, a 5- to 10-minute period of induced AFL is associated with a significant reduction in atrial refractoriness. This "electrical remodeling" reverses within 5 minutes of resumption of sinus rhythm in most patients.
In patients with chronic AFL, atrial refractoriness increases significantly 3 weeks after AFL termination compared with 30 minutes after cessation of the arrhythmia. However, there was no difference between ERPs measured 15 and 30 minutes after reversion. Three weeks after termination of AFL, cSNRT increases significantly compared with values soon after reversion. These findings suggest that chronic AFL promotes reversible remodeling of atrial electrical properties with a time course of recovery distinctly different from that of paroxysmal AFL.
Previous Studies of Atrial Electrical Remodeling Associated
With AFL
Franz et al11 examined the monophasic action
potential duration at 90% repolarization (MAPd90) in patients 15 to 30
minutes after cardioversion of AFL and compared measurements with
patients cardioverted from AF and control subjects. Chronic AFL was
clearly associated with shortening of the MAPd90 and depressed atrial
MAPd-CL relations paralleling those observed in patients cardioverted
from AF. However, serial measurements were not made to determine
whether MAPd90 changed after cardioversion, and an assessment of the
temporal recovery of refractoriness was not
possible.16
Electrical Remodeling Associated With Paroxysmal Atrial
Arrhythmias in Man
Studies in humans have demonstrated that a 5- to 10-minute period
of AF produces a fall in atrial ERPs that reverses over a similar
period after resumption of sinus rhythm.3 4 The magnitude
and duration of ERP reduction were similar to those observed in most
patients in the present study as a result of paroxysmal AFL. As in
prior studies, autonomic blockade was administered to control for
potential fluctuations in autonomic tone resulting from the induced
arrhythmia.3 Our observations suggest that
paroxysmal AFL is of sufficiently short CL (241±14 ms) to induce
atrial electrical remodeling. However, prior studies of short-duration
AF have been conducted in patients without atrial arrhythmias
or structural heart disease. In the present study, electrical
remodeling was observed in patients with a clinical history of
paroxysmal AFL as a result of a paroxysm of their clinical
arrhythmia.
The observed interpatient variability in baseline and subsequent ERP measurements from a single fiducial right atrial site probably reflects the considerable electrical heterogeneity that exists in patients with atrial arrhythmias.17 However, the dynamic trends in refractoriness after a paroxysm of AFL were consistent across the study population, suggesting that electrical remodeling develops regardless of baseline ERPs. No specific reason for failure of refractoriness to return to normal after AFL induction could be delineated in the 4 patients in whom this was observed. Age and left atrial size were comparable to those in whom refractoriness returned to baseline. Failure to observe a return to baseline may have been a function of the time limits of our clinical protocol.
Electrical Remodeling Associated With Chronic Atrial
Arrhythmias in Humans
That atrial electrical remodeling develops as a consequence of
chronic AFL may be inferred from the observation that refractoriness
increases 3 weeks after termination of the arrhythmia. In
contrast to the rapid restitution of atrial refractoriness occurring
after termination of paroxysmal AFL, significant shortening of
refractoriness persisted for 30 minutes in the chronic AFL group.
This suggests that more prolonged AFL is associated with more slowly
reversing electrical remodeling and possibly a different mechanism.
Because autonomic blockade was administered at the time of ERP
assessments, changes in autonomic tone are unlikely to have contributed
to the changes in refractoriness. Our observations support other
evidence from humans demonstrating that chronic AF–related electrical
remodeling develops and may reverse after
cardioversion.18
The present study suggests that adaptation of ERP to rate is present after termination of chronic AFL. This observation is consistent with the work of Pandozi et al18 and Kamalvand et al,19 who demonstrated ERP adaptation to rate after cardioversion of AF. However, our observations contrast with those of Franz et al11 and Attuel et al20 in humans and of animal studies that demonstrate loss or reversal of rate adaptation.1 2
After termination of chronic AFL, cSNRT increased after 3 weeks of sinus rhythm. This finding is consistent with animals studies demonstrating reversible sinus node dysfunction after a period of chronic AF and suggests that AFL may also induce reversible remodeling of sinus node function.21 The persistence of sinus node dysfunction in the presence of autonomic blockade also suggests that AFL causes significant depression of sinus node automaticity and/or sinoatrial conduction.
Relationship Between AFL and AF
Several studies have attempted to clarify the mechanistic
relationships between AFL and AF. AFL may serve as a trigger for AF,
with organized macro-reentrant wave fronts of AFL splitting over
anatomic obstacles such as the crista terminalis or pectinate muscles
to generate daughter wavelets of AF or short-circuiting through gaps in
constraining barriers to yield tighter reentrant
circuits.22 23 24 AFL may disorganize into AF through a
reduction in the length of functional barriers around which atrial wave
fronts propagate.25 Cheng et al23 and
Scheinman et al26 have hypothesized that some forms of
atypical AFL may develop when caudal boundaries of the crista
terminalis are breached during times of reduced atrial refractoriness.
A reduction in atrial ERP like that found in the present study
after a paroxysm of AFL might contribute to the promotion of AF soon
after AFL onset and possibly some atypical forms of AFL by decreasing
the size of such functional barriers in the human heart. The
present study also suggests that AF inducibility may be heightened
for up to 10 minutes after a paroxysm of AFL and for 30 minutes after
termination of chronic AFL owing to the effects of electrical
remodeling. This process may contribute in part to the high rates of AF
inducibility observed immediately after AFL
ablation.7 8 9
Study Limitations
The present study did not control for the potential
confounding effect of multiple ERP determinations on refractoriness. No
significant changes in atrial ERPs were demonstrated after repeated ERP
assessments in previous studies, suggesting that the methodology used
in this study was unlikely to influence the observed changes in
refractoriness3 4 In the chronic AFL group, a threshold
<2 mA at the septal site could be achieved in only 6 patients at 15
and 30 minutes and in 4 patients at 3 weeks. Hence, electrical
remodeling of the septum has not been conclusively demonstrated.
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Acknowledgments |
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Dr Sparks was funded by The National Heart Foundation of Australia as a postgraduate medical research scholar.
Received January 7, 2000; revision received May 19, 2000; accepted May 19, 2000.
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 J. P. Brown, D. E. Krummen, G. K. Feld, and S. M. Narayan Using Electrocardiographic Activation Time and Diastolic Intervals to Separate Focal From Macro-Re-Entrant Atrial Tachycardias J. Am. Coll. Cardiol., May 15, 2007; 49(19): 1965 - 1973. [Abstract] [Full Text] [PDF]
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H. Dobrzynski, M. R. Boyett, and R. H. Anderson New Insights Into Pacemaker Activity: Promoting Understanding of Sick Sinus Syndrome Circulation, April 10, 2007; 115(14): 1921 - 1932. [Full Text] [PDF]
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H. M. Haqqani and J. M. Kalman Aging and Sinoatrial Node Dysfunction: Musings on the Not-So-Funny Side Circulation, March 13, 2007; 115(10): 1178 - 1179. [Full Text] [PDF]
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Y. M. Kim, T. J. Guzik, Y. H. Zhang, M. H. Zhang, H. Kattach, C. Ratnatunga, R. Pillai, K. M. Channon, and B. Casadei A Myocardial Nox2 Containing NAD(P)H Oxidase Contributes to Oxidative Stress in Human Atrial Fibrillation Circ. Res., September 30, 2005; 97(7): 629 - 636. [Abstract] [Full Text] [PDF]
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 J P Bourke, A Dunuwille, D O'Donnell, S Jamieson, and S S Furniss Pulmonary vein ablation for idiopathic atrial fibrillation: six month outcome of first procedure in 100 consecutive patients Heart, January 1, 2005; 91(1): 51 - 57. [Abstract] [Full Text] [PDF]
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P. Sanders, P. M. Kistler, J. B. Morton, S. J. Spence, and J. M. Kalman Remodeling of Sinus Node Function in Patients With Congestive Heart Failure: Reduction in Sinus Node Reserve Circulation, August 24, 2004; 110(8): 897 - 903. [Abstract] [Full Text] [PDF]
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C. Scharf, S. Veerareddy, M. Ozaydin, A. Chugh, B. Hall, P. Cheung, E. Good, F. Pelosi Jr, F. Morady, and H. Oral Clinical significance of inducible atrial flutter during pulmonary vein isolation in patients with atrial fibrillation J. Am. Coll. Cardiol., June 2, 2004; 43(11): 2057 - 2062. [Abstract] [Full Text] [PDF]
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 P. Spurrell, K. Kamalvand, M. Higson, and N. Sulke Temporal changes in atrial refractoriness following DC cardioversion of persistent atrial fibrillation in man Europace, January 1, 2004; 6(3): 229 - 235. [Abstract] [Full Text] [PDF]
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M. Hocini, P. Sanders, I. Deisenhofer, P. Jais, L.-F. Hsu, C. Scavee, R. Weerasoriya, F. Raybaud, L. Macle, D. C. Shah, et al. Reverse Remodeling of Sinus Node Function After Catheter Ablation of Atrial Fibrillation in Patients With Prolonged Sinus Pauses Circulation, September 9, 2003; 108(10): 1172 - 1175. [Abstract] [Full Text] [PDF]
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T. Korte, M. Niehaus, G. Borchert, and J. Tebbenjohanns Significant prolongation of atrial monophasic action potential duration: short-term reverse electrophysiological changes after internal cardioversion of atrial fibrillation Cardiovasc Res, March 1, 2002; 53(4): 944 - 951. [Abstract] [Full Text] [PDF]
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J. B. Morton, M. J. Byrne, J. M. Power, J. Raman, and J. M. Kalman Electrical Remodeling of the Atrium in an Anatomic Model of Atrial Flutter: Relationship Between Substrate and Triggers for Conversion to Atrial Fibrillation Circulation, January 15, 2002; 105(2): 258 - 264. [Abstract] [Full Text] [PDF]
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Prof. F. Lombardi Atrial fibrillation and sinus node dysfunction: Reply J. Am. Coll. Cardiol., November 1, 2001; 38(5): 1585 - 1586. [Full Text] [PDF]
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A. J Workman, K. A Kane, and A. C Rankin The contribution of ionic currents to changes in refractoriness of human atrial myocytes associated with chronic atrial fibrillation Cardiovasc Res, November 1, 2001; 52(2): 226 - 235. [Abstract] [Full Text] [PDF]
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V. L.J.L. Thijssen, J. Ausma, and M. Borgers Structural remodelling during chronic atrial fibrillation: act of programmed cell survival Cardiovasc Res, October 1, 2001; 52(1): 14 - 24. [Abstract] [Full Text] [PDF]
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P. B. Sparks and J. M. Kalman Is atrial flutter a risk factor for stroke? J. Am. Coll. Cardiol., September 1, 2001; 38(3): 785 - 788. [Full Text] [PDF]
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