(Circulation. 1999;99:1255-1264.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Regional Differences in the Recovery Course of Tachycardia-Induced Changes of Atrial Electrophysiological Properties
From the Institute of Clinical Medicine of National Yang-Ming University, Veterans General Hospital–Taipei, Shin-Kong Memorial Hospital, and National Taiwan University, Taipei, Taiwan.
Correspondence to Shih-Ann Chen, MD, Division of Cardiology, Veterans General Hospital–Taipei, 201 Sec 2, Shih-Pai Rd, Taipei, Taiwan. E-mail sachen{at}vghtpe.gov.tw
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Abstract |
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Background—Regional differences in recovery of tachycardia-induced changes of atrial electrophysiological properties have not been well studied.
Methods and Results—In the control group (5 dogs), atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) were assessed before and every 4 hours for 48 hours after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. In experimental group 1 (15 dogs), AERP and inducibility of AF were assessed before and after complete AVJ ablation with 8-week rapid right atrial (RA) pacing (780 bpm) and VVI pacing. In experimental group 2 (7 dogs), AERP and inducibility of AF were assessed before and after 8-week rapid left atrial (LA) pacing and VVI pacing. AERP and inducibility and duration of AF were obtained from 7 epicardial sites. In the control group, atrial electrophysiological properties obtained immediately and during 48-hour measurements after pacing did not show any change. In the 2 experimental groups, recovery of atrial electrophysiological properties included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease of duration and episodes of reinduced AF. However, recovery of shortening and maladaptation of AERP and inducibility of AF was slower at the LA than at the RA and Bachmann's bundle.
Conclusions—The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF.
Key Words: tachycardia • electrophysiology • atrium
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Introduction |
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It has recently been demonstrated that prolonged episodes of atrial fibrillation (AF) induced shortening of atrial effective refractory period (AERP) and loss of the physiological rate-related shortening of AERP.1 2 3 4 5 This effect results in shorter wavelengths for the multiple wavelets during AF.6 7 8 Some studies have demonstrated that tachycardia-induced shortening of AERP was reversible after restoration of sinus rhythm.2 9 However, the time course of recovery of AERP shortening has not been well studied. It is still unknown whether there are regional differences in the course of recovery of tachycardia-induced changes of atrial electrophysiological properties.
The purposes of this study were to assess the time course of recovery of electrophysiological properties at multiple atrial sites after chronic rapid atrial pacing and to investigate possible changes of electrophysiological properties that resulted in initiation and maintenance of AF after chronic rapid atrial pacing.
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Methods |
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Study Groups
(1) Control group AERP and inducibility of AF were assessed in 5 dogs before and after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. (2) Experimental group 1 AERP and inducibility of AF were assessed in 15 dogs before and after complete AVJ ablation with 8-week rapid atrial pacing at the right atrium (RA) and VVI pacing. (3) Experimental group 2 AERP and inducibility of AF were assessed in 7 dogs before and after complete AVJ ablation with 8-week rapid atrial pacing at the left atrium (LA) and VVI pacing.
Experimental Preparation
Twenty-seven mongrel dogs of either sex weighing 20 to 25 kg
were anesthetized with an injection of thiopental sodium 25
mg/kg IV. The chest was opened through the right fifth intercostal
space, and the pericardium was incised to expose the heart. A
quadripolar electrode catheter (Mansfield, Boston Scientific) was
inserted through the left femoral vein and positioned in the RA to
record an atrial electrogram. Seven bipolar pacing wires for
measuring AERP were sutured to the RA and LA (Figure 1
).
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) and 1 pacing lead for rapid atrial pacing at RA or LA (*). IVC
indicates inferior vena cava; PV, pulmonary vein;
and SVC, superior vena cava.
Baseline Electrophysiological Study
Each dog was pretreated with atropine and
propranolol (0.04 and 0.2 mg/kg, respectively) followed by
maintenance infusion (0.007 and 0.04 mg ·
kg-1 · h-1,
respectively).10 AERP was measured by a decremental
technique with 2-ms steps at pacing cycle lengths of 200 ms (PCL 200),
250 ms (PCL 250), and 350 ms (PCL 350) for 8 beats. AERP was defined as
the longest S1-S2 coupling
interval that failed to result in atrial capture. Pacing was performed
at twice diastolic threshold. Baseline AERP at each
epicardial site was measured 3 times and averaged.
Dispersion of AERP was defined as the longest minus the shortest AERP at the same PCL of an individual heart.11 AF was considered to be inducible if a single premature stimulus was followed by rapid irregular atrial activity lasting for >1 second.2 Inducibility and duration of AF were assessed by premature atrial stimulation during AERP testing. If induced AF persisted >20 minutes, electrical cardioversion was performed, and duration of AF was treated as 20 minutes in the calculation. Maladaptation of AERP was considered to be present if AERP failed to adapt or adapted inversely to change in heart rate.2 12 13
Pacemaker Implantation
After complete AV block was created by radiofrequency ablation,
1 unipolar epicardial pacing lead (Capsure 4965, Medtronic) was sutured
to the right ventricular apex, connected to a programmable
VVI pacemaker (Prevail 8086, Medtronic) in a subcutaneous pocket, and
set at 80 pulses per minute.9 In study groups, 1 unipolar
epicardial pacing lead (Capsure 4965, Medtronic) was sutured to the RA
or LA (Figure 1
); the lead was then connected to a pulse
generator (Itrel 7425, Medtronic) that was implanted in a subcutaneous
pocket and programmed to pace at a rate of 780 bpm, 2-ms pulse
duration, and an output of 3 times diastolic threshold.
Seven pacing wires were tunneled subcutaneously to the right chest.
After all the incisions were closed in layers, dogs were returned to
animal quarters. Atrial capture rates immediately and 8 weeks after
pacemaker implantation were 464±48 (range, 418 to 521) and 452±42
(range, 404 to 500) bpm.
Electrophysiological Study After 8-Week Rapid
Atrial Pacing
After intubation and mechanical ventilation, each dog was
treated with atropine and propranolol (0.04 and 0.2 mg/kg,
respectively), followed by maintenance infusion (0.007 and 0.04
mg · kg-1 ·
h-1, respectively). Epicardial pacing wires in
the baseline study were exposed for AERP measurements. In 2
experimental groups, AERP was measured immediately and every 4 hours
for 48 hours after termination of rapid atrial pacing. In the control
group, AERP was also measured every 4 hours for 48 hours. AERP
measurements were performed randomly from different atrial sites.
Temperature, blood pressure, arterial blood gas, sugar, and
electrolyte levels were monitored continuously. We did not complete the
whole procedure in 7 dogs (5 in experimental group 1 and 2 in
experimental group 2).
Statistical Analysis
Continuous variables were expressed as mean±SD. The
2 test with Yates' correction or Fisher's
exact test was used to assess nonparametric data.
Student's t test was used for continuous variables. A
2-way repeated-measures ANOVA with Student-Newman-Keuls test was used
to analyze postpacing AERP and dispersion of AERP. Comparisons
of AF duration before and after pacing were made by Wilcoxon
signed rank test. Linear or nonlinear regression analysis was
used to assess the correlation between 2 parameters. A
value of P<0.05 was considered statistically
significant.
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Results |
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Control Group
AERP, rate adaptation and dispersion of AERP, and inducibility and duration of AF did not change after 8-week complete AV block with VVI pacing (Table
).
Furthermore, these parameters did not change at PCL 200,
250, or 350 ms during 48-hour measurements (Figure 2A).
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Experimental Group 1
Shortening, Dispersion, and Maladaptation of AERP After RA
Pacing
AF appeared after termination of rapid atrial pacing in the
15 dogs, and it terminated spontaneously within 20 minutes in 13 dogs
(442±312 seconds). Electrical cardioversion was performed in the other
2 dogs. AERP at any of the 3 PCLs measured immediately after
termination of rapid atrial pacing was significantly shorter than that
before pacing at any of the 7 atrial sites (all, P<0.01).
AERP shortening at the RA and Bachmann's bundle (BB) recovered faster
than that at the LA at any of the 3 PCLs (Figure 2B). Increased
dispersion of AERP persisted for 20 hours after termination of rapid
atrial pacing at any of the 3 PCLs (Figure 3A). Maladaptation of AERP recovered
faster at the RA and BB than at the LA (Figure 4).
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Inducibility of Secondary AF
Inducibility of AF recovered faster at the RA and BB than at
the LA at any of the 3 PCLs (Figure 5).
Local AERP at the sites with secondary AF was shorter than those
without secondary AF at PCL 200 (88±10 versus 119±12 ms,
P<0.01), PCL 250 (94±12 versus 130±13 ms,
P<0.01), and PCL 350 (102±12 versus 138±14 ms,
P<0.01). Dispersion of AERP in dogs with secondary AF was
significantly greater than in those without secondary AF at PCL 200
(48±6 versus 32±5 ms, P<0.01), PCL 250 (60±5 versus
46±6 ms, P<0.01), and PCL 350 (70±7 versus 54±6 ms,
P<0.01). During 48-hour measurements, secondary AF was
inducible at 564 of the total 1260 epicardial sites at PCL 200. Of the
564 sites with inducible secondary AF, maladaptation of AERP was noted
at 314 sites, and maladaptation of AERP was noted at 132 of the 696
sites without inducible secondary AF. Thus, sites with secondary AF at
PCL 200 had a significantly higher incidence of maladaptation of AERP
than those without secondary AF (314/564 versus 132/696,
P<0.01). Sites with secondary AF had a significantly higher
incidence of maladaptation of AERP than those without secondary AF at
PCL 250 (296/540 versus 150/720, P<0.01) and PCL 350
(280/521 versus 166/739, P<0.01). Furthermore, there was a
significant inverse relationship between time after termination
of rapid atrial pacing and percentage of sites in which secondary
episodes of AF were induced at any of the 3 PCLs during postpacing
measurements (Figure 6A).
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Duration of Secondary AF
Duration of secondary AF at any of the 3 PCLs remained
significantly longer for 4 hours after termination of rapid atrial
pacing at any of the 7 atrial sites. However, there was no significant
difference in duration of secondary AF at any of the 3 PCLs among the 7
atrial sites (Figure 7).
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Average duration of secondary AF induced at the 7 atrial sites was
significantly correlated with AERP of BB at PCL 200 (r=0.54,
P<0.05), PCL 250 (r=0.63, P<0.01),
and PCL 350 (r=0.62, P<0.01), but average
duration of secondary AF induced at the 7 atrial sites did not
correlate with AERP at other sites or dispersion of AERP at any of the
3 PCLs (Figure 8A and Figure 9A). Furthermore, there was a significant
inverse relationship between time after termination of rapid atrial
pacing and average duration of secondary AF induced at the 7 atrial
sites at any of the 3 PCLs (Figure 10A).
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Experimental Group 2
Shortening, Dispersion, and Maladaptation of AERP After LA
Pacing
AF appeared after termination of rapid atrial pacing in the 7
dogs, and it terminated spontaneously within 20 minutes in 5 dogs
(483±298 seconds). Electrical cardioversion was performed in the other
2 dogs. AERP at any of the 3 PCLs measured immediately after
termination of rapid atrial pacing was significantly shorter than that
before pacing at any of the 7 atrial sites (all showed
P<0.01). AERP shortening at the RA and BB recovered faster
than that at the LA at any of the 3 PCLs (Figure 2C).
Increased dispersion of AERP persisted for 16 hours after termination
of rapid atrial pacing at any of the 3 PCLs (Figure 3B).
Maladaptation of AERP recovered faster at the RA and BB than at the LA
(Figure 4).
Inducibility of Secondary AF
Inducibility of AF recovered faster at the RA and BB than at the
LA at any of the 3 PCLs (Figure 5). Local AERP at the sites with
secondary AF was shorter than those without secondary AF at PCL 200
(86±11 versus 115±13 ms, P<0.01), PCL 250 (96±11 versus
129±14 ms, P<0.01), and PCL 350 (104±13 versus 135±15
ms, P<0.01). Dispersion of AERP in dogs with secondary AF
was significantly greater than in those without secondary AF at PCL 200
(50±8 versus 34±5 ms, P<0.01), PCL 250 (59±8 versus
44±7 ms, P<0.01), and PCL 350 (73±9 versus 55±8 ms,
P<0.01). Sites with secondary AF had a significantly higher
incidence of maladaptation of AERP than those without secondary AF at
PCL 200 (134/259 versus 60/343, P<0.01), PCL 250 (128/247
versus 66/355, P<0.01), and PCL 350 (117/232 versus 77/370,
P<0.01). Furthermore, there was a significant inverse
relationship between time after termination of rapid atrial pacing and
percentage of sites at which secondary episodes of AF were induced at
any of the 3 PCLs during postpacing measurements (Figure 6B).
Duration of Secondary AF
Duration of secondary AF at any of the 3 PCLs remained
significantly longer for 4 hours after termination of rapid atrial
pacing at any of the 7 atrial sites. However, there was no significant
difference in duration of secondary AF at any of the 3 PCLs among the 7
atrial sites (Figure 7).
Average duration of secondary AF induced at the 7 atrial sites was
significantly correlated with AERP of BB at PCL 200 (r=0.52,
P<0.05), PCL 250 (r=0.60, P<0.01),
and PCL 350 (r=0.61, P<0.01), but average
duration of secondary AF induced at the 7 atrial sites did not
correlate with AERP at other sites or dispersion of AERP at any of the
3 PCLs (Figures 8B and 9B). Furthermore, there was a
significant inverse relationship between time after termination of
rapid atrial pacing and average duration of secondary AF induced at the
7 atrial sites at any of the 3 PCLs (Figure 10B).
Comparisons Between Experimental Groups 1 and 2
There was no significant difference in percentage change of any of
the atrial electrophysiological
parameters in any time period after termination of rapid
atrial pacing between the 2 groups (Figures 2 through 10).
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Discussion |
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Major Findings
Recovery of atrial electrophysiological properties after chronic rapid atrial pacing included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease in the episodes and duration of reinduced AF. Tachycardia-induced shortening and maladaptation of AERP and increased inducibility of AF recovered faster at the RA and BB than those at the LA.
Recovery of AERP Shortening
Morillo et al1 first used continuous rapid atrial
pacing at 400 bpm for 6 weeks in 22 dogs to study the changes of AERP.
They found that AERP decreased by an average of 23 to 25 ms at the RA
appendage and lower RA. Wijffels et al2 found that AERP of
goat hearts was still shorter than baseline data 1 day after cessation
of AF induced by 2 to 3 weeks of rapid atrial pacing. Our results
showed that AERP shortening recovered faster at the RA and BB than at
the LA. Previous studies have suggested that cytosolic calcium overload
was an important mediator of AERP shortening after rapid atrial pacing;
furthermore, different shapes and durations of atrial action potentials
were found at different atrial sites.3 4 14 15 Regional
differences in ionic channel density, intracellular calcium, and course
of recovery from cytosolic calcium overload between the RA and LA were
possible.14 15
Experimental studies showed that administration of acetylcholine and increase of sympathetic activity could change AERP.16 17 In the present study, propranolol and atropine were administered to minimize the possibility that the course of recovery of tachycardia-induced changes of atrial electrophysiological properties was influenced by changes in autonomic tone. Previous studies have demonstrated that autonomic blockage did not prevent tachycardia-induced shortening of AERP.3 5 Elvan et al9 assessed AERP shortening in dog hearts after 2 to 6 weeks of rapid atrial pacing, and the autonomic system was blocked only during AERP measurements. They found that tachycardia-induced shortening of AERP was still noted 2 days after conversion to sinus rhythm. We assessed the course of recovery of tachycardia-induced changes of atrial electrophysiological properties, and the autonomic nervous system was continuously blocked during 48-hour measurements. We found that changes of atrial electrophysiological properties induced by 8-week rapid atrial pacing recovered completely within 48 hours. These findings suggested that the autonomic nervous system probably influenced the course of recovery of tachycardia-induced changes of atrial electrophysiological properties.
Attuel et al12 demonstrated maladaptation and shortening of AERP in patients with atrial tachyarrhythmia. Recently, Daoud et al18 showed that in humans, 7±2 minutes of AF shortened AERP for up to 8 minutes, and they also demonstrated that recovery of AERP shortening decreased inducibility and duration of secondary AF. Our laboratory demonstrated similar findings.19 These results suggest that a similar recovery process of tachycardiainduced changes of atrial electrophysiological properties may take place in humans.
Dispersion of AERP After Rapid Atrial Pacing
Experimental animal studies have shown that AF is based on
multiple wavelet reentry.20 During AF, many independent
wavelets might propagate in an ever-changing pattern around
continuously shifting areas of conduction block. Dispersion in
refractoriness was considered to favor induction and
maintenance of reentrant arrhythmias.21 22
This study did not find significant correlation between dispersion of
AERP and duration of secondary AF. However, our results suggested that
increased dispersion of AERP played an important role in induction of
secondary AF.
Recovery of AERP Maladaptation
Attuel et al12 found that maladaptation of AERP might
be a marker of atrial pathology causing a propensity to AF. Le Heuzey
et al13 measured the effects of heart rate on action
potential recorded from isolated strips of human atrial
myocardium, and they suggested that maladaptation of AERP
might be the cause of AF in humans. Wijffels et al2
demonstrated that artificial maintenance of AF in goat hearts
for 2 to 3 weeks led to maladaptation of AERP. We first demonstrated
that tachycardia-induced maladaptation of AERP recovered
faster at the RA and BB than at the LA.
Inducibility and Duration of Secondary AF
Both animal and clinical studies have demonstrated that AF is
based on multiple reentrant wavelets wandering throughout the
atria.20 The wavelength of these wavelets, defined as the
distance traveled by the depolarization wave during the duration of its
refractory period (wavelength=conduction velocityxrefractory period),
is an important factor to determine the induction of these reentrant
arrhythmias.6 The smaller the wavelength of the
circulating wavelets, the more easily AF could be
induced.7 8 In the present study, AF was
induced by extrastimulation at the sites with shorter AERP and
maladaptation of AERP. Differences in recovery of AERP shortening and
maladaptation between RA and LA might explain regional differences in
recovery of inducibility of secondary AF. Similar to our results,
Morillo et al1 found that in dogs after 6 weeks of rapid
atrial pacing, the inferoposterior LA showed rapid activation during AF
and that cryoablation of this area could prevent inducibility of AF.
Although conduction velocity was not measured in the present
study, changes of conduction velocity after rapid atrial pacing were
controversial.2 23 Wijffels et al2 showed
that conduction velocity did not change in a goat model of chronic
rapid atrial pacing, but Gaspo et al23 showed a
significant decrease of conduction velocity in a canine model of
chronic rapid atrial pacing. The present study also demonstrated
significant correlation between duration of secondary AF and AERP at
BB. Previous studies in a canine pericarditis model demonstrated that
activation of BB by reentrant wave fronts was critical for
maintenance of AF and that sustained AF could not be induced
after ablation of BB.24 25 These results suggest that BB
may be critical for maintenance of AF in the 2 canine AF
models. The role of BB in maintenance of secondary AF may
explain regional similarities in duration of secondary AF. Wijffels et
al2 showed that AF appeared and persisted for >24 hours
in most goat hearts after 2 to 3 weeks of rapid atrial pacing. It is
possible that we did not establish a chronic AF model in our dogs as
was the case in the goat model of Wijffels et al. It is possible that
>8-week rapid atrial pacing is needed to establish a chronic AF model
in dogs.
Clinical Implications
To the best of our knowledge, this study is the first to show
electrophysiological properties that
account for induction and maintenance of secondary AF in a
canine model after 8-week rapid atrial pacing. Our data suggested that
prevention of fibrillation-induced shortening and maladaptation of AERP
and dispersion of AERP after conversion might help to prevent early
recurrences of AF.
Study Limitations
First, only 7 pairs of electrodes were used in this study; a
detailed atrial mapping using computerized multielectrode mapping and
interelectrode conduction-velocity data is absent. However, this study
still could provide a clear concept about the relation between AF and
shortening, maladaptation, and dispersion of AERP. Although previous
studies and this laboratory also showed that anisotropy, conduction
velocities in different directions, and different atrial structures are
relevant to the occurrence of AF, these issues are beyond the scope of
this study.26 27 28 Second, secondary AF induced during AERP
measurements might affect the course of recovery of
tachycardia-induced changes of atrial
electrophysiological properties. Third,
compared with dogs paced from the LA, atrial
electrophysiological
parameters, except for duration of secondary AF, remained
significantly changed compared with prepacing values for 4 to 8 hours
longer in dogs paced from the RA. However, percentage changes of these
parameters were similar in any time period after
termination of rapid atrial pacing between the 2 groups. Fourth,
mechanisms leading to regional differences and extrapolation of our
results to human AF need further study.
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Acknowledgments |
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This study was supported in part by grants from the National Science Council (NSC88-2314-B-010-094 and 88-2314-B-341-002), Taipei, Taiwan.
Received July 2, 1998; revision received September 30, 1998; accepted October 22, 1998.
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 A. Nygren, A. E. Lomax, and W. R. Giles Heterogeneity of action potential durations in isolated mouse left and right atria recorded using voltage-sensitive dye mapping Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2634 - H2643. [Abstract] [Full Text] [PDF]
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A. E. Lomax, C. S. Kondo, and W. R. Giles Comparison of time- and voltage-dependent K+ currents in myocytes from left and right atria of adult mice Am J Physiol Heart Circ Physiol, November 1, 2003; 285(5): H1837 - H1848. [Abstract] [Full Text] [PDF]
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 S. M. Narayan, F. Bode, P. L. Karasik, and M. R. Franz Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation Circulation, October 8, 2002; 106(15): 1968 - 1973. [Abstract] [Full Text] [PDF]
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K. Fan, K. L. Lee, W.-H. Chow, E. Chau, and C.-P. Lau Internal Cardioversion of Chronic Atrial Fibrillation During Percutaneous Mitral Commissurotomy: Insight Into Reversal of Chronic Stretch-Induced Atrial Remodeling Circulation, June 11, 2002; 105(23): 2746 - 2752. [Abstract] [Full Text] [PDF]
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K. Shinagawa, Y.-F. Shi, J.-C. Tardif, T.-K. Leung, and S. Nattel Dynamic Nature of Atrial Fibrillation Substrate During Development and Reversal of Heart Failure in Dogs Circulation, June 4, 2002; 105(22): 2672 - 2678. [Abstract] [Full Text] [PDF]
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T.-J. Wu, J. J. C. Ong, C.-M. Chang, R. N. Doshi, M. Yashima, H.-L. A. Huang, M. C. Fishbein, C.-T. Ting, H. S. Karagueuzian, and P.-S. Chen Pulmonary Veins and Ligament of Marshall as Sources of Rapid Activations in a Canine Model of Sustained Atrial Fibrillation Circulation, February 27, 2001; 103(8): 1157 - 1163. [Abstract] [Full Text] [PDF]
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B. J. J. M. Brundel, I. C. Van Gelder, R. H. Henning, R. G. Tieleman, A. E. Tuinenburg, M. Wietses, J. G. Grandjean, W. H. Van Gilst, and H. J. G. M. Crijns Ion Channel Remodeling Is Related to Intraoperative Atrial Effective Refractory Periods in Patients With Paroxysmal and Persistent Atrial Fibrillation Circulation, February 6, 2001; 103(5): 684 - 690. [Abstract] [Full Text] [PDF]
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M. A. Allessie, P. A. Boyden, A. J. Camm, A. G. Kleber, M. J. Lab, M. J. Legato, M. R. Rosen, P. J. Schwartz, P. M. Spooner, D. R. Van Wagoner, et al. Pathophysiology and Prevention of Atrial Fibrillation Circulation, February 6, 2001; 103(5): 769 - 777. [Full Text] [PDF]
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T. H. Everett IV, H. Li, J. M. Mangrum, I. D. McRury, M. A. Mitchell, J. A. Redick, and D. E. Haines Electrical, Morphological, and Ultrastructural Remodeling and Reverse Remodeling in a Canine Model of Chronic Atrial Fibrillation Circulation, September 19, 2000; 102(12): 1454 - 1460. [Abstract] [Full Text] [PDF]
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 H. J. Sih, D. P. Zipes, E. J. Berbari, D. E. Adams, and J. E. Olgin Differences in organization between acute and chronic atrial fibrillation in dogs J. Am. Coll. Cardiol., September 1, 2000; 36(3): 924 - 931. [Abstract] [Full Text] [PDF]
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 E. G. Manios, E. M. Kanoupakis, G. I. Chlouverakis, M. D. Kaleboubas, H. E. Mavrakis, and P. E. Vardas Changes in atrial electrical properties following cardioversion of chronic atrial fibrillation: relation with recurrence Cardiovasc Res, August 1, 2000; 47(2): 244 - 253. [Abstract] [Full Text] [PDF]
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D. Li, A. Benardeau, and S. Nattel Contrasting Efficacy of Dofetilide in Differing Experimental Models of Atrial Fibrillation Circulation, July 4, 2000; 102(1): 104 - 112. [Abstract] [Full Text] [PDF]
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S.-A. Chen, M.-H. Hsieh, C.-T. Tai, C.-F. Tsai, V. S. Prakash, W.-C. Yu, T.-L. Hsu, Y.-A. Ding, and M.-S. Chang Initiation of Atrial Fibrillation by Ectopic Beats Originating From the Pulmonary Veins : Electrophysiological Characteristics, Pharmacological Responses, and Effects of Radiofrequency Ablation Circulation, November 2, 1999; 100(18): 1879 - 1886. [Abstract] [Full Text] [PDF]
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W.-C. Yu, S.-H. Lee, C.-T. Tai, C.-F. Tsai, M.-H. Hsieh, C.-C. Chen, Y.-A. Ding, M.-S. Chang, and S.-A. Chen Reversal of atrial electrical remodeling following cardioversion of long-standing atrial fibrillation in man Cardiovasc Res, May 1, 1999; 42(2): 470 - 476. [Abstract] [Full Text] [PDF]
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 D. Li, L. Zhang, J. Kneller, and S. Nattel Potential Ionic Mechanism for Repolarization Differences Between Canine Right and Left Atrium Circ. Res., June 8, 2001; 88(11): 1168 - 1175. [Abstract] [Full Text] [PDF]
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