(Circulation. 1995;91:1588-1595.)
© 1995 American Heart Association, Inc.
Articles |
Chronic Rapid Atrial Pacing
Structural, Functional, and Electrophysiological Characteristics of a New Model of Sustained Atrial Fibrillation
From the Departments of Medicine (C.A.M., G.J.K., D.L.J.), Physiology (D.L.J.), and Pathology (C.M.G.), University of Western Ontario, and the Heart and Circulation Group, The John P. Robarts Research Institute (C.A.M., G.J.K., D.L.J), London, Ontario, Canada.
Correspondence to Carlos A. Morillo, MD, Cardiovascular Physiology, Rm 3C-124, McGuire VA Medical Center, 1201 Broad Rock Blvd, Richmond, VA 23249.
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Abstract |
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Background Despite the clinical importance of atrial fibrillation (AF), the development of chronic nonvalvular AF models has been difficult. Animal models of sustained AF have been developed primarily in the short-term setting. Recently, models of chronic ventricular myopathy and fibrillation have been developed after several weeks of continuous rapid ventricular pacing. We hypothesized that chronic rapid atrial pacing would lead to atrial myopathy, yielding a reproducible model of sustained AF.
Methods and Results Twenty-two halothane-anesthetized
mongrel dogs underwent insertion of a transvenous lead at the right
atrial appendage that was continuously paced at 400 beats per minute
for 6 weeks. Two-dimensional echocardiography was performed in 11 dogs
to assess the effects of rapid atrial pacing on atrial size. Atrial
vulnerability was defined as the ability to induce sustained repetitive
atrial responses during programmed electrical stimulation and was
assessed by extrastimulus and burst-pacing techniques. Effective
refractory period (ERP) was measured at two endocardial sites in the
right atrium. Sustained AF was defined as AF 
15 minutes. In animals
with sustained AF, 10 quadripolar epicardial electrodes were surgically
attached to the right and left atria. The local atrial fibrillatory
cycle length (AFCL) was measured in a 20-second window, and the mean
AFCL was measured at each site. Marked biatrial enlargement was
documented; after 6 weeks of continuous rapid atrial pacing, the left
atrium was 7.8±1 cm2 at baseline versus 11.3±1
cm2 after pacing, and the right atrium was 4.3±0.7
cm2 at baseline versus 7.2±1.3 cm2 after
pacing. An increase in atrial area of at least 40% was necessary to
induce sustained AF and was strongly correlated with the inducibility
of AF (r=.87). Electron microscopy of atrial tissue
demonstrated structural changes that were characterized by an increase
in mitochondrial size and number and by disruption of the sarcoplasmic
reticulum. After 6 weeks of continuous rapid atrial pacing, sustained
AF was induced in 18 dogs (82%) and nonsustained AF was induced in 2
dogs (9%). AF occurred spontaneously in 4 dogs (18%). Right atrial
ERP, measured at cycle lengths of 400 and 300 milliseconds at baseline,
was significantly shortened after pacing, from 150±8 to 127±10
milliseconds and from 147±11 to 123±12 milliseconds,
respectively (P<.001). This finding was highly predictive
of inducibility of AF (90%). Increased atrial area (40%) and ERP
shortening were highly predictive for the induction of sustained AF
(88%). Local epicardial ERP correlated well with local AFCL
(R2=.93). Mean AFCL was significantly shorter in
the left atrium (81±8 milliseconds) compared with the right atrium
94±9 milliseconds (P<.05). An area in the posterior left
atrium was consistently found to have a shorter AFCL (74±5
milliseconds). Cryoablation of this area was attempted in 11 dogs. In 9
dogs (82%; mean, 9.0±4.0; range, 5 to 14), AF was terminated and no
longer induced after serial cryoablation.
Conclusions Sustained AF was readily inducible in most dogs (82%) after rapid atrial pacing. This model was consistently associated with biatrial myopathy and marked changes in atrial vulnerability. An area in the posterior left atrium was uniformly shown to have the shortest AFCL. The results of restoration of sinus rhythm and prevention of inducibility of AF after cryoablation of this area of the left atrium suggest that this area may be critical in the maintenance of AF in this model.
Key Words: fibrillation • electrophysiology
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Atrial fibrillation (AF) remains the most frequently encountered arrhythmia in the clinical setting.1 2 3 Despite this, the management of AF remains less than satisfactory. Most AF animal models have been developed in the short-term setting, and AF has been maintained in these models by pharmacological or electrical stimulation of the vagus nerve.4 5 6 7 Cox et al8 recently developed an AF model in anesthetized dogs after surgically inducing mitral regurgitation. AF was induced by programmed electrical stimulation in 19 of 22 (75%) dogs. The major limitation of these models is failure to sustain AF over prolonged periods.
Conversely, the study of ventricular arrhythmias, particularly ventricular fibrillation, has been strengthened by the development of reproducible animal models. Tachycardia-induced cardiomyopathy achieved by chronic rapid ventricular pacing has been reported recently.9 10 11 In this model, marked structural, functional, and electrophysiological changes were documented and are associated with ventricular fibrillation.10 We therefore hypothesized that chronic rapid atrial pacing would lead to atrial myopathy, thus yielding a reproducible model of sustained AF.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Study Animals
Twenty-two adult mongrel dogs weighing 16 to 30 kg each were used. Baseline 12-lead ECG, white blood cell count, and hemoglobin, serum creatinine, and electrolyte levels were measured to exclude unhealthy animals. The protocol was approved by the University Council on Animal Care of the University of Western Ontario and was completed in accordance with the Guidelines to the Care and Use of Experimental Animals of the Canadian Council on Animal Care.
Baseline Study
The dogs were tranquilized with an injection
of acepromazine
(0.3 to 0.4 mg/kg body wt IM) for transportation to the laboratory and
then anesthetized with a mixture of 4% halothane, 2 L/min nitrous
oxide, 1 L/min oxygen, and 2 L/min medical air administered by mask.
The dogs were then intubated and ventilated at a rate of 10 to 12
breaths per minute and a tidal volume of 12 to 15 mL/kg with a Hospital
300 Anesthesia Ventilator (Hospital Medical Corporation). The halothane
level was subsequently reduced to 0.5% to 1%. A circulating water
blanket and controller were used to maintain body temperature at
37±1°C. Lactated Ringer's solution was infused throughout the
procedure.
Two-dimensional echocardiography was performed in 11 dogs. Atrial size was assessed by calculating the atrial area by planimetry in the apical four-chamber view (Hewlett Packard 77025A U/S system, 2.5-mHz transducer). At least four repeated measurements were performed for both atria, and an average was calculated. Doppler ultrasound flow studies of the mitral and tricuspid valves were also performed.
Arterial pressure was continuously monitored by an indwelling catheter placed in the right femoral artery through a cut-down. Two 6F quadripolar catheters were inserted through direct cut-down of the left internal jugular vein and were fluoroscopically advanced to the right atrial (RA) appendage and lower RA, respectively. All data were continuously displayed on an Electronics for Medicine VR-16 switched-beam oscilloscope and were recorded periodically on photographic paper at 50 to 100 mm/s. The data were also recorded simultaneously on FM tape with a 16-channel Ampex PR 2230 recorder. The RA was stimulated at a pulse duration of 2 ms and twice diastolic threshold with a Grass S88 stimulator (Grass Medical Instruments). A custom-designed timer was used to trigger the stimulator.
Baroreceptor reflex sensitivity was assessed in all dogs by the method of Smyth et al.12 The dogs were given 10 to 40 µg/kg phenylephrine HCl (Neo-Synephrine, Winthrop Laboratories) until an increase of 30 to 40 mm Hg was achieved.13 The dose that achieved the targeted increase in blood pressure was repeated three times. Each RR interval was plotted as a function of the preceding systolic blood pressure, and beat-by-beat analysis was performed when the RR interval changed. A least-squares-fit linear regression was performed, and reflex control of the heart rate was expressed as the slope of the linear regression line. The three slopes obtained were averaged, and a mean baroreceptor slope was calculated for each dog.
Electrophysiological Study
P-wave duration was measured from
the surface ECG at baseline
and after pacing. The PA interval was measured from the onset of the P
wave on the surface ECG to the onset of the atrial electrogram recorded
at the lower RA.
The atrial effective refractory period (ERP) was measured at two endocardial sites, the RA appendage and the lower RA, by delivering a train of eight atrial paced beats S1 at two cycle lengths (400 and 300 ms), followed by an extrastimulus (S2) introduced at coupling intervals decremented by 10 ms to scan the entire atrial diastolic interval. Responses were monitored on a Tektronix 5513 storage oscilloscope. Atrial ERP was defined as the longest S1-S2 interval that failed to result in atrial depolarization.
Atrial vulnerability was defined as the ability to induce sustained atrial repetitive responses during programmed electrical stimulation. Inducibility of AF was determined by programmed electrical stimulation at basic cycle lengths of 400 and 300 ms with up to three extrastimuli (S4) delivered. The second extrastimulus (S3) was introduced with the S1-S2 interval fixed at 30 ms longer than the atrial ERP. The S2-S3 interval was set at 80% of the basic cycle length, introducing the extrastimulus with 10-ms scanning decrements. If double extrastimuli failed to induce arrhythmia, a third extrastimulus (S4) was introduced by use of the same protocol. If the latter protocol failed to induce AF, burst pacing at a cycle length of 100 ms for 20 to 30 seconds was tried. Nonsustained AF was defined as repetitive atrial responses lasting <5 minutes and spontaneously terminating. Sustained AF was defined as irregular repetitive atrial responses lasting >15 minutes.
After the programmed stimulation protocol was completed, all catheters were withdrawn and the right femoral artery was ligated. A unipolar screw-in Medtronic J pacing lead was inserted through the left jugular vein incision, and the tip of the lead was fluoroscopically placed and fixed in the RA appendage. The proximal end of the pacing lead was connected to a custom-modified Medtronic programmable pulse generator (5941,8322,8329) and subsequently implanted in a subcutaneous pocket in the neck. The pacemaker was set at 70 beats per minute (bpm) in the demand mode. After all the incisions were closed, the dogs were allowed to recover from anesthesia and were returned to the animal quarters.
Twenty-four hours were allowed for lead stabilization, and then the pacemaker was programmed to 400 bpm (150 ms) and maintained at this rate for 6 weeks. This invariably resulted in a mean ventricular rate of approximately 130 bpm. The surface ECG was checked at 2-week intervals to ensure constant pacing.
Restudy
Six weeks after the initial study, the pacemaker was
programmed
to the lowest rate attainable and the dogs were studied by use of the
same procedure described for the baseline study. Two-dimensional
echocardiography was assessed in the 11 dogs with baseline echo. P-wave
duration and PA interval were measured before electrophysiological
study. Baroreceptor reflex sensitivity was evaluated in all dogs by use
of the protocol previously described. Atrial ERP and AF vulnerability
were determined by insertion of a catheter through the right jugular
vein. Once sustained AF was induced, the chest was opened by means of a
median sternotomy and the heart was exposed and suspended in a
pericardial sling. Sinus rhythm was restored by electric cardioversion
delivered with epicardial paddles when necessary. Ten quadripolar
plaque electrodes (interelectrode distance, 10 mm) were surgically
attached to the RA and left atrial (LA) walls (Fig 1
).
Bipolar epicardial electrograms were continuously recorded on magnetic
tape and stored on diskette for off-line signal processing by a
computerized mapping system (CMS 1000, Biomedical Instrumentation).
Local epicardial AF cycle length (AFCL) was calculated by measuring the
interval between the steepest negative deflection of each activation
point in a 20-second window and averaged to obtain the mean AFCL. In 8
dogs, local epicardial ERP was measured at each site and correlated
with the local AFCL. In 11 dogs, cryoablation at -30° to
-45°C
with a 10-mm probe (Frigitronics model CCS 100) for 120 seconds was
serially applied to the area with shortest AFCL.
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After the restudy was completed, the heart was excised and examined for size and gross abnormalities. Both atria were removed and sent to the pathology department for light and electron microscopic studies.
Statistical Analysis
Values are expressed as mean±SD.
Paired Student's t
test was used to compare mean values between baseline and restudy.
Linear regression analysis was used to evaluate the relation
between epicardial ERP and local mean AFCL. Baroreceptor reflex
sensitivity was assessed by a least-squares-fit linear regression, and
reflex control of heart rate was expressed as the slope of the linear
regression line. Only slopes with a correlation coefficient of .80
were accepted for analysis. The slopes were averaged, and a mean
baroreceptor slope was calculated for each dog by one-way ANOVA. The
null hypothesis was rejected at the P=.05 level.
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Results |
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Two-dimensional Echocardiography
After 6 weeks of continuous rapid atrial pacing, biatrial enlargement was documented in the 11 dogs assessed by echocardiography (Fig 2
). The areas of both atria were markedly
increased: the LA increased from 7.8±1 to 11.3±1 cm2
(45%) and the RA from 4.3±0.7 to 7.2±1.3 cm2 (67%,
P<.001). Mild tricuspid regurgitation was documented after
pacing in 3 of 11 dogs (25%). No evidence of significant mitral or
tricuspid valve dysfunction was observed at either baseline or
restudy.
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Baroreceptor Reflex Sensitivity
After 6 weeks of continuous
rapid atrial pacing, no changes in the
baroreceptor reflex sensitivity slopes were observed (26.39±14.87
versus 28.08±12.38 ms/mm Hg at baseline, P=NS).
Structural Changes
Light Microscopy
Focal and
early hypertrophy were observed in both atria. Also, in
most cases, large mural thrombi were also found in either the LA or RA.
No evidence of increased connective tissue content was documented.
Electron Microscopy
Severe changes in the
architecture of both LA and RA were
documented by electron microscopy after 6 weeks of rapid atrial pacing.
These changes were characterized by a marked increase in the number and
size of the mitochondria and by disruption of the sarcoplasmic
reticulum (Fig 3). Enlarged nuclei and dilatation of the
rough endoplasmic reticulum were also observed. These changes are
consistent with hypertrophy and perturbation of the cellular metabolic
activity. No changes were observed in ventricular samples assessed
randomly in eight dogs.
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Electrophysiological Findings
P-wave duration and PA interval
were assessed at baseline and
after 6 weeks of chronic rapid atrial pacing. Significant increases in
P-wave duration and PA interval were observed after pacing (55.5±7.5
versus 88.8±8.5 ms and 36.8±10.6 versus 55.5±9.8 ms,
respectively,
P<.05). A significant reduction in endocardial RA ERP was
documented after chronic rapid atrial pacing at cycle length drives of
400 and 300 ms (150±8 to 127±10 ms and 147±11 to
123±12 ms,
respectively, P<.001). Sustained AF was not induced by
programmed electrical stimulation at baseline study in any dog. In
contrast, sustained AF was readily inducible by programmed electrical
stimulation in 11 of 22 dogs (Fig 4). Of 11 total dogs,
AF was induced by a single extrastimulus in 6 dogs, by two extrastimuli
in 3, and by three extrastimuli in 2. Burst pacing was necessary to
induce AF in another 7 dogs. AF was induced at least twice with the
same extrastimulation protocol in 15 of 18 (83%) dogs. Nonsustained
atrial flutter was induced in 2 of the remaining 4 dogs. The mean
ventricular response during sustained AF was 595±85 ms. Nonsustained
AF was induced in 2 dogs (9%). After programming the pacemaker to the
lowest heart-rate setting, AF occurred spontaneously in 4 dogs (18%).
These episodes of spontaneous AF were not initiated or preceded by
premature atrial contractions. Overall, sustained AF was induced at
restudy in 18 of 22 (82%) dogs at a mean duration of 45±7
minutes.
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An increase in atrial area of at least 40% was strongly correlated with the inducibility of sustained AF (r=.87). A 15% reduction in ERP was associated with increased atrial vulnerability. When these variables were combined, the positive predictive value for the induction of sustained AF was 88%.
Mean AFCL was significantly
shorter in the LA (81±8 ms) compared with
the RA (94±9 ms, P<.05). Mean AFCL was correlated with the
local epicardial refractory period in 8 dogs, and a strong correlation
(R2=.93) between these two measurements was
achieved (Fig 5). Epicardial AFCL showed a significant
variance (SD2) between sites (LA, 36.5 ms2; RA,
30.5 ms2), suggesting increased dispersion in
refractoriness. Detailed analysis of the mean AFCL showed that an
area localized to the posterior LA (74±6 ms) had a consistently faster
AFCL than the rest of the epicardial sites (Fig 6). This
area was always localized to the inferoposterior LA adjacent to the
left inferior pulmonary vein. Cryoablation of this area was attempted
in 11 dogs (Fig 7), with a mean of 9
applications.5 6 7 8 9 10 11 12 13 14
The area ablated was between 
5 and 8
cm2. Before AF was terminated, AFCL was significantly
prolonged in both atria (LA, 81±8 to 132±5 ms; RA, 94±9
to 136±4
ms, P<.0001). AF was terminated in 9 of 11 (82%) dogs (Fig
8). Sustained AF was no longer inducible by either
programmed electrical stimulation or burst pacing; instead,
nonsustained atrial flutter was induced in 7 of 9 (77%) dogs.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The present study describes the characteristics of a new canine model of sustained AF. This model may be the experimental counterpart of clinically observed cardiomyopathy induced by tachycardia.14 15 16 Our model is highly reproducible, and sustained AF is readily inducible and can be maintained for prolonged periods of time.
Structural Changes
The marked changes in atrial architecture
that were documented by
electron microscopy, such as fiber disarray and early hypertrophy, may
contribute to the maintenance of AF in this model. Disorganization of
atrial fiber orientation may slow the rate of conduction, facilitating
reentry.17 Similarly, alterations observed at the cellular
level, such as the increase in mitochondrial size and disruption of the
sarcoplasmic reticulum, may create ionic alterations that increase
atrial vulnerability, triggering AF.
A marked increase in atrial size was documented by two-dimensional echocardiography. A 40% increase in atrial area was strongly correlated with the inducibility of sustained AF. This finding may contribute to the maintenance of AF in this model. This finding provides further support for the critical atrial mass hypothesis.18
A high incidence of mural thrombi in both atria was observed by light microscopy. However, two-dimensional echocardiography did not show any evidence of mural thrombi, and no clinical findings suggesting systemic embolization were documented. This model may further expand our understanding of the development of systemic emboli in the presence of chronic nonvalvular AF.
Baroreceptor Reflex Sensitivity
Depressed baroreceptor reflex
sensitivity has been reported in the
paced model of induced heart failure.19 Interestingly, no
changes in baroreceptor function were noted after 6 weeks of continuous
rapid atrial pacing. It is possible that the development of
baroreceptor alterations in the paced induced heart failure model may
be mediated by the presence of heart failure and not by the tachycardia
per se. Finally, increased atrial vulnerability in our AF model cannot
be attributed to alterations in autonomic balance, as evidenced by a
preserved baroreceptor reflex sensitivity after pacing.
Electrophysiological Changes
Prolonged P-wave duration
and PA interval were noted after
pacing. A significant shortening of the RA ERP was also documented at
restudy. A minimal reduction of 15% in ERP associated with an increase
of at least 40% in atrial area was highly predictive of sustained AF.
Similarly, local epicardial ERP measured at five sites in each atrium
showed a marked dispersion of refractoriness. Local epicardial ERP was
strongly correlated with local AFCL, a measure previously used in
experimental20 21 22 and human
studies23 as an
index of local refractoriness. We found a significantly shorter AFCL in
the LA compared with the RA. Further analysis of the mean AFCL
demonstrated that an area localized to the posterior LA was
consistently faster than the rest of the epicardial sites analyzed (Fig
6
). The significant difference between the AFCL of the LA and
RA may be
explained by a shorter refractory period in the LA, modulated in part
by differences in autonomic innervation.24 However, the
exact mechanism leading to this difference remains unclear. The use of
the AFCL as an index of refractoriness is based on the concept that,
during fibrillation, a wandering wavelet will reexcite the cells as
soon as they recover their
excitability.20 21 22 23
Cryoablation
of this area significantly prolonged AFCL in both atria and
successfully restored sinus rhythm in most dogs (82%), rendering
sustained AF noninducible. The ablated area may have been large enough
to prevent reentry of multiple wavelets. These findings suggest that
the ability to maintain AF in this model may be related to an area
localized in the posterior LA that can sustain rapid atrial rates. It
is possible to speculate that the increased susceptibility to AF in
this model was triggered by alterations in the wavelength mediated by a
shortened refractoriness and conduction depression. Although we did not
determine the wavelength in this set of experiments, we did note a
dispersion of refractoriness of 30.5 ms2 in the RA and 36.5
ms2 in the LA and increased right intra-atrial conduction
delay, suggested by the increase in PA interval. The role of triggered
activity as a potential mechanism in the generation of AF in this model
cannot be entirely ruled out. Alterations in the microarchitecture and
anisotropic properties may cause inhomogeneous and discontinuous
propagation of the impulse.25 26 27
Depression of conduction
in our model may be expected and could be related to the marked
ultrastructural changes documented by electron microscopy. Altogether,
these findings may be responsible for the increased atrial
vulnerability noted in this model.
Previous Models
Previous AF models have been developed in dogs with structurally
normal hearts. In these models, AF was generally sustained by electric
or pharmacological stimulation of the parasympathetic nervous
system.4 5 6 7 Allessie et
al28 recently reported
the induction of sustained AF by periodic burst pacing of the LA in
five chronically instrumented dogs. These dogs were restudied 3 days
after implanting a series of epicardial electrodes. Continuous atrial
pacing was not performed in this model, and no evidence of structural
changes in the atria was reported. These authors reported a
significantly shorter AFCL in the LA, comparable to that reported in
the present study. The same group recently developed a model of
chronic AF by repeatedly inducing AF in chronically instrumented
goats.29 In this model, AF was maintained by an external
fibrillation pacemaker. Interestingly, the development of chronic AF
was associated with a significant shortening of the atrial ERP and
shortening of the AFCL. These findings are similar to those in the
present study and provide further support for our model. Similarly,
a model of acute AF achieved by rapid atrial pacing recently has been
used to evaluate different atrial defibrillation
waveforms.30 31 Cox et al8 recently
developed
an AF model in anesthetized dogs subjected to surgically inducing
mitral regurgitation. AF was induced by programmed electrical
stimulation in 19 of 22 (75%) dogs 3 months after the surgical
procedure. We are aware of only one other "chronic" AF model,
which used continuous bipolar 60-Hz AC atrial stimulation for the
development of AF.32 In this model, in 4 of 6 dogs, AF
persisted after the stimulation protocol was terminated. LA enlargement
documented by two-dimensional echocardiography and comparable to that
observed in our study was also reported. Although this model was
reported in abstract form several years ago, no detailed data or a
follow-up on this model is presently available. The model of AF
described herein is unique, in that AF was associated with marked
biatrial myopathy and increased atrial vulnerability in dogs without
valvular disease.
Study Limitations
Insight into the mechanism leading to
sustained AF in this model
is limited by the lack of extensive atrial mapping and interelectrode
conduction-time data. Nonetheless, we describe a reproducible new model
of sustained AF and the functional, structural, and
electrophysiological characteristics of this model.
Clinical Implications
The present study demonstrated the
feasibility of developing a
reproducible model of sustained AF without valvular disease. AF without
overt underlying disease has been increasingly recognized in humans,
and the possibility of expanding our understanding of the mechanisms
leading to AF in this setting may be enhanced by the present model.
Also, new therapeutic modalities may be facilitated by the use of the
present novel model.
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Acknowledgments |
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This work was supported by the Heart and Stroke Foundation of Canada. Dr C.A. Morillo is the recipient of a research fellowship award from the Heart and Stroke Foundation of Canada, Ottawa. Dr G.J. Klein is the recipient of a distinguished professorship of the Heart and Stroke Foundation of Ontario, Toronto, Canada. The authors thank G.K. Wood and R. Kaleda for excellent technical assistance.
Received June 1, 1994; revision received August 24, 1994; accepted September 5, 1994.
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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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D. M. Todd, A. C. Skanes, G. Guiraudon, C. Guiraudon, A. D. Krahn, R. Yee, and G. J. Klein Role of the Posterior Left Atrium and Pulmonary Veins in Human Lone Atrial Fibrillation: Electrophysiological and Pathological Data From Patients Undergoing Atrial Fibrillation Surgery Circulation, December 23, 2003; 108(25): 3108 - 3114. [Abstract] [Full Text] [PDF]
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P. Chandra, T. S Rosen, B. Herweg, P. Danilo Jr., and M. R Rosen Left atrial pacing induces memory and is associated with atrial tachyarrhythmias Cardiovasc Res, November 1, 2003; 60(2): 307 - 314. [Abstract] [Full Text] [PDF]
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H.-M. Lo, F.-Y. Lin, and Y. Z. Tseng Atrial compartment operation for atrial fibrillation: to isolate the left atrium or not? Ann. Thorac. Surg., October 1, 2003; 76(4): 1259 - 1263. [Abstract] [Full Text] [PDF]
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W. Dun, P. Chandra, P. Danilo Jr., M. R. Rosen, and P. A. Boyden Chronic atrial fibrillation does not further decrease outward currents. It increases them. Am J Physiol Heart Circ Physiol, October 1, 2003; 285(4): H1378 - H1384. [Abstract] [Full Text] [PDF]
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M. C. Sanguinetti and P. B. Bennett Antiarrhythmic Drug Target Choices and Screening Circ. Res., September 19, 2003; 93(6): 491 - 499. [Abstract] [Full Text] [PDF]
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S. Verheule, E. Wilson, T. Everett IV, S. Shanbhag, C. Golden, and J. Olgin Alterations in Atrial Electrophysiology and Tissue Structure in a Canine Model of Chronic Atrial Dilatation Due to Mitral Regurgitation Circulation, May 27, 2003; 107(20): 2615 - 2622. [Abstract] [Full Text] [PDF]
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J. Ausma, H. M.W. van der Velden, M.-H. Lenders, E. P. van Ankeren, H. J. Jongsma, F. C.S. Ramaekers, M. Borgers, and M. A. Allessie Reverse Structural and Gap-Junctional Remodeling After Prolonged Atrial Fibrillation in the Goat Circulation, April 22, 2003; 107(15): 2051 - 2058. [Abstract] [Full Text] [PDF]
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L.-P. Lai, C.-C. Tsai, M.-J. Su, J.-L. Lin, Y.-S. Chen, Y.-Z. Tseng, and S. K. S. Huang Atrial Fibrillation Is Associated With Accumulation of Aging-Related Common Type Mitochondrial DNA Deletion Mutation in Human Atrial Tissue Chest, February 1, 2003; 123(2): 539 - 544. [Abstract] [Full Text] [PDF]
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N. Sulke, P. Spurrell, K. Kamalvand, A. Mitchell, M. Higson, J. Gill, and V. Paul The effect of endocardial defibrillator shocks on basic atrial electrophysiology in man: Is post cardioversion atrial electrical 'remodelling' artefact? Europace, January 1, 2003; 5(1): 33 - 37. [Abstract] [PDF]
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R. Mantovan, M. A. Gatzoulis, A. Pedrocco, P. Ius, C. Cavallini, A. De Leo, R. Zecchel, V. Calzolari, C. Valfre, and P. Stritoni Supraventricular arrhythmia before and after surgical closure of atrial septal defects: spectrum, prognosis and management Europace, January 1, 2003; 5(2): 133 - 138. [Abstract] [PDF]
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T. H. Everett IV, J. G. Akar, L.-C. Kok, J. R. Moorman, and D. E. Haines Use of global atrial fibrillation organization to optimize the success of burst pace termination J. Am. Coll. Cardiol., November 20, 2002; 40(10): 1831 - 1840. [Abstract] [Full Text] [PDF]
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E. Bertaglia, D. D'Este, F. Zerbo, F. Zoppo, P. Delise, and P. Pascotto Success of serial external electrical cardioversion of persistent atrial fibrillation in maintaining sinus rhythm. A randomized study Eur. Heart J., October 1, 2002; 23(19): 1522 - 1528. [Abstract] [Full Text] [PDF]
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S. Zhou, C.-M. Chang, T.-J. Wu, Y. Miyauchi, Y. Okuyama, A. M. Park, A. Hamabe, C. Omichi, H. Hayashi, L. A. Brodsky, et al. Nonreentrant focal activations in pulmonary veins in canine model of sustained atrial fibrillation Am J Physiol Heart Circ Physiol, September 1, 2002; 283(3): H1244 - H1252. [Abstract] [Full Text] [PDF]
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S. Verheule, E. E Wilson, R. Arora, S. K Engle, L. R Scott, and J. E Olgin Tissue structure and connexin expression of canine pulmonary veins Cardiovasc Res, September 1, 2002; 55(4): 727 - 738. [Abstract] [Full Text] [PDF]
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A. Goette, M. Arndt, C. Rocken, T. Staack, R. Bechtloff, D. Reinhold, C. Huth, S. Ansorge, H. U. Klein, and U. Lendeckel Calpains and cytokines in fibrillating human atria Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H264 - H272. [Abstract] [Full Text] [PDF]
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O. Berenfeld, A. V. Zaitsev, S. F. Mironov, A. M. Pertsov, and J. Jalife Frequency-Dependent Breakdown of Wave Propagation Into Fibrillatory Conduction Across the Pectinate Muscle Network in the Isolated Sheep Right Atrium Circ. Res., June 14, 2002; 90(11): 1173 - 1180. [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. Oahara, Y. Miyauchi, T. Ohara, M. C. Fishbein, S. Zhou, M.-H. Lee, W. J. Mandel, P.-S. Chen, and H. S. Karagueuzian Downregulation of Immunodetectable Atrial Connexin4O in a Canine Model of Chronic Left Ventricular Myocardial Infarction: Implications to Atrial Fibrillation Journal of Cardiovascular Pharmacology and Therapeutics, June 1, 2002; 7(2): 89 - 94. [Abstract] [PDF]
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G. Schram, M. Pourrier, P. Melnyk, and S. Nattel Differential Distribution of Cardiac Ion Channel Expression as a Basis for Regional Specialization in Electrical Function Circ. Res., May 17, 2002; 90(9): 939 - 950. [Abstract] [Full Text] [PDF]
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J. Kneller, R. Zou, E. J. Vigmond, Z. Wang, L. J. Leon, and S. Nattel Cholinergic Atrial Fibrillation in a Computer Model of a Two-Dimensional Sheet of Canine Atrial Cells With Realistic Ionic Properties Circ. Res., May 17, 2002; 90 (9): e73 - e87. [Abstract] [Full Text] [PDF]
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J. Jalife, O. Berenfeld, and M. Mansour Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation Cardiovasc Res, May 1, 2002; 54(2): 204 - 216. [Abstract] [Full Text] [PDF]
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M. Allessie, J. Ausma, and U. Schotten Electrical, contractile and structural remodeling during atrial fibrillation Cardiovasc Res, May 1, 2002; 54(2): 230 - 246. [Abstract] [Full Text] [PDF]
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A. Goette, U. Lendeckel, and H. U Klein Signal transduction systems and atrial fibrillation Cardiovasc Res, May 1, 2002; 54(2): 247 - 258. [Abstract] [Full Text] [PDF]
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J. E. Olgin and S. Verheule Transgenic and knockout mouse models of atrial arrhythmias Cardiovasc Res, May 1, 2002; 54(2): 280 - 286. [Abstract] [Full Text] [PDF]
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P.-S. Chen, T.-J. Wu, C. Hwang, S. Zhou, Y. Okuyama, A. Hamabe, Y. Miyauchi, C.-M. Chang, L. S. Chen, M. C. Fishbein, et al. Thoracic veins and the mechanisms of non-paroxysmal atrial fibrillation Cardiovasc Res, May 1, 2002; 54(2): 295 - 301. [Abstract] [Full Text] [PDF]
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B. J.J.M. Brundel, R. H. Henning, H. H. Kampinga, I. C. Van Gelder, and H. J.G.M. Crijns Molecular mechanisms of remodeling in human atrial fibrillation Cardiovasc Res, May 1, 2002; 54(2): 315 - 324. [Abstract] [Full Text] [PDF]
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