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(Circulation. 1999;100:87-95.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Promotion of Atrial Fibrillation by Heart Failure in Dogs
Atrial Remodeling of a Different Sort
From the Research Center (D.L., S.F., S.N.), Department of Medicine (D.L., S.N.), and Department of Pathology (T.K.L.), Montreal Heart Institute and University of Montreal, and the Department of Pharmacology and Therapeutics (S.N.), McGill University, Montreal, Quebec, Canada.
Correspondence to Stanley Nattel, MD, Research Center, Montreal Heart Institute, 5000 Belanger St E, Montreal, Quebec H1T 1C8, Canada. E-mail nattel{at}icm.umontreal.ca
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Abstract |
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Background—Studies of atrial fibrillation (AF) due to atrial tachycardia have provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before remodeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block plus ventricular pacemaker at 80 bpm).
Methods and Results—CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8±4 seconds in control dogs to 535±82 seconds; P<0.01), similar to the effect of 1 week of RAP (713±300 seconds). In contrast to RAP, CHF did not alter atrial refractory period, refractoriness heterogeneity, or conduction velocity at a cycle length of 360 ms; however, CHF dogs had a substantial increase in the heterogeneity of conduction during atrial pacing (heterogeneity index in CHF dogs, 2.76±0.16 versus 1.46±0.10 for control and 1.51±0.06 for RAP dogs; P<0.01) owing to discrete regions of slow conduction. Histological examination revealed extensive interstitial fibrosis (connective tissue occupying 12.8±1.9% of the cross-sectional area) in CHF dogs compared with control (0.8±0.3%) and RAP (0.9±0.2%) dogs.
Conclusions—Experimental CHF strongly promotes the induction of sustained AF by causing interstitial fibrosis that interferes with local conduction. The substrates of AF in CHF are very different from those of atrial tachycardia–related AF, with important potential implications for understanding, treating, and preventing AF related to CHF.
Key Words: arrhythmia • antiarrhythmia agents • conduction • remodeling • heart failure • electrocardiology
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Our understanding of atrial fibrillation (AF) has been advanced by studies showing that rapid atrial activation, whether by AF itself1 2 or by rapid atrial pacing (RAP),3 4 5 causes AF-promoting electrical alterations, including decreased atrial effective refractory period (ERP),1 2 3 4 5 slowed atrial conduction,2 3 4 and increased electrophysiological heterogeneity.4 6 These results provide insight into how AF alters atrial electrophysiology to promote its own maintenance but do not account for the substrate supporting the AF that induces remodeling. Congestive heart failure (CHF) is a particularly common clinical cause of AF.7 Very little is known about the mechanisms by which CHF promotes AF. Preliminary studies suggest that experimental CHF promotes AF without reducing refractoriness, leaving the underlying mechanisms unclear.8 The present study was designed to assess the changes in atrial electrical function and structure caused by experimental CHF, determine whether these changes are part of an atrial substrate that supports AF, and compare the atrial remodeling caused by CHF with that resulting from rapid atrial activation.
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Methods |
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Animal Preparation
Thirty-six mongrel dogs (weight, 22 to 30 kg) were studied in 3 groups, as follows: (1) There were 8 dogs in the control group. Three of the control dogs were instrumented and monitored like CHF dogs but without pacemaker activation. The results in these sham dogs were the same as in 5 acute control animals; therefore, the results of all 8 control dogs were grouped together for analysis purposes. We4 have previously shown that atrial pacemaker implantation without activation does not alter atrial electrophysiology for periods of
6 weeks. (2) The CHF group comprised 18 dogs, each
with a ventricular pacemaker (model 8084, Medtronic)
implanted in a subcutaneous pocket in the neck under pentobarbital
anesthesia (30 mg/kg IV) and attached to a pacing lead in
the right ventricular (RV) apex. The pacemaker was
programmed to capture the RV at 240 bpm for 3 weeks, followed by 2
weeks at 220 bpm. CHF was established by clinical signs (lethargy,
dyspnea, and edema) and confirmed by hemodynamic
measurements. (3) Finally, the RAP group consisted of 10 dogs. Right
atrial (RA) pacing at 400 bpm was performed for 1 week as previously
described3 4 except that the ventricular
response was controlled to prevent ventricular dysfunction
due to a rapid response to AF. Radiofrequency ablation of the AV node
was performed, and a programmable ventricular VVIP pacemaker was
implanted to pace the RV at 80 bpm. All tachycardia pacemakers
were kept on standby for 24 hours after implantation before the
initiation of RAP or ventricular pacing.
On study days, dogs were reanesthetized with morphine (2 mg/kg
SC) and 
-chloralose (120 mg/kg IV, followed by 29.25 mg ·
kg-1 · h-1) and
ventilated to maintain physiological
arterial blood gases. Body temperature was maintained at
37°C, and the left femoral artery and both femoral veins were
cannulated for pressure monitoring and drug administration. A median
sternotomy was performed, and bipolar, Teflon-coated, stainless steel
electrodes were hooked into the right and left atrial appendages for
recording and stimulation. A programmable stimulator was used
to deliver 2-ms pulses at twice-threshold current. In CHF and RAP dogs,
the surface ECG was recorded before surgery to confirm 1:1 pacing,
and atrial electrograms were recorded in CHF dogs to check the
atrial rate during ventricular pacing. The implanted
pacemaker was then deactivated. Five silicon sheets containing
240 bipolar electrodes were attached, and stimulation and
recording were performed as previously described (Figure 1
).6
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Electrophysiological Study
ERPs were measured at the left atrial (LA) appendage (LAA) and
the RA appendage (RAA) with a train of 15 basic
(S1) stimuli followed by a premature
(S2) stimulus and a 1-second pause, with the ERP
defined as the longest S1S2
interval that failed to produce a propagated response. The spontaneous
cycle length between trains averaged 432±10 ms (control), 438±6 ms
(RAP), and 430±8 ms (CHF), which was not significantly different among
groups. The mean of 3 ERP values at each basic cycle length (BCL) was
used for data analysis. On rare occasions when the 3 ERP values
differed by >10 ms, 1 or 2 additional ERP measurements were obtained,
and the mean of all determinations was taken to represent ERP.
To determine ERP dispersion, ERPs were measured at a BCL of 300 ms at 8
stimulation sites (Figure 1
): RAA, RA posterior wall (RA-PW), RA
inferior wall (RA-IW), RA Bachmann's bundle (RA-BB), LAA,
LA-PW, LA-IW, and LA-BB. ERP and conduction velocity (CV) measurements
were obtained after 2 minutes at each BCL.
AF induction was attempted with up to 3 consecutive extrastimuli at a
BCL of 360 ms and then atrial burst pacing (10 Hz for 1 to 10 seconds).
AF was considered sustained if it required electrical cardioversion for
termination (cardioversion was never performed until 
30 minutes had
passed since AF onset). To estimate the mean duration of AF, AF was
induced 10 times if AF duration was <20 minutes and 5 times if AF
lasted between 20 and 30 minutes. When electrical cardioversion was
applied, a 30-minute rest period was allowed before the experiment was
continued.
Histology
At the end of experiments, the atria were isolated and immersed
in 10% neutral buffered formalin for 24 hours. Tissue samples were
obtained from BB, the appendages, the PW and IW of the LA, and the
crista terminalis and free wall (FW) of the RA. From each of 6 tissue
zones, longitudinal and transverse sections were obtained, cut at
5-µm intervals and stained with Masson trichrome. Microscopic images
were qualitatively analyzed by an experienced cardiac
pathologist (T.-K.L.) and then subjected to quantitative
analysis.
Microscopic images were scanned into a Power personal computer with Scion Image software. Image files were analyzed with Sigma-Scan 4.0 (Jandel Scientific). Connective tissue was differentiated on the basis of its color and was expressed as a percentage of the reference tissue area. There was <5% variability for repeated measures of the same sample. Blood vessels and perivascular interstitial cells were excluded from the connective tissue quantification.
Data Analysis
The distance of each of 3 to 4 consecutive sites in the
direction of longitudinal propagation was plotted against activation
time, and CV was determined from the slope of the best-fit regression
line,4 with a clear linear relation (r>0.99)
required for analysis. The local wavelength was calculated as
the product of local CV and local ERP.9
To evaluate spatial conduction inhomogeneities, phase maps were
constructed based on previously reported methods.10 Figure 2A shows activation during RAA
pacing at a BCL of 150 ms in a control dog. For each electrode, the
phase differences (activation time difference between the central
electrode and each of the surrounding sites) were determined (Figure 2B) and divided by interelectrode distances. The largest value
at each site was then used to create a phase map as shown in Figure 2C, with values also displayed as a histogram (Figure 2D). The P5–95, expressing the range
between the 5th and 95th percentiles of the phase-difference
distribution, was used to express absolute
heterogeneity. The variation coefficient
(P5–95/P50) was used as a
heterogeneity index to express
heterogeneity independently of CV, as previously
described.10
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We calculated AF cycle length (AFCL) at each epicardial
recording site by counting the number of activations over a
5-second recording. We assessed regional variability in AFCL by
calculating the SD of the mean AFCL in each of the 8 zones in which ERP
was measured directly, ie, RAA, RA-PW, RA-IW, RA-BB, LAA, LA-PW, LA-IW,
and LA-BB (Figure 1).
Statistical Analysis
Statistical comparisons of multiple group means were obtained by
variance analysis (ANOVA). A t test with Bonferroni
correction was used to evaluate the significance of differences between
individual mean values. 
2 tests were used for
contingency comparisons. All results were expressed as mean±SEM, and
P<0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Changes in Hemodynamic Indexes
Overall group characteristics and hemodynamic data are provided in the Table
. LV
weight and ventricular diastolic and atrial
pressures increased in CHF dogs, whereas arterial and
ventricular systolic pressures decreased. RAP dogs
showed no significant hemodynamic alterations. The
atrial rate during ventricular pacing at 220 bpm in CHF
dogs was not different from the spontaneous unpaced sinus rate,
excluding significant retrograde conduction.
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General Electrophysiological Variables and
Properties of AF
Both RAP and CHF dogs had significantly increased AF duration
(Figure 3A). AF was sustained in 10 of 18
CHF dogs and 3 of 10 RAP dogs versus none of the control dogs. RAP
decreased ERP, wavelength, and AFCL (Figure 3B and 3C) and
increased the regional dispersion in ERP and AFCL (Figure 3D and 3E). CHF did not affect any of these variables. Figure 4 shows typical ECG and pressure and
atrial electrogram recordings during sustained AF from an RAP
and a CHF dog. Atrial electrograms were more organized and AFCL was
longer in CHF dogs. AF was induced by burst pacing in all 18 CHF dogs
and by single premature atrial beats in 4 (22%). AF was induced by
single extrastimuli in all RAP dogs. Extrastimuli failed to induce AF
in any control animals. AFCL averaged 103±4 ms in control dogs, 106±4
ms in CHF dogs (P=NS), and 83±4 ms in RAP dogs
(P<0.05 versus control, P<0.01 versus CHF).
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Cycle-Length Dependence and Regional Variability in Atrial
Electrophysiological Properties
Rate-dependent ERP adaptation was obvious in control dogs,
slightly reduced in CHF dogs, and strongly attenuated in RAP dogs
(Figure 5A). ERP was significantly
reduced at all BCLs in RAP dogs, whereas it was unchanged at longer
BCLs and increased at short BCLs in CHF dogs. CV remained unaltered in
both CHF and RAP dogs (Figure 5B). Wavelength was not altered by
CHF but was shortened at all BCLs in RAP dogs (Figure 5C).
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Figure 6 displays regional values of
atrial ERP (A), CV (B), and wavelength (C). CHF slightly increased ERP
at some LA sites and did not affect overall regional ERP variability.
RAP shortened ERP considerably in some regions without affecting it in
others, increasing regional ERP variability. Neither CHF nor RAP
significantly altered CV in any region. Wavelength was not
substantially altered by CHF but was significantly decreased,
particularly in RA-FW, LA-FW, and RA-IW, in RAP dogs. Overall, RAP dogs
displayed a variety of alterations (decreased ERP and wavelength and
increased ERP heterogeneity) that promote multiple
wavelet reentry, whereas CHF dogs did not. To gain insights into the
potential substrate for AF in CHF dogs, we investigated further the
finer properties of conduction.
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Local Conduction Abnormalities
Figure 7 shows isochronal
activation maps (A), phase maps (B), and phase-time histograms (C)
during 1:1 pacing at the RAA with BCLs of 360 ms from
representative control, RAP, and CHF dogs. In the
control and RAP dogs, conduction was homogeneous, phase
maps showed a narrow range of values (<2 ms/mm), and phase-time
histograms were narrow. In the CHF dog, local regions of conduction
slowing were apparent, producing zones of marked phase delay on the
phase map and a broad phase-time histogram.
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Figure 8 provides mean data for the
phase-delay analysis in 18 CHF, 10 RAP, and 8 control dogs.
Neither CHF nor RAP significantly changed the median phase time
(P50), consistent with the lack of change
in overall CV. The absolute range of phase delays
(P5–95) and the heterogeneity
index (P5–95/P50)
increased at all BCLs in CHF dogs. P95 increased
significantly in heart failure dogs (eg, 3.07±0.18 versus 1.74±0.14
ms/mm at BCL of 360 ms; P<0.01), whereas
P5 remained unchanged. Thus, the increases in
heterogeneity indexes were due to the appearance of
large regional phase delays in heart failure dogs, reflecting localized
regions of slow conduction.
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Histology
Histological studies were performed to identify
the potential pathological substrate underlying conduction
abnormalities and AF in CHF dogs. Representative
histological sections from each group are shown in
Figure 9. Both control (Figure 9A)
and RAP (Figure 9B) atria appeared grossly normal under light
microscopy. In CHF dogs (Figure C), there was extensive
interstitial fibrosis accompanied by cell loss,
degenerative changes, and hypertrophy. Bundles of myofibers
were packed less tightly than in control animals and were separated by
thick layers of fibrous tissue. There was also an increase in
connective tissue between individual cells. The connective tissue was
composed of increased numbers of fibroblasts, large amounts of
collagen, ground substance, and occasionally fat cells.
Hypertrophy was frequently present, and cell size
varied considerably within specimens. Band contraction necrosis was
observed in some isolated cells. Degenerating cells were characterized
by a focal to extensive disruption of sarcomeres and loss of
myofibrils. Cell-to-cell junctions appeared intact.
Histological changes were similar in both atria but
were more extensive in the LA.
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A quantitative analysis of fibrosis is shown in Figure 10. The percentage of fibrosis was
significantly greater in all atrial regions in CHF dogs (Figure 10A), and fibrosis was greatly increased overall (Figure 10B). There were no discernible differences between control and
RAP atria.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In the present study, we explored the effects of CHF on the atrial substrate for AF and found that consistent with clinical experience, CHF promotes the maintenance of AF. In contrast to chronic atrial tachycardia, which promotes AF maintenance by reducing the wavelength for reentry and increasing the regional disparity of refractoriness, heart failure does not alter these variables in a fashion that would be expected to favor AF. Rather, the key changes in atrial electrophysiology caused by heart failure appear to involve alterations in local atrial conduction properties caused by interstitial fibrosis.
Substrate for AF in Experimental Models
In the present study, RAP dogs with a controlled
ventricular response showed reduced atrial ERP, reduced ERP
rate adaptation, reduced wavelength, and increased ERP
heterogeneity, consistent with previous
observations of atrial tachycardia–induced
remodeling.1 2 3 4 5 6 The principal factor that induces
remodeling during AF appears to be atrial
tachycardia,11 possibly causing
Ca2+ overload.5 Like remodeling
caused by atrial tachycardia, vagal stimulation decreases
ERP and increases the dispersion of atrial
refractoriness.12 The
electrophysiological changes associated
with RAP and vagal stimulation promote multiple wavelet reentry, which
is suggested by activation mapping during AF.4 12 The
substrate of CHF-related AF in the present study was quite
different: ERP was not reduced, and ERP heterogeneity
was not increased. Rather, local conduction abnormalities and fibrosis
were prominent in CHF dogs and absent in control and RAP animals. The
ultrastructural changes that we observed were qualitatively similar to
those noted by Boyden et al in studies of atria from dogs with mitral
insufficiency13 and from cats with
cardiomyopathy,14 both of which
develop spontaneous AF. Fibrosis may impair atrial conduction at a
local level and permit the induction of
microreentry.15
Atrial Electrophysiological Alterations Induced
by CHF and Potential Relationship to AF Maintenance
There has been extensive investigation of the
electrophysiological abnormalities caused
by CHF at the ventricular level.16 17 Much
less information is available about the effects of CHF on atrial
electrophysiology, despite the clinical importance of CHF as a cause of
AF. Boyden et al13 reported that action potential duration
was not altered in the RA of cats with primary myocardial disease and
was slightly increased in LA cells of animals with severe LA
enlargement. These observations are consistent with the
regional distribution of ERP alterations that we observed, although a
contribution of direct myocardial disease to Boyden's observations
cannot be excluded. Preliminary findings have been published that
suggest that heart failure combined with tricuspid valve avulsion does
not alter mean atrial ERP but may increase ERP
heterogeneity.8 We found that CHF did not
alter ERP at longer cycle lengths and actually increased ERP at shorter
cycle lengths. CHF effects on atrial ERP were regionally variable,
but because of the distribution of ERP values under control conditions,
CHF did not alter overall heterogeneity. Fenelon et
al18 reported preliminary findings that suggest that heart
failure may cause atrial tachycardias related to triggered
activity. We did not observe atrial tachycardias in our
dogs; all of the prolonged atrial arrhythmias that we were able
to induce in CHF dogs had the properties of AF. We have also found that
dofetilide, a class III agent, strongly suppresses CHF-related AF,
consistent with a reentry mechanism, whereas flunarizine, a
drug that suppresses abnormal automaticity, has no significant effect
on AF duration or inducibility in this model.19
Localized conduction abnormalities have been related to fibrotic tissue infiltration in atrial tissue preparations,20 in ventricular tissue from patients with idiopathic dilated cardiomyopathy,21 and in animal models of myocardial infarction.22 Localized atrial conduction abnormalities have been suggested to provide the basis for unidirectional conduction slowing or block and the initiation and maintenance of atrial reentrant arrhythmias.10 15 Given the extensive nature of the atrial histological abnormalities and associated local conduction disturbances caused by CHF, it is plausible that these stabilized reentry and thereby promoted AF. This idea is consistent with preliminary mapping studies pointing to macroreentry and fibrillatory conduction as the mechanism of CHF-related AF,19 although additional work, particularly involving endocardial mapping, is needed to define the mechanism more fully.
Clinical Relevance and Potential Significance
Although studies of atrial remodeling caused by
tachycardia have provided valuable insights into how AF
promotes its own maintenance, they do not explain the
occurrence of the AF that causes remodeling. CHF is one of the most
common clinical causes of AF. In addition, many other conditions
predisposing to AF, including rheumatic valve disease23
and the aging process,24 are associated with atrial
ultrastructural abnormalities (particularly fibrous tissue
infiltration) like those observed in the present study. Our
observations are therefore relevant to understanding how heart failure,
and possibly a variety of other common causes of AF, creates a
substrate for the arrhythmia. Furthermore, our findings are
significant in demonstrating that the
electrophysiological changes produced by
tachycardia-induced remodeling are not essential for the
initiation of sustained AF.
Drug therapy to prevent AF has traditionally targeted atrial electrophysiological properties to promote sinus rhythm maintenance. Collateral changes in ventricular electrophysiology have produced undesirable consequences, particularly ventricular proarrhythmia and potential increases in mortality.25 If, however, structural changes of the type we observed play an important role in AF promotion, drug therapy could potentially be directed against structural remodeling. For example, the renin-angiotensin system is believed to be important in ventricular remodeling, including fibrotic changes, caused by CHF.26 There is evidence that ACE inhibitors can reduce the prevalence of AF in patients with CHF.27 Additional studies of the biochemical mechanisms underlying atrial structural remodeling may lead to novel therapeutic approaches to AF prevention that target substrate development rather than the final electrical consequences.
Potential Limitations
We studied CHF with the use of a well-established (but quite
specific) animal model. The histological changes we
observed are similar to those noted previously in animal and clinical
studies of subjects with atrial volume and/or pressure
overload.13 14 23 Nevertheless, it would be incorrect to
assume that our results can be directly extrapolated to AF substrates
in clinical heart failure or necessarily to AF in other animal models.
The chronic atrial stretch caused by CHF in our dogs could have
contributed to electrophysiological
changes.
Sustained AF was readily induced by burst pacing in a majority of dogs
with CHF; however, premature extrastimuli induced AF relatively
infrequently. This observation is likely due to the lack of ERP
abbreviation in dogs with heart failure: short ERPs appear to be an
important determinant of vulnerability to AF induction by premature
complexes.6 Clinical studies have shown that AF induction
with single premature extrastimuli is uncommon, whereas prolonged
atrial tachyarrhythmias can be induced by burst pacing
in 
80% of patients with a history of atrial
arrhythmias.28 The limited ability of single
premature beats to induce AF may be a protective mechanism that limits
the occurrence of AF in patients with CHF. AF might be initiated by a
brief run of atrial tachycardia due to another mechanism or
by a premature beat in the face of a transient neurohormonal or
autonomic alteration that abbreviates atrial refractoriness. Once AF
occurs, electrical remodeling would likely follow as a result of
sustained atrial tachycardia. Thus, AF in association with
heart failure might begin with the pathophysiology demonstrated in the
present study, but subsequent atrial remodeling could change the
electrophysiological substrate, with
multiple circuit reentry eventually supervening. The potentially
dynamic nature of the substrate for AF may need to be considered in
treating the arrhythmia.
Conclusions
Our study provides the first detailed insights into the functional
and structural changes underlying the ability to sustain AF in an
animal model of CHF. These results are important in pointing toward
potentially different electrical and structural substrates of AF in
different settings and the need for considering such differences to
understand the mechanisms and potential treatment of the
arrhythmia.
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Acknowledgments |
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The authors thank the Medical Research Council and Quebec Heart Foundation for operating funds, Emma De Blasio and Mirie Levi for technical assistance, Luce Bégin and France Thériault for secretarial help, Christine Villemaire for assistance with computer software, and Gaetan Tremblay for programming support.
Received December 21, 1998; revision received March 18, 1999; accepted March 23, 1999.
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P. Milliez, N. DeAngelis, C. Rucker-Martin, A. Leenhardt, E. Vicaut, E. Robidel, P. Beaufils, C. Delcayre, and S. N. Hatem Spironolactone reduces fibrosis of dilated atria during heart failure in rats with myocardial infarction Eur. Heart J., October 2, 2005; 26(20): 2193 - 2199. [Abstract] [Full Text] [PDF]
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S. Saba, A. M. Janczewski, L. C. Baker, V. Shusterman, E. C. Gursoy, A. M. Feldman, G. Salama, C. F. McTiernan, and B. London Atrial contractile dysfunction, fibrosis, and arrhythmias in a mouse model of cardiomyopathy secondary to cardiac-specific overexpression of tumor necrosis factor-{alpha} Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1456 - H1467. [Abstract] [Full Text] [PDF]
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T. H. Everett IV, E. E. Wilson, S. Foreman, and J. E. Olgin Mechanisms of Ventricular Fibrillation in Canine Models of Congestive Heart Failure and Ischemia Assessed by In Vivo Noncontact Mapping Circulation, September 13, 2005; 112(11): 1532 - 1541. [Abstract] [Full Text] [PDF]
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R. Zou, J. Kneller, L. J. Leon, and S. Nattel Substrate size as a determinant of fibrillatory activity maintenance in a mathematical model of canine atrium Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1002 - H1012. [Abstract] [Full Text] [PDF]
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W. Anne, R. Willems, T. Roskams, P. Sergeant, P. Herijgers, P. Holemans, H. Ector, and H. Heidbuchel Matrix metalloproteinases and atrial remodeling in patients with mitral valve disease and atrial fibrillation Cardiovasc Res, September 1, 2005; 67(4): 655 - 666. [Abstract] [Full Text] [PDF]
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J. S. Healey, A. Baranchuk, E. Crystal, C. A. Morillo, M. Garfinkle, S. Yusuf, and S. J. Connolly Prevention of Atrial Fibrillation With Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: A Meta-Analysis J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1832 - 1839. [Abstract] [Full Text] [PDF]
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B. J. Scherlag, W. Yamanashi, U. Patel, R. Lazzara, and W. M. Jackman Autonomically Induced Conversion of Pulmonary Vein Focal Firing Into Atrial Fibrillation J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1878 - 1886. [Abstract] [Full Text] [PDF]
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J. Kneller*, J. Kalifa*, R. Zou, A. V. Zaitsev, M. Warren, O. Berenfeld, E. J. Vigmond, L. J. Leon, S. Nattel, and J. Jalife Mechanisms of Atrial Fibrillation Termination by Pure Sodium Channel Blockade in an Ionically-Realistic Mathematical Model Circ. Res., March 18, 2005; 96(5): e35 - e47. [Abstract] [Full Text] [PDF]
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S. Geidel, J. Ostermeyer, M. Lass, M. Betzold, A. Duong, F. Jensen, S. Boczor, and K.-H. Kuck Three years experience with monopolar and bipolar radiofrequency ablation surgery in patients with permanent atrial fibrillation Eur. J. Cardiothorac. Surg., February 1, 2005; 27(2): 243 - 249. [Abstract] [Full Text] [PDF]
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A. Verma, O. M. Wazni, N. F. Marrouche, D. O. Martin, F. Kilicaslan, S. Minor, R. A. Schweikert, W. Saliba, J. Cummings, J. D. Burkhardt, et al. Pre-existent left atrial scarring in patients undergoing pulmonary vein antrum isolation: An independent predictor of procedural failure J. Am. Coll. Cardiol., January 18, 2005; 45(2): 285 - 292. [Abstract] [Full Text] [PDF]
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A. M. Pritchett, D. W. Mahoney, S. J. Jacobsen, R. J. Rodeheffer, B. L. Karon, and M. M. Redfield Diastolic dysfunction and left atrial volume: A population-based study J. Am. Coll. Cardiol., January 4, 2005; 45(1): 87 - 92. [Abstract] [Full Text] [PDF]
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H.-R. Neuberger, U. Schotten, S. Verheule, S. Eijsbouts, Y. Blaauw, A. van Hunnik, and M. Allessie Development of a Substrate of Atrial Fibrillation During Chronic Atrioventricular Block in the Goat Circulation, January 4, 2005; 111(1): 30 - 37. [Abstract] [Full Text] [PDF]
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S. G. Williams, D. T. Connelly, M. Jackson, A. Bennett, K. Albouaini, and D. M. Todd Does treatment with ACE inhibitors or angiotensin II receptor antagonists prevent atrial fibrillation after dual chamber pacemaker implantation? Europace, January 1, 2005; 7(6): 554 - 559. [Abstract] [Full Text] [PDF]
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