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(Circulation. 2001;103:2120.)
© 2001 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
Nonpharmacological Approaches to Atrial Fibrillation
From the Cardiovascular Research Institute, University of California, San Francisco (M.M.S.), and Division of Cardiology, University of Michigan Medical Center, Ann Arbor, Mich (F.M.).
Correspondence to Fred Morady, MD, Cardiology, B1F245, University of Michigan Medical Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0022. E-mail fmorady{at}umich.edu
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Abstract |
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Top
Abstract
Atrioventricular Junction...The mainstay of managing atrial fibrillation (AF) is drug therapy. In some patients, drug therapy is ineffective or not tolerated. This article reviews the current status of various nonpharmacological options for the treatment of AF.
Key Words: atrial fibrillation • ablation • pacing
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Atrioventricular Junction Ablation |
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Transvenous ablation of the atrioventricular (AV) junction was first performed with direct-current shocks in 1981.1 Radiofrequency energy replaced direct-current shocks for AV junction ablation because of improved efficacy and safety.2 Radiofrequency ablation of the AV junction has a success rate >95% and is associated with a low incidence of adverse effects.3 Although sudden death due to ventricular tachycardia/fibrillation may occur after successful ablation of the AV junction,3 this risk may be minimized by pacing at a lower rate limit of 80 to 90 beats/min for several days to weeks after ablation.
Long-Term Observations
Retrospective studies have documented long-term
improvement in quality-of-life, functional capacity, and left
ventricular function in patients with impaired
systolic function who undergo AV junction ablation. A
prospective study confirmed an improvement in both quality-of-life and
ventricular function in these patients, and it also
demonstrated a reduction in long-term costs compared with standard drug
therapy.4 These findings are
supported by a recent meta-analysis, which also found no
evidence of a higher mortality rate in patients who had undergone AV
junction ablation than in those in large anticoagulant
trials.5
Summary
The available data indicate that AV junction ablation
improves quality-of-life, functional capacity, and
ventricular function. Compared with other types of
nonpharmacological therapy for AF, a major advantage of AV junction
ablation is that its success rate approaches 100%. However, the
disadvantages of AV junction ablation include the lifelong need for a
pacemaker and an ongoing risk of thromboembolic
complications.
AV junction ablation is appropriate in symptomatic patients with AF and an uncontrolled ventricular rate who have failed treatment with several antiarrhythmic drugs (often including amiodarone), particularly when there is evidence of a tachycardia-induced cardiomyopathy. Because of lifelong pacemaker dependency, an alternative form of nonpharmacological therapy may be more suitable for the younger patient with drug-refractory AF.
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AV Node Modification |
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Several studies have demonstrated that radiofrequency energy applied to the right posterior or midseptal regions results in a significant and sustained reduction in ventricular rate during AF in 60% to 85% of patients.6 7 8 In one study, this procedure was associated with a 21% incidence of either early or late AV block.6 Compared with AV junction ablation, the advantage of AV node modification is the achievement of rate control during AF without the need for long-term pacing. However, AV node modification has not achieved widespread use because of a high recurrence rate and because symptoms caused by an irregular rhythm may persist. An attempt at AV node modification is most appropriate in patients who are appropriate candidates for AV junction ablation and who wish to avoid pacemaker implantation. Because of a high risk of AV block, AV node modification should not be recommended in patients who consider the possibility of pacemaker implantation unacceptable.
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Atrial Pacing to Prevent AF |
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Vagotonic AF
Coumel et al9 demonstrated the efficacy of atrial pacing in patients with AF of vagal origin. These patients have AF triggered by sinus bradycardia or atrial bigeminy, usually at rest, during sleep, or after meals. Typically, vagotonic AF is paroxysmal and occurs in men without the sick sinus syndrome or structural heart disease. If treatment with a vagolytic antiarrhythmic drug such as disopyramide is ineffective, atrial pacing may be appropriate.
Pacing in Patients With the Sick Sinus
Syndrome
Retrospective studies have shown that atrial-based
pacing in patients with the sick sinus syndrome is superior to
ventricular demand pacing with respect to the incidence of AF
and the risk of cerebrovascular accidents, congestive heart failure,
and overall mortality. This has been confirmed in prospective,
randomized
trials.10 11
However, when bradycardia is not an indication for pacing, atrial-based
pacing may not prevent episodes of
AF.12
Dual-Site Atrial Pacing
Dual-site atrial pacing results in more
homogeneous atrial depolarization and repolarization than
conventional pacing, and it is more efficacious than single-site pacing
for preventing
AF.13 14 However,
it is important to note that the patients in these studies had a
bradycardia indication for pacing, and they continued to require
treatment with antiarrhythmic drugs.
Summary
The bulk of available data supports the use of
atrial-based pacing for the purpose of decreasing the incidence of AF
episodes in patients with vagotonic AF or sinus node disease. Atrial
pacing cannot be justified on the basis of existing data in patients
with nonvagotonic AF or those without sinus node disease. Although
dual-site atrial pacing remains an intriguing and potentially important
treatment modality, its efficacy requires confirmation in prospective,
randomized trials.
Patients should be informed that antiarrhythmic drug therapy often continues to be required after pacemaker implantation. If AF remains troublesome despite pacing, AV junction ablation can be considered as a next step in management.
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Internal Atrial Defibrillator |
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By preventing remodeling, rapid conversion of AF may decrease the predisposition toward additional episodes of AF. An implantable atrial defibrillator in theory is an excellent modality for the detection and rapid conversion of AF. Implanted atrial defibrillators are safe and have an 80% efficacy in terminating AF.15 Limited data suggest that early cardioversion by the implanted atrial defibrillator prolongs the interval between recurrent episodes of AF.16 The drawbacks of the implanted atrial defibrillator include discomfort from the shocks, early recurrence of AF, and technical problems with the device.
Because frequent shocks are undesirable, the ideal candidate for an implanted atrial defibrillator has infrequent episodes of symptomatic, drug-refractory AF. However, if episodes of AF are rare, it is difficult to justify implanting a device. At present, the implanted atrial defibrillator is available only in combination with a ventricular defibrillator.
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Surgical Treatment of AF |
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Maze Procedure
Creating anatomic barriers in the atria may decrease the number of circulating wavelets to a level below the critical number required to sustain AF. Accordingly, Cox et al17 demonstrated that a series of atrial incisions in patients with AF was often effective in restoring and maintaining sinus rhythm long-term. This "maze" procedure has been refined, and it is typically performed in association with mitral valve or coronary bypass surgery. In recent studies of 39 to 100 patients undergoing the maze procedure, 74% to 90% of patients were in sinus rhythm at 2 to 3 years postoperatiely.18 19 The operative mortality rate is
1%, but up to 6% of patients have
required a
pacemaker.18 19
In >90% of patients, the right and left atria regain mechanical
function.20 The maze
procedure has also been performed in patients with lone paroxysmal AF,
with a 95% success
rate.21
Other Surgical Approaches
Another intraoperative approach for treating AF in
patients undergoing valve surgery has consisted of cryoablation limited
to the posterior left atrium. Linear cryolesions connecting the 4
pulmonary veins and the posterior mitral annulus were effective
in restoring sinus rhythm long-term in 69% of patients with chronic
AF.22
At the time of mitral valve repair or replacement, endocardial isolation of the pulmonary veins was performed under direct visualization using an electrode catheter in 43 patients with chronic AF and dilated atria.23 At 1 year postoperatively, 30% of patients were in sinus rhythm and had functioning atria. Although this is a low success rate, the study demonstrates that the pulmonary veins may sometimes play a critical role in maintaining AF, even in patients with mitral valve disease and a dilated left atrium. In such patients, chronic atrial remodeling might have been expected to make AF permanent, independent of the pulmonary veins.
Summary
Surgical therapy for AF is most appropriate in patients
who require open-heart surgery for another indication. In such
patients, AF is often eliminated with little or no increase in
morbidity or mortality. In patients with lone AF or no other indication
for surgery, an intraoperative approach for the treatment of AF may be
unattractive because of the potential risks, discomfort, and prolonged
convalescence associated with heart
surgery.
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Focal Catheter Ablation of AF |
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Background
There are 2 different types of arrhythmias that may play a role in generating AF, and both may be addressed by focal ablation. One type of arrhythmia is a premature depolarization that initiates AF.24 A second type is a focal tachycardia that either induces fibrillation in the atria or mimics AF by creating a pattern of rapid and irregular depolarization wavefronts in the atria.25 Focal tachycardias that initiate or mimic AF can be recognized in the electrophysiology laboratory because they are frequently associated with exit block between the site of origin of the tachycardia and the rest of the atria.26
Although focal sources of AF may be found in the right
atrium, left atrium, coronary sinus, superior vena cava, or
vein of Marshall, 95% of foci are located within a pulmonary
vein.27 The
pulmonary veins are covered by myocardial sleeves formed by one
or more layers of myocardial fibers oriented in circular, longitudinal,
oblique, or spiral
directions.28 These sleeves
vary from 2 to 25 mm in length, with a mean length of 
10 to
20 mm in the superior pulmonary veins and 5 to 10 mm
in the inferior pulmonary
veins.28 29 The
difference in the length of the sleeves may explain why arrhythmogenic
foci are found more often in the superior than in the
inferior pulmonary veins. The arrhythmogenic nature
of these myocardial sleeves may be due in part to their embryonic
origin from the same substrate that gives rise to the conduction
system, which may be subject to abnormal
automaticity.30 However, it
is unclear whether the arrhythmias that arise in
pulmonary veins are most often due to automaticity, reentry, or
triggered activity, and it is possible that more than one mechanism
plays a role in generating these
arrhythmias.
Focal Ablation Within Pulmonary
Veins
One approach to the ablation of a pulmonary
vein arrhythmia that triggers or simulates AF is to target the
site of origin of the arrhythmia within the pulmonary
vein directly. Localization of the site of origin of the
arrhythmia is guided by the endocardial activation
time.31 Two published
studies have described the results of focal ablation within a
pulmonary vein with 
6 months of follow-up. These studies
consisted of 41 to 79 patients who had frequent atrial ectopy and
episodes of paroxysmal AF, and 65 to 103 ectopic foci originated within
a pulmonary
vein.24 32
Radiofrequency ablation was guided by activation mapping, and a mean of
4 to 7 applications of radiofrequency energy was delivered in the
pulmonary veins. In one of the studies, 75% of patients
required a second or third ablation procedure, and after a mean
follow-up interval of 8 months, 62% of patients were free of
symptomatic AF in the absence of antiarrhythmic drug
therapy.24 The results were
more impressive in the other study, with only 7% of patients needing a
second ablation procedure and a success rate of 86% at a mean of 6
months of follow-up.32
However, in a later publication from the same laboratory, the
recurrence rate at a mean of 8 months of follow-up had
increased to
25%.33
The most common complications associated with the focal
ablation of arrhythmias arising within the pulmonary
veins are pericardial effusion (4%), transient ischemic
episodes (2%), and symptomatic pulmonary vein
stenosis
(2%).24 25 32
Although asymptomatic pulmonary vein
stenosis may occur at as many as 40% of sites at which focal
ablation is performed,32 the
risk of symptomatic pulmonary vein stenosis
seems to be small if the number of radiofrequency applications
delivered within pulmonary veins is kept to a
minimum.
The early experience with the focal ablation of pulmonary vein arrhythmias indicates that the recurrence rate is high and the success rate only modest, even in experienced laboratories. The suboptimal results can be attributed to the limitations of the technique, which include the following: (1) many patients have multiple foci; (2) there may be a paucity of spontaneous or inducible arrhythmias during the procedure; (3) new foci may emerge after the procedure; (4) the risk of pulmonary vein stenosis limits the amount of radiofrequency energy that can be safely delivered within a pulmonary vein; and (5) mapping may be made difficult by frequent recurrences of persistent AF.
Pulmonary Vein Isolation
The limitations associated with focal ablation within
pulmonary veins have prompted the development of other
techniques for eliminating the pulmonary vein
arrhythmias that trigger or mimic AF. One alternative is
electrically isolating the pulmonary veins by circumferential
ablation at their ostia. An anatomically based procedure eliminates the
need for spontaneous or induced arrhythmias, eliminates the
need for mapping, and would be effective in preventing recurrent AF
caused by multiple pulmonary vein foci, even if new foci emerge
at some future time.
Two techniques have been used to isolate pulmonary veins electrically. One technique involves the delivery of multiple, contiguous point applications of radiofrequency energy in a circumferential fashion in the left atrium near the ostia of the pulmonary veins.34 Another technique uses ultrasound energy to create a circumferential lesion with a catheter that has an ultrasound transducer mounted near its tip.35 The transducer is inside an inflatable balloon that is used to occlude the pulmonary vein and to stabilize the transducer at the left atrial–pulmonary vein junction. This technique was successful in 67% of 15 patients with paroxysmal or persistent AF.35
In theory, anatomically based techniques for pulmonary vein isolation have significant advantages over focal ablation within the pulmonary veins. However, the published experience with these techniques is minimal, and their feasibility and safety remain to be established.
Segmental Isolation of Pulmonary
Veins
The myocardial fibers that envelope the
pulmonary veins may not be present along the entire
circumference of the pulmonary vein ostia. Therefore, to
eliminate conduction in and out of a pulmonary vein, ablation
along the entire circumference of the ostium may not be necessary.
Instead, radiofrequency energy can be targeted to the segments of the
ostium at which muscle fibers are present. These sites are
identified by the presence of high-frequency depolarizations, which
likely represent pulmonary vein muscle potentials. The
recording of ostial pulmonary vein potentials is
facilitated by catheters that have multiple electrodes along a distal
loop that fits within the ostium. There is compelling evidence that
electrical pulmonary vein isolation can be achieved by
selective ablation of ostial sites where a pulmonary vein
potential is recorded, which may encompass as little as 25% of the
circumference of the
ostium.36 In the experience
of the authors, complete electrical isolation may be achieved with as
few as 1 to 5 applications of radiofrequency energy.
Because ostial pulmonary vein potentials can be recorded during sinus rhythm or atrial pacing, a segmental approach to pulmonary vein isolation does not require detailed mapping of spontaneous ectopy. It is sufficient to identify which veins are arrhythmogenic, which is usually a much simpler task than pinpointing the site of origin of a focus within a pulmonary vein. If no ectopy is present during the ablation procedure, it may be appropriate to perform empiric segmental isolation of the left and right superior and left inferior pulmonary veins, because these are the most common sources of the arrhythmias that trigger AF.
Another advantage of this technique is that the end point of
ablation is unambiguous. The elimination of all pulmonary vein
potentials within the pulmonary vein indicates that there are
no remaining muscle fibers at the ostium that are capable of conducting
impulses in or out of the pulmonary veins. In one study of 90
patients with paroxysmal AF, the success rate in preventing recurrent
AF in the absence of drug therapy at a mean of 8 months of follow-up
was 90% when pulmonary vein potentials were eliminated in all
arrhythmogenic pulmonary veins, compared with only 55% when
pulmonary vein potentials were still present in 1
pulmonary
veins.36
In that study, no instances of pulmonary vein stenosis occurred when the power of radiofrequency applications was limited to 30 W, even when ostial ablation was circumferential.36
The initial experience with segmental ostial ablation of pulmonary veins guided by pulmonary vein potentials is encouraging, with a long-term success rate of 90% in patients with paroxysmal AF and with minimal or no risk of pulmonary vein stenosis when the power of radiofrequency energy applications is limited to 30 W. Major advantages of this technique are that it eliminates the need for detailed mapping of all pulmonary vein foci and that there is a clear-cut end point of ablation, even when spontaneous arrhythmias are absent. Furthermore, the procedure can be performed with conventional ablation catheters and does not require specialized tools such as a balloon ultrasound ablation catheter. However, occasional patients may remain symptomatic from AF triggered by ectopy arising at sites other than the pulmonary veins.
Chronic AF
Little data are available as yet regarding the efficacy
of radiofrequency ablation within pulmonary veins in the
electrophysiology laboratory in patients with chronic AF. In 2 studies,
an arrhythmogenic pulmonary vein was identified in a total of
18 patients with chronic AF by mapping the ectopy that resulted in
early recurrence of AF after repeated transthoracic
or transvenous
defibrillation.37 38
Radiofrequency ablation, either at the pulmonary vein ostia or
within the pulmonary veins, resulted in long-term sinus rhythm
in 60% to 67% of patients.
The early experience with focal ablation in patients with chronic AF is not sufficient to justify its widespread clinical application. The proportion of patients with chronic AF in whom a focal reinitiating trigger can be identified and the long-term outcome after the radiofrequency ablation of these triggers remain to be determined. Also unclear at this time is whether chronic AF is more amenable to a focal approach directed at the pulmonary veins or to linear ablation in the atria.
Summary
At present, the best candidates for the elimination
of focal triggers of AF are symptomatic, drug-refractory
patients with paroxysmal AF and normal or only mildly enlarged left
atria. On the basis of the limited data available to date, the most
appropriate ablation strategy that is currently feasible in clinical
practice may be to identify the pulmonary vein or veins that
are arrhythmogenic and to attempt to isolate these veins with segmental
ostial lesions guided by pulmonary vein potentials aimed at
eliminating all conduction pathways in and out of the
veins.
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Linear Catheter Ablation of AF |
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Background
Attempts to replicate the results of the maze procedure in the electrophysiology laboratory have consisted of the creation of linear lesions in the left and/or right atria. The linear lesions have been produced either with individual, contiguous applications of radiofrequency energy on a point-by-point basis or with multiple catheters with coil electrodes that are positioned against the atrial wall and that produce a linear lesion without having to repeatedly reposition the catheter.
Right Atrial Ablation
In some studies, linear ablation for AF has been
confined to the right atrium. Although AF is probably never an
exclusively right atrial arrhythmia, by eliminating the
circulating wavelets in the right atrium, linear ablation confined to
the right atrium may be helpful by either promoting early conversion of
AF or improving the response to drug therapy. The number of linear
lesions created in the right atrium most commonly has been 3, with a
range of 1 to
4.39 40 41 42 43
The most common locations of the ablation lines are between the
inferior and superior vena cava; the septum; and the cavotricuspid
isthmus.
In 5 studies, 8 to 45 patients underwent linear ablation in only the right atrium.39 40 41 42 43 In most patients in these studies, AF was idiopathic and paroxysmal. During mean follow-up intervals of 6 to 21 months, only 6% to 25% of patients remained free of symptomatic AF in the absence of antiarrhythmic drug therapy. An additional 20% to 58% of patients had a marked improvement in AF-related symptoms during treatment with antiarrhythmic medications that had been ineffective before the ablation procedure. Therefore, although linear ablation confined to the right atrium eliminates AF in only a small percentage of patients, it more often may be helpful in a palliative fashion by improving the response to drug therapy.
Left Atrial Ablation
Studies of linear left atrial ablation (with or without
right atrial ablation) have included 10 to 19 patients followed for a
mean of 6 to 11
months.39 41 43
The ablation technique has been either to encircle all 4
pulmonary vein ostia and connect this encircling lesion with
the mitral annulus or to create linear lesions from the superior
pulmonary veins through the ostia of the inferior
pulmonary veins to the mitral annulus and between the 2
superior pulmonary veins. In 2 studies, 40% to 58% of
patients had no recurrences of AF in the absence of
antiarrhythmic drug therapy, and another 10% to 20% had an
improvement during treatment with previously ineffective
drugs.39 41
However, these results have not been reproducible, and in a third
study, none of the 12 patients who underwent a combined right and left
atrial approach had a successful
outcome.43
Complications
Because there have been only a small number of clinical
studies describing the results of linear ablation of AF and because
these studies have included small numbers of patients and have used
different techniques, a reliable estimate of the magnitude of risk
associated with linear ablation is not yet available. The most common
complication that has been reported to occur as a result of linear
ablation of AF in the left and/or right atria has been pericardial
effusion, which occurred 11% of
patients.39 40 41 42 43
A complication limited to linear ablation in the right atrium has been
sinus node dysfunction, which has occurred in 8% of
patients.39 40 41 42 43
Two serious types of complications limited to left atrial ablation are
cerebral infarction, which has been reported in 8% of
patients,39 41 43
and pulmonary vein stenosis, the incidence of which is
unclear. An anecdotal report documented the occurrence of
pulmonary vein stenosis causing symptomatic
pulmonary hypertension in 2 patients who underwent linear
ablation in the left
atrium,44 but this
complication was not observed in any of the published series of
patients who underwent linear ablation of AF.
Limitations of Linear Ablation of AF
Conduction block across a linear radiofrequency lesion
in the atrium usually requires continuous transmural necrosis. In the
electrophysiology laboratory, continuous lesions that result in
complete conduction block are difficult to achieve, particularly in the
left atrium and when using individual, contiguous applications of
radiofrequency energy with a conventional ablation catheter. Precise
manipulation and stabilization of an electrode catheter in the left
atrium is a technically challenging and lengthy process, even in the
hands of experienced operators using specialized guiding sheaths and
sophisticated mapping systems that allow tagging of ablation sites. In
a study in which an electroanatomic mapping system was used to guide
the creation of linear ablation lines in the left atrium, the mean
procedure duration exceeded 7 hours, and yet a set of ablation lines
associated with complete conduction block could not be achieved in any
of the 13 patients in the
study.43
Even when linear radiofrequency lesions are created under optimal conditions with a hand-held probe in the operating room, the ablation lines may often be discontinuous. An ablation line that creates incomplete conduction block may be sufficient to prevent AF, but it may be proarrhythmic, allowing new atrial reentrant tachycardias to emerge. Among 25 patients in whom linear, endocardial radiofrequency lesions were created under direct visualization in the left and right atria during open heart surgery, AF was successfully eliminated in 91% of patients.45 However, 6 of the 25 patients (24%) had postoperative atrial flutter that was attributable to reentry through a gap in an ablation line. The frequent failure to achieve complete conduction block, even when radiofrequency lesions are created under direct visualization in the open heart, emphasizes the tremendous challenge associated with creating complete lines of block in the electrophysiology laboratory.
Summary
The risk-benefit ratio of linear ablation in the left
and/or right atrium remains to be defined. At present, this
technique should be viewed as an investigational procedure and should
be restricted to patients with symptomatic AF who have been
refractory to multiple antiarrhythmic
drugs.
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Conclusions |
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In the minority of patients in whom AF cannot be adequately managed by pharmacological therapy, the most appropriate type of nonpharmacological therapy must be selected on an individualized basis. For example, in a cardiomyopathy patient with chronic AF and an uncontrolled ventricular rate, AV junction ablation may be the optimal therapy. In a patient with the sick sinus syndrome, atrial-based pacing (perhaps biatrial) may be the most appropriate option. In a patient who requires an implantable cardioverter-defibrillator and who has occasional episodes of AF, implantation of a device capable of both atrial and ventricular defibrillation should be considered.
If the patient has idiopathic AF, an attempt at curative therapy is often the most attractive option. In the opinion of the authors, the best technique currently available for curing paroxysmal AF (assuming it originates from the pulmonary veins) is segmental isolation of the pulmonary veins by discrete applications of radiofrequency energy at the ostia, guided by pulmonary vein potentials. Other techniques for pulmonary vein isolation, such as a balloon catheter used to create a circumferential lesion at the ostium, hold promise but require further development.
In the patient with idiopathic AF that is persistent or chronic, the best curative catheter ablation technique remains to be determined. On the basis of surgical experience and preliminary results with catheter techniques, it may be that the most effective curative catheter technique for chronic AF will be found to be pulmonary vein isolation in combination with linear ablation in the right and/or left atria. In the occasional patient who is disabled by chronic AF, referral for surgical treatment may be appropriate. However, at present, the most appropriate option for most patients with idiopathic chronic AF may be the use of pharmacological therapy to minimize symptoms as much as possible, prevent tachycardia-induced cardiomyopathy, and avoid thromboembolic complications, awaiting further improvements in curative catheter techniques.
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References |
|---|
1. Scheinman MM, Morady F, Hess DS, et al. Catheter-induced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias. JAMA. 1982;248:851–855.
2. Morady F, Calkins H, Langberg JJ, et al. A prospective randomized comparison of direct current and radiofrequency ablation of the atrioventricular junction. J Am Coll Cardiol. 1993;21:102–109.[Abstract]
3. Scheinman MM, Huang S. The NASPE prospective catheter ablation registry. Pacing Clin Electrophysiol. 2000;1998:23:1020–1028.
4. Kay GN, Ellenbogen KA, Giudici M, et al. The ablate and pace trial: a prospective study of catheter ablation of the AV conduction system and permanent pacemaker implantation for treatment of atrial fibrillation. J Interv Card Electrophysiol. 1998;2:121–135.[Medline] [Order article via Infotrieve]
5.
Wood MA,
Brown-Mahoney C, Kay GN, et al. Clinical outcomes after ablation and
pacing therapy for atrial fibrillation: a meta-analysis.
Circulation. 2000;101:1138–1144.
6.
Williamson BD, Man
CK, Daoud E, et al. Radiofrequency catheter modification of
atrioventricular conduction to control the
ventricular rate during atrial fibrillation.
N Engl J Med. 1994;331:910–917.
7.
Feld GK, Fleck RP,
Fujimura O, et al. Control of rapid ventricular response by
radiofrequency catheter modification of the
atrioventricular node in patients with medical
refractory atrial fibrillation.
Circulation. 1994;90:2299–2307.
8. Della Bella P, Carbucicchio C, Tondo C, et al. Modulation of atrioventricular conduction by ablation of the "slow" atrioventricular node pathway in patients with drug-refractory atrial fibrillation or flutter. J Am Coll Cardiol. 1995;25:39–46.[Abstract]
9. Coumel P, Friocourt P, Mugica J, et al. Long-term prevention of vagal atrial arrhythmias by atrial pacing at 90/minute: experience with 6 cases. Pacing Clin Electrophysiol. 1983;6:552–560.[Medline] [Order article via Infotrieve]
10. Andersen HR, Nielsen JC, Thomsen PE, et al. Long-term follow-up of patients from a randomized trial of atrial versus ventricular pacing for sick sinus syndrome. Lancet. 1997;350:1210–1216.[Medline] [Order article via Infotrieve]
11. Gillis AM, Kerr CR. Whither physiologic pacing? Implications of CTOPP. Pacing Clin Electrophysiol. 2000;23:1193–1196.[Medline] [Order article via Infotrieve]
12.
Gillis AM, Wyse
DG, Connolly SJ, et al. Atrial pacing periablation for prevention of
paroxysmal atrial fibrillation.
Circulation. 1999;99:2553–2558.
13. Levy T, Walker S, Rochelle J, et al. Evaluation of biatrial pacing, right atrial pacing, and no pacing in patients with drug refractory atrial fibrillation. Am J Cardiol. 1999;84:426–429.[Medline] [Order article via Infotrieve]
14. Friedman PA, Hill MRS, Hammill SC, et al. Randomized prospective pilot study of long-term dual-site atrial pacing for prevention of atrial fibrillation. Mayo Clin Proc. 1998;73:848–854.[Abstract]
15.
Wellens HJJ, Lau
C-P, Luederitz B, et al. Atrioverter: an implantable device for the
treatment of atrial fibrillation.
Circulation. 1998;98:1651–1656.
16.
Timmermans C,
Levy S, Ayers GM, et al. Spontaneous episodes of atrial fibrillation
after implantation of the Metrix Atrioverter: observations on treated
and nontreated episodes. J Am Coll
Cardiol. 2000;35:1428–1433.
17. Cox JL, Boineau JP, Schuessler RB, et al. Five year experience with the Maze procedure for atrial fibrillation. Ann Thorac Surg. 1993;56:814–824.[Abstract]
18.
Handa N, Schaff
HV, Morris JJ, et al. Outcome of valve repair and the Cox maze
procedure for mitral regurgitation and associated
atrial fibrillation. J Thorac
Cardiovasc Surg. 1999;118:628–635.
19. McCarthy PM, Gillinov AM, Castle L, et al. The Cox-Maze procedure: the Cleveland Clinic experience. Semin Thorac Cardiovasc Surg. 2000;12:25–29.[Medline] [Order article via Infotrieve]
20. Cox JL, Ad N, Palazzo T, et al. Current status of the Maze procedure for the treatment of atrial fibrillation. Semin Thorac Cardiovasc Surg. 2000;12:15–19.[Medline] [Order article via Infotrieve]
21.
Jessurun ER, van
Hemel NM, Defauw JA, et al. Results of maze surgery for lone paroxysmal
atrial fibrillation.
Circulation. 2000;101:1559–1567.
22.
Gaita F, Gallotti
R, Calo L, et al. Limited posterior left atrial cryoablation in
patients with chronic atrial fibrillation undergoing valvular
heart surgery. J Am Coll
Cardiol. 2000;36:159–166.
23. Melo J, Adragao P, Neves J, et al. Surgery for atrial fibrillation using radiofrequency catheter ablation: assessment of results at 1 year. Eur J Cardiothorac Surg. 1999;15:851–855.
24.
Haissaguerre M,
Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation
by ectopic beats originating in the pulmonary veins.
N Engl J Med. 1998;339:659–666.
25.
Jais P,
Haissaguerre M, Shah DC, et al. A focal source of atrial fibrillation
treated by discrete radiofrequency ablation.
Circulation. 1997;95:572–576.
26. Tse HF, Lau CP, Kou W, et al. Prevalence and significance of exit block during arrhythmias arising in pulmonary veins. J Cardiovasc Electrophysiol. 2000;11:379–386.[Medline] [Order article via Infotrieve]
27. Shah DC, Haissaguerre M, Jais P. Catheter ablation of pulmonary vein foci for atrial fibrillation. Thorac Cardiovasc Surg. 1999;47(suppl):352–356.
28.
Nathan H, Eliakim
M. The junction between the left atrium and the pulmonary
veins: an anatomic study of human hearts.
Circulation. 1966;34:412–422.
29. Ho SY, Sanchez-Quintana D, Cabrera JA, et al. Anatomy of the left atrium: implications for radiofrequency ablation of atrial fibrillation. J Cardiovasc Electrophysiol. 1999;10:1525–1533.[Medline] [Order article via Infotrieve]
30.
Blom NA,
Gittenberger-de Groot AC, DeRuiter MC, et al. Development of the
cardiac conduction tissue in human embryos using HNK-1 antigen
expression: possible relevance for understanding of abnormal atrial
automaticity. Circulation. 1999;99:800–806.
31. Tse HF, Lau CP, Kou W, et al. Comparison of endocardial activation times at effective and ineffective ablation sites within the pulmonary veins. J Cardiovasc Electrophysiol. 2000;11:155–159.[Medline] [Order article via Infotrieve]
32. Chen SA, Hsieh MH, Tai CT, et al. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation. 199;100:1879–1886.
33. Chen SA, Tai CT, Tsai CF, et al. Radiofrequency catheter ablation of atrial fibrillation initiated by pulmonary vein ectopic beats. J Cardiovasc Electrophysiol. 2000;11:218–227.[Medline] [Order article via Infotrieve]
34.
Pappone C,
Rosanio S, Oreto G, et al. Circumferential radiofrequency ablation of
pulmonary vein ostia.
Circulation. 2000;102:2619–2628.
35.
Natale A, Pisano
E, Shewchik J, et al. First human experience with pulmonary
vein isolation using a through-the-balloon circumferential ultrasound
ablation system for recurrent atrial fibrillation.
Circulation. 2000;102:1879–1882.
36.
Haissaguerre M,
Jais P, Shah DC, et al. Electrophysiological end
point for catheter ablation of atrial fibrillation initiated from
multiple pulmonary venous foci.
Circulation. 2000;101:1409–1417.
37.
Lau CP, Tse HF,
Ayers GM. Defibrillation-guided radiofrequency ablation of atrial
fibrillation secondary to an atrial focus.
J Am Coll Cardiol. 1999;33:1217–1226.
38. Haissaguerre M, Jais P, Shah DC, et al. Catheter ablation of chronic atrial fibrillation targeting the reinitiating triggers. J Cardiovasc Electrophysiol. 2000;11:2–10.[Medline] [Order article via Infotrieve]
39. Haissaguerre M, Jais P, Shah DC, et al. Right and left atrial radiofrequency catheter ablation therapy of paroxysmal atrial fibrillation. J Cardiovasc Electrophysiol. 1996;7:1132–1144.[Medline] [Order article via Infotrieve]
40.
Gaita F, Riccardi
R, Calo L, et al. Atrial mapping and radiofrequency catheter ablation
in patients with idiopathic atrial fibrillation.
Circulation. 1998;97:2136–2145.
41.
Pappone C, Oreto
G, Lamberti F, et al. Catheter ablation of paroxysmal atrial
fibrillation using a 3D mapping system.
Circulation. 1999;100:1203–1208.
42. Garg A, Finneran W, Mollerus M, et al. Right atrial compartmentalization using radiofrequency catheter ablation for management of patients with refractory atrial fibrillation. J Cardiovasc Electrophysiol. 1999;10:763–771.[Medline] [Order article via Infotrieve]
43.
Ernst S,
Schlutter M, Ouyang F, et al. Modification of the substrate for
maintenance of idiopathic human atrial fibrillation: efficacy
of radiofrequency ablation using nonfluoroscopic catheter guidance.
Circulation. 1999;100:2085–2092.
44.
Robbins IM,
Colvin EV, Doyle TP, et al. Pulmonary vein stenosis
after catheter ablation of atrial fibrillation.
Circulation. 1998;98:1769–1775.
45.
Thomas SP,
Nunn GR, Nicholson IA, et al. Mechanism, localization, and cure of
atrial arrhythmias occurring after a new intraoperative
endocardial radiofrequency ablation procedure for atrial fibrillation.
J Am Coll Cardiol. 2000;35:442–450.
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