Europace Advance Access originally published online on March 12, 2008
Europace 2008 10(4):425-432; doi:10.1093/europace/eun063
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'ABLATE AND PACE': STILL A VALID TREATMENT FOR AF
Atrioventricular junction ablation and pacemaker implant for atrial fibrillation: still a valid treatment in appropriately selected patients
Department of Cardiology, John Radcliffe Hospital, Headley Way, Headington, Oxford OX3 9DU, UK
Manuscript submitted 7 February 2008. Accepted after revision 19 February 2008.
* Corresponding author. Tel: + 44 1865 220256; fax: + 44 1865 221194. E-mail address: tim.betts{at}orh.nhs.uk
| Abstract |
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This review explores the current techniques of atrioventricular junction ablation, pacemaker prescription and implant, the role of anti-arrhythmic drugs, long-term outcomes, potential complications and adverse effects (including sudden cardiac death), and how these may be overcome, and examines the alternative strategies that are now available.
Key Words: Ablation, Atrial fibrillation, Atrioventricular node, Pacemaker, Heart block
| Introduction |
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Deliberate destruction of the atrioventricular (AV) junction to create complete AV conduction block has been used as a form of ventricular rate control for patients with atrial fibrillation for over 25 years.1
| Technique of atrioventricular junction ablation |
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The standard approach
Complete heart block is achieved by permanently destroying the AV node or His bundle. This is almost universally achieved by using percutaneous catheter radiofrequency ablation. For patients who usually receive formal anticoagulation for thromboprophylaxis, oral anticoagulant medication is stopped 3–5 days before the procedure to minimize the risk of pacemaker haematoma. As the procedure does not influence the underlying rhythm, cardioversion will not occur. It is conventional for the entire procedure to be performed under conscious sedation. The most common approach is right-sided with access via the femoral vein. Two venous punctures and catheters are required: one to perform the ablation and one to pace the right ventricle temporarily once heart block has been achieved and the patient is awaiting permanent pacemaker implant. The temporary pacing wire threshold should be checked prior to ablation and the rate set to 40 bpm so that heart block can be recognized. Some patients may already have permanent ventricular pacemakers in place. In this case, the device should be programmed to VVI mode at 40 bpm. There may be concern that the radiofrequency current will cause oversensing and inappropriate inhibition of the pacing wire. Although it is rare for this to occur, it has been observed in older generators and is probably more likely to occur with unipolar leads. If inappropriate inhibition does occur, the system should be reprogrammed immediately to VOO mode. With permanent pacemakers, this can also be achieved by placing a pacemaker magnet over the pulse generator.
The position of the AV node and His bundle is identified by using fluoroscopic landmarks and electrogram recordings. In a posteroanterior view, the junction is typically at the apex of the curve of the temporary pacing catheter and overlying the vertebrae. In a left anterior oblique view, clockwise twist of the catheter will ensure it is placed on the septal aspect of the tricuspid annulus (Figure 1; R). An annular electrogram signal will demonstrate an atrial component and a ventricular component. When positioned correctly (around 1 oclock on the tricuspid valve annulus on the left anterior oblique view), a His bundle electrogram will be clearly seen in between the atrial and ventricular signals (Figure 2). The AV node is in atrial tissue at the apex of the Triangle of Koch and does not have a characteristic electrogram. Ablation of the AV node may produce a slightly faster, more stable escape rhythm from the His bundle which is often narrow complex, whereas ablation lower down the hierarchy at the His bundle is likely to result in a slower, broad complex ventricular escape rhythm which may be less reliable. An atrial-to-ventricular electrogram ratio of >1:1 indicates an atrial position that favours AV node ablation, a ratio of 1:2 to 1:5 suggests an annular position favouring the His bundle, and a very small or absent atrial signal means the catheter is probably too far into the ventricle and is recording a right bundle branch potential rather than the His bundle. The presence of atrial fibrillation can make the electrograms difficult to interpret due to the presence of high frequency, small amplitude atrial potentials. The His bundle electrogram can be identified by the consistent timing interval between it and the ventricular electrogram or onset of the surface ECG QRS complex.
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Application of radiofrequency energy may cause a transient accelerated junctional rhythm and then heart block should occur within 10 s (Figure 3). If not, the catheter is probably not positioned correctly and the energy should be discontinued and a better position sought. If heart block appears, the energy application should be continued for 60 s. It is then important to observe the rhythm for 20–30 min to ensure heart block is permanent before moving on to pacemaker implant.
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Alternative routes
An alternative route to the His bundle is the retrograde transaortic approach via the femoral artery (Figure 1; L). The aortic valve is crossed and the anterior (membranous) septum explored a few millimetres below the aortic valve. A right-sided His bundle catheter may act as a fluoroscopic reference. The target is a signal with atrial and ventricular potentials and the largest His bundle electrogram. The size of the atrial electrogram is not important. The left-sided approach may be attempted if heart block is not achieved from the right side. A randomized trial of the two approaches showed a higher success rate using fewer lesions with the left-sided approach.2
Atrioventricular junction ablation from the subclavian or axillary vein approach has also been described. An asymmetric curve ablation catheter is inserted through the same venous access site that is used for pacing. The permanent right ventricular (RV) pacing lead is positioned first and then the ablation catheter is steered through a second axillary or subclavian vein sheath. After heart block is achieved, the ablation catheter is removed and an atrial lead placed using the same sheath, or the sheath simply removed. This technique was used successfully in a consecutive series of 17 patients with a median of 3 (range 1–10) burns required for heart block.5
In one patient, AV conduction returned and further ablation was performed through the femoral route. The disadvantage of this technique is that there is a redundant venous access site if only single-chamber pacing is required.
Difficult cases
Overall, there is a 98–99% success rate in achieving complete AV block, although there is a reported 7–10% incidence of conduction recurrence necessitating a second ablation procedure.6
,7
Despite its apparent ease and simplicity, occasionally it can be difficult to achieve permanent AV junction ablation. If this is due to an inability to identify the His bundle electrogram or differentiate it from atrial signals during atrial fibrillation, it may help to perform internal or external DC cardioversion so that mapping can be performed in sinus rhythm. This may be impossible to achieve in long-standing permanent atrial fibrillation, but only a short period of sinus rhythm is required. Care must be taken however to observe proper anticoagulation protocols for cardioversion, and for persistent fibrillation, this may require transoesophageal echocardiography to exclude left atrial thrombus, followed by immediate anticoagulation. The most effective His bundle ablation site may be identified by using unipolar electrogram recordings rather than the standard bipolar approach, particularly if a QS morphology is present.8
Recently, ablation catheter technology has been developed that can create larger and deeper lesions. Saline-irrigated catheters or 8 mm tip catheters may be used rather than the conventional 4 mm tip catheter. Ablation of the His bundle may be successfully performed from the aortic root, at the level of the non-coronary cusp.9
It is very rare nowadays to need to resort to intracoronary alcohol ablation.10
If ablation proves to be unsuccessful, it may still be prudent to implant the pacemaker and then return after 1–3 months with a second attempt, either right- or left-sided.
| Pacemaker implant |
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Timing of pacemaker implant
When ablation is performed from the femoral route, a temporary transvenous RV pacing wire is required. The permanent pacemaker is typically implanted immediately following AV junction ablation to minimize the period of temporary pacing. An alternative strategy is to implant the permanent pacemaker either 6–8 weeks before the ablation procedure or in a single session but prior to the ablation. This avoids the need for a temporary pacing wire and if performed weeks before the ablation, could allow for ongoing anticoagulation if a left-sided approach or DC cardioversion is required as part of the ablation procedure. The natural concern is that the ablation procedure could inadvertently damage or dislodge the permanent pacing leads, however this did not occur in a series of 70 patients in whom the pacemaker was implanted immediately prior to the ablation.11
Pacing mode
Patients with permanent atrial fibrillation will require only a single-lead system. Rate response is an obvious requirement due to the underlying complete heart block. A dual chamber AV sequential pacemaker would usually be considered the mode of choice for patients with paroxysmal atrial fibrillation.3
Dual-chamber pacing allows AV synchrony during sinus rhythm and physiological changes in heart rate determined by sinus node activity. It also avoids pacemaker syndrome which may otherwise occur in 20–25% of patients.14
Although VVIR pacing in patients with paroxysmal atrial fibrillation may abolish symptomatic palpitations, it is not as effective at improving other symptoms, such as fatigue and dyspnoea, as DDD pacing, presumably due to the loss of AV synchrony during sinus rhythm.14
Mode-switching algorithms must be turned on and rate response is still required during periods of atrial fibrillation. Mode-switching at the onset and offset of atrial fibrillation episodes needs to be rapid to minimize symptoms.15
The particular algorithm used does not appear to be important.16
Appropriate atrial sensitivity and blanking and refractory periods must be programmed to allow arrhythmia detection and ensure correct mode-switching function. VDDR pacing is an alternative option with the benefits of a single-lead and AV synchrony, however the inability to pace the atrium may be a disadvantage.17
Although retrospective analysis has suggested that VVI pacing in paroxysmal atrial fibrillation is associated with an increased risk of progression to permanent atrial fibrillation, this has not been borne out in other studies.18
–20
Even when dual chamber pacing is used, there remains a 10–24% incidence of progression to permanent atrial fibrillation and this increases as follow-up continues.18
–22
This may make the symptomatic benefits of AV synchronous pacing transient, arguing the case for a single-lead VDDR or VVIR pacemaker.23
,24
Another potential advantage of dual-chamber pacing in patients with paroxysmal atrial fibrillation is the ability to choose a device with atrial fibrillation prevention or treatment algorithms. The overall reduction in arrhythmia burden is small at best and has not been consistent across a number of studies, and these more sophisticated pulse generators are typically more expensive.25
–27
Acute procedure-related complications
Acute complications of an ablate and pace approach can be subdivided into those associated with the ablation and those associated with pacing. Although very early series reported failure to achieve heart block in up to 18.5% of cases, modern technology and techniques now make this an extremely rare occurrence, occurring in only 1–2%.6
,7
Bleeding at venous or arterial access sites may be limited by stopping anticoagulation prior to the procedure. Pacemaker complications include lead displacement, haematoma, infection, pneumothorax, and pericardial effusions.
Role of ongoing anti-arrhythmic drug therapy
Patients with permanent atrial fibrillation who undergo AV junction ablation can have their rate-controlling medications stopped unless they are required for other indications such as angina, heart failure, or hypertension. Patients with paroxysmal atrial fibrillation have the option of stopping anti-arrhythmics or continuing them with the aim of reducing atrial fibrillation burden. Many patients will be undergoing AV junction ablation because they cannot tolerate anti-arrhythmic drug therapy; however, a proportion will be doing so as drug therapy has been partially effective, but not enough to provide satisfactory rhythm control. Continuing anti-arrhythmic drug therapy may reduce symptoms that result from the loss of atrial contraction and AV synchrony that have not been addressed by AV junction ablation and prevent progression to permanent atrial fibrillation. A randomized trial comparing withdrawal to continuation of anti-arrhythmic drugs did indeed show a reduction in progression to permanent atrial fibrillation with anti-arrhythmic medication (21 vs. 37% at 12 months) but this was at the expense of a higher incidence of heart failure (22 vs. 10%) and hospitalizations, with no difference in quality of life scores or adverse outcomes.28
Other authors have shown in retrospective studies that continuation of anti-arrhythmic drugs is not associated with a reduction in progression to permanent atrial fibrillation.20
,29
Although there is some evidence that permanent atrial fibrillation at the time of AV junction ablation is associated with an increased risk of thrombo-embolism, there is no evidence to suggest that ongoing anti-arrhythmic therapy in patients with paroxysmal atrial fibrillation will reduce the risk.30
The lack of clinical benefit and the risk of potential harm would therefore suggest that anti-arrhythmic medication should be stopped after AV junction ablation in most individuals.
| Outcomes |
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Symptoms and quality of life
Many retrospective studies have documented significant acute and long-term improvement in haemodynamics, symptoms, and quality of life score in selected patients with paroxysmal and persistent drug-refractory atrial fibrillation who have undergone AV junction ablation and pacemaker insertion.31
Patients included in ablate and pace studies were typically enrolled, as they had symptoms due to a rapid ventricular rate that was not satisfactorily controlled with drug therapy. The mechanism by which patients improve is principally through better ventricular rate control, however withdrawal of rate-controlling drugs may also improve quality of life by the abolition of negative inotropic, chronotropic (in sinus rhythm), and systemic side effects.46
Regularization of the ventricular rate may also play a part, potentially even offering symptomatic and haemodynamic improvement in patients with ventricular rates that lie within the normal range.47
,48
Sudden cardiac death
There has been some concern that AV junction ablation and pacemaker insertion may predispose patients to an increased risk of sudden cardiac death.49
Early studies are conflicting however, with 1 year sudden death rates varying from 0 to 9%.45
,50
The majority of those who suffered sudden death in the initial published series had a significant number of risk factors, including reduced LV function, symptomatic heart failure, and a history of ventricular arrhythmias.51
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The proposed mechanism of sudden death is bradycardia-dependent prolongation of the QT interval.49
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This may be overcome by setting the ventricular pacing rate to a minimum of 80 or 90 bpm for the first 1–2 months following the ablation, then reducing it to a conventional 60–70 bpm.49
,54
Recent large studies with long-term follow-up that adopted this approach have subsequently demonstrated a low incidence of sudden death.55
,56
Overall, the 1 year total mortality is 6.3% and sudden death rate is 2%, which is similar to that of control patients with atrial fibrillation who remain on drug therapy.45
,55
Heart failure
In recent years, it has become widely publicized that RV pacing can result in harm by causing ventricular dyssynchrony.57
Constant RV pacing may lead to increased heart failure admissions or death in patients who already have significantly impaired LV function.58
There is therefore concern that rendering a patient dependent upon RV pacing following AV junction ablation may lead to deterioration in LV function. The effect on LV function and heart failure symptoms are not consistent in the literature, with some studies showing a deterioration,44
,59
others no change39
,42
and many an overall improvement.36
,39
,41
,45
This disparity may relate to the initial mechanism of LV impairment and heart failure symptoms in patients undergoing ablate and pace treatment, i.e. tachycardia cardiomyopathy, which is reversed by achieving rate control, and the high proportion of patients with normal LV function included in the majority of studies.
A number of approaches have been used to overcome the potential deleterious effects of RV apical pacing, including right septal, RV outflow tract, para-Hisian, direct His bundle, or biventricular pacing. Direct His bundle pacing produces an activation sequence closest to normal physiological activation, and in dilated cardiomyopathy, patients can avoid a further deterioration in LV function.60
,61
In patients with cardiac co-morbidities and reasonably well-preserved LV function, para-Hisian pacing produces improvements in functional status and exercise capacity which are not seen with RV apical pacing.62
The challenge with His bundle pacing is that success is dependent upon an intact His-Purkinje system distal to the pacing site. Atrioventricular junction ablation needs to be performed at the level of the AV node rather than His bundle. There are also concerns about the stability of an active fixation lead at a site so close to the tricuspid valve in patients who may otherwise be pacing dependent. The results of septal and outflow tract pacing are inconclusive.63
,64
Biventricular pacing offers haemodynamic and symptomatic improvement to patients with severely impaired LV function, symptomatic heart failure, and ventricular dyssynchrony. It would seem logical that biventricular pacing rather than RV apical pacing would offer a greater improvement in LV performance and symptoms, or at least prevent deterioration, in heart failure patients undergoing ablate and pace procedures. The PAVE study65
tested this hypothesis by randomizing 184 patients with a mean LVEF of 46% to biventricular or RV pacing. NYHA class II or III heart failure was present in 83%. Both groups showed an improvement in 6 min walk distance compared with baseline which was immediate. The two pacing modalities did not differ until 6 months after the procedure, when a small deterioration in the RV pacing group resulted in a significant difference between the two. Within 6 weeks, the RV pacing group showed a significant fall in LV ejection fraction which persisted at 6 months, whereas the biventricular pacing group did not change from baseline values. Close analysis shows however that the differences in exercise capacity are due to patients with good LV function or NYHA class I heart failure who received only RV pacing suffering from a fall in exercise capacity between 3 and 6 months while all other groups stayed the same. Patients with impaired LV function at baseline who underwent biventricular pacing showed the greatest improvement and those with NYHA class II or III heart failure who received biventricular pacing improved significantly more than those who received RV pacing. It would therefore seem prudent to consider LV lead placement or His bundle pacing for patients with LV ejection fractions <45% and are NYHA class II or III. It should be pointed out however that in the PAVE study, 14% of randomized patients failed to have an LV lead successfully implanted.
| Alternatives to ablate and pace |
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Atrioventricular nodal modification
Selective ablation of atrial inputs to the AV node (the slow pathway area adjacent to the anterior border of the coronary sinus ostium) has been investigated as a rate-control strategy that may avoid the need for permanent pacemaker insertion.50
Pulmonary vein isolation/left atrial circumferential ablation
Once thought to be beyond the reach of catheter ablation, it is now possible to achieve rhythm control in a significant proportion of patients with highly symptomatic, drug-refractory paroxysmal or persistent atrial fibrillation. A number of different techniques have been described, yet all have in common extensive ablation in the left atrium around the orifices of the pulmonary veins.68
–70
Depending upon the nature of the atrial fibrillation, the institution and operators experience, and the length of follow-up, rhythm control may be achieved in 70–90% of patients. This degree of rhythm control often necessitates multiple ablation procedures, with each procedure carrying a risk of major complications, including stroke, of 6%.71
As yet, no randomized controlled trials have compared an ablate and pace rate-control approach with a left atrial ablation rhythm-control approach. One retrospective comparative case series in elderly patients with cardiac co-morbidities suggested that ablate and pace has better rate control at the expense of increased heart failure symptoms and a higher degree of progression to permanent atrial fibrillation, however all the pacemakers used were single-chamber, many without rate response, unfairly disadvantaging the ablate and pace group.72
Left atrial ablation is continuing to emerge as a viable treatment, particularly in patient groups in which ventricular pacing is best avoided (the young or those with heart failure) and in which atrial systole and AV synchrony is desired.
Indications for atrioventricular junction ablation and pacemaker insertion
Patients suitable for AV junction ablation fall into a number of different categories (Table 1).
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Patients with pacemakers or implantable cardioverter-defibrillators with poor rate control during paroxysmal or persistent atrial fibrillation
If a device is already implanted, the decision to perform AV junction ablation is often easier to make. Paroxysmal atrial fibrillation with a rapid ventricular rate may cause inappropriate shock therapy in patients with implantable cardioverter-defibrillators (ICDs). If this cannot be controlled with drug therapy, AV junction ablation will ensure a constant, paced ventricular rate. As the majority of ICD recipients have impaired LV function, upgrading to a biventricular device may be necessary to avoid worsening of heart failure.
Sinus node disease often accompanies paroxysmal atrial fibrillation and there may be a valid bradycardia indication for pacemaker insertion. Incorporating AV junction ablation may abolish symptoms enough to avoid anti-arrhythmic drug medication with all of its potential side effects.
Patients with persistent atrial fibrillation who undergo biventricular pacing for heart failure
Cardiac resynchronization therapy is only effective if there is close to 100% ventricular pacing. Patients with atrial fibrillation, left bundle branch block, and intact AV conduction may not benefit from CRT if more than 5–10% of ventricular activation is sensed intrinsic conduction. In this situation, AV junction ablation increases the likelihood of a symptomatic response.
Patients with drug-refractory atrial fibrillation with a rapid ventricular rate who do not wish to undergo or are unsuitable for pulmonary vein isolation
The decision to attempt pulmonary vein isolation or AV junction ablation is not always clear cut. If the principle problem is symptomatic palpitations due to a rapid ventricular rate and the patient is elderly, an ablate and pace approach offers good symptomatic benefit with a minimal procedural risk. Those whose symptoms are due in part to the loss of atrial contractile function may be better off attempting a rhythm control strategy with pulmonary vein isolation. In young patients, it is advisable to avoid pacemaker insertion if at all possible in view of the risk of long-term complications such as lead failure, axillary vein thrombosis, pacemaker endocarditis, and the need for multiple generator changes.
Patients with tachycardia cardiomyopathy due to drug-refractory recurrent, persistent, or permanent atrial fibrillation
A proportion of patients with tachycardia cardiomyopathy develop LV impairment, as they are unaware of their arrhythmia and the rapid ventricular rate. They only notice symptoms once the cardiomyopathy has developed. Initial treatment is the restoration and maintenance of sinus rhythm with cardioversion and anti-arrhythmic drug therapy, but if this is unsuccessful and atrial fibrillation with a rapid ventricular rate returns, more definitive action is required. In younger patients, pulmonary vein isolation may be preferable, however recurrent arrhythmias are common and repeated procedures may be required. An ablate and pace approach may be more appropriate, particularly in the elderly.
Pulmonary vein isolation and ablate and pace need not be exclusive. If acceptable rhythm control cannot be achieved after one or two left atrial ablation procedures, AV junction ablation and pacemaker insertion may offer at least some improvement. In the AFFIRM study,73
5% of patients in the rate control group required AV junction ablation after failing a mean of 2.4 ± 0.7 medications. Even in the modern era of drug therapy, complex devices, and sophisticated ablation techniques, the elegant simplicity of the ablate and pace approach should not be ignored. Current published guidelines support the appropriate use of this therapy, which remains a valuable tool in the treatment of atrial fibrillation.3
,74
Conflict of interest: T. R. B. has received a grant from Boston Scientific to fund research that is not related to the subject matter of this review.
| References |
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[1] Gallagher JJ, Svenson RH, Kasell JH, German LD, Bardy GH, Broughton A, et al. Catheter technique for closed-chest ablation of the atrioventricular conduction system. N Engl J Med (1982) 306:194–200.[Abstract]
[2] Kalbfleisch SJ, Williamson B, Man KC, Vorperian V, Hummel JD, Calkins H, et al. A randomized comparison of the right- and left-sided approaches to ablation of the atrioventricular junction. Am J Cardiol (1993) 72:1406–10.[CrossRef][Web of Science][Medline]
[3] Brignole M, Gammage M, Jordaens L, Sutton R. Report of a study group on ablate and pace therapy for paroxysmal atrial fibrillation. Barcelona Discussion Group. Working Group on Arrhythmias of the European Society of Cardiology. Europace (1999) 1:8–13.
[4] Zivin A, Knight BP, Souza J, Bahu M, Weiss R, Goyal R, et al. Predictors of crossover to a left ventricular approach for atrioventricular junction ablation. Am J Cardiol (1997) 80:1611–2.[CrossRef][Web of Science][Medline]
[5] Issa ZF. An approach to ablate and pace: AV junction ablation and pacemaker implantation performed concurrently from the same venous access site. Pacing Clin Electrophysiol (2007) 30:1116–20.[CrossRef][Medline]
[6] Brignole M, Gianfranchi L, Menozzi C, Alboni P, Musso G, Bongiorni MG, et al. Assessment of atrioventricular junction ablation and DDDR mode-switching pacemaker versus pharmacological treatment in patients with severely symptomatic paroxysmal atrial fibrillation: a randomized controlled study. Circulation (1997) 96:2617–24.
[7] Olgin JE, Scheinman MM. Comparison of high energy direct current and radiofrequency catheter ablation of the atrioventricular junction. J Am Coll Cardiol (1993) 21:557–64.[Abstract]
[8] Ito S, Tada H, Naito S, Kutsumi Y, Miyamori I, Nogami A, et al. Randomized comparison of bipolar vs. unipolar plus bipolar recordings during atrioventricular junction ablation: importance and efficacy of unipolar recording. Circ J (2007) 71:874–9.[CrossRef][Web of Science][Medline]
[9] Cuello C, Huang SK, Wagshal AB, Pires LA, Mittleman RS, Bonavita GJ. Radiofrequency catheter ablation of the atrioventricular junction by a supravalvular noncoronary aortic cusp approach. Pacing Clin Electrophysiol (1994) 17:1182–5.[CrossRef][Medline]
[10] Strickberger SA, Foster PR, Wang PJ, Okishige K, Friedman PL. Intracoronary infusion of dilute ethanol for control of ventricular rate in patients with atrial fibrillation. Pacing Clin Electrophysiol (1993) 16:1984–93.[CrossRef][Medline]
[11] Proclemer A, Facchin D, Pagnutti C, Fioretti P, De Michele C. Safety of pacemaker implantation prior to radiofrequency ablation of atrioventricular junction in a single session procedure. Pacing Clin Electrophysiol (2000) 23:998–1002.[CrossRef][Medline]
[12] Padeletti L, Michelucci A, Pieragnoli P, Colella A, Musilli N. Atrial septal pacing: a new approach to prevent atrial fibrillation. Pacing Clin Electrophysiol (2004) 27:850–4.[CrossRef][Medline]
[13] Ramdat MA, Beukema WP, Oude Luttikhuis HA. Multisite or alternate site pacing for the prevention of atrial fibrillation. Am J Cardiol (1999) 83:237D–240D.[CrossRef][Web of Science][Medline]
[14] Marshall HJ, Harris ZI, Griffith MJ, Holder RL, Gammage MD. Prospective randomized study of ablation and pacing versus medical therapy for paroxysmal atrial fibrillation: effects of pacing mode and mode-switch algorithm. Circulation (1999) 99:1587–92.
[15] Kamalvand K, Tan K, Kotsakis A, Bucknall C, Sulke N. Is mode switching beneficial? A randomized study in patients with paroxysmal atrial tachyarrhythmias. J Am Coll Cardiol (1997) 30:496–504.[Abstract]
[16] Marshall HJ, Harris ZI, Griffith MJ, Gammage MD. Prospective, randomized study of atrioventricular node ablation and mode-switching, dual chamber pacemaker implantation using two different algorithms in patients with paroxysmal atrial fibrillation. Europace (1999) 1:20–1.
[17] Buys EM, van Hemel NM, Jessurun ER, Kelder JC, Bakema L, Kingma JH. VDDR pacing after His-bundle ablation for paroxysmal atrial fibrillation: a pilot study. Pacing Clin Electrophysiol (1998) 21:1869–72.[CrossRef][Medline]
[18] McComb JM, Gribbin GM. Chronic atrial fibrillation in patients with paroxysmal atrial fibrillation, atrioventricular node ablation and pacemakers: determinants and treatment. Europace (1999) 1:30–4.
[19] Mitchell MA, Ackerman SJ, Nath S, Haines DE, DiMarco JP. Atrial rhythm after atrioventricular junctional ablation. Am J Cardiol (1996) 78:1251–4.[CrossRef][Web of Science][Medline]
[20] Queiroga A, Marshall HJ, Clune M, Gammage MD. Ablate and pace revisited: long term survival and predictors of permanent atrial fibrillation. Heart (2003) 89:1035–8.
[21] Gianfranchi L, Brignole M, Menozzi C, Lolli G, Bottoni N. Progression of permanent atrial fibrillation after atrioventricular junction ablation and dual-chamber pacemaker implantation in patients with paroxysmal atrial tachyarrhythmias. Am J Cardiol (1998) 81:351–4.[CrossRef][Web of Science][Medline]
[22] Wood MA, Curtis AB, Takle-Newhouse TA, Ellenbogen KA. Survival of DDD pacing mode after atrioventricular junction ablation and pacing for refractory atrial fibrillation. Am Heart J (1999) 137:682–5.[CrossRef][Web of Science][Medline]
[23] Gillis AM. Selection of pacing mode after interruption of atrioventricular conduction for atrial fibrillation: observations from the PA3 clinical trial. Card Electrophysiol Rev (2003) 7:312–4.[CrossRef][Medline]
[24] Gillis AM, Connolly SJ, Lacombe P, Philippon F, Dubuc M, Kerr CR, et al. Randomized crossover comparison of DDDR versus VDD pacing after atrioventricular junction ablation for prevention of atrial fibrillation. The atrial pacing peri-ablation for paroxysmal atrial fibrillation (PA (3)) study investigators. Circulation (2000) 102:736–41.
[25] Hemels ME, Wiesfeld AC, Inberg B, van Dessel PF, Nieuwland W, Tan ES, et al. Right atrial overdrive pacing for prevention of symptomatic refractory atrial fibrillation. Europace (2006) 8:107–12.
[26] Lewalter T, Yang A, Pfeiffer D, Ruiter J, Schnitzler G, Markert T, et al. Individualized selection of pacing algorithms for the prevention of recurrent atrial fibrillation: results from the VIP registry. Pacing Clin Electrophysiol (2006) 29:124–34.[CrossRef][Medline]
[27] Redfearn DP, Yee R. Pacing delivered rate and rhythm control for atrial fibrillation. Curr Opin Cardiol (2006) 21:83–7.[Web of Science][Medline]
[28] Brignole M, Menozzi C, Gasparini M, Bongiorni MG, Botto GL, Ometto R, et al. An evaluation of the strategy of maintenance of sinus rhythm by antiarrhythmic drug therapy after ablation and pacing therapy in patients with paroxysmal atrial fibrillation. Eur Heart J (2002) 23:892–900.
[29] Gribbin GM, Bourke JP, McComb JM. Predictors of atrial rhythm after atrioventricular node ablation for the treatment of paroxysmal atrial arrhythmias. Heart (1998) 79:548–53.
[30] Gasparini M, Mantica M, Brignole M, Gianfranchi L, Menozzi C, Pizzetti F, et al. Thromboembolism after atrioventricular node ablation and pacing: long term follow up. Heart (1999) 82:494–8.
[31] Kay GN, Bubien RS, Epstein AE, Plumb VJ. Effect of catheter ablation of the atrioventricular junction on quality of life and exercise tolerance in paroxysmal atrial fibrillation. Am J Cardiol (1988) 62:741–4.[CrossRef][Web of Science][Medline]
[32] Rodriguez LM, Smeets JL, Xie B, De Chillou C, Cheriex E, Pieters F, et al. Improvement in left ventricular function by ablation of atrioventricular nodal conduction in selected patients with lone atrial fibrillation. Am J Cardiol (1993) 72:1137–41.[CrossRef][Web of Science][Medline]
[33] Twidale N, Sutton K, Bartlett L, Dooley A, Winstanley S, Heddle W, et al. Effects on cardiac performance of atrioventricular node catheter ablation using radiofrequency current for drug-refractory atrial arrhythmias. Pacing Clin Electrophysiol (1993) 16:1275–84.[CrossRef][Medline]
[34] Brignole M, Gianfranchi L, Menozzi C, Bottoni N, Bollini R, Lolli G, et al. Influence of atrioventricular junction radiofrequency ablation in patients with chronic atrial fibrillation and flutter on quality of life and cardiac performance. Am J Cardiol (1994) 74:242–6.[CrossRef][Web of Science][Medline]
[35] Jensen SM, Bergfeldt L, Rosenqvist M. Long-term follow-up of patients treated by radiofrequency ablation of the atrioventricular junction. Pacing Clin Electrophysiol (1995) 18:1609–14.[Medline]
[36] Fitzpatrick AP, Kourouyan HD, Siu A, Lee RJ, Lesh MD, Epstein LM, et al. Quality of life and outcomes after radiofrequency His-bundle catheter ablation and permanent pacemaker implantation: impact of treatment in paroxysmal and established atrial fibrillation. Am Heart J (1996) 131:499–507.[CrossRef][Web of Science][Medline]
[37] Buys EM, van Hemel NM, Kelder JC, Ascoop CA, van Dessel PF, Bakema L, et al. Exercise capacity after His bundle ablation and rate response ventricular pacing for drug refractory chronic atrial fibrillation. Heart (1997) 77:238–41.
[38] Kim SG, Sompalli V, Rameneni A, Gadde MK, Pamidi M, Pathapati R, et al. Symptomatic improvement after AV nodal ablation and pacemaker implantation for refractory atrial fibrillation and atrial flutter. Angiology (1997) 48:933–8.[Web of Science][Medline]
[39] Manolis AG, Katsivas AG, Lazaris EE, Vassilopoulos CV, Louvros NE. Ventricular performance and quality of life in patients who underwent radiofrequency AV junction ablation and permanent pacemaker implantation due to medically refractory atrial tachyarrhythmias. J Interv Card Electrophysiol (1998) 2:71–6.[CrossRef][Web of Science][Medline]
[40] Marshall HJ, Harris ZI, Griffith MJ, Gammage MD. Atrioventricular nodal ablation and implantation of mode switching dual chamber pacemakers: effective treatment for drug refractory paroxysmal atrial fibrillation. Heart (1998) 79:543–7.
[41] Twidale N, Manda V, Nave K, Seal A. Predictors of outcome after radiofrequency catheter ablation of the atrioventricular node for atrial fibrillation and congestive heart failure. Am Heart J (1998) 136:647–57.[CrossRef][Web of Science][Medline]
[42] Brignole M, Menozzi C, Gianfranchi L, Musso G, Mureddu R, Bottoni N, et al. Assessment of atrioventricular junction ablation and VVIR pacemaker versus pharmacological treatment in patients with heart failure and chronic atrial fibrillation: a randomized, controlled study. Circulation (1998) 98:953–60.
[43] Brignole M, Gianfranchi L, Menozzi C, Alboni P, Musso G, Bongiorni MG, et al. Prospective, randomized study of atrioventricular ablation and mode-switching, dual chamber pacemaker implantation versus medical therapy in drug-resistant paroxysmal atrial fibrillation. The PAF study. Paroxysmal Atrial Fibrillation. Europace (1999) 1:15–9.
[44] Vanderheyden M, Goethals M, Anguera I, Nellens P, Andries E, Brugada J, et al. Hemodynamic deterioration following radiofrequency ablation of the atrioventricular conduction system. Pacing Clin Electrophysiol (1997) 20:2422–8.[CrossRef][Medline]
[45] Wood MA, Brown-Mahoney C, Kay GN, Ellenbogen KA. Clinical outcomes after ablation and pacing therapy for atrial fibrillation: a meta-analysis. Circulation (2000) 101:1138–44.
[46] Natale A, Zimerman L, Tomassoni G, Newby K, Leonelli F, Fanelli R, et al. AV node ablation and pacemaker implantation after withdrawal of effective rate-control medications for chronic atrial fibrillation: effect on quality of life and exercise performance. Pacing Clin Electrophysiol (1999) 22:1634–9.[CrossRef][Medline]
[47] Natale A, Zimerman L, Tomassoni G, Kearney M, Kent V, Brandon MJ, et al. Impact on ventricular function and quality of life of transcatheter ablation of the atrioventricular junction in chronic atrial fibrillation with a normal ventricular response. Am J Cardiol (1996) 78:1431–3.[CrossRef][Web of Science][Medline]
[48] Ueng KC, Tsai TP, Tsai CF, Wu DJ, Lin CS, Lee SH, et al. Acute and long-term effects of atrioventricular junction ablation and VVIR pacemaker in symptomatic patients with chronic lone atrial fibrillation and normal ventricular response. J Cardiovasc Electrophysiol (2001) 12:303–9.[CrossRef][Web of Science][Medline]
[49] Geelen P, Brugada J, Andries E, Brugada P. Ventricular fibrillation and sudden death after radiofrequency catheter ablation of the atrioventricular junction. Pacing Clin Electrophysiol (1997) 20:343–8.[CrossRef][Medline]
[50] Twidale N, McDonald T, Nave K, Seal A. Comparison of the effects of AV nodal ablation versus AV nodal modification in patients with congestive heart failure and uncontrolled atrial fibrillation. Pacing Clin Electrophysiol (1998) 21:641–51.[CrossRef][Medline]
[51] Yeung-Lai-Wah JA, Qi A, Uzun O, Humphries K, Kerr CR. Long-term survival following radiofrequency catheter ablation of atrioventricular junction for atrial fibrillation: clinical and ablation determinants of mortality. J Interv Card Electrophysiol (2002) 6:17–23.[CrossRef][Web of Science][Medline]
[52] Ozcan C, Jahangir A, Friedman PA, Hayes DL, Munger TM, Rea RF, et al. Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation. J Am Coll Cardiol (2002) 40:105–10.
[53] Peters RH, Wever EF, Hauer RN, Wittkampf FH, Robles de Medina EO. Bradycardia dependent QT prolongation and ventricular fibrillation following catheter ablation of the atrioventricular junction with radiofrequency energy. Pacing Clin Electrophysiol (1994) 17:108–12.[CrossRef][Medline]
[54] Nowinski K, Gadler F, Jensen-Urstad M, Bergfeldt L. Transient proarrhythmic state following atrioventricular junction radiofrequency ablation: pathophysiologic mechanisms and recommendations for management. Am J Med (2002) 113:596–602.[CrossRef][Web of Science][Medline]
[55] Ozcan C, Jahangir A, Friedman PA, Patel PJ, Munger TM, Rea RF, et al. Long-term survival after ablation of the atrioventricular node and implantation of a permanent pacemaker in patients with atrial fibrillation. N Engl J Med (2001) 344:1043–51.
[56] Gasparini M, Mantica M, Brignole M, Coltorti F, Galimberti P, Gianfranchi L, et al. Long-term follow-up after atrioventricular nodal ablation and pacing: low incidence of sudden cardiac death. Pacing Clin Electrophysiol (2000) 23:1925–9.[Medline]
[57] Healey JS, Yee R, Tang A. Right ventricular apical pacing: a necessary evil? Curr Opin Cardiol (2007) 22:33–8.[Web of Science][Medline]
[58] Wilkoff BL, Cook JR, Epstein AE, Greene HL, Hallstrom AP, Hsia H, et al. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA (2002) 288:3115–23.
[59] Tops LF, Schalij MJ, Holman ER, van Erven L, van der Wall EE, Bax JJ. Right ventricular pacing can induce ventricular dyssynchrony in patients with atrial fibrillation after atrioventricular node ablation. J Am Coll Cardiol (2006) 48:1642–8.
[60] Deshmukh P, Casavant DA, Romanyshyn M, Anderson K. Permanent, direct His-bundle pacing: a novel approach to cardiac pacing in patients with normal His-Purkinje activation. Circulation (2000) 101:869–77.
[61] Catanzariti D, Maines M, Cemin C, Broso G, Marotta T, Vergara G. Permanent direct His bundle pacing does not induce ventricular dyssynchrony unlike conventional right ventricular apical pacing. An intrapatient acute comparison study. J Interv Cardiac Electrophysiol (2006) 16:81–92.[CrossRef][Web of Science][Medline]
[62] Occhetta E, Bortnik M, Magnani A, Francalacci G, Piccinino C, Plebani L, et al. Prevention of ventricular desynchronization by permanent para-Hisian pacing after atrioventricular node ablation in chronic atrial fibrillation: a crossover, blinded, randomized study versus apical right ventricular pacing. J Am Coll Cardiol (2006) 47:1938–45.
[63] Stambler BS, Ellenbogen K, Zhang X, Porter TR, Xie F, Malik R, et al. Right ventricular outflow versus apical pacing in pacemaker patients with congestive heart failure and atrial fibrillation. J Cardiovasc Electrophysiol (2003) 14:1180–6.[CrossRef][Web of Science][Medline]
[64] Mera F, DeLurgio DB, Patterson RE, Merlino JD, Wade ME, Leon AR. A comparison of ventricular function during high right ventricular septal and apical pacing after His-bundle ablation for refractory atrial fibrillation. Pacing Clin Electrophysiol (1999) 22:1234–9.[CrossRef][Medline]
[65] Doshi RN, Daoud EG, Fellows C, Turk K, Duran A, Hamdan MH, et al. Left ventricular-based cardiac stimulation post AV nodal ablation evaluation (the PAVE study). J Cardiovasc Electrophysiol (2005) 16:1160–5.[CrossRef][Web of Science][Medline]
[66] Williamson BD, Man KC, Daoud E, Niebauer M, Strickberger SA, Morady F. Radiofrequency catheter modification of atrioventricular conduction to control the ventricular rate during atrial fibrillation. N Engl J Med (1994) 331:910–7.
[67] Morady F, Hasse C, Strickberger SA, Man KC, Daoud E, Bogun F, et al. Long-term follow-up after radiofrequency modification of the atrioventricular node in patients with atrial fibrillation. J Am Coll Cardiol (1997) 29:113–21.[Abstract]
[68] Nademanee K, McKenzie J, Kosar E, Schwab M, Sunsaneewitayakul B, Vasavakul T, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol (2004) 43:2044–53.
[69] Pappone C, Rosanio S, Oreto G, Tocchi M, Gugliotta F, Vicedomini G, et al. Circumferential radiofrequency ablation of pulmonary vein ostia: a new anatomic approach for curing atrial fibrillation. Circulation (2000) 102:2619–28.
[70] Haissaguerre M, Jais P, Shah DC, Takahashi A, Hocini M, Quiniou G, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med (1998) 339:659–66.
[71] Cappato R, Calkins H, Chen SA, Davies W, Iesaka Y, Kalman J, et al. Worldwide survey on the methods, efficacy, and safety of catheter ablation for human atrial fibrillation. Circulation (2005) 111:1100–5.
[72] Hsieh MH, Tai CT, Lee SH, Tsao HM, Lin YK, Huang JL, et al. Catheter ablation of atrial fibrillation versus atrioventricular junction ablation plus pacing therapy for elderly patients with medically refractory paroxysmal atrial fibrillation. J Cardiovasc Electrophysiol (2005) 16:457–61.[CrossRef][Web of Science][Medline]
[73] Olshansky B, Rosenfeld LE, Warner AL, Solomon AJ, ONeill G, Sharma A, et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: approaches to control rate in atrial fibrillation. J Am Coll Cardiol (2004) 43:1201–8.
[74] Fuster V, Ryden LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: full text: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Europace (2006) 8:651–745.
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