Open access peer-reviewed chapter

Transcatheter Ablation of Atrial Fibrillation in Patients with Chronic Heart Failure

Written By

Antonio Di Monaco, Federico Quadrini, Nicola Vitulano and Massimo Grimaldi

Submitted: May 24th, 2016 Reviewed: November 23rd, 2016 Published: February 15th, 2017

DOI: 10.5772/67024

Chapter metrics overview

1,566 Chapter Downloads

View Full Metrics


Atrial fibrillation (AF) is the most frequent of all cardiac arrhythmias and it is associated with an increased risk of stroke, systemic embolism and heart failure. Patients with AF have a twofold increased risk of death and fivefold increased risk of stroke compared with those without AF. In patients with heart failure (HF), AF ablation improves left ventricular (LV) function over short- and long-term follow-ups, especially compared with medical treatment. Furthermore, AF ablation in HF patients relates to a significant improvement in quality of life, functional class and exercise tolerance, possibly related to the improvement in LV function and hemodynamic status of the patients. Finally, data showed that restoration of sinus rhythm in this setting of patients reduced the incidence of stroke and death. In this review, we reported all the major data regarding atrial fibrillation therapy in patients with heart failure.


  • atrial fibrillation ablation
  • heart failure
  • quality of life
  • left ventricular function
  • atrial fibrosis

1. Incidence and pathogenesis of atrial fibrillation in heart failure

Atrial fibrillation (AF) is defined as a cardiac arrhythmia characterized by the surface ECG showing ‘absolutely’ irregular RR intervals and absence of distinct P waves. Irregular atrial electrical activity, represented by the “f” waves, may be seen in some ECG leads, most often in lead V1, the “f-f” interval is variable and usually shorter than 200 ms [1]. An irregular pulse should always raise the suspicion of AF, but an ECG recording is necessary to diagnose AF [1].

From a clinical point of view, AF can be categorized into five subtypes based on the presentation and duration of the arrhythmia: (1) patient who presents with AF for the first time; (2) paroxysmal AF is self-terminating, usually within 48 h, but it may continue for up to 7 days; (3) persistent AF is present when an AF episode either lasts longer than 7 days or requires termination by cardioversion; (4) AF is considered as long-standing persistent when the arrhythmia has lasted for ≥1 year; (5) permanent AF, when the presence of the arrhythmia is accepted by the patient (and physician) and when it is decided to adopt a rate control strategy [1] (Figure 1).

Figure 1.

European Society of Cardiology guidelines for classification of atrial fibrillation [1].

Atrial fibrillation, the most frequent of all cardiac arrhythmias, is associated with an increased risk of stroke, systemic embolism (SE) and heart failure (HF). Patients with AF have a twofold increased risk of death and fivefold increased risk of stroke compared with those without AF [16].

Atrial fibrillation has multiple adverse clinical implications. The loss of atrial systole and the irregular, fast heart rate contribute to symptoms such as palpitations and reduced exercise tolerance and also predispose to the development of intracardiac thrombus and systemic thromboembolism. Atrial fibrillation can also cause tachycardia-mediated cardiomyopathy or worsening of preexisting heart failure [3].

Whereas anticoagulation treatment reduced the risk for stroke, large randomized trials failed to demonstrate any significant mortality benefit of a pharmacologically based rhythm control strategy even in patients with left ventricular dysfunction when compared with a rate control strategy [711].

This has led to a widespread belief that restoration of sinus rhythm (SR) does not improve prognosis. However, in-depth analysis of these trials demonstrated that the restoration of SR was associated with a 47% lower risk for death compared with continuing AF.

Besides having a good safety profile, catheter ablation therapy for AF has proved effective in establishing and maintaining SR. Induction of AF requires an initiating trigger and perpetuation occurs because triggering activity is sustained or because of the presence of a susceptible atrial substrate. Premature atrial ectopy has been shown to be the most frequent trigger for AF. Observations in patients with dual-chamber pacemakers revealed that 48% of AF episodes were triggered by premature atrial beats, 33% were preceded by bradycardia and 17% were sudden in onset [12]. Also, continuous cardiac monitoring in postoperative patients demonstrated that supraventricular premature beats induced AF in 72–100% of cases [13].

Endocardial mapping revealed that the origin of ectopic activity initiating AF is located inside the pulmonary veins (PV) in 89–94% of cases and that AF is most often triggered by repetitive focal PV discharges [1418].

Catheter ablation targeting the fascicles, which connect the PVs to the left atrium, leads to electrical isolation of the PVs. Interestingly, after electrical isolation, up to 58% of PVs display slow, dissociated activity and some sustain ongoing tachycardia dissociated from the left atrium in SR, emphasizing the arrhythmogenic potential of these structures [19, 20].

Indeed, besides being triggers for AF, PVs can also be responsible for the perpetuation of AF. In a small series of patients who had irregular focal discharges initiating and perpetuating AF, foci at the ostium of PVs were found to be the drivers of sustained AF in 66%. Focal radiofrequency (RF) delivery targeting these foci eliminated AF in all these patients [21].

In addition, a spatial gradient in cycle length, with the PVs activating at a higher frequency than the nearest atrial tissue, has been found in some patients and this reinforces the role of PVs as AF perpetuators [2225].

The involvement of the PVs in the maintenance of AF was further emphasized by the observation that PV isolation in paroxysmal AF led to a progressive increase in the AF cycle length, culminating in the termination of AF in 75% of patients. PV isolation rendered AF noninducible in 57% of patients and prevented relapse in 74% of patients [26]. These findings led to the venous wave hypothesis, postulating a role for PVs in maintenance of AF in most patients with paroxysmal AF [27]. Later, spectral analysis and dominant frequency mapping revealed that the dominant frequency and the highest dominant frequency were spatially distributed near the PVs in most of patients with paroxysmal AF [28]. Put together, these observations emphatically substantiate the role of PVs in the initiation and maintenance of nonpermanent forms of AF.

Although elimination of PV arrhythmogenicity has been highly effective for paroxysmal AF, it has modest efficacy for persistent AF suggesting that mechanisms beyond the PVs also contribute to perpetuation of AF in these patients. A number of ablation strategies have been proposed: linear ablation, ablation of complex fractionated atrial electrograms, ablation of intrinsic cardiac autonomics and ablation of rotors. Frequently these approaches are performed in combination, to target these substrate-related mechanisms beyond the PV arrhythmogenicity, particularly in patients with persistent AF [1].

In the setting of heart failure, the increased filling pressure of atrial and ventricle contributes to the electroanatomic disarrangement of the muscle fibers providing a substrate for reentry and imparts electrical heterogeneity and arrhythmogenicity to onset AF. Histological examinations of atrial tissue in patients with AF show patchy fibrosis, which may contribute to the nonhomogeneity of conduction. Atrial biopsies from patients undergone to cardiac surgery show increase in cell size, loss of sarcoplasmic reticulum and atrial myofibrils, changes in mitochondrial shape, accumulation of glycogen granules, alteration in connexin expression and increase in extracellular matrix [1]. A multicenter trial has demonstrated that atrial fibrosis, as estimated by magnetic resonance imaging (MRI), is independently associated with the likelihood of recurrent AF and in particular an extensive fibrosis caused a low success rate after catheter ablation [29]. Furthermore, recent studies showed that transmural conduction is the predominant mechanism of breakthrough during atrial fibrillation demonstrating the substrate complexity of this arrhythmia [30].

Heart failure increases the risk of AF, with the mechanism of the arrhythmia being multifactorial. Furthermore, AF is an independent risk factor for the development of heart failure and both conditions frequently coexist. Atrial fibrillation in patients with heart failure predisposes to episodes of worsening heart failure and increases the risk of thromboembolic events [1]. Hospitalizations due to AF account for one-third of all admissions for cardiac arrhythmias. Acute coronary syndrome, aggravation of heart failure, thromboembolic complications and acute arrhythmia management are the main causes. In 30% of patients with AF, it is possible to find HF with NYHA II-IV and at the same time, in 30–40% of heart failure patients, AF is found. Heart failure can be both a consequence of AF (e.g., tachycardiomyopathy or decompensation in acute onset AF) and a cause of the arrhythmia due to increased atrial pressure and volume overload, secondary valvular dysfunction, or chronic neurohumoral stimulation.

In the past decade, it showed an increase of the incidence of AF, above all in patients with HF. Many factors have contributed to these epidemiological changes; first of all, the new therapeutic approach to the cardiovascular disease and the following growing average age of patients. A recent comparison between two survey showed a significant increase in the incidence of AF in patients with HF between 38.4% in 2005 and 50.4% in 2013 [31]. Marked unexplained interregional variations in the occurrence of stroke and mortality suggest that factors other than clinical variables might be important [31]. Prevention of death from heart failure should be a major priority in the treatment of atrial fibrillation.


2. Pharmacological treatment of atrial fibrillation in heart failure

2.1. Rhythm control vs. rate control

The optimal resting ventricular rate in patients with AF and HF could be between 60 and 100 bpm [3234]. Van Gelder et al. [35] suggested that a resting ventricular rate of up to 110 bpm might still be acceptable and 2016 ESC AF guidelines recommend this threshold as the target for rate control therapy [33, 3640], but a lower rate for patients with HF may be preferable (60–100 bpm). The optimal ventricular rate during exercise is also uncertain, but may be 110 bpm during light exercise [34].

Sinus rhythm, theoretically, offers physiological rate control, normal atrial activation and contraction, a normal sequence of atrioventricular (AV) conduction and AV valvular function and a regular rhythm.

Most clinical trials (PIAF, STAF, RACE, HOT CAFÉ, CABANA and AFFIRM) [1, 911, 41, 42] have reported no clear superiority of rhythm control. Furthermore, Crijns have reported that patients with AF and HF are unlikely to remain in sinus rhythm in the long-term and 2012 focus updated of ESC guidelines of the management of atrial fibrillation, that rhythm control should not be vigorously pursued in this clinical setting [1].

However, a subgroup analysis of AFFIRM reported that rhythm control may be useful in patients with left ventricular dysfunction. In this study, patients with depressed left ventricular function benefited significantly from rhythm control compared to rate control. The presence of sinus rhythm was associated with a lower risk of death [43].

2.2. Practical approach to rate control

Rate control in AF is based mainly on pharmacological depression of conduction through the AV node. In the presence of HF, this requires careful dose titration and can result in symptomatic bradycardia requiring permanent pacing. Beta-blockers are the preferred drugs in combination with digoxin (adjunctive therapy), because they provide optimal rate control at rest and during exercise in this setting of patients [1]. The AFFIRM study showed during long-term follow-up that beta-blockers achieved optimal rate control in 58% of patients [44]. In a subgroup analysis, patients with a history of HF and left ventricular ejection fraction <40%, successful rate control was observed with beta-blocker, with or without digoxin in 81% and with digoxin alone in 54%, at 1-year follow-up.

Atrioventricular (AV) nodal ablation may be the treatment of choice in the presence of symptoms intolerable to higher rates, despite the use of rate slowing agents. Investigators compared pharmacological rate control vs. AV node ablation in 66 patients with CHF and AF [45]. In this randomized study, both treatment arms were associated with alleviation of symptoms and an increase in functional capacity. Patients treated with the “ablate and pace” strategy had fewer symptoms with no changes in cardiac performance and quality of life. This strategy was not associated with a reduction of mortality.

2.3. Practical approach to rhythm control

The potential of amiodarone to maintain sinus rhythm in patients with AF and HF has been repeatedly shown in observational and prospective randomized controlled studies.

In CTAF study, therapy with amiodarone reduced the incidence of recurrent AF by 57% when compared with sotalol and propafenone [46]. In the CHF-STAT study, patients treated with amiodarone, converted to sinus rhythm more frequently (31.3% vs. 7.7% on placebo) compared to placebo, experienced fewer recurrences of AF and were less likely to develop new AF [47]. Amiodarone is a drug of choice for the management of AF associated with HF. In addition to its antiarrhythmic effects, it is useful in controlling ventricular rate response during recurrences [47].

Dronedarone is a drug similar to amiodarone, though is devoid of iodine with a theoretically safer adverse effect profile [1]. In the dronedarone atrial fibrillation study after electrical cardioversion (DAFNE) trial, dronedarone prolonged the mean interval to recurrence of AF by 55% compared with placebo, resulting in the spontaneous conversion to sinus rhythm in high percentage of patients. The results of the European trial in atrial fibrillation or flutter patients receiving dronedarone for the maintenance of sinus rhythm (EURIDIS) and American-Australian-African equivalent ADONIS showed that dronedarone was superior to placebo in the prevention of recurrent AF and effective in controlling the ventricular rate in over 1200 patients. However, the dronedarone in moderate to severe HF evaluating morbidity decrease (ANDROMEDA) study was stopped prematurely, as an interim safety analysis suggested an excess risk of death in patients on active treatment.


3. Ablation of atrial fibrillation in HF patients

Rhythm control with antiarrhythmic drugs has not been shown to confer benefit in randomized trials, neither in patients with HF nor in those without HF [7, 8]. The lack of benefits of antiarrhythmic drugs might reflect their poor (<50%) efficacy in maintaining sinus rhythm [8]. Conversely, ablative treatment in these patients can be highly effective in reducing morbidity and improving quality of life and functional capacity [79, 4152]. However, patients with AF and left ventricular ejection fraction have more recurrences after a single procedure, thus requiring more repeat procedures, which increase costs and risks [53]. Recent studies [5460] have demonstrated that nonpulmonary vein foci firing from the atrial chambers or other thoracic veins play an important role in initiating and maintaining AF in 3.2–62% of patients, depending on age, sex and comorbidities. Patients with HF usually have a more complex and diseased atrial substrate harboring more nonpulmonary vein foci, which could be responsible for the observed recurrence of AF or atrial tachyarrhythmia AT after pulmonary vein antrum isolation.

In a recent study, Zhao et al. [61] demonstrated that patients with left ventricular ejection fraction more often presented nonpulmonary vein triggers than in patients with normal ejection fraction; in patients with the long-term procedural outcome of pulmonary vein isolation ablation alone remain unsatisfactory with a 32.2% single-procedure success rate, whereas pulmonary vein isolation plus nonpulmonary vein triggers ablation significantly increases the success rate to 75.0%, which is comparable with the success rate of pulmonary vein isolation alone in patients with normal ejection fraction (75.0% vs. 81.7%).

Patients with low ejection fraction and paroxysmal atrial fibrillation had a higher prevalence of nonpulmonary vein triggers than patients with normal ejection fraction (69.1% vs. 26.6%). Many investigators [5460] have addressed the importance of nonpulmonary vein triggers for atrial fibrillation initiation and the reported incidence of nonpulmonary vein triggers in paroxysmal atrial fibrillation.

The basis for extensive left atrial ablation lies in the pathophysiology of atrial fibrillation itself [62]: atrial fibrillation perpetuating in a left atrium with significant substrate modifications and advanced structural and electrical remodeling has historically been targeted by linear lesions [63]. However, linear lesions and CFAE ablation may increase the risk of iatrogenic atypical atrial re-entries (flutter) or atrial tachycardias if not transmural, incomplete, or not perfectly anchored to electrically inert structures, counterbalancing the benefit derived by extensive atrial substrate modification [64].

Among the studies reporting AF ablation in patients with HF, 55% of the patients underwent PV isolation alone, with a large heterogeneity among studies (6–89%). None of the observational studies were designed to compare the efficacy of different AF ablation approaches. However, in the meta-analysis by Anselmino et al. [65] including the largest available population, there was no difference in AF ablation outcome, performing PV isolation alone when compared with additional linear ablation. Moreover, no data compared the different techniques to perform AF ablation (radiofrequency, cryoablation, laser, rotors and surgery) in patients with HF. Finally, recent data reported a higher success rate after AF ablation with a hybrid approach (percutaneous and surgical), but no data were published regarding patients with HF [1].

Larger randomized studies are needed to understand the optimal procedural protocol to adopt in patient with HF and symptomatic AF.

3.1. Paroxysmal vs. persistent atrial fibrillation ablation in heart failure

Several studies have suggested that catheter ablation of AF in the context of HF is relatively safe reporting that the complication rate was not different from that in patients with structurally normal hearts [7, 4853, 6585]. The success rate for catheter ablation of paroxysmal AF was similar in HF patients compared with non-HF patients (70–80%), whereas the success rate for persistent AF was markedly worse. In randomized studies, the success rate following a single procedure has been reported at 38–68%, rising to 50–88% after repeated procedures (2 or 3) at 6–12 months [52, 7981]. Ullah et al [84] published an international multicenter registry from seven centers for patients with HF undergoing AF ablation (Figure 2). In this study with 1273 patients (171 with HF and 1102 without HF) and a median follow up of 3.1 years, the final procedure success rate was no different from paroxysmal AF (78.7% vs. 85.7%, p = 0.186), but significantly different for persistent AF (57.3% vs. 75.8%, p < 0001).

Figure 2.

Freedom from atrial fibrillation and atrial flutter after ablation in patients with and without heart failure [84].

However, despite a lower success rate in patients with HF ablated for persistent AF, Zhu et al. [85] published a meta-analysis of three randomized controlled trials showing a significant improvement of LVEF (6.22%) and reduction of NYHA class and Minnesota living with heart failure questionnaires scores in patients with HF ablated for persistent AF compared with the medical rate control.

The lower success rate for catheter ablation for persistent AF in the HF group is likely multifactorial. Both HF and the conditions leading to HF increase the left atrial pressure and wall stress that causes progressive mitral regurgitation, which further impacts on left atrial pressure and remodeling. The result of these factors is more scarred and remodeled atria, which are more inclined to support AF.

3.2. Improvement in left ventricular function and heart failure

3.2.1. Symptoms after atrial fibrillation ablation

Atrial fibrillation ablations have been shown to improve the LV function during short- and long-term follow-up, when compared to medical therapy. Several meta-analyses regarding the usefulness of AF ablation in HF patients have been published [53, 65, 82, 83, 85]. In the first two works, including maximum 800 patients, the authors concluded that single AF ablation procedure in HF patients is less effective in patients without structural disease, but improves including redo procedures, obtaining a significant improvement in LV ejection fraction over follow-up [53, 82]. The third multicenter, collaborative meta-analysis, including more than 1800 patients [65], reported over a mean follow-up of 2 years a significant improvement in LV ejection fraction and a reduction in the proportion of patients with severely depressed LV function. This finding is very important since potentially confers to ablation the ability to reduce the proportion of patients requiring implantation of cardioverter defibrillators. Moreover, the authors reported that time to first AF diagnosis and heart failure diagnosis was significantly related to ablation outcome, highlighting the importance of prompt optimal treatment of both HF and AF to achieve the best clinical benefit.

Ganesan et al. [83], furthermore, reported meta-analyses including more than 900 patients with HF-ablated for AF showing a LVEF improvement of 13%.

Ullah et al [84] in their multicentric registry reported a significant LV ejection fraction increasing from 34.4 ± 9 to 45.8 ± 12.8% (p < 0.001).

One small observational prospective study specifically investigated patients with preserved LVEF [75]. This study, including 73 patients with a mean follow-up of 34 months, reported 27% efficacy after the first procedure which further raised to 73% with redo procedures and antiarrhythmic drugs. On note, LV diastolic function and systolic function measured with strain and strain rate improved only in patients maintaining stable sinus rhythm.

Moreover, data reported that effective sinus rhythm restoration after AF ablation was useful to improve LVEF in patients with tachycardiomyopathy [48, 65].

Furthermore, AF ablation in HF patients relates to a significant improvement in quality of life, functional class and exercise tolerance, which possibly relates to the improvement in LV function and hemodynamic status of the patients. In general, shorter history of HF and AF is both associated with improved outcome: AF ablation in HF patients should be considered precociously to avoid progression of atrial substrate alteration. Left atrial dimension is a marker of advanced substrate alteration; in fact, patients with severe LA dilation present lower rate of sinus rhythm maintenance.

In particular, Ullah et al. [84] reported a reduction in NYHA class from 2.3 ± 0.7 at baseline to 1.5 ± 0.8 at follow up. This was the first study to examine specifically the impact of maintaining sinus rhythm on rates of stroke and death after catheter ablation of AF patients with HF showing that restoration of sinus rhythm reduced the incidence of stroke and death (Figure 3).

Figure 3.

Factors predicting stroke and death in patients with heart failure [84].

3.3. Indications for transcatheter ablation of atrial fibrillation in patients with heart failure

Within the general population, the safety and efficacy rates of AF ablation promoted this procedure to the first choice following one antiarrhythmic drug failure and in selected patients, even the first option before drugs [1]. Its role within HF, instead, is less well defined due to small randomized trials and observational studies [4853, 6585]. The revised European recommendations for antiarrhythmic drug therapy leave amiodarone as the only available antiarrhythmic agent in this setting [1]. In patients who suffer from symptomatic AF recurrences on amiodarone therapy, catheter ablation remains as the sole choice for rhythm control therapy [1] (Figure 4). In the last guidelines, AF ablation is indicated in symptomatic patients with reduced ejection fraction in order to improve symptoms and cardiac function (class IIa, level of evidence C) [36].

Figure 4.

European Society of Cardiology guidelines for atrial fibrillation ablation [1].

3.4. Catheter ablation of atrial fibrillation in specific cardiomyopathies populations

Some observational studies reported the outcome of AF ablation among patients with hypertrophic [65, 83, 86, 88]. All studies reported low efficacy after a single ablation procedure, especially during long-term follow-up. However, the efficacy raised up to 70–80% including the over 30% redo procedures and the prevalence of extensive left atrial ablation, including linear lesions or CFAEs, which was higher when compared with the general HF population. This finding reflects a complex substrate typical of this specific cardiomyopathy, characterized by severe left atrial enlargement. Being AF detrimental on both the quality of life and prognosis of HCM patients, its effective treatment warrants careful attention and ablation may be considered precociously to achieve rhythm control.

Moreover, although AF standard treatment in valvular cardiomyopathies is more commonly surgical, performed concomitantly to heart surgery, some studies reported the outcome of AF ablation among patients with significant valvular disease. Two studies, including patients with prosthetic valves or previous percutaneous intervention for mitral rheumatic disease, reported a very low efficacy after a single procedure, raising up to 70% at a mean follow-up of 24 months including over 50% repeated procedures [87, 88]. Other two studies including patients with moderate aortic or mitral defects, instead, reported outcomes similar to the general population [87, 89].

3.5. Future perspectives

Catheter ablation of AF is gaining a significant role in HF treatment of patients with concomitant AF, as confirmed by the latest ESC guidelines. However, the following points remains of concern. First of all, pulmonary vein isolation alone and/or additional non-PV targets, as in the general population, need to be tested in prospective randomized trials on HF patients.

Further studies, moreover, should define the optimal timing to perform AF ablation in these patients to increase the success rate and reduce mortality.

In the future, technological innovations may contribute to rise AF ablation safety, for example, new irrigated catheters able to significantly reduce the fluid administration during procedure, particularly relevant among HF patients.

Finally, due to the complexity of this procedure, the suggestion is to refer to experienced, high volume centers, also skilled to manage plausible complications.


  1. 1. Camm AJ, Lip GY, De Caterina R, Savelieva I, Atar D, Hohnloser SH, Hindricks G, Kirchhof P; ESC Committee for Practice Guidelines (CPG). 2012 focused update of the ESC guidelines for the management of atrial fibrillation: an update of the 2010 ESC guidelines for the management of atrial fibrillation. Developed with the special contribution of the European Heart Rhythm Association. Eur Heart J. 2012;33:2719–2747.
  2. 2. Schnabel RB, Yin X, Gona P, Larson MG, Beiser AS, McManus DD, Newton-Cheh C, Lubitz SA, Magnani JW, Ellinor PT, Seshadri S, Wolf PA, Vasan RS, Benjamin EJ, Levy D. 50 year trends in atrial fibrillation prevalence, incidence, risk factors and mortality in the Framingham Heart Study: a cohort study. Lancet. 2015;386:154–162.
  3. 3. Grogan M, Smith HC, Gersh BJ, et al. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol. 1992;69:1570–1573
  4. 4. Kannel WB, Abbott RD, Savage DD, McNamara PM. Epidemiologic features of chronic atrial fibrillation: the Framingham study. N Engl J Med. 1982;306:1018–1022.
  5. 5. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke. 1991;22:983–988.
  6. 6. Benjamin EJ, Wolf PA, D’Agostino RB,Silbershatz H, Kannel WB, Levy D.Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation. 1998;98:946–952.
  7. 7. Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD; Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347:1825–1833.
  8. 8. Roy D, Talajic M, Nattel S, Wyse DG, Dorian P, Lee KL, Bourassa MG, Arnold JM, Buxton AE, Camm AJ, Connolly SJ, Dubuc M, Ducharme A, Guerra PG, Hohnloser SH, Lambert J, Le Heuzey JY, O'Hara G, Pedersen OD, Rouleau JL, Singh BN, Stevenson LW, Stevenson WG, Thibault B, Waldo AL; Atrial Fibrillation and Congestive Heart Failure Investigators. Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med. 2008;358:2667–2677.
  9. 9. Van Gelder IC, Hagens VE, Bosker HA, Kingma JH, Kamp O, Kingma T, Said SA, Darmanata JI, Timmermans AJ, Tijssen JG, Crijns HJ; Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study Group. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002;347:1834–1840.
  10. 10. Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in atrial fibrillation. Pharmacological Intervention in atrial fibrillation (PIAF): a randomized trial. Lancet. 2000;356:1789–1794.
  11. 11. Corley SD, Epstein AE, DiMarco JP, Domanski MJ, Geller N, Greene HL, Josephson RA, Kellen JC, Klein RC, Krahn AD, Mickel M, Mitchell LB, Nelson JD, Rosenberg Y, Schron E, Shemanski L, Waldo AL, Wyse DG; AFFIRM Investigators. Relationships between sinus rhythm, treatment and survival in the atrial fibrillation follow-up investigation of rhythm management (AFFIRM) study. Circulation. 2004;109:1509–1513.
  12. 12. Hoffmann E, Sulke N, Edvardsson N, Ruiter J, Lewalter T, Capucci A, Schuchert A, Janko S, Camm J; Atrial Fibrillation Therapy Trial Investigators. New insights into the initiation of atrial fibrillation: a detailed intraindividual and interindividual analysis of the spontaneous onset of atrial fibrillation using new diagnostic pacemaker features. Circulation. 2006;113:1933–1941.
  13. 13. Jidéus L, Kesek M, Joachimsson PO, Ericson M, Nilsson L, Blomström-Lundqvist C.The role of premature atrial contractions as the main triggers of postoperative atrial fibrillation. J Electrocardiol. 2006;39:48–54
  14. 14. Haïssaguerre M, Jaïs P, Shah DC, Takahashi A, Hocini M, Quiniou G, Garrigue S, Le Mouroux A, Le Métayer P, Clémenty J. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med. 1998;339:659–666.
  15. 15. Chen SA, Hsieh MH, Tai CT, Tsai CF, Prakash VS, Yu WC, Hsu TL, Ding YA, Chang MS. Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses and effects of radiofrequency ablation. Circulation. 1999;100:1879–1886.
  16. 16. Valles E, Fan R, Roux JF, Liu CF, Harding JD, Dhruvakumar S, Hutchinson MD, Riley M, Bala R, Garcia FC, Lin D, Dixit S, Callans DJ, Gerstenfeld EP, Marchlinski FE. Localization of atrial fibrillation triggers in patients undergoing pulmonary vein isolation: importance of the carina region. J Am Coll Cardiol. 2008;52:1413–1420.
  17. 17. Hocini M, Haïssaguerre M, Shah D, Jaïs P, Peng JT, Yamane T, Deisenhofer I, Garrigue S, Fuimaono K, Pike R, Clémenty J. Multiple sources initiating atrial fibrillation from a single pulmonary vein identified by a circumferential catheter. Pacing Clin Electrophysiol. 2000;23:1828–1831.
  18. 18. Haïssaguerre M, Jaïs P, Shah DC, Garrigue S, Takahashi A, Lavergne T, Hocini M, Peng JT, Roudaut R, Clémenty J. Electrophysiological end point for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci. Circulation. 2000;101:1409–1417
  19. 19. Ouyang F, Bänsch D, Ernst S, Schaumann A, Hachiya H, Chen M, Chun J, Falk P, Khanedani A, Antz M, Kuck KH. Complete isolation of left atrium surrounding the pulmonary veins: new insights from the double-Lasso technique in paroxysmal atrial fibrillation. Circulation. 2004;110:2090–2096.
  20. 20. Weerasooriya R, Jaïs P, Scavée C, Macle L, Shah DC, Arentz T, Salerno JA, Raybaud F, Choi KJ, Hocini M, Clémenty J, Haïssaguerre M. Dissociated pulmonary vein arrhythmia: incidence and characteristics. J Cardiovasc Electrophysiol. 2003;14:1173–1179.
  21. 21. Jaïs P, Haïssaguerre M, Shah DC, Chouairi S, Gencel L, Hocini M, Clémenty J. A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation. 1997;95:572–576.
  22. 22. Kumagai K, Yasuda T, Tojo H, Noguchi H, Matsumoto N, Nakashima H, Gondo N, Saku K. Role of rapid focal activation in the maintenance of atrial fibrillation originating from the pulmonary veins. Pacing Clin Electrophysiol. 2000;23:1823–1827.
  23. 23. O’Donnell D, Furniss SS, Bourke JP. Paroxysmal cycle length shortening in the pulmonary veins during atrial fibrillation correlates with arrhythmogenic triggering foci in sinus rhythm. J Cardiovasc Electrophysiol. 2002;13:124–128.
  24. 24. Oral H, Ozaydin M, Tada H, Chugh A, Scharf C, Hassan S, Lai S, Greenstein R, Pelosi F Jr, Knight BP, Strickberger SA, Morady F. Mechanistic significance of intermittent pulmonary vein tachycardia in patients with atrial fibrillation. J Cardiovasc Electrophysiol. 2002;13:645–650.
  25. 25. Nault I, Wright M, Hocini M, Haïssaguerre M, Jaïs P. Extreme firing in a pulmonary vein during atrial fibrillation. J Cardiovasc Electrophysiol 2009;20:696.
  26. 26. Haïssaguerre M, Sanders P, Hocini M, Hsu LF, Shah DC, Scavée C, Takahashi Y, Rotter M, Pasquié JL, Garrigue S, Clémenty J, Jaïs P. Changes in atrial fibrillation cycle length and inducibility during catheter ablation and their relation to outcome. Circulation. 2004;109:3007–3013.
  27. 27. Haïssaguerre M, Sanders P, Hocini M, Jaïs P, Clémenty J. Pulmonary veins in the substrate for atrial fibrillation: the “venous wave” hypothesis. J Am Coll Cardiol. 2004;43:2290–2292.
  28. 28. Sanders P, Berenfeld O, Hocini M, Jaïs P, Vaidyanathan R, Hsu LF, Garrigue S, Takahashi Y, Rotter M, Sacher F, Scavée C, Ploutz-Snyder R, Jalife J, Haïssaguerre M. Spectral analysis identifies sites of high-frequency activity maintaining atrial fibrillation in humans. Circulation. 2005;112:789–797.
  29. 29. Marrouche NF, Wilber D, Hindricks G, Jais P, Akoum N, Marchlinski F, Kholmovski E, Burgon N, Hu N, Mont L, Deneke T, Duytschaever M, Neumann T, Mansour M, Mahnkopf C, Herweg B, Daoud E, Wissner E, Bansmann P, Brachmann J. Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. JAMA. 2014;311:498–506.
  30. 30. Eckstein J, Zeemering S, Linz D, Maesen B, Verheule S, van Hunnik A, Crijns H, Allessie MA, Schotten U. Transmural conduction is the predominant mechanism of breakthrough during atrial fibrillation: evidence from simultaneous endo-epicardial high-density activation mapping. Circ Arrhythm Electrophysiol. 2013;6:334–341.
  31. 31. Rewiuk K, Wizner B, Fedyk-Lukasik M, Zdrojewski T, Opolski G, Dubiel JS, Grodzicki T. The growing rate of atrial fibrillation among heart failure patients in polish primary health care - data from 2005 and 2013. J Hypertens. 2016;34:e23.
  32. 32. Li SJ, Sartipy U, Lund LH, Dahlström U, Adiels M, Petzold M, Fu M. Prognostic significance of resting heart rate and use of β-blockers in atrial fibrillation and sinus rhythm in patients with heart failure and reduced ejection fraction: findings from the Swedish Heart Failure Registry. Circ Heart Fail. 2015;8:871–879.
  33. 33. Mareev Y, Cleland JGF. Should β-blockers be used in patients with heart failure and atrial fibrillation? Clin Ther. 2015;37:2215–2224.
  34. 34. Van Gelder IC, Wyse DG, Chandler ML, Cooper HA, Olshansky B, Hagens VE, Crijns HJ; RACE and AFFIRM Investigators. Does intensity of rate-control influence outcome in atrial fibrillation? An analysis of pooled data from the RACE and AFFIRM studies. Europace. 2006;8:935–942.
  35. 35. Van Gelder IC, Groenveld HF, Crijns HJGM, Tuininga YS, Tijssen JGP, Alings AM, Hillege HL, Bergsma-Kadijk JA, Cornel JH, Kamp O, Tukkie R, Bosker HA, Van Veldhuisen DJ, Van den Berg MP, RACE II Investigators. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010;362:1363 – 1373.
  36. 36. Kirchhof P, Benussi S, Kotecha D, Ahlsson A, Atar D, Casadei B, Castella M, Diener HC, Heidbuchel H, Hendriks J, Hindricks G, Manolis AS, Oldgren J, Popescu BA, Schotten U, Van Putte B, Vardas P, Agewall S, Camm J, Baron Esquivias G, Budts W, Carerj S, Casselman F, Coca A, De Caterina R, Deftereos S, Dobrev D, Ferro JM, Filippatos G, Fitzsimons D, Gorenek B, Guenoun M, Hohnloser SH, Kolh P, Lip GY, Manolis A, McMurray J, Ponikowski P, Rosenhek R, Ruschitzka F, Savelieva I, Sharma S, Suwalski P, Tamargo JL, Taylor CJ, Van Gelder IC, Voors AA, Windecker S, Zamorano JL, Zeppenfeld K. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J 2016;37:2893–2962.
  37. 37. Kotecha D, Holmes J, Krum H, Altman DG, Manzano L, Cleland JGF, Lip GYH, Coats AJS, Andersson B, Kirchhof P, von Lueder TG, Wedel H, Rosano G, Shibata MC, Rigby A, Flather MD. Efficacy of β blockers in patients with heart failure plus atrial fibrillation: an individual-patient data meta-analysis. Lancet. 2014; 384:2235– 2243.
  38. 38. Allen LA, Fonarow GC, Simon DN, Thomas LE, Marzec LN, Pokorney SD, Gersh BJ, Go AS, Hylek EM, Kowey PR, Mahaffey KW, Chang P, Peterson ED, Piccini JP. Digoxin use and subsequent outcomes among patients in a contemporary atrial fibrillation cohort. J Am Coll Cardiol 2015;65:2691–2698.
  39. 39. Gheorghiade M, Fonarow GC, van Veldhuisen DJ, Cleland JGF, Butler J, Epstein AE, Patel K, Aban IB, Aronow WS, Anker SD, Ahmed A. Lack of evidence of increased mortality among patients with atrial fibrillation taking digoxin: findings from post hoc propensity-matched analysis of the AFFIRM trial. Eur Heart J. 2013;34:1489–1497.
  40. 40. Turakhia MP, Santangeli P, Winkelmayer WC, Xu X, Ullal AJ, Than CT, Schmitt S, Holmes TH, Frayne SM, Phibbs CS, Yang F, Hoang DD, Ho PM, Heidenreich PA. Increased mortality associated with digoxin in contemporary patients with atrial fibrillation. J Am Coll Cardiol. 2014;64:660–668.
  41. 41. Carlsson J, Miketic S, Windeler J, et al. STAF Investigators. Randomized trial of rate control versus rhythm control in persistent atrial fibrillation: the strategies of treatment in atrial fibrillation (STAF) Study. J Am Coll Cardiol. 2003;41:1690–1696.
  42. 42. Opolski G, Torbicki A, Kosior D, et al. Rhythm control versus rate control in patients with persistent atrial fibrillation. Results of the HOT CAFE Polish study. Pol Heart J. 2003;59:15–16.
  43. 43. The AFFIRM Investigators. Relationships between sinus rhythm, treatment and survival in the atrial fibrillation follow-up investigation of rhythm management (AFFIRM) study. Circulation. 2004;109:1509–1513.
  44. 44. Olshansky B, Rosenfeld LE, Warner AK; AFFIRM Investigators. The atrial fibrillation follow-up investigation of rhythm management (AFFIRM) study: approaches to control rate in atrial fibrillation. J Am Coll Cardiol. 2004;43:1201–1208.
  45. 45. Brignole M, Menozzi C, Gianfranchi L, 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;98:953–960.
  46. 46. Roy D, Talajic M, Dorian P, et al., Canadian Trial of Atrial Fibrillation Investigators. Amiodarone to prevent recurrence of atrial fibrillation. N Engl J Med. 2000;342:913–920.
  47. 47. Deedwania PC, Singh BN, Ellenbogen K, et al. for the Department of Veterans Affairs CHF-STAT Investigators. Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: observations from the veterans affairs congestive heart failure survival trial of antiarrhythmic therapy (CHF-STAT). Circulation. 1998;98:2574–2579.
  48. 48. Choi AD, Hematpour K, Kukin M, Mittal S, Steinberg JS. Ablation vs medical therapy in the setting of symptomatic atrial fibrillation and left ventricular dysfunction. Congest Heart Fail. 2010;16:10–14.
  49. 49. Gentlesk PJ, Sauer WH, Gerstenfeld EP, Lin D, Dixit S, Zado E, Callans D, Marchlinski FE. Reversal of left ventricular dysfunction following ablation of atrial fibrillation. J Cardiovasc Electrophysiol. 2007;18:9–14.
  50. 50. Hsu LF, Jaïs P, Sanders P, Garrigue S, Hocini M, Sacher F, Takahashi Y, Rotter M, Pasquié JL, Scavée C, Bordachar P, Clémenty J, Haïssaguerre M. Catheter ablation for atrial fibrillation in congestive heart failure. N Engl J Med. 2004;351:2373–2383.
  51. 51. Tondo C, Mantica M, Russo G, Avella A, De Luca L, Pappalardo A, Fagundes RL, Picchio E, Laurenzi F, Piazza V, Bisceglia I. Pulmonary vein vestibule ablation for the control of atrial fibrillation in patients with impaired left ventricular function. Pacing Clin Electrophysiol. 2006;29:962–970.
  52. 52. MacDonald MR, Connelly DT, Hawkins NM, Steedman T, Payne J, Shaw M, Denvir M, Bhagra S, Small S, Martin W, McMurray JJ, Petrie MC. Radio-frequency ablation for persistent atrial fibrillation in patients with advanced heart failure and severe left ventricular systolic dysfunction: a randomized controlled trial. Heart. 2011;97:740–747.
  53. 53. Wilton SB, Fundytus A, Ghali WA, Veenhuyzen GD, Quinn FR, Mitchell LB, Hill MD, Faris P, Exner DV. Meta-analysis of the effectiveness and safety of catheter ablation of atrial fibrillation in patients with versus without left ventricular systolic dysfunction. Am J Cardiol. 2010;106:1284–1291.
  54. 54. Lin WS, Tai CT, Hsieh MH, Tsai CF, Lin YK, Tsao HM, Huang JL, Yu WC, Yang SP, Ding YA, Chang MS, Chen SA. Catheter ablation of paroxysmal atrial fibrillation initiated by non-pulmonary vein ectopy. Circulation. 2003;107:3176–3183.
  55. 55. Yamaguchi T, Tsuchiya T, Miyamoto K, Nagamoto Y, Takahashi N. Characterization of non-pulmonary vein foci with an EnSite array in patients with paroxysmal atrial fibrillation. Europace. 2010;12:1698–1706.
  56. 56. Chen SA, Tai CT. Catheter ablation of atrial fibrillation originating from the non-pulmonary vein foci. J Cardiovasc Electrophysiol. 2005;16:229–232.
  57. 57. Patel D, Mohanty P, Di Biase L, et al. Outcomes and complications of catheter ablation for atrial fibrillation in females. Heart Rhythm. 2010;7:167–172.
  58. 58. Santangeli P, Di Biase L, Mohanty P, et al. Catheter ablation of atrial fibrillation in octogenarians: safety and outcomes. J Cardiovasc Electrophysiol. 2012;23:687–693.
  59. 59. Takigawa M, Kuwahara T, Takahashi A, et al. Differences in catheter ablation of paroxysmal atrial fibrillation between males and females. Int J Cardiol. 2013;168:1984–1991.
  60. 60. Elayi CS, DI Biase L, Bai R, et al. Administration of isoproterenol and adenosine to guide supplemental ablation after pulmonary vein antrum isolation. J Cardiovasc Electrophysiol. 2013;24:1199–1206.
  61. 61. Zhao Y, Di Biase L, Trivedi C, et al. Importance of non-pulmonary vein triggers ablation to achieve long-term freedom from paroxysmal atrial fibrillation in patients with low ejection fraction. Heart Rhythm. 2016;13:141–149.
  62. 62. Allessie M, Ausma J, Schotten U. Electrical, contractile and structural remodeling during atrial fibrillation. Cardiovasc Res. 2002;54:230–246.
  63. 63. Knecht S, Hocini M, Wright M, Lellouche N, O’Neill MD, Matsuo S et al. Left atrial linear lesions are required for successful treatment of persistent atrial fibrillation. Eur Heart J. 2008;29:2359–2366.
  64. 64. Tamborero D, Mont L, Berruezo A, Matiello M, Benito B, Sitges M et al. Left atrial posterior wall isolation does not improve the outcome of circumferential pulmonary vein ablation for atrial fibrillation: a prospective randomized study. Circ Arrhythm Electrophysiol. 2009;2:35–40.
  65. 65. Anselmino M, Matta M, D'Ascenzo F, Bunch TJ, Schilling RJ, Hunter RJ, Pappone C, Neumann T, Noelker G, Fiala M, Bertaglia E, Frontera A, Duncan E, Nalliah C, Jais P, Weerasooriya R, Kalman JM, Gaita F. Catheter ablation of atrial fibrillation in patients with left ventricular systolic dysfunction: a systematic review and meta-analysis. Circ Arrhythm Electrophysiol. 2014;7:1011–1118.
  66. 66. Chen MS, Marrouche NF, Khaykin Y, Gillinov AM, Wazni O, Martin DO, Rossillo A, Verma A, Cummings J, Erciyes D, Saad E, Bhargava M, Bash D, Schweikert R, Burkhardt D, Williams-Andrews M, Perez-Lugones A, Abdul-Karim A, Saliba W, Natale A. Pulmonary vein isolation for the treatment of atrial fibrillation in patients with impaired systolic function. J Am Coll Cardiol. 2004;43:1004–1009.
  67. 67. Efremidis M, Sideris A, Xydonas S, Letsas KP, Alexanian IP, Manolatos D, Mihas CC, Filippatos GS, Kardaras F. Ablation of atrial fibrillation in patients with heart failure: reversal of atrial and ventricular remodelling. Hellenic J Cardiol. 2008;49:19–25
  68. 68. Nademanee K, Schwab MC, Kosar EM, Karwecki M, Moran MD, Visessook N, Michael AD, Ngarmukos T. Clinical outcomes of catheter substrate ablation for high-risk patients with atrial fibrillation. J Am Coll Cardiol. 2008;51:843–849.
  69. 69. Lutomsky BA, Rostock T, Koops A, Steven D, Müllerleile K, Servatius H, Drewitz I, Ueberschär D, Plagemann T, Ventura R, Meinertz T, Willems S. Catheter ablation of paroxysmal atrial fibrillation improves cardiac function: a prospective study on the impact of atrial fibrillation ablation on left ventricular function assessed by magnetic resonance imaging. Europace. 2008;10:593–599.
  70. 70. De Potter T, Berruezo A, Mont L, Matiello M, Tamborero D, Santibañez C, Benito B, Zamorano N, Brugada J. Left ventricular systolic dysfunction by itself does not influence outcome of atrial fibrillation ablation. Europace. 2010;12:24–29
  71. 71. Cha YM, Wokhlu A, Asirvatham SJ, Shen WK, Friedman PA, Munger TM, Oh JK, Monahan KH, Haroldson JM, Hodge DO, Herges RM, Hammill SC, Packer DL Success of ablation for atrial fibrillation in isolated left ventricular diastolic dysfunction: a comparison to systolic dysfunction and normal ventricular function. Circ Arrhythm Electrophysiol. 2011;4:724–732.
  72. 72. Anselmino M, Grossi S, Scaglione M, Castagno D, Bianchi F, Senatore G, Matta M, Casolati D, Ferraris F, Cristoforetti Y, Negro A, Gaita F. Long-term results of transcatheter atrial fibrillation ablation in patients with impaired left ventricular systolic function. J Cardiovasc Electrophysiol. 2013;24:24–32.
  73. 73. Calvo N, Bisbal F, Guiu E, Ramos P, Nadal M, Tolosana JM, Arbelo E, Berruezo A, Sitges M, Brugada J, Mont L. Impact of atrial fibrillation-induced tachycardiomyopathy in patients undergoing pulmonary vein isolation. Int J Cardiol. 2013;168:4093–4097.
  74. 74. Nedios S, Sommer P, Dagres N, Kosiuk J, Arya A, Richter S, Gaspar T, Kanagkinis N, Dinov B, Piorkowski C, Bollmann A, Hindricks G, Rolf S. Long-term follow-up after atrial fibrillation ablation in patients with impaired left ventricular systolic function: the importance of rhythm and rate control. Heart Rhythm. 2014;11:344–351.
  75. 75. Kosiuk J, Nedios S, Darma A, Rolf S, Richter S, Arya A, Piorkowski C, Gaspar T, Sommer P, Husser D, Hindricks G, Bollmann A. Impact of single atrial fibrillation catheter ablation on implantable cardioverter defibrillator therapies in patients with ischaemic and non-ischaemic cardiomyopathies. Europace. 2014;16:1322–1326.
  76. 76. Lobo TJ, Pachon CT, Pachon JC, Pachon EI, Pachon MZ, Pachon JC, Santillana TG, Zerpa JC, Albornoz RN, Jatene AD. Atrial fibrillation ablation in systolic dysfunction: clinical and echocardiographic outcomes. Arq Bras Cardiol. 2015;104:45–52.
  77. 77. Bunch TJ, May HT, Bair TL, Jacobs V, Crandall BG, Cutler M, Weiss JP, Mallender C, Osborn JS, Anderson JL, Day JD. Five-year outcomes of catheter ablation in patients with atrial fibrillation and left ventricular systolic dysfunction. J Cardiovasc Electrophysiol. 2015;26:363–370.
  78. 78. Machino-Ohtsuka T, Seo Y, Ishizu T, Sugano A, Atsumi A, Yamamoto M, Kawamura R, Machino T, Kuroki K, Yamasaki H, Igarashi M, Sekiguchi Y, Aonuma K. Efficacy, safety and outcomes of catheter ablation of atrial fibrillation in patients with heart failure with preserved ejection fraction. J Am Coll Cardiol. 2013;62:1857–1865.
  79. 79. Khan MN, Jaïs P, Cummings J, Di Biase L, Sanders P, Martin DO, Kautzner J, Hao S, Themistoclakis S, Fanelli R, Potenza D, Massaro R, Wazni O, Schweikert R, Saliba W, Wang P, Al-Ahmad A, Beheiry S, Santarelli P, Starling RC, Dello Russo A, Pelargonio G, Brachmann J, Schibgilla V, Bonso A, Casella M, Raviele A, Haïssaguerre M, Natale A; PABA-CHF Investigators. Pulmonary-vein isolation for atrial fibrillation in patients with heart failure. N Engl J Med. 2008;359:1778–1785.
  80. 80. Jones DG, Haldar SK, Hussain W, Sharma R, Francis DP, Rahman-Haley SL, McDonagh TA, Underwood SR, Markides V, Wong T. A randomized trial to assess catheter ablation versus rate control in the management of persistent atrial fibrillation in heart failure. J Am Coll Cardiol. 2013;61:1894–1903.
  81. 81. Hunter RJ, Berriman TJ, Diab I, Kamdar R, Richmond L, Baker V, Goromonzi F, Sawhney V, Duncan E, Page SP, Ullah W, Unsworth B, Mayet J, Dhinoja M, Earley MJ, Sporton S, Schilling RJ. A randomized controlled trial of catheter ablation versus medical treatment of atrial fibrillation in heart failure (the CAMTAF trial). Circ Arrhythm Electrophysiol. 2014;7:31–38.
  82. 82. Dagres N, Varounis C, Gaspar T, Piorkowski C, Eitel C, Iliodromitis EK, Lekakis JP, Flevari P, Simeonidou E, Rallidis LS, Tsougos E, Hindricks G, Sommer P, Anastasiou-Nana M. Catheter ablation for atrial fibrillation in patients with left ventricular systolic dysfunction. A systematic review and meta-analysis. J Card Fail. 2011;17:964–970.
  83. 83. Ganesan AN, Nandal S, Lüker J, Pathak RK, Mahajan R, Twomey D, Lau DH, Sanders P. Catheter ablation of atrial fibrillation in patients with concomitant left ventricular impairment: a systematic review of efficacy and effect on ejection fraction. Heart Lung Circ. 2015;24:270–280.
  84. 84. Ullah W, Ling LH, Prabhu S, Lee G, Kistler P, Finlay MC, Earley MJ, Sporton S, Bashir Y, Betts TR, Rajappan K, Thomas G, Duncan E, Staniforth A, Mann I, Chow A, Lambiase P, Schilling RJ, Hunter RJ. Catheter ablation of atrial fibrillation in patients with heart failure: impact of maintaining sinus rhythm on heart failure status and long-term rates of stroke and death. Europace. 2016;18:679–686.
  85. 85. Zhu M, Zhou X, Cai H, Wang Z, Xu H, Chen S, Chen J, Xu X, Xu H, Mao W. Catheter ablation versus medical rate control for persistent atrial fibrillation in patients with heart failure: a PRISMA-compliant systematic review and meta-analysis of randomized controlled trials. Medicine (Baltimore). 2016;95:e4377.
  86. 86. Santangeli P, Di Biase L, Themistoclakis S, Raviele A, Schweikert RA, Lakkireddy D, Mohanty P, Bai R, Mohanty S, Pump A, Beheiry S, Hongo R, Sanchez JE, Gallinghouse GJ, Horton R, Dello Russo A, Casella M, Fassini G, Elayi CS, Burkhardt JD, Tondo C, Natale A. Catheter ablation of atrial fibrillation in hypertrophic cardiomyopathy: long-term outcomes and mechanisms of arrhythmia recurrence. Circ Arrhythm Electrophysiol. 2013;6:1089–1094.
  87. 87. Khaykin Y, Marrouche NF, Saliba W, Schweikert R, Bash D, Chen MS, Williams-Andrews M, Saad E, Burkhardt DJ, Bhargava M, Joseph G, Rossillo A, Erciyes D, Martin D, Natale A. Pulmonary vein antrum isolation for treatment of atrial fibrillation in patients with valvular heart disease or prior open heart surgery. Heart Rhythm. 2004;1:33–39.
  88. 88. Wang X, Liu X, Shi H, Gu J, Sun Y, Zhou L, Hu W. Heart rhythm disorders and pacemakers: pulmonary vein isolation combined with substrate modification for persistent atrial fibrillation treatment in patients with valvular heart diseases. Heart. 2009;95:1773–1783.
  89. 89. Okamatsu H, Ohara T, Kanzaki H, Nakajima I, Miyamoto K, Okamura H, Noda T, Aiba T, Kusano K, Kamakura S, Shimizu W, Satomi K. Impact of left ventricular diastolic dysfunction on outcome of catheter ablation for atrial fibrillation in patients with hypertrophic cardiomyopathy. Circ J. 2015;79:419–424.

Written By

Antonio Di Monaco, Federico Quadrini, Nicola Vitulano and Massimo Grimaldi

Submitted: May 24th, 2016 Reviewed: November 23rd, 2016 Published: February 15th, 2017