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The management of atrial fibrillation in patients with heart failure
Author:
Brian Olshansky, MD
Section Editors:
Wilson S Colucci, MD
Bradley P Knight, MD, FACC
Deputy Editor:
Gordon M Saperia, MD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2018. | This topic last updated: Mar 19, 2018.

INTRODUCTION — For patients with atrial fibrillation (AF), the main goals of therapy are control of symptoms, prevention of cardiac dysfunction, and prevention of arterial thromboembolism, particularly stroke. These goals are also appropriate for the relatively large subset of AF patients with heart failure (HF). In these individuals, symptoms are frequent and potentially disabling due to the interaction between the two processes.  

This topic will focus on the management of AF in patients with HF. There are few differences in management between those with heart failure with preserved or reduced ejection fraction. (See "Overview of the therapy of heart failure with reduced ejection fraction" and "Use of beta blockers in heart failure with reduced ejection fraction" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Pathophysiology of heart failure with preserved ejection fraction" and "Clinical manifestations and diagnosis of heart failure with preserved ejection fraction".)

The reader will be referred to other AF topics for which care is relatively similar irrespective of the presence of HF. (See "Atrial fibrillation: Anticoagulant therapy to prevent embolization", section on 'Summary and recommendations' and "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy" and "Catheter ablation to prevent recurrent atrial fibrillation: Clinical applications", section on 'Efficacy'.)

PREVALENCE — Atrial fibrillation (AF) and heart failure (HF) often co-exist. The presence of one increases the likelihood of the other [1].

The temporal associations of AF and HF and potential differences in preserved (HFpEF) versus reduced ejection fraction (HFrEF) were examined in an analysis of over 10,000 individuals in the original Framingham Heart Study with new onset AF or HF between 1980 and 2012 [2]. The following was noted in this study:

Among 1737 individuals with new AF, 37 percent had HF.

Among 1166 individuals with new HF, 41 percent had HFpEF and 44 percent HFrEF (15 percent could not be classified); 57 percent had AF.

Using no AF as the referent, prevalent AF was more strongly associated with incident HFpEF compared with HFrEF (hazard ratios 2.34 versus 1.48).

The presence of both AF and HF predicted greater mortality risk compared with neither condition, particularly among individuals with HFrEF. (See 'Prognosis' below and "Pathophysiology of heart failure with preserved ejection fraction" and "Clinical manifestations and diagnosis of heart failure with preserved ejection fraction" and "Treatment and prognosis of heart failure with preserved ejection fraction".)

The prevalence of AF in patients with HF varies from <10 to 57 percent, depending in part upon the severity of HF [3-8] (eg, the prevalence of AF increased from 4 to 50 percent as the NYHA functional class increased from I to IV [9-16]). (See "Predictors of survival in heart failure with reduced ejection fraction", section on 'NYHA functional class'.)

EFFECT ON CARDIAC FUNCTION — Atrial fibrillation (AF) can impair myocardial function by multiple mechanisms and heart failure may result or worsen [17] (see "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm"):

Tachycardia and bradycardia, and abrupt change in rate and the ensuing irregular rhythm, may decrease cardiac output.

Persistent tachycardia may lead to tachycardia mediated cardiomyopathy [18-20]. (See "Arrhythmia-induced cardiomyopathy".)

Loss of atrial systole (also called the atrial "kick") required for optimal ventricular filling. This is particularly important in patients with diastolic heart failure where left ventricular filling occurs largely in late diastole and is therefore more dependent than normal hearts on atrial contraction. (See "Clinical manifestations and diagnosis of heart failure with preserved ejection fraction", section on 'Pathophysiology'.)

Activation of neurohumoral vasoconstrictors such as angiotensin II and norepinephrine, as well as other maladaptive and procoagulant biochemical mechanisms.

Heart failure is a risk factor for AF. While multiple mechanisms are likely, left atrial stretch is certainly contributory. (See "Mechanisms of atrial fibrillation", section on 'Triggers of AF'.)

PROGNOSIS — Most observational studies evaluating the impact of atrial fibrillation (AF) in patients with heart failure (HF), and the converse, were performed many years ago. They present conflicting data as to whether AF is an independent predictor of mortality in patients with HF [3-5,21-24]. A 2009 meta-analysis of 16 studies involving 53,969 patients concluded that AF was independently associated with all-cause mortality with an odds ratio of 1.4 for seven randomized trials and 1.15 for nine observational studies [25]. There is some evidence that new-onset AF predicts HF progression [26].

These studies come to differing conclusions with regard to the impact on mortality of the development of HF in patients with AF. In one registry study of nearly one million patients, 3.4 percent were in AF without HF, 2.2 percent had HF in sinus rhythm, and 1.2 percent had HF in AF [27]. Patients that developed new-onset AF, HF, or both had significantly worse mortality (58.5, 70.7, and 74.8 percent, respectively) compared with those already with the condition at baseline (48.5, 63.7, and 67.2 percent, respectively).

CORRECTION OF REVERSIBLE CAUSES OF AF AND HF — Atrial fibrillation (AF) may worsen symptoms in patients with heart failure (HF) and uncontrolled HF can accelerate the ventricular response of AF or precipitate AF in patients in sinus rhythm. For these reasons, all reversible causes of AF and HF should be identified and corrected when possible. (See "Overview of the therapy of heart failure with reduced ejection fraction" and "Treatment of acute decompensated heart failure: General considerations" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Overview of atrial fibrillation" and "Management of new onset atrial fibrillation".)

ACUTE MANAGEMENT — Management of patients with acutely worsening heart failure and uncontrolled rates in atrial fibrillation (AF) is a clinical challenge. The initial strategy should be to treat the heart failure with diuretics, vasodilators, and other agents while also slowing the ventricular response of the AF. In patients with heart failure with preserved ejection fraction  with congestion or hypotension, intravenous digoxin or intravenous amiodarone are recommended to acutely control the heart rate. Beta blocker therapy should be instituted only following stabilization of patients with decompensated heart failure. Generally, nondihydropyridine calcium channel antagonists should be avoided due to their negative inotropic effects. Once the acutely decompensated heart failure has been adequately treated, amiodarone as an agent for chronic control of ventricular rate should be reserved for patients who do not respond to or are intolerant of digoxin or beta blockers.

Treatment of the heart failure patient with drugs to slow the ventricular response in AF is usually successful as the initial strategy to improve the clinical status. It is rarely necessary acutely to perform cardioversion from AF to normal sinus rhythm with acutely decompensated heart failure; hemodynamic instability is one exception. Cardioversion in the setting of acutely decompensated heart failure is commonly accompanied by early recurrence of AF. However, after stabilization of heart failure, cardioversion should generally be considered unless the patient has had drug resistant or longstanding persistent AF.  

In some patients, persistent rapid ventricular rates in AF may contribute to myocardial dysfunction despite optimal medical therapy. In these patients, a strategy of rhythm control should be attempted. If unsuccessful, atrioventricular (AV) node ablation may be considered when rate cannot be controlled and tachycardia-mediated cardiomyopathy is suspected. However, AV node ablation should not be performed without a pharmacological trial to control ventricular rate. (See "Rhythm control versus rate control in atrial fibrillation", section on 'Summary and recommendations'.)

ANTICOAGULATION — We anticoagulate patients with atrial fibrillation and heart failure (irrespective of ejection fraction) to reduce the risk of thromboembolization [28]. This includes patients with a CHA2DS2-VASc score of 1. (See "Atrial fibrillation: Anticoagulant therapy to prevent embolization", section on 'Our approach to anticoagulation'.)

In addition, effective anticoagulation is required prior to, during, and after cardioversion, whether it be pharmacological or electrical. (See "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation".)

HFpEF or HFrEF — While the clinical presentation and prognosis of atrial fibrillation (AF) patients with preserved or reduced ejection fraction (HFpEF or HFrEF)are similar, some differences in management exist. (See "Overview of the therapy of heart failure with reduced ejection fraction" and "Use of beta blockers in heart failure with reduced ejection fraction" and "Treatment and prognosis of heart failure with preserved ejection fraction" and "Pathophysiology of heart failure with preserved ejection fraction" and "Clinical manifestations and diagnosis of heart failure with preserved ejection fraction".) For HFpEF, calcium channel blockers may be more appropriate but for HFrEF, beta blockers and/or digoxin may be first choice therapy.

Rhythm versus rate control — While rhythm and rate control strategies are reasonable for AF patients with HF, irrespective of whether HFpEF or HFrEF is the cause, we prefer a rhythm control strategy, particularly in younger patients, for several reasons:

The presence of an atrial contraction may provide better long-term symptom and HF control at rest.

Due to the presence of generally higher levels of physical activity in younger people, rate response is better controlled and hemodynamic response improves more substantially in sinus rhythm.  

Ventricular function may improve after rhythm control.

There is evidence that quality of life is improved with rhythm control. For some patients, a dramatic improvement with sinus rhythm is apparent. Thus, we have a lower threshold for rhythm control in patients with HF, as they are often more symptomatic than those without. Symptoms of irregular palpitations or racing heart, fatigue, weakness, shortness of breath, or exercise intolerance may be due to either AF or HF [29]. (See "Rhythm control versus rate control in atrial fibrillation", section on 'Summary and recommendations'.)

The AF-CHF trial was the first large, randomized trial to test the hypothesis that long-term rhythm control with drug therapy is better than rate control in patients with HF and paroxysmal AF [30]. In this trial, 1376 patients with a left ventricular ejection fraction (LVEF) <35 percent, HF symptoms, and a history of paroxysmal (or persistent) AF were assigned to a strategy of either rhythm control (amiodarone, sotalol, or dofetilide) or rate control (with beta blockers). At a mean follow-up of 37 months, there was no significant difference in the primary outcome of death from cardiovascular causes between the rhythm- and rate-control groups (27 versus 25 percent, respectively) or the outcome of the event-free survival. Improvements in quality of life and functional capacity were similar in treatment arms, as were assessments of the six-minute walk distance and New York Heart Association functional class [31].

Rhythm control can also be achieved with catheter ablation. Four small randomized trials, each with methodological limitations, and one observational study have compared catheter ablation with rate control in patients with HF and found benefit [32-36]. (See "Catheter ablation to prevent recurrent atrial fibrillation: Clinical applications", section on 'Efficacy' and 'Catheter ablation' below.):

Irrespective of whether the patient has HF with preserved or reduced ejection fraction, we make an initial attempt at rhythm control. This will allow for a determination if a symptom-rhythm correlation exists and whether a patient’s HF symptoms can improve. If rhythm control (either using anti-arrhythmic drugs or catheter ablation) is not possible, then rate control may be preferred through more definitive means, including atrioventricular node ablation with pacing support. However, for these patients, unopposed right ventricular pacing can have a deleterious effect and even cardiac resynchronization pacing may not emulate electrical activation via the His Purkinje system. (See 'AV node ablation with pacing' below.)

In our experience some, if not many, patients with AF who have HF improve markedly with sinus rhythm restoration (if possible). For those with recent onset or symptomatic AF or with persistent symptomatic HF, cardioversion makes sense at least once as a test of therapeutic efficacy. Furthermore, in many instances, repeat cardioversion is therapy enough as long as AF recurrence is not frequent. Sinus rhythm maintenance can be associated with improvement in symptoms as well as left and even right ventricular dysfunction.

PATIENTS WITH REDUCED EJECTION FRACTION — Assuming optimal management of heart failure and anticoagulation to prevent embolization (see 'Anticoagulation' above), the most important issue in patients with reduced left ventricular ejection fraction (LVEF) and heart failure and persistent AF is restoration and maintenance of sinus rhythm when possible. Sinus rhythm is preferred to AF for most patients with reduced ejection fraction.

For patients with symptomatic AF who have heart failure and failure of antiarrhythmic drug therapy (see 'Antiarrhythmic drug therapy' below), we treat with catheter ablation.

Rhythm control — Rhythm control, which can be achieved with antiarrhythmic drug therapy, catheter ablation, or surgical ablation, is the preferred approach in patients with HF who are hemodynamically unstable or who are persistently symptomatic despite adequate rate control [1]. It is the treatment of choice in patients with recent onset AF in whom there is an exacerbation of HF even if rate control is achieved.

In some instances, direct current cardioversion may be necessary prior to or in conjunction with rhythm control, and this may even be necessary acutely for patients who have sudden precipitation of HF or the development of pulmonary edema. The trial of rate control, even under these circumstances, with attempted stabilization of the patient is recommended before acute cardioversion is anticipated. (See "Cardioversion for specific arrhythmias", section on 'Atrial fibrillation' and "Atrial fibrillation: Cardioversion to sinus rhythm", section on 'DC cardioversion'.)

In general, the efficacy of successful restoration and long-term maintenance of sinus rhythm is dependent in part on how long a patient has been in persistent AF, but several other predictors exist including left atrial size. Both antiarrhythmic drug therapy and catheter ablation are available to achieve this end in select patients.

Initial approach to rhythm control — We take the following sequential steps to achieve rhythm control in AF patients with HF:

Electrical cardioversion. Consider cardioversion without antiarrhythmic drug therapy if AF is not well tolerated, if it is difficult to manage heart failure otherwise, if this is the first episode, or if there is little evidence of mitral regurgitation or left atrial enlargement as long as appropriately anticoagulated. (See 'Electrical cardioversion' below.)

Choose an antiarrhythmic drug (eg, amiodarone, sotalol, or dofetilide) for maintenance control. For patients with rapid rates in AF prior to cardioversion, not controllable by beta blockers or digoxin, amiodarone, either oral or intravenous, can help rate control before electrical cardioversion. There is also a small chance that amiodarone may pharmacologically cardiovert the patient to sinus rhythm.  

For maintenance therapy to help keep a patient in sinus rhythm, we generally start with dofetilide based on its relatively good side effect profile and efficacy; however, its use is limited by stringent guidelines for administration and the fact that it needs to be adjusted based on renal function. There are also concerns about the potential for prolongation of the QT interval and for cost. It must be initiated in the hospital and five to six dosages must be given before discharge to ascertain that the QTc interval does not exceed 500 ms at peak dosing. Sotalol is a reasonable choice for individuals with mild renal dysfunction and left ventricular ejection fractions exceeding 30 percent. It should not be used in patients with more advanced heart failure. Amiodarone can be started as an outpatient and can be used in patients with renal failure. However, side effects are potentially serious and it takes days to weeks to effectively load the drug. It is preferred for older individuals although risks of serious side effects are potential in all patients. (See 'Antiarrhythmic drug therapy' below.)  

Electrical cardioversion — For the first episode of AF, electrical cardioversion may be performed without initiation of antiarrhythmic drug therapy but  the patient must be effectively anticoagulated. (see 'Anticoagulation' above). For those patients who have recurrent episodes of paroxysmal AF or who are cardioverted to AF , amiodarone or dofetilide may help maintain sinus rhythm and prevent AF recurrences. In most cases, patients with persistent AF do not return to normal sinus rhythm with medical therapy alone. Electrical cardioversion can be performed in patients in whom it is not clear that the AF is specifically responsible for the symptoms but cardioversion can be useful to determine if AF is of importance in restoring functional

Cardioversion is not appropriate in those who have short episodes of paroxysmal AF (it may be if episodes last days and there is precipitous change in condition and if patients do not respond to an antiarrhythmic). Most AF patients with HF will have recurrent AF unless it was due to an acute precipitant (acute pulmonary edema, myocardial infarction, pulmonary embolus, cardiac surgery, etc).

Cardioversion has a limited role in the initial management of a patient with acute HF decompensation. We stabilize the patient as best possible and try heart failure management. If the patient does not improve, cardioversion (with or without a transesophageal echocardiogram) is performed.

Antiarrhythmic drug therapy — As discussed above, many patients with AF and HF have been treated with long-term antiarrhythmic drugs based upon the assumption that the restoration and maintenance of sinus rhythm will lead to improved outcomes, such as fewer symptoms or admissions for HF. Also, concerns have been raised about increased mortality with rhythm control when antiarrhythmic drugs are used [37]. Nevertheless, these data are older, retrospective, and suspect. It does appear that antiarrhythmic drug selection is important, since some drugs (propafenone, dronedarone, flecainide, etc) have been shown to worsen outcomes in HF patients while other drugs (dofetilide) may not.  

Our authors and reviewers use amiodarone, sotalol, or dofetilide as the first antiarrhythmic drug in patients with persistent AF and HF or for those with symptomatic paroxysmal AF. Dofetilide is usually tried first, especially in younger patients with preserved kidney function. Given the beta blocker effects of sotalol, many patients do not tolerate the doses often necessary for rhythm control, especially in those with poor left ventricular function and highly symptomatic HF.

The following is a brief discussion of the antiarrhythmic drugs that could be considered for patients with AF and HF:

Dofetilide – Dofetilide, a class III antiarrhythmic drug, is effective for preventing recurrent AF in patients with HF. This was illustrated in a review of 506 patients enrolled in the DIAMOND-CHF or DIAMOND-MI trials who had left ventricular dysfunction and were initially in AF or atrial flutter [38]. Over the course of the study, patients treated with dofetilide were significantly more likely to convert to sinus rhythm (59 versus 34 percent with placebo). Among these 234 patients, the probability of maintaining sinus rhythm at one year was greater with dofetilide (79 versus 42 percent). (See "Therapeutic use of dofetilide".)

Dofetilide is relatively safe in patients with HF. This was established by the DIAMOND-CHF trial, which enrolled 1518 patients with symptomatic HF, including 391 with AF at baseline; the patients were randomly assigned to dofetilide or placebo [39]. Dofetilide was more likely to be associated with reversion to sinus rhythm at one month (12 versus 1 percent) and one year (44 versus 13 percent), but at a mean follow-up of 18 months, there was no overall difference in mortality between the dofetilide and placebo groups (41 versus 42 percent). The most important side effect of dofetilide was torsades de pointes, which was seen in 25 cases (3.3 percent); three-quarters of episodes occurred within the first three days while the patient was in the hospital. (See "Acquired long QT syndrome: Definitions, causes, and pathophysiology", section on 'Torsades de pointes'.)

The recommended dose of dofetilide is 500 micrograms twice daily in the absence of renal insufficiency but it is adjusted based on renal function.

The United States Food and Drug Administration (FDA) has approved the use of dofetilide for the conversion of AF and atrial flutter to normal sinus rhythm and for maintenance of normal sinus rhythm in those with persistent AF. Because of the risk of torsades de pointes, the FDA approval for dofetilide was contingent upon the following restrictions:

Dofetilide is available only to hospitals and subscribers that have received dosing and treatment initiation education and certification.

Patients must be hospitalized for a minimum of three days for dofetilide initiation (to give six pills, one every 12 hours) at a facility that can provide measurement of creatinine clearance, cardiac monitoring, and cardiac resuscitation. The majority of episodes of torsades de pointes occur within this three-day period, the time of peak increase in the QT interval [39]. A QT of >500 ms may be an indication for discontinuation. (See "Therapeutic use of dofetilide" and "Therapeutic use of dofetilide", section on 'Safety'.)

Our authors and reviewers are more comfortable using dofetilide for HF patients with an implantable cardioverter defibrillator in place or in younger patients with less severe impairment of left ventricular systolic function.

Amiodarone – When used for preventing recurrence of AF, amiodarone, particularly in lower doses (less than 400 mg/day and occasionally less than 200 mg/day), has the advantages of lack of a negative inotropic effect and little or no proarrhythmia, despite a low incidence of QT prolongation. The near absence of proarrhythmia was illustrated in a meta-analysis of four trials of low-dose amiodarone therapy for a minimum of one year in patients with underlying HF or myocardial infarction; there were no cases of torsades de pointes in the 738 patients treated with amiodarone [40]. In addition, since amiodarone has beta blocking and calcium channel blocking activity, the ventricular rate is usually slow and well tolerated if AF does recur. Its use in HF patients does not necessarily require hospitalization, but careful monitoring of the international normalized ratio is necessary, as amiodarone can potentiate the effects of warfarin. (See "Amiodarone: Monitoring and management of side effects", section on 'Drug interactions'.)

The efficacy of amiodarone was illustrated in a subset analysis from the CHF-STAT trial in which 15 percent of patients had AF at baseline [41]. Among these 103 patients, 51 were randomly assigned to amiodarone and 52 to placebo. The following significant benefits were noted with amiodarone:

A greater likelihood of reverting to sinus rhythm (31 versus 8 percent) during the course of the study. Patients treated with amiodarone who converted to sinus rhythm had a lower total mortality than those who did not convert. It is not clear if reductions in mortality were because patients who converted were less sick to begin with or if restoration of sinus rhythm was causative.

During AF, a 16 to 20 percent reduction in the mean ventricular rate and a 14 to 22 percent reduction in the maximum ventricular rate.

In addition, among 531 patients initially in sinus rhythm, amiodarone was associated with a lesser likelihood of developing AF (4.1 versus 8.3 percent). There are, however, potential complications associated with amiodarone therapy in patients with HF, particularly during the loading phase. These were illustrated in a report of 37 patients with HF and an average LVEF of 24 percent who presented with AF or atrial flutter [42]. During the period of loading with amiodarone (1.2 g/day), 32 percent developed a bradycardia requiring discontinuation of digoxin and 19 percent required a permanent pacemaker. After 9.5 months, 57 percent of patients remained in sinus rhythm and 14 percent developed complications, including hypothyroidism and neurotoxicity.

Side effects with maintenance therapy are less likely with lower doses but still occur (table 1). Advantages to amiodarone compared to dofetilide include the ability to start therapy as an outpatient, once-a-day dosing, and a lower risk of torsades de pointes. (See "Amiodarone: Monitoring and management of side effects".)

Sotalol – Sotalol should be used with caution in HF patients who have very poor left ventricular function (LVEF <30 percent) based on a report of possible increased risk for torsades de pointes [43]. This is especially true if there are marked fluctuations electrolyte levels, if there is a low LVEF (≤30 percent), if there is acute onset of heart failure, if there is decompensated HF, or if there is evidence of renal dysfunction. (See "Drugs that should be avoided or used with caution in patients with heart failure", section on 'Antiarrhythmic agents' and "Therapeutic use and major side effects of sotalol", section on 'Heart failure'.)

Dronedarone – Dronedarone should not be used in patients with New York Heart Association (NYHA) class III to IV HF or left ventricular systolic dysfunction (LVEF <0.40), as efficacy is poor and safety is a concern. It should also not be used in patients with longstanding persistent AF. This recommendation is consistent with that made by the European Medicines Agency in September of 2011 and that made by the United States FDA in December of 2011 [44,45]. While the available data do not do not allow for firm recommendations regarding the use of dronedarone in patients with NYHA class I to II HF or mild left ventricular systolic dysfunction, we suggest that the drug be used with caution in these patients if at all. (See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations", section on 'Concerns about dronedarone'.) In the general population of patients with AF, a 2009 meta-analysis found a significantly lower rate of recurrent AF with amiodarone compared to dronedarone (odds ratio 0.49; 95% CI 0.37 to 0.63) [46]. (See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials" and "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials", section on 'Dronedarone'.)

Strong evidence for an adverse effect from its use in patients with HF comes from results of the ANDROMEDA trial, which evaluated the safety and efficacy of dronedarone compared to placebo in patients with symptomatic HF and left ventricular systolic dysfunction (LVEF ≤35 percent) [47]. The trial was discontinued early due to a significant increase in the incidence of death in the patients assigned to dronedarone (8.1 versus 3.8 percent) during a median follow-up of two months. It should be noted that in the ATHENA trial, in which approximately 20 percent of patients with NYHA functional class I or II HF, dronedarone appeared safe, but not necessarily effective. The rationale to use dronedarone in symptomatic HF patients is extremely weak and analyses are post-hoc from ATHENA. We believe that patients with severe HF, generally those with NYHA class III or IV HF, or those who have been hospitalized with HF in the past four weeks, should not receive dronedarone. Patients with lesser degrees of HF may receive the drug cautiously. Benefits are uncertain. Symptoms may not be reduced. It should never be used in patients with suspected permanent AF and HF. In general, dronedarone has no role in the management of AF in a HF patient.

Class IC drugs – Class IC drugs (flecainide, propafenone) are associated with an increased risk for proarrhythmia and risk for sudden cardiac death and should not be used in this setting (table 2).

Ibutilide for acute conversion should generally not be used in decompensated HF due to the risks of torsades de pointes. (See "Therapeutic use of ibutilide", section on 'Proarrhythmia'.)  

Beta blockers – There is evidence that chronic beta blocker therapy may reduce the likelihood of the development of AF in patients with HF due to systolic dysfunction. (See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials", section on 'Beta blockers'.)

Catheter ablation — For patients with symptomatic AF who have heart failure with reduced ejection fraction and failure of antiarrhythmic drug therapy who are candidates for the procedure, we perform catheter ablation (CA) of AF rather than continued attempts with antiarrhythmic drug therapy or no antiarrhythmic drug therapy. (See "Primary prevention of sudden cardiac death in heart failure and cardiomyopathy", section on 'Use of an ICD' and "Maintenance of sinus rhythm in atrial fibrillation: Catheter ablation versus antiarrhythmic drug therapy", section on 'Summary and recommendations'.)

The strongest evidence supporting the use of CA in these patients comes from the CASTLE-AF trial, which randomly assigned 363 patients with symptomatic paroxysmal or persistent AF; New York Heart Association class II, III, or IV HF; an LVEF of 35 percent or less; failure or unwillingness to take antiarrhythmic drug therapy; and prior placement of an implantable cardioverter-defibrillator (ICD) to CA or medical therapy [48]. After a median follow-up of nearly 38 months, the primary composite end point of death from any cause or hospitalization for worsening heart failure occurred in fewer patients in the ablation group (28.5 versus 44.6 percent; hazard ratio [HR] 0.62, 95% CI 0.43-0.87). Fewer patients in the ablation group died from any cause (13.4 versus 25.0 percent; HR 0.53; 95% CI 0.32-0.86). The time in AF, as detected by the ICD (or cardiac resynchronization therapy), was significantly lower with CA (25 versus 60 percent). The principal limitation of the trial is its small sample size.

Our recommendation for ablation includes appropriate candidates for the procedure with an LVEF less than 35 percent with or without an ICD. Some patients with advanced heart failure, such as the very elderly, those on inotropic support, or those with left ventricular assist device destination therapy, may not be appropriate candidates.

Other studies provide less strong support for the use of CA in patients with AF:

In a 2014 meta-analysis of 26 randomized trials and observational studies (mean follow-up of 23 months), which included 1838 AF patients with a mean LVEF of 40 percent, LVEF improved from 40 to 53 percent and there was a fall in pro-brain natriuretic peptide levels from 1187 to 567 pg/mL [49]. (See "Natriuretic peptide measurement in heart failure".)

The relative efficacy of CA and antiarrhythmic drug therapy with amiodarone was evaluated in the AATAC trial, which randomly assigned 203 patients with persistent AF and NYHA II to III HF (as well as either dual chamber implantable cardioverter defibrillator or cardiac resynchronization therapy defibrillator) to CA or amiodarone [50]. The mean ejection fraction was about 30 percent. The primary end point of freedom from recurrence of AF after 24 months of follow-up occurred more often with CA (70 versus 34 percent; p<0.001). The ablation group had a lower mortality (8 versus 18 percent).

Three small randomized trials comparing CA with medical rate control have shown improvement in exercise ability, LVEF, and quality of life [32,34,35].

The relative efficacy of CA for rhythm and rate control using AV node ablation with biventricular pacing was addressed in a prospective, randomized trial of 81 patients with class II or III HF who had symptomatic, drug-refractory AF [33]. At six months, catheter ablation was associated with statistically significant improvements in LVEF (35 versus 28 percent), six-minute walk distance (340 versus 297 meters), and score on the Minnesota Living With Heart Failure questionnaire. The role of biventricular pacing in patients with AF is discussed in detail elsewhere. (See "Cardiac resynchronization therapy in atrial fibrillation", section on 'Evidence of CRT benefit in patients with atrial fibrillation'.)

Rate control — Rate control to prevent rapid AF acutely and/or chronically usually leads to an improvement in symptoms in patients with HF. In addition, slowing of the ventricular rate often leads to a moderate or, in some cases, marked improvement in left ventricular function [6,19,20]. (See 'Effect on cardiac function' above.)

While improvement in symptoms with rate control, and with beta blockers in particular, has been well documented, improvement in survival has not. In a meta-analysis of AF patients in 11 randomized trials (n = 3065), beta blockers reduced the ventricular rate by about 12 beats per minute [51]. Beta blockers had no effect on mortality in patients with AF (hazard ratio 0.96, 95% CI 0.81-1.12). This finding was consistent with that in a prior report [52].

While the use of one rate slowing drug is preferred, a combination of drugs may be required to achieve adequate heart rate control. It is important to measure heart rate during moderate exercise and not to base heart rate control solely on values obtained in the resting state.

The potential benefit of rate control was demonstrated in a post-hoc analysis from the randomized United States Carvedilol Heart Failure Trials in which 136 of 1094 patients with HF due to systolic dysfunction had AF [6]. Patients treated with carvedilol had a significant increase in the LVEF (from 23 to 33 percent compared with 24 to 27 percent with placebo); there was also an almost significant trend toward a reduction in the combined end point of death and HF hospitalization (7 versus 19 percent). This study does not prove that the improved outcomes are due to rate control, but rather a beneficial effect of the use of one beta blocker in this setting. (See "Use of beta blockers in heart failure with reduced ejection fraction" and "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy".)

Our approach to rate control — For patients with compensated HF due to systolic dysfunction and AF requiring rate control, our approach is as follows:

Anticoagulate

Choose a rate control goal (see 'Rate-control goal' below)

Choose a beta blocker as first therapy.

The rationale for doing so stems from the fact that, although they do not appear to improve mortality in this setting, there is no evidence of harm with their use. In addition, the alternatives of calcium channel blockers (greater mortality), digoxin (lesser efficacy), and amiodarone (more side effects) have significant limitations. (See "Use of beta blockers in heart failure with reduced ejection fraction".)

We start with carvedilol, extended release metoprolol succinate, or bisoprolol. The doses should be optimized before considering a second agent. The use of these drugs is discussed in detail separately. (See "Use of beta blockers in heart failure with reduced ejection fraction", section on 'Initiation of therapy'.)

The nondihydropyridine calcium channel blockers (verapamil and diltiazem) should be avoided in patients with decompensated HF or those with reduced left ventricular systolic function. They may be considered in patients with preserved left ventricular systolic function and compensated HF. (See "Calcium channel blockers in heart failure with reduced ejection fraction" and "Drugs that should be avoided or used with caution in patients with heart failure".)

In patients who cannot receive either a beta blocker or a calcium channel blocker, and in whom rhythm control will not be attempted, digoxin may be considered. (See "Treatment with digoxin: Initial dosing, monitoring, and dose modification" and "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy", section on 'Digoxin'.)

If two drugs are needed to control the rate, we suggest adding digoxin to a beta blocker

For patients with decompensated HF, the initiation or increase of beta blockers is contraindicated. If such a patient also has rapid AF requiring rate control, use of digoxin is suggested. However, digoxin is often ineffective when used alone, especially in patients in whom sympathetic tone is elevated.

The adequacy of rate control in AF should be assessed both at rest and with typical exertion for the patient [1].

In the event that rate control with either beta blockers or a combination of beta blockers and digoxin has not been achieved, amiodarone may be useful either alone or in combination with other rate-slowing agents. Amiodarone is not recommended as a chronic rate-control medication, but in the acute setting can assist with rate control as it is being loaded or can be used as a temporary rate-control agent in a patient who is unable to tolerate other therapies [41]. The use of amiodarone may prove helpful for rate control in this setting, but care must be exercised when using these agents, especially in those without adequate anticoagulation since there is the possibility of pharmacologically restoring sinus rhythm. If amiodarone is used for rate control, an attempt to load the drug and cardiovert should be considered for those with recent onset AF. (See 'Antiarrhythmic drug therapy' above.)

Dronedarone should be avoided in patients with HF or left ventricular systolic dysfunction. (See 'Antiarrhythmic drug therapy' above.)

For those whose ventricular rate varies markedly with minimal changes in activity, especially if associated with symptoms, a rhythm control strategy may be necessary.

Rate-control goal — Similar to AF patients without HF, the optimal heart rate in patients with HF is not known. There are no well-performed studies that have addressed this issue in these patients.

The broad goal of rate control is to minimize symptoms with exercise and rest. Thus, the adequacy of rate control should be assessed in both circumstances [1]. (See "Control of ventricular rate in atrial fibrillation: Pharmacologic therapy".)

Our reviewers generally start with a heart rate goal of<85 beats per minute at rest and <110 beats per minute during moderate exercise (the strict approach). If this is not possible, the goal becomes <110 beats per minute at rest (the lenient approach).

AV node ablation with pacing — Rate control can also be achieved with radiofrequency ablation of the atrioventricular node and permanent pacemaker placement. This strategy may be useful in patients (usually with permanent AF) in whom rate control with antiarrhythmic drug or catheter ablation has failed or been contraindicated.

In HF patients with AF who undergo atrioventricular node ablation, if the LVEF is below 45 percent and there is an expectation that ventricular pacing will occur more than 50 percent, strong consideration for a biventricular pacing system (also called cardiac resynchronization therapy) should be made as opposed to a standard right ventricular pacing system. (See "Control of ventricular rate in atrial fibrillation: Nonpharmacologic therapy" and "Cardiac resynchronization therapy in heart failure: Indications" and "Cardiac resynchronization therapy in heart failure: Implantation and other considerations" and "Cardiac resynchronization therapy in atrial fibrillation", section on 'Evidence of CRT benefit in patients with atrial fibrillation' and "Cardiac resynchronization therapy in heart failure: Indications", section on 'Rationale for CRT'.)

For patients who can potentially benefit from cardiac resynchronization therapy (CRT) but have AF, it may be necessary to ablate the atrioventricular node so that a high percentage of ventricular pacing can be insured since patients with AF may "override" the pacing and reduce the efficacy of the CRT device. Compelling data would suggest that atrioventricular junctional ablation in patients who are not pacing at rates of upwards of 90 percent with CRT pacing may benefit from radiofrequency catheter ablation [53].

His bundle pacing has become an option.

PATIENTS WITH PRESERVED EJECTION FRACTION — Our approach to heart failure (HF) in patients with preserved ejection fraction is nearly identical to that for those with HF with preserved ejection fraction. Rhythm control is preferred to rate control for most patients.

The efficacy and safety of catheter ablation has been evaluated in patients with diastolic HF. In a study of 74 patients with HF and left ventricular ejection fraction >50 percent, single- and multiple-procedure drug-free success rates were 27 and 45 percent, respectively, during a mean follow-up of 34 months [54]. No major complications were noted.

Our approach to rate control is also similar. Our rate control goal may be more lenient in some patients with preserved ejection fraction. We typically start with a beta blocker; for patients who cannot receive a beta blocker due to issues such as bronchospasm, a nondihydropyridine calcium channel blocker may be used. We use digoxin more cautiously in this group. (See 'Rate-control goal' above.)

RECOMMENDATIONS OF OTHERS — Except as noted, our recommendations are similar to those made in the 2014 American Heart Association/American College of Cardiology/Heart Rhythm Society guideline and the joint European Heart Rhythm Association/Heart Failure Association consensus document on atrial fibrillation [55-57].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links: Arrhythmias in adults" and "Society guideline links: Heart failure in adults".)

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Basics topic (see "Patient education: Heart failure and atrial fibrillation (The Basics)")

SUMMARY AND RECOMMENDATIONS

Atrial fibrillation (AF) is often present in patients with heart failure (HF). It can worsen symptoms, and is associated with a poorer prognosis. Rate- and rhythm-control strategies can be effective in controlling symptoms and have comparable survival rates. (See 'Rhythm versus rate control' above.)

We anticoagulate AF patients with HF irrespective of whether a rate- or rhythm-control strategy is employed or the baseline ejection fraction. (See 'Anticoagulation' above.)

For patients with AF and compensated HF, we suggest rhythm rather than rate-control as an initial treatment strategy (Grade 2B). A rate control strategy is a reasonable approach in older patients who prefer to avoid the potential burdens of rhythm control. (See 'Rhythm control' above and 'Rhythm versus rate control' above and "Overview of atrial fibrillation", section on 'Rate versus rhythm control'.)

For patients with symptomatic AF who have heart failure with reduced ejection fraction, and failure of antiarrhythmic drug therapy, we suggest catheter ablation of AF rather than continued attempts with antiarrhythmic drug therapy or no antiarrhythmic drug therapy (Grade 2B). This recommendation assumes that the patient is a reasonable candidate. (See 'Catheter ablation' above.)

For patients who are chosen for a rhythm control strategy using an antiarrhythmic drug, we suggest dofetilide as the antiarrhythmic drug of choice (Grade 2C). Amiodarone is a reasonable choice for older individuals and sotalol is a reasonable choice for patients with mild renal dysfunction. (See 'Rhythm control' above.)

For patients in whom a rate-control strategy is chosen, we recommend beta blockers rather than calcium channel blockers or digoxin as initial therapy (Grade 1B). (See 'Rate control' above.)

For patients who fail a rate-control strategy using medication and are either not candidates for or have failed a rhythm-control strategy, atrioventricular nodal ablation with pacing is a reasonable therapeutic option. (See 'AV node ablation with pacing' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff would like to thank Dr. Alan Cheng for his contributions as an author to prior versions of this topic review.

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