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Treatment Strategies Of Atrial Fibrillation In Patients With Heart Failure

R.Pancheva, D.Vassilev

Cardiology Clinic, “Alexandrovska” University Hospital, Sofia Bulgaria

 

Abstract

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, occurring in 1–2% of the general population. Its prevalence is estimated to at least double in the next 50 years as the population ages. Approximately the same is frequency of heart failure. Typical of these is the presence of common risk factors and mutual potentiation. Rhythm control in patients with heart failure and atrial fibrillation leads to improved left ventricular ejection fraction, quality of life and its longevity. Because many antiarrhythmic drugs are contraindicated in patients with structural heart disease, their suboptimal efficacy and significant adverse effects, we focus on non-pharmaceutical interventions as an opportunity to change the risks and benefits associated with the maintenance of sinus rhythm.

Keywords: atrial fibrillation, heart failure, rhythm control, rate control, catheter ablation

 

ABBREVIATIONS AND ACRONYMS

AF = atrial fibrillation

EF = ejection fraction

FIRM = focal impulse and rotor modulation

HF = heart failurе

HFpEF = heart failure with preserved ejection fraction

HFrEF= heart failure with reduced ejection fraction

LV = left ventricular

LVEF = left ventricular ejection fraction

NYHA = New York HeartAssociation

PVI = pulmonary vein isolation

QOL = quality of life

RAAS = renin-angiotensinaldosterone system

 

Atrial fibrillation (AF) and heart failure (HF) loom as 2 burgeoning public health problems afflicting our society. They often occur together, and their combination is associated with increased morbidity and mortality1 compared with each disorder alone2. They share common mechanisms and treatment strategies. Consequently, therapies directed toward heart failure may protect the heart against the occurrence of AF. Although restoration of sinus rhythm in patients with heart failure may offer hemodynamic and clinical benefits, recent clinical trials have failed to demonstrate the clinical advantage of sinus rhythm over optimal rate control. The deleterious effects of currently available antiarrhythmic drugs, coupled with their low efficacy, may blunt the potential benefit of sinus restoration. Curative ablation for atrial fibrillation offers the unique opportunity to maintain sinus rhythm without antiarrhythmic drugs. Recent advances in catheter-based ablative therapies for AF have been demonstrated to be effective in well-selected patients with heart failure, resulting in significant improvements in cardiac function, symptoms, and quality of life.

 

Epidemiology

AF is the most common cardiac arrhythmia and affects more than 33 million individuals across the globe. Due in part to the aging population, each year more than 5 million people develop AF worldwide3. In persons ages 55 years and older, the lifetime risk of AF is approximately 25% in men and 22% to 23% in women4-5. AF is an independent predictor of stroke and mortality (twice higher probability of death compared to those with sinus rhythm).

The risk for the occurrence of these complications increases in patients with structural heart disease, especially heart failure. The risk of ischemic stroke in non-valvular AF is five times higher and its incidence increases with age. It is estimated that 15-20% of all strokes (one of six) are secondary complication of this arrhythmia. The Framingham Heart Study reported 10-year death rates in individuals with AF at 61% and 58% in men and women, respectively, compared with 30% and 21% in men and women without AF.

Approximately 1–2% of the adult population in developed countries has HF, with the prevalence rising to 10% among persons 70 years of age or older. At least half of patients with HF have a low EF (i.e. HFrEF). Population studies suggest that the prevalence of HF has doubled over the past decade6,7. As the care for coronary artery disease and acute coronary syndromes improves, the incidence of ischemic cardiomyopathy has increased accordingly. Coronary artery disease (CAD) is the cause of approximately two-thirds of cases of systolic HF, although hypertension and diabetes are probable contributing factors in many cases. There are many other causes of systolic HF, which include previous viral infection (recognized or unrecognized), alcohol abuse, chemotherapy (e.g.doxorubicin or trastuzumab), and ‘idiopathic’ dilated cardiomyopathy8 (although the cause is thought to be unknown, some of these cases may have a genetic basis). Irrespective of etiology, a diagnosis of HF carries a poor prognosis, with an estimated 5-year survival of 25% to 38%7.

 

Shared mechanisms in AF and HF

As heterogeneous syndromes, AF and HF often represent the culmination of many adverse physiological conditions, including common cardiovascular disorders such as hypertension and coronary ischemia. Multiple large cohorts have described obesity, tobacco use, hypertension, diabetes, kidney disease, sleep apnea, and coronary disease as independent risk factors for both AF and HF. Fig. 1 illustrates the relationship between risk factors in the pathogenesis of AF and HF.


Fig. 1 The relationship between risk factors in the pathogenesis of AF and HF

 

Among persons with HF, the prevalence of AF ranges between 15% and 50% . Although it remains uncertain whether AF independently portends increased mortality in patients with HF, it is an independent predictor of worsening left ventricular (LV) function and impaired QOL. In a retrospective analysis of the SOLVD (Studies Of Left Ventricular Dysfunction) trial, Dries et al.9 found that AF was significantly associated with increased mortality in patients with AF versus sinus rhythm who had underlying asymptomatic or symptomatic LV dysfunction. There exist numerous mechanisms through which a LV dysfunction may promote atrial tachyarrhythmias. Fig.2. Hemodynamically, elevated ventricular filling pressures, functional valvular regurgitation, and renin-angiotensin-aldosterone system (RAAS)-induced volume retention promote left atrial dilation. Mechanically, stretching of the myocardium enhances pulmonary venous ectopy (the most common AF trigger)10, promotes re-entry, and slows conduction11-13; all of these actions promote the onset of AF . Neurohormonally, RAAS activation and increased circulating levels of angiotensin II lead to atrial fibrosis and anisotropy. Myocardial fibrosis heralds electrical dysfunction, including slowed and heterogenous conduction times that facilitate wave break. These changes expedite the development and persistence of additional AF triggers and AF perpetuators, including electrical spiral waves (rotors) and focal sources14. Finally, cellular calcium dysregulation occurs in HF as a result of altered myocardial contraction function and modified calcium channel concentration, but has important electrophysiological consequences as well. Calcium overload likely facilitates abnormal action potential durations within the atria that have been associated with both increased AF triggers as well as enablement of reentry15. Atrial contraction plays an important role in ventricular filling. Loss of atrial systole can lead to as much as a 25% reduction in cardiac output16. Irregular, and rapid ventricular conduction in the setting of inefficient and impaired cardiac output can lead to additionally reduction in cardiac output16-18.

 


Fig. 2 Shared pathophysiological mechanisms between AF and HF

However, immediately after cardioversion, increases in stroke volume and left ventricular ejection fraction (LVEF) are observed, despite the absence of demonstrable improvement in contractility. These physiological observations serve as the primary rationale behind strategies to prevent recurrent arrhythmia and maintain sinus rhythm in AF patients with and without underlying cardiovascular disease.

Treatment Strategies

 

Among the most important decisions that must be made by a patient and care provider when choosing a treatment plan for AF is the choice between rate and rhythm control. Rate control is typically a simpler strategy than rhythm control, involving the use of generally less toxic medications and fewer medical procedures, although rate control strategies can result in adverse drug side effects and toxicities and, in some cases, may require interventions such as pacemaker implantation and atrioventricular (AV) nodal ablation. Rhythm control strategies typically involve potentially riskier antiarrhythmic medications or invasive procedures such as catheter ablation or surgery, but, when successful, provide the benefits of sinus rhythm. AF and HF, both alone and in concert are responsible for impaired quality of life, disability and financial burden on society. AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial demonstrated improved QOL in those treated with either rate or rhythm control therapies19. The failure of rhythm control to yield superior QOL compared with rate control may have been due to the limited effectiveness or adverse effects of antiarrhythmic therapy despite the advantages of sinus rhythm. Rhythm control strategy provided no benefit and actually showed a trend toward harm in the general population of patients compared with rate control. Similar results were reported in the AF-CHF (Atrial Fibrillation and Congestive Heart Failure) trial20,where both rate and rhythm control improved symptoms, but sinus rhythm had the added benefit of being associated with improved New York Heart Association functional class and QOL.

 

AF increases stroke risk several fold22, and AF related strokes are associated with significantly reduced QOL, disability, and mortality. Not surprisingly, an analysis of the AFFIRM study failed to show a significant difference in stroke risk between the rate and rhythm control arms, although a posthoc analysis suggested that the presence of AF was associated with an increased risk of ischemic stroke,whereas sinus rhythm and systemic anticoagulation were associated with a lower risk of stroke23. Subsequent studies have continued to raise the hypothesis that the reduction and/or elimination of AF decreases stroke risk. Recently, a retrospective observational analysis of age- and sex-matched patients suggested that catheter ablation of AF was associated with a lower risk of incident stroke24. Across all CHADS2 profiles, patients who underwent ablation demonstrated lower long-term risk of stroke than those with AF who did not undergo ablation. Other studies also have reported very low rates of thromboembolic events after successful AF ablation25-26. Whether or not AF ablation can reduce the risk of stroke in patients with and without HF will require large randomized studies such as the CABANA, RAFT and the CASTLE-AF trials.

Several lines of evidence support the hypothesis that maintenance of sinus rhythm could result in better patient outcomes in comparison with rate control for AF, if sinus rhythm could be maintained with a high success rate and with a therapy that has a better safety profile than currently available antiarrhythmic drugs. Observational studies have demonstrated higher morbidity and mortality among patients with a history of AF, in particular, if they have coexistent CHF, in comparison with those without AF. Among patients with symptomatic paroxysmal AF, symptoms are worse during periods of AF in comparison with sinus rhythm. Analyses of the AFFIRM database demonstrated that patients who maintained sinus rhythm in the study (regardless of rate versus rhythm control strategy) had reduced mortality and heart failure symptoms compared with patients who remained in AF, and that CHF symptoms were worse in the rate control arm in comparison with the rhythm control arm.

 

Pharmacological rhythm control strategy for atrial fibrillation

Antiarrhythmic drug therapy is indicated as firstline therapy for AF that remains symptomatic (EHRA score >2) despite adequate rate control27. Unfortunately, many antiarrhythmic drugs are contraindicated in patients with structural heart disease, because of a risk of ventricular proarrhythmia. Amiodarone and dofetilide are the lone guideline-recommended antiarrhythmic medications for patients with symptomatic HF or significant LV dysfunction, yet they have significant adverse effects and drug–drug interactions28. Amiodarone, for example, carries the risk of pulmonary, hepatic, and thyroid toxicity29. Despite its potency, recurrence rates in patients with AF and HF are 50% or greater at 1 year. Equally concerning, a chief risk of dofetilide therapy is that it prolongs the QT interval and can lead to torsades in 0.8% to 3.3% of those treated. Moreover, dofetilide is renally cleared and must be adjusted in patients with renal dysfunction, which commonly accompanies HF.

 

Pre-clinical development of AF therapies has increased significantly, and there are several novel therapeutic modalities on the horizon. Well-known for its antianginal properties and limited side-effect profile, ranolazine is being studied increasingly in HF and AF. A late sodium-channel antagonist, ranolazine promotes myocardial relaxation by decreasing intracellular calcium and has been shown to reduce atrial and ventricular arrhythmias30,31. It has been reported as an effective synergistic adjunct to amiodarone for AF and is currently being studied as a lone antiarrhythmic drug and in fixed-dose combination with dronedarone.

Dronedarone is a benzofuran derivative, structurally related to amiodarone, which has been approved for the treatment of paroxysmal or persistent AF. Dronedarone is a ‘multichannel blocker’ that inhibits sodium and potassium channels, shows a noncompetitive antiadrenergic activity, and has calcium antagonist properties.The drug is more effective in maintaining sinus rhythm than placebo but inferior to amiodarone in that respect. For patients in NYHA functional class III or IV, there is evidence from the ANDROMEDA32 (ANtiarrhythmic trial with DROnedarone in Moderate-to-severe congestive heart failure Evaluating morbidity DecreAse) trial that these patients may derive harm from dronedaron therapy. On the other hand, in patients with NYHA class I or II heart failure, or with HF-PEF, there is no clear scientific evidence for harmful effects of the drug. Use of dronedarone as an antiarrhythmic agent in patients with recurrent AF and less severe heart failure (NYHA class I–II) is not appropriate unless there is no suitable alternative.

Budiodarone, an amiodarone analogue with a shorter half-life and alternative metabolism, has been investigated for AF rhythm control with the hope of producing fewer side effects33. To date, studies aimed primarily at an HF population do not exist.

 

Catheter ablation for rhythm control

Given the limitations of current antiarrhythmic drug therapy, clinicians have shown great interest in the use of nonpharmacological rhythm control interventions in patients with AF and HF. The role of catheter ablation is not simply to restore and maintain sinus rhythm, but more importantly, to ameliorate symptoms and improve QOL. Catheter ablation remains as the sole choice for escalated rhythm control therapy in patients who suffer from symptomatic

AF recurrences on amiodarone therapy.The main principles of rhythm control therapy apply to this group of patients as well, specifically that rhythm control therapy is indicated to improve AF-related symptoms (EHRA score II–IV), and that OAC therapy should be maintained, as the arrhythmia is likely to recur. It should be emphasized that the likelihood of maintaining sinus rhythm after catheter ablation is lower and the procedure-related risks may be higher in heart failure patients. In addition, correct assessment of AF-related symptoms may be more difficult with overlapping heart failure symptoms, emphasizing the need for an individual and informed decision for catheter ablation in patients with heart failure. In selected patients suffering from heart failure and treated in highly experienced centres, catheter ablation of AF may confer an improvement in left ventricular function34. The percutaneous technique, at a minimum, employs circumferential ablation and hence electrical isolation of the pulmonary veins and their connection to atrial myocardium. Pulmonary vein isolation is often sufficient to eliminate paroxysmal AF but is usually insufficient for persistent AF35.

 

A variety of ablation strategies have been used for persistent AF after the pulmonary veins have been isolated: linear ablation across the left atrial roof, mitral isthmus, or cavotricuspid isthmus; ablation of CFAEs in the left atrium, coronary sinus, or right atrium; various combinations of linear and CFAE ablation; and ablation of ganglionated plexuses36-39. The endpoint of catheter ablation of persistent AF is either completion of a prespecified lesion set (in which case sinus rhythm is restored by cardioversion) or stepwise ablation until the AF converts to sinus rhythm. A novel approach to ablation of AF is FIRM ablation, which is based on the hypothesis that AF is sustained by localized sources, either rotors and/or focal impulses. Signal processing with proprietary software allowed identification of focal impulses and rotors, which were then targeted for radiofrequency ablation during ongoing episodes of AF. A mean of 2.1 localized sources per patient were identified in 97% of 101 patients40. Termination or slowing of AF was successfully achieved by ablation of the localized sources in 86% of cases. At a median of 9 months of follow-up, 82% of patients were free of AF versus 45% of those in a control group who underwent conventional ablation40. These early results suggest that focal impulse and rotor modulation can improve outcomes of catheter ablation of AF. Based on an extensive review of a large number of published reports, the overall single-procedure success rate of radiofrequency catheter ablation of AF without antiarrhythmic drug therapy is 57%, and the multiple-procedure success rate is 71%. Efficacy is strongly influenced by the type of AF being ablated. For paroxysmal AF, a single-procedure success rate of 60% to 75% is expected at experienced centers, whereas for persistent AF, the single-procedure success rate is typically 50% or lower.

 

Cohort studies (Chen et al. 2004, Gentlesk et al. 2007)41,42 compared PVI in patients with reduced vs. normal EF, found no difference in success rates of catheter ablation (86% vs. 87%), though patients with reduced EF more often required repeat ablation. In patients with LV dysfunction, maintenance of sinus rhythm resulted in an average absolute increase in EF of 14%. Randomized trials CAMTAF and ARC-HF43,44, compared PVI with or without linear and focal CFAE ablation vs. pharmacological rate control reported a trend toward significant increase in LVEF, improved LV ESV, functional capacity, and QOL in the PVI group. AF-free survival at 6 months is 81% in the PVI group (ARC-HF)44 and 88% at 12 months (CAMTAF)43. Furthermore, it’s been observed increase in peak VO2, BNP, and NT pro-BNP in the PVI group compared with rate control arm.

 

According to results of a randomised, open-label, parallel-group study presented at the 64th Annual Scientific Session of the American College of Cardiology (ACC), treating persistent atrial fibrillation (AF) with catheter ablation rather than amiodarone reduces hospitalisations and mortality in patients who also have heart failure45. For this study, which included eight centers in the US and Europe, the investigators enrolled 203 adult patients who had a dual-chamber implantable cardioverter defibrillators (ICDs) or biventricular pacemakers with defibrillators (CRT-Ds), NYHA class 2 or 3 heart failure, <40% LVEF, and symptomatic persistent or permanent AF. A particular strength of the AATAC study was that all participants had an implantable cardioverter-defibrillator and/or cardiac resynchronization therapy device, permitting detection of AF with a much higher degree of accuracy than possible in most AF ablation trials. All were randomly assigned to receive either catheter ablation (n=102; 75% men; mean age 62 years; mean AF duration 8.6 months; LVEF 29%) or daily oral amiodarone (n=101; 73% men; mean age 60 years; mean AF duration 8.4 months; LVEF 30%). After 2 years of follow-up, the primary endpoint of freedom from AF was reported in 70% of patients receiving catheter ablation and in 34% of patients receiving amiodarone (P < .001). Secondary endpoints were, hospitalisation for arrhythmia or worsening heart failure (31% vs 57%, P < .001) and all-cause mortality (8% vs 18%, P = .037) were significantly lower in the group receiving catheter ablation. In the catheter-ablation group, 80% of patients also had received additional linear lesions, ablation of complex fractionated electrogram, and elimination of non-pulmonary vein triggers while pulmonary-vein isolation alone was performed in the other 22 patients. At 26 months, success rates were higher among those patients receiving the more extensive ablations (78% vs 36.4%, P < .001).

Patients receiving amiodarone were 2.5 times more likely to have recurrent AF. A total of 10.4% patients in the amiodarone group discontinued the medication due to adverse side effects, including thyroid toxicity, pulmonary toxicity, and liver dysfunction.

Results of AATAC-AF study. Source Dr. Di Biase

 

Among recurrence-free patients, LVEF improved by an average of 9.6% compared with a 4.2% for patients who experienced recurrence (P < .001). Similarly, 6-minute walk distance (mean change, 27 vs. 8; P < .001) and Minnesota functioning score (mean reduction, 14 vs. 2.9; P < .001) were also improved in recurrence-free patients compared with those who experienced recurrence45.

 

As alternative procedure, atrioventricular node ablation with pacing, has shown efficacy in patients with refractory AF and HF46. To compare the extremes of rate and rhythm control strategies, the PABA-CHF (Pulmonary Vein Antrum Isolation versus AV Node Ablation with Bi-Ventricular Pacing for Treatment of Atrial Fibrillation in Patients with Congestive Heart Failure) study randomized 41 patients to atrioventricular node ablation and subsequent

biventricular pacing versus PVI47. At 6-month follow-up, the PVI group had 88% AF-free

survival and an absolute increase in LVEF of 8% versus no change in the biventricular pacing/nodal ablation group (p < 0.001). Functional capacity was enhanced with PVI based on significant improvements in both the 6-min walk test and QOL. The outcomes suggest that atrioventricular node ablaion and pacing was inferior to PVI, but the study did not evaluate the less invasive, more common strategy of pharmacological rate control.

 

Hybrid and surgical ablation approaches

 

Beyond pharmacological and catheter ablation approaches, there exist other methods of rhythm control in order to attenuate AF. The hybrid endocardial–epicardial ablation, or “convergent” procedure, was designed to be less invasive and avoid the need for chest incisions, lung deflation, and heart dissection48. A transdiaphragmatic endoscopic approach is

utilized to make gapped epicardial lesions, which are later connected via percutaneous mapping and endocardial ablation. Two prospective nonrandomized studies have demonstrated the general safety and efficacy of this procedure for treatment of drug refractory

AF83,84, but only 16% of patients in these studies had comorbid HF, and the average LVEF was 55% to 58%. Gehi et al.49 found similar results in a cohort of 101 patients, 30% of which had comorbid HF with an average pre-procedural EF of 50%. Arrhythmia-free survival was 66% at 12 months after a single procedure and 71% after repeat ablation with a major periprocedural complication rate of 6%.

The Cox-Maze III procedure is the surgical standard for medical-refractory AF. It is most often performed in the setting of concomitant valve surgery and/or revascularization procedures, and is associated with decreased AF burden without significant complications when compared with usual surgical care50. The traditional cut-and-sew approach serves as the gold standard for conduction block because it provides definitive transmural injury to cardiac tissue, whereas catheter ablation and hybrid approaches create endocardial and endocardial/epicardial lesions, respectively. Overall, the strength of evidence for surgical maze procedures versus usual surgical care, in regard to restoration and maintenance of sinus rhythm, is reasonable yet insufficient when considering post-procedural HF symptoms and QOL. There are surgical modalities with radiofrequency energy, microwave or cryothermy. Few data are available describing outcomes in patients with LV dysfunction and/or HF who undergo surgical ablation. In a series of 42 patients with AF, a LVEF <40% and symptomatic HF undergoing cardiac surgery with concomitant Cox-Maze III/IV procedures, 86% of patients were in sinus rhythm at a median of 6 months51. The average improvement in LVEF was 15%, and perioperative mortality was 2%.

 

Conclusion

In this ever-expanding population of patients with concomitant AF and HF, it is apparent that that restoration and long-term maintenance of sinus rhythm are associated with significant improvement in cardiac function, symptoms, exercise capacity, and quality of life in patients with congestive heart failure, even in the presence of concurrent heart disease and adequate rate control. Curative ablation for atrial fibrillation offers the unique opportunity to maintain sinus rhythm without antiarrhythmic drugs, which can have deleterious effects. Although there are limited studies reporting on major cardiovascular outcomes following catheter ablation in patients with HF, recent trials note improvement in prognostic surrogates for HF outcomes as well as QOL. Future studies, including large randomized trials, will help delineate the utility of this procedure in reducing morbidity and, perhaps, mortality in patients with concomitant AF and HF.

 

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