We performed a retrospective observational cohort study of consecutive patients with HF symptoms and LVEF <50% who underwent AF catheter ablation between July 2016 and November 2018 in a tertiary referral center. Procedural endpoints and mid-term follow-up results were assessed.

Patients were eligible for inclusion in the study if they met the following criteria: drug-refractory AF or intolerance to AAD therapy; LVEF <50%; and symptoms of HF (New York Heart Association [NYHA] functional class ≥2). All patients provided written informed consent prior to the procedure.

Paroxysmal AF was defined as AF lasting less than seven days, persistent AF as AF lasting between seven days and one year, and long-standing persistent AF as lasting for more than one year before a decision to attempt rhythm control was made.9

All patients underwent assessment for any underlying structural heart disease, and significant coronary artery disease had to be ruled out by cardiac angiography or stress testing.

Exclusion criteria were the following: age <18 years; severe valvular disease; ischemic cardiomyopathy (defined as a history of documented >75% left main or proximal left anterior descending artery stenosis, >75% two-vessel stenosis or a previous history of myocardial infarction and/or revascularization16 or a documented area of ischemia >10% of the left ventricle);5,17 hypertrophic cardiomyopathy; neuromuscular disease; congenital heart disease; other apparent cause for systolic dysfunction (apart from tachycardia-induced cardiomyopathy); and left atrial thrombus.

Data required for cohort characterization were collected from patients’ clinical records. Echocardiographic data including LVEF, left atrial (LA) diameter (LAD) and LV end-diastolic diameter (LVEDD) were also collected. These measurements were performed by specialized operators blinded to the study endpoints. LA anteroposterior diameter and LVEDD were measured at end-systole in M-mode images in parasternal long-axis views. LVEF was calculated according to current recommendations.18

In order to reduce time in AF, electrical cardioversion was performed in all patients with persistent AF before intervention. For this reason, a large number of patients were in sinus rhythm at the time of ablation. All procedures were conducted under general anesthesia and patients suspended AAD therapy at least five half-lives before the procedure, except for amiodarone.

All patients were under oral anticoagulation (OAC) for at least two months prior to the procedure. In patients taking vitamin K antagonists (VKAs), OAC was continued in the periprocedural period with an international normalized ratio within the 2.0-3.0 range. In patients taking non-VKA OAC (NOAC), the last NOAC dose before the procedure was omitted. The presence of intracardiac thrombus was excluded prior to the procedure by transesophageal echocardiography or cardiac computed tomography (CT). During catheter ablation, unfractionated heparin was administered immediately after transseptal puncture and adjusted as needed for a target activated clotting time >300 s.

Anatomical mapping data were collected using a three-dimensional mapping system – CARTO 3 (Biosense-Webster, Irvine, CA, USA) or NavX (Abbott, Chicago, IL, USA) – and integrated with a CT imaging reconstruction of the left atrium, when available.

Each patient underwent a tailored approach, according to our institutional protocol, irrespective of AF type (persistent or paroxysmal) and duration. Briefly, if patients were in sinus rhythm, bipolar voltage mapping was performed. LA mapping was considered to be adequate when >500 voltage points were acquired. Voltage criteria for healthy and scarred tissue were >0.5 mV and <0.2 mV, respectively. After LA mapping, point-by-point pulmonary vein isolation (PVI) was carried out.

If the patient was in AF at the beginning of the procedure, PVI was performed first. Electrical cardioversion was subsequently performed if patients remained in AF after PVI, and a voltage map was obtained in sinus rhythm.

In the presence of low voltage areas, if the patient remained in AF or AF remained inducible with atrial burst pacing, these areas were ablated to achieve tissue homogenization, and if necessary lines were created connecting areas of scar to previous ablation lines (with the aim of achieving bidirectional block). In the absence of low voltage areas but persisting AF inducibility, ablation of complex fractionated atrial electrograms (CFAEs) was performed.19 If AF was converted to a regular atrial arrhythmia, this was mapped and ablated. Likewise, in the presence of typical flutter, ablation of the cavotricuspid isthmus was also performed. When AF persisted or was inducible at the end of the procedure, electrical cardioversion was performed.

The primary endpoint was improvement in LVEF, of at least 5% in order to reduce inter-operator variability.20

Secondary endpoints included improvement in NYHA class and reductions in LVEDD and maximum anteroposterior LAD. AF recurrence after catheter ablation was also analyzed in this population subset.

Safety endpoints included any major procedure-related complications (death, cardiac tamponade, stroke or systemic embolism, or vascular injury requiring transfusion or intervention).

Patients were assessed before discharge and at three, six and 12 months after the procedure. Transthoracic echocardiography (TTE) and 24-hour Holter monitoring were performed before discharge. Information collected during follow-up included clinical data, 24-hour or seven-day Holter monitoring at each visit, and TTE at six or 12 months. Recurrence of AF was defined as the documentation of at least 30 s of AF, atrial tachycardia or atrial flutter, irrespective of symptoms, in accordance with the Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation.21

No AADs were prescribed after ablation in paroxysmal AF patients. In those with persistent AF, AADs were prescribed on discharge at the discretion of the operator (particularly in patients with low voltage areas or persistence of AF at the end of the procedure requiring electrical cardioversion). The first three months after the procedure were considered the blanking period. The anticoagulation strategy after the first three months was based on the CHA2DS2-VASc and HAS-BLED scores.9

Statistical analysis was performed using IBM SPSS Statistics version 20 (IBM, Armonk, NY, USA). Categorical variables are expressed as frequencies and percentages and continuous variables as median and interquartile range (IQR), for variables with or without a normal distribution, respectively. The chi-square test was used to assess differences between categorical variables and the Student's t test or the Wilcoxon test were used to compare continuous variables with or without a normal distribution, respectively. The Kolmogorov-Smirnov test was used to test for normality of distribution of continuous variables. Statistical significance was accepted for p-values <0.05.

Median LVEF was 40% (IQR 34.5-40.2); 41% of the patients had HFrEF (i.e. LVEF ≤40%) and the remainder had HF with mid-range ejection fraction (HFmrEF), as defined by the 2016 European guidelines.5 Median LAD was 48.0 (IQR 43.5-51.5) mm and median LVEDD was 51.0 mm (IQR 54.0-64.8). Data regarding baseline echocardiographic parameters are presented in Table 2.

Details of the technical aspects of the procedures are presented in Table 3. A significant proportion of patients (54%) were in sinus rhythm at the beginning of the procedure, reflecting the high percentage of patients who had undergone electrical cardioversion in the preceding months. All patients underwent a single procedure. A voltage map was acquired in sinus rhythm in all patients, and low-voltage areas outside the pulmonary veins were detected in seven (32%) and CFAEs in five (23%). Antral PVI was performed successfully in all patients, with bidirectional block being obtained at first passage in 73% of cases. Low-voltage homogenization and lines were performed in six (27%) patients, CFAE ablation in five (23%) and cavotricuspid isthmus line ablation in eight (36%). At the end of the procedure, AF was still inducible in four patients (18%), and these underwent successful electrical cardioversion.

There were no immediate procedural or in-hospital complications.

Median follow-up was 11.1 (IQR 6.1-19.0) months.

LVEF assessment after catheter ablation was available in all cases. Improvement was observed from 40% (IQR 33-41) to 58% (IQR 55-62) (median 20% [IQR 15-26], p<0.01). Changes in LVEF before and after the procedure are shown in Figure 1A. Importantly, in 21 cases (95%), LVEF after catheter ablation was >50%. In fact, improvement in LVEF was observed even in patients with AF recurrence. Of the four patients with AF recurrence documented during follow-up, only one still had LVEF <50% (this patient had a considerable improvement from 16% to 43%), while in the remainder LVEF improved to >50%.

Figure 1.

Improvements after catheter ablation in left ventricular ejection fraction (A), left atrial diameter (B) and left ventricular end-diastolic diameter (C). CI: confidence interval; LVEF: left ventricular ejection fraction.

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LAD and LVEDD measurements were available in 21 (95%) and 20 (91%) patients, respectively. LAD decreased from 48.0 (IQR 43.5-51.5) mm to 44 (IQR 40-49) mm (p<0.01), while LVEDD decreased from 61.0 (IQR 54.0-64.8) mm to 55.0 (52.2-58.0) mm (p<0.01). Changes in LAD and LVEDD are shown in Figure 1B and C.

Mean NYHA class improved from 2.35±0.49 to 1.3±0.47 (p<0.01) after catheter ablation. Figure 2 shows improvements in NYHA class pre- and post-ablation. At last follow-up, diuretic doses were reduced or discontinued in 55% of the patients.

Figure 2.

Improvement in New York Heart Association (NYHA) functional class after catheter ablation. Red and blue arrows represent patients with and without recurrence of atrial fibrillation after the blanking period, respectively.

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Recurrence after the blanking period was documented in 18% of patients, four in total – three in AF (two of whom were in paroxysmal AF) and one in paroxysmal atrial tachycardia; one patient was under AAD therapy at the time of recurrence.

All recurrences were in patients with a history of persistent AF (three with long-standing persistent AF), meaning that freedom from symptomatic and/or documented AF at last follow-up was 78% for patients with persistent AF and 100% for those with paroxysmal AF with a single ablation procedure. Only two patients remained under amiodarone at follow-up.

There were no major procedure-related complications. No patients died during follow-up and there were no hospital admissions due to cardiovascular causes.

We acknowledge several limitation of our work. First, this was a retrospective study involving a small number of patients treated in a single center without a control group, which precludes an objective assessment of the impact of ablation compared with medical treatment alone. Second, since our patients did not undergo cardiac magnetic resonance imaging prior to AF ablation, we could not differentiate between patients with tachycardia-induced cardiomyopathy and those with dilated cardiomyopathy due to other causes. However, it may still be possible to reverse LV dysfunction to some extent in the latter group. Third, our follow-up duration was relatively limited and we are thus unable to comment on the benefit of ablation in the mid to long term. Fourth, systematic monitoring using an implantable loop recorder could have documented a higher rate of asymptomatic AF recurrence and provided more objective information regarding AF burden in follow-up. Lastly, electrical cardioversion performed pre-ablation may have contributed to the improvements in functional class and LVEF, as well as atrial and ventricular remodeling. However, even on AADs, almost half of our patients had AF recurrence and were in AF at the beginning of the procedure, which strengthened the indication for it and clearly demonstrates that a similar level of benefit would not have been achieved with electrical cardioversion plus AAD therapy alone.