Summary
Background
Pericardial effusion (PE) can occur during or after atrial fibrillation (AF) ablation, and may induce atrial arrhythmia.
Aim
To characterize the impact of PE on arrhythmia recurrences following AF ablation.
Methods
Patients referred for a first radiofrequency AF ablation were studied prospectively. Transthoracic echocardiography was performed before and 24 h after the procedure. If PE was present, transthoracic echocardiography was repeated at 1 month to evaluate PE evolution. Early arrhythmia recurrences (EARs) were defined as any arrhythmia documented within 1 month of the procedure.
Results
PE was diagnosed in 18/81 patients (22%); and was present in significantly more patients with persistent versus paroxysmal AF (14/40 [35%] vs 4/41 [10%]; P = 0.008). PEs were mild (mean 6 ± 3 mm), mainly asymptomatic (89%), and none required pericardiocentesis. Early and late arrhythmia recurrences were present in 25/81 (31%) and 29/81 (36%), respectively. The incidence of PE was significantly higher among patients with EARs versus those without (12/25 [48%] vs 6/56 [11%]; P = 0.0004). By multivariable analysis, PE and duration in AF were the two independent predictors of EARs. PE incidence was similar in patients with and without late arrhythmia recurrences. At 1 month, no patients had PE on transthoracic echocardiography.
Conclusion
PE following radiofrequency AF ablation is frequent, particularly following persistent AF ablation. This effusion is generally mild, mainly asymptomatic, and independently associated with EARs.
Résumé
Contexte
Un épanchement péricardique peut survenir pendant ou après la réalisation d’une ablation de fibrillation atriale et peut induire des arythmies atriales.
Objectifs
Pour caractériser les épanchements péricardiques survenant après cette intervention et d’étudier leur relation avec la survenue d’arythmie postablation.
Méthodes
Nous avons étudié de manière prospective des patients adressés dans notre centre pour ablation de fibrillation atriale. Une échocardiographie transthoracique a été réalisée avant et 24 heures après l’intervention. Une récidive d’arythmie précoce était définie par une arythmie atriale documentée dans le mois suivant l’ablation. Quatre-vingts un patients ont été inclus dans cette étude.
Résultats
Un épanchement péricardique a été diagnostiqué dans 22 % des cas et plus particulièrement 35 % des patients avec fibrillation atriale persistante et 10 % paroxystique ( p = 0,008). Ces épanchements péricardiques étaient le plus souvent modérées (6 ± 3 mm), asymptomatiques (89 %) et aucun n’a nécessité de drainage. Des récidives d’arythmie précoce et tardive étaient présentes chez 31 et 36 % respectivement dans notre population. L’incidence d’épanchement péricardique était plus élevée chez les patients présentant une récidive précoce d’arythmie comparé aux patients n’ayant pas de récidive précoce (48 % versus 11 %, p = 0,0004). En analyse multivariée, la présence d’un épanchement péricardique et l’ancienneté de la fibrillation atriale étaient les deux seuls facteurs prédictifs indépendants de récidive d’arythmie précoce. L’incidence d’épanchement péricardique était identique chez les patients présentant une récidive tardive d’arythmie ou non. Aucun de nos patients n’avait d’épanchement péricardique un mois après l’intervention.
Conclusion
Un épanchement péricardique est fréquemment rencontré après ablation de fibrillation atriale avec radiofréquence surtout après ablation de fibrillation atriale persistante. Ces épanchements sont modérés, le plus souvent asymptomatiques et associés de manière indépendante à la survenue d’arythmie précoce postablation.
Background
Catheter ablation of AF is an established therapy for patients with both paroxysmal and persistent AF . However, numerous complications have been associated with this procedure, including PE . It has recently been reported that PE is common (10–14%) following AF ablation, but is mainly mild and asymptomatic .
EARs are common during the first month following AF ablation . However, the significance of these EARs in predicting the long-term success of the procedure is controversial . Consistent with this, the consensus document on catheter and surgical ablation of AF has suggested a uniform ‘blanking period’ of 3 months . The pathophysiology of these early arrhythmias is also unclear. Transient autonomic neural modifications or acute tissue inflammation have been suggested as possible mechanisms .
We have studied the incidence and characteristics of PE following paroxysmal and persistent AF ablation. As PE is known to be a common cause of atrial arrhythmias , we also evaluated the relationship between early and late arrhythmia recurrences and the occurrence of acute PE following AF ablation.
Methods
Study population
We prospectively studied patients referred to our centre for a first radiofrequency AF ablation between September 2008 and January 2010. Patients undergoing paroxysmal AF ablation with cryotherapy were excluded in order to homogenize our population, as radiofrequency and cryotherapy create different tissue lesions that can influence arrhythmia recurrences after ablation, and also because persistent AF ablation could not be performed with cryotherapy. Patients with PE before AF ablation were also excluded. The study was approved by an institutional review committee, and all subjects gave written informed consent.
Echocardiography data
Comprehensive echocardiography examination including transoesophageal echocardiography before AF ablation to exclude left appendage thrombus and standard TTE before and 24 h after AF ablation procedure were performed for each patient, with a particular focus on the presence of a new PE. Left ventricular function was assessed by the Simpson biplane method and LA diameter was measured on the parasternal long-axis view. PE was assessed from standard TTE using parasternal long-axis, short-axis and subcostal views, and was quantified during diastolic timing using M mode on the posterior wall. To differentiate PE from pericardial fat, echocardiography data before and after AF were compared. The diagnosis of epicardial fat tissue was retained if the echo-free space was located anteriorly, tended to move in concert with the heart, and remained stable compared to echocardiography data before AF ablation.
Electrophysiological study
All patients received effective anticoagulation therapy (target international normalized ratio 2–3) for at least 1 month before AF ablation. All antiarrhythmic drugs, with the exception of amiodarone, were discontinued five half-lives before the procedure. Oral anticoagulation was stopped 2 days before the procedure, and low-molecular-weight heparin was started. The electrophysiological study was performed under conscious sedation using remifentanyl.
The following catheters were introduced via the right femoral vein for electrophysiological study: (i) a steerable quadripolar or decapolar catheter (Xtrem; Ela Medical, Le Plessis-Robinson, France) was positioned within the coronary sinus, positioned at 4–5 o’clock along the mitral annulus in a left anterior oblique projection; (ii) a circumferential mapping catheter (Lasso; Biosense Webster, Diamond Bar, CA, USA) was introduced following transseptal access and stabilized using a long sheath (SL0 sheath; St Jude Medical, Sylmar, CA, USA) continuously perfused with heparinized saline solution; and (iii) a 3.5 mm externally irrigated tip ablation catheter (Celsius Thermocool; Biosense Webster) used for mapping and ablation.
Transseptal puncture was performed with the guidance of intracardiac echocardiography used transoesophageally . Following transseptal access, a single bolus of 100 IU/kg body weight of heparin was administrated and repeated if activated clotting time was < 300 ms.
Monitoring with a surface electrocardiogram (ECG) and bipolar endocardial electrogram was carried out continuously and recorded on a computer-based digital amplifier/recorder system for off-line analysis (Bard Electrophysiology, Lowell, MA, USA). Intracardiac electrograms were filtered from 30–500 Hz and measured at a sweep speed of 100 mm/s.
Ablation of paroxysmal and persistent atrial fibrillation
Radiofrequency energy was delivered at up to 35 W using an irrigation rate of ≥ 20 mL/min (0.9% saline via Cool Flow; Biosense-Webster) to achieve the desired power delivery. Temperature was limited to 45 °C.
For paroxysmal AF ablation, the procedure was considered successful when all the pulmonary veins were isolated electrically. If a patient experienced AF during the procedure, AF ablation was continued until termination of AF was achieved as described for persistent AF ablation.
Ablation of persistent or long-lasting persistent AF was performed sequentially as described previously , and involved pulmonary vein isolation, electrogram-based ablation, and linear ablation, with termination of AF via catheter ablation being the endpoint (stepwise approach). If the patient converted into atrial tachycardia, this arrhythmia was mapped and ablated until sinus rhythm was restored. Finally, if patient was still in AF after 5 h of procedure, an external cardioversion was performed.
Follow-up
Patients were followed at 1 month and then every 3 months with systematic 12-lead ECG and 24-hour Holter monitoring in our centre for 1 year. They also underwent routine follow-up by their referring cardiologist. From 1 year after the last procedure, they were followed every 6 months by their referring cardiologist.
All patients had antiarrhythmic therapies, including flecainide and beta-blockers for 1 month (for paroxysmal AF) and amiodarone for 3 months (for persistent or long-lasting persistent AF). If arrhythmia recurred after stopping these drugs, antiarrhythmic therapies were restarted. Further ablation was performed if arrhythmias were still present. Oral anticoagulation treatment was restarted 1 day following the procedure, and was continued for at least 3 months.
Patients with PE following AF ablation systematically had another TTE to study PE evolution 1 month after the index procedure. Patients with significant pericarditis pain associated with PE had non-steroidal anti-inflammatory drugs for 1 month.
Definition of early and late arrhythmias
Recurrences were defined as documented atrial arrhythmias after the index AF ablation that lasted for ≥ 3 minutes . The arrhythmia recurrences were characterized as follows: AF defined as chaotic and uncoordinated activity of the atrium and atrial tachycardia defined as a monomorphic atrial activity on 12-lead surface ECG. EARs were defined as any arrhythmia documented within 1 month of the procedure.
Statistical analysis
Continuous variables are expressed as mean ± SD, or median ± interquartile range [IQR] when variables appeared to be non-normally distributed. Statistical significance was assessed using the unpaired Student’s t test or Mann-Whitney test, if necessary. Categorical variables, expressed as numbers or percentages, were analysed with the Chi 2 test or Fisher’s exact test. Univariate factors presenting P < 0.1 were analysed using a logistic regression method for multivariable analysis (performed with StatView Software). All tests were two-tailed and P < 0.05 was considered statistically significant.
Results
Study population
A total of 98 consecutive patients were referred for a first AF ablation from September 2008 to January 2010. Among these, 17 underwent cryoablation for paroxysmal AF and were therefore excluded from our analysis. No patients had PE on TTE before AF ablation. Therefore, 81 patients were included in the analysis. For each patient, only the first procedure was analysed in this study. The median follow-up for our population was 8 (range 6–23) months. Four patients were lost during our long-term follow-up.
Table 1 describes the characteristics of the total study population, as well as in patients with paroxysmal AF ( n = 41) or persistent AF ( n = 40; including 15 with long-lasting persistent AF).
| All patients ( n = 81) | Paroxysmal AF ( n = 41) | Persistent AF ( n = 40) | p | |
|---|---|---|---|---|
| Male | 57 (70) | 28 (68) | 29 (72) | 0.67 |
| Age (years) | 56 ± 11 | 56 ± 12 | 56 ± 11 | 0.99 |
| Hypertension | 34 (42) | 18 (44) | 16 (40) | 0.72 |
| Diabetes | 8 (10) | 4 (10) | 4 (10) | 0.97 |
| Hypercholesterolaemia | 27 (33) | 12 (29) | 15 (37) | 0.43 |
| History of AF (months) | 64 ± 66 | 66 ± 79 | 61 ± 49 | 0.76 |
| Structural heart disease | 31 (38) | 12 (29) | 19 (48) | 0.09 |
| Ischaemic cardiomyopathy | 8 (10) | 2 (5) | 6 (15) | 0.13 |
| LVEF (%) | 55 ± 10 | 58 ± 7 | 52 ± 12 | 0.01 |
| LA diameter (mm) | 43 ± 5 | 42 ± 6 | 44 ± 5 | 0.31 |
| Beta-blockers | 42 (52) | 18 (44) | 24 (60) | 0.14 |
| Amiodarone | 30 (37) | 13 (32) | 17 (42) | 0.32 |
| Oral anticoagulation | 75 (93) | 37 (90) | 38 (95) | 0.41 |
| Antiplatelet therapy | 19 (23) | 14 (34) | 5 (12) | 0.02 |
| Radiofrequency time (min) | 70 ± 36 | 48 ± 26 | 92 ± 30 | < 0.0001 |
| Fluoroscopy time (min) | 75 ± 25 | 62 ± 21 | 88 ± 22 | 0.007 |
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