Risk of Atrial Fibrillation After Atrial Flutter Ablation
The major findings of this study are that: (1) AF occurrence after AFL ablation is a frequent (>20%) event in patients without AF history prior to the ablation, (2) in patients without AF history, the risk of AF occurrence after AFL ablation is particularly high in women and in patients treated with class I AAD or amiodarone prior to AFL ablation, probably because previous AF episodes were masked by this treatment, and (3) most patients who experience AF after AFL ablation have a CHA2DS2-VASc score ≥1, suggesting moderate to high risk of embolic events.
There was a high prevalence of AF history in our population of patients referred for AFL ablation (32%). A higher than 20% prevalence of AF history has also been observed in several other studies.
In our population, higher age was not associated with a higher risk of AF history prior to ablation. In contrast, female gender was associated with a higher risk of AF history. This finding could be related to the higher probability of AF-associated symptoms in women. We also identified that chronic pulmonary disease and ischemic or congenital HD were independently associated with a lower risk of AF history, i.e., patients with these conditions were more likely to have isolated AFL. These results are in keeping with the known high risk for macroreentrant circuits observed in patients with congenital HD and in patients with chronic obstructive pulmonary disease. A history of cardiac surgery (including atriotomy) has also been previously identified to be more common in patients with isolated AFL than in those with AFL combined with AF. With regard to the association between ischemic HD and AF history, Peyrol et al. found a similar prevalence of coronary HD in patients suffering from AFL with or without AF history in a sample of 76 patients referred for AFL.
We found, as in previous studies, that AF history was a strong predictor of AF occurrence after AFL ablation, with an almost 2-fold increase in the risk of subsequent AF in patients with AF history prior to ablation. This finding is in contradiction with the hybrid therapy concept put forward in the late 1990s and early 2000s, in order to reduce the risk of AF recurrences. However, several studies have shown that the risk of AF recurrence in patients with a history of AF was elevated, reaching as high as 70% at 3 years. Our results confirm the limited impact of hybrid therapy on the long-term control of AF.
Combined pulmonary vein-left atrial junction disconnection and cavotricuspid isthmus ablation has also been proposed in patients presenting with typical AFL and AF. However, AFL ablation remains the procedure usually indicated as the first line of treatment.
Several risk factors for AF occurrence after AFL ablation have been identified in previous studies. Reithmann et al. reported that decreased left ventricular ejection fraction was an independent predictor of AF after AFL ablation in a population including only patients with AF and AFL. In a similar population, Della Bella et al. identified that the presence of structural HD, increased left atrial dimension and volume, failure of multiple AAD, as well as inducibility of AF were associated with a higher risk of AF occurrence after ablation. Longer fluoroscopy times, lack of bidirectional block, and significant mitral regurgitation have also been reported to be associated with an increased risk of AF after AFL ablation.
In a previous study, we reported that women had a higher risk of AF occurrence after AFL ablation. We further show that female gender is a particularly strong predictor of AF occurrence in patients without AF history prior to AFL ablation (OR = 1.93, CI = 1.29–2.89, P = 0.001 in the multivariable model). The conjunction of a higher probability of documented AF after AFL ablation in female patients and of a higher AF-related embolic risk in female patients might encourage clinicians to reassess the benefit-to-risk ratio of long-term anticoagulants in this subset of patients.
We also identified that AAD treatment prior to AFL ablation was associated with a higher risk of AF occurrence in patients without AF history. Patients treated with amiodarone or class I AAD before AFL ablation had, respectively, a 1.5- to 2-fold increase in the risk of developing AF later. To the best of our knowledge, this study is the first to report such an association between AAD prior to AFL ablation and subsequent risk of AF occurrence. We can hypothesize that class I and III AAD likely masked previous episodes of AF. As a result, AAD treatments may have decreased or suppressed the AF load prior to AFL ablation or, alternatively, may have decreased symptoms related to AF. Therefore, patients without AF history treated with class I AAD or amiodarone before AFL ablation may have a higher risk of AF after ablation because of an atrial substrate equivalent to that observed in patients with AF history.
The incidence of AF after AFL ablation remains lower than the incidence reported by Ellis at a long-term follow-up of 39 ± 11 months: approximately 82% of patients post-cavotricuspid isthmus ablation for AFL developed drug-refractory AF. This finding suggested that elimination of AFL possibly delayed but did not prevent AF. The same group reported in patients with both AFL and AF that pulmonary vein-left atrial junction disconnection alone could be sufficient to control both arrhythmias. Isthmus block reduced early postablation recurrence of arrhythmias, which in the majority of patients reflected a short-term clinical problem.
Two-thirds (77.3%) of patients herein who suffered from AF after AFL ablation had a CHA2DS2-VASc score ≥1, i.e., the majority of patients with AF occurrence after AFL ablation are at moderate to high risk for embolic events. This result suggests that patients with AF occurrence after AFL ablation, and in whom oral anticoagulants are generally stopped soon after the ablation, are at moderate risk for stroke before the formal diagnosis of AF occurrence and its subsequent treatment. Thus, given the embolic risk of patients referred for AFL ablation (mean CHA2DS2-VASc score greater than 1.5 in our entire population), we can suspect a meaningful risk for stroke associated with these asymptomatic AF episodes.
Patients should be informed regarding the likelihood of AF occurrence after AFL ablation. As the overall risk of AF occurrence after AFL is greater than 20% and since most patients would be at moderate to high risk for stroke if AF occurs, long-term anticoagulation might be systematically discussed on an individual basis. Several authors who reported similarly elevated postprocedural AF occurrence also advocated for a long-term continuation of anticoagulants in certain patients after AFL ablation. This high risk of AF after AFL is easily explained by the well-established pathophysiological interplay between AF and AFL. The need for a cautious and careful benefit-to-risk ratio assessment when considering anticoagulant discontinuation appears especially true in 3 categories of patients: (1) patients with a history of AF prior to AFL ablation, (2) female patients, and (3) patients without AF history but treated with class I AAD or amiodarone, in whom concealed AF episodes hidden by AAD can be suspected. In these subsets of patients, long-term anticoagulants should be considered.
Thus, from our point of view, it is time to reconsider the accepted strategy of anticoagulant discontinuation after successful AFL ablation in patients without AF history.
Discussion
The major findings of this study are that: (1) AF occurrence after AFL ablation is a frequent (>20%) event in patients without AF history prior to the ablation, (2) in patients without AF history, the risk of AF occurrence after AFL ablation is particularly high in women and in patients treated with class I AAD or amiodarone prior to AFL ablation, probably because previous AF episodes were masked by this treatment, and (3) most patients who experience AF after AFL ablation have a CHA2DS2-VASc score ≥1, suggesting moderate to high risk of embolic events.
History of AF Prior to AFL Ablation
There was a high prevalence of AF history in our population of patients referred for AFL ablation (32%). A higher than 20% prevalence of AF history has also been observed in several other studies.
In our population, higher age was not associated with a higher risk of AF history prior to ablation. In contrast, female gender was associated with a higher risk of AF history. This finding could be related to the higher probability of AF-associated symptoms in women. We also identified that chronic pulmonary disease and ischemic or congenital HD were independently associated with a lower risk of AF history, i.e., patients with these conditions were more likely to have isolated AFL. These results are in keeping with the known high risk for macroreentrant circuits observed in patients with congenital HD and in patients with chronic obstructive pulmonary disease. A history of cardiac surgery (including atriotomy) has also been previously identified to be more common in patients with isolated AFL than in those with AFL combined with AF. With regard to the association between ischemic HD and AF history, Peyrol et al. found a similar prevalence of coronary HD in patients suffering from AFL with or without AF history in a sample of 76 patients referred for AFL.
We found, as in previous studies, that AF history was a strong predictor of AF occurrence after AFL ablation, with an almost 2-fold increase in the risk of subsequent AF in patients with AF history prior to ablation. This finding is in contradiction with the hybrid therapy concept put forward in the late 1990s and early 2000s, in order to reduce the risk of AF recurrences. However, several studies have shown that the risk of AF recurrence in patients with a history of AF was elevated, reaching as high as 70% at 3 years. Our results confirm the limited impact of hybrid therapy on the long-term control of AF.
Combined pulmonary vein-left atrial junction disconnection and cavotricuspid isthmus ablation has also been proposed in patients presenting with typical AFL and AF. However, AFL ablation remains the procedure usually indicated as the first line of treatment.
Occurrence of AF After AFL Ablation
Several risk factors for AF occurrence after AFL ablation have been identified in previous studies. Reithmann et al. reported that decreased left ventricular ejection fraction was an independent predictor of AF after AFL ablation in a population including only patients with AF and AFL. In a similar population, Della Bella et al. identified that the presence of structural HD, increased left atrial dimension and volume, failure of multiple AAD, as well as inducibility of AF were associated with a higher risk of AF occurrence after ablation. Longer fluoroscopy times, lack of bidirectional block, and significant mitral regurgitation have also been reported to be associated with an increased risk of AF after AFL ablation.
In a previous study, we reported that women had a higher risk of AF occurrence after AFL ablation. We further show that female gender is a particularly strong predictor of AF occurrence in patients without AF history prior to AFL ablation (OR = 1.93, CI = 1.29–2.89, P = 0.001 in the multivariable model). The conjunction of a higher probability of documented AF after AFL ablation in female patients and of a higher AF-related embolic risk in female patients might encourage clinicians to reassess the benefit-to-risk ratio of long-term anticoagulants in this subset of patients.
We also identified that AAD treatment prior to AFL ablation was associated with a higher risk of AF occurrence in patients without AF history. Patients treated with amiodarone or class I AAD before AFL ablation had, respectively, a 1.5- to 2-fold increase in the risk of developing AF later. To the best of our knowledge, this study is the first to report such an association between AAD prior to AFL ablation and subsequent risk of AF occurrence. We can hypothesize that class I and III AAD likely masked previous episodes of AF. As a result, AAD treatments may have decreased or suppressed the AF load prior to AFL ablation or, alternatively, may have decreased symptoms related to AF. Therefore, patients without AF history treated with class I AAD or amiodarone before AFL ablation may have a higher risk of AF after ablation because of an atrial substrate equivalent to that observed in patients with AF history.
The incidence of AF after AFL ablation remains lower than the incidence reported by Ellis at a long-term follow-up of 39 ± 11 months: approximately 82% of patients post-cavotricuspid isthmus ablation for AFL developed drug-refractory AF. This finding suggested that elimination of AFL possibly delayed but did not prevent AF. The same group reported in patients with both AFL and AF that pulmonary vein-left atrial junction disconnection alone could be sufficient to control both arrhythmias. Isthmus block reduced early postablation recurrence of arrhythmias, which in the majority of patients reflected a short-term clinical problem.
Risk of Stroke for Patients With AF During Follow-Up
Two-thirds (77.3%) of patients herein who suffered from AF after AFL ablation had a CHA2DS2-VASc score ≥1, i.e., the majority of patients with AF occurrence after AFL ablation are at moderate to high risk for embolic events. This result suggests that patients with AF occurrence after AFL ablation, and in whom oral anticoagulants are generally stopped soon after the ablation, are at moderate risk for stroke before the formal diagnosis of AF occurrence and its subsequent treatment. Thus, given the embolic risk of patients referred for AFL ablation (mean CHA2DS2-VASc score greater than 1.5 in our entire population), we can suspect a meaningful risk for stroke associated with these asymptomatic AF episodes.
Clinical Implications
Patients should be informed regarding the likelihood of AF occurrence after AFL ablation. As the overall risk of AF occurrence after AFL is greater than 20% and since most patients would be at moderate to high risk for stroke if AF occurs, long-term anticoagulation might be systematically discussed on an individual basis. Several authors who reported similarly elevated postprocedural AF occurrence also advocated for a long-term continuation of anticoagulants in certain patients after AFL ablation. This high risk of AF after AFL is easily explained by the well-established pathophysiological interplay between AF and AFL. The need for a cautious and careful benefit-to-risk ratio assessment when considering anticoagulant discontinuation appears especially true in 3 categories of patients: (1) patients with a history of AF prior to AFL ablation, (2) female patients, and (3) patients without AF history but treated with class I AAD or amiodarone, in whom concealed AF episodes hidden by AAD can be suspected. In these subsets of patients, long-term anticoagulants should be considered.
Thus, from our point of view, it is time to reconsider the accepted strategy of anticoagulant discontinuation after successful AFL ablation in patients without AF history.