CLINICAL RESEARCH: HEART RHYTHM DISORDERS
The need for atrial flutter ablation following pulmonary vein antrum isolation in patients with and without previous cardiac surgery
Fethi Kilicaslan, MD*,
Atul Verma, MD*,
Hirosuke Yamaji, MD*,
Nassir F. Marrouche, MD*,
Oussama Wazni, MD*,
Jennifer E. Cummings, MD*,
Steven Hao, MD ,
Michelle Williams Andrews, RN*,
Salwa Beheiry, RN,
Ahmad Abdul-Karim, MD*,
William A. Belden, MD*,
Stephen Minor, MD*,
J. David Burkhardt, MD*,
Walid Saliba, MD*,
Robert A. Schweikert, MD* and
Andrea Natale, MD*,*
* Cleveland Clinic Foundation, Section of Pacing and Electrophysiology, Cleveland, Ohio
Sutter Pacific Heart Centers, San Francisco, California
Manuscript received August 23, 2004;
revised manuscript received October 20, 2004,
accepted November 15, 2004.
* Reprint requests and correspondence: Dr. Andrea Natale, Section of Pacing and Electrophysiology, Cleveland Clinic Foundation, Desk F15, 9500 Euclid Avenue, Cleveland, Ohio 44195. (Email: natalea{at}ccf.org).
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Abstract
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OBJECTIVES: The aim of this study was to assess the incidence of atrial flutter (AFL) after pulmonary vein antrum isolation (PVAI) in patients with previous cardiac surgery (PCS) in comparison to patients without PCS and to assess the need for AFL ablation in both groups.
BACKGROUND: Atrial fibrillation (AF) and AFL often co-exist. Pulmonary vein antrum isolation may be sufficient to control both arrhythmias. However, in patients with PCS, atrial incisions, cannulations, and scar areas may cause AFL recurrence despite elimination of pulmonary vein triggers.
METHODS: Data from 1,345 patients who had PVAI were analyzed. Patients with a history of AFL ablation and patients who had concomitant AFL ablation during PVAI were excluded from analysis. Sixty-three patients constituted the PCS group (Group 1, age 57 ± 13 years, 12 female) and 1,062 patients constituted the non-PCS group (Group 2, age 55 ± 12 years, 212 female). Patients in Group 1 had larger left atria, higher incidence of AFL pre-PVAI, and lower ejection fraction.
RESULTS: There was no significant difference in post-PVAI AF recurrence between Groups 1 and 2, but AFL incidence after PVAI was higher in Group 1 (33% vs. 4%, p < 0.0001). Ablation of AFL in Group 1 patients resulted in an 86% acute success rate and 11% recurrence over a mean follow-up of 357 ± 201 days.
CONCLUSIONS: In patients with PCS, post-PVAI AF recurrence is similar to patients without PCS. However, history of PCS is associated with a higher recurrence of AFL after PVAI. In a significant number of patients with PCS, AFL ablation is required to achieve a cure.
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Abbreviations and Acronyms
| | AF = atrial fibrillation | | AFL = atrial flutter | | ASD = atrial septal defect | | AVR = aortic valve replacement | | CABG = coronary artery bypass graft surgery | | LA = left atrium/atrial | | MVR = mitral valve replacement | | PCS = previous cardiac surgery | | PV = pulmonary vein | | PVAI = pulmonary vein antrum isolation | | RA = right atrium/atrial | | RF = radiofrequency |
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Atrial flutter (AFL) is an important late complication after cardiac surgery with increasing morbidity and mortality over time (1–3). The mechanism of AFL occurring after a remote previous cardiac surgery (PCS) is well characterized. The AFL in these patients is re-entrant, and the flutter circuit may involve atypical isthmuses between natural barriers, atrial incisions, and scar areas as well as the cavotricuspid isthmus (2–5).
There is a close relationship between atrial fibrillation (AF) and AFL. They often co-exist in the same patient and may degenerate into each other (6–9). Pulmonary vein (PV) triggers may be responsible for initiation of AFL as well as AF (7,10,11). Pulmonary vein antrum isolation (PVAI) is a feasible and effective treatment for patients with symptomatic and drug-resistant AF, even for patients with PCS (12,13). In patients without a history of PCS, we have shown previously that PVAI is sufficient to control both AF and AFL (10). However, in patients with PCS, the potential for AFL isthmuses secondary to PCS and a very unstable substrate may predispose to AFL recurrence despite the elimination of PV triggers. Whether AFL recurrence after PVAI is different in patients with and without PCS is unknown.
We sought to: 1) assess the incidence of AFL after PVAI in patients with PCS in comparison to patients without PCS, and 2) establish whether additional AFL ablation is required in these patients.
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Methods
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Patient population.
Data from 1,345 patients who had PVAI at two institutions between October 2000 and December 2003 were analyzed. Patients with a history of AFL ablation and patients who had concomitant AFL ablation during PVAI were excluded from analysis. Seventy patients had a history of PCS >6 months ago. Among them, five patients were excluded because of a history of AFL ablation and two patients were excluded because of concomitant AFL ablation during the PVAI procedure, leaving 63 patients in the PCS group (Group 1, age 57 ± 13 years, 12 female). Of the remaining 1,275 patients, 189 were excluded because of either a previous AFL ablation or a concomitant AFL ablation during the PVAI procedure, leaving 1,062 patients in the non-PCS group (Group 2, age 55 ± 12 years, 212 female). Patients who had AF and AFL recurrence concomitantly were considered for repeat PVAI and AFL ablation. An AFL ablation alone was considered if AFL was the only arrhythmia documented with recurrence. The PVAI result, AFL recurrence, and result of additional AFL ablation in both groups were compared. All patients signed written informed consent before the procedure, and patient data were collected in accordance with institutional ethics guidelines.
PVAI.
All patients underwent PVAI using an intracardiac echocardiography-guided technique as described previously (12). Briefly, a 10-F 64-element phased-array ultrasound catheter (Siemens AG, Malvern, Pennsylvania) was positioned in the right atrium (RA) via the right femoral vein. A decapolar circular (Lasso) mapping catheter and an 8-mm-tip ablation catheter (Biosense Webster, Diamond Bar, California) were advanced into the left atrium (LA) via two trans-septal punctures. Radiofrequency (RF) ablation was performed wherever PV potentials were recorded around the PV antrum. Intracardiac echocardiography was used to guide trans-septal puncture, to define the pulmonary venous antra, to guide sequential placement of the Lasso catheter in all positions around PV antra, and to detect microbubble formation for RF energy titration. The RF isolation of the PV was considered complete when all PV potentials surrounding the vein antrum were abolished. All four PVs and the superior vena cava were isolated in every patient. Patients were heparinized during the procedure to maintain an activated clotting time of 350 to 400 s.
Warfarin was discontinued 48 h before the procedure. All antiarrhythmic drugs except amiodarone (which was discontinued four to five months before) were discontinued at least five half-lives before the ablation procedure. All patients had transesophageal echocardiography before the PVAI procedure to exclude intracardiac thrombi.
Mapping and ablation of AFL.
The mapping and ablation of AFL was performed as described in detail elsewhere (5,14). All patients had standard electrophysiologic testing with electrode catheters placed in the coronary sinus, high RA, and His bundle positions. Intracardiac electrograms as well as simultaneous electrocardiographic leads were recorded using a multi-channel recording system (CardioLab, Prucka GE Medical, Waukesha, Wisconsin). Three-dimensional electroanatomic mapping was performed in all patients using the CARTO electromagnetic mapping system (Biosense Webster Inc.). Mapping was performed with a 4-mm-tip ablation catheter (Navistar, Biosense Webster Inc.). On CARTO, "electrically silent areas" were defined as areas with no electrogram or with bipolar voltage amplitude indistinguishable from noise ( 0.05 mV).
If the patient presented in normal sinus rhythm, AFL was induced by atrial programmed stimulation or burst pacing. An electroanatomic activation map of the RA was created during AFL; potential critical isthmuses were identified by concealed entrainment mapping as previously described (2,15). If there were no critical RA isthmuses, LA access was obtained via trans-septal puncture and electroanatomic mapping, and entrainment mapping was repeated in the LA.
The RF lesions were applied depending on the underlying AFL mechanism: 1) between the tricuspid annulus and the Eustachian ridge, 2) between two scars, or 3) between a scar and an anatomic barrier (valve, vena cava, or PV). In patients with typical right AFL, bidirectional block was demonstrated by pacing at different sites and using the CARTO system. In patients with atypical AFL, ablation was continued until there was at least 90% reduction of electrographic amplitude along the ablation line. Block across the line was demonstrated using the CARTO mapping system when possible. Double potentials with a separation of >90 ms were required along the ablation line. To assess the success of the ablation, inducibility of AFL was tested after ablation using both programmed and burst pacing.
Follow-up.
All patients were discharged home the day after the procedure. Patients were followed in the outpatient clinic at 3, 6, and 12 months after ablation. A rhythm transmitter was used in all patients to monitor events during three months after ablation, and this was extended by another three months for patients with recurrence of symptoms. Patients were asked to transmit their rhythm three times per day and every time they had symptoms compatible with arrhythmia. In all patients, 48-h Holter recording was done routinely immediately after the procedure and at the 3-, 6-, and 12-month follow-up visits. For analysis, recurrence of AFL and AF was considered only after eight or more weeks after PVAI (10,12). Warfarin (international normalized ratio 2 to 3) was restarted in all patients the day of PVAI and was continued for a minimum of four to six months. Antiarrhythmic drugs were restarted in all patients the day of PVAI and continued only for two months; these drugs were chosen from sotalol, propafenone, flecainide, or dofetilide. Amiodarone was not used after ablation.
Statistical analysis.
Continuous variables are expressed as mean values ± SD. Continuous variables were compared by the independent-samples unpaired Student t test. Categorical variables were compared by chi-square analysis. A value of p < 0.05 was considered significant for all statistical determinations.
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Results
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Baseline characteristics.
Group 1 and Group 2 patients did not differ in their age, duration, and type of AF, but Group 1 patients had larger LA diameter (4.7 ± 0.7 cm vs. 4.4 ± 0.6 cm, p < 0.0001), higher incidence of AFL diagnosis before PVAI (38% vs. 22%, p = 0.005), and lower ejection fraction (49 ± 10 vs. 54 ± 8, p < 0.0001). Twenty-four (38%) patients in Group 1 had documented AFL at baseline (16 typical, 8 atypical) compared with 234 (22%) patients in Group 2 (230 typical, 4 atypical) (p = 0.005). The baseline demographics of the groups are shown in Table 1.
In patients with PCS, the cardiac surgery was coronary artery bypass graft surgery (CABG) in 26, mitral valve replacement (MVR) in 22, aortic valve replacement (AVR) in 5, AVR + CABG in 1, MVR + CABG in 1, MVR + atrial septal defect (ASD) in 1, MVR and AVR in 1, combined MVR + AVR + ASD in 1, ASD in 4, and tricuspid valve surgery in 1. The mean time period between cardiac surgery and the PVAI date was 7.6 ± 5.2 years.
PVAI results.
All four PVs were isolated successfully in all patients in Group 1 and Group 2 (fluoroscopy time 80 ± 27 min vs. 79 ± 25 min, p = 0.84). After PVAI, 13 (21%) patients in Group 1 and 201 (19%) patients in Group 2 had recurrence of AF during a mean follow-up period of 508 ± 299 days and 548 ± 282 days, respectively (p = 0.31). No major complication related to PVAI was seen in Group 1. In Group 2, seven patients (0.7%) had cerebroembolic complications, four patients (0.4%) had moderate to severe PV stenosis, and two patients (0.2%) had pericardial effusion. Data regarding PVAI results are summarized in Table 2.
The AFL recurrence after PVAI was significantly higher in Group 1 compared with Group 2 (33% vs. 4%, p < 0.0001). In Group 1, 21 patients had AFL recurrence (typical in 7, atypical in 14), whereas in Group 2, 43 patients had AFL recurrence (typical in 28, atypical in 15). Among patients who had AFL diagnosis before PVAI, 15 of 24 patients (63%) in Group 1 and 219 of 234 patients (94%) in Group 2 were free of AFL after PVAI.
AFL ablation.
All 21 Group 1 patients who had AFL recurrence underwent AFL ablation. Four patients in this group had concomitant AF recurrence and a second PVAI was done before AFL ablation at the same session. Details of the ablation procedure and AFL are given in Table 3. During the ablation procedure, a total of 33 AFLs (15 typical, 18 atypical) were identified in the 21 patients. Ten of 21 Group 1 patients (48%) with AFL recurrence had multiple AFL isthmuses and required multiple isthmus ablations. Of all the AFLs, 30 of 33 (91%) were ablated successfully without complication, representing 18 of 21 patients (86%). Interestingly, all three patients with unsuccessful AFL ablation had a history of MVR and had AFL, which was atypical and mapped to LA. During a mean follow-up of 357 ± 201 days, 2 of 18 patients (11%) who had successful AFL ablation had AFL recurrence.
All 43 patients in Group 2 who had AFL recurrence underwent AFL ablation. Three of 43 patients (7%) in Group 2 had multiple AFL isthmuses and needed multiple isthmus ablations. In this group, 22 patients had concomitant AF recurrence and a second PVAI was performed concomitant with AFL ablation at the same session. The AFL ablation was successful in all (100%), and no complication related to AFL ablation was noted. During a mean follow-up of 378 ± 197 days, 2 of 43 patients (5%) had AFL recurrence.
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Discussion
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Main findings.
The main finding of this study is that patients with PCS have higher AFL recurrence after PVAI compared with patients without previous PCS. In addition, AFL ablation is needed in a higher number of patients with PCS and can be performed effectively. To our knowledge, this is the first study to compare AFL occurrence after PVAI in patients with and without PCS.
PVAI as a treatment for AFL.
It is well recognized that AFL and AF often co-exist and may degenerate into each other (6–9). Also, a considerable number of patients have AF recurrence after ablation of typical AFL (16). The reasons for co-existence are not entirely clear, but it is possible that PV triggers may initiate AFL as well as AF, or may convert AFL to AF (7,10,11). We have reported, for example, that in patients with both typical AFL and AF, PVAI alone was sufficient to control both arrhythmias (10). The results presented in this series are consistent with our previous report. Indeed, 94% (219 of 234) of patients who had pre-existing AFL were cured by PVAI alone in the control group (Group 2). In contrast, only 15 of 24 PCS patients (63%) with pre-PVAI AFL were free of AFL after PVAI. Furthermore, 21 (33%) PCS patients experienced AFL occurrence after PVAI. These results demonstrate that the elimination of PV triggers may not prevent the occurrence of AFL in a significant number of patients with PCS.
Possible mechanisms of high AFL incidence in PCS patients after PVAI.
A substrate and a trigger are essential prerequisites to initiate re-entrant AFL (9,17). The PCS patients may be predisposed to AFL because of the co-existence of incision lines, cannulation sites, scars, and conventional anatomic barriers (4,5,17,18). Areas of low voltages may also be found at discrete areas other than incisions and cannulation sites (4,18). Scars may result from interruption of arterial supply, insufficient protection during cardioplegia, and other surgical trauma (4,18). Furthermore, scar areas may be a manifestation of the underlying structural heart disease (19). Concordant with these hypotheses, the present study found that patients with PCS were more likely to have electrically silent areas and larger LA diameter compared with patients without PCS. These associations may reflect a more vulnerable substrate for AFL in patients with PCS (20).
In patients who have AF and AFL postoperatively, a high incidence of premature atrial beats has been reported before the onset of atrial arrhythmias (21). Premature atrial beats from areas other than the PVs may predispose patients to AFL if the appropriate substrate exists to perpetuate AFL (21,22). Indeed, it has been previously observed that premature atrial beats and irregular atrial activity often precede AFL (9,23,24). Because PCS patients have the appropriate arrhythmogenic substrate, they may have higher AFL recurrence as a result of triggers outside of the PVs.
Early recurrence of AF and AFL is more common after PVAI for the first two months. This is considered a transient finding and may not require long-term treatment (10,12). In the study by Wazni et al. (10), for example, early AFL recurrence (within the first two months after the PVAI procedure) was seen in 55% of patients, but long-term AFL recurrence was seen in only 5% of patients. In the present study, 18% (192 of 1,062) of patients without previous PCS and 60% (38 of 63) of patients with PCS had early AFL during the first two months. However, only 4% of patients without PCS continued to have AFL, whereas 33% of PCS patients had long-term AFL that required ablation. This indicates the persistent nature of the arrhythmogenic substrate in patients with PCS.
AFL ablation in patients with and without PCS.
Both the cavotricuspid isthmus-related circuit and other atypical circuits can cause AFL in patients with PCS, and both types of circuits might co-exist in the same patient (5). An AFL recurrence rate of 10% to 60% after AFL ablation has been reported in patients with PCS (3,5,25,26). Several groups have shown that to achieve long-term cure, all potential isthmuses have to be identified and ablated in these patients (5,27,28). Indeed, in the present study, 48% of Group 1 patients with AFL recurrence had multiple AFL isthmuses. On the other hand, only 7% of Group 2 patients had multiple AFL isthmuses requiring ablation.
Study limitations.
This was a retrospective study, and it is therefore subject to limitations inherent in retrospective data analysis. However, all of the data used in this study were collected prospectively in a systematic database.
The AFL after PV isolation has been reported as a complication secondary to RF ablation around the PV ostia, and it could be argued that the AFL occurring after PVAI were secondary to this mechanism (29). However, only half of the atypical AFLs in Group 1 (9 of 18) occurred in the LA, and 28% of the patients had documentation of AFL even before the PVAI. Furthermore, in our "control" group, the rate of LA AFL after PVAI was only 1.2% (n = 13), and of these patients, 31% (n = 4) had evidence of AFL before PVAI. Therefore, we believe that PVAI itself does not explain the occurrence of the vast majority of post-procedural AFL.
Clinical implications.
Patients with PCS are at increased risk of developing AFL recurrence after successful PVAI. This clinical finding is relevant when counseling these patients before PVAI. In this subgroup, concomitant AFL ablation with PVAI should be considered to maximize cure with a single procedure. After isolating PVs, an attempt at inducing AFL with programmed atrial stimulation would be reasonable in PCS patients presenting with AF and AFL. Furthermore, in patients with PCS it is important to detect the nature of the recurrent arrhythmia after PVAI. Careful documentation of the arrhythmia in this group would be helpful when planning further ablative treatment.
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Conclusions
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In patients with PCS, post-PVAI AF recurrence is similar to patients without PCS. However, post-PVAI AFL recurrence is higher in PCS patients. Additional AFL ablation is needed to cure this subset of patients.
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Abstract
Methods