Radiofrequency Catheter Ablation of Type 1 Atrial Flutter
Prediction of Late Success by Electrophysiological Criteria
Background Radiofrequency energy has demonstrated its efficacy in catheter ablation of atrial flutter (AFl). However, long-term recurrences of AFl have been reported frequently after initial, apparently successful ablation. To date, criteria for prediction of late recurrences are lacking.
Methods and Results Twelve patients (10 men; mean age, 53.6 years; range, 26 to 69 years) were referred for AFl ablation. Duodecapolar and decapolar catheters were used for detailed mapping of the tricuspid ring, the inferior vena cava–tricuspid annulus (IVC-TA) isthmus, and the coronary sinus ostium (CSOs) area. Additional multipolar catheters were used for recording activation of the coronary sinus and the CSOs-TA isthmus. AFl was present at baseline in 9 patients and was induced by proximal coronary sinus (PCS) pacing in 3. Counterclockwise right atrial activation was recorded in all patients. Primary success of ablation was defined as when AFl was no longer inducible even during isoproterenol infusion. AFl was successfully ablated in all 12 patients, with a median of 4 pulses delivered at the IVC-TA isthmus. In the 3 patients in whom AFl was induced, during PCS pacing in sinus rhythm before ablation, a collision of descending and ascending wave fronts was observed at the middle lateral right atrium (LRA). This activation pattern of the LRA also was noted after unsuccessful radiofrequency applications. Noninducibility of AFl after radiofrequency applications was associated with a change of activation pattern at the LRA and with an inversion of the activation sequence of the IVC-TA isthmus (from clockwise to counterclockwise) in 9 patients when pacing from the PCS. In 2 of 3 patients, despite noninducibility of atrial flutter, ablation was pursued to obtain evidence of permanent block of conduction at the IVC-TA isthmus. Finally, a completely descending LRA wave front was observed when pacing from the PCS in all patients except one. Low LRA pacing was also performed in 4 patients and showed evidence for block in the counterclockwise direction at the isthmus. During a follow-up of 9±3 months, AFl recurred in 1 patient; this was the only patient who showed no conduction block at the isthmus after the procedure.
Conclusions Direction of impulse propagation at LRA and block of propagation at the IVC-TA isthmus during PCS and low LRA pacing appear to be of interest in predicting long-term success of AFl ablation.
Type 1 atrial flutter is considered to result from a reentrant circuit localized in the right atrium, the left atrium being passively activated.1 The lower part of the right atrium has been shown to be crucial for development of atrial flutter, with interaction of both anatomic (inferior vena cava) and functional (line of block at the posterior right atrial wall and slow conduction zone at the low right atrium) obstacles.2 3 4 5 Initial experience of atrial flutter ablation was done with DC shocks targeting at fragmented electrograms in the low posteroseptal right atrium.6 Long-term results of DC ablation showed a 50% efficacy with a nonnegligible number of late atrial fibrillation episodes.7 Radiofrequency ablation then was applied, with the use of anatomic and/or electrophysiological targets.8 9 10 11 12 13 Cosio et al8 proposed to ablate a zone considered to represent an obligatory route for flutter, that is, the inferior vena cava–tricuspid annulus (IVC-TA) isthmus. Delivery of radiofrequency applications to this purely anatomic target resulted in a reasonable ablation success rate and gave credence to this hypothesis of obligatory route. However, if the acute success rate of atrial flutter ablation (defined by acute termination and/or inability to reinduce atrial flutter) is fairly high, ranging between 65% and 100%, the recurrence rate is not negligible. This probably is partly due to the lack of markers of long term-success. Because the ultimate goal of this type of procedure is to modify conduction at the IVC-TA isthmus, we decided to test the hypothesis that evidence of block at this isthmus after the ablation is a useful marker of long-term success.
Twelve patients were referred to our center for radiofrequency ablation of type 1 atrial flutter from November 10, 1993, to February 20, 1995. Ten men and 2 women, aged 26 to 69 years (mean, 53±15), had documented frequent episodes of type 1 atrial flutter for a period of 58±51 months despite a mean of 3.4±1.5 antiarrhythmic drugs. No episodes of atrial fibrillation had been documented in our patients before the ablation. Three patients previously had undergone a radiofrequency ablation procedure for atrial flutter, but recurrence occurred after 1, 2, and 7 months. Symptoms during flutter were palpitations in 11 patients, dyspnea in 4, cardiogenic shock in 1, and exacerbation of angina pectoris in 2. Structural heart disease was present in 6 of 12 patients: coronary artery disease in 3, hypertensive cardiomyopathy in 2, and dilated cardiomyopathy in 1. Mean left ventricular ejection fraction (measured by two-dimensional echocardiography) in our population was equal to 65% (range, 46% to 75%), and the mean left atrial diameter was 36 mm (range, 24 to 42 mm).
The electrophysiological evaluation was done after all patients had given informed verbal consent. A duodecapolar catheter Halo (Webster Laboratories), 20 poles, 10-mm paired spacing, or decapolar catheters were inserted in 9 and 3 patients, respectively, for detailed mapping of the lateral right atrial wall and the IVC-TA isthmus and in some patients the anterior portion of the tricuspid ring (Fig 1a⇓). Additional multipolar catheters were introduced to record activation of the coronary sinus ostium–TA isthmus and to obtain reference electrograms at the His bundle region and in the coronary sinus. Recordings were made on computerized multichannel systems (Midas, PPG Hellige Biomedical, and Lab 24, BARD Medical System) with use of a configuration allowing up to 32 simultaneous recordings filtered between 30 and 250 Hz. Electrical stimulation was delivered via a stimulator (Bloom Associates, Ltd) with a pulse duration of 2 ms at twice diastolic threshold. Standard 12-lead ECGs were recorded for all atrial flutter episodes. If the patient was in sinus rhythm at the electrophysiological study, incremental atrial pacing at progressively shorter cycle lengths (from 350 to 180 ms) or atrial programmed stimulation (1 to 3 extrasystoles at two different cycle lengths) were performed from the proximal coronary sinus to induce atrial flutter.
Radiofrequency ablation was performed with an Osypka H.A.T. 200-S generator that delivered continuous unmodulated current at 500 KHz. Radiofrequency energy was applied in the power mode (power output, 50 W) when using an 8-mm tip electrode catheter (EP Technology) or in a temperature-guided mode with a 6-mm tip electrode catheter (OSYPKA), the power output being titrated to achieve a temperature of 60° to 70°C at the ablation site. Pulse duration was preset at 90 seconds. Ablation was anatomically guided and directed to the IVC-TA isthmus. The ablation catheter was introduced into the right atrium via the right femoral approach in 11 patients and via the left subclavian approach in 1. This catheter was positioned at the IVC-TA isthmus, where a large ventricular potential and a small atrial electrogram were recorded (Fig 1a⇑), and radiofrequency energy was first applied at that site. The catheter then was slowly withdrawn toward the IVC, with multiple stops during radiofrequency application. If atrial flutter did not terminate, we applied the subsequent line of lesion at the same location or just beside but still at the IVC-TA isthmus relatively far from the coronary sinus ostium and lateral. Attempts to reinduce flutter were performed by pacing from different sites in the right atrium (including the proximal coronary sinus in 12 patients and the lateral right atrium in 7 patients). Pacing protocol consisted of incremental atrial pacing (from 350 to 180 ms) or programmed atrial stimulation (1 to 3 extrasystoles at two different cycle lengths), and it was repeated during isoproterenol infusion (0.5 to 6 μg/min) in case of noninducibility at baseline. Patterns of activation of the lateral right atrial wall and of the IVC-TA isthmus were analyzed during these pacing maneuvers. Block of impulse propagation at the IVC-TA isthmus was revealed by a change in activation pattern at the lateral right atrial wall from a partially ascending wave front to a completely descending one during proximal coronary sinus pacing (Fig 1c⇑ and 1d⇑). An increase of activation time between the low lateral right atrium and the pacing site at the proximal coronary sinus also was observed in this case. Goal of the ablation procedure was to render atrial flutter noninducible after its termination and to obtain evidence of block at the IVC-TA isthmus during proximal coronary sinus pacing.
All patients underwent ECG monitoring for 1 or 2 days and two-dimensional echocardiography before hospital discharge without antiarrhythmic drug therapy. All patients then had a close follow-up control at periodic intervals by us and by their own physicians. This follow up-control included at least one 24-hour ECG monitoring in all patients except one. A repeat electrophysiological study was not systematically performed during follow-up.
Nine patients were initially in tachycardia; three others were in sinus rhythm, and flutter was induced. When pacing from the proximal coronary sinus during sinus rhythm before ablation, two wave fronts of activation were noted. Impulse propagated in a clockwise direction toward the IVC-TA isthmus to the lateral right atrial wall and upward in the septum to the high right atrium in a counterclockwise direction, with collision of wave fronts in the middle of the lateral right atrial wall (Fig 1c⇑). Three patients in our study population had undergone a previous successful ablation but experienced recurrence of flutter. Two of them underwent constant pacing from the proximal coronary sinus at the end of the previous ablation procedure with, at retrospective analysis, absence of evidence of conduction block at the IVC-TA isthmus. All patients showed a counterclockwise atrial activation during flutter, with coronary sinus catheter activation from the proximal to the distal bipole. Flutter episodes observed in our population fulfilled the requirements set forth by Wells et al1 for type 1 definition because we were able to entrain flutter during rapid constant pacing from different sites in the atrium. Atrial flutter cycle lengths ranged between 205 and 310 ms, which also fits with the range described by Wells and colleagues for type 1 atrial flutter. The atrioventricular ratio during flutter was 2:1 in 6 patients, whereas in 6 other patients, various ratios including 2:1, 3:1, and 4:1 and complex alternate Wenckebach phenomena were observed. All our flutters can be categorized as common type (with inverted F waves in the inferior leads), with limitations caused by difficulties in analyzing the shape of the flutter wave when only 2:1 atrioventricular ratio was present.
Radiofrequency applications delivered at the IVC-TA isthmus terminated atrial flutter in all patients. Interruption of tachycardia was due to block of wave front propagation at the ablation site (Fig 2a⇓). Atrial flutter then could be reinduced by proximal coronary sinus pacing in 3 patients. During pacing, a collision of counterclockwise and clockwise wave fronts at the lateral right atrial wall was noted before flutter initiation. A median of 4 pulses (range, 1 to 15) was necessary to prevent inducibility of atrial flutter, which was the initial end point. In 3 patients, despite the noninducibility of flutter, evidence of absence of conduction block at the isthmus was observed as indicated by a persistent collision of two wave fronts at the lateral right atrial wall (Fig 1c⇑). In 2 of 3 patients, additional pulses (1 and 2, respectively) delivered at the IVC-TA isthmus were able to create a block of impulse propagation at this isthmus. The ablation was performed during fixed-rate proximal coronary sinus pacing while monitoring the activation pattern of the lateral right atrial wall (Fig 2b⇓). This block of impulse propagation at the ablation site resulted in a sudden emergence of delay of the low lateral right atrium activation by a mean of 84.3±9 ms. During constant pacing from the proximal coronary sinus, slight movements of the ablation catheter from the septal to the lateral side of the ablation site showed a sudden dramatic prolongation of the stimulus to local A interval, further denoting the presence of conduction block at this isthmus. The third patient complained of back pain, and the procedure had to be stopped before achievement of block at the IVC-TA isthmus. After flutter interruption, pacing also was performed at the lateral right atrial wall in 7 patients (high lateral in 3 and low lateral wall in 4 others). Evidence for conduction block in a counterclockwise direction at the isthmus was present during pacing from the low lateral right atrium. Indeed, the proximal coronary sinus electrogram recorded in the vicinity of the ostium was activated successively after the high right atrium and the His bundle region. In 1 patient, counterclockwise block was rate dependent and was not present at long (>330 ms) cycle lengths. When pacing rate was increased, the direction of impulse propagation abruptly changed with a sudden increase of conduction time between the low lateral right atrial pacing site and the low septal region. This conduction block was associated with a change of the septal activation wave front from ascending to descending and a positivation of the P wave during low lateral right atrial pacing. Pacing the high lateral right atrium, inducing simultaneously descending wave fronts at the lateral wall and at the atrial septum, was not found to be useful for analyzing conduction properties of the IVC-TA isthmus. Finally, the ablation procedure was stopped when flutter was rendered noninducible and in all patients except one, when evidence of block at the IVC-TA isthmus was noted. Successful ablation was achieved with a mean procedure duration of 205±77 minutes and a mean fluoroscopy time of 42±28 minutes.
During a mean follow-up of 9±3.4 months, recurrence of atrial flutter was observed in one patient. This patient was the only one who did not show evidence of conduction block at the ablation site during pacing despite the final noninducibility of tachycardia. This episode occurred the day after the ablation procedure; a second ablation session successfully terminated flutter with one pulse, and three additional applications created a block at the isthmus.
This study supports the concept that anatomically guided radiofrequency ablation of atrial flutter is associated with a high initial success rate. The initial series were carried out with the use of DC shocks; more recently, radiofrequency energy with the use of various electrophysiological criteria (fragmented electrograms in the low posteroseptal right atrium, entrainment pace mapping looking for a short pacing stimulus to P interval, or earliest local activation time compared with F-wave onset) are used to define the target zone. The IVC-TA isthmus has been shown to close the caudal part of the circuit in counterclockwise rotation flutter and therefore to be critical for the circuit of type 1 atrial flutter. Cosio et al8 were the first to apply the anatomic dependence concept of atrial flutter for ablation by defining an anatomic target rather than an electrophysiological one. In our series, atrial flutter was rendered noninducible in all patients, with a relatively small number of radiofrequency applications when large distal electrode catheters were used. No complications were noted in our population, suggesting that these catheters with a large distal electrode can be used safely and increase the success rate.11 Another critical isthmus for atrial flutter ablation has been described, and is located between the TA and the coronary sinus ostium. It is smaller than the IVC-TA isthmus (considered to measure 20 to 25 mm) and may represent an easier area to ablate. Validity of this isthmus depends on the presence of a line of block between the coronary sinus ostium and the IVC during tachycardia. This blocking line recently described by Nakagawa et al13 can delineate a crucial area in maintaining the reentrant circuit. However, precise mapping of the isthmus between the IVC and the coronary sinus ostium was not consistently performed in this study, and in our opinion, concerns remain whether this line of block is constantly found during counterclockwise atrial flutter.14
Criteria to Predict Long-term Success
If acute results of ablation have been reported to be satisfactory, recurrence rate is estimated to be between 7% and 44%.8 9 10 11 12 13 Termination of atrial flutter during radiofrequency application and/or noninducibility of the arrhythmia until now have been considered criteria for acute success. However, recurrence of apparently identical arrhythmia raises questions about these criteria. Acute termination of flutter during energy delivery may be due to the acute, transient effect of radiofrequency on the flutter circuit. In addition, reproducibility of inducibility of atrial flutter is not precisely known and the probability of inducing atrial fibrillation or nonclinical flutter probably is not negligible and is so in our experience. On the other hand, individualization of an obligatory route during atrial flutter was considered to be of great potential to predict absence of recurrence if completely damaged. Demonstration of conduction block in the IVC-TA isthmus by pacing maneuvers (from the low lateral right atrium and the proximal coronary sinus) was the final end point of our study.
Our experience suggested that achieving block at the IVC-TA isthmus may prove to be beneficial in preventing recurrences after radiofrequency ablation of atrial flutter as (1) none of the patients who achieved this end point have had a recurrence at a mean follow-up of 9±3 months; (2) the only reccurrence occurred in a patient in whom this end point could not be achieved at the time of ablation; and (3) in the three patients who had been taken up for ablation for recurrence after previous successful procedures, all showed persistent conduction at the IVC-TA isthmus at repeat study. Pacing from the septal (proximal coronary sinus) and the lateral (low lateral right atrium) sides of the ablation site was useful to evaluate block of impulse propagation, whereas pacing from the high lateral right atrium failed. During pacing from the proximal coronary sinus, a collision of a counterclockwise and a clockwise wave fronts at the lateral right atrial wall occurred before the ablation and after unsuccessful pulses. In three patients, radiofrequency applications were pursued despite noninducibility of atrial flutter in order to obtain evidence of block of conduction at the isthmus. This end point was fulfilled when a completely descending wave front at the lateral right atrial wall and at the IVC-TA isthmus occurred.
Limitations of the Study
Late control electrophysiological study has not been done, and strict correlation cannot be drawn between lack of tachycardia recurrence and the persistence of a conduction block at the IVC-TA isthmus. Also, our results have to be confirmed with a longer follow-up period.
A limited number of radiofrequency applications, when using a large distal electrode catheter, can successfully terminate type 1 atrial flutter and prevent its recurrence. Evidence of conduction block at the IVC-TA isthmus, which is the target site, appears to represent a reliable marker of permanent modification of this region. Creation of block of impulse propagation at this isthmus may prevent late recurrences of flutter and therefore may represent a goal of ablation procedure.
- Received April 10, 1995.
- Revision received June 23, 1995.
- Accepted July 10, 1995.
- Copyright © 1995 by American Heart Association
Wells JL, McLean WAH, James TN, Waldo AL. Characterization of atrial flutter: studies in man after open heart surgery using fixed atrial electrodes. Circulation. 1979;60:655-673.
Puech P, Latour H, Grolleau R. Le flutter et ses limites. Arch Mal Coeur. 1970;63:116-144.
Chauvin M, Brechenmacher C, Voegtlin JR. Application de la cartographie endocavitaire à l’étude du flutter auriculaire. Arch Mal Coeur. 1983;76:1020-1030.
Saoudi N, Mouton Schleiffer D, Letac B. Direct catheter fulguration of atrial flutter. Lancet. 1987;2:558-559.
Feld GK, Fleck P, Chen PS, Boyce K, Bahnson TD, Stein JB, Calisi CM, Ibarra M. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Circulation. 1992;86;1233-1240.
Lesh MD, Van Hare GF, Epstein LM, Fitzpatrick AP, Scheinman MM, Lee RJ, Kwasman MA, Grogin HR, Griffin JC. Radiofrequency catheter ablation of atrial arrhythmias: results and mechanisms. Circulation. 1994;89:1074-1089.
Nakagawa H, McClelland J, Beckman K, Wang X, Lazzara R, Hazlitt A, Santoro I, Arruda M, Abdalla I, Singh A, Sweidan R, Gossinger H, Hirao K, Widman L, Jackman W. Radiofrequency catheter ablation of common type atrial flutter. PACE Pacing Clin Electrophysiol. 1993;16:II-85. Abstract.
Saoudi N, Poty H, Anselme F, Letac B. Endocardial activation mapping of the area posterior to the coronary sinus ostium in type 1 atrial flutter. J Am Coll Cardiol. 1995;25:168A. Abstract.