Successful Atrial Flutter Ablation Research Articles

Effect of Radiofrequency Ablation of Atrial Flutter on the Natural History of Subsequent Atrial Arrhythmias

Flutter Ablation and Subsequent Arrhythmia. Patients with atrial flutter (AFL) treated medically are at high risk for subsequent development of atrial fibrillation (AF). Whether curative radiofrequency ablation of AFL can modify the natural history of arrhythmia progression is not clear. We aimed to determine whether ablation of AFL decreases the subsequent development of AF in patients without previous AF. Patients with AFL as the sole atrial arrhythmia were selected from patients who underwent successful AFL ablation at Mayo Clinic between 1997 and 2003 (N = 137). The cohort was divided by presence (n = 50) or absence (n = 87) of structural heart disease. A control group comprised 59 patients with AFL and no history of paroxysmal AF, who received only medical therapy. Occurrence of AF after AFL ablation was compared among study groups and controls. Symptomatic AF occurred in 49 patients during 5 years of follow-up after AFL ablation, with similar frequency in both study groups. The cumulative probability of paroxysmal and chronic AF was similar in controls and each study group. By multivariate analysis, the AFL ablation procedure carries significant risk of AF occurrence during follow-up. Fifty patients discontinued antiarrhythmic drugs after AFL ablation, and the rate of cardioversions decreased. Successful ablation of AFL does not improve the natural history of atrial arrhythmia progression; postablation AF is frequent. This suggests that AFL may be initiated by bursts of AF and that in the absence of AFL substrate the AF continues to progress.

Severe Left Ventricular Systolic Dysfunction Increases Atrial Fibrillation After Ablation of Atrial Flutter

Atrial fibrillation (Afib) that occurs after a successful atrial flutter (AFL) ablation may negate the potential benefits of the ablation. Afib occurs more often when severe left ventricular systolic dysfunction (LVSD) is present. We hypothesized that even after a successful AFL ablation, the incidence of postablation Afib is increased when severe LVSD is present. Ninety consecutive patients with LVSD who underwent ablation for AFL at Montefiore Medical Center from August 2001 to January 2005 were classified according to the severity of LVSD. Group 1 (n = 36) consisted of patients with EF < or = 35%, and group 2 (n = 54) consisted of patients with EF 36-55%. There were no statistically significant differences in baseline patient characteristics between the two groups. During a mean follow up of 350 days, Afib occurred in 31% (n = 11; 8 with prior history of AFib) in group 1, and 7.4% (n = 4; all with prior history of Afib) in group 2. Cumulative probability of remaining Afib-free in group 1 versus group 2 was 75% versus 96% at 365 days, and 69% versus 91% at 600 days (P = 0.01). A prior history of Afib did not interact with EF when analyzed with a logistic regression analysis. After an AFL ablation, the incidence of Afib is increased, and the probability of remaining free of Afib is decreased, when severe LVSD is present, independent of a prior history of Afib. This finding may have implications for optimal patient selection for AFL ablation, and the use of adjunctive therapies.

Effects of left atrial ablation of atrial fibrillation on size of the left atrium and pulmonary veins

The purpose of this study was to determine the effect of left atrial circumferential ablation on the size of the left atrium and pulmonary veins (PVs). The long-term effects of left atrial circumferential ablation on left atrial and PV size and anatomy have not been analyzed in quantitative fashion. PV and left atrial sizes were analyzed in 41 consecutive patients (mean age 54 +/- 12 years) with paroxysmal (n = 25) or chronic (n = 16) atrial fibrillation. Computed tomography of the chest with three-dimensional reconstruction was performed before and 4 +/- 2 months after left atrial circumferential ablation. Left atrial circumferential ablation was performed to encircle the PVs 1 to 2 cm from the ostia, using a power output of 70 W. Additional ablation lines were created in the posterior left atrium and mitral isthmus. Radiofrequency energy also was delivered within the circles and at the PV ostia in 51% of patients at a reduced power output of 35 W. At 6 months, 36 patients (88%) were in sinus rhythm without antiarrhythmic drug therapy, including 3 patients (7%) who developed persistent left atrial flutter and underwent subsequent successful ablation of atrial flutter. There was a 15 +/- 16% decrease in left atrial volume (P < .01) and 10 +/- 35% decrease in PV ostial area (P < .01), without focal narrowing, in patients with a successful outcome. Focal PV stenosis did not occur in any of the 41 patients. Maintenance of sinus rhythm after left atrial circumferential ablation is associated with reduced left atrial and PV ostial size. Left atrial circumferential ablation for atrial fibrillation does not cause PV stenosis.

The usefulness of surface 12-lead electrocardiogram to predict intra-atrial conduction block after successful atrial flutter ablation

Intraatrial conduction block at the inferior vena cava-tricuspid annulus isthmus was shown to predict successful atrial flutter ablation. However, its demonstration requires the use of several electrode catheters. Thus, a simple approach using surface 12-lead ECG to prove the conduction block would be valuable. Twenty-two patients were prospectively studied during low septal and low lateral atrial pacing before and after successful atrial flutter ablation. Creation of the conduction block was confirmed by comparing the sequence of atrial activation using 3 multipolar catheters during atrial pacing before and after ablation. During low septal pacing, there was no significant difference before and after ablation in P-wave width, axis, or morphology. During low lateral atrial pacing, there was a significant P-wave axis rotation towards the right (from −67 ± 27° to +13 ± 35°, P < .001), and P-wave polarity in limb lead II changed from predominantly negative to predominantly positive in 21 of 22 patients. There was also an increase in P-wave width (from 136 ± 32 to 169 ± 36 ms, P < .001) and stimulus-to-QRS interval (from 268 ± 61 ms to 343 ± 95 ms, P < .001) during low lateral pacing that was not observed during low septal pacing. We conclude that creation of a conduction block in the inferior vena cava-tricuspid annulus isthmus modifies surface 12-lead ECG during low lateral atrial pacing only. We also suggest that P-wave polarity in limb lead II during low lateral pacing could be used as a noninvasive marker of unidirectional counter-clockwise conduction block during atrial flutter ablation.

Acute resumption of conduction in the cavotricuspid isthmus after catheter ablation in patients with common atrial flutter. Real-time evaluation and long-term follow-up.

Cavotricuspid isthmus conduction (CIC) is closely associated with the maintenance and recurrence of common atrial flutter (AFL). This study systematically sought to assess the prevalence and characteristics of acute CIC recovery during AFL ablation and to define its predictors and its relationship with the results of long-term follow-up. A total of 124 consecutive patients (105 men, 19 women, mean age 58 +/- 11 years) who underwent successful AFL ablation were included. The procedure endpoint was defined as complete bi-directional CIC block. During an observation period of 30 min, the incidence of CIC restoration was 34.% in patients and 39.8% in applications. It increased with increasing block time and decreased over time during the observation period. Block time in successful burns followed by persistent block was shorter than in those followed by CIC resumption (12 +/- 6 vs 33 +/- 12 s, P<0.0001). A negative correlation between block time and resumption time was found (r = - 0.57, P<0.001). Patients with permanent pacemakers had a higher incidence of acute CIC resumption than those without pacemakers (5/7 vs 29/117, P = 0.007). The AFL recurrence rate was 4.8% during a mean follow-up period of 21 +/- 8 months. Our results suggest that acute CIC resumption may be a potential risk for clinical AFL recurrence during long-term follow-up. Acute CIC resumption in common AFL ablation varies in terms of incidence and time course. Block time has a predictive value for acute CIC recovery. Observation time can be shortened if block time is short. With longer block time, it is essential to observe for a longer period in order to minimize CIC resumption.

Progressive isthmus delay during atrial flutter ablation: the critical importance of isthmus spanning electrodes for distinguishing pseudoblock from block.

Bidirectional isthmus block is associated with successful atrial flutter ablation, whereas creation of increased isthmus conduction delay without block can be proarrhythmic. Often, halo catheter electrodes fail to provide adequate sub-Eustachian isthmus recordings. The aim of this study was to determine if progressive isthmus conduction delay results in the false appearance of block during atrialflutter ablation. A 20-pole deflectable catheter was prospectively positioned across the sub-Eustachian isthmus (from the coronary sinus os [CSO] to 7:00 on the tricuspid valve annulus [TVA] clock face in the left anterior oblique [LAO] projection) in nine patients undergoing atrial flutter ablation. During sinus rhythm, conduction time was measured from the CSO to the 7:00 position while pacing the CSO. Measurements were repeated after each linear lesion and after conduction block was achieved. Transisthmus conduction time at baseline, just prior to success, and after the presence of complete block was 54 +/- 9, 123 +/- 39, and 155 +/- 30 ms, respectively (P < or = 0.01). The marked delay prior to complete block resulted in reversal of the activation sequence in electrodes at TVA 7:00, creating the false appearance of isthmus block; the isthmus electrodes clearly distinguished delay from block. Catheter ablation results in progressive isthmus conduction delay prior to the creation of complete block. Electrodes spanning the isthmus and line of block are critical for distinguishing conduction delay (and pseudoisthmus block) from block.

Atrial fibrillation after atrial flutter ablation.

Typical atrial flutter is caused by a re-entrant circuit confined to the right atrium (RA). It involves the “atrial flutter isthmus” which is a protected narrow isthmus of conduction, bounded on one side by the inferior vena cava, the eustachian ridge and the coronary sinus ostium and by the tricuspid valve annulus on the other. Clinically atrial flutter is frequently associated with atrial fibrillation and the mechanism for this association has yet to be elucidated. Several types of atrial flutter exist. Typical atrial flutter, or counterclockwise atrial flutter is characterized by negative “sawtooth” flutter waves in leads II, III and aVF on the electrocardiogram. In this form of flutter the impulse is conducted counterclockwise up the atrial septum, with epicardial breakthrough superiorly in the right atrium where it then travels down the free wall of the RA to re-enter the atrial septum. Reverse typical atrial flutter, with positive “sawtooth” flutter waves in leads II, III and aVF on an electrocardiogram, is characterized by impulse conduction opposite to that in typical atrial flutter, in the clockwise direction. In incisional atrial flutter, after repair of congenital heart defects, the re-entrant circuit involves areas of block caused by the incision and interestingly often involves the atrial flutter isthmus as well. A left atrial flutter exists but has not been well characterized, and involves a circuit around one or more of the pulmonary veins or the mitral valve annulus [1,2]. Standard treatment for atrial flutter with antiarrhythmics has changed over time. As compared to class IA agents, class I and class III agents have been shown to be more effective and safer in supression of atrial flutter. Despite the availability of these pharmacologic agents, it is difficult to suppress atrial flutter completely with pharmacotherapy even when multiple agents are used and antiarrhythmics are no longer the treatment of choice for typical atrial flutter. Prospective studies comparing catheter ablation and anti-arrhythmic therapy have shown catheter ablation to be associated with a lower recurrence rate of atrial flutter and fibrillation, a lower rehospitalization rate and improved sense of well being [3‐5]. Thus radiofrequency catheter ablation at the ‘atrial flutter isthmus’ is now considered the treatment of choice, with successful ablation occurring in >90% of patients. Successful ablation of atrial flutter is confirmed by the presence of bidirectional conduction block in the flutter isthmus. Recurrence of atrial arrhythmias following successful ablation of atrial flutter is related to ei

Catheter ablation of atrial flutter and macroreentrant atrial tachycardia.

Catheter ablation has evolved from an experimental technique to first-line therapy for the treatment of atrial flutter. Atrial flutter is characterized by a macroreentrant atrial tachycardia circuit. Successful ablation of atrial flutter involves (1) mapping the atrial flutter to define the conduction zones within the re-entrant circuit to determine whether the atrial flutter is isthmus-dependent, non-isthmus-dependent, or atypical; (2) interrupting the atrial flutter macroreentrant circuit with an ablation catheter by creating either focal or linear lesions within a critical zone of slow conduction that extends to anatomical borders; and (3) terminating the tachycardia and demonstrating conduction block within the atrial flutter circuit after ablation. This update discusses the classification schemes of atrial flutter and macroreentrant atrial tachycardias, reviews the technique of radiofrequency catheter ablation, and highlights recent ablation approaches for atrial flutters and macroreentrant atrial tachycardias.

Early versus late atrial fibrillation after atrial flutter ablation.

Radiofrequency catheter ablation of atrial flutter (AFl) has high initial success with a 10-15% recurrence. Atrial fibrillation (AFib) after radiofrequency catheter ablation of AFl can occur but may be transient (lasting no more than four weeks). Of one hundred seventeen consecutive patients studied, one hundred and four consecutive patients with sustained, symptomatic AFl, as the predominant rhythm disturbance (some of whom had transient pre-ablation AFib), referred for radiofrequency catheter ablation, had clinical follow-up. All had evidence for successful AFl ablation. Patients were followed prospectively. Over a mean follow-up of 28 months, 28 patients developed AFib after ablation of AFl [12 early AFib (<2 months) and 16 late AFib (>2 months)]. Seven of 12 (58%) patients in the early onset group reverted to normal sinus rhythm; none required long-term antiarrhythmic therapy. Only one (8%) developed permanent AFib. No patient in the late onset group remained in sinus rhythm without an antiarrhythmic drug. Three (19%) developed permanent AFib despite therapy among those with late onset AFib. Two (17%) patients with early onset AFib reverted to normal sinus rhythm with treatment versus 5 (31%) in the late onset group. Finally, only 2 patients (17%) with paroxysmal/persistent episodes of Afib from the early onset group stayed in normal sinus rhythm despite therapy, while 8 patients (50%) with paroxysmal/persistent AFib episodes from the late onset group required therapy to maintain normal sinus rhythm. Early onset AFib after ablation of AFl is likely to be transient and self-limited. Late onset AFib after ablation of AFl can persist and require chronic therapy.

Identification of extremely slow conduction in the cavotricuspid isthmus during common atrial flutter ablation.

Complete isthmus block has been used as an endpoint for radiofrequency ablation for common atrial flutter (AF). We sought to systematically evaluate extremely slow conduction (ESC), which is easily misinterpreted as complete block. We studied 107 consecutive patients (92 men, 15 women, 58 +/- 11 years) who had undergone a successful AF ablation procedure. A 24-pole catheter was positioned along the tricuspid annulus spanning the isthmus. Complete isthmus block was defined as the presence of a complete corridor of double potentials along the ablation line. Activation delay time (AT), activation difference (deltaA) between two adjacent dipoles, maximum activation difference (deltaA(max)), change in polarity (CP) and change in amplitude (CA) of the bipolar atrial electrogram were recorded and P-wave morphology in the surface electrocardiogram was analyzed. ESC was observed in 16 patients. Between ESC and complete block, differences were found on the two lateral dipoles adjacent to the ablation line (AT: 148 +/- 17 vs. 183 +/- 27 ms and 155 +/- 18 vs. 170 +/- 28 ms, P < 0.01; deltaA: -91 +/- 22 vs. -126 +/- 28 ms and -7 +/- 13 vs. 13 +/- 6 ms, P < 0.01). Statistically significant differences in CP were detected on the relevant dipoles (7/16 vs. 14/16 and 6/16 vs.13/16, P < 0.05). No significant difference was found either in CA or in terminal P wave positivity. Mean deltaA(max) were 13.8 +/- 5.0 and 27.8 +/- 9.5 ms (P < 0.001) respectively in ESC and complete block. Two types of ESC, regular and irregular, were demonstrated during the ablation procedure. (1) ESC was observed in 15% of the patients during the AF ablation procedure. (2) The parameters of AT, deltaA, and CP may help to differentiate ESC from complete block. DeltaA(max) might be the most powerful indicator. (3) To verify complete block, it is essential to position the mapping catheter across the CTI in order to demonstrate the activation sequence up to the ablation line.

Frequency of subacute resumption of isthmus conduction after ablation of atrial flutter

Achievement of complete bidirectional conduction block in the right atrial isthmus, bordered by the tricuspid valve annulus and the inferior vena cava, is an accepted predictor of long-term efficacy after atrial flutter ablation.1–6 However, in follow-up studies performed in patients at 1 to 12 months after successful ablation,1,2,5,7 isthmus conduction resumes in as many as 50% and is associated with a 10% incidence of recurrent atrial flutter during the first year after ablation.1,3,5 The time course for resumption of isthmus conduction is unknown. Therefore, we sought to determine the incidence of resumption of isthmus conduction within the first 24 hours after successful atrial flutter ablation and to determine whether early repeat ablation would preclude long-term recurrence of atrial flutter.

Catheter ablation of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation

Antiarrhythmic drug treatment for atrial fibrillation can cause atrial flutter-like arrhythmias. The aim of this study was to clarify the effect of catheter ablation of the tricuspid annulus-vena cava inferior isthmus on amiodarone-induced atrial flutter and to determine the incidence of atrial fibrillation after catheter ablation of amiodarone-induced atrial flutter in comparison to regular typical flutter. Among 92 consecutive patients with typical atrial flutter who underwent isthmus ablation 28 patients had atrial flutter without a history of previous atrial fibrillation (group I), 10 patients had atrial flutter following the initiation of amiodarone therapy for paroxysmal atrial fibrillation (group II) and 54 patients had atrial flutter and atrial fibrillation (group III). Atrial cycle length during atrial flutter in amiodarone-treated patients (group II) (277+/-24 ms) was significantly longer as compared to the cycle length of atrial flutter in group I (247+/-33 ms) and group III patients (235+/-28 ms). The rate of successful transient entrainment and overdrive stimulation to sinus rhythm was not different between patients with (60%) or without amiodarone therapy (group I: 71%, group III: 53%). Successful isthmus ablation with bidirectional conduction block eliminating right atrial flutter was achieved in 90% of amiodarone-treated patients and 93% of patients without amiodarone therapy. In the amiodarone-treated patient group atrial conduction times during pacing in sinus rhythm were significantly prolonged by 20-30% before and after ablation in all regions of the reentrant circuit. During a mean follow-up of 8+/-3 months post-ablation, atrial fibrillation recurred in two of 10 patients on continued amiodarone therapy after successful isthmus ablation. Thus, successful catheter ablation of atrial flutter due to amiodarone therapy was associated with a markedly lower recurrence rate of paroxysmal atrial fibrillation (20%) as compared to patients with atrial flutter plus preexisting paroxysmal atrial fibrillation (76%) and was similar to the outcome of patients with successful atrial flutter ablation without preexisting atrial fibrillation (25%). These data suggest that isthmus ablation with bidirectional block and continuation of amiodarone therapy is an effective therapy for the treatment of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.

Basket Catheter Localization of the Origin of Atrial Tachycardia with Atypical Morphology After Atrial Flutter Ablation

Atrial activation from a site in the low lateral right atrium will typically proceed in a superior direction. We present a case of a low lateral right atrial tachycardia with a surface electrocardiographic P wave morphology that appeared to have an inferiorly directed axis. The tachycardia occurred 2 years after successful atrial flutter ablation. The use of a multipolar basket catheter allowed confirmation of the focal origin of the tachycardia, permitted its rapid localization, facilitated catheter ablation, and provided clues to atrial activation that helped describe the appearance of the P wave.

Cavotricuspid Isthmus Mapping to Assess Bidirectional Block During Common Atrial Flutter Radiofrequency Ablation

We sought to compare published methods to an alternative approach ascertaining cavotricuspid isthmus (CTI) block during atrial flutter ablation. In 39 consecutive patients who underwent an atrial flutter ablation procedure, a 24-pole mapping catheter was positioned so that 2 adjacent dipoles were bracketing the targeted CTI line of block (LOB), with proximal dipoles lateral to the LOB and distal dipoles in the coronary sinus. Two pacing sites were lateral (positions A and B) and 2 were septal (positions C and D) to the LOB, with locations A and D closest to the LOB. A resulting CTI block was accepted when 3 criteria were fulfilled: (1) complete reversal of the right atrial depolarization on the 24-pole catheter when pacing in the coronary sinus, (2) conduction delays from A to D greater than from B to D, and (3) conduction delays from D to A greater than from C to A. A successful CTI block was obtained in all patients. Before CTI block was obtained, a progressive CTI conduction delay was observed in 11 patients (28.2%). During the procedure, the 3 criteria defined above were either all present or all absent. This study establishes that reversal of the atrial depolarization sequence up to the LOB is a definitive and mandatory criteria of successful atrial flutter ablation.

Isoproterenol to Evaluate Resumption of Conduction After Right Atrial Isthmus Ablation in Type I Atrial Flutter

After radiofrequency (RF) ablation of atrial flutter (AFL), the demonstration of bidirectional isthmus conduction (BIC) block is considered the hallmark of a successful procedure. The purpose of our study was to test the persistence of BIC block after isoproterenol administration and to evaluate the importance of this finding with regard to AFL recurrences. RF ablation of AFL was performed in 44 consecutive patients with type I AFL by linear ablation of the posterior isthmus (n=29 patients), septal isthmus (n=4 patients), or both right atrial (RA) isthmi (n=11 patients). The procedural end point was complete BIC block and noninducibility of AFL. In case of noninducibility and apparent BIC block, the pacing protocol was repeated under isoproterenol infusion (1 to 3 microgram/min). Reversal of apparent BIC block occurred in 7 (15.9%) of 44 patients. Six patients had bidirectional and 1 had unidirectional resumption of isthmus conduction. Counterclockwise AFL could be reinduced in 4 of these patients. Two to 24 (median, 4) additional RF applications were required to achieve permanent BIC block. At a mean follow-up of 7.3+/-7.6 months (range, 2 to 31 months), 2 (4.5%) of 44 patients had AFL recurrences. Partial linear RF ablation could possibly aggravate preexisting nonuniform anisotropic conduction in the RA isthmus, resulting in profound conduction slowing and apparent BIC block. Isoproterenol can unmask apparent BIC block, thus providing an opportunity to assess the possibility of reversal of BIC block and completeness of isthmus ablation during the same procedure. The low incidence (4.5%) of AFL recurrences at follow-up suggests that noninducibility and BIC block under isoproterenol infusion may be a better end point for successful AFL ablation.

Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter.

The electrophysiological mechanisms for successful catheter ablation of atrial flutter (AFI) targeting the inferior vena cava-tricuspid annulus (IVC-TA) isthmus have not been determined. Twenty patients with common AFI were studied. All had inducible common AFI, and 8 of them had both common and reverse AFI. Right atrial (RA) activation sequences were investigated during pacing from sites proximal (low lateral RA) and distal (proximal coronary sinus) to the IVC-TA isthmus both during entrainment of common or reverse AFI and during pacing in sinus rhythm. This was repeated after ablation. During pacing in sinus rhythm from the low lateral RA, the septum was activated by caudocranial and craniocaudal wave fronts. Similarly, during pacing from the proximal coronary sinus, the lateral RA was activated by two wave fronts. Catheter ablation of the IVC-TA isthmus induced dramatic changes in mapping due to the loss of caudocranial wave front in all but 1 patient. The septum and the lateral RA were activated by a single craniocaudal front as during entrainment of reverse or common AFI, respectively. After a follow-up of 8 +/- 2 months, common or reverse AFI occurred in 4 patients. Two had no or only unidirectional changes in the isthmus conduction induced by ablation. The other 2 had a late recovery of conduction. The present study provides evidence that the mechanism of successful AFI ablation targeting the IVC-TA isthmus is local bidirectional conduction block. This change can be used as a new and complementary electrophysiological end point for the procedure. AFI recurrences are associated with failure to achieve a permanent block.

The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter.

Although radiofrequency catheter ablation of atrial flutter is associated with a high rate of initial success, several clinical issues regarding this therapy remain to be defined. For example, the risks of recurrent atrial flutter and of developing atrial fibrillation after flutter ablation are unknown. In addition, it is not known whether elimination of atrial flutter will modify the natural history of atrial fibrillation in patients who experience both of these arrhythmias. The purpose of the present study was to determine the actuarial freedom from recurrent or new atrial arrhythmias in patients with atrial flutter undergoing catheter ablation. The study population consisted of 59 consecutive patients (mean age, 61.9 +/- 12.6 years) with typical atrial flutter who underwent catheter ablation of the reentrant circuit. Catheter ablation was not advised for patients in whom paroxysmal atrial fibrillation had been a major clinical problem. The inducibility of atrial fibrillation and atrial flutter was assessed after successful atrial flutter ablation with programmed atrial stimulation and rapid atrial pacing to a cycle length of 180 ms or 2:1 atrial capture. Atrial flutter was successfully ablated and rendered noninducible in 53 of 59 patients (90%). Over a mean follow-up period of 13.2 +/- 6.6 months, atrial flutter recurred in 5 patients (9.4%). Atrial fibrillation occurred in 14 of 53 patients after successful ablation (26.4%). Four clinical variables were associated by univariate analysis with the late occurrence of atrial fibrillation: (1) the presence of structural heart disease, (2) a history of atrial fibrillation before ablation of atrial flutter, (3) inducible sustained atrial fibrillation after ablation, and (4) a greater number of failed antiarrhythmic drugs. By multivariate analysis, only the persistent inducibility of sustained atrial fibrillation predicted the later development of atrial fibrillation. Although atrial flutter ablation is highly effective and associated with a low risk of recurrent atrial flutter, atrial fibrillation continues to be a long-term risk for individuals undergoing this procedure. The risk of later atrial fibrillation is especially high for patients in whom sustained atrial fibrillation remains inducible after ablation of atrial flutter.