Characteristics of Cavotricuspid Isthmus–Dependent Atrial Flutter After Left Atrial Ablation of Atrial Fibrillation
Background— Patients who have previously undergone ablation of atrial fibrillation may experience cavotricuspid isthmus (CTI)-dependent atrial flutter during follow-up. The effects of left atrial (LA) ablation on the characteristics of CTI-dependent flutter have not been described.
Methods and Results— Fifteen patients underwent ablation of CTI-dependent flutter late after LA ablation of AF. The ECG, biatrial activation patterns, and LA voltage maps during flutter were analyzed. Thirty age- and gender-matched patients who underwent ablation of CTI-dependent flutter without prior LA ablation served as control subjects. Among the patients with prior LA ablation, mapping revealed counterclockwise activation around the tricuspid annulus in 12 of 15 patients (80%) and clockwise activation in 3 of 15 patients (20%). The flutter waves in the inferior leads were upright in 9 of the 15 patients (60%) with prior LA ablation and in none of the control subjects (P<0.001). The upright flutter waves in the inferior leads in patients with counterclockwise flutter corresponded to craniocaudal activation of the right atrial free wall. LA activation contributed little to the genesis of the flutter waves in these patients because of a significant reduction in bipolar LA voltage (0.44±0.20 versus 1.54±0.19 mV in patients with biphasic/negative flutter waves; P<0.001).
Conclusions— CTI-dependent flutter that occurs after LA ablation of atrial fibrillation often has atypical ECG characteristics because of altered LA activation. In patients presenting with atrial flutter after LA ablation, entrainment mapping should be performed at the CTI even if the ECG is uncharacteristic of CTI-dependent flutter.
Received August 4, 2005; revision received November 6, 2005; accepted November 18, 2005.
A typical left atrial (LA) flutter may occur as a proarrhythmic complication of LA ablation of atrial fibrillation (AF).1–3 However, patients also may experience typical atrial flutter arising from the cavotricuspid isthmus (CTI) after ablation of AF.4 Because LA ablation may alter the normal activation pattern of the LA,2 it is possible that the 12-lead ECG of CTI-dependent flutter may not appear “typical” after AF ablation. However, the effects of LA ablation on the characteristics of CTI-dependent atrial flutter have not been described. Therefore, the purpose of this study was to describe the features of CTI-dependent flutter that occurs after LA ablation.
Clinical Perspective p 615
Fifteen patients underwent mapping and ablation of CTI-dependent flutter late after LA ablation of AF. LA circumferential ablation was performed as previously described.5 Briefly, circular lesions were created around the left- and right-sided pulmonary veins with an electroanatomic mapping system (CARTO, Biosense Webster) and an 8-mm-tip ablation catheter (Navistar, Biosense Webster). A posterior line connecting the 2 circles and a mitral isthmus line also were created. After the risk of LA-esophageal fistula was recognized,6 an ablation line across the posterior wall was no longer performed. The end point of ablation was voltage abatement of the local atrial electrogram by >80% or to <0.1 mV.
The 15 patients in this study were part of a group of 65 consecutive patients who underwent a repeat procedure for atrial flutter after LA ablation of AF. These 65 patients in turn were part of a group of 552 consecutive patients who underwent LA ablation of AF. Among the 65 patients with postablation atrial flutter, 54 patients (83%) had undergone 1 LA procedure and 11 patients (17%) had undergone 2 LA procedures for AF. Eleven of the 54 patients (20%) who underwent 1 procedure were found to have CTI-dependent atrial flutter compared with 4 of the 11 patients (36%) with 2 LA procedures for AF (P=0.25). One study patient (patient 12) had undergone CTI ablation for “typical” atrial flutter before the LA procedure for AF.
Atrial flutter was considered CTI dependent if the postpacing interval at the CTI matched the flutter cycle length and if an activation map was consistent with clockwise or counterclockwise atrial flutter. Table 1 describes the clinical characteristics of the 15 patients. Thirty age- and gender-matched patients who underwent ablation of CTI-dependent flutter and had no history of LA ablation served as control subjects. Patients in the control group did not undergo detailed 3D mapping of the right atrium.
Mapping and Ablation of Atrial Flutter
Antiarrhythmic medications were discontinued at least 5 half-lives before the procedure. In the study group, 2 of the 15 patients (13%) had been treated with amiodarone compared with 5 of the 30 patients (17%) in the control group (P=1.0). Among the former, amiodarone therapy was discontinued 8 to 12 weeks before the procedure.
An activation map was performed with an electroanatomic mapping system during atrial flutter. Entrainment mapping was performed to identify sites within the reentry circuit.7 Sites harboring split, fragmented, or diastolic potentials were labeled on the activation map. Right atrial flutter was suspected if the entire tachycardia cycle length could not be accounted for with a detailed activation map of the LA. CTI dependence was confirmed by entrainment mapping. Twelve of the 15 study patients with CTI-dependent atrial flutter underwent activation mapping of both atria. Bipolar voltage maps of the posterior LA during CTI-dependent flutter also were analyzed.
Radiofrequency current was delivered along the CTI with an 8-mm-tip ablation catheter (Navistar, Biosense Webster) with a target temperature of 50°C to 55°C and power of 60 to 70 W (Stockert 70 RF generator, Biosense Webster). Procedural success was defined as termination of atrial flutter during radiofrequency application and the creation of bidirectional CTI block.8
Twelve-lead ECGs during CTI-dependent flutter were analyzed offline at a paper speed of 25 mm/s. If the flutter waves were not apparent, transient AV block was created by either adenosine administration or ventricular pacing. Flutter waves were designated as being upright, negative, biphasic, isoelectric, or multicomponent. The ECG analysis was performed by 2 investigators (R.L., E.G.) who were blinded to the demographic and electrophysiological data. In case of disagreement between the reviewers, a consensus was reached by input from another blinded investigator (H.O.).
Patients were seen in an outpatient clinic at 3 and 6 to 9 months after the procedure. All patients were instructed to contact a nurse if arrhythmic symptoms recurred, and these patients underwent an ECG and/or 30 days of monitoring with a continuous-loop recorder.
Continuous variables are expressed as mean±SD and were compared by use of the Student t test. Categorical variables were compared by the 2-sided Fisher’s exact test. A value of P<0.05 indicated statistical significance.
Eleven of the 15 study patients (73%) presented to the laboratory with spontaneous CTI-dependent flutter; in the other 4 patients, it was induced by rapid atrial pacing. The mean cycle lengths of CTI-dependent flutter in the study and control groups were 253±26 and 235±29 ms, respectively (P=0.05). In 12 of the 15 study patients (80%), 3D mapping revealed counterclockwise activation around the tricuspid annulus (Figure 1), and in the remaining 3 patients (20%), there was clockwise activation (Figure 2).
The average numbers of points used to construct the left and right atrial activation maps were 63±16 and 66±19, respectively. LA mapping accounted for 51±15% of the tachycardia cycle length. In patients with counterclockwise flutter, LA mapping accounted for 44±8% of the tachycardia cycle length compared with 67±17% in patients with clockwise flutter (P=0.02). Right atrial mapping accounted for 97±5% of the tachycardia cycle length.
Among the 15 study patients with CTI-dependent flutter, the inferior ECG leads displayed biphasic (−/+) or negative flutter waves in 6 patients (40%) and upright flutter waves in 9 patients (60%) (Figure 3). None of the control patients with CTI-dependent flutter showed upright flutter waves in the inferior leads (P<0.001). The classic “sawtooth” morphology (Figure 3A) was not seen in any of the study patients. Six of the 11 patients (55%) with spontaneous CTI-dependent flutter had upright flutter waves in the inferior leads compared with 3 of the 4 patients (75%) with inducible CTI-dependent flutter (P=0.60).
In lead I, the flutter waves were isoelectric in 6 of the 15 patients in the study group (40%) compared with 20 of the 30 patients (67%) in the control group (P=0.12) (Table 2). In lead aVL, the flutter waves were negative in 9 of the 15 study patients (60%) compared with 2 of the 30 control subjects (7%; P<0.001). The flutter waves in lead V1 were positive in 13 of the study patients (87%) compared with 20 of the 30 control patients (67%; P=0.28). Among the remaining 10 patients in the control group, 5 had biphasic flutter waves, 3 had negative, and 2 had isoelectric flutter waves in lead V1. At least 1 precordial lead showed negative flutter waves in 8 of the 15 study patients (53%) compared with 27 of the 30 control patients (90%; P=0.009).
Among the 12 patients with counterclockwise CTI-dependent flutter, the flutter waves in the inferior leads were biphasic or negative in 5 patients (42%; Figure 3B) and upright in 7 patients (58%; Figure 3C and 3D). In the 5 patients with counterclockwise flutter and a biphasic or negative morphology in the inferior leads, the flutter wave was further characterized as having a sharp negative deflection at its nadir (Figure 3B). Among the control patients, this sharp potential was seen in 2 of the 30 patients (7%; P=0.03). In the 3 patients with clockwise CTI-dependent flutter, the flutter waves in the inferior leads were upright in 2 patients and negative in the other. In 2 of the 15 study patients, there was a late potential after the flutter wave (Figure 3E).
Biatrial Activation and Flutter Wave Morphology
Biatrial activation maps during CTI-dependent flutter were available in 12 of the 15 patients. In patients with counterclockwise flutter and biphasic flutter waves in the inferior leads, the flutter wave coincided first with caudocranial activation of the septum/LA, followed by craniocaudal activation of the right atrial free wall. In patients with counterclockwise flutter and upright flutter waves in the inferior leads, the flutter wave coincided with craniocaudal activation of the right atrial free wall (Figure 4). In the patient with clockwise flutter and negative flutter waves in the inferior leads, the flutter wave corresponded to caudocranial activation of the right atrial free wall (Figure 5).
In all 9 patients with counterclockwise flutter in whom an LA activation map was available, the earliest LA activation occurred at the inferoposterior region of the LA. In all 3 patients with clockwise flutter, the earliest LA activation was found at the anterosuperior portion of the LA. In the 2 patients with a late potential after the flutter wave, the late potential coincided with dyssynchronous, late activation of the posterolateral LA (Figure 5C).
Bipolar LA Voltage
The mean bipolar voltage of the posterior LA during CTI-dependent flutter was 0.72±0.50 mV. The mean bipolar voltage was 0.77±0.56, and 0.56±0.08 mV among patients with counterclockwise and clockwise flutter, respectively (P=0.54). In patients with counterclockwise flutter, the mean bipolar voltage of the posterior LA was 1.54±0.19 mV among those with biphasic/negative flutter waves compared with 0.44±0.20 mV among those with upright flutter waves in the inferior leads (P<0.001; Figure 6).
Catheter Ablation and Follow-Up
Catheter ablation terminated CTI-dependent flutter in each of the 15 patients. With additional ablation, complete bidirectional CTI block was achieved in all 15 patients. During a mean follow-up of 6.1±4.4 months, none of the 15 patients had a recurrence of CTI-dependent atrial flutter.
One of the main findings of the study is that the ECG during CTI-dependent flutter that arises after LA ablation of AF frequently shows atypical findings. Specifically, in >50% of the patients with counterclockwise CTI-dependent flutter, the inferior leads had upright flutter waves as opposed to the classic sawtooth morphology. Furthermore, 60% of the study patients compared with only 7% of controls had ECGs with negative flutter waves in lead aVL. This feature is usually associated with arrhythmias arising in the LA.9
These atypical ECG features of CTI-dependent flutter may incorrectly suggest that the tachycardia is arising in the LA1 or coronary sinus,2 as often is the case after LA ablation of AF. In patients with proarrhythmic atrial flutter, entrainment mapping at the CTI early in the procedure, even in the absence of negative flutter waves in the inferior leads, may prevent unnecessary transseptal catheterization and LA mapping.
ECG Characteristics and Biatrial Activation
More than 50% of the study patients with counterclockwise atrial flutter had upright flutter waves in the inferior leads. The earliest LA activation in all patients with counterclockwise atrial flutter occurred at the inferoposterior LA. Flutter wave morphology in CTI-dependent flutter is thought to be primarily determined by LA activation10; therefore, it may be difficult at first glance to explain the upright flutter waves in patients with counterclockwise flutter. One would expect caudocranial activation of the LA and negative flutter waves given the inferoposterior breakthrough in patients with counterclockwise flutter.
The most likely explanation for the upright flutter waves is the debulking effect of LA ablation, which led to a marked reduction in LA voltage. This explanation is supported by the fact that the mean bipolar posterior LA voltage was significantly lower in patients with upright versus negative/biphasic flutter waves in the inferior leads. The manifestation of caudocranial LA activation on the surface ECG was therefore overshadowed by the craniocaudal activation that occurred in the right atrium. This is supported by the results of biatrial propagation mapping. Furthermore, the small amplitude and sharp, negative flutter waves that had a positive terminal component, ie, biphasic flutter waves, in patients with counterclockwise flutter most likely reflected atrial activation over a voltage-attenuated LA mass. Analogously, the negative flutter waves in the inferior leads in the patient with clockwise atrial flutter were likely inscribed as a result of unopposed caudocranial right atrial activation.
Interatrial Conduction During CTI-Dependent Flutter
In patients with counterclockwise flutter, the LA breakthrough occurred at the inferoposterior region. This is consistent with interatrial conduction over the musculature of the coronary sinus, as previously described in patients who had not undergone LA ablation.11,12 In patients with clockwise atrial flutter, the earliest LA activation was at the anterosuperior region, consistent with conduction over Bachmann’s bundle.11,12 One might speculate that interatrial conduction would be altered by extensive LA ablation. However, the results of this study show that the major routes of interatrial conduction are at least qualitatively undisturbed by LA ablation. This supports the conclusion that the unusual flutter wave characteristics observed in this study were caused more by altered intra-atrial conduction than by altered interatrial conduction.
Failure to account for >50% of the tachycardia cycle length usually implies that the tachycardia circuit is located in the chamber opposite the one being mapped.13 Although this seems to hold for patients with counterclockwise flutter, an average of 67% of the tachycardia cycle length was accounted for with LA mapping during clockwise CTI-dependent flutter. This difference implies that interatrial conduction during CTI-dependent flutter is more efficient over Bachmann’s bundle than the musculature of the coronary sinus. This observation confirms the preeminence of Bachmann’s bundle in providing synchronous atrial activation.14
An earlier study by Milliez et al15 differentiated counterclockwise CTI-dependent flutter on the basis of terminal positivity in the inferior leads. In that study, terminal positivity was found to correlate with LA enlargement or disease. The authors postulated that the positivity was due to delayed LA activation over Bachmann’s bundle. However, direct LA mapping was not performed in that study. The results of the present study are consistent with the prior study in that positivity in the inferior leads is related to an abnormal LA, in this case related to ablation. However, results of biatrial mapping during counterclockwise flutter in the present study suggest that the continuum from terminal positivity to frankly upright flutter waves in the inferior leads is related to prevailing activation of the right atrial free wall.
CTI-Dependent Versus LA Flutter After LA Ablation of AF
Because CTI-dependent flutter after LA ablation may mimic proarrhythmic LA flutter, it would be helpful to distinguish the 2 on the basis of the ECG. A prior study on the ECG characteristics of atypical flutter arising from the LA and coronary sinus noted that none of the patients demonstrated negative flutter waves in the inferior leads.2 In the present study, 6 of the 15 patients (40%) with CTI-dependent flutter after LA ablation showed at least partly negative flutter waves in the inferior leads. Also, a negative flutter wave in the precordial leads was not observed in any of the patients in the prior study. Among patients in the present study, a negative flutter wave in the precordial leads was seen in &50% of the patients. Therefore, negativity in the inferior or precordial leads may help to distinguish between atrial flutter arising from the CTI versus the LA/coronary sinus in patients who have undergone LA ablation of AF.
The main implication of this study is that in patients presenting with atrial flutter after LA circumferential ablation, the CTI should be the first place from which entrainment mapping is performed. CTI-dependent flutter should be suspected even in the absence of negative flutter waves in the inferior leads or the presence of negative flutter waves in lead aVL. This strategy may avoid the need for transseptal catheterization and LA mapping in some patients.
Although the ECG during CTI-dependent flutter after LA ablation of AF may resemble that of arrhythmias originating from the LA/coronary sinus, it often contains clues that help distinguish the two. Negative flutter waves in the inferior (particularly with a sharp component at the nadir) or precordial leads point to the CTI as being part of the circuit. This information may facilitate mapping and ablation of atrial flutter arising after a LA ablation procedure.
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Saoudi N, Cosio A, Waldo A, Chen S, Iesaka Y, Lesh M, Saksena S, Salerno J, Schoels W. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. Eur Heart J. 2001; 22: 1162–1182.
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Marine JE, Korley VJ, Obioha-Ngwu O, Chen J, Zimetbaum P, Papageorgiou P, Milliez P, Josephson ME. Different patterns of interatrial conduction in clockwise and counterclockwise atrial flutter. Circulation. 2001; 104: 1153–1157.
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Common atrial flutter that revolves around the tricuspid annulus gives rise to stereotypical flutter waves. It is referred to as CTI dependent because ablation that interrupts conduction through the isthmus between the annulus and inferior vena cava abolishes the arrhythmia. In this study, the ECG and atrial activation sequence of CTI-dependent atrial flutter were studied in 15 patients who developed this arrhythmia late after extensive LA ablation of atrial fibrillation. In contrast to the typical negative flutter waves in the inferior leads present in 30 control patients who had not had AF ablation, the flutter waves were upright in 60% of patients with prior LA ablation. Atrial mapping suggested that the upright flutter waves corresponded to craniocaudal activation of the right atrial free wall that was more prominent because extensive LA ablation diminished the contribution of LA activation to the flutter wave. Mapping indicated that the LA was activated by conduction over the coronary sinus musculature and Bachman’s bundle region at the roof of the atria. In lead aVL, the flutter waves often were negative. These findings further elucidate genesis of the flutter wave morphology. After extensive LA ablation for AF, common atrial flutter, which can be ablated from the right atrium, often has an atypical ECG appearance that may falsely suggest an LA origin. The unusual flutter wave characteristics appear to be due to abnormal intra-atrial rather than interatrial conduction.