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Typical Atrial Flutter: Antiarrhythmic Drugs
or Ablation as First-Line Therapy?

Nassir F. Marrouche, MD; Andrea Natale, MD

Electrophysiology Laboratories, Department of Cardiology, Section of Electrophysiology
and Pacing, The Cleveland Clinic Foundation, Cleveland, OH, USA

   Since Lewis postulated in 1920 that atrial flutter is due to reentrant circuit a large body of evidence has advanced our understanding of the electrophysiologic substrate of typical atrial flutter and has enhanced our ability to treat this arrhythmia. Rosenblueth and Garcia-Ramos (1) and Frame (2,3) first described in an animal model the critical role of the anatomical boundaries in maintaining the flutter circuit. By creating a lesion between the orifices of the venae cavae and extending the lesion to the appendage a model of atrial flutter was developed. Interesting enough the tricuspid annulus served as the anterior barrier and the crush lesion or incision served as the posterior barrier of the macroreentrant flutter circuit. These models raised the concept that atrial flutter is a macroreentrant circuit maintained by anatomical barriers including: 1) the tricuspid annulus; 2) the cavity of the right atrium; 3) the induced surgical barrier that prevents short-circuiting of the macroreentrant circuit within the right atrial free wall. Boineau demonstrated in a canine model that the crista terminalis could replace the crush incision as the posterior barrier of the flutter circuit (4).

   Multiple mapping studies in humans with typical isthmus dependent atrial flutter defined the functional and anatomical boundaries of the flutter circuit. Kalman and colleagues elegantly show by using activation and entrainment mapping that the tricuspid annulus constitutes a continuous anterior anatomical barrier constraining the reentrant wave front of human typical atrial flutter (5). The eustachian ridge and the crista terminalis define the posterior barriers of the flutter circuit, as reported by Nakagawa and colleagues (6). The typical atrial flutter wave propagates in a caudocranial direction from the coronary sinus along the right atrial septum towards the vena cava and comes back along the free wall towards the cavotricuspid isthmus bounded by the crista terminalis posteriorly and the tricuspid annulus anteriorly. The wave front finally enters the narrow isthmus of atrial tissues protected by the eustachian ridge posteriorly and the tricuspid annulus anteriorly.

ELECTROPHYSIOLOGIC CHARACTERISTICS OF ATRIAL FLUTTER
   Waldo and colleagues first demonstrated the classic criteria of concealed entrainment of typical atrial flutter by rapid atrial pacing from high right atrium in an animal model (7). Concealed entrainment predicts that the pacing site is located within the critical flutter isthmus. In case of typical atrial flutter the critical isthmus is between the eustachian ridge and the tricuspid annulus. Applying the technique of transient entrainment, Kalman et al showed that post pacing intervals at all sites of the tricuspid annulus was within the flutter circuit (5).

   Nakagawa and colleagues reported double potentials with widely separated isoelectric interval along the eustachian ridge that extended from the coronary sinus ostium to the inferior vena cava in patients with typical atrial flutter. Arenal et al demonstrated the importance of the double potentials along the crista terminalis and the eustachian ridge, showing, by rapid pacing at both sides of the crista terminalis, that this structure serves as a functional barrier (8). The inducibility of atrial flutter is dependent on both the site of pacing and the number of stimuli, which are required to develop the functional block along the crista terminalis. For this reason burst pacing is more effective than atrial extrastimulus in inducing atrial flutter. Another important factor for initiating atrial flutter is the site of pacing. Pacing from the coronary sinus or the low lateral right atrium are more likely to develop unidirectional block across the cavotricuspid isthmus allowing the flutter circuit to propagate in one direction.

ABLATION OF TYPICAL ATRIAL FLUTTER
   The understanding of the reentrant circuit of typical atrial flutter led to the present treatment strategy, which relies on the ability to create a lesion that transects the critical isthmus by connecting two anatomical barriers. Multiple reports demonstrated that dragging a radiofrequency lesion from the tricuspid annulus to the inferior vena cava and/or eustachian ridge and coronary sinus would interrupt the typical flutter circuit (9-12). The anatomical target for ablation of typical atrial flutter although relatively complex is surrounded by fixed anatomical landmarks, which facilitate placement of the linear lesion. Wang and coworkers examined the dimensions of this anatomical structure defining the flutter isthmus in 51 postmortem hearts (13). They reported a wide variation in the distance between the tricuspid annulus and the eustachian ridge ranging between 1.8 and 4.2 cm. Therefore at times a lesion many centimeters long is needed. These findings have important clinical implications and may explain the relatively high recurrence rates reported in some series.

   Catheter ablation can be conducted either in atrial flutter or during pacing from the coronary sinus or the low right lateral atrium. Understanding the anatomical barriers involved in the substrate for typical atrial flutter lead to the development of new endpoints to establish successful atrial flutter ablation. These include: 1) demonstration of bi-directional conduction block in the flutter isthmus during coronary sinus and low lateral atrial pacing; 2) change to upright P wave with low lateral right atrial pacing; 3) split potentials with wide and fixed timing between the two components along the linear lesion in the isthmus with coronary sinus ostium and/or low lateral right atrial pacing; 4) change in circumannular activation sequence with low lateral right atrial and coronary sinus pacing after ablation (14-19).

   Radiofrequency (RF) is the energy source generally used for treatment of atrial flutter. Monitoring of the catheter tip-tissue temperature interface is particularly important, with the goal of keeping the temperature between 55-60º. The long-term success rates of atrial flutter ablation using RF energy delivery by creating an isthmus line vary between 70 and 95% (11,20-22).

   In our and others preliminary experience (23), the use of cooled-tip catheters, or large-tip catheters (8-10 mm) with a high power generator, appeared to reduce greatly the recurrence rate and to facilitate acute procedural success (Table 1).

MANAGEMENT OF ATRIAL FLUTTER
   Due to the high success rates and low complication rates associated with typical flutter ablation, this therapy modality is becoming the preferred approach. At present, several antiarrhythmic drugs are available to treat typical atrial flutter. In the absence of heart disease the class IC drugs associated with AV node blocking agents are probably the best choice, because better tolerated and the lower organ toxicity compared to class IA drugs, sotalol and amiodarone. Only one retrospective study by Wood and colleagues suggested that the stroke rate in patients with atrial flutter is comparable to that with atrial fibrillation (24). Although at present there is no clear agreement on the use of anticoagulation in patients with atrial flutter, warfarin therapy should be considered in the same fashion as in atrial fibrillation.

ANTIARRHYTHMIC THERAPY VERSUS FIRST-LINE RADIOFREQUENCY ABLATION
   Despite the high cure achieved by radiofrequency catheter ablation, pharmacologic therapy is still considered the standard initial therapeutic approach for atrial flutter. We conducted a study to assess and compare the clinical efficacy of conventional drug therapy versus first-line catheter ablation to treat atrial flutter in a prospective randomized manner.

   This was a multicenter prospective randomized study. Patients were considered eligible for the study if they had at least two symptomatic episodes of atrial flutter in the last four months. Exclusion criteria included the following; 1) prior evidence of atrial fibrillation (AF); 2) the presence of significant left atrial enlargement (> 4.5 cm); and 3) previous treatment with antiarrhythmic medications (AAD). Sixty-one patients were included in the study (42 men; mean age 66±10 years). Mean left ventricular ejection fraction was 49 ± 3 %. After entering the study each patient was randomized to either AAD therapy or to first-line RF catheter ablation. Drug therapy was given based on the physician's preference. An effort was made to keep each patient in the same treatment groups for at least one year. Each investigator was required to attempt sinus rhythm maintenance with at least two drugs, including amiodarone before resorting to rate control medications. Recurrence of atrial flutter during amiodarone therapy was not considered a failure during the initial two months of treatment with this drug. Following enrollment in the study, institution or change of AAD therapy was performed on an outpatient basis unless hospitalization was required by the patients' symptoms. Quality of life and symptoms questionnaires were administered before institution of therapy, six and 12 months thereafter. The study endpoints were as follows: 1) recurrence of atrial flutter; 2) need for rehospitalization; 3) quality of life and symptom scales.

   Radiofrequency catheter ablation was performed by creating a linear lesion from the tricuspid annulus to the inferior vena cava using 4- and/or 8 mm tip electrode catheters advanced in the right atrium with a long 8F sheath (SRO, Daig Corp). The 8 mm tip was used if with the 4 mm tip catheter adequate RF energy delivery could not be achieved due to immediate impedance rise even at low power setting. RF ablation was continued until either no electrogram or consistent reduction of the electrograms amplitude of at least 90% was present across the isthmus. We also assessed inducibility post ablation using extrastimulus testing and burst pacing. To prove bi-directional isthmus block a 20-pole halo catheter (Cordis-Webster, Inc.) was used in 11 patients, where a custom-made catheter with eight proximal and eight distal electrodes separated by a 9-cm gap (Cardiac Assist Device Inc, Cleveland) was used in 15 patients. In these 15 patients the distal electrodes were placed in the coronary sinus and the proximal electrodes were placed along the right lateral atrial wall anterior to the crista terminalis. In the remaining 3 patients isthmus conduction block was proven using the electroanatomical mapping system CARTO (Biosense-Webster).

   An assessment of the patients' quality of life before and after the procedure was performed using a questionnaire that included 16 items to evaluate the physical, social, economics and psychological impairment (Endicott, Quality of Life Enjoyment and Satisfaction Questionnaire).

   All patients were followed up in the outpatient clinic at regular intervals. In case of recurrence of AFL after ablation, the procedure was repeated. In case of recurrence of AFL in patients treated with AAD therapy, a different AAD was initiated. If patients experienced atrial fibrillation after entering the study, the arrhythmia was treated with medical therapy.

   The clinical characteristics between the two study groups are summarized in Table 2.

   Acute successful ablation was obtained in all 31 patients undergoing RF ablation. Twenty-six patients out of 31 had typical isthmus dependent flutter. In the remaining five patients incisional atrial flutter was induced and documented as the only arrhythmia (3 patients) or in combination with typical flutter (2 patients). In all patients, the ablation was initiated with a 4-mm tip electrode and concluded with an 8-mm tip electrode in five of them.

   Among the 26 patients undergoing verification of bidirectional block along the ablation line we observed the following: 1) bidirectional block was present immediately following termination of atrial flutter by cathter ablation only in 11 patients (42%); 2) after demonstration of bidirectional block, additional lesions were required in four patients (15%) to satisfy the electrogram amplitude endpoint; and 3) uniform reduction of the electrogram amplitude across the isthmus was never associated with persistence of conduction throughout this region.

   At the end of the one year follow-up two patients experienced recurrence of AFL (6.4%) and both were successfully treated with a successful ablation. Nine patients experienced atrial fibrillation after successful catheter ablation of atrial flutter (29%). Of these nine patients, five were treated with AAD with long-term persistence of sinus rhythm. Three patients had sporadic episodes of self-terminating AF and were treated with rate control drugs. One patient did not respond to AAD and because rate control was difficult to achieve with medication, he underwent AV node ablation and implantation of a single-chamber permanent pacemaker nine months after the initial ablation for atrial flutter.

   The mean number of drugs initiated in the AAD group was 3.4±1.1. The type of drugs administered in individual patients is shown in Table 3. At follow-up, 16 (53%) of these patients were treated with rate control drugs due to the inefficacy of active AAD in maintenance of sinus rhythm. Of these 16 patients, 15 had both recurrence of atrial flutter and development of atrial fibrillation. At the time of the first arrhythmia recurrence, atrial fibrillation was observed in one patient, whereas all the remaining patients had atrial flutter. Two patients crossed over to AFL ablation group before the end of the first year of follow-up and one patient required AV node ablation and pacemaker due to the inability to maintain sinus rhythm and achieve adequate rate control. Of the remaining 11 patients, 8 were treated with amiodarone, 1 with propafenone and atenolol, and 2 with procainamide and digoxin. Of the 16 patients receiving rate control drugs, 2 were treated with digoxin alone, 7 with diltiazem or verapamil combined with digoxin, 4 with beta-adrenergic blocking agents alone and 3 with a combination of beta-blocker and digoxin.

   In the patients randomized to drug therapy, with the exception of palpitations, there was no statistically significant change in all the quality of life variables (Table 4). Differently, the patients treated with catheter ablation reported a significant improvement in their quality of life and symptoms scores (Table 5).

   After a mean follow-up of 22±11 months, 25 patients (80%) who underwent catheter ablation were in sinus rhythm without the need of active AAD, whereas only 11 (36%, p<0.01) of those receiving AAD remained in sinus rhythm. At follow-up, AF was seen in 9 patients undergoing catheter ablation (29%) versus 18 of those receiving AAD therapy (60%, p<0.05). Eight of the nine patients (88%) experiencing AF following catheter ablation had this arrhythmia controlled by medical therapy. Differently in the drug therapy group, only 1 of the 18 patients (6%) developing AF had this arrhythmia successfully managed with drugs. During the follow-up period, hospitalization was required for occurrence of severely symptomatic arrhythmia in 7 patients (22%) undergoing catheter ablation and 19 (63%, p<0.01) of those receiving medication. Among the patients treated with AAD, recurrence of AFL was never associated with 1:1 AV conduction.

   These data support the use of catheter ablation as the first-line therapy for treatment of AFL as compared with AAD. As shown in our study, AFL ablation was not only more effective in the long-term management of this arrhythmia, but patients treated with this approach experienced less rehospitalizations, and lower occurrence of AF during the follow-up. This clinical beneficial effect appeared to have a more positive impact on the quality of life.

   Of interest is the lower rate of atrial fibrillation after cure of atrial flutter with ablation. This finding may suggest that ineffective prevention of AFL by AAD therapy may potentiate an unfavorable electrical remodeling of the atrium which, in turn, could facilitate degeneration to AF at follow-up. On the other hand, pure atrial flutter could be the early manifestation of an atrial electrical disease, which may lead to atrial fibrillation over time. A longer-term follow-up is needed to exclude or confirm this hypothesis.

   In conclusion, catheter-based treatment of atrial flutter appears superior to conventional drug therapy and should be considered the first line approach. Whether cure of atrial flutter has long-term affect in preventing development of atrial fibrillation remains unclear.

REFERENCES

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2nd Virtual Congress of Cardiology

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