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At least 19 recordsLinked to original sources
PubMed2001

Thromboembolic risk in atrial flutter. The FLASIEC (FLutter Atriale Società Italiana di Ecografia Cardiovascolare) multicentre study.

AIMS: Patients with atrial flutter are believed to be at lower risk of thromboembolism than patients with atrial fibrillation. However, the incidence of atrial thrombi and the need for anticoagulation in patients with atrial flutter is not well established. METHODS AND RESULTS: A prospective observational multicentre study was undertaken to assess the frequency of atrial thrombi and spontaneous echocontrast and the prevalence for aortic complex atherosclerotic lesions in a cohort of unselected patients with atrial flutter. We evaluated 134 patients (102 male, aged 70+/-9 years); exclusion criteria were history of atrial fibrillation, rheumatic mitral valve disease and mitral mechanical prosthesis. The median of atrial flutter duration was 33 days. Twelve patients had been taking warfarin for more than 7 days. One hundred and twenty-four patients (94%) underwent a transoesophageal echocardiogram, which revealed left atrial appendage thrombi in two patients (1.6%) and right atrial thrombi in one patient (1%). At least moderate left atrial echocontrast was found in 16/124 patients (13%). Complex atherosclerotic aortic plaques were detected in 10 patients (8%). Atrial flutter conversion was attempted in 93/134 patients (69%). At the 1-month follow-up, two patients experienced a thromboembolic event following restoration of sinus rhythm. CONCLUSIONS: Atrial thrombi and echocontrast, and complex aortic atherosclerotic plaques are relatively uncommon in patients with atrial flutter. Post-cardioversion embolism was observed in two patients in our study population.

Aged↗
PubMed1997

Pharmacologic management of supraventricular tachycardias in children. Part 2: Atrial flutter, atrial fibrillation, and junctional and atrial ectopic tachycardia.

OBJECTIVE: To review the literature regarding the use of antiarrhythmic agents in the management of atrial flutter (AF), atrial fibrillation (Afib), junctional ectopic tachycardia (JET), and atrial ectopic tachycardia (AET) in infants and children. To discuss the advantages and disadvantages of specific agents in each type of arrhythmia in an effort to develop treatment guidelines. DATA SOURCE: A MEDLINE search encompassing the years 1966-1996 was used to identify pertinent literature for discussion. Additional references were found in the articles, which were retrieved via MEDLINE. STUDY SELECTION: Clinical trials that address the use of antiarrhythmic agents for the treatment of supraventricular tachycardia, AF, Afib, JET, and AET in children were selected. Literature pertaining to dosage, pharmacokinetics, efficacy, and toxicity of antiarrhythmic agents in children were considered for possible inclusion in the review; information judged to be pertinent by the authors was included in the discussion. DATA EXTRACTION: Although there are numerous reports of antiarrhythmic use in children, there are very few large studies designed that evaluate the use of specific antiarrhythmic agents in the treatment of AF, Afib, JET, or AET. Ideally, controlled clinical trials are used to develop clinical guidelines; however, in this situation, most data and information must be obtained from case series of children treated. Although the results from these types of studies may be useful in developing guidelines for the optimal use of these agents for the treatment of AF, Afib, JET, and AET, controlled trials are required for establishing standard treatment guidelines for all patients. DATA SYNTHESIS: Despite limited scientific evaluation of conventional agents in the treatment of AF, Afib, JET, or AET in children, they continue to be the standards of care. Most information regarding the use of conventional agents in children has been extrapolated from the adult literature. Little justification for the use of the agents or dosing in children is available. Controlled trials regarding the use of newer antiarrhythmic agents (propafenone, amiodarone, flecainide) are available; however, the variance in dosing schemes, presence of structural heart disease, and patient age may confound the results. CONCLUSIONS: Because of greater clinical experience, conventional antiarrhythmic agents generally remain as first-line therapy in the management of most supraventricular tachycardias in children. Atrial pacing or cardioversion to reestablish sinus rhythm is indicated for initial episodes of AF in infants, followed by chronic prophylactic therapy in those with significant structural heart disease or in infants in whom AF recurs. Attempts to eliminate AF in children outside the neonatal or infancy period should begin with trials of traditional agents such as digoxin or procainamide, and if unsuccessful, subsequent trials of amiodarone. Digoxin and beta-blockers remain the mainstay of therapy for children with Afib, followed by procainamide for treatment failures. Intravenous amiodarone, the newest addition to our antiarrhythmic armamentarium, is the most promising agent in the treatment of postoperative JET. This arrhythmia has been traditionally managed with corporal cooling and/or digoxin therapy; however, intravenous amiodarone may now be a valuable option. Although relatively unsuccessful in the management of congenital JET and AET, conventional agents are typically used prior to the initiation of long-term therapy with potentially more toxic agents such as amiodarone or propafenone. Additional well-designed, controlled trials are needed to further evaluate the comparative efficacy of agents such as flecainide, sotalol, moricizine, propafenone, and amiodarone in the management of AF, Afib, JET, and AET in children, as well as to evaluate the dosing and toxicity in various age groups.

Anti-Arrhythmia Agents↗
PubMed2001

[Atrial tachycardia, atrial flutter, atrial fibrillation: curative therapy by focal ablation in a pulmonary vein].

We describe the case of a 50-year-old woman with the clinical diagnosis of cardiomyopathy associated with supraventricular tachycardia refractory to pharmacological treatment. The totally irregular tachyarrhythmia was the result of different episodes of atrial tachycardia, atrial flutter and atrial fibrillation that could be identified in the surface ECG. These findings and the patient's symptoms were all caused by a single focal tachycardia originating from the left upper pulmonary vein. Ablation of this focus represented a curative antiarrhythmic therapy also restoring a normalized ventricular function. Thus, an ablation of the AV node with consecutive pacemaker implantation could be prevented.

Atrial Fibrillation↗
PubMed1993

Electrophysiologic effects of a new class III antiarrhythmic agent, E-4031, on atrial flutter, atrial refractoriness, and conduction delay in a canine sterile pericarditis model.

Numerous studies have shown that E-4031 generally prolongs the atrial effective refractory period (AERP) without affecting cardiac conduction. The effects of E-4031 on AERP and cardiac conduction at short cycle lengths (CLs) close to the AERP were measured in 12 dogs with sterile pericarditis. Three pairs of electrodes were sutured at three sites in the atria 4 days after the model was created. We measured AERP and maximum conduction delay (MCD) after 8 beats train at CLs of 400, 300, 200 and 150 ms before and during continuous infusion of E-4031 (0.1 microgram/kg/min) that followed an initial dose of 10 micrograms/kg/min/5 min. E-4031 interrupted sustained atrial flutter (AF) (> or = 10 min) in 4 of 5 episodes and atrial fibrillation (> or = 10 min) in 4 of 4. The CL of AF defined as a rapid atrial rhythm (rate > or = 240 beats/min) in five episodes studied in the sterile pericarditis model was significantly (p < 0.005) prolonged from 120 +/- 8 to 160 +/- 17 ms. There were significant (p < 0.005) increases in AERP at each CL, and prolongation of AERP was 39 +/- 18, 31 +/- 14, 23 +/- 14, and 16 +/- 14 ms at CL 400, 300, 200, and 150 ms, respectively. E-4031 produced less prolongation of AERP at short pacing CLs and had no effect on conduction time during atrial rapid pacing at CLs > 150 ms. E-4031 did not prolong MCD at CL 400 ms, but did prolong MCD at CLs of 300, 200, and 150 ms, despite prolongation of AERP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Atrial flutter, atrial fibrillation, and other primary atrial tachycardias.

Traditional classifications of atrial tachycardias include not only rhythm disturbances arising primarily within the atria, but also dysrhythmias in which it is now recognized that participation of both atrial and non-atrial tissue is required. We prefer to consider those arrhythmias in which the atria are the principal site of electrophysiologic disturbance as "primary" atrial tachyarrhythmias. The mechanisms, diagnosis, and treatment of these "primary" atrial tachycardias are the subject of this article.

Anti-Arrhythmia Agents↗
PubMed1994

Mapping the conversion of atrial flutter to atrial fibrillation and atrial fibrillation to atrial flutter. Insights into mechanisms.

It is not generally believed that there is a relation between atrial flutter, thought to be due to a single reentrant circuit, and atrial fibrillation, thought to be due to simultaneously circulating multiple-reentrant wave fronts. However, there are many reasons to suggest that these rhythms are more closely related than previously thought. To test the hypothesis that the length of an area of functional block in the right atrial free wall is critical to the conversion of atrial flutter to atrial fibrillation and of atrial fibrillation to atrial flutter, we studied spontaneous and ATP-induced conversion of stable atrial flutter to sustained atrial fibrillation and spontaneous conversion of sustained atrial fibrillation to stable atrial flutter. We studied 13 episodes of the conversion of stable atrial flutter to sustained atrial fibrillation and sustained atrial fibrillation to stable atrial flutter in seven dogs with sterile pericarditis. Six episodes were spontaneous and seven were ATP related. All episodes were studied by using a multisite mapping system to record 190 unipolar electrograms (converted in the software to 95 bipolar electrograms) from the right atrial free wall along with ECG lead II. Atrial flutter induction was attempted by atrial stimulation (S1S2 or S1S2S3) or by rapid atrial pacing for > or = 20 beats from selected sites at selected rates. For both the spontaneous and the ATP-related episodes, stable atrial flutter was defined as any episode of > or = 5 minutes, and sustained atrial fibrillation was any episode of > or = 1 minute. During all the episodes of stable atrial flutter, a line of functional block with a mean length of 24 +/- 4 mm was localized on the right atrial free wall. When the previously stable line of functional block decreased to a mean of 16 +/- 3 mm (P < .05), either spontaneously or after ATP administration (40 mg i.v.), the new line of functional block was not long enough to maintain stable atrial flutter, and conversion to atrial fibrillation resulted. This shortened line of functional block continued to change and migrate over the right atrial free wall throughout sustained atrial fibrillation. These observations were similar for both spontaneous and ATP-induced conversions. When sustained atrial fibrillation evolved to stable atrial flutter, there was reformation of a long line of functional block, long enough (> or = prior length) to create a stable reentrant circuit, which then captured the right atrial free wall and subsequently both atria.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed2004

Different clinical courses and predictors of atrial fibrillation occurrence after transisthmic ablation in patients with preablation lone atrial flutter, coexistent atrial fibrillation, and drug induced atrial flutter.

The aim of this prospective study was to compare the long-term follow-up after transisthmic ablation of patients with preablation lone atrial flutter, coexistent AF, and drug induced atrial flutter to determine if postablation AF followed a different clinical course and displayed different predictors in these groups. The study evaluated 357 patients who underwent transisthmic ablation for typical atrial flutter. These were divided into four groups according to their preablation history. Group A included patients with typical atrial flutter and without preablation AF (n=120, 33.6%). Group B included patients with preablation AF and spontaneous atrial flutter (n=132, 37.0%). Group C patients had preablation AF and atrial flutter induced by treatment with IC drugs (propafenone or flecainide) (n=63, 17.6%) Group D included patients with preablation AF and atrial flutter induced by treatment with amiodarone (n=42, 11.8%). During a mean follow-up of 15.2 double dagger 10.6 months (range 6-55 months) AF occurred more frequently in groups B (56.1%) and C (57.1%) patients than in groups A (20.8%, P <0.0001) and D (31.0%, P <0.0001) patients. The results of multivariate analysis revealed that different clinical and echocardiographical variables were correlated with postablation AF occurrence in the different groups. Patients with atrial flutter induced by amiodarone have a significantly lower risk of postablation AF than patients with spontaneous atrial flutter and AF, and those with atrial flutter induced by IC drugs. Different clinical and echocardiographical variables predict postablation AF occurrence in different subgroups of patients.

Aged↗
PubMed2006

Common atrial flutter and atrial fibrillation are not always two stages of the same disease. A long-term follow-up study in patients with atrial flutter treated with cavo-tricuspid isthmus ablation.

OBJECTIVE: Both atrial flutter and atrial fibrillation (AF) frequently develop in the same patient. There is therefore reasonable doubt that flutter ablation may not solve the clinical problem, owing to the occurrence/recurrence of AF. The aim of this study was to establish whether cavo-tricuspid isthmus ablation is curative in patients with common atrial flutter alone or combined with AF. METHODS: One hundred and forty-one patients (114 male, 27 female, mean age 63 +/- 10 years) who had cavo-tricuspid isthmus ablation were followed up for 44 +/- 20 months. Before ablation, 48 patients had only atrial flutter (group A), whereas 93 patients had both atrial flutter and AF. Among the latter, during antiarrhythmic therapy, 31 patients had only atrial flutter (group B1), whereas 62 patients (group B2) continued to experience both arrhythmias. RESULTS: During follow-up, 27% of group A and 61% of group B patients had documented recurrent AF (P < 0.001). AF recurred in 51% of group B1 and in 66% of group B2 patients (P = NS). Permanent AF occurred in 6% of group A, 3% of group B1 and 21% of group B2 (P < 0.01). Specific symptom scale scores significantly decreased in all groups, particularly in group A. Two patients of group B had cerebral ischaemic attacks. CONCLUSIONS: Over a long-term follow-up, cavo-tricuspid isthmus ablation is curative in >70% of patients with atrial flutter alone. Therefore, if no AF is documented, more extensive ablation is not needed. By contrast, cavo-tricuspid isthmus ablation is frequently unable to prevent AF in patients with both atrial flutter and AF, although in some cases a significant clinical benefit may be obtained.

Atrial Fibrillation↗
PubMed2003

Inter-relationships between atrial flutter and atrial fibrillation.

It has been appreciated for a long time that atrial flutter and atrial fibrillation have a clinical relationship. Now, with the technological advances that permit more sophisticated electrophysiological studies, especially mapping studies, we have significantly advanced our understanding of this interrelationship. Regarding the relationship at atrial fibrillation to atrial flutter: Atrial fibrillation of variable duration (very brief to prolonged episodes) precedes the onset of atrial flutter in most instances. It seems that during the period of atrial fibrillation, the functional components of the atrial flutter reentrant circuit are formed. This is principally a line of block between the venae cavae. If this line of block does not form, classical atrial flutter does not form. And if this line of block shortens or disappears, classical atrial flutter disappear as well. In fact, it might be said that the major difference in whether classical atrial flutter or atrial fibrillation develops is whether a line of block forms between the venae cavae. Regarding the relationship of atrial flutter to atrial fibrillation: Studies have demonstrated that a driver (a single focus or reentrant circuit of very short cycle length) can be responsible for causing atrial fibrillation by producing fibrillatory conduction to the rest of the atria. In experimental models and now beginning to be demonstrated in patients, this driver may be a stable reentrant circuit of very short cycle length, i.e., a fast form of atrial flutter, if you will. In fact, there is probably a spectrum of these short cycle lengths that depend, in part, on where the reentrant circuit (i.e., "atrial flutter") exists. When the stable reentrant circuit is of sufficiently short cycle length, it will only activate small portions of the atria in a 1 : 1 manner. The rest of the atria will be activated irregularly, resulting in atrial fibrillation. Unstable reentrant circuits can also do the same thing. In short, it appears that there are several mechanisms of atrial fibrillation, one of which is due to a form of very rapid atrial flutter.

Animals↗
PubMed2006

Electrophysiological mechanisms of atrial flutter.

Atrial flutter (AFL) is a common arrhythmia in clinical practice. Several experimental models such as tricuspid regurgitation model, tricuspid ring model, sterile pericarditis model and atrial crush injury model have provided important information about reentrant circuit and can test the effect of antiarrhythmic drugs. Human atrial flutter has typical and atypical forms. Typical atrial flutter rotates around tricuspid annulus and uses the crista terminalis and sometimes sinus venosa as the boundary. The IVC-tricuspid isthmus is a slow conduction zone and the target of radiofrequency ablation. Atypical atrial flutter may arise from the right or left atrium. Right atrial flutter includes upper loop reentry, free wall reentry and figure of eight reentry. Left atrial flutter includes mitral annular atrial flutter, pulmonary vein-related atrial flutter and left septal atrial flutter. Radiofrequency ablation of the isthmus between the boundaries can eliminate these arrhythmias.

Journal Article↗
PubMedDate not supplied

Management of atrial flutter.

Atrial flutter is a macroreentrant arrhythmia that is associated with cardiovascular and pulmonary disease. In the United States, 200,000 new cases of atrial flutter can be expected to develop every year with a male to female ratio of over 2:1. This arrhythmia is associated with atrial fibrillation in over half the cases. It is also associated with an increased risk of thromboembolic complications, but less than that is seen with atrial fibrillation. The most common form of atrial flutter involves a large reentrant circuit within the right atrium, encircling the tricuspid annulus. Other, less common forms of atrial flutter may involve other anatomic barriers, atriotomy scars, and infarcted areas of the atria. Treatment of atrial flutter often involves electrical cardioversion and/or antiarrhythmic medications. Type I and Type III antiarrhythmic drugs are often used to terminate or prevent recurrent episodes and Type II (beta-blockers) and Type IV (calcium channel blockers) can be used to control the ventricular rate during atrial flutter. However, antiarrhythmic drugs alone control atrial flutter in only 50% to 60% of patients. Since the early 1990s, radiofrequency catheter ablation has been used to interrupt the reentrant circuit and prevent recurrences of atrial flutter. Radiofrequency ablation is acutely successful in over 90% of cases and avoids the long-term toxicity seen with antiarrhythmic drugs. Advanced mapping techniques and newer methods of delivering the radiofrequency lesions are being used to delineate unusual forms of atrial flutter and to minimize fluoroscopic exposure during the procedure.

Anti-Arrhythmia Agents↗
PubMed2001

[Usefulness of a VDD defibrillation electrode in recording atrial electrograms during atrial flutter and atrial fibrillation].

BACKGROUND: Monitoring of atrial signals improves the accuracy in identifying supraventricular tachyarrhythmias to prevent inappropriate therapies in patients with implantable cardioverter-defibrillators (ICD). Since complications due to the additional atrial lead were found in dual chamber ICD systems with 2 leads, we designed a single-pass VDD-lead for use with dual chamber ICDs. PATIENTS AND METHODS: After promising animal experiments in a German multicenter study a prototype VDD lead (single-coil defibrillation electrode with 2 additional fractally coated rings for bipolar sensing in the atrium) was temporarily used in 20 patients. Atrial and ventricular signals were recorded during sinus rhythm, atrial flutter, atrial fibrillation and ventricular tachycardia or ventricular fibrillation. Terminations of ventricular arrhythmias were performed by internal DC shock. RESULTS: The implantation of the electrode was successful in 18 of 20 patients. Mean atrial pacing threshold was 2.45 +/- 0.9 V/0.5 ms, mean atrial impedance was 215 +/- 31 Ohm. Atrial amplitudes were greater during sinus rhythm (2.7 +/- 1.6 mV) than during atrial flutter (1.36 +/- 0.28 mV, p < 0.05) or atrial fibrillation (0.92 +/- 0.29 mV, p < 0.01). During ventricular fibrillation atrial "sinus"-signals had significantly (p < 0.01) lower amplitudes than during sinus rhythm. Mean ventricular sensing was 13.3 +/- 7.9 mV, mean ventricular impedance was 577 +/- 64 Ohm. Defibrillation was successful with 20 J shock. 99.6% of P waves could be detected in sinus rhythm and 85 +/- 9.9% of flutter waves during atrial flutter. During atrial fibrillation 55% of atrial signals could be detected without modification of the signal amplifier. CONCLUSIONS: A new designed VDD dual chamber electrode provides stable detection of atrial and ventricular signals during sinus rhythm and atrial flutter. For reliable detection of atrial fibrillation modifications of the signal amplifier are necessary.

Aged↗
PubMed1998

Radiofrequency ablation of atrial flutter.

Atrial flutter can be understood as atrial tachycardia due to a single intra-atrial macroreentrant circuit that is determined by fixed or functional boundaries. In various types of atrial flutter, radiofrequency ablation has become an established curative therapy. During the course of an ablation procedure, five steps can be distinguished: (1) determination of the reentrant circuit; (2) identification of the boundaries; (3) proof of the participation of an isthmus between the boundaries in the reentrant circuit; (4) connection of the barriers by a linear lesion; and (5) proof that the line of block is complete. After establishing these five steps, the acute and long-term results of atrial flutter ablation are comparable to those of other supraventricular tachycardias. In this review, we discuss these principles of atrial flutter ablation with an emphasis on typical atrial flutter.

Atrial Flutter↗
PubMed2000

Risk of thromboembolism in acute atrial fibrillation or atrial flutter.

Atrial fibrillation (AF) is the most common sustained cardiac dysrhythmia, predominating in the elderly, with stroke as a potentially devastating complication. Prevention of the thromboembolic sequelae from AF remains a central focus of practicing clinicians. Although the risk of thromboembolism in chronic AF is well recognized, less is known about the potential risk of systemic embolism in acute AF. In addition, recent data support the notion of a group at considerable risk of embolism from atrial flutter, an arrhythmia typically believed to bestow little increased risk of thromboembolism. The mechanism of thrombus formation, embolization, and resolution in atrial arrhythmias is not well defined, particularly in that of acute AF or atrial flutter. The traditional concept proposes that atrial thrombus forms only after > 2 days of AF and embolizes by being dislodged from increases in shear forces. This widely accepted concept further holds that newly formed atrial thrombus, in the setting of AF, organizes over a span of 14 days. The results of studies based on observations from transesophageal echocardiography examinations have provided provocative insight into the temporal sequence of atrial thrombus formation, embolization, and resolution in AF or atrial flutter and have expanded the traditional concept of thromboembolism in these atrial dysrhythmias. Namely, left atrial thrombus may form before the onset of AF in the face of sinus rhythm. Conversion to sinus rhythm may increase the thrombogenic milieu of the left atrium. Importantly, atrial thrombus may form in the acute phase of AF. Last, thrombi may require > 14 days to become immobile or to resolve. Findings similar to those of acute AF have been reported in patients with atrial flutter and coexisting cardiac pathology. On the basis of these emerging insights fostered by the use of transesophageal echocardiography, it appears appropriate to consider anticoagulation in patients presenting with acute AF or atrial flutter with coexisting cardiac pathology predisposing to left atrial thrombus.

Acute Disease↗
PubMed1992

Comparison of atrial overdrive pacing with and without extrastimuli for termination of atrial flutter.

Atrial overdrive pacing has been successfully used to terminate atrial flutter. This study compared the efficacy of atrial extrastimuli following a rapid pacing train to overdrive pacing without atrial extrastimuli for the termination of atrial flutter. Patients were randomized to treatments of short or long burst atrial overdrive pacing or atrial overdrive pacing followed by atrial extrastimuli in a crossover study design. A total of 22 patients (73%) had successful conversion of atrial flutter to sinus rhythm. The success rates in patients exposed to each therapy, including crossover therapies, were 62% with the atrial extrastimuli method, 8% with the short burst pacing method, and 8% with the long burst pacing method (p less than 0.001). Transient atrial fibrillation developed in 15 patients and in 9 of these this arrhythmia preceded conversion to sinus rhythm. Sustained atrial fibrillation was induced in 3 additional patients but never with the atrial extrastimuli method. In conclusion, the method of delivering atrial extrastimuli after a rapid pacing train is highly efficacious for the termination of atrial flutter. Furthermore, this method is more effective than atrial overdrive pacing methods delivered at the same pacing cycle length. These observations have important implications for the programming of antitachycardia pacemakers.

Aged↗
PubMed2001

Mechanisms of antiarrhythmic drug action on termination of atrial flutter.

Atrial flutter is an important arrhythmia in clinical practice. Although the reentrant circuit of human typical atrial flutter is well characterized, the action of antiarrhythmic drugs on this tachycardia is less understood. Based on the recent clinical trials, pure Class III drugs like ibutilide or dofetilide are more effective in acute termination of human atrial flutter than Class I drugs like procainamide or flecainide. The mechanisms of drug induced termination of atrial flutter include refractory block due to cycle length oscillation, fixed block due to a reduced safety factor for conduction, or a collision of opposing wavefronts due to loss of the lateral boundaries or return reexcitation. Because ventricular proarrhythmia is a major concern with ibutilide or dofetilide therapy, development of new drugs with more specific target profiles is a future direction for treatment of human atrial flutter.

Animals↗
PubMed1998

[Radiofrequency catheter ablation of atrial flutter and atrial fibrillation].

Radiofrequency catheter ablation is now considered as a curative approach in patients with typical atrial flutter. Typical atrial flutter is due to a macrore-entrant circuit within the right atrium and it can be eliminated by a linear lesion in the isthmus between the tricuspid annulus and the vena cava inferior. The electrophysiological criterion of a bidirectional isthmus block has been shown to reduce the recurrence rate of atrial flutter after catheter ablation, thus achieving long-term cure of typical atrial flutter. Acute success rates of 85 to 90% and recurrence rates of 10 to 15% have been reported. The risk of paroxysmal atrial fibrillation continues to be clinically relevant in patients who underwent successful ablation of atrial flutter, in particular in patients with previously documented atrial fibrillation. The incidence of a new onset of atrial fibrillation after ablation of atrial flutter seems to be approximately 20%. Isthmus ablation has also been shown to be beneficial for the majority of patients with typical atrial flutter and atrial fibrillation: In addition to an elimination of typical atrial flutter the isthmus ablation apparently reduces the incidence of paroxysmal atrial fibrillation. At present, atrial fibrillation can only be treated by catheter ablation as a curative approach in the rare cases where an accessory pathway, an AV nodal re-entrant tachycardia, typical atrial flutter or an ectopic atrial tachycardia is the induction mechanism of the atrial fibrillation. The majority of patients with atrial fibrillation is apparently not amenable to a curative local ablation. While AV junction ablation and AV node modification can palliate some of the symptoms of atrial fibrillation by a control of ventricular rate, the arrhythmia persists with the loss of AV synchrony and continued risk of thromboembolism. The surgical MAZE procedure implies a compartimentation of the atria by surgical incisions resulting in areas to small to sustain the arrhythmia. Based on this procedure experimental and clinical studies are currently performed in order to develop catheter ablation cure of atrial fibrillation.

Atrial Fibrillation↗