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PubMed2003

Review of diagnosis, treatment, and outcome of fetal atrial flutter compared with supraventricular tachycardia.

OBJECTIVE: To review the diagnosis, treatment, and outcome of fetal atrial flutter compared with supraventricular tachycardia. DESIGN: Retrospective review of published reports: 11 papers about fetal tachyarrhythmia published between 1991 and 2002 were selected for review. MAIN OUTCOME MEASURES: All selected studies were analysed for the type of arrhythmia, degree of atrioventricular block in atrial flutter, occurrence of hydrops fetalis, gestational age at diagnosis, first and second line drug treatment, associated cardiac and extracardiac malformations, and mortality of the fetuses. RESULTS: Atrial flutter accounted for 26.2% of all cases of fetal tachyarrhythmias, and supraventricular tachycardia for 73.2%. Hydrops fetalis was reported in 38.6% and 40.5% of fetuses with atrial flutter and supraventricular tachycardia, respectively (NS). Hydropic fetuses with atrial flutter had higher ventricular rates (median 240 beats/min, range 240-300) than non-hydropic fetuses (220 beats/min, range 200-310) (p = 0.02), whereas the atrial rates were not significantly different (median 450 beats/min, range 370-500). Digoxin treatment resulted in a higher conversion rate in non-hydropic fetuses with fetal tachyarrhythmias than in hydropic fetuses (p < 0.001). The overall mortality of atrial flutter was similar to that of supraventricular tachycardia, at 8.0% v 8.9% (p = 0.7). CONCLUSIONS: The prevalence of hydrops fetalis did not differ in fetal atrial flutter and supraventricular tachycardia with 1:1 conduction. There was no difference between the response rate to digoxin in fetus with atrial flutter or supraventricular tachycardia. Mortality was similar in the two types of tachyarrhythmia.

Anti-Arrhythmia Agents↗
PubMed2005

Clinical comparison of ibutilide and propafenone for converting atrial flutter.

OBJECTIVE: To evaluate the efficacy and safety of intravenous ibutilide and propafenone for immediate treatment of atrial flutter. METHODS: Forty patients with atrial flutter with an arrhythmia duration of three hours to 90 days were randomized to receive up to two 10-minute infusions of ibutilide (1 and 1 mg) or propafenone (70 and 70 mg) with a 10-minute interval. RESULTS: Ibutilide was superior to propafenone for treating atrial flutter (90% vs. 30%, p < 0.01). The median conversion time in the ibutilide group was 11 min (the 25th and 75th percentile was 10 and 45 min), and the median conversion time in the propafenone group was 35 min (range 20-55 min). In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was more obvious in the group that received ibutilide. Conversion of atrial flutter by ibutilide was characterized mainly by increased cycle length variability. Bradycardia (2/20) and hypotension (4/20) were more common side effects with propafenone. Of 20 patients given ibutilide, 8 (40%) who developed monomorphic ventricular extrasystoles or repetitive atrial flutter with aberrant conduction tachycardia, no one required any specific treatment except for the interruption of ibutilide infusion. CONCLUSION: Ibutilide is highly effective for rapidly terminating atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.

Adult↗
PubMed1998

Unipolar waveforms and monophasic action potentials in the characterization of slow conduction in human atrial flutter.

Anisotropic propagation may be involved in the development of areas of slow conduction in atrial flutter. We evaluated monophasic action potentials (MAPs) and simultaneous unipolar (0.2-400 Hz) and bipolar electrograms from multiple atrial sites of patients undergoing RF ablation of idiopathic atrial flutter. Nine patients (mean age 46 +/- 20 years) with typical atrial flutter (one with both types) were studied. Unipolar electrograms with triphasic complexes of small amplitude and with a slow, negative deviation of the baseline preceding the rS deflection indicated transversal conduction in relation to the orientation of cardiac fibers; smooth rS complexes longitudinal conduction; QS complexes onset of activation; and R complexes end of activation or collision. In all patients with typical atrial flutter, slow conduction occurred in the corridor between the inferior vena cava, the tricuspid annulus, and the coronary sinus. Transversal conduction was observed in this area, whereas the remaining sites showed longitudinal conduction. Anatomically guided RF ablation was successful in five patients. Transversal conduction was recorded in all successful sites. In the patient with atypical atrial flutter, slow conduction was noted in the high lateral right atrium, also exhibiting transversal conduction. Ablation at this area terminated the arrhythmia. All the areas of transversal conduction during flutter displayed longitudinal conduction after restoration of sinus rhythm. MAPs were normal in all patients during atrial flutter and sinus rhythm, even at the areas where transversal conduction was recorded. These findings suggest that anisotropic propagation is involved in the genesis of functionally determined areas of slow conduction during typical atrial flutter.

Action Potentials↗
PubMed1993

A shared pathway in atrioventricular nodal reentrant tachycardia and atrial flutter: implications for pathophysiology and therapy.

Atrioventricular (AV) nodal reentrant tachycardia and atrial flutter are considered 2 distinct supraventricular tachycardias. Recent clinical and experimental data suggest that both these tachycardias include an area in the lower right atrial septum in their reentrant pathways. This study was designed to test the hypothesis that there is an association between the mechanisms of AV nodal reentrant tachycardia and atrial flutter because of a shared pathway of reentry. Consecutive patients referred for evaluation and management of supraventricular tachycardia, thought to be due to AV nodal reentry, underwent electrophysiologic testing protocols designed to induce both AV nodal reentrant tachycardia and atrial flutter, if present. Fifteen of 29 patients (52%) had both AV nodal reentrant tachycardia and atrial flutter induced during electrophysiologic testing. Seven of these 15 patients (47%) underwent transcatheter radiofrequency current application (mean power 34 +/- 4 W) against the tricuspid annulus above the coronary sinus. In each patient, neither AV nodal reentrant tachycardia nor atrial flutter could be induced after the procedure. Repeat study after successful ablation (mean 6 days) showed no inducible supraventricular arrhythmia of either type at baseline study or during isoproterenol infusion. Atrial flutter occurs frequently (15 of 29 patients; 52%) in patients with AV nodal reentrant tachycardia, because of a shared pathway in their reentry circuits. Because of this shared pathway, both arrhythmias can be ablated at the same site. These observations promote new insights into the mechanism and therapeutics of supraventricular tachycardias.

Adult↗
PubMed1993

Characterization and surgical ablation of acute atrial flutter following the Mustard procedure. A canine model.

BACKGROUND: A high incidence of refractory atrial flutter has been reported as a late postoperative complication of the Mustard procedure. The objective of this study was to reproduce experimentally the long-cycle-length atrial flutter that occurs in these patients and attempt to ablate the arrhythmia surgically. METHODS AND RESULTS: Nine dogs underwent a simulated Mustard procedure, which included a longitudinal right atriotomy, a septectomy, and a continuous suture line placed in the usual baffle location. All animals were subsequently inducible into sustained atrial flutter after surgery. Activation-time electrophysiological maps of the various pathways of atrial reentry were determined using atrial endocardial molds containing 252 bipolar electrodes. Four distinct reentrant circuits were observed in the following locations: (1) around the tricuspid value annulus (n = 5; cycle length, 175 +/- 5 milliseconds), (2) around the atriotomy incision (n = 2; cycle length, 208 +/- 3 milliseconds), (3) in a pathway involving both atria (n = 1; cycle length, 180 milliseconds), and (4) around the mitral valve (n = 1; cycle length, 135 milliseconds). A common pathway for eight of the nine reentrant circuits included the free-wall segment of the right atrium (excluding the mitral valve circuit). In the first three animals, surgical ablation of the atrial flutter was not attempted, but an incision made perpendicular to the atriotomy down to the tricuspid valve annulus resulted in termination of the atrial flutter in the other six animals. One of these animals was subsequently inducible into an atrial flutter of different morphology (cycle length, 125 milliseconds) that involved an isolated left atrial reentrant circuit. CONCLUSIONS: The Mustard procedure creates several anatomic substrates that increase the probability of the heart to develop atrial flutter, and these may be amenable to subsequent surgical correction.

Animals↗
PubMed2004

Results of catheter ablation of typical atrial flutter.

The purpose of this study was to evaluate the safety and efficacy of radiofrequency (RF) ablation of typical atrial flutter by using an 8-mm electrode catheter and a 100-W RF power generator. A limitation of previous trials of catheter ablation of atrial flutter is that the data were not collected as part of a prospective multicenter clinical trial. The study results associated catheter ablation of typical atrial flutter in a cohort of 150 patients with an 88% acute efficacy rate. At 6-month follow-up, recurrent typical atrial flutter was observed in 13% of patients. Of the 12 patients with typical atrial flutter recurrence, 4 were symptomatic and 8 were asymptomatic. Procedure duration was a significant predictor of typical atrial flutter recurrence. The 12-month rate for development of atrial fibrillation was 30%. Catheter ablation of atrial flutter was associated with significant improvements in 5 of 8 domains of the Short Form 36 Survey (quality of life) and significant decreases in 13 of the 16 symptoms of the Symptom Checklist. The device- or procedure-related complication rate was 2.7%. Skin burns occurred at the dispersive pad site due to stronger RF power in 3 patients. Use of a dual dispersive pad system mitigated this problem. Thus, the results of this study associated catheter ablation of atrial flutter with high acute efficacy, a small risk of recurrent atrial flutter, and an important risk of atrial fibrillation during follow-up.

Aged↗
PubMed2002

[A case of atrial flutter after umbilical venous catheterization].

UNLABELLED: Isolated atrial flutter is an extremely rare form of supraventricular tachycardia in the neonatal period. It may be initiated by central venous catheterization. CASE REPORT: A male infant was born at 35 weeks by cesarean section for placenta praevia. He was eutrophic. Apgar score was 10 at 1 and 5 minutes. He secondary developed a respiratory distress syndrome. He was then ventilated by nasal CPAP. Immediately after an umbilical venous catheterization, a tachycardia appeared without preexistent cardiac dysfunction. An intravenous dose of adenosine (Striadyne) showed a characteristic sawtooth pattern of P waves on inferior leads. The cardiac-US examination was normal. This atrial flutter was converted to normal sinus rhythm by transoesophageal pacing, without adjunction of antiarrhythmic drugs. The newborn was weaned from mechanical ventilation 48 hours later and discharged from hospital at seven days post natal age. His development and clinical examination were normal two months later. CONCLUSION: The isolated atrial flutter is rare in the neonate. It may be triggered by a venous catheterization. Transoesophageal atrial pacing is safe and effective for conversion.

Adenosine↗
PubMed1994

[Intracardiac treatment of atrial flutter by radiofrequency currents].

Though not as common as atrial fibrillation, atrial flutter is frequently encountered in everyday cardiological practice. Though generally thought to be benign, it may be difficult to treat both in respect to its conversion to sinus rhythm and prevention of recurrences. It is often poorly tolerated. There are resistant, invalidating forms for which catheter ablation of the His bundle may be considered as a last resort. This is only a palliative measure even if effective from the functional point of view. A new technique for treating atrial flutter by a direct action on the atrial tissue has been recently introduced. The basis of this method is the concept of circus movement of the activation in the right atrium, the wave front circulating in an anti-clockwise direction in common atrial flutter. The postero-inferior region of the right atrium, at Koch's triangle, is the site of slow conduction and the target of choice for catheter ablation. The detection of this zone is determined by the endocavitary recording of fragmented, prolonged electrogrammes and by atrial stimulation techniques. The application of radiofrequency currents on these bases (high energy shocks are rarely used nowadays) results in interruption of atrial flutter. However, there are no data available concerning the long-term efficacy of this technique. Since 1992, our group has used an anatomical approach for catheter ablation. This aims to apply the radiofrequency current on the isthmus of atrial tissue between the orifice of the inferior vena cava and the tricuspid annulus through which the flutter wave front passes to reach the interatrial septum.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗
PubMed1978

Atrial pacing for cardioversion of atrial flutter in digitalized patients.

To test the safety and reliability of atrial pacing as a conversion technique in patients with atrial flutter who are receiving digitalis therapy, atrial pacing conversion was attempted for 49 episodes of atrial flutter in 32 consecutive patients. All patients except one were receiving digitalis. To control ventricular rates most patients had received larger than usual therapeutic doses of digitalis glycoside before pacing. Fourteen of the 25 patients whose serum levels were measured had glycoside concentrations greater than 2 ng/ml. Before atrial pacing the mean atrial and ventricular rates were, respectively, 290 +/- 20.6 and 134 +/- 27.9/min (mean +/- standard deviation). Successful rhythm conversion was achieved on 48 occasions (98%) in 31 patients. One patient required transthoracic direct current synchronized countershock cardioversion. With atrial pacing, the atrial flutter rhythm reverted immediately to sinus mechanism in 23 instances, and there were 25 episodes of atrial fibrillation. Among those who experienced atrial fibrillation, the rhythm spontaneously reverted to sinus mechanism within 24 hours on 14 occasions; on 11 occasions; the rhythm reverted to atrial flutter and repeat pacing was required. Sinus mechanism was eventually established in all 31 patients.

Adult↗
PubMed2003

[Systemic embolism after reversion to sinusal rhythm of persistent atrial flutter].

BACKGROUND: The incidence of embolism in atrial flutter has been underestimated in the routine clinical practice. PATIENTS AND METHODS: In this study the incidence of thromboembolic events after restoration of sinus rhythm (by catheter ablation or cardioversion) was compared in two groups of consecutive patients, with a different anticoagulation protocol. A total of 169 patients were evaluated. A first retrospective analysis of 79 non anticoagulated patients (group I). A second prospective group of 90 patients who were treated with an anticoagulation protocol (group II) similar to that for patients with atrial fibrillation. All had typical atrial flutter of at least one month's duration before the procedure. RESULTS: The mean age of patients in group I was 61 12 years and the mean left ventricular ejection fraction was 57 6%. Patients in group II had a mean age of 61 10 years and the mean left ventricular ejection fraction was 56 9%. No differences were observed regarding prevalence of structural cardiopathy, arterial hypertension, diabetes mellitus, left ventricular dysfunction, atrial size or atrial fibrillation between the two groups of patients. Four patients in the retrospective analysis (5%) had an embolic event associated with the procedure, compared with 0 (0%) in the group of patients treated with the anticoagulation protocol. The efficient anticoagulation was associated with a lower risk of thromboembolic events (p < 0.05). CONCLUSIONS: The incidence of embolic events after reversion to sinusal rhythm of persistent atrial flutter can be decreased. These patients should follow the same recommendations of anticoagulation that apply for patients with persistent atrial fibrillation that are going to be reverted to sinus rhythm.

Anticoagulants↗
PubMedDate not supplied

Organised atrial fibrillation simulating atrial flutter.

We present a case of drug-refractory paroxysmal atrial fibrillation in which episodes of AF spontaneously alternated with a regular arrhythmia resembling atrial flutter. Isthmus-dependent atrial flutter was initially diagnosed and the patient was treated with cavotricuspid isthmus ablation. Two months later the patient returned with recurrent arrhythmias. On the 12-lead ECG there was again evidence of atrial flutter with both typical and atypical characteristics. On electrophysiological study, careful mapping revealed that the regular rhythm actually represented organised slow atrial fibrillation. Circumferential pulmonary vein ablation resulted in the abolition of both arrhythmias.

Atrial Fibrillation↗
PubMed1999

[Radiofrequency ablation as the first line of treatment in patients with common atrial flutter. The arguments pro].

Radiofrequency ablation of atrial flutter may be performed nowadays with 90% probability of success, 10% of recurrences and a very low risk of complications; thus the indications of the procedure have lately expanded. However, there are still many discrepancies among different groups in the way to approach the acute and the chronic therapy for atrial flutter. Acute as well as chronic antiarrhythmic therapy has a limited effectivity and carries a risk of proarrythmia and extracardiac secondary effects. On the other hand, the potential risk of embolism during chronic therapy and after cardioversion is often underestimated. Another important issue often neglected is the tachycardiomyopathy secondary to the sustained high rate at the atrium and also at the ventricular level. The delay in the definitive therapy worsens the atrial remodelling and may promote the development of atrial fibrillation. We consider that radiofrequency ablation of atrial flutter is the first therapeutic option, and it should be attempted when the patient is seen, without further delay. In that way, the above mentioned potential risks are avoided, and for this reason, this is our common approach to therapy.

Anticoagulants↗
PubMed1991

Natural history of isolated atrial flutter in infancy.

To clarify the natural history of isolated (i.e., without associated congenital cardiac anomalies) atrial flutter in infancy, we reviewed the clinical course in nine patients who were seen with this arrhythmia in the first year of life (range 1 day to 4 months). Atrial flutter was identified by the typical sawtooth pattern in leads II, III, and aVF of the surface electrocardiogram or the pattern of atrial flutter on an atrial electrogram recorded through the esophagus. The mean cycle length of the atrial flutter was 151 msec (atrial rate 397 beats/min). Six of the nine patients had other perinatal problems, such as immune and nonimmune hydrops fetalis (two patients), pneumonia (one patient), anemia (five patients), or low birth weight (one patient). In all patients the rhythm reverted to normal, either spontaneously (two patients), with overdrive pacing (four patients), or after oral digoxin therapy (three patients). No consistent temporal relationship between digoxin administration and conversion was observed; conversion was instantaneous in the four patients who received atrial overdrive pacing. Four patients were discharged receiving digoxin therapy (6 months to 1 year). One patient had supraventricular tachycardia after discharge that was controlled with digoxin. No recurrence of atrial flutter was observed among the nine patients during a mean follow-up of 6.8 years (range 0.2 to 20 years). We conclude that isolated atrial flutter in infancy is rare, has a good prognosis, may be related to transient perinatal events, and often spontaneously converts to normal sinus rhythm; however, when it does not, it will respond to transesophageal pacing. Acute and chronic digoxin therapy is probably unnecessary.

Apgar Score↗
PubMed1997

Atrial flutter: historical background.

For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiology in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified inferiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.

Animals↗
PubMed1992

Autodecremental pacing for the interruption of ventricular tachycardia and atrial flutter.

The efficacy and safety of autodecremental pacing (ADP) to interrupt ventricular tachycardia (VT) and atrial flutter was examined. Once tachycardia was recognized, ADP was initiated using a short train of stimuli with gradual shortening (3%) of the interstimulus interval. ADP was applied to 13 consecutive patients during 75 episodes of VT (mostly following induction by ventricular stimulation). Successful interruption of VT occurred in 88% of the episodes. In 6 episodes (8%), ADP resulted in ventricular fibrillation and in 3 episodes VT was unaffected by ADP. The only significant discriminator between the failure or success of ADP was the rate of VT. ADP was also applied to 17 consecutive patients with an atrial flutter that was resistant to conventional antiarrhythmic agents. Successful conversion of atrial flutter to sinus was seen in only 8 patients (47%). A temporary acceleration to atrial fibrillation appeared in 3 patients (18%), and in 6 patients atrial flutter was unaffected by ADP. ADP was successful in 70% (7/10) of patients with type 1 (< 300 beats/min) atrial flutter. The authors conclude that ADP is beneficial in the interruption of VT and atrial flutter in a selected group of patients, especially with a slower rate of tachyarrhythmia (atrial rate during atrial flutter < 300 beats/min and ventricular tachycardia < 180 beats/min).

Adult↗
PubMed1999

New insights regarding the atrial flutter reentrant circuit : studies in the canine sterile pericarditis model.

Background-We studied atrial activation during induced atrial flutter in the canine sterile pericarditis model to test the hypothesis that the atrial flutter reentrant circuit includes a septal component. Methods and Results-We studied 10 episodes of induced, sustained (>5 minutes) atrial flutter in 9 dogs. In all episodes, the reentrant circuit included a septal component. In 6 episodes, there were 2 reentrant circuits, one in the right atrial free wall and the second involving the atrial septum, Bachmann's bundle, and the right atrial free wall; both circuits shared a pathway in the right atrial free wall (figure-of-eight). The direction (superior or inferior) of the septal wave front of the second circuit correlated with the direction (clockwise or counterclockwise, respectively) of the right atrial free-wall circuit. A line of functional block in the right atrial free wall was part of both reentrant circuits. In the other 4 atrial flutter episodes, only 1 reentrant circuit was present, with activation in an inferior-to-superior direction in the septum and a superior-to-inferior direction in the right atrial free wall in 2 episodes and in the opposite direction in the other 2 episodes. In all atrial flutter episodes, the flutter wave polarity in ECG lead II was determined by the direction of activation in the left atrium; polarity was positive when the direction was superior to inferior and negative when the direction was inferior to superior. Conclusions-In this model of atrial flutter, the reentrant circuit (1) always included a septal component, (2) did not always require a right atrial free-wall reentrant circuit, (3) demonstrated figure-of-eight reentry when a reentrant circuit was present in the right atrial free wall, and (4) was associated with a line of functional block in the right atrial free wall.

Animals↗
PubMed1998

Impaired atrial contraction in patients with atrial flutter and gradual recovery after cardioversion.

The risk of thromboembolism after cardioversion of atrial flutter is controversial. The present study provides evidence for blood stasis in the atria of patients with atrial flutter and for gradual recovery of atrial contraction after cardioversion, which justifies prophylactic treatment at cardioversion, as for atrial fibrillation. We examined atrial thrombi and peak flow velocity in the left atrial appendage as an index of blood stasis in 5 consecutive patients with atrial flutter. Transesophageal echocardiography revealed a thrombus in 1 patient, and peak flow velocity in the left atrial appendage was inversely correlated with left atrial dimension (r = -0.90, p < 0.05). After restoration of sinus rhythm, transmitral flow velocity in late diastole was also examined to evaluate the recovery of atrial contraction. The recovery of transmitral flow velocity the next day and 1 week after cardioversion was correlated with flow velocity in the left atrial appendage before cardioversion (r = 0.89, p < 0.05; r = 0.97, p < 0.01, respectively). These findings suggest that some patients with atrial flutter have impaired atrial contraction and that prolonged impairment after cardioversion is also possible. Atrial enlargement and low flow velocity in the atrial appendage were predictive factors for such patients.

Aged↗
PubMed1985

Atrial flutter in the young: a collaborative study of 380 cases.

As children with cardiac disease grow older, atrial flutter becomes more prevalent. A collaborative study was performed in 19 institutions to determine the clinical characteristics of these children and the factors affecting prognosis. There were 380 patients with one or more electrocardiographically documented episodes of atrial flutter that first occurred between ages 1 and 25 years (mean age at onset 10.3). Episodes of flutter continued to occur for a mean of 2.5 years after the onset. Of the 380 patients, 60% had repaired congenital heart disease, 13% palliated congenital heart disease, 8% unoperated congenital heart disease, 8% an otherwise normal heart, 6% cardiomyopathy, 4% rheumatic heart disease and 2% other lesions. Overall, drugs were effective in eliminating atrial flutter in 58% of patients; specifically, amiodarone and digoxin plus quinidine were effective in 53%, digoxin alone in 44% and propranolol in 21%. Amiodarone was effective in seven (78%) of nine patients. Corrective surgery was performed after the onset of atrial flutter in 66 patients; in 52% the atrial flutter was easier to control or it resolved and in only 4% it was worse. At follow-up (mean 6.5 years), 83% of the patients were alive (49% without atrial flutter and 34% with atrial flutter) and 17% died (10% suddenly, 6% of nonsudden cardiac cause and 1% of noncardiac cause). Cardiac death occurred in 20% of those for whom an effective drug could not be found to eliminate atrial flutter compared with 5% of those who were treated with an effective drug (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗