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PubMed1984

Sustained atrial flutter after cardiac surgery: successful termination by rapid atrial pacing.

For termination of sustained atrial flutter, 28 rapid atrial stimulations were performed in 26 patients undergoing cardiac surgery, including coronary bypass surgery, and valvular heart surgery as well as surgery for primum and secundum atrial septal defect and anomalous connection of the pulmonary veins. In 18 patients rapid atrial pacing was successful in directly converting a flutter to a sinus rhythm, in 5 patients after a short period of transient atrial fibrillation. Atrial flutter could be changed to atrial fibrillation in a further 3 patients who remained in permanent atrial fibrillation and subsequently underwent DC cardioversion. Our results demonstrate that rapid atrial pacing is very effective in the treatment of sustained atrial flutter in patients following cardiac surgery and may be used alternatively to DC countershock.

Adolescent↗
PubMed1997

Relation between left atrial size and secondary atrial arrhythmias after successful catheter ablation of common atrial flutter.

Catheter ablation provides an effective cure for patients with typical atrial flutter. However, these patients may have the potential to develop atrial tachyarrhythmias other than common atrial flutter. This study examines clinical and echocardiographic predictors for the occurrence of uncommon atrial flutter or atrial fibrillation after abolition of common atrial flutter. The study population comprised 17 patients (12 men, 5 women, age 32-74 years) who underwent successful radiofrequency catheter ablation of common atrial flutter. Common atrial flutter did not recur in any patient during a median follow-up time of 8 (range 1-25) months. Within a median of 7 (range 1-223) days, however, symptomatic atrial tachyarrhythmias occurred in 8 of 17 patients (47%): uncommon atrial flutter (n = 4); atrial fibrillation (n = 3); and both uncommon atrial flutter and atrial fibrillation in one patient. Preablation left atrial volume was significantly larger in patients who developed secondary arrhythmias compared with patients who remained in sinus rhythm (57.9 +/- 15.6 vs 43.7 +/- 16.4 cm3, P < 0.05). Enlarged left atrial volume dichotomized at 51 cm3 independently predicted postablation atrial arrhythmias (X2 = 5.11, rel. risk = 5.3, P < 0.05). On Kaplan-Meier analysis, time to occurrence of postablation atrial arrhythmias was significantly shorter in patients with enlarged left atrium (P < 0.02). In conclusion, symptomatic uncommon atrial flutter and atrial fibrillation develops in a substantial proportion of patients after successful ablation of common atrial flutter. Out of a series of clinical and echocardiographic parameters, preablation left atrial size is the best predictor for the occurrence of these postablation atrial arrhythmias.

Adult↗
PubMed2001

Class IC antiarrhythmic drug induced atrial flutter: electrocardiographic and electrophysiological findings and their importance for long term outcome after right atrial isthmus ablation.

OBJECTIVE: To describe the electrocardiographic and electrophysiological findings of new atrial flutter developing in patients taking class IC antiarrhythmic drugs for recurrent atrial fibrillation, and to report the long term results of right atrial isthmus ablation in relation to the ECG pattern of spontaneous atrial flutter. DESIGN: Retrospective analysis. SETTING: Tertiary care academic hospital. PATIENTS: 24 consecutive patients with atrial fibrillation (age 54 (12) years; 5 female, 19 male) developing atrial flutter while taking propafenone (n = 12) or flecainide (n = 12). RESULTS: The ECG was classified as typical (n = 13; 54%) or atypical atrial flutter (n = 8) or coarse atrial fibrillation (n = 3). Counterclockwise atrial flutter was the predominant arrhythmia. Acute success after isthmus ablation was similar in patients with typical (12/13) and atypical (8/8) atrial flutter. After long term follow up (13 (6) months, range 6-26 months), continuation of antiarrhythmic drug treatment appeared to result in better control of recurrences of atrial fibrillation in patients with typical atrial flutter (11/13) than in those with atypical atrial flutter (4/8), but the difference was not significant. Ablation for coarse atrial fibrillation was unsuccessful. CONCLUSIONS: New atrial flutter developing in patients taking class IC antiarrhythmic drugs for recurrent atrial fibrillation has either typical or atypical flutter wave morphology on ECG. The endocardial activation pattern and the acute results of ablation suggest that the flutter circuit was located in the right atrium and that the isthmus was involved in the re-entry mechanism. There appeared to be better long term control of recurrent atrial fibrillation in patients with typical (85%) as compared with atypical atrial flutter (50%). Patients developing coarse atrial fibrillation may not be candidates for this strategy.

Adult↗
PubMed1984

[Use of transesophageal atrial stimulation in the treatment of atrial flutter. Clinical experience].

Transesophageal atrial pacing with relatively low current output and wide pulse duration has been recently reported. With this method supraventricular tachycardias can be successfully induced and terminated. In this study 23 episodes of spontaneous common atrial flutter (21 patients) were treated by rapid transesophageal atrial pacing (output of 16 Volts and pulse duration of 10 msec). Sinus rhythm resumption was obtained in 18 episodes (78.2%), directly after interruption of stimulation in 7 and following brief periods of atrial fibrillation in 11. All patients tolerated the procedure well with moderate discomfort; no complications were observed. Esophageal pacing offers a useful, rapid, minimally invasive, well tolerated method of terminating atrial flutter in the clinical practice.

Adult↗
PubMed2005

Clinical prediction of cavotricuspid isthmus dependence in patients referred for catheter ablation of "typical" atrial flutter.

INTRODUCTION: Typical atrial flutter (AFL) can be cured by catheter ablation of the cavotricuspid isthmus (CTI). The surface electrocardiogram (ECG) is not always diagnostic of isthmus dependence of AFL. The aim of this study was to evaluate clinical parameters for the prediction of isthmus-dependent AFL. METHODS AND RESULTS: Sixty consecutive adult patients without suspected atriotomy-related AFL, congenital heart disease, or previous AFL ablation, referred for catheter ablation of presumed typical AFL were studied. All patients had distinct flutter waves in the inferior leads, suggestive of CTI-dependent AFL, either on presentation to the electrophysiology (EP) lab or documented on prior ECG. Electrophysiology study was performed in the standard fashion. Patients who presented to the EP laboratory not in AFL underwent arrhythmia induction with a burst pacing protocol. A clinical history of persistent AFL (P = 0.0001) and existence of AFL on presentation to the EP laboratory (P = 0.0001) were strong predictors of CTI dependence. History of atrial fibrillation (P = 0.19), structural heart disease (P = 0.6), hypertension (P = 0.4), and previous cardiac surgery (P = 0.5), as well as the nature of AFL-related symptoms (P = 0.5), were not predictors of CTI-dependent AFL documented during EP study. CONCLUSION: In patients with ECG suggestive of typical AFL, the presence of persistent rather than paroxysmal AFL and presentation to the EP laboratory in AFL are strong predictors of CTI-dependent AFL. A paroxysmal pattern of AFL predicts noninducibility of CTI-dependent AFL during EP study. CTI ablation may therefore be less effective in these patients.

Atrial Flutter↗
PubMed2004

Atrial flutter ablation: correlation between isthmic activation times and flutter cycle.

BACKGROUND: Ablation of typical atrial flutter relies on the suppression of electrical conduction along the cavo-tricuspid isthmus. Bidirectional isthmus block is a criterion of successful ablation and is associated with the presence of different activation times on each side of the ablation line. OBJECTIVE: The aim of this study was to determine whether the difference in isthmic activation times correlates with the length of the atrial flutter cycle. POPULATION AND METHODS: We studied 31 patients with typical atrial flutter (93.6% male, mean age 66 +/- 9 years) who underwent successful ablation during tachycardia. CARTO electroanatomic mapping was used to confirm diagnosis of isthmus-dependent atrial flutter, guide the ablation line creation and assess its efficacy. At the end of the procedure, a three-dimensional activation map of the right atrium was constructed, under pacing from the coronary sinus ostium (with a 500 ms cycle). Activation times on the lateral (right) and septal (left) sides of the ablation line were measured. The difference between these two activation times was termed the difference in isthmic activation times (delta IAT), and was compared to the flutter cycle length. RESULTS: Mean activation times were 173.7 +/- 34.3 ms on the lateral border of the ablation line and 19.1 +/- 12.5 ms on the septal border. Mean delta IAT was 154.6 +/- 27.8 ms and mean atrial flutter cycle length was 257.5 +/- 30.6 ms. delta IAT and flutter cycle length were significantly correlated (r = 0.503, p = 0.0039). The linear regression equation that best described this result was: delta IAT = 37 + (0.46 x flutter cycle). CONCLUSION: After atrial flutter ablation, a difference in isthmic activation times of more than half the flutter cycle length was associated with isthmus conduction block.

Aged↗
PubMed1992

Atrial flutter--update on the mechanism and treatment.

Atrial flutter is a common and usually benign but symptomatic supraventricular tachycardia. There is a striking similarity between patients with atrial flutter suggesting a common substrate despite the presence or absence of underlying heart disease. In man, the mechanism is a single reentrant circuit originating in the right atrium whose center appears to be functional within the anatomical constraints of the right atrium. The reentrant circuit of atrial flutter contains an area of slow conduction in the inferior right atrium but the size and exact location is uncertain. Drug therapy directed at terminating and preventing atrial flutter has been available for many years. The efficacy and safety of this therapy is not as well tested as is the same therapy for atrial fibrillation. The most effective way to terminate atrial flutter is a nonpharmacological approach. Several nonpharmacological methods provide new treatment options in the management of patients with drug resistant or hemodynamically unstable atrial flutter. The use of anticoagulation for this disorder is still evolving. There is a risk of clinically apparent thromboemboli in some patients with atrial flutter although the risk appears less than that for atrial fibrillation. In the future, refinements and improvements in therapy for atrial flutter will likely be derived from a better understanding of its mechanism.

Animals↗
PubMed1991

Atrial activation sequence during atrial flutter in the canine pericarditis model and its effects on the polarity of the flutter wave in the electrocardiogram.

Stable atrial flutter induced in both conscious and open chest states was studied in 30 mongrel dogs after production of sterile pericarditis. During the conscious state studies, induced atrial flutter (mean cycle length 128 +/- 15 ms) was always sustained greater than 15 min and was stable. Three types of flutter wave polarity were noted in electrocardiogram (ECG) lead II: positive in 16 dogs, negative in 3 and flat or slightly positive in 11. Sequential site atrial mapping during atrial flutter (mean cycle length 133 +/- 18 ms) in the open chest state showed either clockwise (18 dogs) or counterclockwise (12 dogs) circus movement in the right atrium. In 19 of 30 dogs, the circus movement clearly did not require any naturally existing anatomic obstacle; in 11, the orifice of the superior vena cava probably was also involved. Double potentials were recorded from the center of the reentrant circuit during atrial flutter, and fractionated electrograms were recorded from a pivot point of the reentrant wave front. A positive flutter wave in ECG lead II (12 dogs with counterclockwise circus movement) was associated with early activation of the Bachmann's bundle region compared with the posteroinferior left atrium and activation of the left atrium mainly in a superoinferior direction. A negative flutter was associated with the early activation of the posteroinferior left atrium compared with Bachmann's bundle and activation of a considerable portion of the left atrium in an inferosuperior direction. A flat or slightly positive flutter wave (14 of 18 with clockwise circus movement) was associated with activation of the left atrium almost simultaneously by two wave fronts coming from both these sites. In conclusion, atrial flutter in this dog model is due to circus movement in the right atrium, the center of which does not necessarily require an anatomic obstacle. Although atrial flutter is generated by circus movement in the right atrium, the flutter wave polarity in the ECG is determined primarily by the activation sequence of the left atrium.

Animals↗
PubMed1996

[Facilitating effect of propafenone pretreatment in the interruption of atrial flutter by transesophageal pacing].

Transesophageal atrial pacing is effective in the interruption of atrial flutter, and being simple and minimally invasive, is easily performed even on outpatients. The influence of antiarrhythmic drugs on this procedure is controversial. We investigated whether the administration of oral propafenone may facilitate the procedure. Thirty patients with type I atrial flutter were randomized into two groups in which transesophageal pacing was attempted, respectively, without treatment (Group A) and after oral administration of propafenone 600 mg (Group B). Transesophageal pacing was effective in interrupting atrial flutter in 53% (8/15) of patients in Group A and in 85% (13/15) of patients in Group B. A significant lengthening of the flutter cycle was observed in patients treated with propafenone (261 +/- 23 vs 217 +/- 25 ms, p < 0.01). Sinus rhythm resumed at a shorter paced cycle in patients of Group A (166 +/- 13 vs 187 +/- 14 ms, p < 0.01). The transesophageal threshold for stable atrial capture was significantly lower in Group A (20.5 +/- 0.2 vs 23.3 +/- 1.2 mA, p < 0.01). In no patient the threshold for atrial capture was higher than the pain threshold. We did not observe abrupt enhancement of atrioventricular conduction. We can conclude that propafenone is effective and safe when used with transesophageal pacing in the termination of atrial flutter. The depressing effect of the drug on intraatrial conduction and the possible stabilizing effect on the reentry circuit appear to be outweighed by the positive effect of propafenone on the excitable gap of the circuit, facilitating its capture and account for the beneficial effect of the drug on arrhythmia termination.

Adult↗
PubMed1990

[Cryosurgical treatment of atrial tachyarrhythmia with atrial flutter].

Two cases of atrial tachyarrhythmias with atrial flutter requiring cryosurgical treatment are reported. In two cases, preoperative electrophysiological studies revealed supraventricular reentrant tachyarrhythmias during atrial flutter and showed enhanced conduction through the AV node that conducted atrial impulses rapidly to the ventricle. Based on intraoperative endocardial mapping, the earliest excitation site was localized along the AV node and His bundle during supraventricular tachyarrhythmias in one case. The cryosurgical treatment was administered at Koch's triangles and in one case additionally at coronary sinus. After the operation, supraventricular tachyarrhythmias were not inducible and no clinical recurrences have occurred. Normal atrioventricular conduction was preserved in two cases. We concluded that cryosurgical treatment is useful for the treatment of the atrial tachyarrhythmias.

Adult↗
PubMed2004

Long term follow up of radiofrequency catheter ablation of atrial flutter: clinical course and predictors of atrial fibrillation occurrence.

OBJECTIVES: To evaluate the time to onset and the predictors of atrial fibrillation (AF) during long term follow up of patients with typical atrial flutter (AFL) treated with transisthmic ablation. DESIGN: Prospective multicentre study. METHODS AND RESULTS: 383 patients (75.4% men, mean (SD) age 61.7 (11.1) years) who underwent transisthmic ablation for typical AFL were investigated. In 239 patients (62.4%) AF was present before ablation. Ablation proved successful in 367 patients (95.8%). During a mean (SD) follow up of 20.5 (12.4) months, 41.5% of patients reported AF. The cumulative probability of postablation AF increased continuously as time passed: it was 22% at six months, 36% at one year, 50% at two years, 58% at three years, and 63% at four years. CONCLUSIONS: AF occurred in a large proportion of patients after transisthmic catheter ablation of typical AFL. The occurrence of AF was progressive during follow up. Preablation AF, age < 65 years, and left atrial size > 50 mm are associated with postablation AF occurrence.

Atrial Fibrillation↗
PubMed1999

Transesophageal pacemaker therapy in atrial flutter after procainamide pretreatment.

Transesophageal atrial stimulation was applied in 56 patients to terminate atrial flutter. Extrastimulation and atrial burst techniques were applied using programmable stimulator (Medtronic 5328) and hexapolar esophageal electrode catheters. Thirty patients were randomized to receive digoxin pretreatment (group A), and 26 patients were randomized to receive procainamide pretreatment (group B). Efficacy of each pretreatment was evaluated by observing the change in the rhythm. In group A, transesophageal pacemaker therapy successfully converted atrial flutter to sinus rhythm in 13 patients and to atrial fibrillation in 14 patients, whereas the arrhythmia remained unchanged in the 3 remaining patients in the digitalized group. In group B, after procainamide pretreatment, sinus rhythm appeared in 19 and atrial fibrillation in 5, and no change was observed in the remaining 2 patients. Procainamide is more efficacious than digoxin (P < 0.05) in facilitating cardioversion by transesophageal stimulation.

Adult↗
PubMed1996

[Conversion rate and prevention of recurrence of paroxysmal and sustained atrial fibrillation or atrial flutter with verapamil/quinidine].

BACKGROUND: Atrial fibrillation (AF) is the most common sustained arrhythmia, occurs in 0.4% of the adult population and in as many as 2% to 4% of those 60 years of age or older. PATIENTS AND METHODS: We studied retrospectively 102 patients, 76 males, 26 females, mean age 56 +/- 12 years, with paroxysmal or sustained atrial fibrillation or atrial flutter (AFlut) treated with verapamil/quinidine (Cordichin) (dosage 3 to 5 times 1 tablet/day). Coronary artery disease was present in 39 patients, dilated cardiomyopathy in 8 patients, valvular disease in 16 patients and various etiologies were present in 13 patients. Twenty-six patients had no discernable heart disease ("Jone atrial fibrillation"). Patients with long QT-syndrome (QT-duration > or = 500 msec; QTc > or = 440 ms) were excluded from this study. RESULTS: Using verapamil/quinidine conversion to sinus rhythm (SR) was possible in 64 patients (63%) within 2 +/- 1 day (range 1 to 6 days). The mean given dosage of quinidine was significantly higher in patients converted to sinus rhythm (762 +/- 129 mg) compared to those without successful conversion (638 +/- 161 mg) (p < 0.001). Diameter of left atrium and left ventricle as well as the degree of heart failure did not influence cardioversion rate significantly. During a mean follow-up of 34 +/- 32 months (range < 1 to 129 months), sinus rhythm remained constant in 28/64 patients (44%) with verapamil/quinidine in whom conversion to sinus rhythm was successful. During follow-up, side effects were present in 20/64 patients who were discharged with verapamil/quinidine: in 2 patients (2%) a torsade de pointes tachycardia was observed (1 patient died suddenly); gastrointestinal side effects were observed in 5 patients (5%); 4 patients had sinuatrial and 3 patients atrioventricular conduction disturbances. An increase in ventricular ectopic beats were present in 3 patients and allergic reactions occurred in 3 patients. CONCLUSIONS: The present data show that verapamil/quinidine is effective in conversion of atrial fibrillation and atrial flutter to sinus rhythm and is associated with an acceptable efficacy rate in preventing recurrences of atrial fibrillation or flutter. Final conclusions concerning side effects are only possible in prospective studies that are ongoing at the present time.

Adult↗
PubMed1988

Activation sequence during atrial flutter in dogs with surgically induced right atrial enlargement: I. Observations during sustained rhythms.

The atrial activation sequences during 15 episodes of sustained atrial flutters were determined in the isolated hearts of four dogs with surgically induced right atrial enlargement (TI/PS dogs). These sequences were compared with the activation sequences of six episodes of nonsustained atrial tachyarrhythmias induced in three control hearts. Total endocardial activation of both atria during normal sinus rhythm and during the arrhythmias was determined first by recording simultaneously from 192 pairs of recording electrodes positioned into egg-shaped electrode arrays, and then by determining the moment of activation from each of the recorded electrograms. Isochronal maps of total activation were constructed by computer. Nonsustained atrial rhythms inducible in control hearts were due to circus movement excitation either in the left atrium (two episodes) or in the right atrium (four episodes). On the other hand, all 15 episodes of sustained atrial flutter induced and mapped in the TI/PS dog hearts were due to reentrant excitation in the enlarged right atrium. The reentrant pattern could be in a clockwise or counterclockwise pattern. In these episodes of stable flutter an area of functional block was an essential component to the reentrant excitation.

Animals↗
PubMed1977

Bi-morphic atrial flutter.

A case of atrial flutter whose classic "saw-tooth" morphology, resistant to full doses of digoxin and quinidine, was changed to an unusual form by low energy direct current shock is presented. The atrial and ventricular rates remained identical in spite of the different F wave pattern before and after attempted cardioversions. 0.5 mg digoxin was given after cardioversion failed and the patient reverted to normal sinus rhythm. This case strengthens the theory of rapidly discharging atrial focus as a mechanism of atrial flutter and the case for a change in intra-atrial conductions as cause for change in atrial electrograms.

Adult↗
PubMed1997

Acute effects of dual-site right atrial pacing in patients with spontaneous and inducible atrial flutter and fibrillation.

OBJECTIVES: We tested the ability of dual-site right atrial pacing to prevent atrial fibrillation (AF) or atrial flutter induced by single-site atrial pacing and correlated its efficacy with clinical patient characteristics, atrial activation times and refractory periods. BACKGROUND: Prevention of recurrent AF with long-term dual-site right atrial pacing has been demonstrated in our previous studies. However, the mechanism of antiarrhythmic benefit is unclear. METHODS: Using standard electrophysiologic methods, baseline electrocardiographic and electrophysiologic measurements (mean +/- SD) were obtained. Programmed atrial stimulation was performed for AF or atrial flutter induction. Atrial pacing was performed at two drive cycle lengths (600 and 400 ms) and followed by one to three atrial extrastimuli at one to four pacing sites in the right atrium. In patients with inducible AF or atrial flutter, reinduction was then attempted during a dual-site atrial pacing drive train. This was achieved by simultaneously pacing at the high right atrium and coronary sinus ostium at an identical rate to the baseline stimulation, with the atrial extrastimuli being delivered at the pacing site responsible for the initial AF episode initiation. RESULTS: Twenty patients (10 men, 10 women, mean [+/- SD] age 64 +/- 16 years) with symptomatic AF (n = 10) or atrial flutter (n = 10) were studied. There was a significant abbreviation of the P wave duration to 103 +/- 17 ms with dual-site pacing compared with sinus rhythm (120 +/- 12 ms, p = 0.005) and high right atrial pacing (121 +/- 17 ms, p = 0.005). This was also associated with a characteristic change in P wave configuration with an inferior and leftward axis shift. The effective refractory period at the high right atrium remained unchanged with dual-site atrial pacing compared with single-site high right atrial pacing. Sixteen patients had inducible AF or atrial flutter and could be tested after dual-site atrial pacing. The induced atrial tachyarrhythmia was suppressed in nine patients (56%), who had either induced AF (n = 5) or atrial flutter (n = 4). The difference in the effective refractory period between the high right atrium and the coronary sinus ostium pacing sites was significantly greater (33 +/- 12 ms) in patients with suppression of atrial tachyarrhythmia with dual-site atrial pacing compared with patients without suppression (15 +/- 13 ms, p = 0.001). P wave abbreviation did not correlate with arrhythmia suppression. There was no correlation between suppression of inducible AF or atrial flutter and demographic or clinical patient characteristics. CONCLUSIONS: Dual-site right atrial pacing from the high right atrium and coronary sinus ostium can suppress inducible AF or atrial flutter elicited after single-site high right atrial pacing in selected patients. Acute suppression is more likely in patients with greater dispersion of right atrial refractoriness between these two sites.

Adult↗
PubMed2006

[Management of atrial flutter in 2006].

Typical or common atrial flutter is a frequent cardiac arrhythmia related to a macroreentrant circuit located entirely within the right atrium. Risks associated with this supraventricular arrhythmia include 1 to 1 conduction with extremely rapid ventricular rates, tachycardia-mediated cardiomyopathy and thromboembolic events. Treatment of choice of atrial flutter is radiofrequency catheter ablation of the cavo-tricuspid isthmus, and this form of treatment may be considered either during the first episode or at the time of the first recurrence of atrial flutter. Anticoagulant therapy is the rule in the presence of atrial flutter because this arrhythmia favors thromboembolic complications and because atrial flutter is frequently associated with atrial fibrillation.

Anticoagulants↗