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PubMed1988

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm.

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.

Adolescent↗
PubMed1998

A canine model of atrial flutter following the intra-atrial lateral tunnel Fontan operation.

Atrial flutter (AFL) is a common problem in children who have undergone a Fontan operation for single ventricle physiology. Although this has been attributed to the atrial stretch inherent in the earlier forms of this operation, AFL has persisted in spite of a modification that minimizes atrial distension. Therefore, it was hypothesized that AFL following the modified Fontan procedure may result from anatomic barriers related to suture lines rather than from atrial stretch or hypertension. In a series of experiments performed in dogs under general anesthesia, the modified Fontan repair was simulated by placing only the suture line of the intra-atrial repair. No baffle was placed, thus avoiding any hemodynamic alterations. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were inserted through the mitral and tricuspid valves via bilateral ventriculotomies. Induction of AFL was attempted with atrial burst pacing and programmed extrastimulation, and activation sequence maps of subsequent reentry were generated from the endocardial electrodes. Atrial flutter was induced in all of 17 dogs, with a median cycle length of 177 +/- 31 ms. Activation sequence maps demonstrated conduction block along the crista terminalis corresponding to the free wall portion of the suture line. This created an isthmus between the suture line and tricuspid annulus, which appeared critical for sustaining AFL, although the circuit used both the septal and free wall surfaces of the right atrium. In seven dogs, a cryolesion was placed from the tricuspid annulus to the free wall segment of the suture line, terminating the AFL, in all seven. When the free wall segment of the suture line was moved 5 mm medial to the crista terminalis, AFL was induced in four of five dogs, but only in the presence of isoproterenol and at a shorter cycle length (136 +/- 8 ms, P < .001). Atrial flutter was not inducible, even with the addition of isoproterenol, in any of five dogs in which the suture line was placed 10 mm anterior to the crista terminalis and incorporated into closure of the atriotomy. This acute canine model of the modified Fontan operation demonstrates that conduction block from the free wall portion of the suture line creates an isthmus of tissue between the suture line and the tricuspid annulus. This is a sufficient substrate to produce AFL; no hemodynamic alteration is required. Injury to the crista terminalis is a significant risk factor in this model, which suggests that a modification of the suture line might reduce the incidence of AFL in patients following this operation.

Animals↗
PubMed1996

Ablation therapy of type I atrial flutter may eradicate paroxysmal atrial fibrillation.

In patients with paroxysms of atrial fibrillation preceded by episodes of atrial flutter on Holter monitoring, eradication of the flutter circuit may also abolish the episodes of atrial fibrillation. At electrophysiology study, these patients are identified by documentation of simultaneous flutter of the right atrium and fibrillation of the left atrium.

Adult↗
PubMed1996

Electrocardiographic patterns and results of radiofrequency catheter ablation of clockwise type I atrial flutter.

INTRODUCTION: Counterclockwise right atrial propagation is usually observed in common atrial flutter, but little is known regarding flutter with clockwise right atrial rotation. The aim of this study is to describe the ECG characteristics and results of catheter ablation of atrial flutter with clockwise right atrial rotation. METHODS AND RESULTS: Among the 38 patients with type I atrial flutter in this study population, right atrial impulse propagation was counterclockwise in 20 and clockwise in 8. In the remaining 10 patients, both clockwise and counterclockwise patterns were seen. Clinical and ECG parameters associated with clockwise flutter were compared to those of 28 cases of counterclockwise atrial flutter. Ablation was performed in 11 of 18 cases using a technique identical to that used for counterclockwise flutter. A classical "sawtooth" pattern of the flutter wave was observed in 28 of 28 counterclockwise and 14 of 18 clockwise flutter. A shorter plateau phase, a widening of the negative component of the F wave in the inferior leads, and a negative F wave in V1 were the most consistent findings in clockwise flutter. Coronary sinus recording always showed septal to lateral left atrial impulse propagation. Ablation was successful in 11 of 11 cases of clockwise flutter in whom this procedure was performed, with 9.5 +/- 11.6 radiofrequency pulses delivered between the tricuspid valve and the coronary sinus ostium (n = 5) or the inferior vena cava (n = 5), and in the proximal coronary sinus (n = 1). After a follow-up of 46.6 weeks, two recurrences of clockwise flutter were encountered, which were successfully treated with a second session. CONCLUSION: Contrary to commonly accepted concepts, clockwise rotation of atrial flutter is not an infrequent phenomenon and can mimic counterclockwise rotation. It can also be successfully ablated by radiofrequency pulses.

Atrial Flutter↗
PubMed2000

Implantable atrial defibrillator and detection of atrial flutter.

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).

Anti-Arrhythmia Agents↗
PubMed2002

Ibutilide in rapid conversion of atrial flutter in octogenarians.

INTRODUCTION: Atrial flutter is a common sustained atrial tachyarrhythmia for which frequency increases with age. Ibutilide is a novel class III antiarrhythmic agent used for the rapid cardioversion of atrial fibrillation or atrial flutter. AIM: The aim of our study was to assess the use of ibutilide in a selected population of very elderly patients (octogenarians) with recent-onset atrial flutter. METHOD: Twenty-nine consecutive elderly patients (11 male, 18 female; mean age 83 +/- 3 years; interquartile range of 10) with recent-onset atrial flutter were included in the study; none of them had signs or symptoms of severe heart failure, angina or impaired renal or hepatic function. All patients underwent a 10-minute intravenous infusion of ibutilide (0.87 mg in 10 ml). RESULTS: The rate of successful arrhythmia termination was 75.9% within a mean time of 31 +/- 20 minutes. No clinical variables were shown to be associated with successful cardioversion, although there was a tendency towards higher efficacy in patients with a shorter duration of arrhythmia. Two female patients (6.9%) developed torsade de pointes, requiring direct current cardioversion under general anaesthesia. Episodes of nonsustained ventricular tachycardia occurred in two other patients. CONCLUSION: Ibutilide appears to be an effective and well tolerated drug for rapid conversion of recent-onset atrial flutter in octogenarian patients, and may represent a valid approach in the acute management of atrial flutter in this particular set of patients.

Aged↗
PubMed2001

Effects of cavotricuspid isthmus ablation on atrioventricular node electrophysiology in patients with typical atrial flutter.

BACKGROUND: The atrial musculature in the cavotricuspid isthmus is a part of posterior inputs to the AV node. In patients with typical atrial flutter, effects of radiofrequency ablation of this isthmus on AV node conduction are still unknown. METHODS AND RESULTS: This study included 16 patients with clinically documented typical atrial flutter. Group 1 had 8 patients without and group 2 had 8 patients with dual AV nodal pathway physiology. Electrical pacing from the interatrial septum and low right atrium was performed to evaluate antegrade AV node function before and after ablation of the cavotricuspid isthmus. In group 1, the AV node conduction properties were similar before and after ablation. In group 2, the AV node Wenckebach cycle length and maximal AH interval during low right atrium (356+/-58 versus 399+/-49 ms, P=0.008; 303+/-57 versus 376+/-50 ms, P=0.008) and interatrial septum (365+/-62 versus 393+/-59 ms, P=0.008; 324+/-52 versus 390+/-60 ms, P=0.008) pacing were significantly longer after ablation. Elimination of the slow pathway after ablation was noted in 2 patients, including 1 with AV nodal reentrant echo beats. CONCLUSIONS: Radiofrequency ablation of the cavotricuspid isthmus was effective in eliminating typical atrial flutter without injury of antegrade fast AV node conduction. The atrial musculature in the cavotricuspid isthmus significantly contributed to the slow AV node conduction.

Aged↗
PubMed1999

Should ablation of atrial flutter be discouraged in patients with documented atrial fibrillation?

Atrial fibrillation and atrial flutter often coexist in the same patient. The purpose of this article is to provide an analysis of the mechanisms underlying the transformation from atrial fibrillation into atrial flutter and to investigate the long-term clinical benefits following ablation of atrial flutter in relation to recurrences of atrial fibrillation. Experimental studies in the human atrium demonstrated that in most instances atrial fibrillation is a triggering rhythm for atrial flutter. However, a review of the most recent studies shows a low percentage of recurrence of atrial fibrillation after successful catheter ablation for atrial flutter. The risk factors for this recurrence are the presence of structural heart disease, increased left atrial dimension and volume, a previous history of atrial fibrillation, and the failure of multiple antiarrhythmic drugs, inducibility of atrial fibrillation by a standard programmed electrical stimulation protocol after catheter ablation. These data, together with the high success rate of catheter ablation for atrial flutter, suggest to perform radiofrequency catheter ablation for atrial flutter in patients with documented atrial fibrillation.

Atrial Fibrillation↗
PubMed1999

Radiofrequency ablation of "class IC atrial flutter" in patients with resistant atrial fibrillation.

In some patients with atrial fibrillation, atrial flutter develops after administration of class IC antiarrhythmic drugs, the so-called class IC atrial flutter. Radiofrequency ablation of the right atrial isthmus results in clinical improvement in 85% of patients and provides an alternative management strategy for a subset of patients with therapy-resistant atrial fibrillation.

Administration, Oral↗
PubMedDate not supplied

Atrial overdrive pacing for reversion of atrial flutter after heart transplantation.

Atrial overdrive pacing is an effective treatment to terminate classic (type 1) atrial flutter. After heart transplantation, the appearance of atrial flutter may be an indication of acute allograft rejection, and in patients who have this arrhythmia we routinely perform endomyocardial biopsy. In this study we examined the efficacy of atrial overdrive pacing performed at the time of endomyocardial biopsy in the termination of atrial flutter. Endomyocardial biopsy was performed with a Caves-Scholten bioptome via a right internal jugular venous sheath. After completion of the biopsy, a J-shaped 5F bipolar pacing lead was inserted via the sheath and positioned with the lead tip directed medially against the interatrial septum or right atrial appendage. Atrial pacing was performed with stimulation rates up to 450 beats/min at 20 mA for 15 seconds. Since July 1989, 16 episodes of atrial flutter have occurred in nine patients. Twelve episodes (75%) were associated with acute rejection, which was moderate or severe in nine cases. Atrial overdrive pacing was successful in restoring sinus rhythm in 13 of 14 episodes during which it was attempted (success rate, 93%). The procedure was uncomplicated and produced minimal patient discomfort. In comparison, of eight episodes of atrial flutter (in six patients) that occurred before the routine use of atrial overdrive pacing, seven were associated with rejection. With treatment of rejection, two episodes reverted spontaneously, but on six occasions cardioversion with patients under general anesthesia was necessary to restore sinus rhythm. In conclusion, atrial flutter occurring after heart transplantation is usually associated with acute allograft rejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗
PubMed2003

Conduction properties of the crista terminalis in patients with atrial flutter due to amiodarone therapy for atrial fibrillation.

Some patients with atrial fibrillation (AF) treated by antiarrhythmic drugs (AAD) can develop typical atrial flutter, but the mechanism is not clear. This study included 21 patients with AF. Group I (n = 7) had typical atrial flutter due to amiodarone therapy. Group II (n = 7) did not develop atrial flutter after amiodarone treatment. Group III (n = 7) did not receive AAD treatment. A 7 Fr, 20-pole electrode catheter was placed along the CT identified by fluoroscopy and intracardiac echocardiography. After restoration of the sinus rhythm, decremental pacing near the CT was performed until 2 to 1 atrial capture. Complete transverse conduction block was defined as the appearance of double potentials with opposite activation sequence along the CT. Focal transverse conduction delay was defined as the appearance of double potentials at > or = 2 recording sites. Focal transverse conduction delay was observed during pacing at the cycle length of 693 +/- 110 ms in group I, 360 +/- 97 ms in group II and 343 +/- 109 ms in group III (P = 0.001). Complete transverse conduction block was observed during pacing at the cycle length of 391 +/- 118 ms in group I and 231 +/- 23 ms in group II (P = 0.001), but not in group III. In conclusion, focal transverse conduction delay in the CT was common in patients with AF. A predisposition to the line of the conduction block in the CT might contribute to the conversion of AF to typical atrial flutter due to amiodarone therapy.

Aged↗
PubMed1999

Maintenance of sinus rhythm with oral d,l-sotalol therapy in patients with symptomatic atrial fibrillation and/or atrial flutter. d,l-Sotalol Atrial Fibrillation/Flutter Study Group.

Currently d,l-sotalol is widely used to prevent recurrence of atrial fibrillation and/or atrial flutter, although a randomized dose-response study has not previously been conducted to guide therapy for this indication. This study summarizes findings of a double-blind, placebo-controlled, multicenter, randomized trial evaluating the efficacy, safety, and dose-response relation of 3 fixed doses of d,l-sotalol (80, 120, and 160 mg twice daily) for the maintenance of sinus rhythm in 253 patients with atrial fibrillation and/or atrial flutter. All patients were in sinus rhythm at randomization. Treatment (69 patients on placebo, 59 on 80 mg, 63 on 120 mg, and 62 on 160 mg given twice daily) was continued for 12 months or until documented recurrence of symptomatic atrial fibrillation and/or flutter. Transtelephonic electrocardiographic monitoring was used to detect symptomatic recurrences. Demographic characteristics were not different in the 4 groups. Structural heart disease was present in 57% of patients. Patients with a history of heart failure were excluded. The time from randomization to symptomatic arrhythmia recurrence was significantly longer in the 2 higher d,l-sotalol dose groups than in the placebo group. The median times to recurrence were 27, 106, 229, and 175 days for the placebo, 80, 120, and 160 mg groups, respectively. There were no deaths or cases of torsade de pointes, sustained ventricular tachycardia, or ventricular fibrillation reported. Thus, d,l-sotalol appeared to be both safe and effective in maintaining sinus rhythm in patients with symptomatic atrial fibrillation and/or flutter. Further, the 120-mg twice daily dose appeared to provide the most favorable benefit and/or risk.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

Effects of pharmacologic agents on induced atrial flutter in dogs with right atrial enlargement.

The effects of selected drugs on the sustained atrial flutter induced in conscious dogs with surgically produced right atrial enlargement (TI dogs) were evaluated. This was done to better understand the electrophysiologic mechanism of the tachyarrhythmias. Agents known to cause a slowing of atrioventricular (AV) nodal conduction--verapamil, methacholine, and phenylephrine--did not significantly decrease the rate of the induced flutter, whereas beta-adrenergic stimulation with an infusion of isoproterenol increased the rate of the flutter in all trials. Propranolol and atropine had little effect on the atrial flutter rate. Agents known to increase atrial refractoriness, such as procainamide, n-acetylprocainamide, bretylium, and clofilium, all increased the cycle length of the induced flutter and, in some cases, terminated the arrhythmia. These results suggest then that the perpetuation of the sustained atrial flutter in the conscious TI dog is not due to a delayed afterdepolarization mechanism but is more likely due to reentrant excitation. Furthermore, it is unlikely that the flutter is due to reentry over a pathway involving the AV node; rather, the arrhythmia seems to be caused by reentrant excitation of the leading circle type.

Acecainide↗
PubMed1990

Demonstration of an area of slow conduction in human atrial flutter.

Ten patients with chronic atrial flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of atrial flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from greater than or equal to 30 right atrial sites for each patient during atrial flutter demonstrated that right atrial free wall activation was craniocaudal and that the interatrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during atrial flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a "missing" interval of electrical activity occurred in the inferior right atrium for an average of 40% of the atrial flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right atrial pacing. The mean activation time from the high right atrial pacing site to the coronary sinus (inferior left atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of atrial flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right atrial pacing during sinus rhythm at rates similar to atrial flutter demonstrated a short activation time to the coronary sinus and low right atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during atrial flutter. Thus, atrial mapping and pacing data were complementary, indicating that human atrial flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during atrial flutter.

Atrial Flutter↗