Termination of atrial flutter by atrial pacing demonstrated through intracavitary recordings.
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Action Potentials↗
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Electroshock for atrial flutter and atrial fibrillation. Follow-up studies on 50 patients.
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Adult↗
Electrophysiologic basis, surgical development, and clinical results of the maze procedure for atrial flutter and atrial fibrillation.
After more than a decade of experimental and clinical research into the basic mechanisms underlying atrial fibrillation, we were able to develop a surgical procedure that appears to cure the arrhythmia. This surgical procedure has been used in 100 patients in our institution and in a total of approximately 130 patients by surgeons in other institutions. The surgical results have been excellent, which indicates the sophisticated electrophysiologic mapping systems are unnecessary and that the results are not surgeon-specific.
Animals↗
Linear ablation of the isthmus between the inferior vena cava and tricuspid annulus for the treatment of atrial flutter. A study in the canine atrial flutter model.
BACKGROUND: The isthmus between the inferior vena cava and the tricuspid annulus has been shown to be involved in the reentry circuit of common atrial flutter. The effects of radio-frequency catheter ablation of this isthmus were examined in the canine model of atrial flutter due to reentry around the tricuspid annulus. METHODS AND RESULTS: A model of atrial flutter was prepared in 11 of 14 dogs by creating intercaval and connected transverse lesions (Y-shaped lesion). Bipolar electrodes were attached at 24 atrial sites, and computer-assisted mapping was performed. Stable atrial flutter with a cycle length of 133 +/- 11 ms was repeatedly induced by rapid atrial pacing in all dogs, and atrial mapping revealed reentry around the tricuspid annulus including the isthmus. In 6 dogs, the isthmus was ligated during atrial flutter (mechanical ablation). In the other 5 dogs, a 7F large-tip electrode catheter was placed at the isthmus under a fluoroscopic control. Radiofrequency energy (25 W for 30 s) was delivered to three sequential sites from the tricuspid annulus to the inferior vena cava to ablate the isthmus linearly. Atrial flutter was terminated in all dogs after mechanical and radio-frequency ablation of the isthmus and was not induced again. Atrial pacing from the posterior left atrium during sinus rhythm demonstrated intra-atrial conduction block at the isthmus after ablation. Pathological examination of the isthmus showed transmural myocardial damage. CONCLUSIONS: Linear radiofrequency ablation of the isthmus can induce intra-atrial conduction block and is effective as a curative therapy for atrial flutter when the reentry circuit involves the isthmus.
Animals↗
Detection of atrial-flutter and atrial-fibrillation waveforms by fetal magnetocardiogram.
Two cases of fetal tachycardia are reported: atrial flutter and fibrillation. The waveforms from each case were detected by fetal magnetocardiograms (FMCGs) using a 64-channel superconducting quantum interference device (SQUID) system. Because the magnitude of supraventricular arrhythmia signals is very weak, two subtraction methods were used to detect the fetal MCG waveforms: subtraction of the maternal MCG signal, and subtraction of the fetal ORS complex signal. It was found that atrial-flutter waveforms showed a cyclic pattern and that atrial-fibrillation waveforms showed f-waves with a random atrial rhythm. Fast Fourier transform analysis determined the main frequency of the atrial flutter to be about 7Hz, and the frequency distribution of atrial fibrillation consisted of small, broad peaks. To visualise the current pattern, current-arrow maps, which simplify the observation of pseudo-current patterns in fetal hearts, of the averaged atrial flutter and fibrillation waveforms were produced. The map of the atrial flutter had a circular pattern, indicating a re-entry circuit, and the map of the atrial fibrillation indicated one wavelet, which was produced by a micro-re-entry circuit. It is thus concluded that an FMCG can detect supraventricular arrhythmia, which can be characterised by re-entry circuits, in fetuses.
Atrial Fibrillation↗
Effects of flecainide on termination of atrial flutter by rapid atrial pacing.
Rapid atrial pacing is effective in terminating atrial flutter, but often results in transient or permanent atrial fibrillation rather than sinus rhythm. Class Ia antiarrhythmic drugs have earlier been shown to facilitate the direct conversion of atrial flutter to sinus rhythm. The present study was performed to test the hypothesis that flecainide, a group 1c antiarrhythmic drug, increases the direct conversion to sinus rhythm. In a series of 30 consecutive clinical episodes of atrial flutter treated with rapid atrial pacing, 12 episodes were in patients on flecainide treatment (group A), while in 13 episodes no patients were on group I antiarrhythmic drugs (group B). Direct conversion to sinus rhythm was achieved more often in group A (75%) than in group B (31%) P = 0.034. Both the flutter rates and the pacing rates used were lower in group A, 240 vs 280 beat.min-1 and 375 vs 430 b.min-1, respectively. Patients with atrial flutter in whom rapid atrial pacing is to be performed should be considered for pretreatment with flecainide.
Adult↗
Response of atrial flutter to overdrive atrial pacing and intravenous disopyramide phosphate, singly and in combination.
Ten patients who suffered spontaneous paroxysms of atrial flutter were investigated by electrophysiological techniques. Two had overt Wolff-Parkinson-White syndrome; three Lown-Ganong-Levine syndrome; and one a concealed accessory atrioventricular connection. Atrial flutter was initiated, at study, by right atrial pacing and electrograms from the right atrium and coronary sinus were observed for at least five minutes to ensure stable flutter in both atria. Atrial flutter was terminated by 2.5 s or 5 s bursts of atrial pacing at rates 10, 50, or 100 beats/min faster than the intrinsic flutter rate in only two patients. Atrial flutter, which was reinitiated in two patients, was then treated with intravenous disopyramide phosphate, 2 mg/kg body weight, infused over five minutes. In all 10 patients the atrial rate slowed from a mean of 310 +/- 39 beats/min to 217 +/- 27 beats/min and atrial flutter terminated in one case. Though the mean ventricular rate fell from 161 +/- 52 beats/min to 156 +/- 45 beats/min the atrioventricular conduction ratio fell from 2.17 +/- 0.86 to 1.55 +/- 0.59 and four patients were left with symptomatically significant increases of ventricular rate. In seven of nine patients overdrive atrial pacing, repeated after disopryamide, resulted in the conversion of atrial flutter to sinus rhythm. In this study, overdrive atrial pacing and intravenous disopyramide, singly and in combination, terminated atrial flutter in nine of the 10 patients and it is suggested that this method may provide an effective alternative to direct current cardioversion.
Adult↗
[Catheter ablation of atrial flutter and paroxysmal atrial fibrillation].
Radiofrequency catheter ablation has emerged as a curative therapy for atrial flutter based on studies demonstrating the role of the cavotricuspid isthmus. With a high rate of success and minimal complications, catheter ablation is the therapy of choice for patients with the common type of atrial flutter. Left atrial flutter, non-cavotricuspid isthmus dependent, and those associated with heart disease have a worst outcome with catheter ablation. Radiofrequency catheter ablation has also emerged as a curative therapy for paroxysmal atrial fibrillation based on studies demonstrating the role of triggering foci in the pulmonary veins for the initiation of atrial fibrillation. Catheter ablation is performed by a transseptal approach using radiofrequency energy at the ostium of each pulmonary vein. Mapping is guided by special catheters. Sequential radiofrequency applications eliminates or dissociates pulmonary vein muscle activity. Although complications exists, this is the only curative method for these patients.
Atrial Fibrillation↗
Chronic nicotine in hearts with healed ventricular myocardial infarction promotes atrial flutter that resembles typical human atrial flutter.
The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were administered nicotine (5 mg.kg(-1).day(-1) sc) for 1 mo using osmotic minipumps. High-resolution epicardial (1,792 bipolar electrodes) and endocardial Halo catheters were used to map activation during induced atrial rhythms. Nicotine promoted inducible sustained AFL at a mean cycle length of 134 +/- 10 ms in all MI dogs (n = 6) requiring pacing and electrical shocks for termination. No AFL could be induced in MI dogs (n = 6), control (non-MI) dogs (n = 3) not exposed to nicotine, and dogs with no MI and exposed to nicotine (n = 3). Activation maps during AFL showed a single reentrant wavefront in the right atrium that rotated either clockwise (60%) or counterclockwise (40%) around the crista terminalis and through the isthmus. Ablation of the isthmus prevented the induction of AFL. Nicotine caused a significant (P < 0.01) but highly heterogeneous increase in atrial interstitial fibrosis (2- to 10-fold increase in left and right atria, respectively) in the MI group but only a 2-fold increase in the right atrium in the non-MI group. Nicotine also flattened (P < 0.05) the slope of the epicardial monophasic action potential duration (electrical restitution) curve of both atria in the MI but not in non-MI dogs. Two-dimensional simulation in an excitable matrix containing an isthmus and nicotine's restitutional and reduced gap junctional coupling (fibrosis) parameters replicated the experiments. Chronic nicotine in hearts with MI promotes AFL that closely resembles typical human AFL. Increased atrial interstitial fibrosis and flattened electrical restitution are important substrates for the AFL.
Animals↗
Dual echocardiographic determination of atrial contraction sequence in atrial flutter and other related atrial arrhythmias.
We have applied the new technique of dual echocardiography to determine the sequence of atrial contraction as reflected in the simultaneously recorded movements of the tricuspid and mitral valves. The study group included 29 normal subjects and 23 patients with either atrial flutter, coarse atrial fibrillation or atrial tachycardia with block. In normal individuals, right atrial contraction preceded left atrial contraction, with an average interatrial contraction time of 17 +/- 8 msec. In contrast, the atrial contraction sequence was reversed in atrial flutter, with left preceding right atrial contraction and a prolonged interatrial contraction time of 82 +/- 20 msec. In two patients with atrial tachycardia with block, atrial contraction was either simultaneous or left preceded right atrial contraction by a brief interval. The sequence of atrial excitation, as determined by electrode catheter recordings from the right and left atria in one patient with atrial flutter and one patient with normal sinus rhythm, was the same as the contraction sequence. Left atrial pacing reversed both excitation and contraction sequences. After cardioversion of three patients from atrial flutter to normal sinus rhythm, interatrial contraction time was shortened but remained longer than in normal subjects, suggesting an interatrial conduction disturbance in patients with atrial flutter. In coarse atrial fibrillation, the contraction sequence varied. Significant motion of both mitral and tricuspid valves coincident with fibrillary waves occurred frequently, especially when the fibrillary waves were coarse and regular. Dual echocardiography permits the noninvasive determination of the sequence of atrial contraction and excitation, and may be useful in studying the characteristics of atrial arrhythmias.
Atrial Fibrillation↗
Catheter ablation of inducible atrial flutter, in combination with atrial pacing and antiarrhythmic drugs ("hybrid therapy") improves rhythm control in patients with refractory atrial fibrillation.
UNLABELLED: Atrial flutter or tachycardia may coexist with atrial fibrillation [AF] and can be treated with ablation techniques in attempt to reduce the total AF burden. The role of ablation of latent atrial tachyarrhythmias elicited at electrophysiologic study in conjunction with atrial pacing and antiarrhythmic drugs in patients with refractory AF has not been evaluated. We evaluated the efficacy of catheter ablation of electrically induced atrial flutter or atrial tachycardia in improving rhythm control in patients with refractory AF. METHODS: Consecutive patients with refractory AF, and spontaneous atrial flutter (Group 1) or without spontaneous atrial flutter (Group 2) underwent programmed stimulation in a baseline drug-free state. All patients had electrically induced atrial flutter or tachycardia. Radiofrequency ablation of the arrhythmia substrate was performed in all patients. Primary endpoints evaluated for patient outcome in both groups included maintenance of rhythm control and freedom from recurrent atrial tachyarrhythmias. RESULTS: Forty-three patients, with a mean age of 66 +/- 13 years were studied. Group 1 consisted of 22 patients while Group 2 had 21 patients. Ablation of the tricuspid valve-inferior venacaval isthmus was performed in 41 patients who had common atrial flutter induced at electrophysiologic study. Ablation of other atrial sites was performed in 8 patients with induced atypical flutter and 4 patients with induced atrial tachycardia. Ten of these patients had ablation of more than one arrhythmia. 17 patients (40%) had atrial pacing instituted and 28 patients remained on a class 1/3 antiarrhythmic drug. During a mean follow-up of 26 +/- 14 months, 33 patients (82.5%) remained in rhythm control. Actuarial analysis showed 96% of patients in rhythm control at 6 months, 94% at 12 months, and 90% at 24 months. Freedom from symptomatic AF recurrence was 64% at 6 months, 58% at 12 months, and 42% at 24 months. The outcome for both of these endpoints was similar for Group 1 and Group 2 (p = NS). The AF free interval increased significantly from 7+/- 9 days to 172 +/- 121 days (p < 0.01) after ablation. This increase was again similar in both the groups. In the 14 patients were who did not receive atrial pacing and who remained on the same class 1/3 antiarrhythmic drug, the AF free interval increased from 18 +/- 17 days to 212+/- 102 days (p < 0.01). CONCLUSIONS: We conclude that electrophysiologic studies can elicit latent atrial flutter or tachycardia in patients with refractory AF without spontaneous monomorphic atrial tachyarrhythmias. Catheter ablation of electrically induced atrial flutter or tachycardia either alone, or with atrial pacing and with antiarrhythmic drug may improve rhythm control and reduce AF recurrences. This is similar in patients with and without spontaneous atrial flutter and refractory AF.
Aged↗
Induction of nonsustained atrial flutter by programmed atrial stimulation in children: incidence, mechanisms, and clinical implications.
Nonsustained atrial flutter was induced by programmed atrial extrastimulation in 6 (4%) of 137 children with preoperative congenital heart defects, who underwent electrophysiologic evaluation as part of cardiac catheterization. None of these patients had ECG or clinical evidence of arrhythmias. Atrial reentry was induced by programmed atrial extrastimulation in these six patients at coupling intervals slightly longer than the coupling interval at which flutter was induced. The flutter cycle length was similar to the atrial refractory periods. The duration ranged between 0.4 second and 60 seconds. The PA interval and the duration of the P wave were normal in all of the patients. Five of the six had normal PR intervals. It is concluded that nonsustained atrial flutter may be induced by programmed atrial extrastimulation in dysrhythmia-free children. The cycle length is determined by atrial refractoriness and, contrary to adults with clinical atrial flutter, prolonged PA and P wave duration are not predisposing factors.
Adolescent↗
Catheter ablation of atypical atrial flutter and atrial tachycardia within the coronary sinus after left atrial ablation for atrial fibrillation.
OBJECTIVES: The goal of this study was to describe the prevalence and ablation of coronary sinus (CS) arrhythmias after left atrial ablation for atrial fibrillation (AF). BACKGROUND: The CS has been implicated in a variety of supraventricular arrhythmias. METHODS: Thirty-eight patients underwent mapping and ablation of atypical flutter that developed during (n = 5) or after (n = 33) ablation for AF. Also included were two patients with focal CS arrhythmias that occurred during an AF ablation procedure. A tachycardia was considered to be originating from the CS if the post-pacing interval in the CS matched the tachycardia cycle length and/or if it terminated during ablation in the CS. RESULTS: Among the 33 patients who developed atypical flutter late after AF ablation, 9 (27%) were found to have a CS origin. Overall, 16 of the 40 patients in this study had a CS arrhythmia. The tachycardia was macro-re-entrant in 14 patients (88%) and focal in two patients. Radiofrequency ablation with an 8-mm-tip catheter was successful in 15 patients (94%) without complication. In eight patients (50%), > or = 45 W was required for successful ablation. Thirteen of the 15 patients (87%) with a successful ablation acutely remained arrhythmia-free during 5 +/- 5 months of follow-up. CONCLUSIONS: The musculature of the CS serves as a critical component of the re-entry circuit in approximately 25% of patients with atypical flutter after ablation for AF. The CS may also generate focal atrial arrhythmias that may play a role in triggering and/or maintaining AF. Catheter ablation of these arrhythmias in the CS can be performed safely.
Arrhythmia, Sinus↗
Conduction velocity in the tricuspid valve-inferior vena cava isthmus is slower in patients with type I atrial flutter compared to those without a history of atrial flutter.
INTRODUCTION: In human type I atrial flutter, the electrophysiologic substrate is unclear. In order to determine if slow conduction is mechanistically important, we evaluated conduction velocity in the tricuspid valve-inferior vena cava (TV-IVC) isthmus, right atrial free wall, and interatrial septum in patients with and without a history of atrial flutter undergoing electrophysiologic study. METHODS AND RESULTS: Nine patients with (group 1) and nine without a history of type 1 atrial flutter (group 2) were studied. Conduction time (msec) in the right atrial free wall, TV-IVC isthmus (bidirectional), and interatrial septum was measured during pacing in sinus rhythm at cycle lengths of 600, 500, 400, and 300 msec from the low lateral right atrium and coronary sinus ostium. Conduction velocity (cm/sec) was calculated by dividing the distance between pacing electrodes and sensing electrodes (cm) by the conduction time (sec). Conduction velocity was slower in the TV-IVC isthmus in group 1 (range 37 +/- 8 to 42 +/- 8 cm/sec) versus group 2 (range 50 +/- 8 to 55 +/- 9 msec) at all pacing cycle lengths (P < 0.05). However, conduction velocity was not different in the right atrial free wall or interatrial septum between groups 1 and 2. Conduction velocity was also slower in the TV-IVC isthmus than in the right atrial free wall and interatrial septum in group 1 patients, at all pacing cycle lengths (P < 0.05). Atrial flutter cycle length correlated with total atrial conduction time (r > or = 0.832, P < 0.05). CONCLUSION: Slow conduction in the TV-IVC isthmus may be mechanistically important for the development of human type I atrial flutter.
Aged↗
Entrainment mapping of dual-loop macroreentry in common atrial flutter: new insights into the atrial flutter circuit.
INTRODUCTION: The aim of this study was to determine using entrainment mapping whether the reentrant circuit of common type atrial flutter (AFL) is single loop or dual loop. METHODS AND RESULTS: In 12 consecutive patients with counterclockwise (CCW) AFL, entrainment mapping was performed with evaluation of atrial electrograms from the tricuspid annulus (TA) and the posterior right atrial (RA) area. We hypothesized that a dual-loop reentry could be surmised from "paradoxical delayed capture" of the proximal part of the circuit having a longer interval from the stimulus to the captured beat compared with the distal part of the circuit. In 6 of 12 patients with CCW AFL, during entrainment from the septal side of the posterior blocking line, the interval from the stimulus to the last captured beat was longer at the RA free wall than at the isthmus position. In these six patients with paradoxical delayed capture, flutter cycle length (FCL) was 227 +/- 12 ms and postpacing interval minus FCL was significantly shorter at the posterior blocking line than at the RA free wall (20 +/- 11 ms vs 48 +/- 33 ms, P < 0.05). In two of these patients, early breakthrough occurred at the lateral TA. A posterior block line was confirmed in all six patients in the sinus venosa area by intracardiac echocardiography. CONCLUSION: Half of the patients with common type AFL had a dual-loop macroreentrant circuit consisting of an anterior loop (circuit around the TA) and a posterior loop (circuit around the inferior vena cava and the posterior blocking line).
Adult↗
Management of atrial flutter.
Typical atrial flutter is a macroreentrant arrhythmia of the right atrium. The isthmus area between the tricuspid annulus, the inferior vena cava, and the ostium of the coronary sinus is a critical zone of the reentry circle. Atrial flutter has been treated with class I and III antiarrhytmic drugs to maintain sinus rhythm, with moderate success. Catheter ablation has been highly successful in treating atrial flutter. A contiguous line of bidirectional electrical block is created in the isthmus area between the tricuspid annulus and the inferior vena cava by application of radiofrequency energy. In patients with both atrial flutter and atrial fibrillation, ablation of the atrial flutter circuit may make the atrial fibrillation more easy to control. Quality of life assessments show improvement after ablation of atrial flutter. With a probability of success of 90%, a recurrence rate of 5% to 15%, and few complications, catheter ablation emerges as the best treatment of recurrent, symptomatic flutter.
Animals↗
The induction of atrial flutter and fibrillation and the termination of atrial flutter by esophageal pacing.
In patients with Wolff-Parkinson-White syndrome (WPW), it is important to assess the ventricular response during atrial flutter or fibrillation since conduction across the accessory pathway during these atrial rhythms may cause hemodynamic impairment or life-threatening ventricular arrhythmias. We have recently reported the effective use of an esophageal electrode in pacing the atrium. In this study we prospectively assessed the ability to induce atrial flutter and fibrillation by esophageal pacing in 23 patients with WPW or other electrophysiological abnormalities. An esophageal bipolar electrode with 29 mm interelectrode distance was positioned in the esophagus to record the most rapid and largest esophageal electrogram (mean distance of 36.6 +/- 2.9 cm (SD) from the nares). Pacing was performed at cycle lengths of 40-340 ms (mean 166 +/- 72), pulse durations of 7.0-9.9 ms, and currents of 10-25 mA. Atrial flutter alone was induced in 6 patients, fibrillation alone in 11 patients, and both arrhythmias in 5 patients. In one patient neither flutter nor fibrillation was induced by esophageal pacing, and fibrillation was induced only with difficulty using intracavitary pacing. Of the 11 patients with flutter, the arrhythmia was terminated in 8 by esophageal pacing at cycle lengths of 160-220 ms (mean 176 +/- 18 ms). All patients tolerated the procedure well with only mild to moderate discomfort. Therefore, esophageal pacing appears to offer an effective, well tolerated method of initiating atrial fibrillation and flutter and terminating atrial flutter and offers a potentially useful noninvasive method of following patients serially.
Adolescent↗
Pseudoatrial flutter: artifact simulating atrial flutter caused by a transcutaneous electrical nerve stimulator (TENS).
A patient with previous actual atrial flutter had what appeared to be atrial flutter seen on Holter monitoring during treatment with a transcutaneous electrical nerve stimulation (TENS) unit. This proved to be artifact caused by the unit rather than a true arrhythmia. The artifact was reproduced in a normal volunteer by application of a TENS unit.
Adult↗