Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Atrial Flutter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed1993

Lessons learned from computerized mapping of the atrium. Surgery for atrial fibrillation and atrial flutter.

The supraventricular arrhythmias of atrial fibrillation (AF), both chronic and paroxysmal, and atrial flutter (AFL) have been more difficult to study than most other clinical arrhythmias. Initial epicardial mapping studies at Washington University in canine models and in patients undergoing surgical ablation of other supraventricular arrhythmias demonstrated that AFL resulted from a macroreentrant circuit that was thought to occur only on the right side of the atrium with passive depolarization of the left atrial tissue. Atrial fibrillation was initially demonstrated to be considerably more complex with multiple circuits present. Furthermore, these circuits occurred simultaneously on both the right and left atria. Inability to map the atrial septum and the orifices of the pulmonary veins, however, led to the development of second-generation form-fitting experimental endocardial templates for the canine studies and an endocardial right atrial template for the patient studies. These second-generation experimental maps demonstrated that AFL circuits could involve the fixed anatomic obstacles of the right and left atria and adjacent areas of conduction block, frequently involving the septal and pulmonary vein tissue, with passive depolarization of the contralateral atrium. In contrast to this single-circuit mechanism, AF was confirmed to result from varying degrees of multiple reentrant circuits, occurring transiently in time and migrating over the surface of both atria. Furthermore, the single clinical arrhythmia of AF could result from a spectrum of endocardially or epicardially mapped arrhythmias, ranging from rapid AFL with variable atrioventricular block on one end to very fine multiple-circuit AF on the other end. It was clear that the development of a surgical procedure to ablate AF would need to isolate the atrial tissue in such a way that the transient reentrant circuits responsible for AF could not form because they were extinguished by a fixed or surgically created (eg, a suture line) anatomic obstacle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Electrocardiographic and electrophysiologic characterization of atypical atrial flutter in man: use of activation and entrainment mapping and implications for catheter ablation.

INTRODUCTION: Although the circuit in typical counterclockwise atrial flutter has been clearly delineated, the mechanisms of "atypical atrial flutters" have been less well characterized. The purpose of this study was to investigate the ECG and electrophysiologic (EP) characteristics of atypical atrial flutter. METHODS AND RESULTS: Thirty-three patients with at least one form of atypical atrial flutter underwent EP evaluation with multipolar atrial activation and entrainment mapping. Nineteen patients with clockwise flutter had: (1) stereotypic ECG morphology; (2) same cycle length as counterclockwise flutter; (3) clockwise activation around the tricuspid annulus; (4) recording of discrete split potentials along the length of the crista terminalis, suggesting the presence of conduction block; (5) concealed entrainment from the low right atrial isthmus; (6) successful ablation in this isthmus. Twenty patients with atypical flutter not consistent with a clockwise mechanism ("true atypical flutter") showed: (1) heterogeneous ECG morphology; (2) cycle length shorter than that of clockwise flutter; (3) frequent transitions from and to atrial fibrillation; (4) could be entrained in only six patients and, when accomplished, demonstrated surface fusion when entraining from the low right atrial isthmus. CONCLUSIONS: Atypical flutter falls into two broad categories. Clockwise flutter uses the same circuit with the same endocardial barriers as its counterclockwise counterpart and is best considered a form of typical flutter. True atypical flutter induced in the EP laboratory is a heterogeneous group of arrhythmias that are transitional to atrial fibrillation. Although it may superficially resemble clockwise or counterclockwise flutter based on the 12-lead ECG alone, the distinction can be readily made from a combined evaluation including activation and entrainment mapping.

Adult↗
PubMed1993

[Atrial flutter and tachy-systole].

Atrial flutter and tachysystoles may complicate the course of all heart diseases or may be discovered independently of any detectable cardiopathy. Functional tolerance mainly depends on the presence and severity of the associated heart disease, if any. A regular cardiac rhythm of 150 beats/minutes at rest suggests a 2:1 block flutter. Electrocardiographic identification of the disorder is usually easy and may lead, in certain cases, to vagal manoeuvres to recognize the atriogramme and the atrium-ventricle relationship. In all cases, 2:1 flutters must be reduced with amiodarone, by electrical stimulation or by electric shock. A prophylactic treatment of recurrences is often, but not always, indicated. The treatment of tachysystoles must take into account the cause of the ventricular rate.

Atrial Flutter↗
PubMed1981

Fetal cardiac arrhythmia: antepartum diagnosis of a case of congenital atrial flutter.

A case of antepartum atrial tachyarrhythmia was detected in the 36th week of pregnancy. Cardiotocograph recordings done twice daily enabled close surveillance of the fetal condition after oxytoxin challenge testing had failed to show evidence of hypoxia. After a diagnosis of fetal cardiac arrhythmia had been made, elective caesarean section in the 40th week of pregnancy resulted in delivery of an infant in atrial flutter and cardiac failure. Both these problems were soon resolved by cardioversion and subsequent treatment with digoxin. Cardiac catheterisation showed no underlying cardiac abnormality. Increasing use of antenatal cardiotocography may show that intrauterine tachyarrhythmias are more common than had generally been believed.

Arrhythmias, Cardiac↗
PubMed1970

Use of propranolol in atrial flutter.

Seven consecutive patients with atrial flutter are described, in six of whom sinus rhythm was restored by a combination of digoxin and propranolol. It is suggested that propranolol, used in this way, is a valuable addition to the available measures for the control of this arrhythmia.

Adult↗
PubMed1984

Atrial flutter and maprotiline: case report.

Atrial flutter developed in an 80-year-old woman after 10 days of treatment with maprotiline at therapeutic concentrations. This cardiac irregularity is extremely rare with the conventional antidepressants. Evidence is reviewed to suggest that the likely mechanism was reuptake blockade of noradrenergic amines stimulating reentrant excitation within the atria.

Aged↗
PubMed2000

Prospective randomized comparison of antiarrhythmic therapy versus first-line radiofrequency ablation in patients with atrial flutter.

BACKGROUND: Despite the high success rate of radiofrequency (RF) ablation, pharmacologic therapy is still considered the standard initial therapeutic approach for atrial flutter. OBJECTIVE: We prospectively compared the outcome at follow-up of patients with atrial flutter randomly assigned to drug therapy or RF ablation. METHODS: Patients with at least two episodes of symptomatic atrial flutter in the last four months were randomized to regimens of either antiarrhythmic drug therapy or first-line RF ablation. After institution of therapy, end points included recurrence of atrial flutter, rehospitalization and quality of life. RESULTS: A total of 61 patients entered the study, 30 of whom were randomized to drug therapy and 31 to RF ablation. After a mean follow-up of 21 +/- 11 months, 11 of 30 (36%) patients receiving drugs were in sinus rhythm, versus 25 of 31 (80%) patients who underwent RF ablation (p < 0.01). Of the patients receiving drugs, 63% required one or more rehospitalizations, whereas post-RF ablation, only 22% of patients were rehospitalized (p < 0.01). Following RF ablation, 29% of patients developed atrial fibrillation which was seen in 53% of patients receiving medications (p < 0.05). Sense of well being (pre-RF 2.0 +/- 0.3 vs. post-RF 3.8 +/- 0.5, p < 0.01) and function in daily life (pre-RF 2.3 +/- 0.4 vs. post-RF 3.6 +/- 0.6, p < 0.01) improved after ablation, but did not change significantly in patients treated with drugs. CONCLUSION: In a selected group of patients with atrial flutter, RF ablation could be considered a first-line therapy due to the better success rate and impact on quality of life, the lower occurrence of atrial fibrillation and the lower need for rehospitalization at follow-up.

Aged↗
PubMed2003

Electrocardiographic and electrophysiological characteristics of atrial fibrillation organized into atrial flutter by oral administration of class I antiarrhythmic agents.

The aim of this study was to evaluate the electrocardiographic (ECG) and electrophysiological characteristics of atrial fibrillation (AF) that organized into atrial flutter during oral administration of class I antiarrhythmic agents. The former clinical study included 72 consecutive patients (58 paroxysmal AF, 14 persistent AF) in whom class I antiarrhythmic agents were orally administered in the outpatient clinic for termination or prophylaxis of AF. The clinical background and ECG variables were compared between the patients with and without atrial flutter during class I antiarrhythmic agents therapy. An electrophysiological study was performed in ten patients with paroxysmal AF (five with [group A] and five without atrial flutter [group B] during oral class I antiarrhythmic agents therapy. Local electrograms from five different atrial sites (high and low right free wall, high and low septum, and distal coronary sinus) were analyzed during induced AF. The activation pattern of the right free wall during AF was also analyzed using a Halo catheter. Atrial flutter was documented during class I antiarrhythmic agents therapy in 14 (24%) patients with paroxysmal AF, whereas in none with persistent AF. The mean cycle length (f-f interval) and amplitude of the fibrillation waves in leads II and V1 from the surface ECG were significantly greater in the patients with than in those without atrial flutter. In the electrophysiological study, the mean cycle lengths for the low and high right free wall were significantly longer in group A than in group B, whereas those for the low septums and distal coronary sinus did not differ between the two groups. During the induced AF, the ratio of time exhibiting a consistent activation pattern (cranio-caudal, caudo-cranial, or undetermined) along the right free wall was significantly greater in group A than in group B. Atrial flutter newly developed during class I antiarrhythmic agents therapy in patients with coarse AF on the surface ECG and a relatively organized activation in the right atrial free wall. The observation of these findings may facilitate the identification of candidates for hybrid pharmacologic and ablative therapies.

Administration, Oral↗
PubMed1990

[Are double potentials an indication of reentry? Intra-atrial catheter mapping in atrial flutter].

A local doubling of atrial potentials was demonstrated in 40 out of 49 electrophysiological investigations with intraatrial catheter-mapping during atrial flutter. Such doubled potentials can be localized in small areas of the right atrium. In these circumscribed areas the distances between the doubled potentials vary. A predilection area inside the right atrium was not detected. The doubled potentials were found in different sites varying from patient to patient: 15 times in the upper, 13 times in the middle, and 12 times in the lower areas of the atrium. In each patient there was a particular reproducible place, where the doubled potentials were found. Sequential activation time mapping seems to show atrial excitation spreading from the area where the doubled potentials were found. We interpreted these findings as evidence of a reentry-circuit. However, the reentry-circuit apparently does not use preexisting anatomical obstacles, but rather a circumscribed pathological alteration in the atrium.

Adult↗
PubMed2005

Mechanism of propensity to atrial fibrillation in patients undergoing isthmus ablation for typical atrial flutter.

UNLABELLED: Mechanism of propensity to atrial fibrillation. BACKGROUND: Patients undergoing isthmus ablation for atrial flutter (AFL) may reveal postablation atrial fibrillation (AF). The electrophysiological mechanism is unclear. In patients with idiopathic AF, enhanced spatial dispersion of right atrial refractoriness was the substrate for the initiation of AF. We hypothesize that dispersion of right atrial refractoriness in patients undergoing AFL ablation is the major cause of postablation AF. METHODS: Consecutive patients (n=42) undergoing isthmus ablation for typical AFL were included. Twelve right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol, starting with one extrastimulus, followed by more aggressive pacing until AF was induced. Mean fibrillatory intervals were used to assess local refractoriness of each recording site. Spatial dispersion of right atrial refractoriness was calculated as the coefficient of dispersion (CD-value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). A CD-value of 3.0 or less was defined as normal, whereas CD-value greater than 3.0 was considered enhanced dispersion. PES and refractoriness analysis were followed by isthmus ablation. RESULTS: Of the 42 patients, 29 had CD-value of 3.0 or less. In these 29 patients, AF was induced with 1 extrastimulus in only 1 patient, with 2 extrastimuli in 4 patients and burst pacing was required to induce AF in 24 of these 29 patients. Prior to the procedure, 5 of 29 patients had AF episodes, after ablation 6 of 29 patients. Of the 42 patients, 13 had CD-value greater than 3.0, AF was induced with a single extrastimulus in 11 patients, with 2 extrastimuli in the remaining 2 patients. Of the 13 patients, 11 had AF episodes both before and after ablation (P<0.001). CONCLUSION: Enhanced spatial dispersion of right atrial refractoriness may be the substrate for propensity to AF in patients with AFL. The substrate was associated with enhanced inducibility of atrial fibrillation.

Atrial Fibrillation↗
PubMed1975

Congenital atrial flutter.

Two cases of congenital atrial flutter, one of which was documented electrocardiographically before birth, are reported. In both patients sinus rhythm was restored with digoxin treatment; in one patient the transition was preceded by various arrhythmias. No cardiac malformation was found in either case, and no materal disease occurred during pregnancy. Both mothers had received medication during pregnancy, but its role as a causative factor is questionable.

Atrial Flutter↗
PubMed1997

[Radiofrequency ablation of resistant atrial flutter: a new anatomical approach].

Several reports have suggested that radiofrequency ablation could prevent atrial flutter resistant to antiarrhythmic therapy. The usual recommendation is to apply the radiofrequency current in a zone situated between the tricuspid valve and orifice of inferior vena cava. The aim of this study was to assess the efficacy of another site of ablation of flutter extending from the tricuspid valve to the orifice of the coronary sinus, either alone or associated with a site between the coronary sinus and the lateral wall of the right atrium. Twenty patients aged 42 to 78 years (mean : 6 +/- 11 years) were included. Atrial flutter was paroxysmal in 15 patients and chronic in 5 patients. Each patients had documented failure of 1 to 5 antiarrhythmic agents (average 3.1 +/- 1.6). The site of ablation was localised by anatomical criteria alone. During follow-up of 7 +/- 5 months (range 1 to 18 months), 13 patients had no recurrence of atrial flutter after ablation, 5 patients had recurrence and 2 patients had paroxysmal atrial fibrillation alone: the success rate was 15/20 (75%). This study suggests that the zone between the tricuspid valve and coronary sinus may be a site for radiofrequency ablation of atrial flutter. It is valuable alternative to the usually recommended technique.

Adult↗
PubMed1981

Double Wenckebach phenomenon in atrioventricular node and His bundle. Electrophysiological demonstration in a case of atrial flutter.

In a case of atrial flutter with a 9:2 atrioventricular response, the only possible way to explain the conduction pattern was 3:1 block in the atrioventicular node (which is 3:2 Wenckebach sequence in the N zone and a 2:1 block at the junction of the node with the bundle of His) plus 3:2 Wenckebach sequence distal to the H deflection. The recording of the His bundle deflection confirmed this analysis.

Aged↗
PubMed1995

Nonpharmacologic approaches to the treatment of atrial fibrillation and atrial flutter.

The high prevalence of atrial fibrillation, the associated morbidity and mortality, the absence of safe and effective drug therapy, and an increased understanding of the pathophysiologic basis of atrial fibrillation and flutter have collectively led to the development of novel nonpharmacologic treatments for the management of these arrhythmias, including the CORRIDOR and MAZE surgical procedures, catheter-based ablation and modification of AV conduction, catheter-based ablation of atrial flutter and fibrillation, and internal atrial defibrillation. These surgical and catheter-based techniques offer potentially curative therapy while sparing the long-term risk of antiarrhythmic drug therapy. For patients with typical atrial flutter, catheter ablation affords to cure rate in excess of 70%. As technological innovations further facilitate identification and ablation of the critical isthmus in the floor of the right atrium, success rates should improve substantially. For patients with atrial fibrillation, AV junction ablation with implantation of a rate-responsive ventricular pacemaker should be considered palliative therapy, as should modification of AV junction conduction. The MAZE procedure offers very high cure rates, but because it currently involves open heart surgery, patient selection is critical. Catheter-based procedures emulating aspects of the MAZE procedure may one day offer cure rates comparable to those of the surgery itself, but additional research and technological development are necessary to further define and refine the minimal effective procedure, and then to facilitate the placement of contiguous, full-thickness lesions in precise three-dimensional configurations. In the interim, the implantable automatic atrial defibrillator may offer a means for rapidly restoring sinus rhythm without the risks of long-term antiarrhythmic drug therapy.

Atrial Fibrillation↗
PubMed1996

Elucidating the mechanisms of atrial flutter cycle length variability using power spectral analysis techniques.

BACKGROUND: The mechanism of the small beat-to-beat variations in cycle length of atrial flutter in humans has not been fully explained. We investigated the beat-to-beat control of atrial flutter cycle length using time and frequency analysis techniques. METHODS AND RESULTS: Mean, SD, and power spectra of atrial cycle lengths were calculated from atrial recordings in 28 patients with type I atrial flutter. In control patients, mean and SD values of atrial cycle length were 265 +/- 37 and 4.9 +/- 1.7 ms. Power spectra contained two or three major peaks with 10.6 +/- 9.2% in band 1 (0.0 to 0.18 Hz), 26.7 +/- 15.9% in band 2 (0.18 to 0.6 Hz), and 63.1 +/- 17.7% in band 3 (0.6 to 2.2 Hz). Isoproterenol infusion (n = 8) increased percentage of total power in band 1 (7.1 +/- 5.6% to 25.7 +/- 18.9%, P < .001). Percentage of total power in band 1 was less in patients receiving (n = 5) versus not receiving (n = 18) oral beta-blockers (2.2 +/- 1.9% versus 10.6 +/- 9.2%, P = .003). Standard deviation (2.5 +/- 1.3 versus 4.9 +/- 1.7 ms, P = .009) and total power (2025 +/- 1350 versus 9768 +/- 8874 ms2, P = .005) were less in heart transplant recipients (n = 5) than control patients. Increases in respiratory rate (n = 6) shifted band 2 frequency peak to higher frequencies (0.26 +/- 0.13 to 0.38 +/- 0.18 Hz, P < .05). Atrial cycle length was longer and monophasic action potential duration was shorter during inspiration than during expiration. Band 3 frequency peak was correlated with heart rate (r = .797, P < .0001). CONCLUSIONS: Atrial flutter cycle length variability has an underlying periodic pattern that is detected by spectral analysis. Atrial flutter is modulated on a beat-to-beat basis by an interplay between the autonomic nervous and respiratory systems and the ventricular rate.

Adrenergic beta-Antagonists↗
PubMed1977

Atrial flutter. Tracing an elusive arrhythmia.

Seven bried case reports representing variations of atrial flutter point up important considerations bearing on diagnosis: situations predisposing individuals to atrial flutter with 1:1 atrioventricular conduction, the need for special care in placing ECG leads for continuous monitoring, the use of carotid sinus massage to unmask atrial flutter, the infrequent but not rare association of Wenckebach block, the possible presence of diffuse disease of the conduction system, the possibility of initiation of atrial tachyarrhythmia by a premature atrial impulse, and possible inherent limitations of routine ECGs.

Aged↗
PubMed1975

Right atrium monophasic action potentials during atrial flutter and fibrillation in man.

Monophasic action potentials recorded in two patients with atrial flutter and one patient with atrial fibrillation showed a nonuniform depolarization of the right atrial wall. In each of the two patients with atrial flutter, there was a site where two separate action potential deflections were recorded for each flutter wave. It was supposed that this was the site of re-entry for a cycling wavelet subsidiary to the main flutter wave. In the patient with atrial fibrillation, three types of electric atrial activity were found: regular activity at 180 per minute similar to that found in flutter, small irregular activity at a rate of 400 per minute, and a mixed type of the former two. The significance of these findings for the mechanism of atrial flutter and fibrillation is discussed.

Action Potentials↗
PubMed1997

The upper link of human common atrial flutter circuit: definition by multiple endocardial recordings during entrainment.

Common atrial flutter is due to a macroreentry circuit in the right atrium, but the cranial path of the circuit has not been defined. The objectives of this article are to determine the cranial turning point of flutter activation in relation to a hypothetic obstacle, the superior vena cava opening, by examining the changes in activation sequence produced by entrainment from different points. In 13 cases of common atrial flutter with typical counter-clockwise right atrial circuits confirmed by endocardial mapping the atrium was paced from the high posterior and mid-septal walls. Entrainment was confirmed by simultaneous recordings of 6-7 right atrial electrograms. Changes in sequence of electrograms from high septum and high anterolateral walls was sought. Electrogram sequence and morphology did not change with entrainment at the posterior wall with respect to the basal flutter or mid-septal wall entrainment. Pacing "below" the superior vena cava did not advance the anterior wall electrogram in relation to the septal electrogram. These findings support the concept that common flutter activation turned around (cranial and anterior to) the superior vena cava opening, and not around the free end of a line of block below the superior vena cava in the posterior wall. Common atrial flutter activation rotates cranial (and anterior) to the superior vena cava opening, through the "right atrial roof." The line of functional block should span from inferior to superior vena cava openings.

Adult↗