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PubMed1996

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success.

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.

Adult↗
PubMed1963

MECHANISM OF ATRIAL FLUTTER AND FIBRILLATION INDUCED BY ACONITINE IN THE DOG, WITH OBSERVATIONS ON THE ROLE OF CHOLINEGIC FACTORS.

The topical application of aconitine nitrate to the right atrial appendage in the "intact" anaesthetized dog produced atrial flutter. Premature systoles with fixed coupling preceded the development of flutter. In early stages of the arrhythmia, atrial rate was irregularly irregular. Also, the form of flutter beats was similar to that of preceding premature systoles. The fibrillatory activity of acetylcholine described by earlier workers has been confirmed. Transient atrial dissociation was seen after intravenous injection or topical application of acetylcholine. The occurrence of fibrillation in the left atrium after focal application of acetylcholine has been demonstrated, while the right atrial appendage containing the ectopic focus induced by aconitine continued to flutter. Aconitine produced slow-rate flutter in dogs treated with atropine or hemicholinium; this flutter was easily distinguishable from the sinus tachycardia produced by these drugs, by recording the electrocardiogram from a direct atrial lead from the area treated with aconitine, but not from limb lead II. The importance of these findings in the interpretation of the mechanism of atrial flutter and fibrillation is discussed.

Acetylcholine↗
PubMed2005

[Atrial flutter and fibrillation].

This article summarizes current understandings and therapies for both arrhythmias. Atrial flutter is most often arising from a macroreentry circuit in the right atrium or around scar tissue in case or previous cardiothoracic surgery. As a macroreentrant tachycardia it is regular and can lead to higher heart rates, especially if occurring with 1:1 conduction. In contrast atrial fibrillation, especially when occurring paroxysmal at the beginning, is arising from triggers within the pulmonary veins. Ablation strategies to electrically isolate those triggers have a treatment success rate of 80%, which is much more than can be achieved with antiarrhythmic medication (success rates 30-50%). Emergency treatment of both arrhythmias include cardioversion and pacemaker implantation with AV node ablation if necessary.

Adrenergic alpha-Antagonists↗
PubMed1992

Detection of reentry currents in atrial flutter by magnetocardiography.

We discuss the use of magnetocardiography to detect reentry currents in cardiac flutter and fibrillation. The magnetic field produced by induced atrial flutter was measured in isolated rabbit hearts. A moving dipole model is proposed to treat the experimental data and to locate the reentry path.

Animals↗
PubMed1996

Atrial flutter in the human fetus: diagnosis, hemodynamic consequences, and therapy.

In the context of a large program of prenatal echocardiographic detection of fetal heart disease, special attention was paid to the in utero detection and identification of fetal heart rate disorders. This article focuses on 18 cases of tachycardiac fetuses. It provides information on how to identify the nature of the detected tachycardia, the hemodynamic consequences of tachycardia, the particular characteristics of fetal atrial flutter, and the efficacy of the transmaternal treatment of fetal tachycardia. It also describes an original way to grade and score the degree of fetal heart failure that proved useful for the assessment and monitoring of in utero therapeutic procedures. The results presented stress the efficacy of digoxin for fetal atrial flutter as well as the usefulness of prenatal echocardiography in the assessment of anatomical, functional, and rhythmic conditions of the fetal heart.

Anti-Arrhythmia Agents↗
PubMed1995

[Ablation therapy of type I atrial flutter with radiofrequency].

PURPOSE--To present initial experience on radiofrequency (RF) ablation of atrial flutter (AFL) guided by anatomic and electrophysiologic parameters. METHODS--Eight patients (six males), mean-age of 42 +/- 17.5 years with chronic type I AFL (mean cycle length of 251 +/- 14.3 msec, range 240 to 280 msec) were undergone to RF catheter ablation applied between inferior vena cava (IVC) and tricuspid annulus (TA). Two had persistent and two the paroxysmal form. Two had surgical corrected congenital heart disease (atrial septal defect in 2 and ventricular septal defect in 1). Four had systolic dysfunction and 2, an atrial tachycardia associated with the AFL. RESULTS--Areas of slow conduction represented by fractionated potentials were recorded between IVC and TA in all patients. RF ablation was successful in 8/8 patients (100%). The mean number of RF applications was 9.2 +/- 6.2 (4-24). The successful ablation site was located in the isthmus between IVC and TA in seven patients and in the lateral wall in the patient with ASD. Successful sites had an early atrial activation preceding the atrial electrogram (range from -65 to -82 ms). In one patient the RF energy was successfully delivered between the atriotomy scar (AS) and IVC. After three months follow-up six remained free of recurrent AFL. One pt had type 1 AFL recurrence and one with ASD had a type II AFL. The Type II AFL was successfully ablated between AS and IVC. CONCLUSION--Fractionated potentials were commonly observed between IVC and T; AFL ablation can be guided by anatomic landmarks or electrophysiologic parameters; electrograms recorded at successful sites were early and never fractionated; the long-term evaluation must be analyzed prospectively.

Adult↗
PubMed1999

Radiofrequency catheter ablation of common atrial flutter: role of the eustachian valve.

INTRODUCTION: During radiofrequency catheter ablation of a common atrial flutter between the tricuspid annulus and the Eustachian valve "septal isthmus", double potentials were recorded along the Eustachian valve, previously described as an anatomical line of conduction block between the coronary sinus ostium and the inferior vena cava. RESULTS: Just before flutter termination, lengthening and beat to beat delay variations between the 2 components of the double potentials were correlated with simultaneous modifications of the flutter cycle length. CONCLUSION: The "septal isthmus" is a common pathway for the flutter wavefront and the impulse generating the second component of the double potential. It is also a good target for flutter ablation.

Adult↗
PubMed2003

Noninvasive, direct visualization of macro-reentrant circuits by using magnetocardiograms: initiation and persistence of atrial flutter.

AIMS: We analysed the cardiac magnetic fields on the body surface to visualize electrical currents noninvasively during reentrant arrhythmias. METHODS AND RESULTS: Seven patients with counterclockwise atrial flutter (AFL) were studied during 17 episodes of AFL using 64-channel magnetocardiograms (MCGs) and electrophysiological study. Eight of the episodes were paroxysmal AFL, in which MCGs were recorded from the time of spontaneous onset to the time of termination. We constructed iso-magnetic field maps of the tangential components and produced MCG animations. With respect to AFL initiation, an atrial premature complex induced AFL. Prior to the initiation of AFL, atrial fibrillation (AF) transiently occurred. The cardiac magnetic fields revealed a single peak during sinus rhythm or with premature complexes but a disorganized pattern during AF. When AF transformed to AFL, the magnetic fields changed from a disorganized pattern to a single peak at first and then evolved to a circular pattern. During persistent AFL, the magnetic source moved in a counterclockwise circuit. CONCLUSION: MCG animation can be used to visualize the sequence in which a premature complex transforms sinus rhythm to AFL via AF. Our findings indicate that MCGs can be used to identify noninvasively the mechanisms responsible for atrial tachyarrhythmias.

Atrial Fibrillation↗
PubMed1996

Type II atrial flutter interruption with transesophageal pacing: use of propafenone and possible change of the substrate.

Type II atrial flutter (AFII) is an arrhythmia which usually cannot be interrupted by atrial pacing: the underlying mechanism is considered to be a leading circle without an excitable gap. We investigated whether the administration of propafenone, an antiarrhythmic drug, which primarily decreases conduction velocity, has a beneficial effect on AFII interruption using transesophageal pacing. Twelve patients with an AFII were randomized into 2 groups in which pacing was performed without treatment (group A) or two hours after the administration of 600 mg of oral propafenone (group B). Sinus rhythm was attained in 0 of 6 patients in group A and in 4 of 6 patients in group B (P < 0.05). The baseline mean cycle length was the same in both groups (175 +/- 7 (A) vs 168 +/- 8 ms (B); it lengthened significantly after the administration of propafenone (219 +/- 33 vs 168 +/- 8 ms; P < 0.05). Propafenone did not significantly lengthen the cycle in the two patients in whom interruption of the arrhythmia was impossible. Our data show that propafenone has a facilitating effect on atrial pacing only when it significantly prolongs the cycle length of the arrhythmia, possible expression of a conversion of AFII into type I, with an anatomical substrate and an excitable gap allowing arrhythmia capture and interruption. In the two patients in whom sinus rhythm was not restored, the absence of a direct dependence of the cycle length on the change in conduction velocity induced by propafenone may be explained by the persistence of a functionally determined circuit, resistant to atrial pacing.

Administration, Oral↗
PubMed1985

Electrophysiologic mechanisms of provoked atrial flutter in mitral valve prolapse syndrome.

To examine the electrophysiologic determinants of provoked atrial flutter (AF) in patients with mitral valve prolapse (MVP), studies were performed in 4 groups of patients: group 1 (n = 5), patients with MVP and AF; group 2 (n = 6), patients without MVP but with AF; group 3 (n = 6), patients with MVP but without AF; and group 4 (n = 5), patients without MVP and without AF. P-wave duration, intraatrial conduction, interatrial conduction and effective refractory periods for both the high right atrium and the low right atrium were longer in group 2 than in group 1. The effective refractory period of the low right atrium was longer in group 3 than in group 1. The interatrial conduction interval was longer in group 2 than in group 4. Thus, in patients without MVP, atrial conduction delay is the predominant determinant of AF, whereas differences in right atrial refractoriness appear to be most important to the provocation of AF in the patient with MVP. These differences in atrial refractoriness may be a result of abnormal autonomic influences in patients with MVP.

Adolescent↗
PubMed1997

Efficacy of intravenous propafenone in termination of atrial flutter by overdrive transesophageal pacing previously ineffective.

Fifty patients with symptomatic type I atrial flutter in whom termination of the arrhythmia with transesophageal stimulation was unsuccessful were randomized to undergo a repeat procedure after intravenous propafenone (n = 25) or placebo (n = 25). Immediate sinus rhythm recovery rate was 36% in the propafenone group and 4% in the placebo group (p = 0.005), indicating that intravenous propafenone increases the rate of successful transesophageal stimulation and can be used when a first attempt at conversion is ineffective.

Aged↗
PubMed1990

Characterization of slow conduction in the common type of atrial flutter--using transient entrainment.

To characterize slow conduction of the common type of atrial flutter (common AF), in which excitation wave propagated in a counterclockwise fashion, transient entrainment during the distal high lateral right atrium (HRAd) pacing and during the proximal coronary sinus (CSp) pacing was studied in 7 patients with common AF. In transient entrainment of common AF, conduction time from stimulus to CSp during HRAd pacing was always longer than that from stimulus to HRAd during CSp pacing. It was also longer than that from stimulus to CSp during HRAd pacing in 5 control patients without common AF in sinus rhythm. Return cycles at HRA and CS after cessation of rapid pacing during transient entrainment were studied. In HRAd pacing, return cycle at the proximal high lateral right atrium was almost equal to the pacing cycle length, or almost equal to or slightly shorter than the flutter cycle length (AFCL). Return cycle at CSp was almost equal to AFCL. In CSp pacing, return cycle at the distal coronary sinus was much longer than AFCL and increased at progressively shorter pacing cycle lengths. In conclusion, slow conduction was demonstrated in the lateral limb (from HRA laterally to CS) of the reentrant circuit in common AF, but it did not exhibit decremental conduction property. Return cycle at an endocardial recording site after transient entrainment in common AF does not always exhibit an uniform pattern, affected by the relative location of and the distance between the recording site, the pacing site, the reentrant circuit and the area of slow conduction.

Aged↗
PubMed2002

Atrial tachycardia with recipient-to-donor atrioatrial conduction and isthmus-dependent donor atrial flutter in a patient after orthotopic heart transplantation. Successful treatment by radiofrequency catheter ablation.

Atrial arrhythmias are common after orthotopic heart transplantation. We report an unusual case of a patient after heart transplantation with 2 types of atrial arrhythmias: one was a macro-reentrant, incisional, recipient-atrial tachycardia conducted to the donor atrium, and the other was a common-type, isthmus-dependent atrial flutter in the donor atrium. These 2 arrhythmias were successfully treated with selective radiofrequency catheter ablation.

Atrial Flutter↗
PubMed2004

Novel pore mutation in SCN5A manifests as a spectrum of phenotypes ranging from atrial flutter, conduction disease, and Brugada syndrome to sudden cardiac death.

OBJECTIVES: The purpose of this study was to determine the clinical and biophysical characteristics of a novel SCN5A mutation. BACKGROUND: Brugada syndrome and isolated cardiac conduction defect have been linked to SCN5A mutations. METHODS: Eleven members of a western European family underwent electrophysiologic investigations and mutation analysis of the SCN5A gene. Wild-type and mutant SCN5A channels were expressed in HEK293 cells, and whole cell currents were studied using patch clamp procedures. RESULTS: A novel mutation, R376H, in the first pore segment of SCN5A variably causes Brugada syndrome and/or conduction disease in a single family. Biophysical analysis demonstrated a significant current reduction for the mutant, a pathophysiologic profile consistent with Brugada syndrome and isolated cardiac conduction defect. Among 11 family members, 9 were carriers of the mutation. The proband's initial presentation was a saddleback Brugada ECG, atrial flutter, and diffuse conduction disturbances. He had no inducible ventricular arrhythmias but experienced sudden cardiac death. His brother was affected by atrial flutter and had a clear conduction disorder, but he did not display baseline or evocable ECG signs of Brugada syndrome. He received an implantable cardioverter-defibrillator that delivered one appropriate shock after 1 year of follow-up. The phenotype in the family members was highly variable and ranged from noninducible and inducible asymptomatic carriers of the mutations to isolated conduction disease and to symptomatic Brugada syndrome. CONCLUSIONS: We describe the functional characterization of a novel SCN5A pore mutation, R376H, with variable clinical expression in the same family. Differentiating between electrophysiologic entities (Brugada syndrome-isolated cardiac conduction defect) is more challenging. Recognition of factors modifying the clinical presentation may be important for clinical decision making.

Adolescent↗
PubMedDate not supplied

Prenatal diagnosis of idiopathic stenosis of the ductus arteriosus associated with fetal atrial flutter.

Antenatal stenosis or closure of the ductus arteriosus unrelated to either congenital heart defects or prostaglandin inhibitors is considered to be uncommon, but may result in congestive heart failure, hydrops fetalis, and perinatal death. We report a case of idiopathic ductal stenosis detected prenatally by two-dimensional and Doppler echocardiography in a fetus presenting atrial flutter and right atrial dilatation at 31 weeks of gestation. Prenatal treatment with digoxin and verapamil resulted in conversion to sinus rhythm. The fetus was closely monitored. Congestive heart failure did not develop, and the fetus was delivered spontaneously in good condition at 39 weeks of gestation. In case of ductal stenosis, the potential risk of congestive heart failure must be considered, and maternal administration of drugs with constrictive effects on the ductus arteriosus, as indomethacin or betamethasone, should be avoided.

Adult↗
PubMed2004

Effectiveness of catheter ablation for coexisting atrial fibrillation and atrial flutter.

In 79 consecutive patients (51 men and 28 women) with paroxysmal (n = 54) or persistent atrial fibrillation (AF) (n = 25) and typical, isthmus-dependent atrial flutter (AFl), pulmonary vein (PV) isolation and anatomically guided linear ablation of the right atrial isthmus was performed during the same procedure. After 208 +/- 331 days of follow-up, 42% remained free of AF and AFl, and a symptomatic lessening was reported by 77%. Paroxysmal AF (beta = 1.682, p = 0.008) and ablation of 3 or 4 PVs (beta = 1.830, p = 0.013) were independent predictors for arrhythmia-free survival. Combined catheter ablation of PVs and the right atrial isthmus for the treatment of patients with mixed AF and AFl is moderately effective in preventing early arrhythmia recurrence but leads to clinical improvement in most patients.

Atrial Fibrillation↗
PubMed2004

Left septal atrial flutter: electrophysiology, anatomy, and results of ablation.

BACKGROUND: We describe the clinical and electrophysiological characteristics of a novel macroreentrant form of left atrial flutter circuit. METHODS AND RESULTS: A total of 11 patients were included in the study. The mean tachycardia cycle length was 278+/-41 ms. Nine of the 11 patients were treated with antiarrhythmic drugs at the time of the study for concomitant atrial fibrillation. With the use of entrainment pacing and either the CARTO Biosense mapping system (9 patients) or conventional mapping (2 patients), the flutter circuit was found to rotate around the left septum primum with a critical isthmus located between the pulmonary veins posteriorly and/or mitral annulus anteriorly and the septum primum. In 5 patients, radiofrequency ablation was performed from the septum primum to the right inferior pulmonary vein (group 1), and in 6 patients, a lesion was made from the septum primum to the mitral annulus (group 2). After a follow-up of 13+/-6 months, 2 patients in group 1 and all patients in group 2 remained in sinus rhythm without recurrence. CONCLUSIONS: Slowing of electric conduction in the left atrial septum due to antiarrhythmic drugs and/or atrial myopathy seems to promote left septal atrial flutter. Radiofrequency ablation of this arrhythmia is usually effective and safe. A line of block between the septum primum and the mitral annulus proved to be effective for cure of tachycardia.

Aged↗
PubMed2005

Construction of a three-dimensional outline of the heart and conduction pathway by means of a 64-channel magnetocardiogram in patients with atrial flutter and fibrillation.

BACKGROUND: Magnetocardiography (MCG) has the potential for collecting three-dimensional (3D) intracardiac electric information, because the magnetic field is unaffected by the shape of the lungs and torso. In the present study, we report on the generation of a 3D heart outline and conduction pathway by means of a current density map using a 64-channel SQUID system, and an evaluation of its significance in patients with atrial flutter (AFL) and atrial fibrillation (AFIB). METHODS: The subjects consisted of 20 healthy volunteers, and 3 patients with AFL and 4 patients with AFIB. A 64-channel MCG was recorded after digitization at 500 Hz, and a 3D current density was reconstructed from the magnetic fields using a space filter in conjunction with the minimum normalization method of Tikhonov. A 3D heart outline was generated from the integrated current density by the space filter. The conduction pathway was superimposed on a heart outline generated by a magnetic field. The heart outline was verified by the silhouette on the magnetic resonance (MR) images. An MCG was recorded pre- and post interventional therapy, and therapeutic efficacy was evaluated. RESULTS: The 3D heart outline of the atrium and ventricle corresponded to the silhouette of the right atrium and left ventricle, respectively, on an MR image. The serial conduction pathway of the QRS segment superimposed on the 3D heart outline map demonstrated the conduction pattern generated within the heart. The MCG revealed a counter-clockwise rotation in patients with AFL, and random micro-reentry in the case of AFIB. After interventional therapy, restoration of the sinus rhythm was verified in patients with both AFL and AFIB. CONCLUSIONS: A 64-channel MCG was used to evaluate the 3D heart outline and conduction pathway in patients with AFL and AFIB without the need for MR images. Condensed Abstract A 64-channel MCG was used to evaluate the 3D heart out line and conduction pathway in patients with AFL and AFIB.

Aged↗