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PubMed1997

Three-dimensional mapping of the common atrial flutter circuit in the right atrium.

BACKGROUND: The full circuit of common atrial flutter using conventional methods of sequential or multielectrode activation mapping is not completely understood. METHODS AND RESULTS: We performed three-dimensional right atrial endocardial activation mapping during common counterclockwise atrial flutter in 17 patients (16 men, 1 woman; mean age, 53+/-11 years) by using the Cordis-Biosense EP Navigation system and assessed the distribution of estimated conduction velocities and double and fractionated potentials. ECG flutter wave morphologies were compared with activation patterns. Points (91+/-29) were sequentially acquired covering 88+/-11% of the flutter cycle length of 239+/-22 ms. A wide and variable posterior zone of double and fractionated potentials coincided with blocking and colliding wave fronts and formed the posterior limit of the circuit. A progressively widening septal (sep) wave front ascending from just beyond the coronary sinus ostium, passed cranially as a broad front anterior to the superior vena cava (SVC) in 14 patients, whereas fusion around the SVC formed the superior (sup) limb of the circuit in 3. Bounded anteriorly by the tricuspid valve, the wave front descended down the lateral (lat) aspect of the right atrium before completing the circuit in all cases through the inferior vena cava-tricuspid annulus isthmus. The estimated conduction velocity in the medial isthmus (0.6+/-0.3 m/s) was lower than in the other limbs of the circuit (sup=1+/-0.5 m/s, lat=1+/-0.5 m/s, sep=0.9+/-0.4 m/s, P=.05). Double and fractionated potentials were constant and more prevalent in the posterior right atrium. ECG flutter wave morphology did not correlate with three-dimensional activation maps. CONCLUSIONS: Interindividual variations occur in the right atrial circuit of common atrial flutter, with constant activation through the cavotricuspid isthmus. A variable zone of block forms the posterior limit. Fusion around the SVC can occur, and ascending medial septal activation does not follow a consistent pattern.

Adult↗
PubMed2004

Typical counterclockwise atrial flutter occurring despite absence of the inferior vena cava.

A 74-year-old man with a structurally normal heart presented with typical atrial flutter, after treatment of atrial fibrillation with propafenone. Catheterization and computed tomographic imaging revealed absence of the inferior vena caval segment that normally traverses the liver to enter the right atrium. Abdominal venous return occurred via the hemi-azygous vein, draining into the superior vena cava. Hepatic veins inserted postero-inferiorly into the right atrium. Pacing atrial myocardium between the hepatic veins and the tricuspid valve resulted in concealed entrainment. Radiofrequency catheter ablation directed (via a superior approach from the right internal jugular vein) to this extraordinary "isthmus" abolished atrial flutter. The implications of this congenital abnormality on posterior barriers maintaining the atrial flutter circuit are discussed.

Aged↗
PubMed1998

Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course.

BACKGROUND: The occurrence of atrial fibrillation after ablation of type I atrial flutter remains an important clinical problem. To gain further insight into the pathogenesis and significance of postablation atrial fibrillation, we examined the time to onset, determinants, and clinical course of atrial fibrillation after ablation of type I flutter in a large patient cohort. METHODS AND RESULTS: Of 110 consecutive patients with ablation of type I atrial flutter, atrial fibrillation was documented in 28 (25%) during a mean follow-up of 20.1+/-9.2 months (cumulative probability of 12% at 1 month, 23% at 1 year, and 30% at 2 years). Among 17 clinical and procedural variables, only a history of spontaneous atrial fibrillation (relative risk 3.9, 95% confidence intervals 1.8 to 8.8, P=0.001) and left ventricular ejection fraction <50% (relative risk 3.8, 95% confidence intervals 1.7 to 8.5, P=0.001) were significant and independent predictors of subsequent atrial fibrillation. The presence of both these characteristics identified a high-risk group with a 74% occurrence of atrial fibrillation. Patients with only 1 of these characteristics were at intermediate risk (20%), and those with neither characteristic were at lowest risk (10%). The determinants and clinical course of atrial fibrillation did not differ between an early (< or = 1 month) compared with a later onset. Atrial fibrillation was persistent and recurrent, requiring long-term therapy in 18 patients, including 12 of 19 (63%) with prior atrial fibrillation and left ventricular dysfunction. CONCLUSIONS: Atrial fibrillation after type I flutter ablation is primarily determined by the presence of a preexisting structural and electrophysiological substrate. These data should be considered in planning postablation management. The persistent risk of atrial fibrillation in this population also suggests a potentially important role for atrial fibrillation as a trigger rather than a consequence of type I atrial flutter.

Aged↗
PubMed2000

Catheter ablation of atrial flutter guided by electroanatomic mapping (CARTO): a randomized comparison to the conventional approach.

INTRODUCTION: Three-dimensional electroanatomic (CARTO) activation mapping of the cavotricuspid isthmus can be helpful to guide atrial flutter ablation, but to date has not been investigated in comparison to conventional strategies. The aim of the present study was to assess the efficacy of the CARTO navigation system, especially with respect to the fluoroscopy time required for successful atrial flutter ablation. METHODS AND RESULTS: Eighty patients with recurrent common-type atrial flutter were randomly assigned to temperature-controlled radiofrequency (RF) catheter ablation, either guided by conventional criteria (group 1) or additionally oriented on electroanatomic mapping (group 2). In all patients, similar multipolar catheters were inserted into the coronary sinus and placed at the tricuspid annulus, respectively. In group 2, positioning of the mapping electrode and delivery of RF pulses within the cavotricuspid isthmus was mainly oriented on the CARTO map to achieve the most linear and continuous RF lesions. Abolition of intra-atrial conduction verified by conventional criteria (group 1) and electroanatomic mapping (group 2) could be verified in all patients. The overall number of RF pulses (group 1: 16.7+/-6.5; group 2: 13.2+/-5.3) and mean procedure duration (group 1: 172.5+/-47.4 min; group 2: 169.3+/-47.3 min) were not different between the two groups, but mean fluoroscopy time was significantly shorter when the CARTO technology was used (group 1: 29.2+/-9.4 min; group 2: 7.7+/-2.8 min; P = 0.0001). Recurrence of atrial flutter was observed in 3 (9%) patients in each group after a mean follow-up of 8.5+/-2.8 months. CONCLUSION: Atrial flutter can be abolished effectively using the conventional technique as well as oriented on electroanatomic mapping. However, overall X-ray exposure can be significantly reduced by the CARTO-guided approach without prolongation of procedure duration.

Aged↗
PubMed1996

[Atrial flutter in young patients after corrective operation of congenital heart defects: therapy by high frequency catheter ablation].

UNLABELLED: Radiofrequency catheter ablation has been used successfully in adult patients for treatment of atrial flutter. Three young patients (mean age 14.6 years) with common type atrial flutter (n = 2) and uncommon type atrial flutter (n = 1) underwent electrophysiologic study. Cardiac diagnoses included tricuspid atresia after Fontan operation, status after closure of an atrial septal defect of secundum type, and status after surgical valvotomy for valvular pulmonary stenosis, respectively. Indication for ablation were syncopal episodes in one and presyncopal episodes in two patients. Flutter cycle length ranged from 280 to 320 ms. Right atrial endocardial mapping revealed areas with local electrograms preceding the onset of the flutter-P-wave by 70 to 80 ms. In these regions pace mapping was performed with the intention to produce an identical P-wave morphology and short stimulus to P-wave interval. Radiofrequency current application (500 kHz) with 30 W for 30 s at theses sites terminated atrial flutter and prevented reinduction in all three patients. No complications were observed. Follow-up (7 to 11 months) revealed recurrence of uncommon type of atrial flutter in one patient who previously had had common type. The remaining two patients are in stable sinus rhythm. CONCLUSION: Radiofrequency catheter ablation appears to be an effective treatment of atrial flutter after surgery for congenital heart defects in young patients.

Adolescent↗
PubMed2006

[Can we cure atrial flutter with radiofrequency ablation in an hour?].

BACKGROUND: Radiofrequency ablation of common atrial flutter requires the creation of a complete transmural ablation line across cavotricuspid region to achieve bidirectional conduction block. Irrigated tip catheters facilitate rapid achievement of this block by creation larger and deeper lesions. The EASTHER registry was organized to collect data about the efficacy of the procedure in small and middle volume centres in Central and Eastern Europe, all using THERMOCOOL catheter technology. METHODS: Easther is a prospective registry (April 2002-February 2003). 133 consecutive patients (81.1% male, age 59.0 +/- 10.4 years, range 30-81 years) with common atrial flutter were enrolled. Coincidence with atypical flutter was observed in 2.7%. Patients had a history of flutter of 31.0 +/- 53.6 month (range 1-403) and concomitant atrial fibrillation was observed in 42.9%. Structural heart disease was present in 38.9%. Amount of re-ablated cases was 14%. RF energy was applied during 60 sec in power-controlled mode at a setting between 40 to 50 W with an average flow rate of 19.0 ml/min. RESULTS: Acute success rate defined as bi-directional block was achieved in 93.1%, although 94.7% of cases were assessed successful by the treating electrophysiologist. Average number of RF applications was 12.0 +/- 7.0 (range 2-40) per procedure. Average delivered power varied between a minimum of 36.1 +/- 15.1 W till a maximum of 45.3 +/- 13.0 W, while the average maximum temperature observed at the same time was varied between 39.0 +/- 3.4 degrees C and 45.4 +/- 4.0 degrees C. Total procedure time was 100.1 +/- 42.7 min (range 20-280 min) and fluoroscopy time was 15.8 +/- 9.6 min (range 4-45 min). In comparable French TC registry Average total and fluoroscopy time were 46.4 +/- 33.6 min, and 10.0 +/- 6.8 min resp. In the Middle European centres total and fluoroscopy time was 96.1 +/- 40.9 min, and 15.0 +/- 8.9 min resp. In centres from Eastern Europe it was 120.3 +/- 51.2 min, and 20.4 +/- 11.9 min resp. Two adverse events were reported. Both patients had strong chest pain during ablation. These results are comparable with the literature data published. CONCLUSIONS: Irrigated tip catheters are effective and safe in ablation of common atrial flutter. This technology helps to accelerate and facilitate achievement of bi-directional isthmus block. Most of procedures were terminated to one hour in experienced centers in France as early as 2002. Procedures not exceeding one hour are feasible in case of spreading this method as method of first choice with gaining of experiences in centres of Middle and Eastern Europe.

Adult↗
PubMed2006

Endurance sports is a risk factor for atrial fibrillation after ablation for atrial flutter.

INTRODUCTION: Sports activity has been associated with the development of atrial arrhythmias. Atrial fibrillation (AF) is frequently observed after successful ablation for atrial flutter. Sports activity as a risk factor for AF development after flutter ablation has not been studied. METHODS: We analyzed outcome in 137 patients (83% men) after ablation for isthmus-dependent atrial flutter (excluding patients with concomitant ablation for atrial tachycardia or fibrillation). Sports activity before and after ablation was evaluated by detailed questionnaires. Endurance sports was defined as (semi-)competitive participation in cycling, running or swimming for > or =3 h/week (and for > or =3 years pre-ablation). Median follow-up was 2.5 years. Survival free of AF was evaluated with Kaplan-Meier curves and log-rank statistics. Multivariate analysis was based on Cox proportional hazard evaluation. RESULTS: Acute ablation success was 99% and flutter recurrence 4.4%. Thirty-one patients (23%) had been regularly engaged in endurance sports before ablation and 19 (14%) continued regular sports activity afterwards. Those performing sports were slightly younger. A history of endurance sports was a significant risk factor for post-ablation AF (univariate HR 1.96 (1.19-3.22), p<0.01, and multivariate HR 1.81 (1.10-2.98), p=0.02). Also continuation of endurance sports activity after ablation showed a trend for increased risk to develop AF despite a relatively small sample size (n=19; multivariate HR 1.68 (0.92-3.06), p=0.08). Cox proportional hazard calculations revealed a 10% and 11% increased risk for AF development per weekly hour sport performed before and after ablation respectively (p<0.01 for both). CONCLUSION: A history of endurance sports activity is associated with the development of AF after ablation of atrial flutter.

Atrial Fibrillation↗
PubMed1984

Body surface maps in 2 cases of atrial flutter.

Body surface maps during one cycle of atrial flutter were recorded in 2 cases. The sequences of movements of the maximum and the minimum were compared to those of the sinus P waves. The maps of normal sinus P waves usually show that a maximum first appears at the anterior chest near the sternum and moves to the left side of the thorax in the later half of the P wave. The maps of atrial flutter in Case 1 showed that a maximum first appeared on the upper right back and then moved to the right side of the anterior chest. The maps of Case 2 showed that a maximum first appeared on the upper right back and then moved down the right side of the posterior thorax. There were no movements of the maxima in either case from the right side of the chest to the left as seen in the sinus P waves.

Adult↗
PubMed2002

Catheter ablation of atrial flutter in a heart transplant recipient.

In the transplanted heart with biatrial anastomosis, atrial flutter is common and is amenable to catheter ablation. Although this arrhythmia is isthmus dependent, the unique atrial architecture with a suture line through the inferior vena cava-tricuspid annulus isthmus makes the substrate atypical. A cardiac transplant recipient with atrial flutter underwent successful catheter ablation. Five weeks after the procedure, the patient died of a myocardial infarction. The autopsy and histological findings are described and correlated with the electroanatomic map obtained during the ablation. Due to the atrial suture lines, atrial flutter following cardiac transplantation is an isthmus dependent arrhythmia with a different arrhythmogenic substrate. The electrical isthmus (atrial tissue from the tricuspid annulus to the suture line) in these hearts is smaller than the anatomic isthmus.

Atrial Flutter↗
PubMed2001

Risk of stroke in patients with atrial flutter.

Using a Medicare-based retrospective cohort study, the stroke risk in patients with atrial flutter (RR = 1.41) was determined to be greater than that in a control group (RR = 1.00) but less than that in an atrial fibrillation group (RR = 1.64). Furthermore, patients with atrial flutter who subsequently had an episode of atrial fibrillation had a higher risk of stroke (RR = 1.56) than patients with atrial flutter who never had a subsequent episode of atrial fibrillation (RR = 1.11).

Aged↗
PubMed1986

Pharmacologic conversion and suppression of experimental canine atrial flutter: differing effects of d-sotalol, quinidine, and lidocaine and significance of changes in refractoriness and conduction.

The electrophysiologic determinants of conversion and the prevention of atrial flutter are poorly defined. This issue was therefore investigated by evaluating the effects of the new class III antiarrhythmic drug d-sotalol and the class I antiarrhythmic drugs quinidine and lidocaine. Atrial flutter was reproducibly induced in the open-chest anesthetized dog with intercaval crush and rapid atrial pacing. In this preparation, intravenous d-sotalol restored sinus rhythm in 14 of 15 (93%) dogs, whereas quinidine converted nine of 15 (60%) and lidocaine two of 10 (20%). d-Sotalol prevented reinduction in eight (53%), whereas quinidine was effective in four (27%) and lidocaine in none (0%). In the atria, d-sotalol induced significant increases in effective refractory period (+32%; p less than .01), functional refractory period (+30%; p less than .01), conduction time at an atrial paced cycle length of 150 msec (+9%; p less than .05), and atrial flutter cycle length (+8%; p less than .01). Quinidine increased effective refractory period (+40%; p less than .01), functional refractory period (+27%; p less than .01), conduction time at sinus cycle length (+13%; p less than .01), conduction time at an atrial paced cycle length of 150 msec (+18%; p less than .01), and atrial flutter cycle length (+31%; p less than .01). Lidocaine decreased functional refractory period (-6%; p less than .05) while lengthening the atrial flutter cycle length (+13%; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Risk factors for recurrence of atrial fibrillation in patients undergoing hybrid therapy for antiarrhythmic drug-induced atrial flutter.

AIMS: Catheter ablation of the inferior vena cava-tricuspid annulus isthmus and continuation of antiarrhythmic drug therapy have been shown to be an effective hybrid therapy for atrial flutter which results from antiarrhythmic drug treatment of atrial fibrillation. The aim of this study was to determine the risk factors for recurrence of atrial fibrillation in patients undergoing hybrid therapy for antiarrhythmic drug-induced atrial flutter. METHODS AND RESULTS: 90 patients with paroxysmal (n=46) or persistent atrial fibrillation (n=44) developed atrial flutter due to the administration of amiodarone (n=48), flecainide (n=22), propafenone (n=14) or sotalol (n=6). Recurrence of atrial fibrillation after ablation was assessed during follow-up on continued antiarrhythmic drug therapy and during long-term follow-up, irrespective of the initial antiarrhythmic medication. During the follow-up on continued antiarrhythmic drug therapy (16+/-13 months), recurrence of atrial fibrillation was documented in 24 of 90 patients (27%). The presence of accompanying pre-ablation episodes of atrial fibrillation on antiarrhythmic treatment (Odds ratio 7.1, 95% confidence interval 2.3 to 25, p=0.001) and decreased left ventricular ejection fraction (Odds ratio 3.7, 95% confidence interval 1.01 to 12.5, p=0.048) were significant and independent predictors of post-ablation atrial fibrillation. Antiarrhythmic medication was discontinued during long-term follow-up due to adverse drug effects (amiodarone, n=12; flecainide, n=1) in 13 patients (14%). During the long-term follow-up, irrespective of the initial antiarrhythmic medication (21+/-15 months), stable sinus rhythm was maintained in 60 of 90 patients (67%). CONCLUSION Hybrid therapy can be considered as the first line therapy for patients with antiarrhythmic drug-induced atrial flutter but patients should be carefully evaluated for accompanying pre-ablation episodes of atrial fibrillation and possible adverse drug effects before initiation of hybrid therapy.

Analysis of Variance↗
PubMed2005

Separating non-isthmus- from isthmus-dependent atrial flutter using wavefront variability.

OBJECTIVES: The aim of this study was to separate isthmus-dependent atrial flutter (IDAFL) from non-isthmus-dependent atrial flutter (NIDAFL) from the electrocardiogram (ECG) based on functional differences. BACKGROUND: The ECG analyses of F-wave shape suboptimally separate NIDAFL from IDAFL. The authors hypothesized that anatomic and functional differences may result in greater wavefront variability in NIDAFL than IDAFL, allowing their separation. The authors tested this hypothesis in patients undergoing ablation for atrial flutter using a novel ECG algorithm to detect subtle F-wave variability, validated by intracardiac measurements. METHODS: In 62 patients (23 NIDAFL, 39 IDAFL) ECG atrial wavefronts were represented as correlations of an F-wave template to the ECG over time. Correlations in orthogonal ECG lead-pairs were plotted at each time point to yield loops reflecting temporal and spatial regularity in each plane. The ECG analyses were compared with intracardiac standard deviations of: 1) atrial electrograms (temporal variability), and 2) bi-atrial activation time differences (spatial variability). RESULTS: Atrial ECG temporospatial loops were reproducible in IDAFL, but varied in NIDAFL (p < 0.01) suggesting greater variability that correctly classified IDAFL (39 of 39 cases) from NIDAFL (22 of 23 cases; p < 0.001). Intra-atrial mapping confirmed greater temporal variability for NIDAFL versus IDAFL, in lateral (p < 0.01) and septal (p = 0.03) right atrium, and proximal (p = 0.02) and distal (p < 0.01) coronary sinus. Spatial variability was greater in NIDAFL than IDAFL (p = 0.02). CONCLUSIONS: Greater cycle-to-cycle atrial wavefront variability separates NIDAFL from IDAFL and is detectable from the ECG using temporospatial analyses. These results have implications for guiding ablation and support the concept that IDAFL and NIDAFL lie along a spectrum of intracardiac organization.

Algorithms↗
PubMed1993

A comparison of transoesophageal atrial pacing and direct current cardioversion for the termination of atrial flutter: a prospective, randomised clinical trial.

OBJECTIVE: To compare the safety and efficacy of transoesophageal atrial pacing (TAP) with an easily swallowed pill electrode and direct current cardioversion (DCC) in patients with atrial flutter that was refractory to appropriate medical treatment. DESIGN: Prospective, randomised clinical trial. SETTING: Community based United States naval hospital. SUBJECTS: Twenty one consecutive patients with refractory atrial flutter selected consecutively from the inpatient cardiology consultation service. All patients were haemodynamically stable and medical treatment with a class IA or IC antiarrhythmic agent had failed. Eleven patients were treated with TAP and 10 patients were treated with DCC. INTERVENTIONS: Digoxin was given to all patients to control the ventricular rate to < 100/minute. MAIN OUTCOME MEASURE: Conversion to normal sinus rhythm and arrhythmias after cardioversion. RESULTS: Conversion to normal sinus rhythm was similar in both groups (TAP 8/11, DCC 9/10, p = 0.31). Arrhythmias after cardioversion including third degree heart block and non-sustained ventricular tachycardia were more frequent in the DCC group (TAP 0/11, DCC 6/10, p = 0.02). CONCLUSION: Transoesophageal atrial pacing with an easily swallowed pill electrode is safe, well tolerated, and is as efficacious as DCC for refractory atrial flutter.

Aged↗
PubMed1995

Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Activation and entrainment mapping guided by intracardiac echocardiography.

BACKGROUND: The importance of barriers in atrial flutter has been demonstrated in animals. We used activation and entrainment mapping, guided by intracardiac echocardiography (ICE), to determine whether the crista terminalis (CT) and eustachian ridge (ER) are barriers to conduction during typical atrial flutter in humans. METHODS AND RESULTS: In eight patients, ICE was used to guide the placement of 20-pole and octapolar catheters along the CT and interatrial septum and a roving catheter to nine sites: just posterior (1) and anterior (2) to the CT along the lateral right atrium, at the fossa ovalis (3), and just posterior and anterior to the ER at the low posterolateral (4 and 5), low posterior (6 and 7), and low posteromedial (8 and 9) right atrium. Entrainment was performed, and each site was considered within the flutter circuit if the postpacing interval-flutter cycle length (PPI-FCL) and the stimulus time-activation time (stim time-act time) were < 10 msec. Split potentials were recorded along the CT with components activated in a low-to-high pattern and a high-to-low pattern. Conduction times, as percentage of FCL, were significantly different at sites on either side of the CT and ER: site 1 (33 +/- 13%) and site 2 (43 +/- 12%) (P = .02), site 4 (48 +/- 24%) and site 5 (75 +/- 8.9%) (P = .02), and site 6 (22 +/- 10%) and site 7 (82 +/- 5.3%) (P = .0009). During entrainment, no surface fusion was observed at sites 5, 7, or 9. The PPI-FCL and stim time-act time were not significantly different than 0 at sites 2, 7, 5, or 9, indicating that they were within the flutter circuit, whereas sites 1, 3, 4, and 6 were not. CONCLUSIONS: ICE enabled the correlation of functional electrophysiological properties with specific anatomic landmarks, identifying the CT and ER as barriers to conduction during human atrial flutter.

Aged↗
PubMed1992

Role of anisotropy in determining the selective action of antiarrhythmics in atrial flutter in the dog.

OBJECTIVE: The aim was to clarify the electrophysiological and anatomical features of the preferential site of action of antiarrhythmic drugs in the re-entrant circuit of canine atrial flutter. METHODS: Electrophysiological and anatomical findings were correlated in 17 anaesthetised adult mongrel dogs with atrial flutter associated with an intercaval anatomical obstacle, before and after intravenous administration of disopyramide (2 mg.kg-1) and flecainide (2 mg.kg-1). RESULTS: Before drug injection, a rate dependent prolongation of conduction time occurred in the low right atrium where the conduction was slow during atrial flutter. Disopyramide (n = 8 dogs) and flecainide (n = 9 dogs) terminated atrial flutter, with conduction block occurring in this slow conduction area in the low right atrium. Although the degree of drug induced prolongation of refractoriness in this particular area was similar to those in other areas of the right atrium, conduction was depressed to a greater extent in this region. Anatomical study revealed that a thick pectinate muscle that branched from the crista or crista terminalis itself ran perpendicular to the wavefront of the pacing impulse and atrial flutter in this slow conduction area. CONCLUSIONS: These data indicated that slow conduction might be attributed, at least in part, to anisotropic conduction over the thick muscle bundle in the low right atrium, and that antiarrhythmic drugs preferentially produced conduction block in this area. Anisotropic conduction in the low right arium is an anatomical substrate for slow conduction in the re-entrant circuit and for the site preference of antiarrhythmic drugs in the present canine model.

Animals↗
PubMed1991

Antiarrhythmic drugs preferentially produce conduction block at the area of slow conduction in the re-entrant circuit of canine atrial flutter: comparative study of disopyramide, flecainide, and E-4031.

STUDY OBJECTIVE: The aim was to test whether antiarrhythmic drugs preferentially suppressed conduction in the area of slow conduction in the re-entrant circuit. DESIGN: Intravenous disopyramide [n = 8, plasma concentrations: 1.4 (SEM 0.2) micrograms.ml-1], flecainide [n = 8, 0.6(0.1) micrograms.ml-1], and E-4031, a new class III antiarrhythmic drug [n = 8, 5.6(1.0) ng.ml-1], were investigated for their effects on atrial flutter due to re-entry in dogs with intercaval crush. In three dogs, detailed atrial activation sequence during atrial flutter was determined with a hand held bipolar electrode and an epicardial isochronal map was drawn. EXPERIMENTAL MATERIAL: 24 anaesthetised adult mongrel dogs were used. MEASUREMENTS AND MAIN RESULTS: There was an area of slow conduction during atrial flutter in the low right atrium. Atrial flutter was terminated in all dogs except for one treated with flecainide. In 92% of the dogs, conduction block occurred in the low right atrium in which the area of slow conduction was located. Increase in local conduction time was greater in the area of slow conduction than other parts of the atria (percent ratio to the increase in cycle length of atrial flutter: 63% with disopyramide, 52% with flecainide, and 99% with E-4031). CONCLUSION: These data suggested antiarrhythmic drugs preferentially suppressed conduction at the area of slow conduction in the re-entrant circuit leading to termination of atrial flutter in this canine model, irrespective of electrophysiological effects of antiarrhythmic drugs.

Animals↗