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PubMed1997

Electrophysiologic effects of SD-3212, a new class I antiarrhythmic drug, on canine atrial flutter and atrial action-potential characteristics.

SD-3212 (levo-semotiadil fumarate) is a newly developed compound that exhibits potent antiarrhythmic activity because of its inhibitory action on sodium and calcium channels. In animal models, SD-3212 suppressed ventricular tachyarrhythmias, but the effects of this drug on atrial tachyarrhythmias have not been reported. We investigated the electrophysiologic effects of SD-3212 on canine atrial flutter induced after placement of the intercaval obstacle and on atrial action-potential characteristics. In all seven dogs, SD-3212 (1.9 +/- 0.3 mg/kg) terminated atrial flutter after significant increase in atrial flutter cycle length from 126 +/- 5 to 166 +/- 14 ms (increase, 31 +/- 8%; p < 0.005). SD-3212 increased right atrial effective refractory period (RAERP) significantly from 126 +/- 7 to 149 +/- 11 ms at a basic cycle length of 300 ms. The increases in RAERP after SD-3212 at basic cycle lengths of 300, 200, and 150 ms did not differ (increase, 18 +/- 4%, 17 +/- 3%, and 19 +/- 3%, respectively). Interatrial conduction time (IACT) was prolonged after SD-3212 from 63 +/- 4 to 81 +/- 6 ms (increase, 31 +/- 6%) at a basic cycle length of 150 ms. Prolongation of IACT was frequency dependent. The plasma concentration of SD-3212 after the termination of atrial flutter was 187 +/- 56 ng/ml in four dogs tested. In vitro study by using standard microelectrode techniques showed SD-3212 at concentrations of 1-3 microM significantly prolonged action-potential duration at 90% repolarization. Vmax was decreased by SD-3212 in a concentration-dependent manner (0.3-3 microM), and the inhibitory effect on Vmax was greatest at the highest stimulation frequency of 3.3 Hz. These results indicate that a new antiarrhythmic drug, SD-3212, is effective in interrupting canine atrial flutter, possibly by suppressing atrial conduction, and might be effective for the treatment of clinical atrial tachyarrhythmias.

Action Potentials↗
PubMed1975

Termination of atrial flutter and atrial tachycardia with rapid atrial stimulation.

The results in this series of fifty-seven patients confirms the safety and reliability of rapid atrial stimulation to terminate atrial flutter and atrial tachycardia. Transthoracic wires implanted at thoracotomy or transvenously placed atrial electrodes can be used for the confident intracardiac electrocardiographic diagnosis of tachyarrhythmias and for atrial stimulation. Our experience represents the second largest reported series of patients to undergo cardioversion by this method. In all but five of fifty-seven patients either the atrial tachyarrhythmia was converted to normal sinus rhythm or the flutter-tachycardia was terminated with resultant atrial fibrillation. In forty-three patients sinus rhythm was eventually re-established after atrial stimulation. Various aspects of rapid atrial stimulation, including it's preference over precordial shock, have been discussed. We feel particular consideration should be given cardioversion by rapid atrial stimulation in patients with possible digitalis toxicity and in all patients who have atrial flutter, atrial tachycardia, or junctional tachycardia after open heart surgery.

Aged↗
PubMed1988

Shift of atrial reentrant tachycardia with transient entrainment to an uncommon and a common type of atrial flutter.

Atrial reentrant tachycardia (ART) which demonstrated transient entrainment shifted to an uncommon type of atrial flutter (AF) with premature atrial stimulation, and then returned to ART spontaneously. Subsequently, this ART shifted to a common type of AF by rapid atrial pacing, which was further transformed into an uncommon type of AF and finally terminated by rapid atrial pacing. The mechanism of AF in clinical cases is still controversial, but in this case, AF, both uncommon and common types, is considered due to macro-reentry within the atria. To explain the shift of ART to AF and mutual transformation between common and uncommon type of AF, we made a schematic figure of reentry loop within the atria of ART and AF.

Aged↗
PubMed1996

Radiofrequency ablation of atrial flutter and atrial tachycardias in patients with permanent indwelling catheters.

UNLABELLED: The presence of chronic indwelling leads in the area targeted for RF ablation may pose a technical challenge and reduce the chance of success of the ablation. In addition, application of lesions in close proximity to pacemaker leads or other permanent catheters could affect their function. Fourteen patients referred for RF ablation of atrial flutter/fibrillation and atrial tachycardia, who had a permanent dual chamber pacemaker (10 patients), ICD (1 patient), or both (3 patients) were studied to assess the safety, efficacy, and effects of the ablative procedure on device function. Lead impedance, R and P wave amplitude, and pacing threshold of the defibrillator and pacemaker were measured before and after ablation. The procedure was successful in all patients. In one patient who underwent both atrial flutter and atrial fibrillation ablation, the atrial pacing threshold increased from 1.0 preablation to 2.0 V postablation. No P wave was detectable after ablation. In another patient, the P wave amplitude went from 4.0 to 2.0 mV postablation. In both patients the device converted to the power reset mode. No changes were observed in the remaining patients. Postablation defibrillator testing showed no malfunction. Follow-up reinterrogation of the devices revealed no alterations. IN CONCLUSION: (1) RF ablation of atrial flutter and/or tachycardia is feasible even in patients with multiple chronic atrial and ventricular indwelling catheters; and (2) RF applications in close proximity of defibrillator and pacing catheters does not appear to alter their function unless lesions are produced in the area surrounding the distal pacing electrode.

Aged↗
PubMed2005

Similarities and differences between atrial flutter and atrial fibrillation.

Atrial flutter and atrial fibrillation have a complex relationship that has mechanistic, diagnostic, therapeutic and prognostic components. While thromboembolic risk management and pharmacological strategies share many similarities, there are important differences. Radiofrequency ablation should be considered to be an early, first-line alternative to pharmacological strategies for many patients with atrial flutter.

Atrial Fibrillation↗
PubMed1998

Conversion efficacy and safety of repeated doses of ibutilide in patients with atrial flutter and atrial fibrillation. Study Investigators.

BACKGROUND: A study was conducted to determine the efficacy and safety of ibutilide fumarate versus placebo in the acute termination of atrial flutter and fibrillation. METHODS AND RESULTS: Two hundred sixty-two patients aged 28 to 88 years with atrial flutter or fibrillation duration of 3 hours to 90 days were randomly assigned in a 5:1 ratio (ibutilide:placebo) to receive two 10-minute infusions, 10 minutes apart, of ibutilide (1 mg) or placebo. Patients were hospitalized and monitored by telemetry for 24 hours, with follow-up 72 hours later. Seventy-three (34.9%) of 209 evaluable ibutilide recipients had termination of atrial flutter or fibrillation within 1.5 hours compared with 0 (0%) of 41 placebo recipients. Those with atrial flutter had a higher success rate. At hour 24, 86.3% remained in normal or alternative sinus rhythm. Of the patients who received ibutilide, 2.3% experienced drug-related sustained polymorphic or monomorphic ventricular tachycardia and recovered after intervention. Additionally, 7.3% experienced nonsustained polymorphic or monomorphic ventricular tachycardia. Other frequent medical events in ibutilide recipients were generally also noted in the placebo group. CONCLUSIONS: Ibutilide is effective and safe for acute termination of atrial fibrillation or atrial flutter.

Adult↗
PubMed2001

Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium.

OBJECTIVES: We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability. BACKGROUND: The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear. METHODS: Isolated canine right atria were perfused with 1 to 5 micromol/l of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD(90) was measured during regular pacing (S(1)) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S(2)). RESULTS: At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD(90) from 124 +/- 15 ms to 72 +/- 9 ms (p < 0.01) with 1 to 2.5 micromol/l of ACh, S(2) pacing induced single, stable and stationary re-entrant wave fronts (307 +/- 277 cycles). They either anchored to pectinate muscles (5 tissues) or used pectinate muscles as part of the re-entry (4 tissues). When ACh was raised to 2.5 to 5 micromol/l, the APD(90) was further shortened to 40 +/- 12 ms (p < 0.01); S(2) pacing induced in vitro AF by two different mechanisms. In most episodes (n = 13), AF was characterized by rapid, nonstationary re-entry and multiple wave breaks. In three episodes with APD(90) <30 ms, AF was characterized by rapid, multiple, asynchronous, but stationary wave fronts. CONCLUSIONS: Progressive APD shortening modulates atrial wave front stability and converts atrial flutter to AF by two mechanisms: 1) detachment of stationary re-entry from the pectinate muscle and the generation of multiple wave breaks; and 2) formation of multiple, isolated, stationary wave fronts with different activation cycle lengths.

Acetylcholine↗
PubMed2004

[Catheter ablation of atrial flutter and atrial fibrillation].

Within the past 20 years, refinements in electrophysiologic mapping techniques have provided a better understanding of the pathophysiology of atrial flutter and atrial fibrillation (AF), which resulted in the development of catheter ablation techniques for this arrhythmias. Nowadays, catheter ablation has become the first line treatment of recurrent symptomatic or hemodynamically significant atrial flutter. In contrast, catheter ablation of AF is still an investigational procedure and should be restricted to patients with symptomatic AF who have been refractory to multiple antiarrhythmic drugs. In symptomatic patients with AF and an uncontrolled ventricular rate who have failed treatment with several antiarrhythmic drugs and who do not fit for primary catheter ablation of AF atrioventricular junction ablation with prior pacemaker implantation is recommended.

Anti-Arrhythmia Agents↗
PubMed1996

[Epidemiology, risk factors, and pathogeny of atrial fibrillation and atrial flutter].

Atrial fibrillation is a frequent arrhythmia which has a high prevalence after 65 years of age, thus the typical patient's age is about 75. There are two atrial fibrillation predictors: traditional factors of cardiovascular risk (age, male sex, high blood pressure, diabetes), and structural heart disorders (heart failure, valvular heart disease). All preventive measures to reduce atrial fibrillation incidence, must be directed towards these factors. Additionally, left atrial size, ejection fraction and ventricular hypertrophy are echocardiographic predictors. Atrial fibrillation doubles the mortality rate and is related to an annual stroke rate of 4.5%. The stroke risk factors are: age, hypertension, diabetes, previous stroke, congestive heart failure, coronary heart disease, mitral stenosis, prosthetic heart valves and thyrotoxicosis. Left atrial size and ventricular disfunction are echocardiographic stroke risk factors. Each patient's risk can be stratified on the basis of these factors. All of this information is essential to handle the arrhythmia appropriately; this arrhythmia may be more important than has been thought. Atrial flutter is not very frequent and so it is less studied; however it is an arrhythmia with a similar clinical context to atrial fibrillation, although, probably, with a smaller embolic risk.

Atrial Fibrillation↗
PubMed1975

Atrial activity during exercise in patients with atrial flutter or atrial fibrillation.

The atrial activity was studied at rest and during exercise in 6 patients with atrial flutter and in 7 patients with atrial fibrillation. In the latter, a special recording technique was used which permitted identification of the f-waves. No increase in the frequency of the atrial waves was found. Thus the increase of the ventricular rate during work in patients with atrial flutter or atrial fibrillation seems to be caused by a change in the atrio-ventricular conduction.

Adult↗
PubMed2001

Effect of autonomic neurotransmitters on excitable gap composition in canine atrial flutter.

Atrial arrhythmias are believed to be influenced by autonomic nervous system tone. We evaluated the effects of sympathetic and parasympathetic activation on atrial flutter (AF1) by determining the effects of norepinephrine (NE) and acetylcholine (ACh) on the composition of the excitable gap. A model of reentry around the tricuspid valve was produced in 17 chloralose anesthetized dogs using a Y-shaped lesion in the intercaval area that extended to the right atrial appendage. Excitable gap characteristics were determined during AF1 by scanning diastole with a single premature extrastimulus at progressively shorter coupling intervals to define the reset-response curve. Measurements were made during a constant infusion of NE (15 microg/min) into the right coronary artery and repeated during ACh infusion (2 microg/min) following a 15 min recovery period. The excitable gap (27 +/- 1 ms) was significantly (P < 0.001) increased by NE (34 +/- 1 ms) and ACh (50 +/- 2 ms). The fully excitable portion (7 +/- 1 ms) was also significantly (P < 0.001) increased by NE (17 +/- 1 ms) and ACh (43 +/- 2 ms). We conclude that both neurotransmitters increase the safety margin of full excitability ahead of the wavefront, demonstrating that parasympathetic and sympathetic activation can facilitate the persistence of this refractory atrial arrhythmia.

Acetylcholine↗
PubMed1987

Effects of N-acetylprocainamide on experimental atrial flutter and atrial electrophysiologic properties in conscious dogs with sterile pericarditis: comparison with the effects of quinidine.

N-acetylprocainamide (NAPA) is said to have class III antiarrhythmic drug properties. The effects of NAPA (25 mg/kg intravenously) on sustained, stable, reentrant atrial flutter induced in 12 conscious dogs using a sterile pericarditis model were studied and compared with the effects of quinidine (5 mg/kg intravenously) given on a different day in 10 of the same 12 dogs. The effects of these drugs on atrial excitability, the atrial effective refractory period and intraatrial conduction time measured during rapid atrial pacing performed during sinus rhythm were also compared. The mean NAPA and quinidine serum levels were 17.7 and 7.1 micrograms/ml, respectively. Both NAPA and quinidine immediately prolonged the atrial flutter cycle length in all dogs, from 118 +/- 15 to 141 +/- 18 ms and from 119 +/- 17 to 153 +/- 21 ms, respectively (both p less than 0.001), and then terminated atrial flutter in 11 of the 12 NAPA studies and in 6 of the 10 quinidine studies. Neither drug affected atrial excitability. Both NAPA and quinidine increased the atrial effective refractory period significantly, from 138 +/- 17 to 168 +/- 20 ms (p less than 0.001) and from 136 +/- 14 to 148 +/- 16 ms (p less than 0.01), respectively. NAPA did not change intraatrial conduction time measured during atrial pacing at 150 beats/min, but during atrial pacing at 300 beats/min, it prolonged it from 51 +/- 9 to 54 +/- 10 ms (p less than 0.05), and at 400 beats/min, from 52 +/- 10 to 64 +/- 13 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1980

Conversion of atrial flutter: rapid atrial pacing as a bedside technique.

Eleven patients with atrial flutter underwent intracardiac right atrial pacing at bedside in an attempt to terminate this dysrhythmia. Nine of the eleven patients were converted to sinus rhythm; the remaining two patients were converted to atrial fibrillation with a slower ventricular rate. There were no complications. The potential hazards of direct current cardioversion (anesthesia, fractures, muscle strain, myocardial injury, etc.) were avoided. In contrast to rapid atrial pacing in the electrophysiology laboratory, the bedside technique did not require a special laboratory setting, electronic or x-ray equipment, or technical personnel. Transportation of critically ill patients was obviated. Atrial flutter can be converted at the bedside to a more favorable rhythm; the expediency, safety, and low cost of this bedside cardioversion technique not only makes it feasible, but also it is often the procedure of choice.

Adult↗
PubMed1999

Atrial Flutter.

Atrial flutter can have serious short- and long-term consequences. Treatment options for an acute attack include direct-current cardioversion, atrial pacing, and intravenous drug therapy. For chronic disease or for recurrence, treatment options include ablation of the flutter, rate-controlling therapy, and antiarrhythmic drugs. Anticoagulation should be considered.

Journal Article↗
PubMed1991

The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation.

Computerized mapping of atrial fibrillation was performed in animals and man. To study atrial fibrillation in a systematic manner, we developed a clinically relevant experimental model of atrial fibrillation. Chronic mitral regurgitation was created surgically in 25 dogs without opening the pericardium. After several months of chronic mitral regurgitation, the atria became enlarged and sustained atrial fibrillation could be induced by standard programmed electrical stimulation techniques. Computerized isochronous activation maps of the atria were recorded during atrial fibrillation from 208 bipolar electrodes simultaneously. In a parallel study, human atrial fibrillation was mapped with a separate 160-channel intraoperative mapping system in patients with paroxysmal atrial fibrillation who were undergoing surgical correction of the Wolff-Parkinson-White syndrome. The canine activation sequence maps demonstrated a spectrum of rhythm abnormalities ranging from simple atrial flutter to complex atrial fibrillation. They also showed that macroreentrant circuits within the atrial myocardium were responsible for the entire spectrum of arrhythmias. Atrial reentry was also documented during human atrial fibrillation. All patients had nonuniform conduction around regions of bidirectional block in both atria resulting in multiple discrete wave fronts. In addition, six patients had a single reentrant circuit in the right atrium in which bidirectional block of the activation wave front occurred along the sulcus terminals between the venae cavae. The left atrium in all patients demonstrated multiple wave fronts and conduction block, but left atrial reentry could not be detected. Both the experimental study and the clinical study demonstrated that multiple wave fronts, nonuniform conduction, bidirectional block, and large (macroreentrant) reentrant circuits occur during atrial fibrillation. The presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation.

Adult↗
PubMed2001

Atrial Flutter.

Atrial flutter (AFl) is an arrhythmia resulting from reentry in a macroreentrant circuit, most commonly in the right atrium. Typical AFl uses the narrow isthmus of right atrial tissue between the tricuspid valve annulus and the inferior vena cava orifice as part of the macroreentrant circuit. The treatment of AFl is directed toward achieving the following four goals. 1) In the presence of AFl, adequate rate control is required, which can be achieved in most but not all patients by oral or intravenous digoxin, calcium channel blockers, or beta-blockers, alone or in combination. 2) Anticoagulation with warfarin should be considered in patients with recurrent AFl, especially those over 70 years of age, and those with a history of atrial fibrillation, stroke, or structural heart disease. 3) Conversion to sinus rhythm can be achieved in up to 70% of patients with intravenous ibutilide, but this should be reserved for patients with either normal hearts or only mild left ventricular dysfunction. Direct-current cardioversion is nearly 100% effective and is ideal for patients with left ventricular dysfunction. 4) Long-term maintenance of sinus rhythm may be achieved in up to 50% to 60% of patients by using antiarrhythmic drugs, including sotalol, amiodarone, dofetilide, propafenone, and flecainide, but with the potential for causing significant proarrhythmia and side effects. Radiofrequency catheter ablation may cure over 90% of patients with type 1 AFl (using the tricuspid valve to inferior vena cava isthmus), and from 70% to 90% of patients with atypical AFl. Newer mapping techniques, such as electroanatomic mapping, are likely to further reduce procedure time and improve success rates.

Journal Article↗
PubMed2002

Catheter ablation of atrial flutter and macroreentrant atrial tachycardia.

Catheter ablation has evolved from an experimental technique to first-line therapy for the treatment of atrial flutter. Atrial flutter is characterized by a macroreentrant atrial tachycardia circuit. Successful ablation of atrial flutter involves (1) mapping the atrial flutter to define the conduction zones within the re-entrant circuit to determine whether the atrial flutter is isthmus-dependent, non-isthmus-dependent, or atypical; (2) interrupting the atrial flutter macroreentrant circuit with an ablation catheter by creating either focal or linear lesions within a critical zone of slow conduction that extends to anatomical borders; and (3) terminating the tachycardia and demonstrating conduction block within the atrial flutter circuit after ablation. This update discusses the classification schemes of atrial flutter and macroreentrant atrial tachycardias, reviews the technique of radiofrequency catheter ablation, and highlights recent ablation approaches for atrial flutters and macroreentrant atrial tachycardias.

Atrial Flutter↗