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PubMed2001

Atrial flutter in fetuses and early childhood: a report of eight cases.

Atrial flutter is an uncommon arrhythmia in children. The presenting features and treatment responses of two fetuses and six children with atrial flutter were presented. Two patients were diagnosed prenatally at 31 and 35 weeks' gestation. One patient was successfully controlled in utero by maternal administration of digoxin and the other by direct current cardioversion after delivery. Two fetuses and 2 of 6 children had normal cardiac structure by echocardiogram. Three patients had right atrial enlargement due to atrial primun septal defect, secundum atrial septal defect with primary pulmonary hypertension, and endomyocardial fibrosis. One patient developed atrial flutter with sinus node dysfunction after surgical correction of total anomalous pulmonary venous connection. Four cases presented as atrial flutter with regular atrioventricular conduction (2:1 or 3:1 conduction) while the remainder presented with irregular atrioventricular conduction. Heart failure was presented in two patients and improved after the arrhythmias were controlled. Successful termination of atrial flutter was accomplished by using DC cardioversion in 4 patients and one patient converted to normal sinus rhythm following combination of digoxin and amiodarone administration. Digoxin was administered for one year as the prophylactic medication in six patients. None had recurrence of atrial flutter during the follow-up period of one to four years. Two patients required chronic digoxin and amiodarone therapy. We concluded that atrial flutter in fetuses and early childhood carries a good prognosis. Acute treatment with direct current cardioversion is sufficient in most patients, combination of digoxin and amiodarone may be an alternative therapy to convert atrial flutter.

Anti-Arrhythmia Agents↗
PubMed1990

Successful treatment of congenital atrial flutter with antitachycardia pacing.

Congential atrial flutter is a condition that rarely requires chronic pharmacological therapy. An unusual case of congenital atrial flutter is described which was resistant to medical therapy, yet responded well to antitachycardia pacing. While most experience with antitachycardia pacing in pediatrics has been with the postoperative congenital heart patient, patients such as the one described with unscarred atria may prove to be the most suitable pediatric candidates for this pacing modality.

Atrial Flutter↗
PubMed2003

Optimizing the detection of bidirectional block across the flutter isthmus for patients with typical isthmus-dependent atrial flutter.

The purpose of this study was to show that multipolar electrographic recordings along the subeustachian isthmus (SI) can better differentiate slow conduction from complete isthmus block after atrial flutter ablation, leading to a lower incidence of recurrent atrial flutter (Afl). Despite the presence of various techniques to identify bidirectional conduction block (BDB) after isthmus ablation for typical Afl, several studies, including a report from a national registry, suggest that radiofrequency ablation is still associated with a 15% recurrence rate. Thus, techniques that can distinguish slow conduction from complete isthmus block have the potential for reducing long-term recurrences. We evaluated patients who underwent radiofrequency ablation for typical isthmus-dependent Afl. Patients were separated into 2 groups. Group A underwent assessment of BDB with conventional methods. In group B, BDB was assessed by placing a multipolar catheter along the floor of the SI, pacing adjacent to the line of radiofrequency application, and assessing electrographic activation on either side. One hundred thirty-one cases of Afl ablation were analyzed (86 in group A, 45 in group B). Over a mean follow-up period of 17 months, recurrence rates of Afl were 16.5% in group A and 4.3% in group B (p = 0.043). Thus, assessment of BDB by placement of a multipolar catheter across the SI after ablation of typical Afl is associated with a significant reduction in long-term recurrence of Afl.

Aged↗
PubMed1996

Atrial flutter: a newly recognized complication of pediatric lung transplantation.

BACKGROUND AND METHODS: Atrial flutter after pediatric lung transplantation has not previously been reported. We reviewed the records of 78 children who underwent lung transplantation at our institution to characterize the incidence and clinical course of postoperative atrial flutter. The diagnosis was based on either a surface or transesophageal electrocardiogram that demonstrated a fixed cycle length atrial tachycardia that did not require ventricular participation. RESULTS: Atrial flutter occurred in seven of 62 (11.3%) patients who underwent bilateral sequential lung transplantation, zero of 10 patients after single lung transplantation, and zero of six patients after heart-lung transplantation. Ages of the patients with atrial flutter ranged from 2.5 months to 14 years. Electrocardiographic findings among patients varied with respect to p-wave morphology and atrioventricular conduction. No patient had a prior atrial arrhythmia or coexisting structural cardiac disease. None had atrial flutter in relation to a rejection episode. Two patients had atrial flutter transiently during the first postoperative day, but it resolved spontaneously. Five patients had recurrent atrial flutter that began 13 +/- 7 days after the operation. The mean cycle length of atrial flutter was 196 +/- 65 msec. The arrhythmia was unresponsive to digoxin in four patients to whom it was administered. It was controlled with procainamide in four patients and with flecainide in one. At 1 and 6 months after lung transplantation, procainamide was discontinued in two patients without recurrence. One patient died of bronchiolitis obliterans 6 months after the operation while still receiving flecainide. Two patients continue to receive procainamide 4 and 7 months after transplantation. CONCLUSIONS: (1) Atrial flutter commonly occurs after bilateral lung transplantation in children. (2) Electrocardiographic manifestations are variable. (3) Type 1 antiarrhythmic agents provide satisfactory control.

Adolescent↗
PubMed1981

Overdrive and programmed atrial electrostimulation in the study of the electrogenetic mechanism of atrial flutter in man.

The response of atrial flutter (AF) to programmed atrial stimulation (PAS) (13 cases) and overdrive atrial pacing (OAP) ws studied in a total of 18 patients. During PAS the return cycle was equal to the basic cycle of AF in six patients, shorter in one patient, and slightly longer in six; it was never compensatory. ATrial flutter terminated in two patients by PAS and by OAP in three. In 4 patients, PAS resulted in an acceleration of the AF rate, followed by spontaneous interruption within 2 seconds. In the remaining patients, the stimulation either converted the AF into an uncommon type of AF (two patients) or into atrial fibrillation that was followed by spontaneous return to sinus rhythm. In two patients it was possible to reproduce the AF with PAS; in one of the patients another type of AF was induced. Some of the data observed suggest a re-entry circuit as the electrogenetic mechanism responsible for AF in man.

Adult↗
PubMed1994

The patient with recurrent atrioventricular nodal reentrant tachycardia or chronic atrial fibrillation or atrial flutter.

Atrioventricular nodal reentry tachycardias, atrial fibrillation, and atrial flutter are common symptomatic arrhythmias encountered in clinical practice. The reentry mechanisms and pathophysiology of atrioventricular nodal reentrant tachycardias, atrial fibrillation, and atrial flutter are described. This article outlines the therapeutic approaches used in the acute phases of presentation. Nursing implications for patients admitted to intensive care/telemetry units are discussed.

Atrial Fibrillation↗
PubMed1996

Atrial flutter after lateral tunnel construction in the modified Fontan operation: a canine model.

Intraatrial reentrant tachycardia, or atrial flutter, is a common postoperative problem after Fontan repair, which involves an atriopulmonary connection. A modification of Fontan repair, total cavopulmonary connection, minimizes the portion of the right atrium exposed to stretch and hypertension; however, atrial flutter continues to occur after this procedure. We postulated that the intraatrial lateral tunnel suture line of total cavopulmonary connection, in the absence of physiologic alterations such as atrial hypertension or stretch, provides the necessary electrophysiologic substrate for atrial flutter. The purpose of this study was to produce a canine model of total cavopulmonary connection (1) to establish that the intraatrial suture line alone is sufficient to permit sustained atrial flutter and (2) to characterize the pathways of resulting reentrant arrhythmias. After induction of general anesthesia, 25 to 30 kg dogs (n = 17) underwent median sternotomy, cradling of the pericardium, and placement of a pacing electrode on the right atrial appendage. Normothermic cardiopulmonary bypass was initiated. The total cavopulmonary connection suture line was placed through a standard right atriotomy,simulating construcion of the lateral tunnel. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were placed through bilateral ventriculotomies. By means of atrial burst pacing and programmed extrastimulation, induction of atrial flutter was attempted. If atrial flutter could not be induced, isoproterenol was infused and the stimulation protocol was repeated. After induction of atrial flutter, mapping of the activation sequence was performed. Before suture line placement, no dog had inducible atrial flutter. After placement of the suture line, sustained atrial flutter was reproducibly induced in every dog, although isoproterenol was required for this in three (17.6%). The mean flutter cycle length was 177 +/- 30 msec. In each case, the atrial flutter circuit was limited to the right atrium, with the left atrium being passively activated. The atrial flutter circuit was dependent on a corridor of myocardium that resulted from conduction block on the free wall, created by the lateral margin of the total cavopulmonary connection. In no case was the atriotomy integral to the atrial flutter circuit. This study establishes that the total cavopulmonary connection baffle suture line alone, without alteration in circulatory physiology, creates a sufficient anatomic substrate for atrial flutter in a short-term canine model. Delineation of the anatomic boundaries of the reentrant circuit raises the possibility of targeting areas within the circuit that could be modified, potentially reducing the incidence of postoperative atrial flutter after total cavopulmonary connection.

Animals↗
PubMed1994

Management of atrial flutter after the Fontan procedure.

OBJECTIVES: The purpose of this study was to review the management of atrial flutter occurring after the Fontan procedure. BACKGROUND: Atrial flutter occurs frequently after the Fontan procedure and is often hemodynamically poorly tolerated. METHODS: The patients' charts were reviewed for relevant information. RESULTS: Between 1984 and 1992, 18 patients had atrial flutter after the Fontan procedure. The underlying heart defect was tricuspid atresia in nine, mitral atresia in six and double inlet left ventricle in three. All but three patients had undergone previous palliative surgery. The time interval from Fontan operation to atrial flutter was < 1 day to 16 years (mean 3.7 years). Seven had early atrial flutter before leaving the hospital. Electrophysiologic study in 15 showed sinus node dysfunction in 12. Atrial flutter was inducible in all patients, and 13 had > 1 flutter configuration. Digoxin and a variety of other antiarrhythmic agents (mean 2.7 drugs/patient) were tried with poor results. Only digoxin, amiodarone, flecainide and propafenone showed some benefit when used alone or in combination. Antitachycardia pacemakers were implanted in 16 patients (endocardial 14, epicardial 2) and, with drugs, were useful in 8 (50%). Because atrial flutter was resistant to treatment, right atriectomy was performed in three patients (with benefit in two, one death), successful radiofrequency catheter His bundle ablation in one patient and catheter ablation of atrial flutter in three patients (two failed, one partial success). One patient underwent heart transplantation, and two died suddenly. Another died of complications after an elective epicardial pacemaker replacement procedure. CONCLUSIONS: Atrial flutter after the Fontan procedure is difficult to control. Aggressive drug and antitachycardia pacemaker therapy help about half of the patients. When these measures fail, other options, such as atriectomy, His bundle ablation or catheter ablation of atrial flutter, need consideration. The risk of sudden death justifies the use of such aggressive treatment methods.

Adolescent↗
PubMed1998

Prevention of acute inducible atrial flutter in dogs by using an ibutilide-polymer-coated pacing electrode.

Atrial arrhythmias (atrial fibrillation or atrial flutter) after coronary artery bypass graft surgery are difficult to prevent or treat and often result in significant morbidity. Prior experimental studies by our group showed improved therapeutic efficacy for antiarrhythmic drugs delivered via controlled-release polymeric matrices implanted on the epicardial surface. These experiments were conducted to test the hypothesis that direct atrial epicardial administration of ibutilide from a controlled-release system (compared with intravenous administration) can reduce the inducibility of atrial flutter in the acute postoperative atrial myocardium. Polymeric sustained-release preparations were formulated by solvent casting of an ibutilide and polyurethane (Pellathane) solution in tetrahydrofurane. Multilayer solvent-casted coatings on pacing electrode wires were carried out to fabricate a sustained-release electrode system. In animal model studies, each dog underwent a thoracotomy, followed by a right atriotomy that was repaired. Induction of atrial flutter was attempted by burst pacing with the bipolar pacing catheter. Sinus rhythm was restored with overdrive pacing. After determining the induction rate (percentage) of atrial flutter in the baseline state, a stainless-steel wire coated with the drug-delivery system, 10% ibutilide/90% polyurethane (n = 7), or without drug (polyurethane coating without ibutilide, n = 5; control) was sewn onto the right atrium. Systemic intravenous administration of ibutilide (1.2 microg/kg/h) also was carried out in a separate group of animals after atriotomy (n = 5). For ibutilide (at an estimated dose of 1.2 microg/kg/h), the atrial-flutter results were 41.85 +/- 2.21% induction for baseline compared with 12.42 +/- 5.26% (p = 0.02) after the ibutilide wire implant. In the control dogs, atrial flutter was induced 29.4 +/- 4.7% at baseline and 25.2 +/- 5.1% after implantation of the control wire (p = 0.4). Ibutilide coronary venous serum concentrations at the end of the ibutilide-polyurethane electrode experiments were 2.25 +/- 0.2 ng/ml (mean +/- SEM) versus systemic levels that were below the limits of detection. Systemic intravenous ibutilide infusions had no effect on the inducibility of atrial flutter. In conclusion, an epicardial implantable electrode coating with an ibutilide controlled drug-release system significantly reduced the inducibility of atrial flutter in an experimental atriotomy model. These results suggest that atrial arrhythmias occurring after coronary bypass surgery may be prevented by local atrial administration of ibutilide from a controlled-release pacing electrode.

Animals↗
PubMed1977

Cardiac malformations presenting as congenital atrial flutter.

A case of congenital atrial flutter with tetralogy of Fallot is presented. Fetal tachycardia was detected three weeks prior to birth and digitalization converted the arrhythmia to a normal sinus rhythm at two days of age. The seven previously reported cases of congenital atrial flutter associated with congenitally malformed hearts are reviewed.

Atrial Flutter↗
PubMed1996

Spontaneous onset of type I atrial flutter in patients.

OBJECTIVES: This study sought to characterize the spontaneous onset of atrial flutter in patients. BACKGROUND: Temporary epicardial electrodes are routinely placed on the atria of patients at the time of open heart surgery and brought out through the anterior chest wall for potential diagnostic and therapeutic use in the postoperative period. We utilized these electrodes to study the spontaneous onset of type 1 atrial flutter in 16 patients in the postoperative period after open heart surgery. METHODS: Twenty-seven episodes of the spontaneous onset of type I atrial flutter from sinus rhythm were studied in these 16 patients by recording bipolar atrial electrograms simultaneously with at least one electrocardiographic lead during each episode. RESULTS: In all 27 episodes, the onset of type I atrial flutter was through a transitional rhythm of variable duration (mean 9.3 s) precipitated by a premature atrial beat. In 21 episodes, the transitional rhythm was atrial fibrillation; in 3 episodes it was type II atrial flutter that appeared to generate atrial fibrillation; and in 3 episodes it was a brief (3 to 6 beats), rapid, irregular arrhythmia. CONCLUSIONS: Type I atrial flutter does not start immediately after a premature atrial beat. Rather, it starts after a transitional rhythm that is usually atrial fibrillation. Extrapolating from mapping studies of the onset of atrial flutter in the canine pericarditis model, we suggest that a transitional rhythm is required for the initiation of type I atrial flutter because during that rhythm, the requisites for development of the atrial flutter reentry circuit evolve.

Atrial Fibrillation↗
PubMed1992

Salvage transvenous rapid atrial pacing to terminate atrial flutter after cardiac operations.

Atrial flutter occurring after cardiac operations normally responds well to atrial overdrive pacing through epicardial atrial pacing wires and medication. When this fails, transvenous atrial overpacing offers an attractive alternative. We performed the procedure 29 times in 25 patients. Sinus rhythm returned acutely after 25 procedures in 21 patients and persisted with medication in 20 patients at follow-up. The procedure was well tolerated by all.

Aged↗
PubMed2000

Incidence and predictors of atrial flutter in the general population.

OBJECTIVES: The goal of our study was to determine the incidence and predictors of atrial flutter in the general population. BACKGROUND: Although atrial flutter can now be cured, there are no reports on its epidemiology in unselected patients. METHODS: The Marshfield Epidemiological Study Area (MESA), a database that captures nearly all medical care among its 58,820 residents was used to ascertain all new cases of atrial flutter diagnosed from July 1, 1991 to June 30, 1995. To identify predisposing risk factors, we employed an age- and gender-matched case-control study design using eight additional variables. RESULTS: A total of 181 new cases of atrial flutter were diagnosed for an overall incidence of 88/100,000 person-years. Incidence rates ranged from 5/100,000 in those <50 years old to 587/100,000 in subjects older than 80. Atrial flutter was 2.5 times more common in men (p < 0.001). The risk of developing atrial flutter increased 3.5 times (p < 0.001) in subjects with heart failure and 1.9 times (p < 0.001) for subjects with chronic obstructive pulmonary disease. Among those with atrial flutter 16% were attributable to heart failure and 12% to chronic obstructive lung disease. Three subjects (1.7%) without identifiable predisposing risks were labeled as having "lone atrial flutter." CONCLUSIONS: This study, the first population-based investigation of atrial flutter, suggests this curable condition is much more common than previously appreciated. If our findings were applicable to the entire U.S. population, we estimate 200,000 new cases of atrial flutter in this country annually. At highest risk of developing atrial flutter are men, the elderly and individuals with preexisting heart failure or chronic obstructive lung disease.

Adult↗
PubMed1996

Left-sided atrial flutter: characterization of a novel complication of pediatric lung transplantation in an acute canine model.

BACKGROUND: Postoperative atrial flutter has been observed in approximately 10% of children undergoing lung transplantation at our institution. We hypothesized that the left atrial anastomoses made to establish pulmonary venous continuity provide the primary electrophysiologic substrates for atrial flutter. OBJECTIVES: Our objectives were (1) to determine whether the left atrial suture lines alone are sufficient to produce atrial flutter in an acute canine model of lung transplantation and (2) to characterize any resulting reentrant circuits to surgically ablate the atrial flutter. METHODS: Supported by cardiopulmonary bypass, adult dogs (n = 10) underwent bilateral pneumonectomies. The left atrial anastomotic suture lines were simulated by dividing the tissue between the ostia of the transected superior and inferior pulmonary veins and closing the resulting defects. Bilateral suture lines were placed in group 1 (n = 6) to simulate bilateral lung transplantation. In group 2 (n = 4), only a left-sided suture line was placed to represent single lung transplantation. Unipolar 253-point biatrial endocardial mapping electrodes were inserted via bilateral ventriculotomies. Atrial flutter was induced by atrial burst pacing, and activation sequence maps were generated. In five of six cases in group 1, a T-incision connecting the two suture lines and the mitral anulus was then made. In group 2, a single incision from the suture line to the mitral anulus was performed in each case. Burst pacing was subsequently repeated. RESULTS: Atrial flutter could not be induced after bypass alone in any case. After simulated lung transplantation, sustained atrial flutter was reproducibly induced in 10 of 10 dogs. The mean cycle length in all dogs was 133 +/- 7 msec. There was no significant difference in mean cycle length or activation sequence patterns between groups 1 and 2. The reentrant circuit was confined to the left atrium. Each simulated left atrial anastomosis created a zone of conduction block around which circus movement could occur. In group 1, either suture line functioned as the central obstacle. Atrial flutter was terminated in five of five dogs in group 1 by means of the T-incision and in all four dogs in group 2 with the incision connecting the suture line to the mitral anulus. CONCLUSIONS: (1) In an acute canine model of lung transplantation, each left atrial suture line alone provides an electrophysiologic substrate for atrial flutter by creating a zone of conduction block around which circus movement can occur. (2) Extending this zone of block to the mitral anulus, together with interruption of the isthmus of tissue between the two suture lines present after bilateral lung transplantation, terminates the atrial flutter in this model and may have an application prophylactically at the time of lung transplantation in children to prevent postoperative atrial flutter.

Anastomosis, Surgical↗
PubMed1996

Effects of azimilide dihydrochloride on circus movement atrial flutter in the canine sterile pericarditis model.

INTRODUCTION: The effects of a Class III agent, azimilide dihydrochloride, on atrial flutter circuits were studies in a functional model of single loop reentrant atrial flutter using dogs, 3 to 5 days after production of sterile pericarditis. METHODS AND RESULTS: A computerized mapping system was used to construct activation maps from 138 to 222 epicardial sites in the right atrium. Doses of 3, 10, and 30 mg/kg i.v. azimilide dihydrochloride were analyzed in 8 dogs in which sustained atrial flutter lasting more than 30 minutes was induced by burst pacing. Atrial flutter was always due to single loop circus movement reentry in the lower right atrium. At 3 mg/kg, azimilide dihydrochloride terminated atrial flutter in 2 dogs; however, atrial flutter was reinduced. At 10 mg/kg, atrial flutter was terminated in all 8 dogs but was reinduced in 4 dogs with slower rate. At 30 mg/kg, atrial flutter was terminated in the remaining 4 dogs and could not be reinduced. Atrial flutter cycle length always increased prior to termination. Isochronal activation maps showed that the increase in cycle length was due to additional conduction delays in the slow zone of the reentrant circuit. The site of termination was always located within the slow conduction zone situated in the lower right atrium between the line of functional conduction block and the AV ring. Effective refractory periods (ERPs) were measured at selected sites in the slow zone and normal zone at twice diastolic threshold for the 10 mg/kg dose. Azimilide preferentially prolonged ERP in the slow zone (42.4 +/- 20.1 msec, mean +/- SD) compared with the normal zone (23.3 +/- 15.4 msec, P < 0.0001). The increase in cycle length corresponded with the increase in ERP in the slow zone. CONCLUSIONS: In a functional model of circus movement atrial flutter, azimilide dihydrochloride terminates and prevents reinduction of atrial flutter by a preferential increase in refractoriness leading to further conduction delay and conduction block in the slow zone of the functional reentrant circuit.

Animals↗
PubMed1998

New electrocardiographic criteria for the differentiation between counterclockwise and clockwise atrial flutter: correlation with electrophysiological study and radiofrequency catheter ablation.

OBJECTIVE: To develop new electrocardiographic (ECG) criteria for the differentiation between counterclockwise and clockwise atrial flutters. BACKGROUND: Traditionally, the ECG differentiation between counterclockwise and clockwise atrial flutters is based on the flutter wave polarity in the inferior leads. However, determination of flutter wave polarity is subjective and sometimes difficult, especially in flutter waves of undulating pattern. PATIENTS: The study comprised 37 consecutive patients with drug resistant atrial flutter; 30 had counterclockwise and 17 had clockwise atrial flutter (10 had both forms of atrial flutter). The isthmus dependence was confirmed by entrainment study and catheter ablation. The ECG patterns of both types of atrial flutter were compared and the flutter wave polarity in the inferior leads was determined by four independent cardiologists. RESULTS: The flutter wave polarity in the inferior leads appeared negative in 24, positive in one, and equivocal in five of the counterclockwise atrial flutters; polarity appeared negative in one, positive in 10, and equivocal in six of the clockwise atrial flutters. However, the aVF/lead I flutter wave amplitude ratio was > 2.5 in all counterclockwise but < 2.5 in all clockwise atrial flutters. The flutter wave nadirs in the inferior leads corresponded to the upstrokes in V1 in all counterclockwise atrial flutters, but corresponded to the downstrokes in V1 in all clockwise atrial flutters. CONCLUSIONS: The flutter wave polarity in the inferior leads does not correlate well with the flutter wave rotating direction. However, counterclockwise and clockwise atrial flutters can be differentiated by new ECG criteria with high accuracy.

Adult↗
PubMed1995

Radiofrequency catheter ablation for the treatment of common atrial flutter in humans.

Endocardial catheter ablation has been recently been proposed for the treatment of arrhythmias originating in the right atrium. In this study, we used this technique in 5 patients with paroxysmal common atrial flutter and 3 patients with paroxysmal uncommon atrial flutter. Various antiarrhythmic agents had failed to prevent the recurrence of these episodes. In each procedure, we used a large-tip 7 F quadripolar catheter electrode that was introduced via the femoral vein into the lower part of the right atrium. The two distal electrodes were used to record double-spike potentials or fragmented electrograms. A unipolar electrogram recording from a distal electrode of the same catheter was also used to identify local activation. The targets for ablation were sites which showed double-spike potential and fragmented electrogram 40-60 msec earlier than the onset of the F wave. Application of radiofrequency (RF) energy (25-40 watts) (3-17 applications) terminated atrial flutter and prevented reinduction of atrial flutter in the 5 patients with common atrial flutter. However, atrial flutter could not be terminated with the application of RF energy in the 3 patients with uncommon atrial flutter. The sites at which ablation was successful were located inferior or posterior to the coronary sinus ostium between the inferior vena cava and the tricuspid valve annulus, and were characterized by double-spike potentials and fragmented electrograms with activation times > or = 40 msec before the onset of the F wave. This area may represent the exit site from the area of slow conduction, since pacing from this site showed concealed entrainment of the F wave, and a local electrogram to the onset of the F wave coincided with the pacing spike to the onset of the F wave. Follow-up of these 5 patients (19.4 +/- 10.4 weeks) revealed recurrence of the original atrial flutter in 1 patient and a new type of atrial flutter in 1 patient. The other 3 patients have been episode-free, although an antiarrythmic agent was given for the treatment of paroxysmal atrial fibrillation in 2 patients. We conclude that the application of RF energy to the presumed critical area in the atrial flutter reentrant circuit seems to be effective in terminating and preventing common atrial flutter. Long-term follow-up is required for the recurrence of atrial flutter.

Adolescent↗
PubMed1996

Use of intravenous dofetilide in atrial flutter with hemodynamic instability.

Paroxysmal atrial flutter is a drug-resistant supraventricular tachyarrhythmia that is often accompanied by hemodynamic instability due to an excessive ventricular response. We report here a case of atrial flutter with 1:1 atrioventricular conduction, in which we were able to rescue the patient from a state of cardiogenic shock by using intravenous dofetilide, a new class III antiarrhythmic agent. Dofetilide was suitable for the treatment because it immediately increased atrioventricular nodal refractoriness without any negative inotropic action.

Adult↗