Atrial Overdrive Pacing Research Articles

Effects of increased heart rate and sympathetic tone on intraventricular electrogram morphology

Electrogram pattern recognition by way of morphologic analysis has been proposed as a technique that may improve discrimination of ventricular tachycardia from sinus rhythm by anti-tachycardia devices. The potential impact that increases in heart rate and sympathetic tone could have on such techniques, however, has not been previously determined. A comparative study was undertaken to quantify possible changes in ventricular electrogram morphology using correlation waveform, area of difference, and amplitude analyses in 6 patients during atrial overdrive pacing at cycle lengths of 600 and 400 ms (group A), in 13 patients during infusions of physiologic doses of epinephrine (group B), and in 20 patients undergoing infusions of isoproterenol (group C). Four patients were in both groups A and B. A bipolar intraventricular template of cardiac depolarization during sinus rhythm at rest was compared with depolarization during subsequent passages of sinus rhythm at rest and subsequently increased heart rate. In 36 of 39 patients, waveform configuration as assessed by correlation waveform analysis remained relatively stable during atrial overdrive pacing, epinephrine infusion, and isoproterenol infusion when compared with sinus rhythm at rest. The correlation value did not fall below 0.950 in any patient. Area of difference values for the same 36 patients changed by an average of 6 and 37% during atrial overdrive pacing at cycle lengths of 600 and 400 ms intervals, respectively, by 3% during epinephrine infusion, and by 17% during isoproterenol infusion. In these same patients, there was an average change in electrogram amplitude of −1% during atrial overdrive pacing at 600 ms, 26% during pacing at 400 ms, −1% during epinephrine infusion, and 12% during isoproterenol infusion. Little or no correlation was found between relative changes of amplitude and changes of correlation coefficient during any intervention. However, changes in amplitude and changes in area of difference exhibited weak to moderate correlation during infusion of epinephrine and isoproterenol. Despite some amplitude variation, overall waveform morphology remains relatively constant during increases in heart rate with or without concurrent changes in sympathetic tone. These findings suggest that heart rate increases are unlikely to confound time-domain detection schemes used in antitachycardia devices.

Natural history of isolated atrial flutter in infancy

To clarify the natural history of isolated (i.e., without associated congenital cardiac anomalies) atrial flutter in infancy, we reviewed the clinical course in nine patients who were seen with this arrhythmia in the first year of life (range 1 day to 4 months). Atrial flutter was identified by the typical sawtooth pattern in leads II, III, and aVF of the surface electrocardiogram or the pattern of atrial flutter on an atrial electrogram recorded through the esophagus. The mean cycle length of the atrial flutter was 151 msec (atrial rate 397 beats/min). Six of the nine patients had other perinatal problems, such as immune and nonimmune hydrops fetalis (two patients), pneumonia (one patient), anemia (five patients), or low birth weight (one patient). In all patients the rhythm reverted to normal, either spontaneously (two patients), with overdrive pacing (four patients), or after oral digoxin therapy (three patients). No consistent temporal relationship between digoxin administration and conversion was observed; conversion was instantaneous in the four patients who received atrial overdrive pacing. Four patients were discharged receiving digoxin therapy (6 months to 1 year). One patient had supraventricular tachycardia after discharge that was controlled with digoxin. No recurrence of atrial flutter was observed among the nine patients during a mean follow-up of 6.8 years (range 0.2 to 20 years). We conclude that isolated atrial flutter in infancy is rare, has a good prognosis, may be related to transient perinatal events, and often spontaneously converts to normal sinus rhythm; however, when it does not, it will respond to transesophageal pacing. Acute and chronic digoxin therapy is probably unnecessary.

Usefulness of excitable gap and pattern of resetting in atrial flutter for determining reentry circuit location

Clinical and experimental data show that type I atrial flutter is due to a reentry mechanism with an excitable gap. To define the location of the reentry circuit of atrial flutter, width of excitable gap, poststimulation cycle and pattern of reset after premature stimulus were analyzed in 18 patients during atrial flutter at multiple atrial sites (high, lateral, posterior and septal right atrium, and coronary sinus). The pattern of reset was defined as flat or increasing whether the return cycle remained unchanged or prolonged with increasing prematurity. Shorter values of the excitable gap were found at the coronary sinus (33 ± 8 ms) and high right atrium (30 ± 10 ms) than at the posterior (43 ± 9 ms) or septal right atrium (45 ± 11 ms). Intermediate values (36 ± 8 ms) were measured at the lateral right atrium. Poststimulation cycle, corrected for atrial flutter cycle length, was shorter in the posterior (6 ± 7 ms) and septal right atrium (5 ± 7 ms) than in the coronary sinus (35 ± 9 ms), and the high (23 ± 10 ms) and lateral right atrium (15 ± 9 ms). A flat pattern of resetting occurred more frequently at the septal (18 of 18 patients) and posterior right atrium (15 of 18) than at the lateral (8 of 18) and high right atrium (2 of 17), and was never observed at the coronary sinus. Atrial flutter was successfully terminated by overdrive atrial pacing in 15 of 18 patients, and termination was more easily obtained from the septal and posterior right atrium. The relation between shortest poststimulation cycle, flat pattern of resetting and widest excitable gap, probably identifies sites closer to the reentry circuit. This pattern is consistently observed at the septal and posterior right atrium. These criteria might be useful to improve efficacy in the electric termination of atrial flutter and in ablative therapy.

Linking in accessory pathways. Functional loss of antegrade preexcitation.

Concealed retrograde activation has been proposed as a mechanism for antegrade conduction block in the bundle branches and atrioventricular accessory pathways. We studied this hypothesis (linking) in 10 patients with the Wolff-Parkinson-White syndrome in whom antegrade preexcitation could be persistently blocked by overdrive atrial pacing. An atrial pacing protocol, with a decremental ramp followed by an incremental ramp, defined a range of atrial paced cycle lengths (linking window) associated with both persistent conduction and block in the accessory pathway. Within the limits of the linking window, the ability of an atrial impulse to conduct over the accessory pathway was dependent on the preceding state (i.e., conduction or block). The observed linking window ranged from 70 to 290 msec (mean, 185 +/- 68 msec) and closely approximated the measured delay in retrograde activation of the accessory pathway during persistent antegrade block. The mean antegrade effective refractory period of the accessory pathways was long (486 +/- 156 msec), and in each case, it exceeded the antegrade refractory period of the normal atrioventricular pathway. Critically timed premature ventricular extrastimuli, delivered while linking was maintained in the accessory pathway, were able to interrupt the linking and restore antegrade accessory pathway conduction. These observations suggest that accessory pathway linking is associated with bidirectional block in the accessory pathway. The ability to initiate linking (and the stability of the phenomenon) depends on a critical relation between antegrade accessory pathway refractoriness and the magnitude of retrograde accessory pathway activation delay.

Life-Threatening Ventricular Arrhythmia (Torsades de Pointes) after Haloperidol Overdose

A 48-year-old woman developed QT prolongation and episodes of life-threatening ventricular tachycardia (torsades de pointes) after intentional overdose of haloperidol and orphenadrine. The arrhythmia did not respond to conventional anti-arrhythmic therapy but was suppressed by atrial overdrive pacing. A literature review identified haloperidol as the most likely cause of the torsades de pointes.

Further observations on entrainment of atrial flutter in the dog

To determine whether the first postpacing interval after entrainment was affected by recording and pacing sites, overdrive atrial pacing was undertaken in 13 episodes of atrial flutter with a mean flutter cycle length (FCL) of 140 ± 8 msec induced in seven dogs. Atrial flutter was induced by means of an anatomic obstacle. Seven recording sites, four in the right atrium and three in the left atrium, and three pacing sites, two in the right atrium and one in the left atrium, were selected. After entrainment from the right atrium at pacing cycle lengths that were 94% of the FCL, the first postpacing interval was not significantly different from the intrinsic FCL at each recording site, but it tended to be shorter than the FCL at the recording sites near pacing sites. For entrainment from the left atrium, the first postpacing interval was longer than the FCL at recording sites in the left atrium ( p < 0.001), but it was not different from the FCL at recording sites in the right atrium. These results are due to differences in placement of recording and pacing electrodes relative to the reentrant circuit. Also we observed that activation sequences involving three appropriately selected recording sites were always identical when paced from two different pacing sites at a single constant pacing cycle length. This new phenomenon may best be explained by postulating reentry as the mechanism for atrial flutter.

Alinidine Reduces the Incidence of Ischemic Ventricular Fibrillation in a Conscious Canine Model, a Protective Effect Antagonized by Overdrive Atrial Pacing

The antiarrhythmic and antifibrillatory effects of the specific bradycardic agent alinidine were evaluated in a conscious canine model of myocardial infarction and sudden death, and by determination of ventricular fibrillation thresholds (VFT) in anesthetized dogs. Programmed electrical stimulation (PES) was performed in conscious animals, 3-5 days after a 2-h occlusion/reperfusion of the left anterior descending coronary artery (LAD). Dogs in which PES resulted in a reproducible nonsustained or sustained ventricular tachycardia (VT) were randomized to receive either intravenous alinidine (1 mg/kg, n = 11) or intravenous vehicle (n = 10). Programmed electrical stimulation and measurement of electrophysiologic parameters were repeated after 30 min, and the animals were entered into the sudden death protocol by introducing a 150 microA anodal current to the lumen of the left circumflex coronary artery (LCX) via a surgically implanted silver wire electrode. A second alinidine-treated group (n = 3) had heart rates controlled by atrial pacing during this period. Alinidine failed to prevent the programmed electrical induction of VT in 10 of 11 animals, but significantly reduced both sudden (less than 1 h ischemia) and 24-h mortality as compared to the ventricle group. Infarct sizes were similar in the two groups, but the ischemia-related increase in heart rate was attenuated (p less than 0.05) by alinidine and the onset of ischemia tended to be delayed. All of the atrial-paced animals died acutely. Heart rate decreased after alinidine (p less than 0.01), but apart from a single index of refractoriness, the drug was without electrocardiographic or electrophysiologic effects. Neither alinidine nor vehicle demonstrated any effect upon VFT in two groups of five animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Automaticity of the SN and A-V Junctional Tissue Before and After Chemical Denervation in the Dog

Automaticity of SN and A-V junctional tissue was studied in 40 dogs in which a stable junctional rhythm was obtained following thermal ablation of the SN and sulcus terminalis. Atrial overdrive pacing studies were performed both before and after chemical denervation of the heart. Control sinus cycle and junctional CL were 438 +/- 13 ms and 751 +/- 23 ms, respectively. Chemical denervation resulted in significant prolongation of both junctional CL and maximal corrected junctional recovery time; junctional rate was down to 46 percent of the sinus rate observed before suppression of SN activity. Neither sinus CL nor maximal corrected SN recovery time changed significantly after administration of drugs. The basal autonomic nervous system has a relatively greater influence on the junctional pacemaker than on the normal SN in the dog and, when SN was suppressed, chemical denervation prolonged the junctional CL by 23 percent and junctional recovery time by 63 percent.

Transesophageal electrocardiography and atrial pacing in acute cardiac care: diagnostic and therapeutic value.

The utility of transesophageal electrocardiography using a bipolar 'pill electrode' was assessed in 17 consecutive patients with tachycardia presenting to our casualty department. Standard 12-lead electrocardiography showed regular narrow QRS tachycardia in 12 patients, and five patients had wide QRS tachycardia. Esophageal atrial electrogram recordings were obtained in 14 patients (82%), and these were helpful in determining the mechanism of tachycardia in 11 patients (78%). Of these 11, seven patients fulfilled criteria for atrioventricular junctional (AVJ) tachycardia based on measurement of the minimum interval between the onset of ventricular depolarisation and earliest atrial (esophageal) activity. One of these patients had presented with a wide QRS tachycardia. The other four patients were diagnosed as having ventricular tachycardia (VT) following diagnosis of AV dissociation. Atrial overdrive pacing, via the pill electrode, successfully reverted four of the nine patients (44%) with narrow QRS tachycardia but no patient with VT. Esophageal recording during tachycardia is a simple, relatively non-invasive technique which is helpful in suggesting the mechanism of tachycardia both in patients with narrow and wide QRS tachycardia, and may have a therapeutic role in patients with AVJ tachycardia.

Reappraisal of Atrioventricular Junctional Pacemaker Automaticity in the Sick Sinus Syndrome: Clinical Significance and the Role of Autonomic Chronotropic Influences

Postpacing impulse recovery times of the junctional tissue (junctional automaticity) were determined by atrial or ventricular overdrive pacing in 27 patients with dysfunction of the sinus node. The maximum junctional recovery time (MJRT) could be measured in 22 patients and ranged from 1,630 to 9,730 ms (mean 3,860 +/- 2,077); the maximum corrected junctional recovery time (MJRTc) could be measured in 18 patients and ranged from 140 to 5,986 ms (mean 2,089 +/- 1,529). Autonomic influence on the JRTs was evaluated by intravenous administration of atropine (1.5 mg) alone or in combination with propranolol (5 to 6 mg). Of the seven patients in whom MJRTc and/or MJRT could be measured before and after drug intervention, the JRTs shortened in four and prolonged in three after combination of atropine and propranolol. Atropine alone shortened MJRT in all eight patients studied. Our data reveal that both vagal and catecholamine-dependent factors (especially vagal over-activity) are operative in the escape mechanism of the junctional tissue.

Facilitating influence of disopyramide on atrial flutter termination by overdrive pacing

Long-lasting (mean 30 days) type I atrial flutter was treated with overdrive pacing in 30 patients (mean age 69 years) with organic heart disease. To evaluate the effect of pretreatment with disopyramide, the study population was divided in 3 groups of 10 patients each: group A, no disopyramide therapy; group B, intravenous disopyramide (maximum dose 250 mg in 1 hour); and group C, oral disopyramide (400 mg daily for 4 days). There were no differences in baseline cycle length of atrial flutter among the 3 groups before drugs were given. The stimulation protocol included overdrive atrial pacing up to the shortest paced cycle of 150 ms performed at a maximum of 3 atrial sites. Reversion to sinus rhythm occurred in 2 patients in group A, 7 in group B (p < 0.01) and 5 in group C. Pacing was performed from a mean number of 2.1 sites/patient in group A, 1.2 in group B and 2.0 in group C. Atrial fibrillation occurred in 7, 3 and 4 patients, respectively. Acceleration to a faster form of atrial flutter occurred in 3, 3 and 4 patients, respectively, and reversion to sinus rhythm occurred in all patients who had intravenous disopyramide and in 1 who took the drug orally. The administration of disopyramide before overdrive pacing improved the rate of conversion to sinus rhythm and allowed an easier stimulation protocol with a lower incidence of pacing-induced atrial fibrillation. Disopyramide is beneficial when overdrive atrial pacing is performed for the treatment of long-standing atrial flutter in patients with organic heart disease.

Validation of double-spike electrograms as markers of conduction delay or block in atrial flutter

Recent mapping studies of atrial flutter have shown that fragmented electrograms can be found in most cases from the posterior, posteroseptal and posterolateral walls of the right atrium. The fragmentation pattern most often consists of a double spike. To further assess double-spike electrograms as a possible marker of conduction delay, bipolar electrograms were continuously recorded during atrial overdrive pacing of common flutter from the right atrium (7 patients) and from the proximal coronary sinus (5). Baseline double-spike separation of 50 to 130 ms was unchanged in 1 patient and slightly increased (5 to 25 ms) in 4 by coronary sinus pacing. The electrogram sequence was unchanged and the surface morphology was similar to that of basal flutter. Right atrial pacing decreased double-spike separation by 25 to 85 ms from basal values of 45 to 175 ms (23 to 83%), suggesting fusion in the area of fragmented electrograms. These findings suggest that double-spike electrograms represent activation on both sides of a conduction delay zone. The changes induced in these electrograms by pacing from the anterior right atrium and the coronary sinus are consistent with flutter circuits rotating counterclockwise (frontal plane) in the posterior right atrial wall in common atrial flutter.

Subthreshold atrial pacing in patients with a left-sided accessory pathway: An effective new method for terminating reciprocating tachycardia

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent suhthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 ± 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 ± 14% of threshold current and the maximal ineffective current was 49 ± 17% of threshold (p < 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 ± 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by suhthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway.It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.

Chronic Idiopathic Idioventricular Tachycardia Caused by Slow Response Automaticity

A 22-year-old female, asymptomatic and without any evidence of cardiac disease, was found to have a persistent idioventricular tachycardia (IVT). Sinus rhythm and IVT rates were similar and showed parallel changes in successive resting electrocardiograms. Both IVT and sinus rhythm were transiently slowed or suppressed by vagal stimulation and accelerated by sympathetic stimulation. Long periods of atrial overdrive pacing, at a rate 62% faster than the spontaneous rate of IVT, depressed both ectopic and sinus activity. Fast channel blocking agents (lidocaine, disopyramide), and digoxin and amiodarone failed to modify IVT significantly. Verapamil, a calcium channel blocking drug, allowed total control of the arrhythmia. These electrophysiologic and pharmacologic responses suggest that the IVT may relate to the automatic activity of a ventricular focus of the "slow response" type, functionally resembling an "additional" sinus node with preserved innervation. During an 88-month follow-up, the patient continued to be asymptomatic, warning arrhythmias were never found and the features of IVT remained unmodified.

ATRIAL FLUTTER IN INFANCY: NO NEED FOR CHRONIC PROPHYLAXIS

Many authorities recommend digoxin for one year for atrial flutter (AT.FL) in infants with normal structural hearts. To re-examine this recommendation the electrocardiogram, response to programmed extrastimulation, (PES) (n=3), and clinical course in six infants with AT.FL. alone were reviewed. AT.FL exhibited a regular sawtooth pattern with a cycle length of 148 msec (range: 130-160 msec). Age at diagnosis was 34 days (range: birth (n=4) to 180 days). There were two males and four females; all were initiallly treated with digoxin but only two converted to sinus rhythm. AT.FL resolved spontaneously in two, two were converted with atrial overdrive pacing. Post-conversion electrocardiogram demonstrated normal P wave axis, PR interval .14 sec (range: .12-.16 sec), P wave duration .08 sec, and P wave amplitude .23 mV (3 > .25 mV) at heart rate 142 bpm. Post-conversion atrial PES with burst pacing in three failed to initiate AT.FL and demonstrated normal atrial effective refractory periods (158 msec; range: 150-173 msec) and normal atrioventricular conduction system effective refractory periods (199 msec; range: 180-216 msec). Only two patients were maintained on digoxin, six months and one year after conversion. Follow-up was 5.5 years (1.5 - 18 years) without recurrence. These data suggest that AT.FL in infants without structural heart disease, following conversion, is self-limited and not easily inducible by extrastimulation. We conclude that infants with atrial flutter alone, following cardioversion, do not require chronic prophylaxis.

The origins of the sinus node pacemaker complex in man: Demonstration of dominant and subsidiary foci

To test the hypothesis that the human sinus node is capable of demonstrating multiple sites of impulse generation, we assessed spontaneous shifts in the sinus node pacemaker complex, and shifts after overdrive atrial pacing, premature atrial stimulation and carotid sinus massage. A total of 24 patients aged 59 +/- 15 years (mean +/- SD) in whom stable sinus node electrograms were obtained were selected for the study. Ten of the 24 patients had sick sinus syndrome, whereas 14 had no sinus node dysfunction. All 24 patients had atrial pacing at cycle lengths of 1,000 to 300 ms; 9 patients had premature atrial stimulation and 12 had carotid sinus massage. Shifts in the sinus node pacemaker complex occurred spontaneously in 4 (17%) of the 24 patients; after atrial pacing at cycle lengths of 800 to 300 ms (mean 387 +/- 92) in 15 (63%) of 24 patients; after premature atrial stimulation at one or more coupling intervals in 5 (56%) of 9 patients and during carotid sinus massage in 9 (75%) of 12 patients. Shifts in the sinus node pacemaker complex lasted one to six beats and returned to the original site within two to seven beats. Spontaneous shifts in the sinus node pacemaker complex occurred in 3 of 14 patients without sick sinus syndrome and were induced in 6 (60%) of 10 patients with sick sinus syndrome and 11 (79%) of 14 patients without sick sinus syndrome. Shifts in sinus node pacemaker complex were characterized by loss of primary negativity, change in P wave morphology, significant (p less than 0.001) prolongation of sinoatrial interval and sinus cycle length.

T Wave Amplitude as a Quantitative Index of Regional Myocardial Sympathetic Responsiveness

Alterations in T wave morphology have been quantitated in seven open chest anesthetized dogs by simultaneous recording of electrograms from 10 epicardial sites across the anterior left ventricular wall under basal conditions, following left sympathetic stimulation (LSS) at 2, 4, 8, 12, and 16 Hz and during noradrenaline infusions (NAI) of 0.125, 0.25, 0.50, and 1.0 micrograms/kg/min. Overdrive atrial pacing at 175 beats/min was employed and rate of rise of left ventricular pressure (dP/dt) monitored. Linear log dose-response relationships were found between both peak T amplitude and left ventricular dP/dt for NAI between 0.125 and 0.50 micrograms/kg/min (peak T wave amplitude 4.0 +/- 0.9 to 1.4 +/- 0.7 mV). Following LSS, T wave amplitude responses were highly variable both between animals and between electrode sites in individual studies. A linear log dose-response relationship was found at stimulation frequencies between 8 and 16 Hz (T amplitude 3.9 +/- 1.4 to 1.8 +/- 1.2 mV). Changes in QT interval were minor and inconsistent. It is concluded that changes in peak T wave amplitude may provide a useful index of regional myocardial sympathetic responsiveness following NAI, but are more variable following LSS.

Termination of Ventricular Tachycardia by an Implantable Atrial Pacemaker and External Pacemaker Activator

An atrial pacemaker was implanted in a patient who had dilated cardiomyopathy, sinus node dysfunction, and drug-resistant ventricular tachycardia (VT). VT episodes were terminated by atrial overdrive pacing using an implanted pacemaker and a newly developed hand-held external programmer/transmitter. Although successful cases of termination of intractable VT by ventricular pacing have recently been reported, the ventricular method might increase the risk of accelerating VT. Atrial overdrive pacing is a safer method since it minimizes the possibility of tachycardia acceleration and, combined with antiarrhythmic drugs, it appeared to be a unique and useful approach for the treatment of drug-resistant VT.

Pacemaker reversion for suspected supraventricular tachycardia.

Overdrive atrial pacing was employed in twelve patients with suspected supraventricular tachycardia resistant to drug therapy. Eleven of these patients reverted to sinus rhythm with pacing either immediately or after a short episode of atrial fibrillation. In one patient, recordings from the atrial electrode indicated that a broad complex tachycardia was of ventricular rather than supraventricular origin. No complications were encountered and the procedure was well tolerated in all. Overdrive pacing is suggested as a safe alternative to DC cardioversion in drug-resistant supraventricular tachycardia, particularly in the presence of digitalis, in the elderly and in patients with chronic lung disease.

Atrial Overdrive Pacing for Conversion of Atrial Flutter in Children

Twenty-three successive patients with 27 different episodes of sustained atrial flutter were treated with atrial pacing for conversion of the tachyarrhythmia; 15 patients with 16 episodes of atrial flutter underwent intracardiac right atrial pacing and eight patients with 11 episodes of atrial flutter were treated with transesophageal atrial pacing. Ten of sixteen episodes (63%) and eight of 11 episodes (73%) were successfully converted using intracardiac and transesophageal techniques, respectively. Mean flutter cycle length for all 27 episodes was 219 ms (mean heart rate 274 beats per minute); successful pacing conversion cycle length (n = 15) was 72% of the flutter cycle length. Hemodynamic, electrophysiologic, and roentgenographic data were not predictive of conversion by either technique. Induction of localized atrial fibrillation or failure to meet critical pacing criteria may explain pacing failures. Based on this experience, a trial of transesophageal atrial pacing for acute conversion of any episode of atrial flutter in children prior to direct current cardioversion is recommended.