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Acute and long-term results of radiofrequency ablation of common atrial flutter and the influence of the right atrial isthmus ablation on the occurrence of atrial fibrillation.

AIMS: The purpose of this study was to evaluate the acute success rate and long-term efficacy of radiofrequency ablation of common type atrial flutter (AFL) by using a standardised anatomical approach in a large series of patients and to assess the influence of right atrial isthmus ablation on the occurrence of atrial fibrillation. There are no large scale prospective or retrospective multicentre studies for radiofrequency ablation of AFL. METHODS AND RESULTS: The study population consisted of 363 consecutive patients with AFL (mean age 58+/-16 years, 265 men) who underwent radiofrequency ablation at the inferior vena cava-tricuspid annulus (IVC-TA) isthmus using a standardised anatomic approach. Bidirectional isthmus block at the IVC-TA was achieved in 328 patients (90%). Following radiofrequency ablation, 343 patients (95%) were followed for a mean of 496+/-335 days. During the follow-up period, 310 patients (90%) remained free of AFL recurrences. Multivariate analysis identified five independent predictors of AFL recurrence: fluoroscopy time (p<0.001), atrial fibrillation after AFL ablation (p=0.01), lack of bidirectional block (p=0.02), reduced left ventricular function (p=0.035) and right atrial dimensions (p=0.046). Atrial fibrillation occurrence was significantly reduced after AFL ablation (112 in 343 patients, 33%) as compared to occurrence of atrial fibrillation before radiofrequency ablation (198 in 363 patients, 55%, p<0.001). CONCLUSIONS: The current anatomical ablation approach for AFL and criteria for evaluation of the IVC-TA isthmus block is associated with an acute success rate of 90% and a long-term recurrence rate of 10%. Radiofrequency ablation of common AFL results in a significant reduction in the occurrence of atrial fibrillation.

Acute 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.

Adolescent↗

Ablation of left atrial flutter in a patient surgically treated for atrial fibrillation. Does it indicate a possible hybrid approach?

Surgical treatment of atrial fibrillation (AF) has a high success rate and nowadays simpler and faster procedures have been proposed. The following is a description of the case of a patient who, after a modified Maze procedure, developed an atypical left atrial flutter and underwent a successful radiofrequency ablation procedure. A 71-year-old male underwent surgical biological valve replacement and a concomitant modified Maze procedure. After surgery the patient developed a persistent atrial arrhythmia with severe symptoms and refractory to any drug. For this reason, an electrophysiological study was planned. We performed a three-dimensional atrial mapping using the real-time position management system (Boston Scientific). Right atrial mapping indicated an early activation area on the septum. After transseptal puncture, left atrial mapping showed a reentry circuit around the mitral annulus with positive entrainment. A linear lesion was made between the mitral annulus and the superior right pulmonary vein and sinus rhythm was restored. After 7 months of follow-up the patient is asymptomatic and still in stable sinus rhythm. In conclusion, the follow-up of surgical AF may be improved by close collaboration between the surgeon and electrophysiologist. The available data suggest that a combined surgical and percutaneous approach could be the strategy of choice.

Aged↗

Atrial flutter in infancy: diagnosis, clinical features, and treatment.

The clinical features and treatment of atrial flutter in eight infants (four male and four female) less than 2 months of age are presented. Atrial flutter was noted during the first week of life in six of the infants and between 6 and 8 weeks of life in the other two infants. Four of the eight infants had associated structural or functional cardiovascular disease, and in three infants a central venous pressure catheter was present in the atrium at the time atrial flutter was diagnosed. Classic flutter waves were apparent on 12-lead ECGs in only two infants. In six infants, flutter waves were not obvious on standard ECGs, but transesophageal electrogram recordings demonstrated the presence of atrial flutter with second degree atrioventricular block. The atrial cycle length during flutter ranged from 135 to 180 ms (mean 149 ms; mean atrial rate 403 beats per minute); there was a 2:1 ventricular response to atrial flutter. Successful termination of atrial flutter was accomplished using three modes of electrical cardioversion in seven of the eight infants: direct current cardioversion in one, transvenous atrial pacing in one, and transesophageal atrial pacing in five. One asymptomatic infant converted to normal sinus rhythm 24 hours following digoxin administration. One infant had multiple atrial flutter recurrences and required chronic procainamide therapy. In seven of the eight infants, no recurrences have been noted in 6 months to 3 1/2 years of follow-up. These results demonstrate that atrial flutter may be difficult to diagnose in infants with tachycardia unless transesophageal electrogram recording is utilized for evaluation.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗

Left atrial flutter after radiofrequency catheter ablation of focal atrial fibrillation.

We report an arrhythmic complication in two patients in whom a procedure directed at isolating one or two pulmonary veins had been performed. The complication was related to pulmonary vein disconnection scars after ablation. Both patients developed new clinical tachycardia (atypical atrial flutter) secondary to a reentrant phenomena in the vicinity of a previously ablated pulmonary vein.

Adult↗

Fetal atrial flutter recorded prenatally by magnetocardiography.

A case of fetal atrial flutter successfully recorded by magnetocardiography (MCG) is reported. Initial ultrasonography revealed frequent fetal atrial extrasystoles at 31 weeks of gestation. Fetal MCG was recorded using a multichannel MCG system at 31, 35 and 38 weeks of gestation. A series of fluctuations in the baseline of the MCG were noted at 35 and 38 weeks of gestation, which were revealed to be atrial flutter P waves. The averaged MCG showed that the fetal arrhythmia was an atrial flutter with a 3:1 atrioventricular block. The diagnosis was confirmed by neonatal electrocardiogram. Fetal MCG may be useful for the diagnosis of fetal atrial flutter.

Adult↗

Alternation in the flutter wave morphology during radiofrequency catheter ablation for common atrial flutter.

A linear lesion created at the right atrial isthmus by radiofrequency current application can successfully eliminate common atrial flutter (AF). The mechanism of unsuccessful cases has not yet been well delineated. This study sought to investigate the cause of unsuccessful cases of radiofrequency catheter ablation of AF. Sixty-six patients with refractory common AF were referred for radiofrequency catheter ablation. Radiofrequency current was applied to the right atrial isthmus between the inferior vena cava and tricuspid annulus or between the coronary sinus orifice and tricuspid annulus. In 5 (8%) of the 66 patients, a morphological change of the flutter wave was observed in the 12-lead ECG concomitant with the change of the atrial excitation sequence during the delivery of radiofrequency energy without the termination of atrial flutter. In 8 (12%) patients, the morphology of the new AF wave, which was provoked electrically after the termination of the original AF, was different, and the average flutter cycle length also differed in 3 cases (2%). The results of radiofrequency application could be misinterpreted as unsuccessful when the occurrence of another, different type of AF has been overlooked following the elimination of the original AF during the radiofrequency catheter ablation procedure. It is possible that the flutter circuit can take an alternative pathway despite the complete conduction block at the right atrial isthmus.

Adult↗

Simultaneous occurrence of atrial fibrillation and atrial flutter.

INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.

Animals↗

Electrical remodeling of the atrium in an anatomic model of atrial flutter: relationship between substrate and triggers for conversion to atrial fibrillation.

BACKGROUND: Atrial flutter (AFL) and atrial fibrillation (AF) frequently coexist, yet the specific relationship between these arrhythmias, and particularly whether sustained AFL leads to AF, is unknown. METHODS AND RESULTS: We investigated the electrophysiological consequences of chronic AFL using an ovine anatomic right atrial Y-lesion model. AFL was induced in 7 animals, and 4 remained in sinus rhythm (controls). Sheep were monitored for spontaneous conversion of AFL to AF. Six of 7 sheep sustained AFL for 28 days. In 1 of 7 sheep, spontaneous conversion of AFL to AF occurred on day 5. AFL produced a highly significant fall in right and left atrial refractoriness (AERP, P<0.001), with 74+/-10% of the reduction occurring by day 3. Right atrial conduction velocity also fell significantly (baseline 89+/-9 cm/s versus day 28 64+/-14 cm/s, P<0.001) but over a slower time course. AERP and conduction velocity changes coincided with a characteristic biphasic decrease and increase in the AFL cycle length. The excitable gap (percent of AFL cycle length) increased from 13+/-3% at baseline to 46+/-8% by day 28 (P<0.001). Sustained AF (>30 seconds) was not inducible at baseline but after 28 days of AFL could be induced in 6 of 6 sheep by critically timed single or multiple extrastimuli delivered either in sinus rhythm or AFL. There was no significant change in any parameter in control sheep. CONCLUSIONS: In this model, AFL produced electrical remodeling and the substrate for sustained AF. However, spontaneous conversion to AF was uncommon, and the development of AF was dependent on specific triggers.

Animals↗

Influence of propafenone on resetting and termination of canine atrial flutter.

Previous studies on atrial flutter (AF) presumed that resetting was due to the prematurity effect (PE) in which the stimulated antegrade wavefront travels in the tail of the AF preexisting wavefront. We studied the collision effect (CE) between the AF and the stimulated retrograde wavefronts, its contribution to resetting, and its relationship to AF termination and how they are affected by the Class IC agent propafenone (PPF). A canine model of AF was created using a Y-shaped lesion in the right atrium in 14 dogs (33 +/- 3 kg). Five atrial bipolar electrodes were positioned around the tricuspid valve. In a subsequent set of 11 dogs, we used 16 bipolar electrodes for recording. AF was induced by burst pacing. Single and multiple stimuli were applied to measure conduction time and reset-response curves (RRCs). This was repeated after the administration of PPF (1 mg/kg loading dose for 10 minutes, followed by 1.8 mg/kg/per hour infusion). Three distinct mechanisms were found to contribute to the RRC: the PE, the CE, and heterogeneity. PPF stabilized the RRC, increased significantly the cycle length (CL), the duration of the effective refractory period, as well as the duration of the excitable gap. However, PPF did not alter the duration of the fully excitable portion. We studied 36 annihilations without and 48 with PPF. Transient fibrillation was found in 75% of the episodes without, compared to 22% with PPF. Other types of termination such as conduction block, CL oscillations, and reversal of activation were found for 25% of the episodes without and 78% with PPF. In many cases, conduction block and CL oscillations were associated with a failure of propagation of the stimulated antegrade wavefront in the region of collision. Termination by reversal of activation suggests that propagation was two dimensional and could not be represented by a one dimensional movement. The average coupling interval (in percent of CL), that induced fibrillation was not significantly different from that at which conduction block occurred. This suggests that transient fibrillation is associated with a weak CE rather than with rapid pacing. The CE is amplified by multiple stimuli and PPF. The incidence of transient fibrillation in AF annihilation diminishes with PPF as the CE becomes more important. This suggests that the evaluation of PE and CE in AF may be an indication of the risk of atrial fibrillation.

Action Potentials↗

Effects of verapamil and diltiazem on the ventricular rate during simulated atrial flutter in isolated guinea pig hearts.

To compare the direct effects of verapamil and diltiazem on the ventricular rate during atrial flutter, we developed an atrial flutter model in guinea pig isolated hearts. Atrial flutter was simulated by rapid atrial pacing (cycle length = 50 ms). At this atrial pacing cycle length, the shape of the frequency of distribution of the ventricular cycle lengths was comparable to that during spontaneous atrial flutter. Verapamil (0.01, 0.03 microM) and diltiazem (0.03, 0.09 microM) caused a comparable prolongation of the atrioventricular conduction time and atrioventricular refractoriness. Also, the anterograde Wenckebach cycle length was increased to a comparable degree by both substances. The mean ventricular cycle length during atrial flutter was comparable prolonged by both substances. The prolongation of the maximal ventricular cycle length was significantly more pronounced in the presence of verapamil. The time dependence of drug-induced alterations in atrioventricular conduction time during abrupt changes of heart rate is significantly more pronounced in the presence of verapamil compared to diltiazem. In conclusion, the more pronounced effect of verapamil on the maximal ventricular cycle length compared to the action of diltiazem may be explained by the slow binding kinetic of this drug to the Ca2+ channel resulting in a longlasting blockade of the Ca2+ channel.

Animals↗

Catheter ablation of common-type atrial flutter guided by three-dimensional right atrial geometry reconstruction and catheter tracking using cutaneous patches: a randomized prospective study.

INTRODUCTION: EnSite NavX (NavX) is a novel mapping and navigation system that allows visualization of conventional catheters for diagnostic and ablative purposes and uses them to create a three-dimensional (3D) geometry of the heart. NavX is particularly suitable for ablation procedures utilizing an anatomic approach, as in the setting of common-type atrial flutter (AFL). The aim of this study was to compare NavX-guided and conventional ablation procedures for AFL. METHODS AND RESULTS: Forty consecutive patients (32 male, 59 +/- 12 years) with documented AFL were randomized to undergo fluoroscopy-guided (group I, 20 patients) or NavX-guided (group II, 20 patients) ablation, including 3D isthmus reconstruction. The same catheter setup was used in both groups. The endpoint of bidirectional isthmus block was obtained in all patients. Compared to conventional approaches, NavX-guided procedures significantly reduced fluoroscopy time (5.1 +/- 1.4 min vs 20 +/- 11 min, P < 0.01) and total x-ray exposure (5.1 +/- 3.1 Gycm2 vs 24.9 +/- 1.6 Gycm2, P < 0.01). Isthmus geometry reconstruction could be performed in all patients of group II. In 4 patients (20%) of group II, anatomic isthmus variations were detected by NavX. No significant differences in radiofrequency current applications and procedural times were found between the two groups. CONCLUSION: NavX technology allows geometry reconstruction of the cavotricuspid isthmus. NavX-guided ablation of AFL reduces total x-ray exposure compared to the fluoroscopy-guided approach but does not prolong procedure time.

Atrial Flutter↗

Catheter inversion: a technique to complete isthmus ablation and cure atrial flutter.

Cure of typical atrial flutter (AFL) by catheter ablation to produce bidirectional block across the tricuspid annulus-inferior vena cava isthmus (IS) is highly effective, but failures may occur. We describe a technique that may allow creation of bidirectional block where a conventional strategy has failed. AFL ablation was performed using the conventional approach with a mapping/ablation (ablation) catheter introduced via the right femoral vein (RFV) to create a line of bidirectional block across the IS. If this was not achieved after five passes of the ablation catheter from the tricuspid annulus to the inferior vena cava (IVC) a catheter inversion technique was used. This allowed stable positioning of the ablation catheter at the IVC end of the isthmus. In 11 patients, a mean of 17 (range 3 to 45) radiofrequency (RF) applications was given before the catheter inversion technique was applied. Following catheter inversion a mean of 4 (1 to 14) further RF applications achieved bidirectional isthmus block in every patient. No complications occurred. Catheter inversion provides a simple, safe, and effective means of achieving bidirectional isthmus conduction block in cases where a conventional ablation strategy might have failed.

Aged↗

Atrial tachycardia masquerading as atrial flutter following ablation of the subeustachian isthmus.

We report a case of atrial tachycardia masquerading as atrial flutter in a man who had previously undergone catheter ablation for atrial flutter. The recurrent arrhythmia was electrocardiographically almost identical to the prior atrial flutter; at repeat electrophysiologic study, although bidirectional conduction block was observed in the tricuspid annulus-inferior vena caval isthmus, the atrial arrhythmia was readily initiated. Activation mapping suggested typical atrial flutter, but entrainment techniques demonstrated intra-atrial reentry not involving the ablated isthmus. This case illustrates the need to apply entrainment techniques even in cases of apparent "typical" atrial flutter to confirm that putative ablation targets are necessary for tachycardia perpetuation.

Aged↗

Mechanism of spontaneous termination of stable atrial flutter in the canine sterile pericarditis model.

BACKGROUND: We tested the hypotheses that spontaneous termination of stable atrial flutter is directly related to spontaneous beat-to-beat cycle length oscillations and that block of the circulating reentrant wave front occurs in an area of slow conduction. METHODS AND RESULTS: We studied 30 episodes of spontaneous termination of stable atrial flutter induced by atrial stimulation in 11 conscious, nonsedated dogs with sterile pericarditis. Additionally, in 5 dogs, 14 episodes of spontaneous termination of stable atrial flutter were studied with a multisite mapping system to record simultaneously from 190 right atrial electrodes. In the conscious-state studies, atrial flutter cycle length oscillations began 6 +/- 1 (mean +/- SEM) beats before termination in 26 episodes, stable atrial flutter evolved into atrial fibrillation in 3 episodes, and no cycle length change occurred before termination in 1 episode. In the open-chest studies, in all instances, spontaneous oscillations began 7 +/- 1 beats before termination. The only consistent oscillation pattern occurred for the last two beats: a long cycle length (149 +/- 9 milliseconds) followed by a much shorter cycle length (110 +/- 6 milliseconds) (P < .01). Activation maps demonstrated that all cycle length oscillations were explained by changes of conduction in an area(s) of slow conduction in the reentrant circuit. In two instances, the last (short) cycle length was associated with disappearance of an area of slow conduction. In all episodes, the last circulating reentrant wave front blocked in an area of slow conduction in the reentrant circuit. Although not tested, during the last beat, the very early arrival of the circulating reentrant wave front at an area of slow conduction suggests an important role for refractoriness, with head and tail interactions, resulting in block. CONCLUSIONS: Spontaneous termination of stable atrial flutter in the sterile pericarditis model (1) is preceded by beat-to-beat cycle length oscillations that result from changes in conduction in areas of slow conduction in the reentrant circuit and (2) results from block of the circulating reentrant wave front in an area of slow conduction.

Animals↗

Prospective evaluation of transesophageal pacing for the interruption of atrial flutter.

PURPOSE: Although transesophageal pacing has been used successfully for the interruption of cardiac arrhythmias, the efficacy of this technique for the interruption of spontaneous atrial flutter remains poorly defined. The utility of transesophageal pacing to interrupt atrial flutter that was persistent despite standard antiarrhythmic drug therapy (mean duration: 70.3 days; range: one day to more than 365 days) was studied prospectively in 39 consecutive patients. PATIENTS AND METHODS: After written informed consent was obtained from each patient, transesophageal pacing was performed with a programmable stimulator, using the distal electrode as the cathode and the proximal electrode as the anode. All patients continued to receive a type 1 antiarrhythmic drug or amiodarone throughout the period of transesophageal pacing. The response to transesophageal pacing was classified as follows: (1) direct conversion; (2) indirect conversion; or (3) failure to interrupt atrial flutter. RESULTS: The mean stimulus amplitude and pulse duration required for atrial capture were 19.8 +/- 7.5 mA and 18.4 +/- 7.9 msec. Atrial flutter was successfully converted to sinus rhythm by transesophageal pacing in 82% of patients. In 38% of patients, atrial flutter was converted directly to sinus rhythm without another intervening arrhythmia (direct conversion). The mean pacing rate required for direct conversion was 341 +/- 27 beats/minute. In 44% of patients, the cycle length of atrial flutter was accelerated to less than 180 msec or was converted to atrial fibrillation with spontaneous conversion to sinus rhythm within 24 hours (mean 8.4 +/- 9.3 hours, indirect conversion). The mean pacing rate inducing accelerated atrial flutter or transient atrial fibrillation was 372 +/- 61 beats/minute (p = NS compared to direct conversion). Atrial flutter was not interrupted or atrial fibrillation was induced that did not spontaneously convert to sinus rhythm within 24 hours in an additional seven patients (18%). The underlying cardiac disease, age, previous drug therapy, atrial size, atrial flutter cycle length, history of prior atrial fibrillation, left ventricular function, and concomitant medical illnesses did not predict the efficacy of transesophageal pacing. CONCLUSION: The present study suggests that transesophageal pacing is highly effective for interrupting spontaneous atrial flutter that does not terminate with standard antiarrhythmic drug therapy.

Adult↗

Atrial and ventricular pressures in atrial flutter.

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 +/- 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Both the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 +/- 15 beats/min) or in those with variable conduction (heart rate 96 +/- 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.

Atrial Flutter↗

Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques.

BACKGROUND: Recent studies of human type 1 atrial flutter demonstrated reentry in the right atrium and an area of slow conduction in the low posteroseptal right atrium. Direct-current catheter ablation of this area has been only moderately successful in preventing recurrence. Therefore, we performed endocardial activation mapping and entrainment pace mapping during atrial flutter to determine the critical site for radiofrequency ablation of this arrhythmia. METHODS AND RESULTS: Twelve consecutive patients (seven men and five women; age, 21-73 years) with type 1 atrial flutter (mean cycle length, 253 +/- 39 msec) underwent right atrial endocardial activation and entrainment pace mapping using standard transvenous catheter techniques to localize the atrial flutter reentrant circuit, the area of slow conduction, and the exit site from the area of slow conduction. Upon identifying appropriate sites, radiofrequency energy (16-29 W) was applied via a 4-mm tipped catheter. Activation mapping of atrial flutter revealed a counterclockwise reentrant wave front originating just inferior or posterior to the coronary sinus ostium, proceeding superiorly in the atrial septum to the right atrial free wall, then inferiorly toward the tricuspid annulus and finally medially between the inferior vena cava and the tricuspid annulus, where low-amplitude fragmented electrical activity was noted. Entrainment pace mapping from this area produced an exact P wave match to atrial flutter on 12-lead ECG with a long (greater than 40 msec) stimulus-to-P interval indicating slow conduction, whereas pacing just inferior or posterior to the coronary sinus ostium produced an exact P wave match with a short stimulus-to-P interval (less than 40 msec), presumably identifying the exit site from the area of slow conduction. Radiofrequency energy (one to 14 applications) was effective in terminating and preventing reinduction of atrial flutter in 10 patients. In two patients, atrial flutter was not terminated during radiofrequency energy application but during subsequent pacing attempts. Sites where ablation was successful, located just inferior or posterior to the coronary sinus ostium, were characterized by discrete electrograms with activation times of -20 to -50 msec before P wave onset and exact entrainment pace maps with a stimulus-to-P interval of 20 to 40 msec, consistent with the exit site from the area of slow conduction. Follow-up (mean, 16 +/- 9 weeks; range, 2-31 weeks) revealed recurrence of the original atrial flutter in two patients, one of whom underwent repeat ablation without further recurrence, self-limited infrequent recurrence of a new atrial flutter or atrial fibrillation in three suppressed by beta-blocker or digoxin, and no recurrence in seven. CONCLUSIONS: 1) Radiofrequency energy applied to a critical area in the atrial flutter reentrant circuit, inferior or posterior to the coronary sinus ostium, will terminate and prevent arrhythmia reinduction. 2) Long-term follow-up in a larger series of patients will be required to confirm efficacy of this technique, although short-term results look promising.

Adult↗