Linear Ablation of the Isthmus Between the Inferior Vena Cava and Tricuspid Annulus for the Treatment of Atrial Flutter
A Study in the Canine Atrial Flutter Model
Background The isthmus between the inferior vena cava and the tricuspid annulus has been shown to be involved in the reentry circuit of common atrial flutter. The effects of radiofrequency catheter ablation of this isthmus were examined in the canine model of atrial flutter due to reentry around the tricuspid annulus.
Methods and Results A model of atrial flutter was prepared in 11 of 14 dogs by creating intercaval and connected transverse lesions (Y-shaped lesion). Bipolar electrodes were attached at 24 atrial sites, and computer-assisted mapping was performed. Stable atrial flutter with a cycle length of 133±11 ms was repeatedly induced by rapid atrial pacing in all dogs, and atrial mapping revealed reentry around the tricuspid annulus including the isthmus. In 6 dogs, the isthmus was ligated during atrial flutter (mechanical ablation). In the other 5 dogs, a 7F large-tip electrode catheter was placed at the isthmus under a fluoroscopic control. Radiofrequency energy (25 W for 30 s) was delivered to three sequential sites from the tricuspid annulus to the inferior vena cava to ablate the isthmus linearly. Atrial flutter was terminated in all dogs after mechanical and radiofrequency ablation of the isthmus and was not induced again. Atrial pacing from the posterior left atrium during sinus rhythm demonstrated intra-atrial conduction block at the isthmus after ablation. Pathological examination of the isthmus showed transmural myocardial damage.
Conclusions Linear radiofrequency ablation of the isthmus can induce intra-atrial conduction block and is effective as a curative therapy for atrial flutter when the reentry circuit involves the isthmus.
Atrial flutter has been shown to be due to reentry in the right atrium, with an area of slow conduction located in the lower part of the right atrium.1 2 3 4 Previous mapping studies of human atrial flutter demonstrated a downward activation in the right atrial free wall and upward activation in the interatrial septum, and the narrow isthmus between the inferior vena cava and the tricuspid annulus seems to be a common, critical pathway for the reentry circuit of atrial flutter.1 3 5 6 7 8 9 As a curative therapy for atrial flutter, surgical ablation of the isthmus was shown to be effective in two patients.6 Recently, catheter ablation with a direct current or application of radiofrequency energy to the area of slow conduction close to the isthmus or to the area between the coronary sinus ostium and the inferior vena cava was shown to be effective for the treatment of atrial flutter.4 9 10 11 12
Frame and coworkers13 have shown that atrial flutter induced in dogs in which a Y-shaped lesion was created in the right atrial free wall was due to reentry around the tricuspid annulus and that the isthmus between the inferior vena cava and the tricuspid annulus was involved in the reentry circuit. They also demonstrated that a ligature placed between the tricuspid valve and the transverse incision of the Y-shaped lesion interrupted atrial flutter in this model, suggesting a rationale for the treatment of atrial flutter caused by reentry around the tricuspid annulus. In the present study, using this well-established model of canine atrial flutter, we examined the efficacy of ablation of the isthmus between the inferior vena cava and the tricuspid annulus for the treatment of atrial flutter. For this purpose, the isthmus was mechanically ligated in 6 dogs. Then, linear radiofrequency catheter ablation of the isthmus was attempted in another 5 dogs, and its electrophysiological and pathological effects were examined.
Fourteen adult mongrel dogs (weight, 19 to 23 kg) were anesthetized with sodium pentobarbital (30 mg/kg IV as a bolus injection followed by 2 mg/kg hourly). Endotracheal intubation and ventilation with oxygen-supplemented air were used to maintain Po2, Pco2, and pH of the atrial blood at their own physiological levels. Right lateral thoracotomy was performed at the fourth intercostal space, and the heart was suspended in a pericardial cradle. As previously reported by Frame and coworkers,13 a Y-shaped incision was created in the right atrial free wall in 11 of 14 dogs: As described by Rosenblueth and Garcia-Ramos,14 an intercaval incision extending from the superior vena cava to the inferior vena cava was first created and then continuously sutured. A second incision was created from the center of the intercaval incision to the right atrial appendage and was continuously sutured. In the remaining 3 dogs, no incision was created in the right atrium, and the influence of ablation of the isthmus to the atrial activation sequence during sinus rhythm was examined.
Twenty-four bipolar electrodes were attached in the atria for both pacing and recording bipolar atrial electrograms (Fig 1A⇓ and 1B⇓). Three types of electrodes were used. One was a silicone pad type on a 3×4-cm rectangular plaque and contained 24 bipolar, platinum-tip electrodes with interelectrode distances of 1 mm within each pair and 8 mm between two neighboring pairs. It was attached on the right atrial free wall, and 14 pairs of electrodes were used for recording electrograms from the atrial tissue around a Y-shaped lesion. In the dogs without a Y-shaped lesion created, 14 of the 24 pairs of the electrodes were used to record electrograms from the whole right atrial free wall. Six hook-type bipolar electrodes with an interelectrode distance of 2 mm were attached on the atrial sites along the tricuspid annulus, including the site under the Bachmann’s bundle, the arch of the crista terminalis, the posterior and anterior aspects of the right atrial appendage, the posteroinferior right atrial wall near the crux, and the posterior left atrium near the crux. One needle-type octapolar electrode (ie, 4 bipolar electrodes with interelectrode distances of 2 mm within each pair and 4 mm between two successive pairs) was inserted from the anterior atrium under the Bachmann’s bundle toward the crux to be attached to the interatrial septum. During the placement of these electrodes, special care was taken to place electrodes around the tricuspid annulus, except for 8 bipolar electrodes placed around the Y-shaped lesion (sites 8 to 11 and 14 to 17 in Fig 1A⇓). Bipolar electrograms from these 24 atrial sites were recorded simultaneously with ECG leads I, II, and III with a multiplex mapping system (HPM 7100, Fukuda-Denshi). All of the bipolar electrograms were filtered by a band-pass filter from 30 to 1000 Hz. Atrial pacing was performed with a programmable stimulator (cardiac stimulator 3F51, San-ei) that delivers rectangular pulses with a 2-ms duration. The stimulus output was set at five times the diastolic threshold.
Induction of Atrial Flutter and Mapping Technique
During sinus rhythm or atrial pacing at 200 beats per minute from the site closest to the sinus node, the bipolar electrograms from 24 atrial sites were taken into the mapping system and the data were saved on a floppy disk for detailed poststudy analysis. The activation sequence was analyzed by measuring the activation time of each site relative to the reference site, and a 5- or 10-ms isochron was drawn automatically.
In dogs in which a Y-shaped lesion was created, induction of atrial flutter was attempted by single– or double–atrial extrastimulus technique or by rapid atrial pacing. An atrial extrastimulus was delivered after 10 basic drive beats at a cycle length of 300 ms until atrial refractoriness was reached. If atrial flutter was not induced, a second extrastimulus was delivered after the first, with a fixed coupling interval set at 20 ms longer than the effective refractory period. When atrial flutter was not induced, rapid atrial pacing at a cycle length of 200 ms was performed for approximately 5 s and terminated abruptly. If atrial flutter was not induced, the pacing cycle length was shortened by 10 ms and the same procedure was repeated until stable atrial flutter was induced, atrial fibrillation was induced, or one-to-one capture by the pacing was lost. These pacing procedures usually were performed through the hook electrodes attached at the right atrial appendage or posterior right atrium. When stable atrial flutter was not induced by pacing from one site, the pacing site was changed and the same pacing protocols were repeated. In this study, stable atrial flutter was defined as a regular atrial tachycardia with a cycle length less than 200 ms, a beat-to-beat cycle length variation less than 10 ms, and a continuation longer than 10 minutes after the initiation.
During induced stable atrial flutter, the activation sequence was analyzed as described above. Rapid atrial pacing at a cycle length 10- to 20-ms shorter than the flutter cycle length was performed during atrial flutter to interrupt it. Induction of stable atrial flutter was attempted at least 30 times in each dog. If stable atrial flutter was not induced, the study was terminated.
In the three dogs in which a Y-shaped lesion was not created, the atrial activation sequence during sinus rhythm was examined before and after mechanical ablation of the isthmus. Right atrial pressure was measured before and after ablation with a catheter inserted in the right atrium through the internal carotid vein.
Analysis of Atrial Activation Sequence During Atrial Pacing
In dogs in which a Y-shaped lesion was created, atrial pacing at a cycle length of 300 ms was performed from the posterior left atrium near the crux (Fig 1A⇑) during sinus rhythm. The atrial activation sequence during this atrial pacing was determined. The conduction time between the pacing site (the posterior left atrium) and the posteroinferior right atrium was also determined during atrial pacing (intra-atrial conduction time). The distance between these two sites was approximately 2 cm.
A hemostatic suture was placed from the inferior vena cava to the posterobasal aspect of the right ventricle in six dogs (Fig 1B⇑). During stable atrial flutter, the isthmus between the inferior vena cava and the tricuspid annulus was ablated by tightening this suture. When atrial flutter was interrupted, rapid atrial pacing was performed from several atrial sites to induce atrial flutter.
Atrial pacing at a cycle length of 300 ms was performed from the posterior left atrium, and the activation sequence in the right atrium and conduction time between the pacing site and posteroinferior right atrium (ie, the sites sandwiching the ablation site) were determined.
Radiofrequency Catheter Ablation
The right femoral vein was exposed and a 7F, 4 mm-tipped, deflectable quadripolar electrode catheter with an interelectrode distance of 5 mm (Elecath) was inserted through a cut-down hole. Under a fluoroscopic control, the electrode catheter was advanced into the cardiac chamber, and the tip of the catheter was placed at the tricuspid annulus as shown in Fig 1C⇑. Radiofrequency energy was applied during stable atrial flutter to three sequential sites in the isthmus between the inferior vena cava and the tricuspid annulus. Thus, the catheter was initially inserted into the right ventricle and pulled back gradually while a bipolar electrogram was recorded from a distal pair of electrodes. When a small atrial potential and a large ventricular potential were recorded, the recording site was considered to be on the tricuspid annulus, and radiofrequency energy of 25 W was applied for 30 seconds. Then, the catheter was pulled back slightly to record an electrogram with an atrial potential amplitude almost equal to a ventricular one and radiofrequency energy was applied for 30 seconds. The catheter was pulled back farther to record an electrogram with an atrial potential larger than a ventricular one, and a third period of radiofrequency energy was applied for 30 seconds. Thus, the isthmus between the tricuspid annulus and the inferior vena cava was linearly ablated during stable atrial flutter. Energy application to the three sites was counted as one ablation session. When atrial flutter was not interrupted by a single ablation session, another session was conducted in the same way. When atrial flutter was interrupted during the first or second energy application of one session, energy delivery to the three sites was completed. Rapid atrial pacing was performed to induce atrial flutter, and when stable atrial flutter was induced, the same ablative procedure was repeated. When atrial flutter was not induced with rapid atrial pacing, atrial pacing at a cycle length of 300 ms was performed from the posterior left atrium and atrial activation sequence and conduction time between two atrial sites were determined as described above.
The radiofrequency energy source used in this study (NL-50, Central Inc) delivers an unmodulated sine waveform at 500 kHz between the tip of the ablation catheter and a large skin electrode. If there was an abrupt impedance increase >30 Ω from the baseline value, the energy delivery was automatically stopped and the ablation catheter was withdrawn to remove the coagulum from the catheter tip.
In dogs in which radiofrequency energy was applied to the isthmus, the heart was excised after the experiment. At least two specimens were obtained from the ablation site, one from the site close to the tricuspid annulus and the other close to the inferior vena cava. Each specimen was fixed in 10% neutral buffer formaldehyde for more than 7 days. Then the specimens were embedded in paraffin, cut into slices 3.5-μm thick, and stained with hematoxylin and eosin.
All data are shown as mean±SEM. For comparison of intra-atrial conduction times, total right atrial activation times, atrioventricular (AV) conduction intervals, and mean right atrial pressures before and after ablation of the isthmus, a two-tailed paired t test was used. For comparison of the change in intra-atrial conduction time after ablation of the isthmus between mechanical and radiofrequency ablation, an unpaired t test was used. A probability of less than .05 was considered significant.
Induction of Atrial Flutter and Atrial Mapping
Stable atrial flutter lasting for >10 minutes was induced in all of the 11 dogs in which a Y-shaped lesion was created. It was not induced by single atrial extrastimulus technique in either group of dogs. It was induced by double atrial extrastimulus technique in 4 dogs and by rapid atrial pacing at a mean cycle length of 130±20 ms (range, 100 ms to 130 ms) in all 11 dogs. A mean of four episodes of stable atrial flutter (range, 2 to 6 episodes) was induced in each dog. Mean atrial flutter cycle length was 134±2 ms (n=45).
Atrial mapping during atrial flutter revealed reentry along the tricuspid annulus in all dogs. From the endocardial view, counterclockwise rotation along the tricuspid annulus was demonstrated in 16 episodes and clockwise rotation in the remaining 29 episodes. Representative examples are shown in Fig 2⇓. Fig 2A⇓ shows a circus movement with counterclockwise rotation and a cycle length of 126 ms; Fig 2B⇓ shows a circus movement with clockwise rotation and a cycle length of 128 ms.
Mechanical and Radiofrequency Catheter Ablation of Atrial Flutter
Mechanical ablation of the isthmus between the tricuspid annulus and the inferior vena cava (n=6) resulted in the abrupt interruption of atrial flutter in all dogs (Fig 3⇓). After ablation, atrial flutter was no longer induced in any dogs by rapid atrial pacing at any pacing cycle length.
Radiofrequency catheter ablation of the isthmus (n=5) resulted in the interruption of atrial flutter in all dogs. Total radiofrequency energy delivered, number of ablation sessions, and the incidence of impedance rise during ablation for each experiment are shown in the Table⇓. In 4 of the 5 dogs, atrial flutter was interrupted during the first ablation session. In one of those 4 dogs, atrial flutter was no longer induced, and the ablation procedure was finished. In the other 3 dogs, however, atrial flutter was again induced: In 2 of the 3, atrial flutter was not induced after the second ablation session, and in the other, it was not induced after the third session. In the remaining dog, atrial flutter was interrupted during the second ablation session and was no longer induced. Thus, one ablation session was required to eliminate atrial flutter in 1 dog, two sessions in 3, and three sessions in the remaining dog.
Atrial Activation Sequence and Intra-atrial Conduction Time During Atrial Pacing Before and After Ablation
Fig 4⇓ shows atrial activation sequences during atrial pacing from the posterior left atrium near the crux before (Fig 4A⇓) and after (Fig 4B⇓) mechanical ablation of the isthmus in 1 dog. Before ablation, the excitation wave front from the pacing impulse spread to the two opposite directions (ie, clockwise and counterclockwise) along the tricuspid annulus. After ablation, the clockwise excitation wave front was blocked at the ablation site, so that most parts of the right atrium were activated by the counterclockwise excitation wave front. A similar observation was made in the other 5 dogs in which the isthmus was mechanically ablated. The intra-atrial conduction time from the pacing site to the posteroinferior right atrium (indicated by an asterisk in Fig 4A⇓) was 35±4 ms before mechanical ablation and was significantly prolonged to 105±4 ms after ablation (P<.001).
Similar findings were obtained from experiments in which radiofrequency catheter ablation was performed. Fig 5⇓ shows atrial activation sequences during atrial pacing before (Fig 5A⇓) and after (Fig 5B⇓) radiofrequency ablation in 1 dog. As noted in mechanical ablation, the atrial activation sequence changed markedly after radiofrequency ablation of the isthmus. The same observation was made in the other 4 dogs. The intra-atrial conduction time was 29±3 ms before radiofrequency ablation and was prolonged significantly to 113±9 ms after ablation (P<.001). The change in the intra-atrial conduction time after radiofrequency ablation did not differ from that after mechanical ablation (P=.292).
After radiofrequency ablation of the isthmus, double potentials were recorded at the ablation site in two dogs in which electrode No. 24 was close to the ablation site. Fig 6⇓ shows bipolar electrograms during atrial pacing after radiofrequency ablation of the isthmus in the experiment shown in Fig 5⇑. The recording sites are identified in Fig 5B⇑. At the site of electrode No. 24, double potentials were noted: The initial, small potential was activated at 27 ms after the pacing stimulus artifact, while the second, large potential was at 99 ms after the stimulus and after the activation of the right atrial free wall, indicating intra-atrial conduction block at the isthmus and activation of the block site from two different directions.
Pathological Examination of the Radiofrequency Ablation Site
The mean width of the isthmus between the inferior vena cava and the tricuspid annulus was 11.0 mm (range, 9 to 15 mm). The thickness of the atrial muscle was maximal at the site near the tricuspid annulus (mean, 2.0 mm; range, 1.7 to 2.2 mm). Atrial muscle thickness in the isthmus became tapered toward the junction between the atrium and the inferior vena cava.
Fig 7⇓ shows typical microscopic findings of the ablation site observed in one dog in which radiofrequency energy was applied to the isthmus six times (ie, two sessions). Fig 7A⇓ (low magnification of the lesion) shows a transmural lesion of the atrial myocardium and a wavy pattern of the myocardial fibers. Fig 7B⇓ shows endocardial degeneration and atrophy. In the myocardial layer (Fig 7B⇓ and 7C⇓), atrophy, waxy degeneration, and pyknosis were observed. Interstitial edema and microvascular red thrombus were also noted. In the periphery of the ablation site (Fig 7D⇓), interstitial hemorrhage, karyolysis, and segmentation of the muscle fibers were observed. In the subepicardial layer (Fig 7E⇓), infiltration of neutrophils was observed.
Similar findings were observed in the other specimens obtained from the ablation site. Degeneration and atrophy of the endocardium were noted in all 5 dogs, and endocardial edema was seen in 4 dogs. A wavy pattern of the muscle fibers and interstitial edema and hemorrhage were noted in all dogs. In the myocardium, waxy degeneration, pyknosis and focal necrosis were noted in all dogs. Segmentation and karyolysis of the myocardium were noted in 4 dogs. Microvascular thrombi were noted in all dogs. Thus, transmural lesions were observed at the ablation site in all dogs.
Influence of Ablation of the Isthmus on the Right Atrial Activation Sequence in Dogs Without a Y-Shaped Lesion
Fig 8⇓ shows the right atrial activation sequences during sinus rhythm before (Fig 8A⇓) and after (Fig 8B⇓) mechanical ablation of the isthmus in 1 dog in which a Y-shaped lesion was not created. No detectable change was noted after ablation of the isthmus. Similar findings were observed in the other 2 dogs. Total right atrial activation times before and after ablation were 40±2 and 37±23 ms, respectively (P=.6). AV conduction intervals measured from the onset of the atrial activation to the onset of the QRS complex on the ECG before and after ablation were 104±3 and 104±4 ms, respectively (P=.67). Mean right atrial pressures before and after ablation were 7±1 and 7±0 mm Hg, respectively.
Reentry Around the Tricuspid Annulus as a Mechanism of the Present Model of Atrial Flutter
Frame and coworkers13 introduced a stable canine model of atrial flutter in which a connected lesion toward the right atrial appendage was added to the intercaval lesion previously described by Rosenblueth and Garcia-Ramos14 (ie, a Y-shaped lesion). Frame et al studied the nature of atrial flutter in this model extensively in both in vivo13 and in vitro experiments15 and found that reentry around the tricuspid annulus was the mechanism of atrial flutter. They further showed that the original wave front of the reentrant impulse circulates through the atrial fibers in the supravalvular lamina that surrounds the tricuspid annulus. Our computer-assisted mapping of atrial activation during stable atrial flutter in the same canine model confirmed the previous findings by Frame and coworkers.13 15
We mechanically ablated the narrow isthmus between the inferior vena cava and the tricuspid annulus during atrial flutter by tightening the ligature placed around the isthmus, which resulted in abrupt termination of atrial flutter in all dogs. Atrial flutter was no longer induced in any of the dogs after the procedure. This finding also confirmed the previous observation made by Frame and coworkers13 that a ligature placed between the tricuspid ring and the transverse incision of the Y-shaped lesion in the right atrial free wall interrupted atrial flutter. Thus, creation of conduction block in the isthmus is indicated to eliminate reentry around the tricuspid annulus.
Radiofrequency Catheter Ablation of the Isthmus
Since mechanical ablation of the isthmus was effective in the cure of atrial flutter in the present model, we attempted catheter ablation of the isthmus with radiofrequency energy and a standard large-tipped electrode catheter. The results showed that radiofrequency catheter ablation of the isthmus is feasible and as effective as mechanical ablation for the treatment of atrial flutter encircling the tricuspid annulus. The width of the isthmus was estimated to be approximately 1 cm, while the tip electrode of the ablation catheter had a 4-mm length. Therefore, energy had to be applied sequentially from the tricuspid annulus to the inferior vena cava to ablate the isthmus linearly. The sequential atrial sites for ablation were carefully selected by measuring the amplitudes of the atrial and ventricular potentials recorded from the distal pair of the electrodes of the ablation catheter (Fig 1C⇑).
Pathological examinations of the isthmus after radiofrequency ablation demonstrated transmural degeneration of the atrial myocardium, including focal necrosis and microvascular thrombosis, in all dogs. Furthermore, inflammation was noted in the subepicardial layer. The radiofrequency energy used in the present experiment was similar to that used in clinical cases9 10 11 and, moreover, was delivered from the endocardium through a standard ablation catheter. Thus, radiofrequency energy applied as in clinical cases resulted in damage of the atrial myocardium from the endocardium to the subepicardium. Because the atrial wall is thin compared with the ventricular wall, transmural damage was caused by radiofrequency catheter ablation from the endocardium.
The right atrial activation sequence during sinus rhythm in the dogs without Y-shaped lesions was little affected by ablation of the isthmus because the isthmus was the last activation site in the right atrium during sinus rhythm. Furthermore, the AV conduction interval was not affected. Therefore, radiofrequency catheter ablation of the isthmus between the inferior vena cava and the tricuspid annulus was found to be an effective method of treatment of circus movement tachycardia around the tricuspid annulus.
Conduction Block at the Isthmus as a Marker of Successful Radiofrequency Ablation
The present study clearly demonstrated that radiofrequency catheter ablation created intra-atrial conduction block at the isthmus, an ablation site, as did mechanical ablation of the isthmus. The atrial activation sequence during atrial pacing from a site close to the isthmus changed markedly after ablation of the isthmus (Fig 5⇑). Conduction time between the two sites sandwiching the isthmus measured during atrial pacing was increased significantly because of the change in the activation sequence. Furthermore, double potentials indicating conduction block and activation of the block site from two different directions16 were recorded at the ablation site. These findings are simple and positive markers of the elimination of conduction through the isthmus. They will therefore be useful markers for the successful ablation of atrial flutter encircling the tricuspid annulus, just as the disappearance of ventriculoatrial conduction through a concealed AV accessory pathway during ventricular pacing is a marker of successful ablation of the accessory pathway. After successful linear radiofrequency ablation of the isthmus in human common type of atrial flutter, we noted the change of the activation sequence in the isthmus lesion and double potentials at the ablation site during atrial pacing from a site adjacent to the isthmus (K. Okumura, MD, et al, unpublished data, 1995).
Relevance to Human Atrial Flutter and Treatment With Catheter Ablation
Recent clinical studies demonstrated that the mechanism of human atrial flutter, especially that of the classic type, is a circus movement in the right atrium with an area of slow conduction in the inferior right atrium, including the isthmus.1 2 3 4 5 6 7 8 9 It was shown that during the classic type of atrial flutter, the excitation wave front travels downward in the anterior wall of the right atrium, transverses the isthmus between the right ventricle and the inferior vena cava to the ostial area of the coronary sinus, and travels upward in the interatrial septum.1 3 5 6 7 8 9 Although the reentry circuit is not confined to the atrial muscle fibers around the tricuspid annulus but uses a larger portion of the right atrium, the isthmus between the inferior vena cava and the tricuspid annulus is involved in the reentry circuit, as it is in the present canine model of atrial flutter. Thus, atrial flutter induced in the present canine model has a clinical counterpart in the mechanism of reentry whose circuit involves the isthmus.
Radiofrequency catheter ablation has now been established as a curative therapy for supraventricular tachycardias including AV reciprocating tachycardia utilizing an accessory pathway,17 18 19 AV nodal reentrant tachycardia,20 21 22 and ectopic atrial tachycardia.23 24 Catheter ablation of atrial flutter with direct and radiofrequency currents has been reported previously. Saoudi and coworkers4 applied direct current to the fragmented electrogram site in the inferior right atrium. Feld and coworkers9 applied radiofrequency energy to the area of slow conduction or its exit site. Calkins and coworkers10 delivered radiofrequency energy to the fractionated site or early activation site during atrial flutter. Cosio and coworkers11 applied radiofrequency energy sequentially to the isthmus between the tricuspid valve and the inferior vena cava to ablate the isthmus linearly. All of these previous ablation procedures were directed to the area in or near the isthmus between the right ventricle and the inferior vena cava because the classic type of atrial flutter uses the isthmus as a critical pathway within the reentry circuit.
Unlike an AV accessory pathway in patients with preexcitation syndrome, the isthmus has a certain width (approximately 1 cm in the dogs used in the present study) and, therefore, radiofrequency catheter ablation of one site within the isthmus with a standard large-tipped electrode catheter seems to be insufficient to eliminate conduction through the isthmus. When slow conduction critical for the initiation and maintenance of reentry is confined to a narrow band of atrial fibers in the isthmus, ablation of one site with a large-tipped catheter may eliminate the reentry circuit for atrial flutter. In three previous clinical trials of radiofrequency catheter ablation of atrial flutter by Feld and coworkers,9 Calkins and coworkers10 and Cosio and coworkers,11 the mean numbers of energy applications were 10, 27, and 21, respectively. Although multiple energy application is required during linear ablation with a standard large-tipped catheter, we suggest that total elimination of conduction through the isthmus between the inferior vena cava and the tricuspid annulus is rational and effective in the treatment of human atrial flutter, as Cosio and coworkers previously reported.11
We thank Kiyoshi Takahashi, MD, professor of the Second Department of Pathology, Kumamoto University School of Medicine, for his critical comments on the pathological findings in this study.
- Received January 23, 1995.
- Accepted March 6, 1995.
- Copyright © 1995 by American Heart Association
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