Author + information
- Received January 30, 2002
- Revision received May 10, 2002
- Accepted May 23, 2002
- Published online August 21, 2002.
- Ching-Tai Tai, MD*,* (, )
- Jin-Long Huang, MD*,
- Yung-Kuo Lin, MD*,
- Ming-Hsiung Hsieh, MD*,
- Pi-Chang Lee*,
- Yu-An Ding, MD*,
- Mau-Song Chang, MD* and
- Shih-Ann Chen, MD*
- ↵*Reprint requests and correspondence:
Dr. Ching-Tai Tai, Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, 201, Sec. 2, Shih-Pai Road, Taipei, Taiwan.
Objectives This study was aimed at delineating the reentrant circuit of right atrial (RA) upper loop re-entry using noncontact three-dimensional mapping.
Background Various forms of atypical atrial flutter including lower loop re-entry and left atrial flutter have been demonstrated. However, little is known about upper loop re-entry in the RA.
Methods The study population consisted of eight patients (65 ± 12 years, seven men) with atypical atrial flutter. Right atrial activation during atrial flutter was visualized using a noncontact mapping system (EnSite-3000 with Clarity Software, St. Paul, Minnesota) for a three-dimensional reconstruction of the endocardial depolarization. The narrowest part of the re-entrant circuit was targeted using radiofrequency catheter ablation.
Results Noncontact mapping showed macro–re-entry confined to the RA free wall with RA activation time accounting for 100% of the cycle length (214 ± 21 ms) in all eight patients. Two patients had counterclockwise activation, and six patients had clockwise activation around the central obstacle, which was composed of the crista terminalis, the area of functional block, and superior vena cava. The lower turn-around points were located at the conduction gap in the crista terminalis. Radiofrequency linear ablation of the conduction gap in the crista terminalis was performed and eliminated atrial flutter in six patients without recurrence during a follow-up of 3.2 ± 1.1 months.
Conclusions Atypical atrial flutter could arise from upper loop re-entry in the RA with conduction through the gap in the crista terminalis. Radiofrequency linear ablation of the conduction gap was effective in eliminating this atrial arrhythmia.
Typical atrial flutter has been well demonstrated as a macro–re-entrant circuit around the tricuspid annulus (1–4). Radiofrequency (RF) catheter ablation of the cavotricuspid isthmus (CTI) is highly effective in eliminating this tachycardia. However, various forms of nonincisional atypical atrial flutter have been reported, including CTI-dependent lower loop re-entry and CTI-independent right atrial (RA) and left atrial free wall flutters (5–8). Using electroanatomic mapping, Kall et al. (6) found a specific type of atypical atrial flutter arising in the RA free wall anterior to the crista terminalis. Yang et al. (8) observed upper loop reentry in the RA, but they did not elucidate the entire re-entrant circuit. Until now, noncontact three-dimensional mapping of atypical atrial flutter has not been reported.
In this study we described the electrophysiologic characteristics and results of RF ablation in a series of patients with upper loop re-entry around the crista terminalis using noncontact three-dimensional mapping.
In 150 consecutive patients with clinically documented atrial flutter referred for RF catheter ablation, eight (5.3%) patients (seven men and one woman, 65 ± 12 years old) were found to have typical and atypical RA flutter (Table 1). These eight patients constituted the study population. One patient had received CTI ablation for typical atrial flutter. Three patients had a history of paroxysmal atrial fibrillation. Six patients had cardiovascular diseases, including two with coronary artery disease, three with hypertension, and one with rheumatic heart disease.
Informed written consent was obtained from all patients. As described previously, all antiarrhythmic drugs were discontinued for at least five half-lives before the study (3,9). In all patients a 7F, 20-pole, deflectable Halo catheter with 10 mm paired spacing (Cordis-Webster Inc., Baldwin Park, California) was positioned around the tricuspid annulus to record the RA activation in the lateral wall and the low RA isthmus simultaneously. A 7F, deflectable, decapolar catheter with 2-mm interelectrode distance and 5-mm space between each electrode pair was also inserted into the coronary sinus via the internal jugular vein. The position of the proximal electrode pair at the ostium of the coronary sinus was confirmed with contrast injection. A 9F sheath placed in the left femoral vein was used to introduce the noncontact mapping catheter.
Noncontact mapping system
The noncontact mapping system (EnSite 3000, Endocardial Solutions, St. Paul, Minnesota) was described in detail previously (10). In brief, the system consists of a noncontact catheter (9F) with a multielectrode array (MEA) surrounding a 7.5-ml balloon mounted at the distal end. Raw data detected by the MEA is transferred to a silicon graphics workstation via a digitalized amplifier system.
Before deployment of the MEA, patients were given 3,000 IU heparin boluses to maintain activated clotting time between 250 s and 300 s throughout the study. The MEA catheter was deployed over a 0.035-in. guidewire, which had been advanced to the superior vena cava (SVC) (Fig. 1). The system locates any catheter in relation to the MEA using a “locator” signal, which serves two purposes. It is used to construct a three-dimensional computer model of the virtual endocardium providing a geometry matrix for the inverse solution. Geometric points are sampled at the beginning of the study during sinus rhythm or atrial flutter. The locator signal is also used to display and track the position of the catheter on the virtual endocardium and allows marking of anatomic locations identified using fluoroscopy and electrogram characteristics.
Using mathematical techniques to process these potentials, the system is able to reconstruct more than 3,000 unipolar electrograms simultaneously and superimpose them onto the virtual endocardium, producing isopotential maps with a color range representing voltage amplitude. Reconstructed electrograms can also be selected from sites on the virtual endocardium and displayed individually. Morphologic components in the virtual electrogram correlate with contact electrogram as previously validated (10).
If spontaneous atrial flutter was found at the onset of study, multicatheter mapping and noncontact mapping were performed simultaneously to investigate the reentrant circuit. If sinus rhythm was present at baseline, low RA or coronary sinus pacing was performed until 2 to 1 atrial capture was attained to induce atrial flutter. At baseline, counterclockwise typical atrial flutter was spontaneous in three patients and induced in four patients. Clockwise typical atrial flutter was induced in two of seven patients. After successful ablation of typical atrial flutter with creation of bidirectional isthmus conduction block, the previous pacing protocol was repeated (9). Sustained atypical atrial flutter was induced in all of these seven patients. The remaining one patient had induced atypical atrial flutter only.
Anatomical nomenclature was used that reflected the true orientation and positioning of the human heart in the thorax. Using this format the SVC and RA appendage are superior, and the inferior vena cava and the CTI are inferior to the tricuspid annulus. The His bundle is positioned in the anterosuperior aspect of the medial tricuspid annulus, the coronary sinus in the posteroinferior aspect of the medial tricuspid annulus, and the crista terminalis is located in the lateral wall of the RA and is oriented from superior to inferior.
Typical atrial flutter was defined as a macro–re-entrant atrial tachycardia circulating around the whole tricuspid annulus with concomitant activation through the posterior and anterior free walls as well as conduction block along the crista terminalis.
Atypical atrial flutter was defined as any macro–re-entrant atrial tachycardia except typical atrial flutter and not produced by prior atriotomy.
Counterclockwise upper loop re-entry was defined as an atypical atrial flutter involving the upper portion of the RA with a descending activation sequence in the free wall anterior to the crista terminalis.
Clockwise upper loop re-entry was defined as an atypical atrial flutter involving the upper portion of the RA with an ascending activation sequence in the free wall anterior to the crista terminalis.
Conduction gap in the crista terminalis was defined as the remnant of conducting tissue bounded on both sides by regions of conduction block as determined from the isopotential map.
Double potentials were defined for conventional bipolar and virtual unipolar atrial electrograms with two discrete deflections per beat either separated by an isoelectric baseline or a low amplitude interval (11).
Scar zones were defined as areas with the amplitude of unipolar peak negative potential between 0 and −1.0 mV with slow conduction or conduction block as determined from the isopotential map.
Atypical atrial flutter ablation and follow-up
Radiofrequency ablation was performed using a 4-mm electrode-tipped ablation catheter connected to an EPT-1000 generator. The critical isthmus for the reentrant circuit was targeted. Energy applications (50W, 60°C, 40 s) were performed sequentially to produce a linear lesion. After ablation, burst pacing was performed from the low RA and coronary sinus to 2 to 1 atrial capture. Successful ablation was defined as bidirectional conduction block along the crista terminalis shown by noncontact mapping and inability to reinduce atrial flutter. After hospital discharge all patients were followed up closely in the outpatient clinic. Long-term efficacy was assessed clinically on the basis of the resting surface electrocardiogram (ECG), 24-h Holter monitoring, and clinical symptoms.
Continuous data are expressed as mean ± SD.
Induction and noncontact mapping
In all eight patients, sustained atypical atrial flutter was induced with burst pacing at cycle lengths of 200 to 250 ms from the proximal coronary sinus. Spontaneous transitions between atypical atrial flutter and atrial fibrillation were observed in three patients. The mean cycle length of atypical atrial flutter was 214 ± 21 ms. The ECGs of induced and previously documented atrial flutter were similar. The flutter waves in the inferior ECG leads were positive in five patients with distal to proximal coronary sinus activation and negative in three patients with proximal to distal coronary sinus activation (Table 1). There was no relationship between the flutter wave morphology in the inferior ECG leads and the direction of upper loop re-entry.
During sustained atypical atrial flutter, RA activation was earlier than coronary sinus activation. Noncontact mapping showed macro–re-entry confined to the RA free wall with RA activation time accounting for 100% of the cycle length in all eight patients. In the left anterior oblique view, there was counterclockwise activation in two patients and clockwise activation in six patients. In two patients with counterclockwise upper loop re-entry, the activation wavefront propagated down the anterior free wall and split into two wavefronts. One crossed the gap of the midcrista terminalis and proceeded up the posterior wall and around the central obstacle, which was composed of the upper crista terminalis, the area of functional block and the SVC, to complete the re-entrant circuit; the other approached the lateral CTI with conduction blocked at the previous ablation line for typical atrial flutter (Fig. 2). Interestingly, one patient had the area of functional block anterior to the crista terminalis and the other had the area of functional block posterior to the crista terminalis. In six patients with clockwise upper loop re-entry, the activation wavefront propagated down the posterior wall and split into two wavefronts. One crossed the gap in the crista terminalis and proceeded up the anterior free wall and around the central obstacle, which was composed of the upper crista terminalis, the area of functional block and the SVC, to complete the reentrant circuit; the other approached the medial CTI with conduction blocked at the previous ablation line for typical atrial flutter (Fig. 3).
In all eight patients, virtual electrograms showed widely split double potentials in the crista terminalis, as well as in areas of functional block, and low amplitude potentials with fractionation at the gap in the crista terminalis during atrial flutter. During sinus rhythm areas of functional block demonstrated wide and low-amplitude potentials consistent with scar formation in two patients and normal atrium in six patients.
RF ablation and follow-up
The ablation procedure did not proceed in two patients because they felt pain during energy application. Thus, RF energy was applied sequentially on the gap in the crista terminalis during sinus rhythm in only six patients. The mean number of RF energy applications was 6 ± 2.1. After ablation, conduction block at the gap in the crista terminalis was confirmed by atrial pacing during sinus rhythm (Fig. 4). There was no complication during the ablation procedure. During a follow-up of 3.2 ± 1.1 months, none of eight patients had recurrence of typical or atypical atrial flutter. In three patients with a history of atrial fibrillation, there has been no recurrence of atrial fibrillation during the follow-up period.
This study demonstrated that atypical right atrial flutter could arise from upper loop re-entry around the combined anatomic and functional central obstacle. The lower turn-around point was located at the conduction gap of the crista terminalis in all eight patients. Radiofrequency linear ablation of this conduction gap was effective in eliminating upper loop re-entry in the RA.
Previous experimental and clinical atypical RA flutters
Several experimental models of right atrial atypical atrial flutter have been described (12–15). In the canine sterile pericarditis model, Shimizu et al. (12) showed that, after induction of unidirectional conduction block in the upper or lower portion of the sulcus terminalis, counterclockwise or clockwise atrial flutter could develop in the RA free wall respectively (12); the re-entrant circuit of this atrial flutter is similar to that of upper loop re-entry in this study. In the other canine sterile pericarditis model, Schoels et al. (13) demonstrated that the induced atrial flutter was single-loop re-entry around an arc of block close to the atrioventricular ring or around a combined functional and anatomic obstacle when the arc joined an atrial vessel. Similar circus movement atrial flutters were also found in the canine RA enlargement model (14,15).
In a series of 28 patients with 36 episodes of atypical right atrial flutter, Yang et al. (8) found that 67% of 36 episodes was CTI-dependent lower loop re-entry, 22% was upper loop re-entry, and 11% was macro–re-entry around low voltage areas (scars) in the posterolateral RA. They speculated that upper loop re-entry was the converse of lower loop re-entry with a clockwise circuit and break over the lateral or anterolateral annulus with impulse collision in the CTI, but the precise path and boundaries of the circuit were not defined. Kall et al. (6) reported six patients with atypical atrial flutter originating in the RA free wall; the electroanatomic mapping demonstrated clockwise or counterclockwise activation around the vertical central line of block, which was located anterior to the crista terminalis with the length of 2.0 cm to 2.4 cm.
In the present study, we first used noncontact three-dimensional mapping to delineate upper loop re-entry in the RA and found that this circus movement tachycardia was different from previously described atypical atrial flutters, showing activation around the central obstacle, which was composed of the crista terminalis, the area of functional block and the SVC. The difference of the mechanism for atypical RA flutter between the study by Kall et al. (6) and ours lies in the role of the crista terminalis. In the Kall et al. (6) study, the crista terminalis was a barrier for the re-entrant circuit, but in our study a portion of the crista terminalis was included in the central obstacle of the re-entrant circuit because of wavefront propagation through the gap.
Role of the crista terminalis in development of atypical atrial flutter
The crista terminalis has been demonstrated to be a posterior barrier and a line of block in typical atrial flutter (1). Furthermore, limited transverse conduction capabilities of the crista terminalis may contribute to the development of typical atrial flutter (16–18). However, the rate-dependent conduction block of the crista terminalis was shown, suggesting that the line of block during typical atrial flutter was functional (16–18). In some patients complete transverse block of the crista terminalis was not achieved even during pacing until 2 to 1 atrial capture or extrastimulation with a short coupling interval (17,18). This finding suggested the presence of a transverse conduction gap in the crista terminalis, especially in patients with atrial fibrillation (18). Why conduction persists in the gap with block in the residual portions of the crista terminalis is unclear. However, the success or failure of propagation is determined by the underlying source-sink relation, which reflects a complex interaction of several factors such as tissue anisotropy, gap junction distribution, and wavefront curvature (12). Thus, the inhomogeneous conduction properties of the crista terminalis provide a predisposition to unidirectional block and induction of circus movement atrial flutter around the crista terminalis as shown in the present study.
In addition, a scar zone was combined with the crista terminalis to become the central obstacle during upper loop re-entry in two of eight patients. During sinus rhythm, the unipolar virtual electrograms in the scar zone demonstrated wide, low-amplitude, and fractionated electrograms, suggesting a delayed and nonuniform anisotropic conduction through the diseased RA. This may be related to severe atrial fibrosis resulting from proliferation of smooth muscle cells and collagen fibers beneath the endocardial lining (19).
Catheter ablation of atypical atrial flutter
For successful elimination of atrial flutter, the narrowest part of the re-entrant circuit is usually targeted for catheter ablation. Yang et al. (8) reported that RF ablation of the CTI with creation of bidirectional block was effective in eliminating lower loop re-entry tachycardia. Kall et al. (6) showed that RF energy application from a discrete midlateral RA central line of conduction block to the inferior vena cave terminated and prevented the reinduction of atypical atrial flutter in all six patients. In the present study the conduction gap in the crista terminalis was targeted for ablation. After ablation no atypical atrial flutter could be induced, and, during the follow-up period, no recurrence of atrial flutter and atrial fibrillation (in three patients) occurred. This finding suggested that the conduction gap in the crista terminalis is critical for maintenance of the re-entrant circuit of atypical atrial flutter and atrial fibrillation. In the canine sterile pericarditis model, sufficiently rapid atrial flutter on the RA free wall could degenerate into atrial fibrillation (20). Thus, the conduction gap in the crista terminalis may lead to breaks in the activation wavefront of upper loop re-entry and the formation of new “daughter” wavelets. After linear ablation of this gap, both arrhythmias disappeared.
Atypical atrial flutter could arise from upper loop re-entry in the RA through the conduction gap in the crista terminalis. Radiofrequency linear ablation of the conduction gap was effective in eliminating this atrial arrhythmia.
The authors would like to thank Graydon Beatty of Endocardial Solutions, Inc., for his technical assistance with this study.
☆ Supported, in part, by grants from National Science Council (NSC 90-2314-B-010-023, 90-2314-B-075-044, 90-2315-B-010-004), Taipei, Taiwan, and Endocardial Solutions, Inc., St. Paul, Minnesota.
- cavotricuspid isthmus
- multiple electrode array
- right atrium
- superior vena cava
- Received January 30, 2002.
- Revision received May 10, 2002.
- Accepted May 23, 2002.
- American College of Cardiology Foundation
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