Activation and Entrainment Mapping Defines the Tricuspid Annulus as the Anterior Barrier in Typical Atrial Flutter
Background The importance of anatomic barriers in the atrial flutter reentry circuit has been well demonstrated in canine models. It has been shown previously that the crista terminalis and its continuation as the eustachian ridge form a posterior barrier. In this study we tested the hypothesis that the tricuspid annulus forms the continuous anterior barrier to the flutter circuit.
Methods and Results Thirteen patients with typical atrial flutter were studied. A 20-pole halo catheter was situated around the tricuspid annulus. A mapping catheter was used for activation and entrainment mapping from seven sequential sites around the tricuspid annulus and from three additional sites including the tip of the right atrial appendage, at the fossa ovalis, and in the distal coronary sinus. Sites were considered to be within the circuit when the postpacing interval minus the flutter cycle length and the stimulus time minus the activation time were ≤10 ms; sites were considered to be outside the circuit when these intervals were >10 ms. All seven annular sites were within the circuit; activation occurred sequentially around the annulus and accounted for 100% of the flutter cycle length. The fossa ovalis, the distal coronary sinus, and the right atrial appendage were outside the circuit.
Conclusions Closely spaced sites around the tricuspid annulus are activated sequentially, and are all within the flutter circuit according to entrainment criteria. This demonstrates that the tricuspid annulus constitutes a continuous anterior barrier constraining the reentrant wave front of human counterclockwise atrial flutter.
The importance of anatomic barriers in the atrial flutter reentry circuit has been well demonstrated in canine models.1 2 3 4 5 We hypothesized that typical human atrial flutter is caused by a broad activation wave front rotating in a counterclockwise direction in the right atrium and constrained between natural endocardial barriers. We have shown previously that the CT and its continuation as the ER form a posterior barrier to the flutter circuit.6 In this study we prospectively tested the hypothesis that the TA forms a continuous anterior barrier to activation and that therefore all sites adjacent to this ring are within the circuit. While activation mapping has shown that during typical atrial flutter, propagation occurs in a counterclockwise direction approximately parallel to the TA,7 sequential activation timing does not prove conclusively that sites are within or critical to the circuit.
Waldo et al8 9 first described the technique of entrainment to characterize reentrant circuits including atrial flutter. Subsequently, entrainment mapping was applied to localize regions of myocardium that are within a reentrant circuit, both during ventricular tachycardia in the setting of coronary artery disease10 11 and more recently during atrial flutter.6 7 12 Entrainment mapping in atrial flutter has demonstrated that sites between the TA and either the IVC or the ostium of the CS are within the flutter circuit. However, entrainment mapping from other sites adjacent to the TA is lacking. In this study we performed systematic entrainment mapping from multiple sites around the TA and compared this with entrainment from other sites considered likely to be outside the circuit.
Thirteen patients (3 women, 10 men; mean age, 64.2±6.8 years; range, 52 to 73 years) with typical atrial flutter who were referred to the University of California, San Francisco, for curative ablation of typical atrial flutter were studied. Typical atrial flutter was defined by the presence of the following characteristics: (1) characteristic surface ECG appearance, (2) counterclockwise activation pattern in the right atrium in the frontal plane, and (3) entrainment characteristics including manifest entrainment from the high right atrium and concealed entrainment from the isthmus between the IVC and the TA. All antiarrhythmic drugs were stopped at least 5 half-lives before study. Informed consent was obtained from all patients before the study according to the protocol approved by the Committee on Human Research.
Fluoroscopic appearance of the catheter placement is shown in Fig 1⇓. A 7F, 20-pole, halo catheter (Cordis-Webster) with 2-mm interelectrode distance was situated in the right atrium around the TA and its annular location confirmed from fluoroscopic projections in the right and left anterior oblique projections. The catheter was placed with the distal tip in the ostium of the CS such that poles 1,2 were located at approximately the 7 o'clock position on the TA and poles 19,20 at approximately the 2 o'clock position, considering the “best-septal” left anterior oblique projection of the TA as the clock face. An 8F roving catheter (EP Technologies) (5-mm electrode tip, other electrodes 2 mm with 2-mm interelectrode spacing) was used for activation and entrainment mapping from seven sites within 0.5 cm of the TA (on the clock face in the left anterior oblique projection these included the 6, 8, 10, 12, 2, 4, and 5 o'clock positions) and from three additional sites including: the tip of the RAA, at the FO, and in the distal CS. To facilitate annular mapping and to stabilize tissue contact, the rove catheter was deployed through a long vascular sheath (Daig Corp) whose curve was chosen according to the site required. Sites were considered to be in close proximity to the TA on the basis of the fluoroscopic appearance in the right anterior oblique projection and by the demonstration of a low-amplitude ventricular electrogram on the distal pair of the entraining catheter. An 8F, open-lumen, decapolar catheter (Elecath; 2-mm interelectrode distance and 5-mm intraelectrode distance) was placed through the internal jugular vein or the left femoral vein into the CS. Positioning of the proximal electrode pair at the ostium of the CS was confirmed with contrast injection viewed with fluoroscopy, with the ostium typically located at the 4:30 position on the left anterior oblique view.
Bipolar intracardiac electrograms filtered between 30 and 500 Hz were recorded and stored digitally on a Cardiolab system (Prucka Engineering) simultaneously with 12-lead surface ECGs. All measurements were performed on the Cardiolab system at screen speeds of 400 to 1600 mm/s with the use of on-screen digital calipers.
Entrainment mapping was performed according to a previously described protocol.6 Briefly, during atrial flutter, unipolar pacing was performed at each site from the distal electrode of the roving catheter. A large patch-skin electrode was used as the indifferent electrode. A custom-made Y-splitter that attached to the lead from the distal electrode allowed simultaneous recording of the distal bipole pair during unipolar pacing. Measurements were made from bipolar recordings filtered at 30 to 500 Hz. Pacing was performed three times at 10, 20, and 40 ms less than the spontaneous FCL for at least 10 beats at twice diastolic threshold for capture thresholds of ≤1 mA with a 2-ms pulse width.
For characterizing entrainment, we adopted definitions as previously described for entrainment of atrial flutter6 and of ventricular tachycardia.10 Manifest entrainment is defined as entrainment demonstrating surface fusion, progressive fusion with faster rates, and in which the last captured flutter wave is entrained without surface fusion. Concealed entrainment is defined as entrainment in which there is no evidence of surface fusion (on a complete 12-lead ECG) and there is a delay between the stimulus artifact and the flutter wave. The first flutter wave after the last paced flutter wave returns at the tachycardia cycle length. Sites demonstrating concealed entrainment at all pacing cycle lengths were considered to be within a relatively protected isthmus of conduction.
PPI is defined as the time necessary to conduct from the pacing site to the reentrant circuit, through the circuit, and back to the pacing site. It was measured from the last stimulus artifact to the first recorded electrogram at the pacing site (distal electrode pair of the pacing catheter). The electrogram was measured with the use of two techniques: (1) to the first sharp component that reached an angle of 45 degrees with the baseline13 14 and (2) to the peak amplitude of the electrogram.15 16 All measurements were made consistently for annular sites and for sites outside the circuit. All data in tables are presented with the use of the first methodology.
FCL was taken as an average of three intervals after the first PPI. When there was >10-ms beat-to-beat variation in the cycle length of these postpacing beats, it was assumed that decremental conduction had occurred and these trials were excluded from analysis. This technique of measurement of the FCL also was compared with FCL from an average of 10 cycles before entrainment.
Stimulus time is defined as time from the pacing artifact to onset of activation in the os of the CS (when capture occurred orthodromically). Because the onset of the flutter wave is often difficult to discern on the surface ECG—either because of rapid AV conduction or lack of a true isoelectric point on the surface flutter wave—the electrogram from the CS os was used as a surrogate marker for the onset of the flutter wave, as previously described.11 12 17
Activation time is defined as time from the electrogram recorded at the pacing site to onset of activation in the os of the CS.
Sites were considered to be within the circuit when the PPI minus the tachycardia cycle length and the stimulus time minus the activation time were ≤10 ms.
Sites were considered to be outside the circuit when the PPI minus the tachycardia cycle length and the stimulus time minus the activation time were >10 ms.
Decremental conduction was considered to be present when there was a >10-ms increase in the PPI when pacing at a cycle length of (a) 20 ms or (b) 40 ms less than the FCL compared with pacing at 10 ms less than the FCL.
Values are expressed as mean±SD. PPI−FCL and stimulus time−activation time were calculated at each site for each patient as an average of values for each pacing rate at each site. Statistical comparisons between two continuous variables were performed with use of the Student's t test (paired or unpaired as appropriate). Statistical analyses between three or more variables were performed with the use of ANOVA with between-group comparisons performed with Scheffe´'s F test. Statistical significance was accepted at the P<.05 level, and all tests were two-tailed.
There were 13 patients (3 women, 10 men; mean age, 64.2±6.8 years; range, 52 to 73 years). Eight patients had no significant associated heart disease, 2 had coronary artery disease, 1 had tachycardia-bradycardia syndrome, 1 had acquired atrioventricular block, and 1 had a prior aortic valve replacement. The mean tachycardia cycle length was 258±24 ms (range, 216 to 292 ms). There was no significant difference in FCL when this was measured from the 10 beats before entrainment (256±24 ms) compared with the 3 beats after entrainment. Radiofrequency ablation was successful in all patients by creation of a linear lesion between the IVC and the TA (one at the 5:30 position on the TA, seven at the 6:00 position on the TA, and five at the 7:00 position on TA). The mean number of radiofrequency applications was 7±4 (range, 1 to 12).
Activation times on the halo catheter are shown in Table 1⇓. Sequential activation was seen on the halo catheter in all patients with activation occurring earliest at poles 19,20 (high septal right atrium) and then continuing sequentially around the TA to distal poles 1,2 (low posterolateral right atrium) (Fig 2⇓). Activation timing at the proximal set of electrodes (19,20) was taken as 0 ms. For this halo catheter, with electrodes deployed from approximately the 2 o'clock position (bipole pair 19,20) counterclockwise to approximately 7 o'clock (bipole pair 1,2), activation times were uniformly distributed and did not demonstrate an area of significantly slower conduction. However, in all patients this catheter was deployed such that the poles did not span the region of the previously described atrial flutter “slow zone.”17 Activation timing around the entire annulus including the slow zone is evaluated from the seven annular sites mapped with the roving mapping catheter. Activation times from each of these seven annular sites and from the three additional sites (tip of the RAA, distal CS, and FO) are shown in Table 2⇓. These activation times are measured to activation at the ostium of the CS. Activation occurred sequentially around the annulus in all patients and accounted for 100% of the FCL. Forty-eight percent (48±5%) of the complete flutter circuit occurred between the 8 and 4 o'clock positions on the annulus, and the percent activation time in this region was significantly longer than for the distance from the 4 to 12 o'clock positions (31±8%) or from the 12 to 8 o'clock positions (21±5%; P<.0001, ANOVA). The difference in activation time between the 4 o'clock to 12 o'clock positions compared with 12 o'clock to 8 o'clock positions was not significant. Activation time was longest in the area between the 6 o'clock position on the TA and the 4 o'clock position (immediately superior to the CS ostium).
Entrainment was established for each patient from one or more of the 10 mapping sites. Results of entrainment mapping are shown in Table 3⇓. The PPI was not significantly different than the FCL and the stimulus time was not different than the activation time at any of the 7 tricuspid annular sites (Table 3⇓, Fig 2A⇑, and Fig 3A through 3C⇓).
Concealed entrainment was observed in all trials at both 5 and 6 o'clock positions on the TA. Manifest entrainment was observed for all trials at tricuspid annular sites 10, 12, and 2 o'clock positions. Interestingly, at the 4 and 8 o'clock positions on the TA, pacing at 10 to 20 ms less than the FCL did not produce manifest fusion on the 12-lead surface ECG. However, at both of these sites, fusion was evident when pacing at 40 ms less than the FCL in all trials.
At the FO, the distal CS, and the tip of the RAA, the PPI was significantly longer than the tachycardia cycle length by a mean of >40 ms at each site, and the stimulus time was significantly longer than the activation time by a mean of >50 ms at each site (Table 3⇑, Fig 2C⇑, and Fig 3D and 3E⇑⇑). Entrainment at all three sites produced manifest fusion on the 12-lead surface ECG at all cycle lengths. When we measured to the electrogram peak, compared with the 45 degree deviation from the baseline, there was a mean increment in the PPI of 4±3 ms for annular sites and 6±4 ms for sites outside the circuit (P=NS). There was no significant difference in the FCL according to the method of electrogram measurement.
Decremental conduction as defined above was observed in 2 of 13 patients when pacing at 20 ms less than FCL (mean increment in the PPI=14±4 ms) and in 5 of 13 patients when pacing at 40 ms less than FCL (mean increment in the PPI=21±6 ms). There was no significant difference in the decrement observed for pacing sites in the isthmus of slow conduction, annular sites outside this isthmus, or sites remote from the circuit.
For a group of patients with typical counterclockwise atrial flutter, we used activation and entrainment mapping to demonstrate that closely spaced sites around the entire TA circumference are activated sequentially, account for 100% of the FCL, and are all within the atrial flutter circuit. Although previous studies have demonstrated counterclockwise activation in the right atrium7 and defined an area of slow conduction17 in the inferoposterior right atrium, this study is unique in that activation mapping was performed from closely spaced sites around the entire circumference of the annulus with entrainment mapping used to confirm that these sites are all within the flutter circuit. The tip of the RAA, the distal CS, and the FO were outside the reentrant circuit. We have demonstrated previously that the CT and its continuation as the ER form a posterior barrier to the reentrant loop, with sites anterior to this being within the flutter circuit and sites posterior being outside the circuit.6 Our findings in the present study extend these results and demonstrate that atrial flutter is a broad reentrant circuit constrained at least in part between barriers and that the TA forms a continuous anterior barrier to constrain the wave front as it rotates.
Use of Entrainment to Define a Reentrant Circuit
Waldo et al8 first described that high right atrial pacing at a rate faster than the spontaneous flutter rate caused acceleration of flutter or “entrainment” to the pacing rate. The pacing wave front enters the circuit in the orthodromic direction, thereby advancing activation, and also in the antidromic direction, colliding with the previous orthodromic wave front. The criteria required to demonstrate entrainment have been described in detail by Henthorn et al.18 Recently, the demonstration of concealed entrainment has been used to identify a narrow or protected isthmus constrained between barriers both during ventricular tachycardia10 and atrial flutter.7 11 17 19 20 Entrainment from these sites is not manifest on the surface ECG because the small area of tissue captured in the antidromic direction is insufficient to affect the P-wave or QRS morphology, respectively. Precisely because this technique identifies a narrow isthmus, ablation at these sites carries a high probability of success. In atrial flutter, this area has been identified between the IVC and the TA.6 11
More recently, the relationships of the PPI to the tachycardia cycle length and of the stimulus time to the activation time have been used to determine whether a particular site is within a reentrant circuit. Inoue et al21 observed that the PPI varied, depending on where the pacing and recording sites were in relation to the reentrant circuit. Stevenson et al10 elegantly demonstrated both in a computer model and in human ventricular tachycardia that the PPI at the pacing site is a useful marker of whether that site is inside or outside of the reentrant circuit. When the PPI was within 30 ms of the tachycardia cycle length, the site was considered to be in the tachycardia circuit. Olgin et al6 recently demonstrated similar findings during entrainment of atrial flutter. The stimulus time (activation time from the stimulus) also can be used to determine sites that are within the reentrant circuit during entrainment.10 22 If atrial flutter is entrained without fusion, the activation time (local electrogram to flutter wave) and the stimulus time (stimulus to flutter wave) both reflect the time necessary for conduction from the pacing site to the exit site from the critical isthmus. When manifest entrainment (ie, fusion) is present, the stimulus time to the onset of the orthodromically captured flutter wave cannot be measured because a P wave will be initiated as soon as the pacing stimulus captures atrium as opposed to when the tachycardia wave front exits the protected isthmus. In this study, we used the CS ostium electrogram recording as a surrogate marker of the exit site as previously described.11 12 17
Role of the Tricuspid Annulus
The importance of barriers, either functional or fixed, in the genesis and perpetuation of atrial arrhythmias has long been recognized both in animal models1 3 4 5 23 and in humans11 17 24 25 26 and has been reviewed recently by Boyden.27 In a model described by Frame et al,3 creation of a Y-shaped incision in the right atrial wall led to reentry around the TA either in a clockwise or counterclockwise direction.2 We have demonstrated recently that the CT forms a posterior line of conduction block during counterclockwise atrial flutter.6 We speculate that the Y-shaped incision created by Frame et al creates a line of block in this model of atrial flutter that serves a similar function to the CT in human atrial flutter (Fig 4⇓). This line of block (either in the animal model or in human atrial flutter) prevents a “short circuiting” of the TA via the posterior smooth-walled right atrium with termination of reentry caused by the wave front encountering refractory tissue. Rather, in the presence of the line of block, the reentrant wave front is “forced” around the TA as the shortest reentrant path (Fig 4⇓). Multipolar endocardial mapping in the Frame model clearly delineated the two boundaries that were necessary for stable reentry.
In the model of Frame et al,3 circus movement occurred in the tissues of the supravalvular lamina of the canine tricuspid ring28 and conduction velocity was relatively uniform around the ring. In human atrial flutter, a zone of slow conduction in the low right atrium between the TA and the IVC has been demonstrated previously,17 and our results also suggest that conduction velocity in this region is slow. This may be due to the presence of anisotropic conduction through the trabeculations of the low right atrium. The demonstration of uniform conduction velocity on the halo catheter probably reflects the fact that this particular catheter did not fully span the slow zone and did not have electrodes within this region.
Recent studies in human atrial flutter have demonstrated that the TA in the low right atrium is an important anatomic barrier.6 7 11 17 25 Feld et al11 demonstrated that concealed entrainment was achieved in the area between the TA and the IVC with a long (>40 ms) stimulus to flutter wave and between the CS os and the TA with a short (<40 ms) stimulus to flutter wave. Cosio et al7 also demonstrated concealed entrainment from within the IVC-tricuspid isthmus and manifest entrainment from high right atrial sites. In the present study we also demonstrated concealed entrainment from within the isthmus between the IVC and the tricuspid valve and manifest entrainment from other annular sites. Interestingly, at the 8 and 4 o'clock positions, manifest entrainment was evident only at the shorter pacing cycle lengths possibly because at these sites, the amount of myocardium captured antidromically at the longer cycle lengths was insufficient to be detected on the surface ECG. In the case of pacing from the 4 o'clock site, this may reflect its proximity to the exit of the slow zone. When pacing from the 8 o'clock site in the vicinity of the entrance to the slow zone, antidromic spread will be relatively limited by the close confines of the CT posteriorly and the TA anteriorly in this region. Annular sites demonstrating manifest entrainment nevertheless showed the entrainment characteristics of being within the circuit.
Cosio et al24 have previously suggested on the basis of activation mapping that human atrial flutter may circulate around the TA. The present study using entrainment techniques provides evidence in support of this hypothesis. However, rather than stating that the wave front travels around the annulus it is perhaps more correct to state that the annulus is the anterior barrier of a broad wave front.
Toward a More Complete Description of the Atrial Flutter Circuit
From the activation and entrainment maps obtained in this study and from the results of extensive previous investigation both in animal models and humans, a more complete understanding of the human atrial flutter circuit is gradually being constructed. Typical atrial flutter occurs in a counterclockwise rotation with the continuous anterior barrier provided by the TA. On the superior and lateral right atrial aspects the flutter wave is a broad, inferiorly directed wave front constrained between the CT posteriorly and the TA anteriorly. Our observations are consistent with those of Arribas et al,29 who have recently demonstrated that the upper link in the atrial flutter circuit is superior rather than inferior to the SVC. These data are consistent with our findings in the current study and in a previous study that the flutter wave front does not activate across the CT at any point. On the lateral atrium, the CT and the TA form a funnel that directs the excitation wave front into the isthmus bounded by the inferior TA and the ER. At this point, the flutter wave front is at its narrowest and is therefore most susceptible to ablation. On the medial or septal aspect, as the reentrant wave front now continues superiorly from between the CS ostium and the TA, the anterior barrier is again the TA. That portion of excitation directed along the medial or septal TA will continue the reentrant circuit anterior to the superomedial portion of the CT. Similar to the situation in the Frame model,3 conduction time around the septal region of the tricuspid ring probably will be shorter than any alternate septal path for the impulse. Hence, the FO is outside the circuit. Boyden27 has described this type of alternate pathway through fully excitable tissue with a longer conduction time as a form of functional barrier. A careful evaluation of the anatomy of the septum does not yield a structure that would be likely to provide any additional fixed anatomic barrier between the ostium of the CS and the superomedial CT. Nevertheless, what role if any is played by such structures as the tendon of Todaro or the limbus of the FO is unknown. This description of the flutter circuit is based on data accumulated from activation and entrainment mapping during electrophysiological studies. Confirmation of this description must await high-density mapping of the circuit such as has been performed during animal studies.3 5 30 31 As has been reviewed recently, the atrial flutter circuit is complex, and some questions remain to be answered.32 For example, although we have demonstrated that activation proceeds around the annulus anterior to the base of the RAA, an alternate path that may be of similar length would be around the posterior base of the RAA. It is possible that the activation wave front splits around the base of the appendage but that both limbs form part of the circuit. Our study has not addressed this question.
Recent reports have demonstrated the high success rates in the cure of atrial flutter by creation of a lesion between the TA and the IVC.11 25 33 34 Nevertheless, procedures can be long and difficult and recurrence rates may be high. Atrial flutter may be cured by any lesion that spans from the posterior barrier to the anterior barrier, the TA. Thus, alternate sites for ablation may exist between the superior CT and the TA at that level or between the CT and the TA on the inferolateral right atrial wall. Although this area is trabeculated and lesion formation potentially difficult, the area between the inferior CT and the TA is relatively narrow and may be no more trabeculated than the area between the IVC and the TA. With the use of newer catheter technologies, access to this area may be facilitated. It should be emphasized that although a site may demonstrate entrainment characteristics of being within the circuit (ie, any annular site) this is an insufficient criterion for successful ablation. In addition, a successful lesion in this area must also span between two barriers.
Recently, an association between atrioventricular nodal reentry tachycardia and inducible atrial flutter has been reported.35 36 Continuation of the atrial flutter circuit around the septal rim of the TA as has been shown in this study (4 o'clock position on the TA) and through the triangle of Koch may account for this observation. A lesion in the region between the CS os and the TA may be expected to cure both arrhythmias.
The limitations of this entrainment technique have been well described previously.6 10 Principally, decrement occurring within the circuit as a result of entrainment may cause prolongation of the PPI leading to sites that are in the circuit appearing to be outside the circuit. For this reason, we used data from pacing at the longest cycle length that reliably entrained the tachycardia.
During entrainment, we used an output current of twice diastolic threshold as has been reported previously10 because pacing at or just above capture threshold6 caused repeated episodes of loss of capture during multiple entrainment episodes and proved to be impractical during a long-term clinical study. In theory, suprathreshold stimulation may lead to a site outside the circuit appearing to be “in.” However, for this to occur, the pacing stimulus would not only need to capture atrial tissue that was within the circuit but was also “orthodromically downstream” by a greater amount than the actual pacing site was outside the circuit. Although this may be theoretically possible, at stimulation thresholds used in the clinical electrophysiology laboratory, it would be very unlikely. In the study by Wikswo et al37 it was shown that the size of the virtual electrode was small (1 mm) and relatively constant over the range of 1 to 7 mA in the longitudinal orientation; at oblique orientations it demonstrated a logarithmic dependence on stimulus strength. Nevertheless, even at maximal stimulation of 7 mA, the size of the virtual electrode was only 3 mm. At twice diastolic threshold, assuming a worst-case scenario of the size of the virtual electrode and the conduction velocity in the direction of the circuit, the time error would only be ≈2 to 4 ms. Furthermore, the same stimulation protocol was used for annular sites as for sites outside the circuit so that any error would be eliminated by comparison.
Although it is well accepted that the most accurate reflection of underlying cellular activity in a unipolar recording is at the intrinsicoid deflection, the best method for measurement of bipolar electrograms is not clear.15 38 We measured to onset of the first sharp component with at least a 45 degree angle with the baseline6 10 13 14 39 and were consistent in all measurements made for all sites. Although there was a 4- to 5-ms increment when we measured to the electrogram peak, this difference was present for both annular sites and sites outside the circuit. Furthermore, in contrast to the minor measurement variations according to how the electrogram is marked, the differences between sites in or out of the circuit differed by >300% (30 to 80 ms) wherever the measurements were made.
The halo catheter is at times somewhat difficult to hold in stable position for the length of an electrophysiology study. Therefore, activation times on the halo catheter were supported by data from the roving mapping catheter, and only this latter catheter was used for entrainment.
To achieve catheter stability and reliable capture of atrial (and not ventricular) myocardium during entrainment of atrial flutter, it was necessary to consider sites as being “annular” if they were within 0.5 cm of the annulus rather than truly abutting the annulus. In this type of macroreentrant circuit, we believe that it is reasonable to assume that sites immediately adjacent to the annulus will be activated with the same characteristics.
We used a definition of atrial flutter based on flutter wave morphology and activation and entrainment mapping characteristics. We have therefore taken a mechanistic approach to the definition of atrial flutter rather than a more arbitrary cycle length definition. Nevertheless, the range of cycle lengths included in our study (216 to 292 ms) is similar to that included in recent studies dealing with mapping or ablation of typical atrial flutter (Kirkorian et al,33 200 to 320; Feld et al,11 200 to 350; Poty et al,40 200 to 350; and Olshansky et al,41 205 to 290).
We have shown that closely spaced sites around the TA are activated sequentially, account for 100% of the FCL, and are all within the flutter circuit according to entrainment criteria. This demonstrates that the TA constitutes a continuous anterior barrier constraining the reentrant wave front of human counterclockwise atrial flutter.
Selected Abbreviations and Acronyms
|FCL||=||flutter cycle length|
|IVC||=||inferior vena cava|
|RAA||=||right atrial appendage|
|SVC||=||superior vena cava|
Dr Kalman was funded as the Ralph Reader Overseas Research Fellow of the National Heart Foundation of Australia.
- Received December 7, 1995.
- Revision received March 8, 1996.
- Accepted March 21, 1996.
- Copyright © 1996 by American Heart Association
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