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Circulation. 1996;93:284-294

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(Circulation. 1996;93:284-294.)
© 1996 American Heart Association, Inc.

Articles

Electrophysiological Effects of Catheter Ablation of Inferior Vena Cava–Tricuspid Annulus Isthmus in Common Atrial Flutter

Bruno Cauchemez, MD; Michel Haissaguerre, MD; Bruno Fischer, MD; Olivier Thomas, MD; Jacques Clementy, MD; Philippe Coumel, MD

From the Cardiology Department, Lariboisière Hospital (B.C., O.T., P.C.), Paris, and Haut-Lévèque Hospital (M.H., B.F., J.C.), Bordeaux-Pessac, France.

Correspondence to Dr Bruno Cauchemez, Service de Cardiologie, Hôpital Lariboisière, 2 rue Ambroise Paré, 75475 Paris Cedex 10, France.


*    Abstract
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 *Abstract
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Background The electrophysiological mechanisms for successful catheter ablation of atrial flutter (AFl) targeting the inferior vena cava–tricuspid annulus (IVC-TA) isthmus have not been determined.

Methods and Results Twenty patients with common AFl were studied. All had inducible common AFl, and 8 of them had both common and reverse AFl. Right atrial (RA) activation sequences were investigated during pacing from sites proximal (low lateral RA) and distal (proximal coronary sinus) to the IVC-TA isthmus both during entrainment of common or reverse AFl and during pacing in sinus rhythm. This was repeated after ablation. During pacing in sinus rhythm from the low lateral RA, the septum was activated by caudocranial and craniocaudal wave fronts. Similarly, during pacing from the proximal coronary sinus, the lateral RA was activated by two wave fronts. Catheter ablation of the IVC-TA isthmus induced dramatic changes in mapping due to the loss of caudocranial wave front in all but 1 patient. The septum and the lateral RA were activated by a single craniocaudal front as during entrainment of reverse or common AFl, respectively. After a follow-up of 8±2 months, common or reverse AFl occurred in 4 patients. Two had no or only unidirectional changes in the isthmus conduction induced by ablation. The other 2 had a late recovery of conduction.

Conclusions The present study provides evidence that the mechanism of successful AFl ablation targeting the IVC-TA isthmus is local bidirectional conduction block. This change can be used as a new and complementary electrophysiological end point for the procedure. AFl recurrences are associated with failure to achieve a permanent block.


Key Words: ablation • catheters • atrial flutter • electrophysiology • conduction


*    Introduction
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 up arrowAbstract
 *Introduction
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down arrowDiscussion
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Previous studies in animals and humans have shown that the mechanism of common AFl is a large reentrant circuit confined to the RA.1 2 3 4 5 6 7 8 The first attempts at AFl ablation were focused on the exit sites from the myocardial isthmus between the IVC and the TA. Initially, surgery was used,9 and then DC shocks.10 11 Later, ablation using RF energy was focused either on the middle of the IVC-TA isthmus or on the exit sites.12 13 14 15 16 The acute success rate was high with both techniques, yet there was a high recurrence rate, between 10% and 35%.12 13 14 15 16

In all these studies, the end point for the procedure was defined by tachycardia termination and inability to induce AFl.9 10 11 12 13 14 15 16 The use of the latter end point is questionable, since the inducibility of AFl is not systematically tested before ablation, and its reproducibility may be low.17 Furthermore, no study has determined the electrophysiological mechanism for successful ablation.

In this prospective study, we describe the modifications induced by catheter ablation of the IVC-TA isthmus in terms of both intra-atrial conduction time and RA activation sequence. This allows the definition of new electrophysiological criteria for the assessment of the AFl ablation procedure and provides new insight into the role of the isthmus in activation of the RA.


*    Methods
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 up arrowAbstract
 up arrowIntroduction
 *Methods
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Patients
Twenty patients were prospectively included in this study. They were part of a cohort of 54 consecutive patients referred to both centers from April 1994 through December 1994 for RF catheter ablation of common AFl. Inclusion required (1) documented common AFl with an inverted P wave in leads II, III, and aVF giving a typical "sawtooth" pattern; (2) inducibility of sustained common AFl during electrophysiological study; and (3) electrophysiological criteria of AFl as described below (see electrophysiological definitions). Thirty-four patients were excluded because common AFl was not inducible (n=2); because sustained and recurrent atrial fibrillation was induced during pacing maneuvers, requiring repeated DC shocks or drug injection (n=30); or because the electrophysiological inclusion criteria were not fulfilled (n=2).

The 20 patients consisted of 16 men and 4 women with a mean age of 58±9 years. Symptoms had been present from 1 to 15 years. Patients were resistant to a mean of 3±1 antiarrhythmic drugs (range, 1 to 5), including amiodarone in 19 patients. Four patients also had episodes of documented paroxysmal atrial fibrillation, but AFl was their predominant clinical arrhythmia. One patient had a ventricular pacemaker for paroxysmal AV block. Structural heart disease was present in 6 patients (3 coronary artery disease, 2 dilated cardiomyopathy, and 1 aortic valve prosthesis) and chronic obstructive pulmonary disease in 3.

Electrophysiological Study
The protocol was approved by the University Committee on Human Research for both centers, and patients gave informed consent. The patients were studied in the postabsorptive state under light sedation with fentanyl and midazolam. Antiarrhythmic drugs were interrupted 5 or more half-lives before the study, except for amiodarone, which was interrupted 5±6 days before ablation in 19 patients. The drug was taken for a mean of 7±10 and a median of 4 months (range, 0.3 to 36 months).

Four or five catheter electrodes were introduced through both femoral and left subclavian veins and positioned in the RA as shown in Fig 1Down. One 6F decapolar catheter with a 2-mm interelectrode distance and a 5-mm interbipole distance was positioned on the lateral RA. Another multipolar catheter was positioned in the coronary sinus, with its proximal bipole located at the ostium, as checked in the 60° left anterior oblique view.18 One deflectable 7F quadripolar catheter with a 2-mm interelectrode distance and a 4-mm tip electrode was used for the mapping of the IVC orifice region and for ablation. A quadripolar catheter was placed in the His bundle region. In 9 patients, an additional "halo" catheter consisting of 10 bipoles (2-mm interelectrode distance, 5-mm interbipole distance; Webster Laboratory) was positioned with one side on the lateral RA and the other on the septal RA. The upper region of the RA was not studied. Care was taken to keep the mapping catheters in the same stable position throughout the study.



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  		Figure 1. Radiograph (60° left anterior oblique) of standard catheter position on the high, mid, and low lateral RA wall (H, M, and L Lat), mid septum in the His bundle region (M Sept), lower septum (L Sept), and PCS, with corresponding sites of atrial electrogram recordings.

Endocardial electrograms were filtered between 30 and 500 Hz and simultaneously recorded with surface leads I, II, III, and aVF on a 12-channel recorder (ES 2000, Gould Instrument, or Midas, PPG Biomedical) at a paper speed of 100 or 250 mm/s.

Atrial electrograms were recorded from three levels of the lateral RA (high, mid, and low) and from various levels on the septum: high, mid in the His bundle region, low at the coronary sinus ostium, and more inferior at the "lower septum" located between the IVC-TA isthmus and the coronary sinus ostium. The local atrial activation time was taken as the first sharp deflection of bipolar electrograms.

Pacing maneuvers were performed with a rectangular stimulus pulse of 1-ms duration at twice diastolic threshold amplitude (Savita VPA Medical). Two sites of pacing were used: the low lateral RA proximal to the IVC-TA isthmus and the PCS distal to it.

Electrophysiological Definitions
Common AFl was defined as a reentrant tachycardia with counterclockwise RA activation in an anterior view. The mean cycle length of common AFl was 253±27 ms, with a high-to-low lateral activation lasting 47±14 ms and a PCS to His bundle region activation occurring in 35±22 ms. The presence of a reentry was demonstrated by the criteria of entrainment described by Waldo and colleagues.2 19 20 The fourth criterion was considered to be present if (1) a change in conduction time and electrogram morphology occurred at a recording site with decreasing pacing cycle lengths and (2) tachycardia returned after pacing.20 21 22 During common AFl, the fourth criterion was observed in all patients during pacing of the low lateral RA, which was orthodromically proximal to the IVC-TA isthmus and to the area of slow conduction, whereas pacing from the PCS induced concealed entrainment.7 21 22

In 8 patients, a reverse AFl with a mean cycle length of 256±21 ms was induced during pacing. This AFl used the same circuit as the common form but in the reverse direction. The low to high lateral RA activation time was 48±10 ms, and the His bundle region to PCS activation time was 43±16 ms. During reverse AFl, the fourth criterion of entrainment was observed during pacing of the PCS, whereas pacing from the low lateral RA induced concealed entrainment.23

With the medial part of the isthmus used as the pacing and recording site, the participation of the IVC-TA isthmus in the circuit was demonstrated by entrainment with exact resetting based on a first postpacing interval in the range of the tachycardia cycle length (no longer than 20 ms).14 24

Assessment of RA Activation Sequence and Conduction Times During Pacing in AFl or Sinus Rhythm
During pacing of the low lateral RA, "anterograde" intra-atrial conduction times were assessed from the stimulation spike to the His bundle region, the lower septum, and the PCS. During pacing of the PCS, "retrograde" conduction times were measured to the high and low lateral RA. Pacing was performed during common or reverse AFl (entrainment) or during sinus rhythm, and conduction times were compared at identical cycle lengths. Unless otherwise specified, pacing refers to pacing in sinus rhythm, whereas entrainment refers to pacing in AFl.

During entrainment, the conduction times were measured on the last captured beat that was entrained but not fused (Fig 2Down).2 20 22 Furthermore, measurements were performed at the longest cycle length that captured the tachycardia to minimize pacing-induced conduction delay and any possible effect of a partially excitable gap.25



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  		Figure 2. Diagrammatic illustration of RA activation during AFl entrainment. Openings of the superior and inferior venae cavae and coronary sinus are shown for reference. Shaded area in posterior (intercaval) RA represents a zone of block. Last paced beat that is entrained but not fused is represented. Thus, the orthodromic wave front is the only one schematized. Top, Entrainment of common AFl is a model of unidirectional counterclockwise RA activation. During pacing from the low lateral RA, conduction times to the lower septum (L Sept), PCS, and His bundle region (M Sept) are representative of activation by a single "anterograde" caudal input. During pacing from the PCS, conduction times to the high and low lateral RA (H, L Lat) are a model of activation via a single "retrograde" cranial input. Bottom, Entrainment of reverse AFl is a model of unidirectional clockwise RA activation. In this circumstance, conduction times are a reference for activation by a single "anterograde" cranial input when pacing the low lateral RA and a single "retrograde" caudal input when pacing the PCS. Dotted lines express uncertainty concerning upper part of circuit that was not studied.

During sinus rhythm, stimulation included incremental pacing up to the rate of AFl entrainment and single extrastimuli delivered after a paced cycle length of 600 ms up to atrial refractoriness. Curves of intra-atrial conduction were constructed by plotting conduction times against the corresponding stimulus coupling interval. A jump in conduction time of more than 40 ms for a decrease in the corresponding coupling interval of 10 ms defined a discontinuity during either incremental pacing or extrastimulation.

Radiofrequency Ablation
Unmodulated 500-kHz RF current was delivered in unipolar fashion from a generator (HAT 200 or OSCOR Medical). RF energy (20 to 30 W for 60 seconds) was applied during common AFl in the IVC-TA isthmus as described by Cosio et al.13 Using a left anterior oblique projection, we took care to deliver RF energy on the same line of the medial part of the IVC-TA isthmus, thus avoiding the more septal and lateral areas. In this location, sharp atrial electrograms occurred in the medial part of the isoelectric portion (plateau) of the surface flutter wave in inferior leads.26 The end point for the procedure was both interruption and inability to reinduce common AFl. The latter was assessed regularly for 30 minutes after the last application to define a successful ablation. The stimulation protocol for AFl induction included burst (10 to 20 beats) and ramp (20 to 40 beats) pacing at progressively shorter cycle lengths until 2:1 capture was noted.

Postablation assessment of RA activation sequences and conduction times was performed 30 minutes after the final RF application. An electrophysiological effect on conduction was not considered an end point for the procedure. Additional "intermediate" assessments were performed during the ablation process, after series of RF applications that terminated AFl (without premature beats) but were not successful in preventing its reinduction.

Follow-up
Patients were monitored for 48 hours after the procedure. They were discharged without antiarrhythmic therapy and seen every 3 months for ECG, Holter monitoring, and physical examination. Additional evaluations were performed if symptoms recurred. A late electrophysiological study was performed in 17 patients a mean of 16±11 weeks after ablation (range, 4 to 39 weeks) and a mean of 17±11 weeks after amiodarone interruption in patients who took this drug. In one patient, induction of a sustained atrial fibrillation prevented determination of intra-atrial conduction. Three patients declined the study.

Statistical Analysis
Continuous variables are expressed as mean±SD. The significance of differences between electrophysiological parameters was assessed by Student's t test for paired data. Fisher's exact test was used for qualitative variables. A value of P<.05 was considered statistically significant.


*    Results
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*Results
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Conduction Times During Transient Entrainment of AFl
During entrainment of common AFl from the low lateral RA, conduction time to the PCS was 123±24 ms, and during entrainment from the PCS, conduction time to the low lateral RA was 190±25 ms. During entrainment of reverse AFl from the low lateral RA, conduction time to the PCS was 186±32 ms, and during entrainment from the PCS, conduction time to the low lateral RA was 131±12 ms (Table 1Down).


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  		Table 1. Conduction Times During AFl Entrainment and Pacing in Sinus Rhythm at the Same Cycle Length

RA Activation Sequence and Conduction Time During Pacing in Sinus Rhythm: Comparison With Data During Entrainment
Conduction during low lateral RA stimulation. In all patients, pacing the low lateral RA produced two caudocranial wave fronts: one clockwise in the lateral wall, the other counterclockwise in the septum activating the lower septum and then the PCS. However, there was a craniocaudal activation of the high septum and His bundle region, with the collision between wave fronts occurring near the PCS (Fig 3Down, left). Activation of the His bundle region occurred only 6±18 ms after the PCS.



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  		Figure 3. Top to bottom, Leads III, aVF, and bipolar electrograms from high, mid, and low lateral RA (H, M, L Lat), high and mid septum 1 and 2 (H, M1, M2 Sept), PCS, and lower septum (L Sept). Drawings schematize RA activation sequence. Left, Pacing from the low lateral RA. Activation of the lateral RA is caudocranial: mid lateral RA is activated first, then high lateral RA. Activation of the septum occurs through dual wave fronts. Low region of septum is activated caudocranially: lower septum is activated first, then PCS. Upper region is activated craniocaudally: high septum is activated first, then mid septum 1 and 2. Right, Pacing from the PCS. Activation of the septum is caudocranial. Activation of the lateral RA is mainly caudocranial, low lateral RA being activated before mid and high lateral RA. Nevertheless, high lateral RA is activated before mid lateral RA, owing to a craniocaudal wave front.

Conduction times to the lower septum and PCS during pacing were identical to those during common AFl entrainment (96±23 and 98±24 ms, respectively, to the lower septum, P=.10; 124±26 and 123±24 ms to the PCS, P=.53). They were shorter to the His bundle region during pacing than during common AFl entrainment (130±25 and 159±30 ms, respectively, P<.001) owing to the earlier capture of the His bundle region by the craniocaudal wave front during pacing (Table 1Up).

No discontinuity was observed in the conduction curves. The conduction times during pacing at a basic cycle length of 600 ms are listed in Table 2Down.


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  		Table 2. Conduction Times During Pacing in Sinus Rhythm at Basic Cycle Lengths

Conduction during PCS stimulation. In all patients, pacing the PCS produced two caudocranial wave fronts: one counterclockwise in the septum, the other clockwise in the lateral RA activating the low lateral and then the mid lateral RA. However, there was a craniocaudal activation of the high lateral RA, with the collision between wave fronts occurring near the mid lateral RA (Fig 3Up, right). The high lateral RA was activated 22±21 ms after the low.

Conduction times to the low lateral RA during pacing were similar to those during reverse AFl entrainment (122±25 and 131±12 ms, respectively, P=.3). Times were shorter to the high lateral RA during pacing than during reverse AFl entrainment (144±26 and 179±15 ms, respectively, P<.001) owing to the craniocaudal wave front during pacing.

In 8 patients, a discontinuity in the conduction times from the PCS to the low lateral RA was observed during incremental stimulation, and in 6 of the 8, this resulted in initiation of common AFl (Fig 4Down). A jump of 69±29 ms in the conduction time to the low lateral RA occurred for a corresponding coupling interval of 204±26 ms with a dramatic change in the lateral RA activation. The high lateral RA became activated 51±12 ms before the low lateral RA, and a change in electrogram morphology of the low lateral RA occurred. This discontinuity suggested retrograde block in the IVC-TA isthmus, with all the lateral RA becoming activated by a craniocaudal wave front. No discontinuity in the conduction curve was observed when extrastimulation was used. Conduction times during pacing at basic cycle lengths are listed in Table 2Up.



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  		Figure 4. Top to bottom, Leads III, aVF, and bipolar electrograms from high, mid 1 and 2, and low lateral RA (H, M1, M2, L Lat). Values are in milliseconds. Proximal coronary sinus is paced at progressively shorter cycle lengths (CL). Drawings schematize RA activation of last paced beat. Top, Ramp pacing until CL 180 fails to induce AFl. For the last paced beat (*), as for the preceding, lateral RA activation occurs through caudocranial and craniocaudal fronts. Similarly, ramp pacing with CL >180 ms leads to the same RA activation sequence and fails to induce AFl (not shown). Bottom, Ramp pacing until CL 170 induces common AFl. On the last paced beat, a jump in conduction time to low lateral RA occurs. The latter is activated after high and mid lateral RA by a single craniocaudal front. Note similarity between the electrogram morphologies on the last paced beat and the ongoing common AFl. The reproducibility of this phenomenon (not shown) illustrates link between unidirectional conduction block and AFl induction.

RA Activation Sequence and Conduction Times After Ablation
In all patients, common AFl was terminated and rendered noninducible after a mean of 15±8 and a median of 14 (range, 3 to 40) RF applications in the IVC-TA isthmus. Dramatic changes in RA activation sequences and conduction times (Table 1Up) were observed after ablation.

Conduction during low lateral RA stimulation. In 17 patients, pacing the low lateral RA after ablation of the isthmus resulted in delayed activation of the lower septum and PCS compared with before ablation; the lower septum and PCS were now activated after the His bundle region (Tables 1Up and 2Up). Conduction times to the His bundle region were not modified, so that all the septum was activated craniocaudally via a single clockwise front (as during reverse AFl) (Fig 5Down, left). This suggested an anterograde conduction block in the IVC-TA isthmus without an alternative conduction pathway in the posterior RA. The postablation conduction times were not significantly different (although slightly shorter) from those observed during entrainment of reverse AFl (182±26 and 186±32 ms, respectively, to the PCS, P=.4) (Fig 6Down). In 2 patients, ablation increased the conduction times to the PCS without change to the lower septum. In one patient (patient 18), ablation failed to induce any significant modification.



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  		Figure 5. Same patient, electrograms, and abbreviations as in Fig 3Up. Left, Pacing from the low lateral RA. After ablation, all the septum is activated craniocaudally via a single clockwise front. Right, Pacing from the PCS. The lateral RA is activated craniocaudally via a single counterclockwise front.



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  		Figure 6. Pacing from the low lateral RA. Top to bottom, Leads III, aVF, and bipolar electrograms from high, mid, and low lateral RA (H, M, L Lat), mid septum 1 and 2 (M1, M2 Sept), lower septum (L Sept), and PCS. Values are in milliseconds. Left, Before ablation. Pacing during sinus rhythm at cycle length (CL) 215. Activation of the septum occurs through caudocranial and craniocaudal fronts. Conduction times are 120 ms to mid septum, 95 ms to lower septum, and 125 ms to PCS. Middle, After ablation. Pacing during sinus rhythm at CL 210. Ablation leads to craniocaudal activation of the septum. Conduction times increase to lower septum and PCS, whereas no change occurs to mid septum. Right, Model of reverse AFl entrainment at CL 210. (*) indicates the last paced beat. Changes in RA activation sequence and conduction times induced by ablation in middle panel fit this model of unidirectional clockwise activation. This illustrates the loss of "anterograde" caudal input.

Conduction during PCS stimulation. In 19 patients, pacing the PCS after ablation of the isthmus resulted in delayed activation of the low lateral RA compared with before ablation; the low lateral RA was now activated after the high lateral RA (Tables 1Up and 2Up). Conduction times to the high lateral RA were not modified, so that all the lateral RA was activated craniocaudally via a single counterclockwise front (as during common AFl) (Fig 5Up, right). This indicated a retrograde conduction block in the IVC-TA isthmus and the absence of an alternative pathway in the posterior RA. Postablation conduction times were not significantly different (although slightly shorter) from those observed during transient entrainment of common AFl (182±27 and 190±25 ms, respectively, to the low lateral RA, P=.14; 41±11 and 46±14 ms for high to low lateral RA interval, P=.16) (Fig 7Down). In 1 patient (patient 18), no modification in conduction occurred.



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  		Figure 7. Same patient, electrograms, and abbreviations as in Fig 6Up. Pacing from the PCS. Left, Before ablation. Pacing during sinus rhythm at CL 215. Activation of high and low lateral RA is nearly simultaneous, indicating a fusion between caudocranial and craniocaudal wave fronts. Middle, After ablation. Pacing in sinus rhythm at CL 210. Ablation leads to craniocaudal activation of lateral RA. Low lateral RA is activated 45 ms after high lateral RA. Right, Model of common AFl entrainment at CL 210. (*) indicates last paced beat. Changes in lateral RA activation sequence induced by ablation in middle panel fit this model of unidirectional counterclockwise activation. This illustrates loss of "retrograde" caudal input.

Heterogeneous conduction changes. In 13 patients, the changes in RA activation were present in both anterograde and retrograde directions at each pacing cycle length without discontinuity in the conduction curve ("apparent complete" block) (Fig 8Down). In 6 patients, the changes occurred at a critical cycle length ("rate-dependent" block) or could be unidirectional, always in anterograde direction. For 2 of these patients (patients 9 and 17), a nonclinical reverse AFl was induced (Fig 9Down).



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  		Figure 8. Conduction curves. Left, Control. Right, After ablation. Cycle length intervals during incremental pacing (S1-S1) are shown on the abscissa and conduction times (S1-A1) on the ordinate. Values are in milliseconds. Top, Conduction times to mid septum (Mid Sept) in the His bundle region, lower septum (Low Sept), and PCS during pacing from the low lateral RA. Conduction time to the mid septum is not affected by ablation, whereas conduction times to lower septum and PCS increase. Bottom, Conduction times to the high and low lateral RA (High, Low Lat) during pacing from the PCS. Ablation leads to longer conduction times to the low lateral RA, whereas no change occurs at the high lateral RA.



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  		Figure 9. Top to bottom, Leads III, aVF, and bipolar electrograms from high, mid, and low lateral RA (H, M, L Lat), distal and proximal mid septum (M Sept), distal and proximal lower septum (Low Sept), and PCS. Values are in milliseconds. Left, Reverse AFl is induced during pacing from the low lateral RA. On the paced beats (*), septum is activated craniocaudally by a single clockwise front as during induced reverse AFl. This indicates "anterograde" conduction block in the IVC-TA isthmus. Right, Pacing from the PCS demonstrates the presence of "retrograde" conduction in the isthmus, the low lateral RA being activated before the high. This asymmetrical effect of ablation elucidates the persistent possibility for reverse AFl induction.

Progressive Conduction Changes During the Ablation Process
In 15 patients, initial RF applications terminated tachycardia without preventing common AFl induction (35 terminations). In 25 terminations, repeated evaluation of conduction times showed various data: (1) no change in anterograde and retrograde conduction times (n=6); (2) a transient conduction block in the IVC-TA isthmus that disappeared within 14 to 30 minutes (n=4); (3) unidirectional changes that became bidirectional with subsequent RF applications (n=12); (4) a progressive prolongation in conduction times (n=12) with a concomitant increase in the induced AFl cycle length (Fig 10Down, left, first termination); (5) a discontinuity occurring at longer cycle lengths than initially, facilitating AFl induction (n=5), either the reverse form during pacing from the low lateral RA or the common form during pacing from the PCS (Fig 10Down, right, second termination); and (6) in one patient, common AFl still inducible, despite a reversal in RA activation sequence suggesting conduction block in the isthmus. The conduction time from the low lateral RA to the PCS was longer during AFl entrainment than during pacing at the same cycle length, suggesting, for this patient, anterograde concealed conduction in the IVC-TA isthmus, ie, a major slowing of the counterclockwise front through the isthmus with longer conduction times than the clockwise wave front outside the isthmus.


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  		Figure 10. (Facing page) Conduction curves during intermediate evaluation. Extrasystolic coupling intervals (S1-S2) are shown on the abscissa and conduction times (S2-A2) on the ordinate. Values are in milliseconds. Left, "Anterograde" conduction times to mid septum (Mid Sept), lower septum (Low Sept), and PCS during pacing from low lateral RA. Right, "Retrograde" conduction times to high and low lateral RA (High Lat, Low Lat) during pacing from PCS. Top to bottom, Control; first, second, and third AFl terminations; and ablation. During control, AFl with a cycle length (CL) of 290 ms is induced by incremental pacing from the PCS for a CL of 220 ms (not shown). First series of RF applications induces a lengthening in anterograde conduction times to lower septum and PCS, whereas no modification occurs in retrograde conduction time to low lateral RA (asymmetrical modification). AFl with a CL of 300 ms was induced for the same critical cycle length of S1-S1. After the second series, a jump of 45 ms in conduction times to low lateral RA occurs for a CL of 260 ms (right, arrow). This illustrates a lengthening of the retrograde "effective refractory period" of the IVC-TA isthmus. For this CL, common AFl (CL, 310) is reproducibly induced by the single extrastimulus S2. The third series leads to conduction block in both directions. Note that modifications in conduction times to low lateral RA are absent for the longest CLs, 400 and 600. No AFl is induced at this time, but 20 minutes later, when conduction curve returns to level of second reduction (transient modifications, not shown). After ablation, modifications are present at every pacing cycle length.

Follow-up
During a mean follow-up period of 8±2 months (range, 5 to 13 months), common AFl recurred in 3 patients 2 weeks to 2 months after ablation, and it did not recur in the 17 others. A reverse AFl occurred in patient 9. There was a trend for a better outcome in patients with an initial "apparent complete" block in the isthmus compared with patients with "rate-dependent" block or unchanged isthmus conduction (one AFl recurrence in 13 patients [8%] and three AFl recurrences or occurrence in 7 patients [43%], respectively, P=.10).

A complete electrophysiological study was done in 16 patients (Fig 11Down). The three patients with AFl recurrence had intact conduction in the IVC-TA isthmus in both the anterograde and retrograde directions. In 1 patient (patient 18), this was already observed immediately after ablation, and in the two others, this was due to a late recovery of conduction. The tachycardia was inducible in 2 of them and not inducible in 1, even during isoproterenol infusion. In patient 9, there was unidirectional retrograde conduction in the isthmus and reverse AFl was inducible, as it was at the time of ablation. The remaining 13 patients had no inducible AFl. An "apparent complete" and bidirectional block was observed in 6 patients and a "rate-dependent" or unidirectional (anterograde) block in the 7 others. Fig 11Down shows the various changes observed between early and follow-up electrophysiological studies. The 4 patients with no electrophysiological data had no AFl recurrence.




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  		Figure 11. Long-term follow-up. Flow chart shows various changes in conduction observed in 16 patients with repeat electrophysiological studies. Eight patients had no modification in the status of conduction in the IVC-TA isthmus, 6 had partial (n=4) or total (n=2) recovery of conduction, and 1 had a late completion of block. *In one patient with unidirectional "anterograde" block, a reverse AFl occurred during the follow-up.


*    Discussion
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 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
By analyzing RA activation sequences and conduction times during pacing in sinus rhythm before and after application of RF energy at the IVC-TA isthmus, the present study specifies the electrophysiological mechanisms for acute successful AFl ablation and provides new insight into the mechanisms of AFl recurrences. Furthermore, the reversal in the RA activation sequence induced by ablation provides new insight into the role of the isthmus in activation patterns of the RA during sinus rhythm.

Mechanism of Successful Ablation of Common AFl
The applications of RF energy at the IVC-TA isthmus produced in all patients an elimination of common AFl, confirming previous studies.13 14 16 In most patients, the mechanism of success is the creation of a persistent bidirectional conduction block in the IVC-TA isthmus. This is demonstrated by dramatic changes in RA activation sequence and conduction times during pacing from sites proximal (low lateral RA) or distal (PCS) to the isthmus. Initially, the septal or lateral end of the isthmus was directly activated within 125 ms from the other end by a caudal input generating a caudocranial RA activation. After ablation, there was an increase of 60 ms in the conduction times in both directions due to a loss of caudal input, each end of the isthmus being activated craniocaudally.

In most patients, an "apparent complete" block was present after ablation, while in the others, the block occurred beyond a critical cycle length, with a possible discrepancy in anterograde and retrograde properties. Only one patient had no significant change. Two patients had a prolongation of conduction time from the low lateral RA to the PCS without any change in the lower septum. This may be due to a longitudinal dissociation in the atrial fibers of the isthmus going to the septum or due to a peculiar activation from the posterior RA.

A tight link between conduction block in the isthmus and AFl elimination is further highlighted by intermediate evaluations and follow-up electrophysiological studies. As long as AFl is inducible during the ablation process, only various degrees of conduction slowing and unidirectional block are observed. Transient AFl noninducibility is due to transient block in the isthmus. Finally, AFl becomes not inducible after completion of isthmus ablation. In some patients, incomplete ablation of the isthmus can be proarrhythmic by increasing the isthmus "refractory period," thus facilitating the induction of tachycardia in either the common or reverse direction.

It is important to note that a total conduction block cannot be differentiated from a major conduction slowing in the isthmus. This concealed conduction in the IVC-TA isthmus was observed in only one patient, as demonstrated by a common AFl still inducible despite a reversal in RA activation sequence. The use of isoproterenol may have been helpful to confirm the presence of conduction block rather than markedly delayed conduction. Because of these limitations, assessment of conduction block cannot be the sole end point for determining successful AFl ablation, and noninducibility of AFl must still be considered as well.

The assessment of conduction times and RA activation sequences is used in patients in sinus rhythm and is particularly useful in patients without inducible AFl or with easily inducible atrial fibrillation. Practically, a craniocaudal activation of the septum (PCS activated after His bundle region) during pacing of the low lateral RA indicates an anterograde block in the isthmus, whereas a craniocaudal activation (low after high RA) of the lateral RA during pacing of the PCS indicates a retrograde block. The nonachievement of these patterns is the proof of persistent conduction in the isthmus, and we think it requires the continuation of the ablation procedure on the basis of the follow-up data.

In one patient discharged despite no change in isthmus conduction, AFl recurred within 2 weeks. Furthermore, the appearance of reverse AFl not previously documented in a patient discharged with persistent "retrograde" isthmus conduction suggests the need to complete isthmus ablation until bidirectional block. The other mechanism for AFl recurrence is a late complete recovery of conduction in the IVC-TA isthmus that we observed only in the patients with AFl recurrence. Regarding the number of recurrences, the present study does not allow determination of the optimal degree of conduction block that must be achieved during the procedure to minimize the risk of late recurrence. It suggests a better outcome for "apparent complete" block, but this point needs further study. Furthermore, the use of amiodarone may have interfered in the mechanism of conduction recurrence. In addition to the electrophysiological end point, more appropriate modes of RF energy application, using larger tips or irrigated electrodes, may also prevent these recurrences by creating larger and deeper atrial lesions with fewer applications.14 27 28 29

Indirect Evidence for Slow Transverse Conduction in the Posterior RA: RA Activation as a Dual-Component Process
The disruption induced by ablation in the RA activation sequence is an impressive finding. Whereas initial RA activation was fusion of different wave fronts, ablation of the isthmus eliminates a caudocranial wave front, with the result that RA activation appears to be dependent on a single craniocaudal wave front. The finding is also confirmed by the comparison at similar cycle lengths of conduction times during pacing with those obtained during AFl entrainment. During entrainment, the conduction times measured on the last paced beat offer a reference point for purely unidirectional conduction times during either counterclockwise (common AFl) or clockwise (reverse AFl) RA activation.2 20 22 30 Nearly identical conduction times in both directions indicate that the impulse travels through the same area at the same velocity in both modes of stimulation. This strongly suggests that in most patients there is no transverse activation going through the posterior intercaval RA wall (or that the latter has a very long conduction time) and that this area of block is present not only during AFl5 6 31 but also during pacing in sinus rhythm. We do not know whether this condition is truly physiological or whether it is peculiar to patients presenting with atrial arrhythmias. In a recent study, the borders of the area of block were the crista terminalis and the eustachian ridge.32

Results of the present study have other implications: (1) The absence of an alternative pathway to the caudal activation front in the low RA strongly supports the rationale for using the IVC-TA isthmus as a target for RF ablation in AFl.13 (2) Because the RA activation behaves like a dual wave front model, the initiation of AFl requires conduction block in one component, as demonstrated by discontinuity in conduction curve in the present study.33 34 35 This was observed mainly during preablation pacing from the PCS that produced a retrograde block in the isthmus region and induced common AFl. Far less frequent was induction of anterograde block with initiation of reverse AFl using lateral RA pacing, which was observed only after energy applications. A different arrangement of longitudinal and transverse myocardial fibers could explain these differences in anterograde and retrograde directions.35 36 37 38 (3) While slow conduction in the IVC-TA isthmus is well accepted during AFl, it is controversial during pacing in sinus rhythm.7 The results of the preablation study, showing similar conduction times to the PCS both during common AFl entrainment and pacing at similar cycle lengths, suggest that there is no additional conduction delay along the isthmus during AFl compared with pacing in sinus rhythm. In a previous report from Olshansky et al,7 the slow conduction was not observed during pacing in sinus rhythm. The differences between the two studies may be due to a different location of the pacing site inducing different wave fronts with different collision sites.39 40 41 42 43 44

Conclusions
The present study provides evidence that the mechanism of successful AFl ablation targeted to the IVC-TA isthmus is local bidirectional conduction block leading to dramatic changes in the RA activation sequence. These changes can be used as new and complementary electrophysiological end points for the procedure.


*    Selected Abbreviations and Acronyms
 
AFl = atrial flutter
IVC = inferior vena cava
PCS = proximal coronary sinus
RA = right atrium
RF = radiofrequency
TA = tricuspid annulus


*    Acknowledgments
 
This work was supported in part by grant P 940906 from the Délégation à la Recherche Clinique de l'Assistance Publique and the Fédération Française de Cardiologie. We wish to thank Dr James Coromilas for his helpful suggestions in the elaboration of this manuscript. We wish to acknowledge Dominique Belly, Dr Janine Bizot, Dr Xavier Copy, Dr Isabelle Denjoy, Agnes Dutrey, and Dr Frank Halimi for their contributions and Annie Gouverneur for assistance with drawings.

Received June 1, 1995; revision received August 21, 1995; accepted September 10, 1995.


*    References
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