Effect of Slow Pathway Ablation on Ventricular Rate During Atrial Fibrillation
Dependence on Electrophysiological Properties of the Fast Pathway
Background Catheter ablation of the posteroseptal right atrium has been proposed for control of ventricular rate in patients with tachycardic atrial fibrillation (AF). However, the exact mechanism of rate control is unclear. Because the ablation site corresponds to the location of the slow pathway in patients with AV nodal reentry tachycardia (AVNRT), we investigated whether selective ablation of this posterior AV nodal input can provide a sufficient reduction in heart rate during AF.
Methods and Results In 30 patients with AVNRT, conduction properties of the AV nodal pathways were determined before and after slow pathway ablation. AF was induced by burst pacing at baseline and after ablation, and the mean ventricular cycle length was determined. After slow pathway ablation, the mean ventricular cycle length during AF increased (449±98 versus 515±129 milliseconds, P<.01). At baseline, the mean ventricular cycle length correlated with the Wenckebach cycle length of both the slow (r=.90) and fast (r=.86) pathways. After ablation, the mean ventricular cycle length was extremely well determined by the Wenckebach cycle length of the fast pathway (r=.94). However, the slope of the regression line was significantly steeper compared with baseline (1.50 versus 0.77, P<.0001), illustrating that the reduction in ventricular rate was not as evident if the fast pathway had a short Wenckebach cycle length.
Conclusions Selective elimination of the slow pathway reduces ventricular rate during AF. However, in patients with a short Wenckebach cycle length of the anterior AV nodal input that causes tachycardic AF, this effect may be insufficient to provide adequate control of ventricular rate.
Under physiological conditions, AV conduction occurs through anatomically distinct AV nodal inputs and the AV node itself.1 Earlier attempts to slow the ventricular rate during tachycardic AF by catheter ablation essentially used titrated delivery of RF energy to impair fast conduction over the anteroseptal AV nodal input.2 However, because the site of ablation was rather close to the area where complete ablation of the AV junction can be accomplished, widespread use of this type of modification of AV conduction has been hampered by a high incidence of inadvertent complete AV block or insufficient rate control in other patients.2
A new catheter technique to modify AV conduction recently was proposed. RF energy was applied to the posteroseptal and midseptal area of the right atrium, ie, the sites typically targeted for ablation of the slow pathway in patients suffering from AVNRT.3 4 5 6 With this posterior approach, AV conduction could be modified successfully in the majority of patients with medically intractable tachycardic AF3 4 5 or atrial flutter.6 The exact mechanism of rate control, however, remains to be elucidated. It is certainly conceivable that ablation of the posterior AV nodal input can result in a slower ventricular rate, provided that it has a higher conduction capacity than the anterior input. However, it is unclear whether the observed decrease in heart rate can be explained solely on this basis.
Therefore, the goals of the present study were to determine the potential effect of selective slow pathway ablation on ventricular rate during AF and to delineate the electrophysiological determinants of ventricular rate during AF both before and after slow pathway ablation in a patient population with proven dual AV nodal pathways and AVNRT.
The study population consisted of 30 patients (age, 50±12 years; 23 women, 7 men) with dual AV node physiology who underwent RF catheter ablation of the slow pathway to eliminate AVNRT. None of them had documented episodes of spontaneous AF. Patients were included only if AVNRT could be induced without pharmacological challenge. Three patients had a history of syncope. Structural heart disease was present in 5 patients: cor pulmonale caused by chronic obstructive pulmonary disease (n=2), left ventricular hypertrophy in the presence of arterial hypertension (n=1), mitral valve prolapse (n=1), and a small atrial septal defect of the secundum type (n=1).
Electrophysiological Study Protocol
The study was approved by an institutional review committee, and written informed consent was obtained from all patients. All antiarrhythmic drugs had been discontinued at least five half-lives before the study. No sedation was used. Under local anesthesia with lidocaine, five multielectrode catheters (Webster Laboratories) were inserted percutaneously into the right subclavian vein and both femoral veins. A dodecapolar orthogonal electrode catheter7 was placed in the coronary sinus. Two quadripolar catheters were placed in the high right atrium and the right ventricular outflow tract. A hexapolar catheter was positioned at the AV junction, and a 4-mm-tip catheter was used for mapping and ablation along the tricuspid annulus. Digitized recordings (Bard Electrophysiology) were stored in a dedicated computer system for further analysis. Measurements were made from the computer screen at a sweep speed of 200 mm/s. The stimulation protocol included determination of the AV conduction curve by atrial extrastimulus testing during sinus rhythm. Measurements of the AH interval were obtained from the distal pair of electrodes of the His catheter. During extrastimulus testing, a discontinuous AV conduction curve was defined in the presence of a sudden prolongation of the A1H1 interval by ≥50 ms in response to a 10-ms decrease in the paced atrial cycle.8 The ERP-fast was defined as the longest AA1 interval that failed to conduct through the fast pathway. The ERP-slow was defined as the longest AA1 interval without propagation to the His-Purkinje system. The functional refractory period of the atrium was determined as the shortest AA1 interval attainable, regardless of the paced coupling interval. Incremental atrial pacing was performed, starting with a rate just below the spontaneous heart rate. Cycle length was decreased by 10 ms after every fourth to fifth beat until tachycardia was initiated or, if possible, until the occurrence of a 2:1 block of AV conduction. Because patients with a dual AV node generally exhibit an atypical Wenckebach periodicity with a sudden increase in AH,9 10 WBCL-fast was estimated to be the longest A1A1 interval at which AV conduction shifted to the slow pathway.11 12 WBCL-slow was reached at the longest A1A1 interval resulting in loss of 1:1 AV conduction. Subsequently, AF was induced by high-rate atrial burst pacing. The first 10 RR intervals during AF were measured to determine both the shortest and the longest ventricular cycle lengths and to calculate the MVCL during AF.
RF Catheter Ablation
After initiation of the tachycardia by atrial pacing and confirmation of the diagnosis of AVNRT, catheter ablation of the slow pathway was performed13 14 15 16 17 with a commercially available RF generator (Radionics). The technique used was a combination of the anatomic and electrogram mapping approaches. The right posteroseptal area along the tricuspid annulus extending from the coronary sinus ostium to the recording site of the His bundle was divided into three regions: posterior, medial, and anterior.14 15 Initially, the most posterior region adjacent to the septal leaflet was mapped for slow pathway potentials similar to those described by Jackman et al.16 During the delivery of RF energy, the catheter usually was moved slowly toward the limbus of the coronary sinus ostium. If unsuccessful or if no satisfactory recordings could be obtained, the mapping and ablation procedure was continued with the catheter placed more anteriorly along the tricuspid annulus. Whenever possible, ablation in this area also was guided by recordings, as done by Jackman et al.16 However, some electrograms obtained in this region resembled more closely those described by Haissaguerre et al,17 which were also believed to represent a marker for the slow pathway. In instances in which no recordings considered to be representative of slow pathway potentials of either type could be obtained, ablation was performed according to the approach using primarily anatomic landmarks.14 15 During each energy application, the tracings were observed for the occurrence of a junctional rhythm with intact retrograde fast pathway conduction. RF pulses were delivered at 30 to 35 W, with a maximum duration of 120 seconds. The end point of the ablation procedure was defined as the inability to induce AVNRT.16 18 This was achieved either by complete elimination of slow pathway conduction, as evaluated by both extrastimulus testing and incremental pacing, or by impairment of the slow pathway to the extent that it could not sustain 1:1 AV conduction.16
Evaluation of AV conduction by atrial extrastimulus testing, incremental atrial pacing, and the induction and analysis of AF was performed in analogy to the baseline study 20 minutes after the last RF application. Finally, the success of the ablation procedure was reevaluated by repetition of the stimulation protocols during an infusion of orciprenaline.
Data are presented as mean±SD unless otherwise specified. Comparisons between groups of data were performed with two-tailed Student’s t test for paired or unpaired data as appropriate. Variables characterizing AV nodal conduction properties were correlated with the parameters obtained during AF. Comparisons of regression lines were performed with standard methods.19 A value of P<.05 was considered statistically significant.
All patients had the common (slow-fast) form of AVNRT. Ablation of the slow pathway, rendering the tachycardia noninducible, was successful in all patients. The ablation site was in the posterior region in 15 patients. In 3 of these patients, energy also was delivered just inside the coronary sinus. In 15 patients, the ablation was successful at the medial third of the triangle of Koch. The number of RF pulses required was 3±2, with a duration of 85±27 seconds per pulse. The slow pathway was completely eliminated in 12 patients, whereas 18 patients still had some evidence of residual slow pathway conduction at extrastimulus testing or incremental atrial pacing (with no demonstrable 1:1 AV conduction). However, single AV nodal reentrant beats were inducible in only 5 of these patients. Control stimulation during the infusion of orciprenaline did not necessitate additional RF application in any patient. During a follow-up period of 5±3 months, no recurrence of tachycardia was observed.
Characteristics of AV Conduction
During the procedure, the sinus cycle length decreased slightly but significantly (750±135 ms before versus 697±108 ms after ablation; P<.01). Table 1⇓ shows the characteristics of AV conduction and refractoriness at baseline and after slow pathway ablation. The AH interval remained unchanged. At baseline, discontinuous conduction curves were demonstrable by extrastimulus testing in 20 patients, whereas in 10 patients the ERP-fast was shorter than the functional refractory period of the atrium, precluding an exact determination. After ablation, the ERP-fast could be measured in 25 patients. Statistical analysis comparing the ERP-fast before and after ablation was performed in those 20 patients in whom data were available both before and after ablation, revealing a significant shortening after slow pathway ablation. At the baseline study, the ERP-slow could generally not be determined, either because of initiation of the tachycardia or because it was less than the functional refractory period of the atrium; thus, it was not used in further analysis. Because all patients displayed at baseline an atypical Wenckebach periodicity during incremental atrial pacing, the WBCL-fast could be estimated in all cases both before and after slow pathway ablation. At baseline, the median of the sudden increase in AH observed during incremental atrial pacing was 75 ms (range, 45 to 190 ms). Table 1⇓ shows that there was a statistically insignificant trend toward a shorter WBCL-fast after the procedure. The WBCL-slow at baseline could be determined in 20 patients in whom incremental pacing could be continued until the occurrence of 2:1 AV block without initiation of the tachycardia. The WBCL-fast and WBCL-slow correlated closely (r=.93). According to the definition of a successful end point of slow pathway ablation, the WBCL-slow after ablation either did not apply (if slow pathway conduction was not present during incremental pacing at all) or was virtually identical to the WBCL-fast (inability to sustain 1:1 AV conduction through the slow pathway).
Ventricular Rate During AF
The durations of the induced episodes of AF were not different before (median, 12 seconds; range, 5 to 720 seconds) and after (median, 12 seconds; range, 5 to 300 seconds) slow pathway ablation. Seventeen episodes of AF lasted for >1 minute (before ablation in 7 patients, after ablation in 4 patients, and both before and after ablation in 3 patients). In these patients, the MVCL calculated over the first 10 RR intervals was correlated with the MVCL determined over 1 minute of AF. Fig 1⇓ shows that there was an excellent correlation with a slope of the regression line close to 1 and an intercept around 0.
Table 2⇓ shows the effects of catheter ablation on ventricular cycle lengths during AF. Catheter ablation of the slow pathway significantly slowed the heart rate during AF, as reflected by a significant prolongation of all the variables evaluated (ie, MVCL and minimal and maximal ventricular cycle lengths). A subgroup analysis with patients stratified according to either complete (n=12) or incomplete (n=18) elimination of slow pathway conduction revealed a significant increase in MVCL during AF for both groups (410±43 ms before versus 496±84 ms after ablation, P<.01; 475±115 ms before versus 528±153 ms after ablation, P<.05). Furthermore, the postablation MVCL was not significantly different between the two groups, indicating that ablation of the slow pathway to the point where 1:1 AV conduction cannot be maintained has the same effect as complete elimination of the slow pathway.
The anatomic location of successful slow pathway ablation had no impact on the degree of slowing of the ventricular rate during AF. In patients ablated in the posterior region (n=15), MVCL increased from 451±84 to 518±128 ms (P<.01). In patients in whom AVNRT was eliminated by ablation within the medial region (n=15), MVCL increased from 446±113 to 512±136 ms (P<.05). Furthermore, there was no correlation between the total amount of energy delivered and the increase in MVCL (r=−.35, P=NS).
Electrophysiological Determinants of Ventricular Rate During AF
At baseline, the ventricular response during AF was determined by the electrophysiological properties of the fast and slow AV nodal pathways. Linear regression analysis revealed a good correlation between ERP-fast (n=20) and both the mean and the minimal ventricular cycle lengths during AF (r=.78 with MVCL; r=.75 with minimal ventricular cycle length). Similarly, WBCL-fast correlated closely with MVCL (r=.86) and minimal ventricular cycle length (r=.80). WBCL-slow (n=20) also was a good predictor of ventricular rate during AF because it correlated well with MVCL (r=.90) and minimal ventricular cycle length (r=.87). Moreover, as Fig 2⇓ shows, the slope of the regression line determining the relation between WBCL-slow and MVCL during AF was significantly steeper compared with the slope of the corresponding regression line using WBCL-fast.
After ablation of the slow pathway, the ventricular rate during AF was extremely well predicted by the electrophysiological properties of the fast pathway. ERP-fast (n=25) correlated with both the mean (r=.86) and minimal (r=.82) ventricular cycle lengths. The strongest determinant of the ventricular response during AF was WBCL-fast (r=.94 with MVCL; r=.93 with minimal ventricular cycle length). Fig 3⇓ illustrates how elimination of the slow pathway affected the relation between the fast pathway and ventricular rate during AF. The slope of the regression line after slow pathway ablation was significantly steeper; in fact, it was even steeper compared with the slope of the regression line characterizing the relation between WBCL-slow and MVCL before ablation (P<.001). Therefore, slow pathway ablation altered the relation between the conduction properties of the fast pathway and the mean heart rate during AF in a way that suggests that the reduction in ventricular rate that can be expected after ablation depends strongly on the characteristics of the fast pathway. It is more pronounced in the presence of a fast pathway with a relatively long WBCL, whereas significant overlap in ventricular rates before and after slow pathway ablation exists if the fast pathway has a high conduction capacity. To further examine the degree of slowing of ventricular rate during AF as a function of the conduction properties of the fast pathway, a subgroup analysis was performed. Group A (n=14) included only patients who had WBCL-fast ≤350 ms both before and after slow pathway ablation; group B (n=8) comprised patients who had WBCL-fast >350 ms both before and after slow pathway ablation. The sinus cycle lengths did not change significantly within these groups (group A, 681±91 ms before versus 657±85 ms after ablation; group B, 892±140 ms before versus 776±106 ms after ablation). Table 3⇓ shows that the MVCL in group A was significantly shorter compared with group B both before and after slow pathway ablation. Although slow pathway ablation resulted in a significant increase in MVCL in both groups, the increase was significantly greater in group B. Moreover, the MVCL in group A after slow pathway ablation (corresponding to a mean heart rate of 138 beats per minute) was significantly shorter than in group B at baseline.
Finally, we evaluated whether the increase in MVCL after slow pathway ablation might be explained simply by the overall increase in the WBCL of the AV node. In 3 of the 20 patients in whom we could obtain WBCL-slow at baseline, the WBCL-fast after ablation was actually shorter than the WBCL-slow before ablation. In the remaining 17 patients, the ΔWBCL of the AV node after versus before ablation (ie, postablation WBCL-fast minus preablation WBCL-slow) was calculated and correlated with ΔMVCL during AF in these patients. The corresponding values are 45±28 ms for ΔWBCL of the AV node and 71±70 ms for ΔMVCL, respectively. As Fig 4⇓ shows, there was some degree of correlation between these two variables. However, the flat slope of the regression line suggests that the changes in MVCL during AF cannot be explained solely by the overall increase in the WBCL of the AV node caused by selective slow pathway ablation.
Effect of Slow Pathway Ablation on Ventricular Rate During AF
The present study shows that before ablation of the slow pathway the ventricular response during AF depends on the conduction properties of both AV nodal pathways, whereas after ablation of the slow pathway, there is a very strong relation between the conduction properties of the fast pathway and the ventricular cycle length. Despite the observed shortening of the ERP-fast and a trend toward a shorter WBCL-fast, which is in agreement with several previous studies,13 16 20 elimination of the slow pathway results in a significant increase in ventricular cycle length during AF. Similarly, a recently published report by Blanck et al,21 who investigated the effects of slow pathway ablation on the ventricular response during AF in a cohort of 18 patients with AVNRT under autonomic blockade, demonstrated a significant prolongation of ventricular cycle lengths during AF after elimination of the slow pathway.
To analyze the changes in AV conduction during AF after slow pathway ablation, three principal factors need to be taken into account: AV nodal refractoriness, concealed AV nodal conduction, and summation of the atrial impulses entering the AV node. The ventricular response in AF is presumably the result of a complex interplay of these variables.22 It was shown previously that the ventricular rate during AF is strongly correlated with the ERP of the AV node21 23 24 and the shortest paced atrial cycle length resulting in 1:1 AV conduction.21 23 It is therefore not surprising that in a patient population with proven dual AV nodal pathways, elimination of the pathway exhibiting the shorter refractory period and the shorter WBCL results in slowing of the ventricular response during AF. However, theoretically this effect might be counteracted if one assumes that during AF the slow pathway contributes significantly to concealed conduction into the AV node. The present data do not prove or disprove the role of concealed conduction. Nevertheless, the observed increase in ventricular cycle length after slow pathway ablation may provide some indirect evidence that a reduction of concealed conduction resulting from elimination of an AV nodal input does not play a principal role. This is in agreement with a study of Brugada et al10 that demonstrated that concealed conduction from one AV nodal pathway to another does not play a role in determining the ventricular response during AF in patients with dual AV node physiology. Although an overall increase in the WBCL of the AV node and an increase in AV nodal refractoriness after elimination of the slow pathway may be factors contributing to the slowing of the ventricular rate, the findings of the present study cannot be explained solely on this basis. This is illustrated, for example, by the rather weak correlation between the ΔWBCL of the AV node and ΔMVCL during AF. In particular, the flat slope of the regression line indicates that the actual increase in MVCL during AF is more pronounced than one might expect from the increase in WBCL of the AV node. Furthermore, the overall increase in AV nodal refractoriness cannot account for the observed impact of slow pathway ablation on the relation between WBCL-fast and the ventricular cycle length during AF, ie, the significant increase in the slope of the regression line. The most likely explanation for these two findings is a reduction in summation of atrial impulses reaching the AV node after elimination of one AV nodal input. Hashida et al25 developed a model of AV nodal conduction that showed that summation of excitatory stimuli needs to occur during AF until a threshold value that leads to conduction of the impulse is reached. Elimination of the posteroseptal approach to the AV node presumably reduces the likelihood of summation, which results in a greater reduction in ventricular rate than can be accounted for by the overall increase in WBCL of the AV node. Furthermore, Zipes et al26 demonstrated that a premature stimulus that is blocked if it approaches the AV node through a single pathway can elicit an impulse propagation if it enters the AV node with the same prematurity through two pathways. Considering that this phenomenon is of significance only if the tissue encountered by the impulse is still refractory, it is conceivable that this concept might explain why the reduction in ventricular rate is more pronounced in the presence of a fast pathway with a longer WBCL. If the remaining anteroseptal AV nodal input blocks antegrade conduction at lower rates, it might depend on summation to conduct to the ventricle more than a fast pathway with an immanent short refractoriness. Elimination of the posteroseptal AV nodal input would therefore lead to an increase in the slope of the regression line between WBCL-fast and ventricular cycle length during AF, as observed in the present study.
Olsson et al27 found a typical bimodal distribution of RR intervals in patients with chronic AF and concluded that this was evidence of dual AV nodal pathways being a ubiquitous phenomenon. In fact, a posterior atrionodal input, corresponding to the location of the slow pathway, has been established as one of the physiological approaches to the AV node.1 28 29 It has been suggested that the functional defect in humans with AVNRT may be an abnormally long refractory period of the fast pathway rather than the presence of an abnormal slow pathway.30 It is conceivable that the posterior AV nodal input also may play a role in determining the ventricular response during AF in patients not exhibiting distinct differences in refractoriness between the anterior and posterior AV nodal pathways. Therefore, attempting to slow the ventricular rate during AF by ablation of this posterior approach to the AV node may seem promising. In fact, several recent publications reported adequate control of heart rate during AF3 4 5 or atrial flutter6 in the majority of patients after RF ablation of the posteroseptal or midseptal right atrium. However, because most of the patients studied by Williamson et al4 and Feld at al5 were in chronic AF, the effect of this ablation on AV nodal conduction and refractoriness could not be evaluated to clarify the exact mechanism of rate control. Based on the present data, the effect of selective elimination of the posterior AV nodal input alone, even if it is known to exhibit a shorter refractory period than the anterior approach to the AV node, may not be sufficient to provide adequate control of ventricular rate in all cases. In fact, it seems particularly insufficient in the presence of tachycardic AF owing to a fast pathway with a short WBCL. Therefore, in patients in whom adequate control of heart rate could be achieved,3 4 5 6 some degree of preexisting impairment of AV conduction caused by the underlying heart disease might have contributed to the success of the procedure. For example, Feld et al5 reported successful modification of the AV conduction in 7 of 10 patients studied. Of note, 2 of these had permanent pacemakers previously implanted for sick sinus syndrome that were programmed to VVI at a low rate.5 However, as suspected by Williamson et al,4 in some patients additional injury to the compact node may have contributed to the reduction in ventricular rate. This would also explain why transient or permanent complete AV block occurred in 6 of 19 patients studied despite application of RF energy in an interrupted, conservative fashion. This incidence of complete AV block usually is not seen in patients undergoing selective ablation of the slow pathway for control of AVNRT. Della Bella et al6 studied a cohort of 14 patients suffering from AF or atrial flutter. Complete AV block occurred in 2 patients.6 In contrast to the previously mentioned studies,3 4 5 several patients were studied during sinus rhythm.6 It is of note that in 4 of 8 patients in whom the AH interval was available after the ablation procedure, AH was ≥100 ms, although it was unchanged from baseline values.6 This prolongation of the AH interval lends further support to the hypothesis that there might have been some preexisting impairment of AV conduction contributing to the success of the procedure. In 6 patients studied during sinus rhythm, the WBCL of the AV node increased from 346±33 to 458±75 ms.6 This postablation value is certainly not considered to be within the normal range. Furthermore, as Della Bella et al pointed out, the AV nodal ΔWBCL is far beyond that reported in patients undergoing selective ablation of the slow pathway for elimination of AVNRT, which is a population known to have a higher conduction capacity through the posteroseptal AV nodal input than through the anteroseptal input. In the study of Della Bella et al,6 no patients in whom it could be tested had evidence of dual AV node physiology. Similarly, in the present study, the overall increase in the WBCL of the AV node was much smaller. Therefore, the reduction in ventricular rate achieved in these patients6 may not have been due solely to selective elimination of a distinct posteroseptal AV nodal input in all cases.
Because the episodes of induced AF were generally short, lasting from a few seconds to <1 minute in most cases, we focused on the analysis of the first 10 RR intervals, which could be obtained in all patients. This may not necessarily be predictive of the events during longer episodes or in chronic AF. However, the findings regarding the relation between AV conduction and refractoriness and the ventricular response during AF may be more valid when only the first few beats are analyzed because hemodynamic alterations secondary to longer AF episodes may be more likely to change the autonomic tone, which influences the conduction properties of the AV node.31 Furthermore, the comparison between the MVCL determined over the first 10 RR intervals with the MVCL during 1 minute of AF demonstrated a rather close relation.
Because the study was not performed under autonomic blockade, as was that of Blanck et al,21 it is possible that the observed small decline in the resting sinus cycle length, which is in agreement with previously published data,13 might indicate a slight increase in sympathetic tone during the procedure. However, it was shown recently that the decrease in refractoriness of the fast pathway is not related to changes of the autonomic tone.20 Nevertheless, we cannot entirely rule out that a small increase in sympathetic tone might have led to slight underestimation of the increase in MVCL during AF in some patients. However, we do not believe that this could have significantly altered the findings of this study. In particular, in the subgroup of patients in whom the procedure seemed least effective, ie, those patients who had a WBCL-fast ≤350 ms before and after ablation, the sinus cycle length remained virtually unchanged.
Selective ablation of the slow pathway in patients with AVNRT significantly reduces ventricular rate during AF. However, this effect is more pronounced if the remaining fast pathway has a relatively long WBCL, leading to lower heart rates to begin with. Selective elimination of this posterior AV nodal input alone may not be sufficient to achieve adequate control of the ventricular rate in patients with tachycardic AF who have a short WBCL of the anteroseptal AV nodal input.
Selected Abbreviations and Acronyms
|AVNRT||=||AV nodal reentry tachycardia|
|ERP-fast||=||effective refractory period of the fast pathway|
|ERP-slow||=||effective refractory period of the slow pathway|
|MVCL||=||mean ventricular cycle length|
|WBCL-fast||=||Wenckebach cycle length of the fast pathway|
|WBCL-slow||=||Wenckebach cycle length of the slow pathway|
- Received January 23, 1995.
- Revision received June 27, 1995.
- Accepted August 29, 1995.
- Copyright © 1996 by American Heart Association
Fleck RP, Chen PS, Boyce K, Ross R, Dittrich HC, Feld GK. Radiofrequency modification of atrioventricular conduction by selective ablation of the low posterior septal right atrium in a patient with atrial fibrillation and a rapid ventricular response. Pacing Clin Electrophysiol. 1993;16:377-381.
Feld GK, Fleck RP, Fujimura O, Prothro DL, Bahnson TD, Ibarra M. Control of rapid ventricular response by radiofrequency catheter modification of the atrioventricular node in patients with medically refractory atrial fibrillation. Circulation. 1994;90:2299-2307.
Jackman WM, Friday KJ, Yeung-Lai-Wah JA, Fitzgerald DM, Beck B, Bowman AJ, Stelzer P, Harrison L, Lazzara R. New catheter technique for recording left free-wall accessory atrioventricular pathway activation: identification of pathway fiber orientation. Circulation. 1988;78:598-610.
Josephson ME. Supraventricular tachycardias. In: Josephson ME, ed. Clinical Cardiac Electrophysiology: Techniques and Interpretations. 2nd ed. Philadelphia, Pa: Lea & Febiger; 1993:191.
Rosen KM, Denes P, Wu D, Dhingra RC. Electrophysiological diagnosis and manifestation of dual A-V nodal pathways. In: Wellens HJJ, Lie KI, Janse MJ, eds. The Conduction System of the Heart. Leiden, Netherlands: HE Stenfert Kroese BV; 1976:453-466.
Sung RJ, Huycke EC, Keung EC, Tseng CD, Lai WT. Atrioventricular node reentry: evidence of reentry and functional properties of fast and slow pathways. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. Philadelphia, Pa: WB Saunders; 1990:514.
Kay GN, Epstein AE, Dailey SM, Plumb VJ. Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia: evidence for involvement of perinodal myocardium within the reentrant circuit. Circulation. 1992;85:1675-1688.
Jazayeri MR, Hempe SL, Sra JS, Dhala AA, Blanck Z, Deshpande SS, Avitall B, Krum DP, Gilbert CJ, Akhtar M. Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia. Circulation. 1992;85:1318-1328.
Kalbfleisch SJ, Strickberger SA, Williamson B, Vorperian VR, Man C, Hummel JD, Langberg JJ, Morady F. Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia. J Am Coll Cardiol. 1994;23:716-723.
Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, Moulton KP, Twidale N, Hazlitt HA, Prior MI, Oren J, Overholt ED, Lazzara R. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med. 1992;327:313-318.
Haissaguerre M, Gaita F, Fischer B, Commenges D, Montserrat P, d’Ivernois C, Lemetayer P, Warin JF. Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy. Circulation. 1992;85:2162-2175.
Sokal RR, Rohlf FJ. Comparison of regression lines. In: Sokal RR, Rohlf FJ, eds. Biometry. 2nd ed. New York, NY: Freeman & Co; 1981:499-509.
Natale A, Klein G, Yee R, Thakur R. Shortening of fast pathway refractoriness after slow pathway ablation: effects of autonomic blockade. Circulation. 1994;89:1103-1108.
Blanck Z, Dhala AA, Sra J, Deshpande SS, Anderson AJ, Akhtar M, Jazayeri MR. Characterization of atrioventricular nodal behavior and ventricular response during atrial fibrillation before and after a selective slow-pathway ablation. Circulation. 1995;91:1086-1094.
Zipes DP, Mendez C, Moe GK. Evidence for summation and voltage dependency in rabbit atrioventricular nodal fibers. Circ Res. 1973;32:170-177.
Olsson SB, Cai N, Dohnal M, Talwar KK. Noninvasive support for and characterization of multiple intranodal pathways in patients with mitral valve disease and atrial fibrillation. Eur Heart J. 1986;7:320-333.
McGuire MA, de Bakker JMT, Vermeulen JT, Opthof T, Becker AE, Janse MJ. Origin and significance of double potentials near the atrioventricular node: correlation of extracellular potentials, intracellular potentials, and histology. Circulation. 1994;89:2351-2360.