Characterization of Atrioventricular Nodal Behavior and Ventricular Response During Atrial Fibrillation Before and After a Selective Slow-Pathway Ablation
Background The presence of atrioventricular nodal dual-pathway physiology in patients with atrioventricular nodal reentrant tachycardia (AVNRT) provides an opportunity to characterize the effect of a selective slow-pathway ablation on the ventricular rate during atrial fibrillation (AF). This may have important clinical implications for the nonpharmacological management of AF with a rapid ventricular rate.
Methods and Results Selective radiofrequency catheter ablation of the atrioventricular nodal slow pathway was performed with a stepwise approach in patients with documented sustained AVNRT. The AV nodal conduction properties and refractoriness and the ventricular rate during induced AF were assessed at baseline and under autonomic blockade before and after a selective slow-pathway ablation in 18 patients (mean age, 34±8 years). Sustained AVNRT was induced with a mean cycle length of 339±58 ms. A slow-pathway ablation was successfully achieved with 5±4 applications of radiofrequency energy. The shortest cycle length of 1:1 AV conduction and the AV nodal effective refractory period significantly prolonged after ablation (367±53 versus 403±55 ms, P<.0001, and 258±55 versus 292±74 ms, P<.05, respectively). Selective slow-pathway ablation significantly prolonged the mean (526±93 versus 612±107 ms, P<.0001), the shortest (378±59 versus 423±73 ms, P<.0001), and the longest (826±150 versus 969±226 ms, P<.01) cycle lengths of the ventricular response to AF. Significant slowing of the ventricular rate during AF occurred in 13 patients (72%), including all eight patients in whom AV nodal dual-pathway physiology was abolished. Five patients did not have a significant change in the ventricular rate during AF; a persistent dual AV nodal pathway physiology was demonstrable in four of these patients. Loss of dual-pathway physiology after ablation had a sensitivity of 77%, specificity of 80%, and positive predictive value of 91% for slowing the ventricular rate during AF.
Conclusions In patients undergoing a slow-pathway ablation for control of AVNRT, selective slow-pathway ablation may cause a significant decrease in the ventricular rate during AF. These effects are primarily due to the prolongation of AV nodal conduction properties and refractory period of the residual AV nodal transmission system. These findings may have important therapeutic implications for the nonpharmacological treatment of AF, particularly in patients with underlying dual AV nodal physiology.
Atrial fibrillation (AF) is the most common form of sustained tachyarrhythmia encountered in clinical practice. It has been estimated that 0.4% of the general population has AF.1 2 Ventricular rate control of AF is one of the major therapeutic objectives when sinus rhythm cannot be restored. Although AV nodal blocking agents are usually considered the first option, pharmacological therapy is ineffective in achieving optimal rate control in many patients with rapid ventricular response to AF. The application of radiofrequency energy to the AV junction has been shown to be a safe and effective modality for creating complete AV block when nonpharmacological management is considered for this arrhythmia.3 However, the most significant drawback of this therapeutic approach is a life-long pacemaker dependency.
A selective ablation of the AV nodal slow pathway in patients with AV nodal reentrant tachycardia (AVNRT) can effectively eliminate the tachycardia.4 5 6 7 8 Theoretically, a similar approach, by modifying the electrophysiological characteristics of the AV node, might lessen the ventricular rate of AF and yet, by maintaining the integrity of AV conduction, obviate the need for a permanent pacemaker. Based on this assumption, a recent case report9 in which radiofrequency pulses were applied to the posteroseptal region of the right atrium showed a significant decrease in the ventricular response to AF. Nonetheless, the impact of a selective slow-pathway ablation on the ventricular response to AF must be tested in patients whose electrophysiological properties of the AV node can be evaluated reliably before and after such an intervention. To this end, we systematically assessed the AV nodal conduction and refractoriness under autonomic blockade in patients undergoing AV nodal modification for control of AVNRT. Furthermore, the ventricular response to AF was analyzed before and after AV nodal modification. The main objective of this study was to characterize the impact of a selective slow-pathway ablation on the ventricular rate of induced AF in such a patient population.
Patients undergoing radiofrequency catheter ablation of the AV nodal slow pathway for documented or suspected AVNRT were invited to participate in this investigational protocol if they met the following criteria: (1) age between 18 and 60 years, (2) inducible sustained AVNRT during electrophysiological studies, (3) no structural heart disease, (4) no contraindications for autonomic blockade, and (5) no prior attempt at fast- or slow-pathway catheter ablation. This protocol was approved by the Institutional Review Board of Sinai Samaritan Medical Center.
Each patient underwent a complete electrophysiological evaluation performed in a postabsorptive state. All antiarrhythmic medications had been discontinued for at least five half-lives before the study. Except for one patient who was sedated with intravenous midazolam, all patients were anesthetized with intravenous propofol. Electrode catheters were introduced percutaneously into femoral and internal jugular veins and positioned under fluoroscopic guidance in the right ventricular apex, high right atrium, and His bundle region. A 6F decapolar catheter was placed in the coronary sinus with the most proximal pair of recordings positioned at the ostium. Surface ECG leads (I, II, and V1), intracardiac electrograms, and time lines were simultaneously displayed on a multichannel oscilloscope (EVR-180, PPG Biomedical) and printed on a thermal recorder. Data were recorded on optical disks (Biomedical Instrumentation Inc) for subsequent reproduction. Electrical stimulation was performed with a programmable digital stimulator (Bloom Associates). Atrial and ventricular extrastimulation and incremental pacing were used to assess the antegrade and retrograde AV nodal conduction and refractoriness. We considered AV nodal dual-pathway physiology to be present when an H1-H2 interval prolongation of ≥50 ms (with or without AVNRT initiation) in response to a 10-ms decrement in A1-A2 interval was demonstrable. The induction of AVNRT was attempted repeatedly to determine the most reliable and reproducible method of tachycardia induction. When tachycardia could not be initiated or sustained, isoproterenol was infused intravenously and titrated to increase the sinus cycle length by a minimum of 20%, and the stimulation protocol was repeated. Intravenous heparin was administered as an initial dose of 2000 U followed by intermittent boluses of 1000 U/h.
Radiofrequency current was delivered between the distal electrode of the ablating catheter and an external adhesive patch electrode (Scotchplate 1149C, 3M Co) placed on the chest wall. The ablation catheter was a 7F deflectable quadripolar catheter with a 4-mm bulbous-tip electrode (Mansfield Scientific). The radiofrequency generator was a LIZ-88 (American Cardiac Ablation Corp), which generates radiofrequency energy at 540 kHz. This unit integrates the power source and energy output monitoring circuitry into a single package and gives direct readouts of the voltage and load impedance.
A slow-pathway ablation was performed by the stepwise approach, as previously described.4 Briefly, the septal annulus of the tricuspid valve, extending from the most posterior region adjacent to the coronary sinus ostium (posterior) to the His bundle recording site (anterior), was divided into posterior (P), medial (M), and anterior (A) zones. Each zone was further divided into two sites. The ablating catheter was initially positioned in the most posterior aspect of the tricuspid septal site (P1), adjacent to the coronary sinus ostium. This site was considered optimal for ablation if the local electrogram showed an A/V ratio of ≈0.5 or less. If the ablation attempt at this site was unsuccessful, the ablation catheter was moved anteriorly while an optimal A/V ratio was maintained to reach sites P2, M1, M2, and A1 if necessary. After the delivery of each pulse of radiofrequency energy, pacing protocols were repeated to assess the inducibility of AVNRT. Radiofrequency pulses were set at 60 to 80 V and delivered for 40 to 60 seconds. Whenever changes in the catheter tip position or impedance rise were noted, the energy delivery was immediately terminated. The end point of the ablative procedure was to render AVNRT noninducible. The presence of a single AV nodal reentrant echo beat or persistent AV nodal dual-pathway physiology was not considered a procedural failure and did not necessitate further radiofrequency applications.4
After completion of the initial electrophysiological evaluation, incremental atrial and ventricular pacing, premature atrial stimulation, and induction of AF were performed under autonomic blockade. The same pacing protocol and AF induction were also repeated under autonomic blockade 30 minutes after successful ablation.
Atrial fibrillation was induced by rapid high right atrial or coronary sinus pacing. The shortest, mean, and longest ventricular cycle lengths were analyzed during the first 60 seconds of induced AF. In addition, the frequency distribution of ventricular cycle lengths during AF was tabulated by 20-ms intervals in each patient at baseline and during autonomic blockade before and after ablation. If spontaneous restoration of sinus rhythm did not occur within 5 to 10 minutes, DC electrical cardioversion was performed. Antiarrhythmic agents were not administered.
Autonomic Nervous System Blockade
Fluctuations in autonomic tone during the procedure may potentially impact on the ventricular rate during AF and may mask the electrophysiological changes resulting from the ablation and preclude a meaningful analysis. Therefore, autonomic blockade was used to eliminate such an interference.
Autonomic blockade was achieved with a combination of esmolol and atropine in all patients before and after a slow-pathway ablation. Because administration of β-adrenergic agents with long half-lives may prevent the inducibility of sustained AVNRT, intravenous esmolol, a nonselective β-blocker with a short half-life (9.5 minutes),10 was used. A loading dose of 500 μg · kg−1 · min−1 was administered for 3 minutes and followed by a maintenance dose of 400 μg · kg−1 · min−1.11 The same dosage was used before and after ablation.
Parasympathetic nervous system blockade was achieved with intravenous atropine, which was administered at a dose of 0.04 mg/kg12 before ablation. A second dose of 0.01 to 0.02 mg/kg was given after ablation. Atropine was administered over 30 seconds approximately 5 minutes after the esmolol maintenance dose was infused. When isoproterenol was used, a period of at least 20 minutes was allowed for its washout before the study protocol was continued.
The atrial refractory period studies were performed at several drive cycle lengths, and only data obtained at identical cycle lengths before and after ablation were compared in each patient. Except for transient blurred vision and dry mouth resulting from the administration of atropine, no side effects or complications occurred from this investigational protocol or the ablative procedures.
All patients underwent a repeat electrophysiological study with and without isoproterenol 30 minutes after slow-pathway ablation and 24 to 48 hours later before hospital discharge.
Data are expressed as mean value ±SD. Paired and unpaired Student’s t tests were used to compare continuous variables. Two different statistical methods were used to compare changes in the ventricular cycle length during AF in all patients as a group and in each patient individually. The changes in the mean, shortest, and longest ventricular cycle lengths were analyzed with a paired two-tailed Student’s t test. The two-sided Kolmogorov-Smirnov nonparametric statistical analysis was used to assess the change in the frequency distribution curve of ventricular cycle lengths tabulated at 20-ms intervals. This method was used because the frequency distribution curve of the ventricular cycle lengths during AF did not follow a normal distribution in all patients. We considered a change in the ventricular cycle length during AF significant in each patient only if both statistical methods showed a P<.05.
The presence of a correlation between electrophysiological parameters and the change in ventricular cycle length during AF was examined by linear regression analysis.
Between March 1992 and August 1993, 20 patients agreed to participate in this study. Two patients were excluded from the subsequent analysis because of the inducibility of AVNRT 24 hours after ablation in 1 patient and inability to induce sustained AF after ablation in the other. The remaining 18 patients form the basis of this study. There were 11 women and 7 men, with a mean age of 34±8 years. None of the patients had a history of heart disease or any structural heart disease demonstrable by two-dimensional echocardiography. Tachycardias induced in the laboratory were sustained AVNRT of the common (16 patients) or uncommon (1 patient) variety. The remaining patient had both common and uncommon (slow-slow) forms of AVNRT. Isoproterenol was required in 8 patients for inducing or maintaining AVNRT. The mean cycle length of the AVNRT was 339±58 ms.
The induction of AVNRT was successfully abolished by a selective slow-pathway ablation in all patients. The patients received a mean of 5±4 (range, 1 to 17; Table 1⇓) radiofrequency applications, the last of which (ie, successful pulse) had a mean voltage, power, and duration of 70±8 V, 49±10 W, and 38±12 seconds, respectively. Successful ablation sites were P1 and P2 in 12 patients and M1 and M2 in 6 patients.4
Electrophysiological Parameters Before and After Ablation
Electrophysiological parameters, including the atrial-His (AH) interval, the shortest cycle length of 1:1 antegrade and retrograde conduction, the AV nodal functional and effective refractory periods, and the presence of AV nodal dual-pathway physiology, were determined in each patient (Table 2⇓).
After autonomic blockade and before ablation, the shortest cycle length of 1:1 AV conduction lengthened from 348±72 to 367±53 ms (P<.05), and antegrade AV nodal dual-pathway physiology was present in 14 patients (versus 13 at baseline). Four patients (patients 2, 9, 10, and 16) demonstrated two or more “jumps” in their discontinuous AV nodal conduction curves during atrial extrastimulation, suggesting the presence of more than one slow pathway. AVNRT remained inducible with a mean cycle length of 390±51 ms in 10 patients.
The electrophysiological parameters measured under autonomic blockade before and after a slow-pathway ablation are listed in Tables 2⇑ and 3⇓. After ablation, there was a significant lengthening in the shortest cycle length of 1:1 AV conduction (403±55 versus 367±53, P<.0001) and in the AV nodal effective refractory period (292±74 versus 258±55, P<.05). There was no significant difference in preablation versus postablation values of the AH interval, the functional refractory period of the AV node, or the shortest cycle length maintaining 1:1 retrograde ventriculoatrial conduction (Table 3⇓).
Atrioventricular nodal dual-pathway physiology was abolished after a slow-pathway ablation in 8 of 14 patients (57%) (Table 2⇑). In these 14 patients, the fast-pathway effective refractory period remained unchanged in 8 patients, prlonged (≥20 ms) in 4, and shortened (≥20 ms) in 2 patients after a slow-pathway ablation (Table 2⇑).
Of the remaining 4 patients with a continuous AV nodal conduction curve under autonomic blockade before ablation, 1 developed the dual-pathway physiology after ablation. It should be pointed out that in 3 of these patients (patients 12, 13, and 17), the AV nodal dual-pathway physiology was demonstrable at baseline (ie, before autonomic blockade).
Data on isoproterenol administered intravenously at 1 to 5 μg/min (mean, 2±1 μg/min) were compared in 8 patients before and after ablation. There was no significant difference in the shortest cycle length of 1:1 AV conduction (291±36 versus 289±44 ms, P=NS) or the AV nodal effective refractory period (209±11 versus 214±12 ms, P=NS) after ablation in any of these 8 patients.
Ventricular Response During Atrial Fibrillation Before and After Slow-Pathway Ablation
The mean, shortest, and longest ventricular (RR) cycle lengths during AF at baseline and after autonomic blockade (before the ablation) were compared. There was a significant lengthening in the mean (526±93 versus 476±78 ms, P=.004) and the shortest (378±59 versus 344±57 ms, P=.004) RR cycle lengths after autonomic blockade. The mean and shortest RR cycle lengths during AF had a better correlation with the shortest cycle length of 1:1 AV conduction (r=.88 and r=.91, with P<.0001 for both) than with the AV nodal effective refractory period (r=.73 and r=.68, with corresponding values of P=.0005 and P=.001, respectively) or functional refractory period (r=.60 and r=.66, with P<.007 and P<.002, respectively). No correlation was found between the AH interval and the RR cycle lengths during AF.
After ablation, there was a statistically significant lengthening of the mean (612±107 versus 526±93 ms, P<.0001), the shortest (423±73 versus 378±59 ms, P<.0001), and the longest (969±226 versus 826±150 ms, P<.004) ventricular cycle lengths during AF (Table 3⇑). In addition, the frequency distribution curve of the ventricular cycle lengths during AF shifted to the right after the ablation (P<.0001, Fig 1⇓).
When the ventricular response during AF before and after ablation was compared in each patient, 13 patients (72%) had significant RR cycle length prolongation after ablation (Table 2⇑, patients 1 through 13). This included all 8 patients in whom AV nodal dual-pathway physiology was abolished after the ablation (Fig 2⇓), 3 patients with persistent AV nodal dual-pathway physiology, and 2 patients in whom this finding was not demonstrable before or after the ablation.
In the remaining 5 patients (Table 2⇑, patients 14 through 18), only one of the statistical methods showed a significant slowing of the ventricular rate during AF (P<.05), and they were considered to have only a trend toward significant slowing of the ventricular rate during AF. Interestingly, 4 (80%) of these 5 patients had AV nodal dual-pathway physiology after ablation (Fig 3⇓), including the patient whose AV nodal dual-pathway physiology was unmasked after a slow-pathway ablation. This was in marked contrast to the 23% incidence of persistent AV nodal dual-pathway physiology among 13 patients with significant RR prolongation (P<.02). In these two subgroups of patients (patients 1 through 13 versus 14 through 18), comparison of the magnitude of change in the shortest cycle length of 1:1 AV conduction and the mean RR cycle length during AF before and after the ablation showed a significant statistical difference (P<.05).
Linear regression analysis demonstrated that the change in the mean RR cycle length during AF before and after ablation had a modest correlation with the change in the AV nodal effective refractory period (r=.67, P=.002). The correlation between the change in mean RR cycle length and the change in the shortest cycle length of 1:1 AV conduction did not reach statistical significance.
The loss of AV nodal dual-pathway physiology after ablation had a sensitivity of 77% and a specificity of 80%, with positive and negative predictive values of 91% and 57%, respectively, for slowing of the ventricular response during AF.
This study demonstrated that a selective ablation of the AV nodal slow pathway in the majority of patients with AVNRT led to a significant slowing of the ventricular rate during induced AF. Among several electrophysiological parameters, the elimination of AV nodal dual-pathway physiology and prolongation of AV nodal effective refractory period were associated with a marked reduction in the ventricular response to AF. These data may have important therapeutic implications for patients suffering from AF with rapid ventricular rate, and they might also provide further insight into the physiological behavior of the AV node in such a prevalent arrhythmia.
Electrophysiological Properties of the AV Node After Modification
A selective slow-pathway ablation not only eliminates AVNRT but also can modify the electrophysiological properties of the residual AV nodal conduction system.4 5 6 7 8 Previous studies have shown that the shortest cycle length of 1:1 AV conduction and the effective refractory period of the AV node are both prolonged after a slow-pathway ablation.13 Interestingly, however, in patients with a demonstrable dual-pathway physiology at baseline, prolongation of these two parameters is of a greater magnitude when the AV nodal dual-pathway physiology is completely abolished.13 The present study, by reaffirming these findings under autonomic blockade, indicates that changes in the AV nodal conduction characteristics and refractory periods observed after a slow-pathway ablation are independent of autonomic influences.
Shortening of the fast-pathway effective refractory period has been previously reported after a selective slow-pathway ablation in patients with AVNRT.5 A recent study14 demonstrated such a phenomenon occurring in 70% of patients with AVNRT undergoing a slow-pathway ablation. The shortening of the fast-pathway effective refractory period in the latter study was demonstrable with and without autonomic blockade. It has been shown in a computer model of dual-pathway physiology that the antegrade activation of the slow pathway may electrotonically delay fast-pathway depolarization.15 Based on this observation, therefore, shortening of the fast-pathway effective refractory period after slow-pathway ablation has been attributed to the elimination of such an electrotonic influence that the slow pathway might exert on the fast pathway.15 This hypothetical interaction may be accountable for shortening of the fast-pathway effective refractory period occurring in the clinical setting. However, in our series of 14 patients with demonstrable dual-pathway physiology at baseline, shortening of the fast-pathway refractoriness after ablation was encountered in only 2 patients (28%) despite a complete loss of the AV nodal dual-pathway physiology in 8 patients (57%). Nonetheless, it should be pointed out that although the initiation and maintenance of AVNRT require the existence of two anatomically and functionally distinct pathways known as fast and slow pathways, the AV nodal structure is probably more complex in patients with AVNRT than can be portrayed as a structure with a single fast and slow pathway. In fact, multiple AV nodal pathways may be demonstrable in as many as one third of patients.13 Therefore, in such a complex structure with possible reciprocal electrotonic interactions between different pathways, it might be difficult at times to assess the effect of a slow-pathway ablation on its faster counterpart and vice versa.
Ventricular Response During Atrial Fibrillation
The ventricular response during AF is typically characterized by irregular RR intervals. Although the exact reason for these irregularities is not well understood, two possible mechanisms have been offered. First, the concept of “concealed conduction” introduced by Langendorf16 17 and supported by several animal studies18 19 20 21 suggested that the degree of concealment in the AV node during rapid and irregular transmission of the fibrillatory atrial impulses was the main determinant of the ventricular rate during AF. On the basis of this hypothesis, therefore, the AV node behaves primarily as an electrical conduit that, depending on its refractoriness and excitability, randomly allows a complete transmission of the atrial impulses. In addition to the phenomenon of concealed conduction occurring in the AV node, the rate and irregularity of the atrial impulses22 and summation or inhibition of the wave fronts approaching the AV node from different inputs20 23 may contribute to the ventricular rate of AF. The second hypothesis suggests that the AV node functions solely as a pacemaker and that its rate or timing of depolarization is electrotonically altered by the atrial impulses.24 25 26
Although the results of the present study cannot prove or disprove the validity of either of the two theories, prolongation of the RR cycles during AF after a selective slow-pathway ablation strongly suggests that the AV nodal conduction plays some role in the ventricular response to AF. Therefore, even if the concept of the electrotonic modulation is valid, our data support the notion that the atrial impulses must propagate through some portion of the AV node before they can modulate the AV nodal pacemaker.21
AV Nodal Modification for Control of Ventricular Response in Atrial Fibrillation
Previous studies have shown that the mean ventricular response during AF correlates with the AV nodal conduction and effective refractory period.27 28 Thus, it seems conceivable to anticipate an increase in the RR cycle length during AF after the AV nodal properties are modified. In this series of patients with AV nodal reentry, we were able to demonstrate a significant reduction of the ventricular rate during AF by ablating the critical slow pathway. These results suggest that before the AV node was modified, the ventricular response of AF was determined predominantly by the electrophysiological properties of the slow pathway. Interestingly, a marked reduction of the ventricular rate during AF was demonstrated in all 8 patients (100%) in whom the AV nodal dual-pathway physiology was completely eliminated, as opposed to only 3 (43%) of 7 patients who had demonstrable dual-pathway physiology after ablation. Therefore, a residual slow pathway after ablation, although unable to maintain sustained AVNRT, was still capable of contributing to a relatively rapid ventricular response during AF in most patients exhibiting dual-pathway physiology. Conversely, among 4 patients without any demonstrable dual-pathway physiology before the ablation, a slow-pathway ablation resulted in a significant decrease of the ventricular rate during AF in 2 patients without any marked prolongation of the AV nodal conduction properties or refractoriness after ablation. One might speculate that although the AV nodal dual-pathway physiology could not be demonstrated in this subset of patients, the slow pathway was probably the predominant pathway determining the ventricular rate during AF before the AV nodal modification.
Although we did not specifically address the effect of a fast-pathway ablation on the ventricular rate during AF, the possibility of achieving rate control seems unlikely, for two reasons. First, several studies have shown that a selective fast-pathway ablation does not alter the shortest cycle length of 1:1 AV conduction or the AV nodal effective refractory period.4 13 29 Second, the result of the present study has clearly shown that complete abolition of slow-pathway conduction leads to a significant slowing of the ventricular response during AF despite intact fast-pathway conduction, suggesting that, at least in this series, the slow pathway was the primary determinant of the ventricular rate in AF before ablation. In fact, one might argue that conduction of the atrial impulses across the fast pathway, by blocking retrogradely in the slow pathway, may ordinarily contribute to its concealment and, therefore, ablation of the fast pathway may potentially enhance the ventricular rate during AF. Obviously, further studies are needed to address this issue.
Radiofrequency energy has been used to modify the AV nodal properties for control of the ventricular rate during atrial tachyarrhythmias. Both the anterior/superior aspect of the interatrial septum and the posterior/inferior aspect of the septal annulus of the tricuspid valve have been targeted for achieving such a rate control.30 31 32 The anterior/superior approach was shown to be initially effective in only 35% of patients with atrial tachyarrhythmias, including AF.30 However, in a long-term follow-up in patients with an initial successful AV nodal modification, a rate control persisted in only one third of patients, and the remaining patients either developed a complete AV block (54%) or had a recurrence of their original symptoms.
Preliminary reports of the posterior/inferior approach have demonstrated a significant slowing of the ventricular response to AF in 70% of patients with chronic AF who were refractory to medical therapy.31 32 The remaining 30% of these patients either did not respond to this intervention or developed a complete AV block during application of radiofrequency energy. It should be pointed out that none of the studies mentioned above have assessed the presence of a dual-pathway transmission system in the study patients before the transcatheter ablation. Therefore, it remains unclear which patient populations will respond to these approaches and whether or not the rate control achieved by a posterior/inferior approach is solely due to a selective AV nodal slow-pathway ablation.
The results of this study clearly demonstrate that in patients with AV nodal reentry, a selective slow-pathway ablation can reduce the ventricular rate during induced AF, particularly when AV nodal dual-pathway physiology is completely abolished or the AV nodal effective refractory period is lengthened after ablation. These data lend support to the hypothesis that a rate control in patients with AF undergoing a posterior/inferior approach is due to a selective slow-pathway ablation.31 32 Furthermore, on the basis of these observations, it seems reasonable to anticipate that patients with an underlying dual-pathway physiology might be more suitable candidates for such a therapeutic modality than those without this phenomenon.
One may argue that the reported success rate of AV nodal modification for rate control in patients with AF31 32 seems exceedingly higher than the incidence of dual-pathway physiology in patients without AVNRT. Although this argument cannot be dismissed entirely, several possibilities may be considered. First, even though the exact incidence of dual-pathway physiology in the general population is unknown, it is not uncommon to find this phenomenon fortuitously in individuals without any documented cardiac arrhythmia who undergo electrophysiological studies.33 Second, patients with a rapid ventricular rate during AF who do not respond adequately to the AV nodal blocking agents should be considered a subgroup of patients with unusual AV nodal electrophysiological properties. Therefore, the incidence of dual-pathway physiology in this patient population who were the subject of previous reports31 32 may be much higher than that in the general population. Third, although patients without dual-pathway physiology may also demonstrate a reduction of the ventricular rate during AF after a slow-pathway ablation, the magnitude of rate reduction may be far more significant in those with dual-pathway physiology.
Knowledge of the presence of dual-pathway physiology may be important in some patients undergoing a posterior/inferior ablation for rate control of AF. A complete abolition of this phenomenon may be used as a therapeutic end point, particularly when AF is paroxysmal and not present at the time of the ablative procedure. Once the AV nodal modification is verified by the loss of dual-pathway physiology, its impact on the ventricular rate of the induced AF can be determined.
Several points in the observations made in this study deserve further comment. First, none of the study patients had documented clinical AF. Therefore, it remains unclear whether the results of the present study can be extended to patients with clinical AF. Second, the impact of a slow-pathway ablation on the ventricular response to AF was assessed during autonomic blockade. Thus, in the absence of autonomic blockade, and especially when the adrenergic tone is enhanced, it remains unknown whether or not the AV nodal modification will lead to any significant reduction of the RR cycle length. Third, we did not specifically attempt to eliminate the AV nodal slow pathway completely, as evidenced by the presence of residual dual-pathway physiology after ablation in 7 patients (39%). It is possible, therefore, that further attempts at a complete abolition of the AV nodal slow pathways would have resulted in a rate control of AF in a higher number of patients. Finally, the vast majority of our patients had a common variety of AVNRT. The impact of a slow-pathway ablation on the ventricular response to AF in patients with an underlying uncommon AVNRT remains to be explored.
Summary and Conclusions
Successful slow-pathway ablation in patients with AVNRT significantly decreased the ventricular rate during induced AF as a result of modifying AV nodal conduction and refractoriness. Notably, ablation of the AV nodal dual-pathway physiology predicted a significant reduction in the ventricular rate during AF. These findings support the potential role of selective slow-pathway ablation as a therapeutic modality for rate control in patients with clinical AF.
We would like to thank Chris Martin, Inga Hawkins, David Krum, MS, Brian Miller, and Brian Schurrer for their help in the preparation of this manuscript.
Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993.
- Received July 5, 1994.
- Revision received September 19, 1994.
- Accepted October 5, 1994.
- Copyright © 1995 by American Heart Association
Onundarson PT, Thorgeirsson G, Jonmudsson E, Sigfusson N, Hardarson TH. Chronic atrial fibrillation: epidemiologic features and 14 year follow-up: a case control study. Eur Heart J. 1987;8:521-527.
Jazayeri M, 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.
Kay NG, Epstein AE, Dailey SM, Plumb VJ. Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia. Circulation. 1992;85:1675-1688.
Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, Moulton KP, Twidale N, Hazlitt A, 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, Caita 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.
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. PACE Pacing Clin Electrophysiol. 1993;16:377-381.
Jose AD, Taylor RR. Autonomic blockade by propranolol and atropine to study intrinsic myocardial function in man. J Clin Invest. 1969;4:2019-2031.
Jazayeri RM, Sra JS, Deshpande SS, Blanck Z, Dhala AA, Krum PD, Avitall B, Akhtar M. Electrophysiological spectrum of atrioventricular nodal behavior in patients with atrioventricular nodal reentrant tachycardia undergoing selective fast or slow pathway ablation. J Cardiovasc Electrophysiol. 1993;4:99-111.
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.
Lesh MD, Gibb WJ, Epstein L. Electrotonic interaction between dual AV nodal pathways: evidence from RF ablation and a computer model. Circulation. 1992;86(suppl I):I-30. Abstract.
Langendorf R, Pick A, Katz LN. Ventricular response in atrial fibrillation: role of concealed conduction in the AV node. Circulation. 1965;32:69-75.
Moe GK, Abildskov JA. Observations on the ventricular dysrhythmia associated with atrial fibrillation in the dog heart. Circ Res. 1964;14:447-460.
Moore EN. Observations on concealed conduction in atrial fibrillation. Circ Res. 1967;21:201-209.
Mazgalev T, Dreifus LS, Bianchi J, Michelson EL. Atrioventricular nodal conduction during atrial fibrillation in rabbit heart. Am J Physiol. 1982;243:H754-H760.
Vereckei A, Vera Z, Pride HP, Zipes DP. Atrioventricular nodal conduction rather than automaticity determines the ventricular rate during atrial fibrillation and atrial flutter. J Cardiovasc Electrophysiol. 1992;3:534-543.
Chorro FJ, Kirchhof CJHJ, Brugada J, Allessie MA. Ventricular response during irregular atrial pacing and atrial fibrillation. Am J Physiol. 1990;259:H1015-H1021.
Zipes DP, Mendez C, Moe GK. Evidence for summation and voltage dependency in rabbit atrioventricular nodal fibers. Circ Res. 1973;32:170-177.
Rowland E, Curry P, Fox K, Krikler D. Relation between atrioventricular pathway and ventricular response during atrial fibrillation and flutter. Br Heart J. 1981;45:83-87.
Lee MA, Morady F, Kadish A, Schamp DJ, Chin MC, Scheinman MM, Griffin JC, Lesh MD, Pederson D, Goldberger J, Calkins H, de Buitlier M, Kou WH, Rosenheck S, Sousa J, Langberg JJ. Catheter modification of the atrioventricular junction with radiofrequency energy for control of atrioventricular nodal reentry tachycardia. Circulation. 1991;83:827-835.
Feld GK, Fujimura O, Fleck PR, Bahnson TD, Prothro DL, Boyce K, Henjum SC. Radiofrequency catheter modification of the AV node for control of rapid ventricular response to atrial fibrillation. Circulation. 1993;88(suppl I):I-584. Abstract.
Denes P, Wu D, Dhingra R, Amat-y-Leon F, Wyndham C, Rosen KM. Dual atrioventricular nodal pathways: a common electrophysiologic response. Br Heart J. 1975;37:1069-1076.