Mechanism of Ventricular Rate Control After Radiofrequency Modification of Atrioventricular Conduction in Patients With Atrial Fibrillation
Background Modification of atrioventricular (AV) conduction during atrial fibrillation (AF) may be achieved by radiofrequency ablation in the posteroseptal region of the tricuspid annulus. We tested the hypothesis that elimination of the posterior atrionodal input rather than direct damage to the compact AV node accounts for the decrease in ventricular rate after AV nodal modification.
Methods and Results Twenty-four patients with the typical form of AV nodal reentrant tachycardia (AVNRT) underwent selective radiofrequency ablation of the slow AV nodal pathway in the posteroseptal tricuspid annulus. AF was induced before ablation (phase 1), 30 minutes after ablation (phase 2), and during follow-up 24 hours after ablation (phase 3), both with and without concurrent infusion of isoproterenol (4 μg/min). Successful elimination of AVNRT was achieved in all patients. During phase 3, 11 patients (46%) had residual dual pathway physiology. AV nodal Wenckebach cycle length (AVNW-CL) increased progressively during each phase of the protocol (356±72 versus 371±78 ms versus 432±104 ms, P<.0001), as did the effective refractory period of the AV node (279±60 versus 304±67 ms versus 372±56 ms, P<.0001). Minimal, mean, and maximal RR intervals during AF progressively increased immediately after ablation and 24 hours later (485±88 versus 533±116 ms versus 637±142 ms for mean RR, P<.0001). The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF were independent of residual dual pathway physiology after ablation. Similar observations were observed during isoproterenol infusion.
Conclusions Modification of AV nodal conduction during AF by radiofrequency ablation in the posteroseptal tricuspid annulus is independent of the presence or absence of a residual slow AV nodal pathway. On the basis of these observations, the mechanism of AV nodal modification is consistent with elimination of the posterior atrionodal input.
Recent studies have demonstrated that RF ablation in the posteroseptal region of the tricuspid annulus may slow the ventricular response during AF,1 2 3 4 5 but the mechanism by which this occurs has not been established. It has been suggested that rate modulation is due to partial damage to the compact AV node.4 Others have proposed that posteroseptal ablation results in selective elimination of the slow AV nodal pathway and that the remaining fast pathway limits AV nodal conduction due to its longer refractory period.2 3 6 Implicit in the latter hypothesis is that dual AV nodal pathway physiology is a required substrate for successful AV nodal modification.
Experimental studies in rabbits and dogs have demonstrated that AV nodal conduction is determined by discrete anteroseptal and posteroseptal atrionodal inputs that are associated with differential functional properties, which are determined by fiber geometry and intercellular connections.7 8 9 10 11 Evidence suggests that the anteroseptal input is characterized by a rapid conduction velocity, a relatively long refractory period, and a low safety factor of conduction. In contrast, the posteroseptal input, comprising the inferoposterior extension of the crista terminalis, is thought to have a slow conduction velocity, a short refractory period, and a high safety factor of conduction.7 8 9 10 11 Consistent with this concept, we have previously demonstrated that RF ablation of posteroseptal accessory pathways (in the region of slow pathway ablation) results in modification of AV nodal conduction in patients without dual pathway physiology, such as prolongation of the AVNW-CL, similar to that observed after slow pathway ablation.12 To test the hypothesis that elimination of the posterior atrionodal input accounts for the decrease in ventricular rate after AV nodal modification for AF, we examined the ventricular response during AF in patients undergoing posteroseptal ablation for AVNRT and compared AV nodal conduction in patients with and without residual dual pathway physiology after ablation.
The study population consisted of 24 consecutive patients (17 women; age, 50±14 years; range, 24 to 68 years) undergoing slow pathway ablation for AVNRT. Duration of symptoms before ablation was 9±11 years (range, 4 weeks to 30 years). Clinical characteristics of the study population are summarized in Table 1⇓.
All patients were studied in the sedated state after informed written consent was obtained. Antiarrhythmic medications and AV nodal blocking agents were discontinued for at least five half-lives before the study in 20 patients. Three patients ( Nos. 13, 21, and 22) were receiving β-blockers (1 for angina and 2 for frequent episodes of supraventricular tachycardia) and 1 patient (No. 24) was on diltiazem (for frequent supraventricular tachycardia) at the time of initial and follow-up studies.
Patients were locally anesthetized with 0.25% bupivacaine and sedated with intravenous midazolam before electrophysiological study. Three quadripolar catheters and one decapolar catheter were introduced percutaneously and positioned in the high right atrium, the right ventricular apex, across the tricuspid valve to record the His bundle potential, and within the coronary sinus under fluoroscopic guidance. Bipolar intracardiac recordings were filtered at 30 to 500 Hz and displayed with three surface ECG leads on a digital monitor. Data were stored on optical disk (Prucka Engineering). Peripheral arterial pressure was continuously monitored (Dinamap, Cirikon). Stimulation was performed with a programmable stimulator and an isolated constant-current source (Bloom Associates). Stimuli were delivered as rectangular pulses of 2-ms duration at four times diastolic threshold. The stimulation protocol included rapid atrial and ventricular pacing and the introduction of single and double extrastimuli from atrial and ventricular sites at multiple paced cycle lengths.
Patients with AVNRT were identified by standard electrophysiological criteria.13 14 15 16 Dual pathway physiology was defined as a discontinuous AV nodal conduction curve during atrial extrastimulus testing (≥50 ms increase in A2-H2 interval for a 10-ms decrement in the A1-A2 interval) or the presence of AV nodal echo beats either during the baseline autonomic state or during isoproterenol infusion. The ERP of the fast AV nodal pathway was defined on the basis of a discontinuous AV conduction curve or, in the case of a continuous conduction curve, by the longest A1-A2 interval resulting in an AV nodal echo beat. The ERP of the AV node was defined as the longest A1-A2 interval failing to result in an H1-H2 response. In patients with discontinuous nodal conduction curves or AV nodal echo beats, the AV nodal ERP therefore reflects the ERP of the slow pathway; in patients with continuous conduction curves and an absence of nodal echo beats, the AV nodal ERP reflects the ERP of the fast pathway. All patients had the typical form of AVNRT (anterograde slow-retrograde fast pathway). No patient demonstrated evidence for an accessory pathway. All patients underwent ablation through the posterior approach.13 15
Current generated by a 500-kHz RF energy source (EPT-1000, EP Technologies) was delivered from the distal 4-mm tip of a steerable mapping catheter (EPT Steerocath-T, EP Technologies) to a left subscapular chest wall patch (7.25×1.5 in). Energy was applied at 10 to 50 W for ≤60 seconds to obtain a distal tip temperature of 60°C (or until an abrupt rise in catheter impedance). Sites for RF ablation were identified anatomically in the inferoposterior aspect of the tricuspid valve annulus anterior to the coronary sinus os (Fig 1⇓), and electrograms at these sites demonstrated an atrio-ventricular ratio of 0.1 to 0.5.15 The location of the ablation site was divided into six equal regions (1 through 6) between the His bundle and the coronary sinus os. RF energy was applied during AVNRT, sinus rhythm, or atrial pacing while monitoring for junctional tachycardia, VA block, or anterograde AV block. If the initial RF application was unsuccessful (usually site 5 or 6), the catheter was moved anteriorly and the procedure repeated. For all applications of RF energy, the tip of the ablation catheter was ≥1.5 cm from the His bundle electrode and in no case was a His bundle electrogram recorded at the ablation catheter. In no patient did transient or delayed AV block occur.
As confirmed by others,13 17 18 19 successful ablation was defined as elimination of dual pathway physiology or the induction of a maximum of a single AV nodal echo beat. All patients underwent testing with single and double atrial extrastimuli 30 minutes after ablation and during a follow-up study (with and without an infusion of isoproterenol). The anterograde AVNW-CL, the ERP of the fast AV nodal pathway, and the ERP of the AV node were assessed at basic cycle lengths of 600, 500, and 400 ms, as dictated by the sinus cycle length and anterograde AVNW-CL. These values were measured before the first application of RF energy (phase 1), 30 minutes after successful ablation (phase 2), and at follow-up 1 day later (phase 3), each time during the baseline autonomic state and during an infusion of isoproterenol (2 to 4 μg/min). The target infusion rate for isoproterenol was 4 μg/min; however, two patients (Nos. 8 and 23) were unable to tolerate this dose and measurements were made at 2 μg/min during each phase of evaluation.
After the procedure, patients were continuously monitored for 24 hours. A follow-up electrophysiological study was performed within 24 hours in 22 patients and at 3 days in 2 patients. During the follow-up study, the long-term success of the ablative procedure was confirmed, and the conduction and refractory properties of the AV node as outlined above were reevaluated, both at baseline and during isoproterenol infusion. In no patient was AVNRT reinduced during follow-up.
Induction of AF
AF was induced during three stages of the protocol: (1) during the initial study before ablation (phase 1), (2) 30 minutes after ablation (phase 2), and (3) during the follow-up study (phase 3). During each phase, AF was induced twice, during the baseline autonomic state and during isoproterenol infusion, resulting in 6 inductions for each patient. AF was induced with rapid atrial pacing from the high right atrium or coronary sinus (burst cycle lengths of 50 to 250 ms). The duration of AF varied from 5 seconds to >20 minutes. Of 144 induced episodes of AF, 126 (87%) were >10 seconds in duration. If AF did not spontaneously terminate within 10 minutes, DC cardioversion was performed (which was required for 8 episodes in 6 patients). During each episode of AF, minimal, maximal, and mean RR intervals were measured during a 10-second period (or less if dictated by the duration of the episode). In addition, sinus cycle length was recorded before each induction of AF.
Data are expressed as mean±SD. Within-group comparisons of variables were performed by ANOVA (Crunch 4.0, Crunch Software Corp) with post hoc analysis by a step-down, multiple-stage F test. Differences in normally distributed variables were assessed by the two-tailed t test for independent groups. Differences in proportions were analyzed with the Fisher exact test. Comparisons of ERP data included only those patients with comparable data during each phase of the protocol (eg, comparable drive cycles and an ERP of the AV node that exceeded the functional refractory period of the atrium) and were analyzed with the Friedman test for nonparametric variables or the Wilcoxon signed rank test. A value of P<.05 was required to reject the null hypothesis.
All 24 patients had the typical form of AVNRT. The mean cycle length during tachycardia was 346±72 ms. In each case, the successful ablation site was in the posteroinferior septum (sites 3 through 6; mean site, 4.4) The number of applications of RF energy ranged from 1 to 6 (mean, 2.7±1.9). Characteristics of AVNRT and RF ablation in each patient are presented in Table 1⇑.
Immediately after RF ablation (phase 2), 18 patients (75%) had residual dual pathway physiology, as defined by either a discontinuous AV nodal conduction curve or the presence of single AV nodal echo beats. During the follow-up study (phase 3), 11 patients (46%) had evidence for dual pathway physiology. This delayed effect of RF energy has been attributed to lesion expansion caused by a progressive inflammatory response or microcirculatory injury.20
Effects of Slow Pathway Ablation on AV Nodal Conduction
Electrophysiological parameters at baseline and after ablation are summarized in Table 2⇓. The sinus cycle length decreased immediately after RF and then increased during follow-up (733±141 versus 685±96 ms versus 810±106 ms, P<.0001) (Fig 2⇓). The AH interval did not change after slow pathway ablation (84±16 ms [phase 1], 85±16 ms [phase 2], 80±17 ms [phase 3], P=NS). As demonstrated in Fig 2⇓, the AVNW-CL prolonged immediately after ablation and prolonged further at the time of follow-up study (356±72 versus 371±78 ms versus 432±104 ms, P<.0001). At follow-up, the AVNW-CL had prolonged in 20 of 24 patients (83%) compared with baseline.
AV nodal ERP could be compared in 15 patients during each phase of the protocol. In the remaining patients, comparison of nodal ERP was limited by the functional refractory period of the atrium. As demonstrated in Fig 2⇑, the ERP of the AV node increased immediately after ablation and increased further at the time of follow-up (279±60 versus 304±67 ms versus 372±56 ms, P<.0001). During follow-up, AV nodal ERP increased in 14 of 17 patients (82%) compared with baseline.
A different pattern was observed for the ERP of the fast pathway (Fig 2⇑). Fast pathway ERP could be compared in 15 patients during the 3 phases of the protocol. Fast pathway ERP decreased immediately after ablation but then increased during follow-up (360±76 versus 312±63 ms versus 373±65 ms, P<.02). The difference between the fast pathway ERP at follow-up (phase 3) and at baseline (phase 1) was not statistically significant.
AV nodal conduction curves before and after ablation were compared in 7 patients with dual pathway physiology during the follow-up study (phase 3). The maximal AH interval during extrastimulus testing, reflecting conduction in the slow AV nodal pathway, decreased from phase 1 to phase 3 (349±81 versus 287±48 ms, P=.10). The maximal AH interval decreased in 5 patients and increased in the remaining 2.
Ventricular Response During AF
Immediately after ablation (phase 2) there was lengthening of the minimal, mean, and maximal RR intervals during induced AF (Fig 4⇓). A more profound effect was observed 1 day after ablation (phase 3), with further lengthening of minimal, mean, and maximal RR intervals during AF (Figs 3 and 4⇓⇓). For example, the mean RR interval during control AF was 485±88 ms, which increased to 533±116 ms during phase 2 and further increased to 637±142 ms during phase 3 (P<.0001, Fig 4⇓). During follow-up (phase 3), the mean RR had increased in 23 of 24 patients (96%), the minimal RR increased in 21 of 24 patients (88%), and the maximal RR increased in 21 of 24 patients (88%).
At follow-up, the mean RR interval during AF increased by 33% (P<.0001), compared with an increase in AVNW-CL of 23% (P<.0001) and an increase in AV nodal ERP of 39% (P<.0001). In contrast, the fast pathway ERP demonstrated no significant change. The ventricular response in AF correlated with AVNW-CL, AV nodal ERP, and fast pathway ERP (Table 3⇓). The strongest correlations were observed immediately after ablation.
Effect of Isoproterenol on AV Nodal Conduction and Ventricular Response in AF
Isoproterenol abolished the difference in sinus cycle length at each phase of the protocol, as shown in Fig 2⇑ (482±76 versus 466±72 ms versus 487±49 ms, P=NS). During isoproterenol infusion, AVNW-CL did not significantly change during any phase after ablation (269±83 versus 248±44 ms versus 261±43 ms, n=8, P=NS). In most subjects, isoproterenol infusion resulted in shortening of the AV nodal ERP and the fast pathway ERP to less than the functional refractory period of the atrium.
During isoproterenol infusion, slowing of the ventricular response during AF was observed after posteroseptal ablation. Although the mean RR during AF increased, as did minimal RR and maximal RR (Figs 3 and 4⇑⇑), the magnitude of reduction in ventricular response during isoproterenol was significantly less than that observed during the baseline autonomic state (19% versus 31% for mean RR, 15% versus 32% for minimal RR, 19% versus 34% for maximal RR, P<.02 for each comparison).
Effect of Residual Dual Pathway Physiology on AV Nodal Conduction
There was no difference with respect to age, sex, number of RF applications, successful RF site, or baseline electrophysiological characteristics between those who demonstrated dual pathway physiology [DP(+)] and those who did not [DP(−)] during phase 3 of the protocol (Table 4⇓). After ablation, there were no significant differences in AVNW-CL or AV nodal ERP between DP(−) and DP(+) subjects. AVNW-CL increased from 365±85 to 431±134 ms in DP(−) patients and from 345±53 to 434±59 ms in DP(+) patients (P=NS between groups). An increase in AVNW-CL was demonstrated in 9 of 13 DP(−) and in 11 of 11 DP(+) patients (P=NS). Similarly, AV nodal ERP increased in both groups, from 298±67 to 364±63 ms for DP(−) patients (n=9, P<.04) and from 239±39 to 361±56 ms for DP(+) patients (n=8, P<.02).
The ventricular response during AF slowed in patients independent of the presence or absence of dual AV nodal pathways (Table 4⇑). The mean RR interval during induced AF prolonged in DP(−) patients from 488±113 ms (phase 1) to 657±180 ms (phase 3) and in DP(+) patients from 481±51 ms to 612±80 ms (P=NS between groups). The mean RR interval during AF increased in 12 of 13 DP(−) patients and in 11 of 11 DP(+) patients (P=NS). Similar increases were observed for minimal RR and maximal RR intervals, and no significant differences were noted between groups. In addition, no differences between DP(−) and DP(+) patients were observed in ventricular response during AF in the presence of isoproterenol infusion.
The findings of this study demonstrate that the ventricular response during AF slows by ≈30% in patients with dual AV nodal physiology in whom AV nodal reentry is successfully ablated in the posteroseptal region of the tricuspid annulus. Significantly, elimination of dual pathway physiology was not required to modulate AV nodal conduction. No substantive differences in AVNW-CL, AV nodal ERP, or ventricular rate during AF were observed between patients with or without dual pathway physiology after ablation. These observations suggest that the decrease in ventricular response during AF cannot be explained solely on the basis of complete elimination of the slow AV nodal pathway and its associated short refractory period but rather are consistent with the presence of dual atrionodal inputs (anterior and posterior) that, while distinct from the compact AV node, play a role in determining its conduction properties. In this model the posterior atrionodal input has a higher safety factor of conduction than the anterior atrionodal input and therefore in part facilitates rapid AV conduction. The success of AV nodal modification in limiting the ventricular response during AF therefore may be due to elimination of the posterior atrionodal input with atrial conduction preferentially proceeding over the anterior atrionodal input with its lower safety factor of conduction.
The feasibility of modifying AV nodal conduction by ablation in the posterior septum has been demonstrated previously.1 2 3 4 5 In ≈75% of patients, ventricular rates decrease by 25% to 35%,2 3 a magnitude similar to that observed in the present study. In these studies, the patients had incessant AF, precluding evaluation of dual pathway physiology. Therefore, the mechanism of AV nodal modification could not be addressed. In contrast, several recent studies have examined the effect of selective slow pathway ablation on ventricular rate of induced AF in patients with dual AV nodal physiology and AVNRT. These studies confirm that selective slow pathway ablation results in modification of ventricular conduction in AF, an increase in the AVNW-CL, and an increase in AV nodal ERP.6 21 22 23 In addition, a recent study reported the feasibility of modifying ventricular response by posteroseptal ablation in patients with paroxysmal AF who did not demonstrate dual pathway physiology.24
Mechanism of Modulation of AV Conduction in AF
Several potential mechanisms may account for modulation of the ventricular response during AF after RF catheter ablation. It has been proposed that this phenomenon may be secondary to partial damage to the compact AV node.4 However, this explanation appears to be an unlikely mechanism in our study for the following reasons: (1) the AH interval and the fast pathway ERP did not change significantly after ablation, indicating that fast pathway conduction and the compact AV node were still intact, and (2) the ablation catheter was remote from the compact AV node. It is possible that in a previously reported study,4 damage to the compact AV node did in fact contribute to rate control, as suggested by the large magnitude of change in ventricular response (43% decrease in maximal rate), the relatively large number of ablative attempts (11 applications of RF energy), and the increased risk of heart block (21%).
An alternative explanation to the compact AV nodal damage hypothesis is that AV nodal modification is achieved by selective ablation of the posterior atrionodal input. Perturbing the posterior input may alter AV nodal conduction in one of several ways. For example, partial injury to the slow pathway or posterior atrionodal input (if it is assumed they are one and the same) may be sufficient to slow the ventricular response in AF, prolong the AVNW-CL, prevent reinduction of AVNRT, and produce a discontinuous AV nodal conduction curve and nodal echo beats (Fig 5B⇓). In this circumstance, and in contradistinction to our findings, one would have expected an increase in the maximal AH interval during slow pathway conduction, reflecting injury to this structure. This latter finding is not consistent with a model of partial injury to the slow pathway.
Another possibility to account for successful AV nodal modification with persistence of dual pathway physiology is the existence of subsidiary inputs to the AV node (Fig 5C⇑).25 A left atrial input has been demonstrated in canine preparations,26 as has the participation of the left atrium in rare forms of AV nodal reentry tachycardia.27 It is conceivable that these atrionodal inputs provide the substrate for dual AV nodal physiology after slow pathway ablation in posterior septum but rarely allow perpetuation of tachycardia because of presumably less favorable conduction and refractory properties than those associated with the posterior atrionodal input. Alternatively, slow pathway conduction after posteroseptal ablation may involve the same structure present before ablation (Fig 5D⇑). In this case, a dual pathway substrate would still exist in the AV node or perinodal tissue, allowing for a discontinuous AV nodal conduction curve and nodal echo beats. However, elimination of the posterior atrionodal input results in a change in the direction of wave front propagation into the AV nodal slow pathway, and therefore AV node reentry fails to sustain. This may explain the seemingly contradictory but consistent observation that successful ablation of AVNRT may be associated with the induction of single AV nodal echo beats.18 19 In this model, the posteroseptal input is contiguous with but different from the slow AV nodal pathway. In this case, it is likely that the ablation site was posterior to the input's nexus with the slow pathway in those patients with residual slow pathway conduction [DP(+)] after ablation; in DP(−) patients, ablation may have been at the site of merger of these two structures.
The models presented in Fig 5⇑ emphasize the role of the posteroseptal atrionodal input in determining AV conduction. The results of the present study, demonstrating slowing of AV nodal conduction during AF, suggest that the posterior atrionodal input facilitates AV nodal conduction at rapid rates. We have previously shown that AV nodal function can be modified in patients without dual AV nodal physiology after ablation of accessory pathways in the right posteroseptal region of the tricuspid annulus, an observation consistent with elimination of a posteroseptal atrionodal input.12
Anatomic and Cellular Basis for Dual Atrionodal Inputs
Evidence has accumulated in animal models to support the presence of distinct atrionodal inputs with different electrophysiological properties. In canine and rabbit preparations, multichannel mapping of impulse propagation into the AV node has demonstrated distinct wave fronts that approach the AV node anterior from the intra-atrial septum and posterior from the crista terminalis.7 8 9 10 11 28 These routes of conduction are determined not by specialized internodal tracts but by anatomic obstacles in the right atrium (the fossa ovale, crista terminalis, and tricuspid annulus).
The success of AV nodal conduction is dependent on the direction of wave front propagation into the AV node.7 9 In a rabbit model of the AV junction, Janse7 demonstrated 2:1 AV block during stimulation of the anterior septum and 1:1 AV conduction during stimulation of the crista terminalis at a comparable cycle length. These findings are consistent with anterior and posterior atrionodal inputs with different safety factors of conduction. A lower safety factor for conduction has been demonstrated in anisotropic tissue with recurrent discontinuities in intercellular connections (caused by a discontinuous array of gap junctions and collageneous septae).29 30 In discontinuous anisotropic tissue, wave fronts that propagate parallel to the long axis of the fiber encounter a lower axial resistivity and are associated with a faster conduction velocity but a lower dV/dt because of the greater coupled effective membrane capacitance or electrical load. Since the amount of depolarizing current is reduced under these circumstances, conduction first fails in the longitudinal direction as opposed to transverse direction, resulting in a lower safety factor of conduction. Conversely, wave fronts that propagate in a direction of higher axial resistivity (transverse to the direction of the long axis of the fiber) have a slower conduction velocity (as is seen in the posterior atrionodal input along the tricuspid annulus) but have a higher dV/dt (due to a lower electrical load resulting from intercellular discontinuities) and therefore a higher safety factor for conduction.30 Slow anterograde conduction in the posteroseptal region of the tricuspid annulus, possibly caused by anisotropic tissue properties, has been demonstrated in dog and rabbit models2 and during intraoperative mapping in humans.31
In this study we did not use autonomic blockade to control for autonomic tone. However, slowing of ventricular response immediately after ablation occurs despite a decrease in sinus cycle length, indicating that AV conduction is modified independent of changes in autonomic tone. Furthermore, although there was no difference in sinus cycle length at each phase of the protocol during isoproterenol infusion, modest changes were still observed in ventricular response to AF. Another potential limitation is the short duration of AF observed in some patients. It is conceivable that the ventricular response during induced AF does not reflect nodal conduction in chronic atrial fibrillation. We believe, however that these measurements are clinically relevant. As reported by others,23 an excellent correlation has been observed between the mean ventricular cycle length over the first 10 RR intervals of induced AF and the mean cycle length computed over 1 minute. In 87% of our patients, the duration of AF was >10 seconds.
The implication of our study is that modification of AV nodal conduction in AF by the present technique is limited by the functional properties of the anterior AV nodal input. It may not be possible to slow ventricular response beyond a certain limit (≈30%) while leaving the anterior atrionodal input and the compact AV node intact, and this may provide a reasonable end point for the procedure. Further modification of nodal conduction might require injury to these structures. In addition, β-adrenergic stimulation attenuates the change in AV nodal conduction, possibly by overcoming the limitations of the anterior atrionodal input (ie, by improving the safety factor of conduction or shortening the refractory period of this tissue). This is supported by the finding that AVNW-CL measured during isoproterenol infusion fails to prolong after ablation, an observation also noted by others.6 This effect of β-adrenergic tone on fast pathway properties may limit the clinical utility of posteroseptal ablation as a therapeutic procedure in some patients.
Selected Abbreviations and Acronyms
|AVNRT||=||atrioventricular nodal reentry tachycardia|
|AVNW-CL||=||atrioventricular nodal Wenckebach cycle length|
|ERP||=||effective refractory period|
This work was supported in part by a grant from the National Institutes of Health (RO1-44747) and the Rosenfeld Heart Foundation. Dr Lerman is an Established Investigator of the American Heart Association.
- Received May 15, 1996.
- Revision received July 2, 1996.
- Accepted July 11, 1996.
- Copyright © 1996 by American Heart Association
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