Atrioventricular Node Reentry With ‘Smooth’ AV Node Function Curves
A Different Arrhythmia Substrate?
Background Some patients with otherwise typical AV node reentry do not manifest discontinuous AV node function curves. We examined the effects of an ablation in the slow-pathway region in patients with smooth AV node function curves.
Methods and Results Fifteen patients with AV node reentrant tachycardia (AVNRT) and discontinuous AV node function curves were compared with 15 patients with AVNRT and smooth AV node function curves. In the group with a discontinuous curve, the “net” anterograde effective refractory period (AERP) of the AV node increased (270±28 versus 304±37 ms, P=.03) and AERP of the remaining fast pathway decreased (367±100 versus 304±37 ms, P=.026) after the ablation. In the group with a smooth curve, the AERP of the AV node increased (266±42 versus 299±76 ms, P=.07) and the anterograde Wenckebach cycle length increased (336±66 versus 379±86 ms, P=.008) after the ablation. Retrograde conduction over the AV node was similar in both groups and was unchanged after ablation. The longest attainable AH interval (AHmax) measured during atrial extrastimulus testing was more prolonged in patients with a discontinuous curve than in patients with a smooth curve (326±48 versus 250±70 ms, P=.002). The AHmax shortened in both groups after ablation (326±48 versus 173±34 ms, P<.0001, and 250±70 versus 179±34 ms, P<.0003, respectively) and were similar. Successful ablation in the slow-pathway zone in patients with a smooth AV node function curve resulted in the loss of the “tail” of the curve representing the slow pathway.
Conclusions These data suggest that the smooth AV node function curve consists of two distinct components representing both fast and slow AV node pathways even when the typical discontinuity is absent.
The mechanism of AV node reentry is based on a substrate with two functionally and anatomically distinct AV node pathways that permit reciprocation.1 2 3 In classic AV node reentry, the curve relating the AH interval to prematurity of an atrial extrastimulus is discontinuous, with a distinct “jump” separating the fast and slow node pathways. Some patients with otherwise typical AV node reentry do not manifest this discontinuity even when tested at multiple cycle lengths and varying pacing sites.4 To explore the mechanism of this phenomenon, we examined the effects of successful ablation in the slow-pathway region in patients with smooth AV node function curves and otherwise typical features of AV node reentry.
The study population consisted of three groups of patients. Group 1 included patients with symptomatic tachycardia who underwent electrophysiological study and were found to have dual AV node pathways and AVNRT. Radiofrequency catheter ablation energy was applied to the slow-pathway area. Group 2 included patients with symptomatic tachycardia who underwent electrophysiological study and were found to have AVNRT in the absence of a clear-cut discontinuity of the AV node function curve. Radiofrequency catheter ablation energy was delivered in the putative slow-pathway area. Group 3 was a control population that underwent an electrophysiological study as part of the investigation for syncope and/or palpitations yet to be diagnosed. The electrophysiological study was within normal limits in all cases.
Written and verbal consents were obtained from all patients. Each patient was studied in the fasting state under sedation with intravenous midazolam and fentanyl or general anesthesia with propofol. All antiarrhythmic medication was discontinued a minimum of five half-lives before the study. Three quadripolar catheters were introduced percutaneously into the right femoral vein and advanced to the high right atrium, His bundle recording position, and right ventricular apex, respectively. An octapolar catheter was placed in the coronary sinus via the left subclavian vein. A baseline study was performed in all patients to confirm the diagnosis of AVNRT5 and to measure anterograde and retrograde conduction parameters. Briefly, the study consisted of high right atrial and right ventricular apical incremental pacing to block and extrastimulus testing with at least two drive cycle lengths. Presence of dual AV node physiology was established by a sudden prolongation of the AH interval of at least 50 ms for a 10-ms decrement during extrastimulus testing. There was no systematic attempt to use multiple atrial sites or further cycle lengths when discontinuous curves were not observed.
A 7F quadripolar deflectable catheter (Mansfield-Webster) with a 4-mm tip electrode was used for ablation. Radiofrequency energy was delivered by a device that operates at 350 kHz and provides continuous monitoring of current, impedance, and energy (RFG-3D, Radionics). The approach used in our laboratory has been described previously.6 A power setting of 30 W was used for each ablation attempt. Current was applied for 40 seconds if junctional tachycardia was observed during ablation. Application of energy was interrupted if junctional tachycardia did not occur within 10 seconds or if impedance rose. Lesions were anatomically guided and directed to the region between the orifice of the coronary sinus and tricuspid annulus. The end point in patients with dual pathways was elimination of the slow pathway as evaluated by atrial extrastimulus testing. In the absence of dual AV node physiology, noninducibility of reentrant tachycardia and elimination of all echo beats served as markers of successful ablation.
Evaluation After Ablation
Thirty to 45 minutes after the last radiofrequency ablation, the presence of slow-pathway conduction was assessed by programmed atrial stimulation. If anterograde slow-pathway conduction was eliminated, electrophysiological evaluation was repeated according to the same protocol as previously described. All patients were monitored continuously for 24 hours after the procedure. Patients were discharged without antiarrhythmic medication and were reevaluated at 3 months. Follow-up electrophysiological testing was not performed unless the patient developed evidence of tachycardia.
Additional Measurements and Definitions
The ERP of the AV node was defined as the longest A1A2 interval measured at the His bundle site that failed to generate a nodal response to a premature atrial extrastimulus (A2). The “net” ERP refers to the shortest ERP regardless of discontinuity and is the slow-pathway ERP in patients with dual pathways. Whenever possible, all ERP measurements were determined with a drive cycle length of 600 ms. For each individual patient, the drive cycle lengths at which ERP measurements were obtained before the ablation were matched and repeated after the ablation. The AV node function curve was defined as the plot of AH interval as a function of prematurity of the atrial extrastimulus as measured at the His bundle site. The maximum AHmax was the longest AH interval (A2H2) measured during atrial extrastimulus testing and was determined both before and after ablation.
Statistical analysis of electrophysiological data before and after ablation was performed by use of the two-tailed paired Student’s t test. Student’s t test for independent samples with Bonferroni’s correction was used when appropriate. ANOVA was used to compare continuous variables in multiple groups. Data were expressed as mean±SD. A value of P<.05 was considered statistically significant.
Group 1 (dual AV node pathways) included 15 patients, 11 women and 4 men, 41.9±13.0 years old (mean±SD). Group 2 (tachycardia without dual pathways) included 15 patients, 12 women and 3 men, 47.8±12.1 years old. Radiofrequency ablation was successful in eliminating inducibility of reentrant tachycardia in all patients. Group 3 (control subjects) consisted of 15 patients, 8 women and 7 men, 46.6±15.6 years old. The three groups did not differ with respect to age, sex, AH interval, His-ventricular interval, or sinus cycle length. The cycle lengths of the reentrant tachycardia induced during electrophysiological study did not differ between groups 1 and 2 (dual, 317±137 versus 334±107 ms, P=NS).
Effects of Slow-Pathway Ablation Group 1
Sustained slow-fast AVNRT was induced in 12 of 15 patients before ablation. Sustained atypical AVNRT was induced in 1 patient, and typical AV node echo beats were observed in 2. Clear evidence of dual AV node physiology was present in all patients before ablation (Fig 1⇓). The effects of ablation on the refractory and conduction properties of the AV node are shown in the Table⇓. Sinus cycle length (779±182 versus 732±146 ms, P=NS), AH interval (65±15 versus 58±13 ms, P=NS), and anterograde Wenckebach cycle length (362±67 versus 368±60 ms, P=NS) remained unchanged. The net AERP of the AV node increased (270±28 versus 304±37 ms, P=.03), whereas the ERP of the remaining fast pathway shortened (367±100 versus 304±37 ms, P=.026).
Before ablation, all patients in group 1 had retrograde ventriculoatrial conduction. After ablation, 1 patient had no retrograde conduction over the AV node. Retrograde Wenckebach cycle length (335±60 versus 323±44 ms, P=NS) and the retrograde ERP of the AV node (282±49 versus 270±34 ms, P=NS) remained unchanged.
Effects of Ablation at the Putative Slow-Pathway Site in Group 2
Sustained slow-fast AVNRT was induced in 10 of 15 patients before ablation. Sustained atypical AVNRT was observed in 4 patients, while typical AV node echo beats were seen in 1. Clear evidence of dual AV node pathways as evidenced by discontinuity of the AV node function curve was not present before ablation (Fig 2⇓). In one case of a patient with recurrent atrial fibrillation, the entire electrophysiological study and ablation were performed while the patient was on a procainamide infusion. In three cases, propranolol and atropine were infused. The latter did not alter individual AV node function curves. The effects of ablation on the refractory and conduction properties of the AV node are shown in the Table⇑. Sinus cycle length (685±101 versus 696±108 ms, P=NS) and the AH interval (65±23 versus 70±17 ms, P=NS) remained unchanged. The anterograde Wenckebach cycle length increased (336±66 versus 379±86 ms, P=.008), and the AERP of the AV node increased (266±42 versus 299±76 ms, P=.07).
Retrograde Wenckebach cycle length increased slightly after ablation (328±55 versus 359±75 ms, P=NS). The retrograde ERP of the AV node (267±38 versus 252±90 ms, P=NS) remained unchanged.
Comparison of Groups 1 and 2
The sinus cycle length did not differ between the two groups either before or after ablation. The net ERP before (dual, 270±27.8 versus 266±42 ms, P=NS) and after (dual, 304±37 versus 299±76 ms, P=NS) ablation remained unchanged. The anterograde Wenckebach cycle length remained unchanged in group 1 (discontinuous AV node function curve) but increased after the ablation in group 2 (smooth AV node function curve) (362±67 versus 368±60 ms, P=NS, and 336±66 versus 379±86 ms, P=.008, respectively).
Retrograde Wenckebach cycle length and retrograde ERP of the AV node were similar and did not change after ablation.
The baseline AHmax was significantly different between groups (ANOVA, P<.001). The AHmax measured during atrial extrastimulus testing before ablation was greater in patients with discontinuous AV node function curves than in patients with a smooth AV node function curve (326±48 versus 250±70 ms, P=.002), and both values were greater than the control group (control, 205±37 ms, P<.05). After ablation in patients with a discontinuous AV node function curve, the AHmax was shortened (326±48 versus 173±34 ms, P<.0001). The AHmax in patients with smooth AV node function curves also shortened significantly after ablation (250±70 versus 179±56 ms, P<.0003). After ablation, the AHmax was similar in both groups (dual, 173±34 versus no dual, 179±56 ms, P=NS). The AHmax measured in the control group was similar to both the treated groups after ablation (control, 205±37 versus dual, 173±34 versus no dual, 179±56 ms; ANOVA, P=.076).
Failure to observe a distinct discontinuity in the curves relating AH interval to prematurity of an atrial extrastimulus in otherwise typical AV node reentry may be related to cycle length tested or atrial pacing site.1 2 3 In other instances, autonomic blockade in such patients may result in transformation of the curve to yield typical discontinuities,7 suggesting that the fast and slow pathways respond uniquely to autonomic influences and that differences in the conduction and refractory properties of the curves are not sufficiently distinct at rest to yield discontinuities.
This study further supports the hypothesis that the smooth AV node refractory curve in fact consists of two distinct components representing both fast and slow AV node pathways even when the typical discontinuity is absent. Successful ablation in the slow-pathway zone in these patients resulted in loss of the “tail” of the curve representing the slow pathway. The AHmax obtained with atrial extrastimuli decreased in a parallel fashion after ablation in patients both with and without dual-pathway curves. The initial longest attainable AHmax was shorter in patients without typical dual-pathway curves, suggesting that the slow pathway in patients without typical discontinuities may be “less decremental.” The remaining fast pathway had a similar ERP in patients with both discontinuous and smooth curves, which was also similar to the ERP of the AV node in control subjects, who presumably do not have a slow pathway. As has been described previously, the ERP of the fast pathway in patients with discontinuous curves initially shortened after ablation of the slow pathway.7 8 The data suggest that patients with smooth AV node function curves differ from those with discontinuous AV node function curves only in magnitude of the difference in conduction time over the two slow pathways. There is no reason to believe that the arrhythmia substrates are different. This is further supported by curve-fitting data suggesting that the slow-pathway component can be distinguished from the fast-pathway component of this curve regardless of the presence of discontinuities.9
This study has important limitations. First, an exhaustive attempt to demonstrate discontinuities in the curve was not made because of reluctance to inadvertently produce atrial fibrillation. It is possible that use of multiple atrial sites, more extrastimuli, or pharmacological maneuvers could have revealed discontinuities in some of the smooth curves. Second, the slow-pathway component of the curves may have a relatively short duration in some individuals. This would make this judgment of “loss of the tail” more tenuous and difficult in these patients.
Loss of the slow pathway is a useful predictor of clinical efficacy in patients undergoing slow-pathway ablation for AV node reentry and is preferred by some investigators.10 11 This end point is less evident when the initial curves do not yield a discontinuity. This study suggests that loss of the “tail” of the curve, as indicated by prolongation of the ERP and failure to attain the AHmax previously observed, can be considered essentially comparable to loss of the slow-pathway portion of the curve in patients with obvious discontinuity.
Persistence of a slow pathway with single echo cycles in some patients suggests the continued presence of the arrhythmia substrate and potential for further clinical occurrence of AV node reentrance.11 Significant shortening of the AHmax in this setting suggests that the slow pathway may have been altered or, alternatively, the slow pathway remaining is not the “clinical” slow pathway that caused the initial tachycardia. This might, in part, explain the clinical observation that persistence of a slow pathway by no means precludes an excellent clinical result.12 13 14 15
Finally, the study suggests that an AHmax in the range of 250 to 300 ms or greater may indicate the presence of a slow pathway whether or not the curve is discontinuous. This merits further observations with larger numbers of patients.
Selected Abbreviations and Acronyms
|AERP||=||anterograde effective refractory period|
|AHmax||=||longest attainable AH interval|
|AVNRT||=||atrioventricular node reentrant tachycardia|
|ERP||=||effective refractory period|
This study was supported by the Heart and Stroke Foundation of Ontario, Toronto, Canada. Dr Klein is a Career Investigator of the Heart and Stroke Foundation. We acknowledge the assistance of Katherina M. Leetch in the preparation of the manuscript.
- Received July 11, 1995.
- Revision received October 4, 1995.
- Accepted October 6, 1995.
- Copyright © 1996 by American Heart Association
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