Histopathological Study Following Catheter Guided Radiofrequency Current Ablation of the Slow Pathway in a Patient with Atrioventricular Nodal Reentrant Tachycardia

The present study examined histological changes induced by catheter guided radiofrequency current in a patient with AV nodal reentrant tachycardia who underwent cardiac transplantation 1 week after ablation of the slow pathway. During the electrophysiology study AV nodal conduction curves were discontinuous and AV nodal reentry was induced. At the conclusion of the procedure there was no evidence of slow pathway function. Histological sections from the explanted heart demonstrated a sharply demarcated atrial lesion (5 × 5 × 4 mm) extending from the septal portion of the tricuspid annulus to the posterior border of the AV node. The lesion did not encompass the compact AV node. These observations support the hypothesis that the slow pathway is comprised of atrial approaches to the AV node and is distinct from the compact AV node.     

Atrioventricular Nodal Physiology After Slow Pathway Ablation

The A V nodal physiology before and 1 week after “slow pathway potential” guided catheter ablation was examined in 32 patients with AV nodal reentrant tachycardia. A mean of 4.9 applications of radiofrequency energy eliminated AV nodal reentrant tachycardia in all patients. There were no significant differences in sinus cycle length (815 ± 159 msec vs 813 ± 162 msec;P = NS) and fast pathway conduction properties before and 1 week after ablation. Slow pathway conduction was completely eliminated in 10 (31%) (group I) of 32 patients after ablation. In the remaining 22 patients residual slow pathway conduction associated with one AV node echo was observed. In 15 patients (47%) (group II), the effective refractory period of the slow pathway showed a change of < 30 msec (265 ± 51 vs 266 ± 51 msec; P = NS), and in 7 patients (22%) (group III), a prolongation of more than 80 msec (247 ± 56 vs 340 ± 42 msec; P = 0.0001) before and 1 week after ablation. Minimal and maximal A₂-H₂ interval over the slow pathway in group II was not significantly changed (Min A₂-H₂:241 ± 37 vs 247 ± 40 msec; P = NS, Max A₂-H₂: 346 ± 79 vs 350 ± 60 msec; P = NS), while a significant prolongation was measured in group III (Min A₂-H₂: 261 ± 53 VS 373 ± 107 msec; P < 0.01. Max A₂-H₂: 359 ± 41 vs 427 ± 63 msec; P < 0.05) before and after ablation. Conclusion: In group II patients there was no evidence shown of impairment of the slow pathway. This suggests that disruption of the link between fast and slow pathways may be responsible for the elimination of AV nodal reentrant tachycardia, besides the elimination or impairment of the slow pathway itself, in “slow pathway potential” guided catheter ablation, and that the slow pathway potential may not necessarily represent activation of the slow pathway itself or of its atrial connection.     

Is Vagal Innervation to the Atrioventricular Node Impaired After Radiofrequency Ablation of the Slow Atrioventricular Nodal Pathway?

To assess the potentially adverse effects of RF catheter ablation (RFCA) of the slow AV nodal pathway on the parasympathetic innervation to the AV node in patients with AV nodal reentrant tachycardia (AVNRT), AV nodal conduction was evaluated following vagal stimulation by means of a phenylephrine bolus injection (200 μg) before and after RFCA in ten patients (mean age, 37 ± 14 years). Nine patients with AV reentrant tachycardia (AVRT) due to a left free wall accessory pathway served as a control group (mean age of 37 ± 12 years). Whereas no prolongation of the AH interval was observed in the AVNRT group following the phenylephrine bolus during sinus rhythm, despite a significant slowing in sinus rate, phenylephrine administration in AVRT patients was associated with both slowing of the sinus rate and prolongation of the AH interval. Following successful RFCA, the same responses were observed. To delineate the indirect effect of heart rate on AV conduction in response to the phenylephrine bolus, the AH interval was also measured during fixed atrial pacing. A marked prolongation of the AH interval occurred in both groups following phenylephrine administration. This prolongation was biphasic in 50% of A VNRT patients before ablation, suggesting a predominant effect of vagal stimulation on the fast AV nodal pathway. RFCA was associated with disappearance of discontinuous AV conduction in all but one patient with AVNRT. Vagal stimulation caused the same amount of AH interval prolongation as before RFCA in both study groups. In conclusion, patients with AVNRT have a preserved modulation of AV nodal conduction in response to vagal stimulation during sinus rhythm. In addition, vagal stimulation seems to exert a predominant effect on the fast A V nodal pathway. RFCA of the slow AV nodal pathway in patients with A VNRT does not cause detectable damage to the vagal innervation to the AV node.     

Shortcut Link Between the Fast and Slow Pathways and the Mechanism of Cure in Atrioventricular Nodal Reentrant Tachycardia by Catheter Ablation

The mechanism of cure in AV nodal reentrant tachycardia (AVNRT) by catheter ablation has not been fully clarified. We hypothesized that disruption of a shortcut link between the fast and slow pathways is responsible for the elimination of tachycardia. Results: AVNRT was eliminated in 20 patients by catheter ablation. In five patients (25%; group 1) slow pathway conduction disappeared 1 week after ablation. In six patients (30%; group II), the effective refractory period of the slow pathway was prolonged by more than 50 ms (212 ± 81 ms vs 340 ± 81 ms; P < 0.05). In the remaining nine patients (45%; group III), there was no change in the refractory period (270 ± 65 ms vs 273 ± 74 ms), although tachycardia was not inducible. A shortcut link between the fast and slow pathways was examined by comparing the A-H intervals over the slow pathway during the tachycardia and during atrial pacing at the tachycardia cycle length. Prior to ablation, a shortcut link was assumed in 1 of group I patients, 2 of group II patients, and 8 of group III patients. Of the 9 patients in whom the slow pathway was not impaired after ablation (group III), 8 patients were found to have a shortcut link, while 8 of 11 patients with impairment of the slow pathway after ablation (groups I and II) had no shortcut link between the fast and slow pathways (P < 0.05). Conclusion: In patients with a shortcut link between the fast and slow pathways, slow pathway conduction itself does not need to be impaired to eliminate the AVNRT, whereas in patients without this shortcut link, slow pathway conduction must be impaired.     

Slow Potential-Guided Radiofrequency Catheter Ablation in Atrioventricular Nodal Reentrant Tachycardia: Characteristics of the Potential Associated with Successful Ablation

To examine the characteristics of Haïssaguerre's slow potential (SP) specific to effective catheter ablation of the slow pathway in AV nodal reentrant tachycardia, the properties of SP and its recording site ware analyzed in 52 patients who underwent successful SP-guided ablation. The properties of SP included the ratio of the amplitude of SP to that of atrial potential (A)(SP/A), the SP duration, the interval between His-bundle potential (HP) and SP (HP-SP), the interval between A and SP (A-SP), the interval between SP and ventricular potential (V) (SP-V), and the ratio of A-SP to the interval between A and the V (A-SP/A-V). The SP recording site was determined by the ratio of the amplitude of A to that of V (A/V) and by the relative position of the ablation catheter on X ray (right anterior oblique projection), expressed as the ratio of the distance between the coronary sinus ostium and SP site to that between the coronary sinus ostium and HP recording site (relative SP position). Twenty-eight slow pathways were ablated with a single energy application, while the other 24 required applications ≥ 2. In all successful applications, SP/A, SP duration, HP-SP, A-SP. SP-V, A-SP/A-V, A/V, and relative SP position were 51 %± 25%, 28 ± 5 ms, -11 ± 9 ms, 57 ± 25 ms, 68 ± 13 ms, 46%± 9%, 15%± 13%, and 51%± 13%, respectively. A significant correlation was observed between the relative SP position and A-SP, and between the relative SP position and A-SP/A-V (r = 0.60 and 0.37, respectively), while it was not between the relative SP position and HP-SP, nor between the relative SP position and SP-V. When the characteristics of SP were comparatively analyzed between the effective and ineffective applications in 24 patients in whom applications ≥ 2 were required, there was no difference observed in HP-SP, A-SP, SP-V, A-SP/A-V, and A/V. However, SP/A, SP duration, and the relative SP position in the effective applications were all greater than those in the ineffective ones (56%± 20% vs 35%± 18%, P < 0.001; 29 ± 4 vs 26 ± 5 ms, P < 0.01; and 52%± 15% vs 33%± 11%, P < 0.001, respectively). These results indicate that SP with an amplitude over a half of A amplitude and recorded at the mid-septum of the tricuspid annulus can be a marker for successful slow pathway ablation. Although the local atrial electrogram appears late as the SP recording site shifts to the lower position, the timing of SP relative to HP and V remained unchanged, suggesting that SP is independent of the local atrial activation.     

Successful Slow Pathway Ablation in a Patient with Atrioventricular Nodal Reentrant Tachycardia Having a Proximal Common Pathway

Radiofrequency catheter ablation was attempted in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). AVNRT was easily inducible but an intermittent loss of the atrial activation was observed during AVNRT suggesting the presence of a proximal common pathway. During sinus rhythm, a relatively delayed activation that was compatible with a slow potential, was recorded anterior to the ostium of coronary sinus, and radiofrequency catheter ablation application (20 watts) to the site induced junction tachycardia. After an additional radiofrequency catheter ablation application to close the site, AVNRT became noninducible without deterioration of atrioventricular conduction through a fast pathway. This is the first case in which radiofrequency catheter ablation application to the slow potential recording site has been successful, even in AVNRT having a proximal common pathway.     

Comparative Atrioventricular Node Properties After Radiofrequency Ablation and Operative Therapy of Atrioventricular Node Reentry

The anatomical substrate for atrioventricular (AV) node reentry is unclear. To gain insights into the mechanism of cure of AV node reentry by nonpharmacological techniques, we compared AV node properties in 53 patients undergoing operative therapy (perinodal dissection) and 43 undergoing radiofrequency ablation (28 posterior approach, 15 anterior approach). Anterior radiofrequency ablation was associated with significant AH prolongation (62 ±18 msec vs 136 ± 64 msec, P < 0.0001), loss of "fast" pathway physiology, and no change in the anterograde refractory period of the AV node (273 ± 24 msec vs 268 ± 28 msec, P = NS). Posterior radiofrequency ablation did not change the AH interval (67 ± 17 msec vs 68 ± 17 msec, P = NS), prolonged AV node effective refractory period (275 ± 48 msec vs 320 ± 55 msec, P < 0.0001), and was associated with loss of "slow pathway" physiology. Operative treatment prolonged the AH interval (66 ±18 msec vs 83 ± 37 msec, P < 0.0001) and the AV node effective refractory period (264 ± 52 msec vs 364 ±112 msec, P < 0.0001), and affected dual pathway physiology inconsistently. These data support the view that the "fast" and "slow" pathways are distinct perinodal entities that can be selectively ablated. The operative approach causes more diffuse and variable injury to the AV node region.     

Coincident Idiopathic Left Ventricular Tachycardia and Atrioventricular Nodal Reentrant Tachycardia: Control by Radiofrequency Catheter Ablation of the Slow Atrioventricular Nodal Pathway

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.     

Atrial Ectopy Originating from the Posteroinferior Atrium During Radiofrequency Catheter Ablation of Atrioventricular Nodal Reentrant Tachycardia

Atrial ectopy sometimes appears during RF ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, its origin, characteristics, and significance are still unclear. To examine these issues, we analyzed 67 consecutive patients with AVNRT (60 with slow-fast AVNRT and 7 with fast-slow AVNRT), which was successfully eliminated by RF ablation to the sites with a slow potential in 63 patients and with the earliest activations of retrograde slow pathway conduction in 4 patients. During successful RF ablation, junctional ectopy with the activation sequence showing H-A-V at the His-bundle region appeared in 52 patients (group A) and atrial ectopy with negative P waves in the inferior leads preceding the QRS and the activation sequence showing A-H-V at the His-bundle region appeared in 15 patients (group B). Atrial ectopy was associated with (10 patients) or without junctional ectopy (5 patients). Before RF ablation, retrograde slow pathway conduction induced during ventricular burst and/or extrastimulus pacing was more frequently demonstrated in group B than in group A (9/15 [60%] vs 1/52 [2%], P < 0.001). Successful ablation site in group A was distributed between the His-bundle region and coronary sinus ostium, while that in group B was confined mostly to the site anterior to the coronary sinus ostium. In group B, atrial ectopy also appeared in 21% of the unsuccessful RF ablations. In conclusion, atrial ectopy is relatively common during slow pathway ablation and observed in 8% of RF applications overall and 22% of RF applications that successfully eliminated inducible AVNRT. Atrial ectopy appears to be closely related to successful slow pathway ablation among patients with manifest retrograde slow pathway function.     

Cryoablation for Presumed Atrioventricular Nodal Reentrant Tachycardia in Pediatric Patients

Background: Little data exist on the outcomes of cryoablation for the treatment of presumptive atrioventricular nodal reentrant tachycardia (AVNRT) in a pediatric population. Methods: We performed a retrospective chart review of patients undergoing cryoablation from January 2006 to October 2010 for presumed AVNRT at the Children's Hospital Colorado. Inclusion criteria were age ≤ 18, normal heart structure, no prior ablation procedures, documented narrow complex tachycardia, and no inducible tachycardia or other tachycardia mechanisms during electrophysiology study. Results: Thirteen patients underwent cryoablation for presumed AVNRT. Cryoablation catheter tip size varied from 4 to 8 mm with a median of eight cryoablation lesions. Isoproterenol was utilized preablation in 54% and none postablation. Procedural endpoints, per written report, were loss of sustained slow pathway, change in Wenckebach cycle length, and no specific endpoint. Procedural endpoints, per measured data, were a decrease in patients exhibiting sustained slow pathway conduction. Maximum atrial‐His (AH) interval with atrial overdrive pacing was reduced from 266 ms preablation to 167 ms postablation, p = 0.006. The number of patients with an AH jump was reduced from 6 to 2. After follow‐up of 13.8 ± 14.3 months, 23% (3/13) had documented tachycardia recurrence. No statistical significance was determined when comparing electrophysiology testing parameters pre‐ and postablation among the group with recurrence versus the group without recurrence. Conclusions: Cryoablation can be considered as a safe alternative to radiofrequency ablation for the treatment of presumed AVNRT among pediatric patients, albeit with a recurrence rate of 23%. (PACE 2012; 35:1319–1325)     

Fast-Slow Type of Atrioventricular Nodal Reentrant Tachycardia: Horizontal Dissociation of the AV Node During Tachycardia

Two patients with recurrent supraventricular tachycardia are presented. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. In patient 1 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response. In patient 2 the ventriculoatrial conduction was not observed. In both patients, the unchanged atrial cycle length during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia the first AH interval was shorter than the subsequent HA interval. In patient 2 verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (280 mg/day) suppressed the tachycardia in patient 1. These findings suggest that the mechanism of tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has tendency to show incessant form.     

Effect of Pacing Site on the Atrial Electrogram at Target Sites for Slow Pathway Ablation in Patients with Atrioventricular Nodal Reentrant Tachycardia

Atrial electrograms recorded from target sites during radiofrequency catheter ablation of the slow atrioventricular (AV) nodal pathway are often fractionated and may be associated with a late, high frequency component (the slow pathway potential). The purpose of the current study was to assess the effects of slow pathway ablation on the morphology of the atrial electrogram and to determine whether target site electrograms display direction dependent changes in morphology during atrial pacing maneuvers. Twenty-six patients with typical AV nodal reentry had electrograms recorded from target sites before and after successful ablation of the slow A V nodal path way and during pacing from the high right atrium and distal coronary sin us at cycle lengths of 500 and 300 msec. There was no significant change in the duration or degree of fractionation of the atrial electrogram as the result of slow pathway ablation. In contrast, the duration and degree of fractionation were less when pacing from the coronary sinus compared with sinus rhythms or right atrial pacing. Pacing rate did not affect electrogram morphology. These data suggest that the morphology of the slow pathway target site electrogram is dependent on the direction of atrial activation and that the "slow pathway potential" does not represent activation of an anatomically discrete pathway.     

Safety of Slow Pathway Ablation in Patients with Long PR Interval: Further Evidence of Fast and Slow Pathway Interaction

Whether the presence of abnormal PR before selective slow pathway ablation for AV node reentrant tachycardia increased the risk of complete heart block remains controversial. We report our experience in seven patients with prolonged PR intervals undergoing catheter ablation for AV reentry tachycardia. Their mean age was 66 ± 12 years; four patients were female and three were male. RF ablation was performed using an anatomically guided stepwise approach. In six patients, common type AV node reentry was induced and uncommon type was observed in the remaining patient. In all seven patients, successful selective slow pathway ablation was associated with no occurrence of complete heart block and was followed by shortening of the AH interval in five patients. In all seven patients, successful ablation was achieved at anterior sites (M₁ in two patients and M₂ in five patients). Despite AH shortening after ablation, the 1:1 AV conduction was prolonged after elimination of the slow pathway, excluding either sympathetic tone activation or parasympathetic denervation. In conclusion, selective slow pathway ablation can be performed safely in the majority of patients with prolonged PR interval before the procedure. Because successful ablation is achieved at anterior sites in most patients, careful selection and monitoring of catheter position is required.     

Radiofrequency Catheter Ablation of the Slow Reentrant Pathway of Sustained Ventricular Tachycardia

The article reports the cases of two patients with severe coronary artery disease and associated recurrent sustained ventricular tachycardia successfully treated with radiofrequency catheter ablation. In the first patient, two different types of ventricular tachycardia (one incessant) were eliminated. In all procedures, an area of slow conduction critical for tachycardia maintenance was localized by endocardial mapping techniques. Radiofrequency energy delivered to this area could permanently modify the anatomical substrate of the arrhythmia. After single follow-ups of 19, 14, and 13 months regarding the arrhythmic entities, the patients are well and free from spontaneous recurrences.     

Ablation of Atrioventricular Nodal Reentrant Tachycardia in a Patient with Reversal of Slow and Fast Pathways Inputs into the Atrioventricular Node

We report a case of atrioventricular nodal reentrant tachycardia (AVNRT) coexistent with His bundle anomaly and atrial septal defects. The His‐bundle potential was recorded at the coronary sinus (CS) ostium. Fractionated atrial potentials and an A:V electrogram ratio 1:3 were recorded at the anterior septum of the tricuspid annulus approximately 2 cm from CS ostium. Radiofrequency catheter ablation at the anterior septum of the tricuspid annulus effectively eliminated AVNRT. (PACE 2012; 35:e17–e19)     

Radiofrequency Catheter Ablation of Atrioventricular Junctional ("AV Nodal") Reentrant Tachycardia in Patients with Implantable Cardioverter Defibrillators

Catheter ablation of tachycardias has been undertaken successfully in patients with ICDs without damage to the ICD or lead. Ablation of the slow AV nodal pathway, however, is technically challenging because the lead of the ICD lies close to the ablation site. We report successful ablation of AV Junctional reentrant tachycardia (AVJRT) in three patients with ICDs, In all cases, the ablation site was within a few millimeters of the ICD lead. The ablation was successful in all cases and did not cause damage to the ICD or lead. The patients have remained free of recurrence of AVJRT during a mean follow-up of 12 months.     

Radiofrequency Catheter Ablation of Atrioventricular Nodal Reentrant Tachycardia in Children

Radiofrequency (RF) catheter ablation has been widely used in the treatment of cardiac arrhythmias. In atrioventricular nodal reentrant tachycardia (AVNRT), the experience has been predominantly in adults. The cardiac electrophysiological records of 18 consecutive children undergoing RF catheter AV node modification for AVNRT were reviewed. The patients (10 females, 8 males) were 8.2–17.9 years of age (mean 13.6 ± 3.0), weight 15.2–88.1 kg (mean 52.2 ± 20.8), and height 103–190 cm (mean 157.1 ± 21.7). Thirteen were on antiarrhythmic medications (1–3, average 1.5 drugs/day). All drugs were discontinued 48 hours prior to the ablations. The procedures were performed under sedation and local anesthesia. Pre- and post-AV node modification electrophysiological studies were performed in all procedures. The 18 patients underwent a total of 25 procedures (1.39 ± 0.61 per patient): the anterior approach aimed at the antegrade fast pathway in the first four patients and the posterior approach aimed at the slow pathway in the remainder. Thenumber of energy applications was 8–54 (19.8 ± 10.7) per procedure. The maximum energy used in each procedure was 30–50 watts (33.8 ± 8.4). The average energy was 24–50 watts (33.0 ± 6.8). The fluoroscopy time was 7.1–73.4 minutes (29.9 ± 20.0) per procedure, for a total catheterization time of 228–480 minutes (300.3 ± 59.1). Preablation spontaneous or induced AVNRT (cycle length 310.4 ± 55.0 msec) was seen in all except one who had the arrhythmia (cycle length 270 msec) on surface ECG. In 22 of 25 studies, the AH interval measured 67.4 ± 13.2 msec pre- and 98.7 ± 58.4 msec post-AV node modification (P < 0.02). Procedures were initially successful in 16 (89%) of 18 patients. One patient developed complete AV block requiring DDD pacemaker and has since recovered normal AV conduction. Transient third- or second-degree block was seen in four. Other complications included airway obstruction in one and excessive emesis in another. In follow-up of 2–26 months (13.0 ± 7.3), one patient underwent surgical ablation for failed initial RF catheter ablation, and two underwent successful RF procedures for recurrences. RF catheter AV node modification for AVNRT in children is a useful technique. Under ideal circumstances, it is safe and efficacious. Follow-up to determine the potential long-term complications is necessary.     

Effects of Pharmacological Autonomic Blockade on Dual Atrioventricular Nodal Pathways Physiology in Patients with Slow-Fast Atrioventricular Nodal Reentrant Tachycardia

The purpose of this study was to investigate the atrioventricular AV nodal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 ± 17 years) with clinical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71 %) of 17 patients still demonstrated AV nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 ± 105 ms vs 630 ± 80 ms, P < 0.005) and AV blocking cycle length (365 ± 64 ms vs 338 ± 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and functional refractory period of the fast pathway (369 ± 67 ms vs 305 ± 73 ms, P < 0.005; 408 ± 56 ms vs 350 ± 62 ms, P < 0.005) and the slow pathway (271 ± 30 ms vs 258 ± 27 ms, P < 0.01; 344 ± 60 ms vs 295 ± 50 ms, P < 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 ± 94 ms vs 326 ± 89 ms, NS) and effective refractory period of retrograde fast pathway (228 ± 38 ms vs 240 ± 80 ms, NS) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the decreased inducibility of clinical AVNRT.