Pacemaker-like syndrome complicating slow pathway ablation for AV nodal reentrant tachycardia

This case report describes pacemaker-like syndrome after successful slow pathway ablation for atrioventricular (AV) nodal reentrant tachycardia due to recurrence of single AV nodal echo beats during sinus rhythm. The resultant AV dyssynchrony was responsible for the symptom complex. Following ablation of retrograde ventriculoatrial conduction, the AV nodal echo beats were eliminated and the pacemaker-like syndrome resolved.     

Atrioventricular Node Reentry: Physiology and Radiofrequency Ablation

Atrioventricular (A V) node reentry has heen recognized as a clinical arrhythmia for many years. Earlier basic investigations identified a dual AV conduction system, and atrial echo beats occurred when the refractory period of the slow conduction pathway was shorter than the fast pathway. Subsequent studies in humans confirmed the concept of dual AV node physiology and AV node reentry. Slow-fast AV node reentry (anterograde conduction over the slow pathway and retrograde conduction over the fast pathway) occurs most frequently. The fast-slow and intermediate varieties are much less common. A high (> 95%) cure rate occurs with radiofrequency catheter ablation with experienced electrophysiologists. Most electrophysiologists prefer the posterior approach, which results in absence or very poor conduction over the slow AV node pathway; the PR interval is minimally changed. This approach is highly successful for all three forms of AV node reentry and associated with a 1%–2% incidence of heart block in most experienced laboratories.     

Acute effects of simvastatin to terminate fast reentrant tachycardia through increasing wavelength of atrioventricular nodal reentrant tachycardia circuit

Simvastatin (SV) leads to reduction of ventricular rhythm during atrial fibrillation on rabbit atrioventricular (AV) nodes. The aim of our study was (i) to determine the frequency‐dependent effects of SV in a functional model, and (ii) to assess the effects of SV to suppress experimental AV nodal reentrant tachycardia (AVNRT). Selective stimulation protocols were used with two different pacing protocols, His to atrial, and atrial to atrial (AA). An experimental AVNRT model with various cycle lengths was created in three groups of perfused rabbit AV nodal preparations (n = 24) including: SV 3 μm , SV 7 μm , and verapamil 0.1 μm . SV increased nodal conduction time and refractoriness by AA pacing. Different simulated models of slow/fast and fast/slow reentry were induced. SV caused inhibitory effects on the slow anterograde conduction (origin of refractoriness) more than on the fast anterograde conduction time, leading to an increase of tachycardia cycle length, tachycardia wavelength and termination of slow/fast reentrant tachyarrhythmia. Verapamil significantly suppressed the basic and frequency‐dependent intrinsic nodal properties. In addition, SV decreased the incidence of gap and echo beats. The present study showed that SV in a concentration and rate‐dependent manner increased the AV effective refractory period and reentrant tachycardia wavelength that lead to slowing or termination of experimental fast AVNRT. The direction‐dependent inhibitory effect of SV on the anterograde and retrograde dual pathways explains its specific antireentrant actions.     

The history of AV nodal reentry

Though patients with AV nodal reentry are now routinely cured by catheter ablation, the basic mechanism of this disorder is still under debate. The putative mechanism of AV node reentry was first discovered by the elegant work of Gordon Moe. He demonstrated the existence of dual pathways and echo beats in rabbits. Building on these seminal observations, the mechanism of AVNRT has burgeoned to include the possibility of left atrial input into the node. The first curative nonpharmacologic procedures involved surgical dissection around the AV node and the procedure was rapidly supplanted by catheter ablation procedures. The initial ablative procedure targeted the fast pathway, but later observations showed that ablation of the slow pathway was more effective and safer. Cure of AV nodal reentry which is the most common cause of paroxysmal supraventricular tachycardia became possible through the cooperative efforts of anatomists, physiologists, surgeons, and clinical electrophysiologists.     

Electrophysiological characteristics of junctional rhythm during ablation of the slow pathway in different types of atrioventricular nodal reentrant tachycardia

BACKGROUND: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. METHODS: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. RESULTS: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). CONCLUSIONS: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.     

Inducible atrioventricular nodal reentrant echo behind organic 2:1 infra-hisian block during sinus rhythm

A 77-year-old male patient with an intermittent 2:1 infra-Hisian block during sinus rhythm was presented with dizziness and near-syncope. During electrophysiological (EP) study, dual atrioventricular (AV) nodal pathways and retrograde fast pathway were easily induced by atrial and ventricular programmed stimulation, respectively. A typical slow-fast AV nodal reentrant echo beat also could be demonstrated by single atrial extrastimulation. Atrioventricular nodal reentrant tachycardia (AVNRT) can occasionally exhibit 2:1 AV block. Conversely, AV nodal reentry property had been rarely reported behind 2:1 infra-Hisian block. The EP presentation from this case may support the notion that tissues below the His are not part of the reentrant circuit of AVNRT.     

Incessant Atrio‐Ventricular Node Reentrant Tachycardia Induced by Unapparent Dual Atrio‐Ventricular Node Conduction

We present the case of a patient with incessant slow‐fast atrio‐ventricular (AV) node reentrant tachycardia induced by dual AV node conduction with aborted conduction to the ventricles. The unapparent conduction over the slow pathway was suspected here because of spontaneous nodal echoes without QRS complexes occurring during sinus rhythm, manifested as isolated premature atrial beats and which repetitively induced the tachycardia.     

Cycle Length Alternation During Supraventricular Tachycardia: Occurrence and Mechanism in a Canine Model of AV Reentrant Tachycardia

Cycle length alternation (CLA) is commonly observed during supraventricular tachycardia (SVT) onset and termination. The present study was designed to gain insights into the mechanism and potential clinical relevance of CLA by comparing computer simulations of tachycardia to directly observed behavior in a canine model of AV reentrant tachycardia (AVRT). The computer model was based on the hypothesis that CLA is secondary to feedback between AV nodal output during SVT and subsequent AV nodal input, and used the measured anterograde AV nodal recovery curve (AV vs A1A2) to predict sequential AV and RR intervals during SVT. Orthodromic AVRT was created experimentally in 11 open-chested, autonomically-blocked (atropine plus nadolol) dogs using a sensing and pacing circuit that mimicked a retrograde-conducting accessory pathway. Steady-state cycle length and AV interval during experimental AVRT closely paralleled predictions made by the computer model. CLA appeared consistently at the onset of experimental AVRT at programmed VA intervals less than or equal to 100 msec (corresponding to VA less than or equal to 150 msec as measured clinically) in all dogs. The amplitude and duration of CLA increased as the VA interval decreased, and closely paralleled predictions based on the computer model. Abrupt accelerations in atrial pacing to the same rate as AVRT did not result in alternation of cycle length. In conclusion, alternation of cycle length results from feedback between AV nodal output and subsequent AV nodal input at the onset of reentrant supraventricular tachycardia, and does not require changes in autonomic tone or dual AV nodal pathways. CLA occurrence, amplitude, and duration are predictable based on AV node recovery properties, and depend on retrograde conduction properties of the reentrant circuit. The presence of CLA suggests that the AV node is an integral component of the SVT reentry circuit, and may be useful clinically to identify the mechanism of supraventricular tachycardias.     

Fast pathway ablation in a patient with PR prolongation

The classical form of typical atrioventricular node reentrant tachycardia (AVNRT) is a “slow-fast” pathways tachycardia, and the usual therapy is an ablation of the slow pathway since it carries a low risk of atrioventricular (AV) block. In patients with long PR interval and/or living on the anterograde slow pathway, an alternative technique is required. We report a case of a 42-year-old lady with idiopathic restrictive cardiomyopathy, persistent atrial fibrillation status post pulmonary vein isolation, and premature ventricular complex ablation with a systolic dysfunction, who presented with incessant slow narrow complex tachycardia of 110 bpm that appeared to be an AVNRT. Her baseline EKG revealed a first-degree AV block with a PR of 320 ms. EP study showed no evidence of anterograde fast pathway conduction. Given this fact, the decision was to attempt an ablation of the retrograde fast pathway. The fast pathway was mapped during tachycardia to its usual location into the anteroseptal region, then radiofrequency ablation in this location terminated tachycardia. After ablation, she continued to have her usual anterograde conduction through slow pathway and the tachycardia became uninducible. In special populations with prolonged PR interval or poor anterograde fast pathway conduction, fast pathway ablation is the required ablation for typical AVNRT.     

Radiofrequency ablation of probable atrioventricular nodal reentrant tachycardia in children with documented supraventricular tachycardia without inducible tachycardia

The reproducible induction of supraventricular tachycardia (SVT) during electrophysiological study is critical for the diagnosis of atrioventricular nodal reentry tachycardia (AVNRT), and for determining a therapeutic endpoint for catheter ablation. In the sedated state, there are patients with reentry SVT due to AVNRT who are not inducible at electrophysiological study. This article reports on the empiric slow pathway modification for AVNRT in six pediatric patients (age 6-17, mean 13.3 years) with documented, recurrent, paroxysmal SVT in the setting of a structurally normal heart who were not inducible at electrophysiological study. Atrial and ventricular burst and extrastimulus pacing at multiple drive cycle lengths were performed in the baseline state, during an isuprel infusion, and during isuprel elimination. Single AV nodal (AVN) echo beats were present in all patients, while classic dual AVN physiology was present in three of six patients. Radiofrequency energy was administered in the right posteroseptal AV groove resulting in accelerated junctional rhythm in five of six patients. Postablation testing demonstrated the elimination of echo beats in four patients, while dual AVN physiology and echo beats persisted in two patients. At follow-up (22-49 months, mean 29.5 months), all patients are asymptomatic without recurrence of SVT and are not taking any antiarrhythmic medication. In selected patients, empiric slow pathway modification may be offered as a potential cure in children with recurrent paroxysmal SVT who are not inducible at electrophysiological study. Elimination of slow pathway conduction may serve as a surrogate endpoint, though is not necessary for long-term success.     

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.     

Transvenous Ablation with High Frequency Energy for Atrioventricular Junctional (AV Nodal) Reentrant Tachycardia

We performed transcatheter AV junction ablation with high frequency energy in four patients with AV nodal reentrant tachycardia where extensive trials of several antiarrhythmic drugs failed to prevent further recurrences of tachycardia. Initially high frequency catheter ablation induced complete AV block in all patients. A recuperation of AV 1:1 conduction followed some time later, persisting in follow-up. No complications have been encountered in either the acute phase or the follow-up (from 6 to 8 months; mean +/- SD: 8.7 +/- 2.5 months). The electrophysiological study was carried out 6 weeks following ablation, and all patients showed AV 1:1 conduction. No dual nodal pathway was encountered and no tachycardia could be triggered. With refinement of the method, the potential application of high frequency energy to interrupt intranodal or perinodal connections responsible for reentrant supraventricular tachycardia or to retard AV nodal conduction appears promising.     

Atypical AV nodal reentry with bystander accessory pathway: an unusual mechanism of preexcited tachycardia

We present an unusual mechanism of preexcited tachycardia--atypical AV nodal reentry with bystander AP. It can be differentiated from other preexcited tachycardias by its variable degree of preexcitation (either spontaneous or in response to atrial pacing), higher degree of preexcitation with pacing near the origin of the AP than during tachycardia, inability to preexcite the tachycardia by either late atrial or ventricular premature beats, the presence of nonpreexcited atypical AV nodal reentry tachycardia following successful AP ablation, and by exclusion of atrial tachycardia.     

Subthreshold Stimulation at the Focal Origin of Para-Hisian-Located Ectopic Atrial Tachycardia

WEISS, C., et al. : Subthreshold Stimulation at the Focal Origin of Para-Hisian-Located Ectopic Atrial Tachycardia. The focal origin of ectopic atrial tachycardia (EAT) is occasionally located in the superoparaseptal region adjacent to the bundle of HIS. Radiofrequency catheter ablation (RFCA) of EAT in this anatomic location implies the potential hazard of adverse impairment of the AV conduction. Therefore, careful precise mapping is mandatory. Subthreshold stimulation as defined as the delivery of noncaptured low energy pulses has been introduced as an additional mapping technique for slow pathway ablation in the setting of AV nodal reentrant tachycardia and other reentrant tachycardia. A patient with a right superoparaseptal EAT focus, in which subthreshold stimulation (STS) could determine the site of successful subsequent RFCA is described. During STS with EAT termination no AV conduction disturbances, junction-escape rhythms or atrial capture could be recorded. Thus STS may be used as an additional mapping tool to identify successful ablation sites in EAT.     

One-to-Two Atrioventricular Conduction Causing Nonreentrant Tachycardia: Successful Treatment with Radiofrequency Ablation

The anatomical substrate for AV nodal reentrant tachycardia (AVNRT) is well known and is due to anterograde conduction through a siow conducting pathway and retrograde conduction using a fast conducting path way. In this report, we describe a patient with AVNRT who also presented with frequent episodes of paroxysmal nonreentrant tachycardia due to the occurrence of two conducted ventricular beats for each sinus depolarization. Palpitations and arrhythmias were abolished after radiofrequency ablation of the slow pathway.     

A Nodoventricular Fiber Associated with Dual AV Nodal Conduction, AV Nodal Reentrant Tachycardia, and Anterior Location of the Slow AV Nodal Pathway

We present a case of a patient with a nodoventricular tract, associated with dual AV nodal conduction and AV nodal reentrant tachycardia, and an anteroseptal location of the slow AV nodal pathway. The remarkable feature of this case is the site of successful ablation, in the anteroseptum just anterior and superior to the His bundle, where both preexcitation and dual AV nodal physiology were abolished.     

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.     

Modification of the DDD Pacing Mode to Prevent Junctional Reentry Tachycardia: Computer Modelling Experiments

This paper examines the possibility of using short atrioventricular (AV) delay dual chamber pacing to prevent junctional reentry tachycardia mediated by an accessory pathway or by an intra-AV nodal circuit. For this purpose, a clinically realistic computer simulation model of cardiac rhythm and heart-pacemaker interactions has been used. The computational experiments compared the actions of two pacemaker models: (A) a clinically realistic DDD mode operating with quasi-Wenckebach prolongation of the AV delay; and (B) a new modification of the DDD mode introducing independent counters for the atrial and ventricular refractory periods of the heart, and the possibility of instantaneous or shortly delayed atrial pacing triggered by a sensed or paced ventricular event. The pathological phenomena modelled in the experiments simulate different possibilities of tachycardia initiation. These disorders include: (1) single atrial premature beats (APBs), (2) salvos of APBs, (3) closely coupled pairs of APBs, (4) ventricular premature beats initiating an antidromic reentry tachycardia, and (5) ventricular ectopic beats initiating an AV nodal reentry tachycardia. The computational results prove that many possible mechanisms of initiation of junctional reentry tachycardia are beyond the prophylactic capabilities of current sophisticated DDD pacemakers (A). The results also show that the suggested pacing mode (B) improves anti-tachycardia prophylaxis even when responding to complex pathological episodes of the natural cardiac activity. Future development of the suggested mode (B) is discussed.     

A Wide QRS Complex Tachycardia with Different Initiation Patterns: What is the Mechanism?

A 47-year-old man with palpitations underwent electrophysiologic testing (EPS). Burst atrial pacing while infusing isoproterenol induced non-reproducible wide QRS tachycardias with an unusual pattern of an H-A-V activation with the same tachycardia cycle length and two different initiation patterns. The tachycardia had the earliest atrial activation at the His bundle region. No dual atrioventricular (AV) nodal physiology was demonstrated by programmed atrial stimulation. Though a definite diagnosis of AV nodal reentrant tachycardia was not obtained, slow pathway ablation was performed in order to avoid inadvertent AV block as a complication. Thereafter, no tachycardias were induced by repeat burst atrial pacing.     

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.