Demonstration of Right and Left Atrial Dissociation by Atrial Rapid Pacing or Extrastimulation During Fast-Slow (Uncommon) Form of Atrioventricular Nodal Reentrant Tachycardia

Some recent works suggest that extranodal atrial fibers may form part of the reenlry circuit in the atrioventricular (AV) nodal reentrant tachycardia (AVNRT). This hypothesis is based on the fact that the perinodal dissection successfully abolished AVNRT while preserving intact AV conduction. Apart from the surgical success, the electrophysiological evidence supporting this hypothesis has not been demonstrated, especially in the uncommon (fast-slow) form of AVNRT. We present some electrophysiological evidence suggesting atrial participation in eight patients with the fast-slow form of AVNRT. During the tachycardia, rapid pacing or extrastimulation was done from the orifice of the coronary sinus (CS) and the right atrium (RA), while recording the electrograms of the CS and the low septal RA. In seven patients, right and left atrial dissociation was demonstrated during pacing from the RA, while in the remaining one this was demonstrated from the CS. The interatrial dissociation will be unlikely if the intranodal reentry circuit connects with the atria via a single upper common pathway. This suggests that the upper turnaround of the reentry circuit involves atrial tissue and that the extranodal accessory pathway with long conduction times may form the ascending limb of the circuit (atrionodal reentry). Alternatively, the reentry circuit is entirely intranodal and two or more connecting pathways are present between the atria and the circuit.     

Wide QRS Supraventricular Tachycardia Due to Coexisting Mahaim and Kent Pathways

In two patients with Wolff-Parkinson-White syndrome, we observed the unusual coexistence of functional Mahaim and accessory atrioventricular pathways. In the first patient, three types of reciprocating tachycardia were demonstrable: (1) anterograde conduction over the atrioventricular (AV) node with right bundle branch block (RBBB) and retrograde conduction via a right-sided atrioventricular accessory pathway; (2) anterograde conduction through the AV node with RBBB and retrograde conduction via two (right-sided and septal) anomalous pathways; and (3) anterograde conduction through nodoventricular fibers and retrograde conduction over a right-sided accessory pathway. In the second patient the reentry circuit was comprised of AV node fasciculoventricular fiber in an anterograde direction and a right-sided accessory pathway in a retrograde direction. We believe this to be the first report of triple accessory pathways, consisting of two atrioventricular and one nodoventricular connection, demonstrated by intracardiac electrophysiologic study.     

"V-H-A Pattern" as a criterion for the differential diagnosis of atypical AV nodal reentrant tachycardia from AV reciprocating tachycardia

BACKGROUND: During ventricular extrastimulation, His bundle potential (H) following ventricular (V) and followed by atrial potentials (A), i.e., V-H-A, is observed in the His bundle electrogram when ventriculo-atrial (VA) conduction occurs via the normal conduction system. We examined the diagnostic value of V-H-A for atypical form of atrioventricular nodal reentrant tachycardia (AVNRT), which showed the earliest atrial activation site at the posterior paraseptal region during the tachycardia. METHODS: We prospectively examined the response of VA conduction to ventricular extrastimulation during basic drive pacing performed during sinus rhythm in 16 patients with atypical AVNRT masquerading atrioventricular reciprocating tachycardia (AVRT) utilizing a posterior paraseptal accessory pathway and 21 with AVRT utilizing a posterior paraseptal accessory pathway. Long RP' tachycardia with RP'/RR > 0.5 was excluded. The incidences of V-H-A and dual AV nodal physiology (DP) were compared between atypical AVNRT and AVRT. RESULTS: V-H-A was demonstrated in all the 16 patients (100%) in atypical AVNRT and in only 1 of the 21 (5%) in AVRT (P < 0.001). DP was demonstrated in 10 patients (63%) in atypical AVNRT and in 4 (19%) in AVRT (P < 0.05). The sensitivity of V-H-A for atypical AVNRT was higher than that of DP (P < 0.05). Positive and negative predictive values were 94% and 100%, respectively, for V-H-A and 71% and 74%, respectively, for DP. CONCLUSIONS: The appearance of V-H-A during ventricular extrastimulation is a simple criterion for differentiating atypical AVNRT masquerading AVRT from AVRT utilizing a posterior paraseptal accessory pathway.     

Atrioventricular nodal re-entrant tachycardia with two functionally discrete fast pathways

We present a case with two forms of atrioventricular nodal re-entrant tachycardia (AVNRT) that revealed similar H-A-V sequences, but could be differentiated only by their retrograde atrial activation sequences. Both tachycardias were induced following anterograde slow pathway conduction, suggesting the slow pathway as the anterograde limb of the re-entry circuit. The earliest atrial activation site of one form was in the same region of the bundle of His as that of the common type of AVNRT, while that of the other form was the ostium of the coronary sinus. Properly timed extra-stimuli delivered from the atrium or ventricle during the latter tachycardia penetrated through the fast pathway without resetting the tachycardia cycle length. These rare phenomena suggest the existence of two functionally discrete fast pathways, of which the alternative pathway alters to become the more predominant retrograde limb according to time and circumstances.     

Specificity of Retrograde Conduction in Screening for Atrioventricular Nodal Reentrant Tachycardia

Baseline AV conduction properties (antegrade and retrograde) are often used to assess the presence of dual AV nodal physiology or concealed AV accessory pathways. Although retrograde conduction (RET) is assumed to be a prerequisite for AV nodal reentrant tachycardia (AVNRT), its prevalence during baseline measurements has not been evaluated. We reviewed all cases of AVNRT referred for radiofrequency ablation to determine the prevalence of RET at baseline evaluation and after isoproterenol infusion. Results: Seventy-three patients with AVNRT underwent full electrophysiological evaluation. Sixty-six patients had manifest RET and inducible AVNRT during baseline atrial and ventricular stimulation. Seven patients initially demonstrated complete RET block despite antegrade evidence of dual AV nodal physiology. In 3 of these 7 patients AVNRT was inducible at baseline despite the absence of RET. In the other four patients isoproterenol infusion was required for induction of AVNRT, however only 3 of these 4 patients developed RET. One of these remaining patients had persistent VA block after isoproterenol. Conclusions: The induction of AVNRT in the absence of RET suggests that this is not an obligatory feature of this arrhythmia. Therefore, baseline AV conduction properties are unreliable in assessing the presence of AVNRT and isoproterenol infusions should be used routinely to expose RET and reentrant tachycardia.     

Mechanism of Double Ventricular Response to a Single Atrial Extrastimulus in Patients with Wolff-Parkinson-White Syndrome

The purpose of this study is to elucidate electrophysiological determinants of double ventricular response (DVR) to a single atrial extrastimulus in Wolff-Parkinson-White (WPW) syndrome. DVR was observed in 5 (3.4%) out of 146 consecutive patients with WPW syndrome. The site of accessory pathway was located in left lateral free wall in four patients and posterior septum in one. DVR was induced by extrastimulus from coronary sinus in four patients with left-sided accessory pathway, and from both coronary sinus and high right atrium in a patient with septal accessory pathway. However, it was not possible to induce DVR from high right atrium in patients with left-sided accessory pathway, because 50 to 80 ms are needed for intra-atrial conduction from high right atrium to coronary sinus. Critical prolongation of normal AV conduction allowing DVR was seen in the slow pathway of AV node in four patients. In the remaining patients requisite conduction delay occurred in both AV node and His-Purkinje system. Single right ventricular extrastimulus could easily elicit orthodromic AV reciprocating tachycardia or echo beat in four out of five patients and incremental ventricular stimulation induced it in the remaining patient, indicating the presence of retrograde block in the normal AV pathway. As requisites of DVR to a single atrial extrastimulus in WPW syndrome: (1) slow antegrade conduction and retrograde block in the normal AV pathway; and (2) stimulation site in the vicinity of accessory pathway, are needed.     

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.     

Atrioventricular Nodal Supraventricular Tachycardia with 2:1 Block above the Bundle of His

A patient with narrow complex supraventricular tachycardia underwent electrophysiological study at which time a tachycardia was initiated which had 2:1 AV conduction, with block occurring above the His bundle. The modes of tachycardia initiation, as well as the responses to atrial and ventricular premature depolarizations during tachycardia, made a diagnosis of atrioventricular nodal reentry as the tachycardia mechanism. The unusual finding of 2:1 supra-His block suggests the presence of tissue situated between the tachycardia circuit and His bundle, and effectively excludes the possibility of a His-atrial bypass tract as the retrograde limb of the tachycardia circuit.     

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.     

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.     

Diagnostic Approach to Narrow Complex Tachycardia with VA Block

Narrow complex tachycardia with VA block is rare. The differential diagnosis usually consists of (1) junctional tachycardia (JT) with retrograde block: (2) AV nodal reentrant tachycardia (AVNRT) with proximal common pathway block; and finally (3) nodofascicular tachycardia using the His-Purkinje system for antegrade conduction and a nodofascicular pathway for retrograde conduction. Analysis of tachycardia onset and termination, the effect of bundle branch block on tachycardia cycle length, and the response to atrial and ventricular premature depolarization must be carefully done. Making the correct diagnosis is crucial as the success rate in eliminating the tachycardia will depend on tachycardia mechanism.     

Variable Effects of Adenosine on Retrograde Conduction in Patients with Atrioventricular Nodal Reentry Tachycardia

Adenosine has been demonstrated to reliably produce transient block of atrioventricular nodal (AVN) conduction, and has been advocated as a method of differentiating retrograde conduction via the atrioventricular node from accessory pathway conduction. However, the response of retrograde AVN to adenosine in patients with typical atrioventricular nodal reentry tachycardia (AVNRT) remains unclear. We evaluated 13 patients (mean age 45 ± 20 years) with typical AVNRT prior to AVN modification. During right ventricular pacing, a rapid bolus of adenosine (0.2 mg/kg; maximum 18 mg) was administered. Adenosine sensitivity, defined by transient ventriculoatrial block, was observed in six patients, while in seven patients ventriculoatrial conduction was unaffected. An adenosine bolus administered during sinus rhythm or atrial pacing resulted in antegrade atrioventricular block in all the adenosine resistant patients in whom this was performed (n = 6). Comparisons of AVN electrophysiological characteristics between the adenosine sensitive and adenosine resistant patients were performed. There was no difference with respect to ventriculoatrial effective refractory period, ventriculoatrial Wenckebach, AVNRT cycle length, and His to atrial echo interval in AVNRT. However, there was a trend toward a longer antegrade fast pathway ERP in the adenosine sensitive group (P = 0.07). Electrophysiological properties do not predict retrograde AVN adenosine sensitivity. Adenosine does not cause retrograde AVN block in all patients with AVNRT, and therefore cannot reliably distinguish between retrograde conduction via the AVN or an accessory pathway.     

Analysis of Atrioventricular Nodal Reentrant Tachycardia with Variable Ventriculoatrial Block: Characteristics of the Upper Common Pathway

Background: The precise nature of the upper turnaround part of atrioventricular nodal reentrant tachycardia (AVNRT) is not entirely understood.
Methods: In nine patients with AVNRT accompanied by variable ventriculoatrial (VA) conduction block, we examined the electrophysiologic characteristics of its upper common pathway.
Results: Tachycardia was induced by atrial burst and/or extrastimulus followed by atrial-His jump, and the earliest atrial electrogram was observed at the His bundle site in all patients. Twelve incidents of VA block: Wenckebach VA block (n = 7), 2:1 VA block (n = 4), and intermittent (n = 1) were observed. In two of seven Wenckebach VA block, the retrograde earliest atrial activation site shifted from the His bundle site to coronary sinus ostium just before VA block. Prolongation of His-His interval occurred during VA block in 11 of 12 incidents. After isoproterenol administration, 1:1 VA conduction resumed in all patients. Catheter ablation at the right inferoparaseptum eliminated antegrade slow pathway conduction and rendered AVNRT noninducible in all patients.
Conclusion: Selective elimination of the slow pathway conduction at the inferoparaseptal right atrium may suggest that the subatrial tissue linking the retrograde fast and antegrade slow pathways forms the upper common pathway in AVNRT with VA block.     

Unusual Mechanism in the Initiation of the Paroxysmal Supraventricular Tachycardia in a Patient with WPW Syndrome

A heretofore unreported unusual mechanism in the initiation of the paroxysmal supraventricular tachycardia (PSVT) in a patient with WPW (Wolff-Parkinson-White) syndrome was observed using His bundle recordings. The patient initially had some degree of AV conduction disturbance at the level of the AV node. A premature atrial impulse initially activated the ventricle exclusively through the accessory pathway and the same impulse re-excited the ventricle via the AV nodal-His axis after finishing the pure pre-excitation with marked prolongation of the AH and the HV intervals. After finishing this double ventricular response it traversed to the atrium to produce the PSVT.     

Pacemaker-mediated Tachycardias: A New Modality of Treatment

Three Patients with pacemaker interactive drug resistant tachycardia underwent invasive electrophysiological studies. In the first patient, the retrograde conduction of the artificial reciprocating tachycardia was provided by two right-sided accessory pathways and the antegrade conduction by an atrial synchronous plus generator. In addition, AV nodal tachycardia occurred alternately. In the second patient with intermittent atrial flutter, the AV node and, coincidentally, an AV sequential pulse generator provided high-rate antegrade conduction to the ventricles. In the third patient with surgical complete heart block, intermittent AV-nodal tachycardia induced retrograde atrial activation while an atrial synchronous pacemaker provided the antegrade conduction. Electrode catheter exploration of the heart allowed localization and closed-chest ablation of the accessory pathways or AV node by delivering two to seven 200-Joule direct-current shocks through the appropriate electrode of the exploring catheter, Thereby, pacemaker-mediated arrhythmias could be controlled in these patients in the follow-up of 6 to 8 months.     

Direct Endocardial Recording and Catheter Ablation of an Accessory Pathway in a Patient with Incessant Supraventricular Tachycardia

A patient presented with incessant supraventricular tachycardia due to a concealed accessory pathway. The His bundle electrocardiogram showed a large discrete accessory pathway potential following ventricular activation and resulting in retrograde atrial activation. Percutaneous catheter ablation in the region of the accessory pathway potential left nodal conduction intact but prevented retrograde activation of the atria. Symptomatic tachycardia has not recurred. Direct endocardial recording of accessory pathway potentials is rare hut may offer the opportunity for catheter ablation.     

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.     

New Observations on Decremental Atriofascicular and Nodofascicular Fibers: Implications for Catheter Ablation

Introduction: The purpose of this study was to characterize the anatomy and physiology of accessory pathways that exhibit anterograde decremental conduction. Results: Among 100 consecutive patients with an accessory pathway undergoing electrophysiological study, six individuals with decremental anterograde accessory pathway conduction were identified. Anterograde accessory pathway effective refractory periods and conduction curves were assessed by atrial extrastimulus testing. Atrial pace mapping and ventricular activation sequence mapping were used to define accessory pathway origin and insertion. Surgical ablation (N = 1) or radiofrequency catheter ablation (N = 3) was performed based on accessory pathway anatomy as determined during electrophysiological study. Four of 6 patients had gaps in anterograde accessory pathway conduction. Two patients had evidence of functional longitudinal dissociation in the accessory pathway. Five of 6 patients had atriofascicular fibers with an atrial rather than AV nodal site of origin of their decrementally conducting accessory pathway and with distal insertions in the right bundle branch. Among these five patients, a right posterior atrial origin was nearly as common as a right anterior atrial origin. One patient had a true nodofascicular fiber that arose from the AV node, inserting distally into the left bundle branch. Conclusion: Most accessory pathways with anterograde decremental conduction arise from the right anterior or right posterior atrium, not the AV node. A gap in anterograde accessory pathway conduction and functional longitudinal dissociation are common in such accessory pathways. Surgical or catheter ablation of such pathways is effective when directed at the atrial origin of the accessory pathway. True nodofascicular fibers arising from the AV node are rare. These may insert distally in the left ventricle. Catheter ablation of the proximal origin of such fibers is likely to result in complete AV block.     

Unmasking of Retrograde Conduction by Isoproterenol in a Concealed Accessory Pathway

A 52-year-old female with no structural heart disease presented with a right bundle branch block (RBBB)/right axis deviation tachycardia with a cycle length of 300 msec. P waves were not discernible on the surface ECG. Baseline electrophysiology study in the drug-free state revealed no evidence for anterograde or retrograde conducting accessory pathways (APs) or for dual AV node physiology. Retrograde VA block with AV dissociation was present at a ventricular paced cycle length of 600 msec (sinus cycle length of 635–700 msec). AV nodal Wenckebach occurred during decremental atrial pacing at a cycle length of 300 msec. During isoproterenol administration, a left lateral AP with retrograde only conduction became manifest with 1:1 VA conduction to 380 msec. No anterograde AP conduction was present. Orthodromic reciprocating tachycardia with a cycle length of 285–315 msec was easily induced. We conclude that total functional conduction block can exist in APs, and unmasking of total conduction block can be accomplished with isoproterenol. All patients with undiagnosed tachycardias should have full repeat stimulation studies during adrenergic stimulation if the initial baseline evaluation is nondiagnostic.     

Dual Accessory Nodoventricular Pathways: Role in Paroxysmal Wide QRS Reciprocating Tachycardia

Clinical electrophysiological study in an otherwise healthy 21 -year-old male with paroxysmal wide QRS tachycardia (cycle length 300 ms. heart rate 200/min) suggested the presence of two nodoventricular (NV) bypass connections. The first NV connection pre-excited the base of the interventricularseptum (NVs), as evidenced by a short HV interval during sinus rhythm (15–20 ms), with local ventricular activation occurring earlier at the septal base than at either the right ventricular apex or the base of the left vcntricle. The second NV connection appeared to connect the AV junction with the right ventricle (NV_RV). Intracardiac recordings from a portion of the right-bundle branch of the interventricular conduction system demonstrated right ventricular pre-excitation by NV_RV during both atrial pacing and reciprocating tachycardia. The latter finding supported participation of NV_RV in the tachycardia. Further, following exclusion of atrial participation in the arrhythmia, premature depolarization of the right ventricle and interventricularseptum appeared to advance the tachycardia without altering the timing of His bundle depolarization, implicating NV_S in the retrograde limb of a re-entry circuit. Consequently, this study demonstrated the presence of two NV connections and provided further support to the concept that NV accessory bypass connections may comprise portions of a re-entry pathway during reciprocating tachycardia in man.