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.     

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.     

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.     

"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.     

Rapid atrial pacing: a useful technique during slow pathway ablation

BACKGROUND: Catheter ablation is the treatment of choice for atrioventricular nodal reentrant tachycardia (AVNRT) with a success rate of 95-98%. The appearance of junctional rhythm during radiofrequency (RF) application to the slow pathway has been consistently reported as a marker for the successful ablation of AVNRT. Ventriculoatrial (VA) conduction during junctional rhythm has been used by many as a surrogate marker of antegrade atrioventricular nodal (AVN) function. However, VA conduction may not be an accurate or consistent marker for antegrade AVN function and reliance on this marker may leave some patients at risk for antegrade AVN injury. OBJECTIVE: The purpose of this study is to describe a technique to ensure normal antegrade AVN function during junctional rhythm at the time of RF catheter ablation of the slow pathway. METHODS: Retrospective review of all patients less than 21 years old who underwent RF ablation for AVNRT at our institution from January 2002 to July 2005. During RF applications, immediately after junctional rhythm was demonstrated, RAP was performed to ensure normal antegrade AVN function. Postablation testing was performed to assess AVN function and tachycardia inducibility. RESULTS: Fifty-eight patients underwent RF ablation of AVNRT during the study period. The mean age +/- SD was 14 +/- 3 years (range: 5-20 years). The weight was 53 +/- 15 Kg (range: 19-89 Kg). The preablation Wenckebach cycle length was 397 +/- 99 msec (range: 260-700 msec). Fifty-four patients had inducible typical AVNRT, and four patients had atypical tachycardia. The mean tachycardia cycle length +/- SD was 323 +/- 62 msec (range: 200-500 msec). Patients underwent of 8 +/- 7 total RF applications (median: 7; range 1 to 34), for a total duration of 123 +/- 118 seconds (median: 78 sec, range: 20-473 sec). Junctional tachycardia was observed in 52 of 54 patients. RAP was initiated during junctional rhythm in all patients. No patient developed any degree of transient or permanent AVN block. Following ablation, the Wenckebach cycle length decreased to 364 +/- 65 msec (P < 0.01). Acutely successful RF catheter ablation was obtained in 56 of 58 patients (96%). CONCLUSION: Rapid atrial pacing during radiofrequency catheter ablation of the slow pathway is a safe alternative approach to ensure normal AVN function.     

Exact Location of the Branching Bundle in the Living Heart

Aims: The His bundle electrogram is believed to reflect the exact location of the His bundle. However, the distinction between distal His bundle potential and proximal right bundle branch potential is challenging. The aim of this study was to pinpoint the location of the branching point of the His bundle, and to compare that site with the site of recording of the largest His bundle electrogram (LH) during sinus rhythm.
Methods: We hypothesized that the site of earliest His activation (EH) during retrograde conduction via the left bundle branch is the branching point. We studied 15 nonconsecutive patients (mean age = 40 ± 22 years; eight men). We performed a programmed stimulation from right ventricular apex until retrograde right bundle branch block appeared. At that point we measured (1) the distance between antegrade LH site and retrograde EH site and (2) the atrial-to-ventricular amplitude ratio (A/V ratio) at both sites.
Results: EH was recorded at the proximal electrode of the His bundle catheter in all patients. Mean distance between EH and LH was 9.8 ± 2.5 mm. The mean A/V ratios at the EH site and the LH site were 1.01 ± 0.42 and 0.08 ± 0.06, respectively.
Discussion: This study showed that the EH site is located approximately 10-mm proximal to the LH site. The mean A/V ratio at the EH site during sinus rhythm is approximately 1.0. These observations suggest that the majority of His potentials reflect proximal right bundle activation. Before delivering radiofrequency energy in the para-Hisian area, attention should be paid to the presence of a His potential and to the A/V ratio, rather to the amplitude of the His electrogram.     

Double Atrial Responses to a Single Ventricular Impulse in Long RP' Tachycardia

Double atrial responses (DARs) to a single ventricular impulse have been described in patients with long RP' tachycardia. To define the determinants for the occurrence of DARs. 8 cases with long RP' tachycardia were examined. The mechanism of long RP' tachycardia was the orthodromic atrioventricular reciprocating tachycardia (AVRT) involving a slow conducting concealed accessory pathway in 4 cases and uncommon (fast-slow) type of atrioventricular nodal reentrant tachycardia (AVNRT) in the other 4 cases. Programmed and rapid ventricular pacing was performed during sinus rhythm and also rapid ventricular pacing during tachycardia (i.e., entrainment). The retrograde effective refractory period (ERP) and the retrograde maximal 1:1 conduction rate of the fast and slow conducting pathways were examined. In 1 of the 4 cases with AVRT, DARs were observed during programmed and rapid ventricular pacing, performed during sinus rhythm and also during entrainment. In 1 of the 4 cases with AVNRT, DARs were observed only during entrainment. The determinants of DARs in cases with long RP' tachycardia were: (1) presence of two different retrogradely conducting pathways; (2) short ERP of the retrograde fast and slow conducting pathways and a short minimal pacing cycle length at which 1:1 ventriculoatrial conduction occurs via these pathways; (3) crucial conduction delay in the slow conducting pathway: and (4) preexisting antegrade unidirectional block in the slow conducting pathway or the antegrade block in the slow conducting pathway produced by collision with a previous retrograde impulse during entrainment.     

Relation between the AH interval and the ablation site in patients with atrioventricular nodal reentrant tachycardia

The determinants of slow pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT) are still unknown, and great differences in the AH interval during slow pathway conduction are observed between patients. In 35 patients with typical AVNRT who underwent successful slow pathway ablation (defined as complete elimination of dual pathway physiology), the A2H2 interval at the "jump" during programmed atrial stimulation and the AH interval during AVNRT (as a reflection of slow pathway conduction time) and the fluoroscopic distance between the successful ablation site and the His-bundle recording site and between the coronary sinus ostium (CSO) and the His-bundle recording site were determined. The mean (+/- SEM) AH interval during slow pathway conduction was 323 +/- 12 ms with programmed stimulation and 310 +/- 10 ms during AVNRT. The mean number of energy applications was 8 +/- 1 (range 1-21). The mean distances between (1) the successful ablation site and the His bundle recording site and (2) between the CSO and the His-bundle recording site were 24 +/- 1 and 28 +/- 1 mm in the RAO and 23 +/- 1 and 28 +/- 1 mm in the LAO projections, respectively. The AH interval during slow pathway conduction correlated significantly with the distance between the successful ablation site and the His-bundle (P < 0.001) but not with the distance between CSO and His-bundle recording site. There is a significant correlation between the AH interval during slow pathway conduction and the distance of the successful ablation site from the His bundle. This relationship (1) suggests that, in addition to functional factors, anatomic factors influence slow pathway conduction and (2) may be helpful in determining the initial energy application site during slow pathway ablation.     

Double Ventricular Responses to a Single Atrial Depolarization in a Patient with Dual AV Nodal Pathways

Electrophysiological study was performed in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). Double ventricular responses through dual AV nodal pathways were observed by atrial extrastimulus technique followed by initiation of AVNRT. The difference in conduction time between the slow and fast AV nodal pathways was longer than 320 msec. A ventricular extrastimulus delivered during sinus rhythm, which was not followed by ventriculoatrial conduction, also induced AVNRT. These findings indicated the presence of an antegrade critical delay and retrograde block in the slow AV nodal pathway, criteria necessary for the occurrence of a double ventricular response.     

Role of Specialized Conducting Fibers in the Genesis of "AV Nodal" Re-entry Tachycardia

Recent reports have suggested that an accessory bypass tract connecting the His bundle to the atrium (His-atrial fiber) may form the retrograde limb of "AV nodal" re-entry tachycardia (AVNRT). We studied 12 patients with AVNRT in whom the presence of an accessory atrioventricular fiber (Kent fiber) was excluded. We investigated the possibility of a His-atrial (H-A) fiber by examining the nature of retrograde conduction and by assessing the necessity of the atrium as a part of the re-entry pathway. Retrograde conduction through the A V node had characteristics similar to retrograde conduction over a Kent bundle; that is, retrograde conduction times were short and did not vary. With echo beats (Ae) evoked during antegrade refractory period determination early premature beats resulted in prolongation of the AH interval with no change in HA_e interval. During AVNRT the A'H':H'A' ratios ranged from 2.0–8.0 (mean 4.0 ± 1.8) and with changes in tachycardia cycle length the H'A interval remained constant. During retrograde refractory period determination, delay occurred below the AV node without change in the H-A interval. Estimations of retrograde conduction times by all 3 methods were not significantly different (p > 0.2). The pattern of retrograde conduction suggests anatomical or functional specialized fibers as the retrograde limb of the tachycardia. The necessity of the atria as a part of the re-entry circuit was assessed by the introduction of atrial premature beats (APBs) in the region of the atrial septum during AVNRT in 10 patients. APBs pre-excited the atria by 40–140 ms without changing the cycle length of the tachycardia, providing strong evidence against the participation of an extranodal His-atrial fiber in AVNRT, In conclusion, retrograde conduction during AVNRT appears to take place over a functional or anatomical specialized fiber within the AV node and not over an extranodal H-A fiber.     

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.     

Determination of Repetitive Slow Pathway Conduction for Evaluation of the Efficacy of Radiofrequency Ablation in AVNRT

LUKAC, P., et al.: Determination of Repetitive Slow Pathway Conduction for Evaluation of the Efficacy of Radiofrequency Ablation in AVNRT. Aims: To determine whether the loss of repetitive slow pathway conduction identifies a successful radiofrequency ablation of atrioventricular nodal reentry tachycardia (AVNRT). Methods and results: Thirty nine consecutive patients undergoing ablation of AVNRT using the slow pathway approach were included. At baseline and after each radiofrequency application with an episode of junctional rhythm, repetitive slow pathway conduction was assessed as follows: Effective refractory period of the fast pathway was determined. The coupling interval of the first atrial extrastimulus (A2) was set at 30 ms below the effective refractory period of the fast pathway to ensure its conduction via the slow pathway. The second atrial extrastimulus (A3) was introduced at progressively longer coupling intervals starting from 200 ms until: (1) it propagated to the His bundle or (2) an anterogradely blocked AV nodal echo of A2 appeared before a conducted A3 depolarized the atrium in the His bundle electrogram. The response was termed repetitive slow pathway conduction if A3 was conducted with an   AH > 200 ms   . Application was considered successful if no AVNRT could be induced. Repetitive slow pathway conduction was present after 1 of 39 successful and after 34 of 40 ineffective applications   (P < 0.0001)   . Repetitive slow pathway conduction identified a successful application with 97% sensitivity, 86% specificity, 86% positive predictive value, and 97% negative predictive value. Conclusion: The presence of repetitive slow pathway conduction identifies an unsuccessful application with a clinically meaningful negative predictive value. (PACE 2003; 26[Pt. I]:827–835)     

The electrophysiological characteristics in patients with ventricular stimulation inducible fast-slow form atrioventricular nodal reentrant tachycardia

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) can usually be induced by atrial stimulation. However, it seldom may be induced with only ventricular stimulation, especially the fast-slow form of AVNRT. The purpose of this retrospective study was to investigate the specific electrophysiological characteristics in patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation. METHODS: The total population consisted of 1,497 patients associated with AVNRT, and 106 (8.4%) of them had the fast-slow form of AVNRT and 1,373 (91.7%) the slow-fast form of AVNRT. In patients with the fast-slow form of AVNRT, the AVNRT could be induced with only ventricular stimulation in 16 patients, Group 1; with only atrial stimulation or both atrial and ventricular stimulation in 90 patients, Group 2; and with only atrial stimulation in 13 patients, Group 3. We also divided these patients with slow-fast form AVNRT (n = 1,373) into two groups: those that could be induced only by ventricular stimulation (Group 4; n = 45, 3%) and those that could be induced by atrial stimulation only or by both atrial and ventricular stimulation (n = 1.328, 97%). RESULTS: Patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a lower incidence of an antegrade dual AVN physiology (0% vs 71.1% and 92%, P < 0.001), a lower incidence of multiple form AVNRT (31% vs 69% and 85%, P = 0.009), and a more significant retrograde functional refractory period (FRP) difference (99 +/- 102 vs 30 +/- 57 ms, P < 0.001) than those that could be induced with only atrial stimulation or both atrial and ventricular stimulation. The occurrence of tachycardia stimulated with only ventricular stimulation was more frequently demonstrated in patients with the fast-slow form of AVNRT than in those with the slow-fast form of AVNRT (15% vs 3%, P < 0.001). Patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a higher incidence of retrograde dual AVN physiology (75% vs 4%, P < 0.001), a longer pacing cycle length of retrograde 1:1 fast and slow pathway conduction (475 +/- 63 ms vs 366 +/- 64 ms, P < 0.001; 449 +/- 138 ms vs 370 +/- 85 ms, P = 0.009), a longer retrograde effective refractory period of the fast pathway (360 +/- 124 ms vs 285 +/- 62 ms, P = 0.003), and a longer retrograde FRP of the fast and slow pathway (428 +/- 85 ms vs 362 +/- 47 ms, P < 0.001 and 522 +/- 106 vs 456 +/- 97 ms, P = 0.026) than those with the slow-fast form of AVNRT that could be induced with only ventricular stimulation. CONCLUSION: This study demonstrated that patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a different incidence of the antegrade and retrograde dual AVN physiology and the specific electrophysiological characteristics. The mechanism of the AVNRT stimulated only with ventricular stimulation was supposed to be different in patients with the slow-fast and fast-slow forms of AVNRT.     

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.     

Alternate Ventriculo-Atrial Wenckebach Conduction during Ventricular Tachycardia

Although pacing-induced ventriculo-atrial (VA) Wenckebach conduction has been previously described, the occurrence of this phenomenon during ventricular tachycardia has received little attention. The latter is defined as 2:1 VA block in which the conducted beats show progressive lengthening of VA conduction until the sequence is terminated by two or three blocked ventricular beats. This phenomenon was observed in a 16-year-old boy who underwent electrophysiologic study for ventricular tachycardia as a late complication of surgical correction of tetralogy of Fallot. During pacing-induced ventricular tachycardia with a morphology similar to that of the spontaneous tachycardia, 8:4 alternating VA block was observed. This sequence suggested that the AV node was the site of block, the 2:1 block being located at the upper level, and the VA Wenckebach block at the lower level. Alternate VA Wenckebach conduction appears as a possible cause of variation in atrial depolarization intervals during ventricular tachycardias with short cycle lengths.     

Mapping and Ablation of Atypical AVNRT from the Morphologic Left Atrium in a Patient with Dextrocardia and Situs Inversus

A 75‐year‐old woman with dextrocardia, situs inversus, and subpulmonic outflow obstruction presented with recurrent supraventricular tachycardia (SVT). This SVT was easily inducible during electrophysiology study, and pacing maneuvers during SVT were consistent with atypical, slow‐slow atrioventricular nodal reentrant tachycardia (AVNRT). The His bundle was identified in the low postero‐septal morphologic right atrium, at the typical anatomic site for slow pathway ablation of AVNRT. Mapping of the retrograde earliest atrial electrogram during AVNRT localized this site to the mid‐septal morphologic left atrium, and cryoablation at this site terminated the AVNRT and rendered it noninducible. (PACE 2010; e106–e109)     

Narrow Complex Tachycardia with VA Block: Diagnostic and Therapeutic Implications

To review our experience with cases of narrow complex tachycardia with VA block, highlighting the difficulties in the differential diagnosis, and the therapeutic implications. Prior reports of patients with narrow complex tachycardia with VA block consist of isolated case reports. The differential diagnosis of this disorder includes: automatic junctional tachycardia, AV nodal reentry with final upper common pathway block, concealed nodofascicular (ventricular) pathway, and intra-Hissian reentry. Between June 1994 and January 1996, six patients with narrow complex tachycardia with episodes of ventriculoatrial block were referred for evaluation. All six patients underwent attempted radiofrequency ablation of the putative arrhythmic site. Three of six patients had evidence suggestive of a nodofascicular tract. Intermittent antegrade conduction over a left-sided nodofascicular tract was present in two patients and the diagnosis of a concealed nodofascicular was made in the third patient after ruling out other tachycardia mechanisms. Two patients had automatic junctional tachycardia, and one patient had atroventricular nodal reentry with proximal common pathway block. Attempted ablation in the posterior and mid-septum was unsuccessful in patients with nodofascicular tachycardia. In contrast, those with atrioventricular nodal reentry and automatic junctional tachycardia readily responded to ablation. The presence of a nodofascicular tachycardia should be suspected if: (1) intermittent antegrade preexcitation is recorded, (2) the tachycardia can be initiated with a single atrial premature producing two ventricular complexes, and (3) a single ventricular extrastimulus initiates SVT without a retrograde His deflection. The presence of a nodofascicular pathway is common in patients with narrow complex tachycardia and VA block. Unlike AV nodal reentry and automatic junctional tachycardia, the response to ablation is poor.     

Fatigue of the His-Purkinje System During Routine Electrophysiologic Studies

In this report we describe fatigue of the His-Purkinje system during retrograde stimulation of the His bundle by ventricular programmed stimulation. The patient underwent electrophysiologic evaluation for syncope. Antegrade conduction and supraventricular studies were normal with the exception of baseline left bundle branch block. During programmed ventricular stimulation, the patient developed intra-Hisian and infra-Hisian block with symptomatic 3:1 atrioventricular heart block requiring insertion of a permanent pacemaker. This case demonstrates the need for careful study of both antegrade and retrograde conduction properties of the His bundle and atrioventricular node when performing standard His bundle studies in evaluation of syncope.     

Prospective Evaluation Of The Length Of The Lower Common Pathway In The Differential Diagnoss Of Various Forms Of AV Nodal Reentrant Tachycardia

The conduction time over the lower common pathway (LCP) in AVNRT can be assessed by subtracting the H A-interval during tachycardia (HA_t) from that during ventricular pacing at exactly the same cycle length (HAp) (ΔHA = HAp - HAt). tt has been suggested that H-A measurements may help in the differentiation of Slow/Fast from Slow/Slow AVNRT. This study evaluated prospectively in 61 consecutive patients with AVNRT (43 ± 15 y; 46 women, all with antegrade conduction during AVNRT over the slaw pathway) how often a reliable measurement of the length of the LCP could be made, and in how far the results were concordant with mapping criteria for the differentiation of Slow/Fast from Slow/Slow A VNRT. A new para-Hisian pacing technique (using only the His bundle catheter) was applied in all patients. Comparison of HAt and HAp was possible in 44 of the 61 patients (72%). In these 44 patients, HAp was longer than HAt in 12 patients, indicating the presence of a LCP. All patients with ΔHA ≥ 15 ms had earliest retrograde atrial activation in the posterior septum (Slow/Slow AVNRT, n = 6) or simultaneously in the anterior and posterior septum (n = 1). On the other hand, 31 of the 32 patients without evidence of a substantial LCP (ΔHA ≤ 0) had typical Slow/Fast AVNRT. Moreover, although it appears logical for Slow/Fast A VNRT to have a shorter HAt than Slow'Slow A VNRT, an HAp of ≥ 70 ms was a better discriminator between the two forms of AVNRT than any HAt value. Therefore, ΔHA ≥ 15 ms (sens. ≥86%; spec. ≥97%) or HAp ≥ 70 ms (sens. = 100%; spec. ≥89%) were highly indicative for the Slow/Slow variant of AVNRT. Using a para-Hisian pacing technique, H-A measurements can be performed in 72% of A VNRT patients. They can be used as an important tool in the differentiation of Slow/Fast and Slow/Slow A VNRT.     

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.