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.     

Supernormal Conduction in the Left Bundle Branch Unmasked by the Linking Phenomenon

This presentation reflects a case of phase-3 left bundle branch block (LBBB). Analysis reveals that relatively early QRS complexes are wide, whereas beats occurring later than a critical time are narrow. There are, however, two unexpected phenomena: (1) an overlap occurs between the range of R-R intervals resulting in normal intraventricular conduction and the range of R-R intervals resulting in LBBB pattern. Complexes that follow a wide beat are often wide although they are associated with relatively long R-R intervals, whereas complexes that follow a normal beat tend to be normal even after relatively short R-R cycles. This is due to concealed retrograde penetration of the bundle branch that is blocked in anterograde direction (the so-called linking phenomenon). (2) Some early supraventricular impulses, paradoxically, resulted in normal intraventricular conduction. The phenomenon is a manifestation of supernormal LBB conduction, and only occurs following a wide QRS complex associated with retrograde activation of the LBB. The linking phenomenon reveals or unmasks the supernormal phase of LBB conduction. Following a retrograde and delayed activation of the LBB, the refractory period of the bundle branch is postponed, in such a way that a supraventricular impulse is allowed to occur during the early phase of supernormal conduction.     

Linking: A Mechanism of Intermittent Preexcitation in the Wolff-Parkinson-White Syndrome

MIDDLEKAUFF, H.R., ET AL.: Linking: A Mechanism of Intermittent Preexcitation in the Wolff-Parkinson-White Syndrome. Intermittent preexcitation in the Wolff-Parkinson-White syndrome has been equated with a long accessory pathway refractory period and long R-R interval between preexcited beats in atrial fibrillation and therefore a low risk for sudden death. A case of Wolff-Parkinson-White syndrome in which preexcitation became intermittent following procainamide infusion, with only moderate prolongation of the accessory pathway refractory period but marked prolongation of the shortest preexcited R-R interval in atrial fibrillation, is described. Programmed ventricular and atrial stimulation demonstrated that intermittent preexcitation was caused by concealed conduction producing a linking phenomenon, facilitated by the antiarrhythmic drug. Linking due to concealed retrograde penetration of a propagated impulse into the accessory pathway may contribute to the disparity between accessory pathway refractory period and shortest preexcited R-R interval in atrial fibrillation in some patients and may be a confounding factor in the interpretation of noninvasive tests of accessory pathway conduction.     

Retrograde Supernormal Conduction, Gap Phenomenon in Concealed Accessory Atrioventricular Pathways

We present four patients with the Wolff-Parkinson-White syndrome who exhibited retrograde supernormal conduction or gap phenomenon in concealed accessory pathways. In the first patient, ventricular extrastimulus testing revealed retrograde block at the coupling interval of 520 msec and reappearance of conduction at the coupling interval of 370 msec. In a second patient, 1:1 retrograde conduction was not present but supernormal conduction was demonstrated at coupling intervals of 360 msec to 310 msec during the ventricular extrastimulus testing when the basic drive consisted of atrioventricular (AV) simultaneous pacing. In a third patient, ventricular extrastimulus testing demonstrated retrograde conduction through the accessory pathway only at coupling intervals of 400 msec to 360 msec. In a fourth patient, retrograde block occurred at the coupling interval of 340 msec and retrograde "slow" conduction reappeared at coupling intervals of 300 msec to 250 msec (gap phenomenon) only when the basic drive consisted of AV simultaneous pacing. Thus, concealed accessory pathways may exhibit retrograde supernormal conduction or gap phenomenon. Ventricular extrastimulus testing consisting of AV simultaneous pacing during the basic drive may facilitate demonstration of these unusual properties.     

Unusual Mechanism of PR Interval Variation and Nonreentrant Supraventricular Tachycardia as Manifestation of Simultaneous Anterograde Fast and Slow Conduction Through Dual Atrioventricular Nodal Pathways

Noninvasive recordings in a 69-year-old woman showed two distinct PR intervals of about 0.21 and 0.58 s, suggestive of dual AV nodal conduction. Various unusual mechanisms of transition from short to long and from long to short conduction intervals and phenomena of concealed conduction were due to the presence of two functionally separated intranodal pathways. Refractoriness of the slow pathway was associated with bradycardia. Episodes of tachycardia exhibited a one-to-two relationship between P-waves and ventricular activations as a consequence of simultaneous anterograde fast and slow conduction leading to double ventricular responses to single P-waves.     

Reentrant Ventricular Arrhythmias in the Late Myocardial Infarction Period: 14. Mechanisms of Resetting, Entrainment, Acceleration, or Termination of Reentrant Tachycardia by Programmed Electrical Stimulation

The mechanisms of resetting, entrainment, acceleration, or termination of reentrant ventricular tachycardia by programmed electrical stimulation were studied in the canine post-infarction model. In this model, reentrant circuits were localized in the epicardial layer overlying the infarction and were accessible to detailed mapping by multiplexer techniques. The reentrant circuit has a characteristic figure-eight configuration in the form of two circulating wavefronts around arcs of functional conduction block that coalesce into a slow common reentrant wavefront. Termination of reentrant tachycardia occurred when a stimulated wavefront arrived earlier to a strategically located area in the proximal portion of the zone of slow conduction, before refractoriness expired distally, resulting in conduction block. The three factors that determined if the stimulated wavefront could reach this zone in time for conduction block were: the cycle length of stimulation; the number of stimulated beats; and the site of stimulation. The most optimal situation for stimulated termination of reentry was a critically coupled single stimulus applied to the ischemic zone close to the proximal side of the zone of slow conduction that captured locally and conducted prematurely to the strategic zone for conduction block. When a single stimulated wavefront failed to terminate reentry, one or more subsequent wavefronts succeeded. However, the stimulated train had to be terminated following the beat that interrupted reentry. Otherwise, a subsequent stimulated beat could reinitiate the same reentrant circuit or induce a different circuit. The new circuit could have a shorter revolution time, resulting in tachycardia acceleration, and occasionally degeneration into ventricular fibrillation. Overdrive termination of reentry required both a critical cycle length of stimulation and a critical number of beats in a stimulated train. Otherwise, the stimulated train could establish a new balance of refractoriness and conduction velocity in the reentrant pathway. This could perpetuate the reentrant process at the shorter cycle length of the stimulated train and spontaneous reentry would resume on termination of the train (entrainment). The study provides better understanding of the mechanisms of action of programmed electrical stimulation on reentrant ventricular tachycardia.     

Quantitative Analysis of Concealed Conduction into Accessory Atrioventricular Pathways in Wolff-Parkinson-White Syndrome

Concealed conduction is demonstrated to occur in an accessory AV pathway (AP). To test the hypothesis that anterograde and retrograde concealed conduction in the AP would have different characteristics, 35 consecutive patients with single APs were studied. The anterograde or retrograde ERP of the AP could be determined in 23 of those patients. Anterograde concealed conduction in the AP was assessed in the first 13 patients with retrograde AP conduction (8 APs with retrograde conduction only and 5 with both directions) (group A). Retrograde concealed conduction in the AP was evaluated in the remaining 10 patients with anterograde AP conduction (6 APs with anterograde conduction only and 4 with both directions) (group B). The concealed conduction in the AP was quantified by determining the ERP of the AP using a “probe” extrastimulus (S_p) introduced in the opposite chamber. The ERP was determined both during conventional extrastimulus (S₁S₂ method; ERP_c) and during that with an S_p (S₁S_pS₂ method; ERP_p). The S_p was delivered before or after the last S₁ with various S₁S_p intervals. The ERP_p was determined at each S₁S_p interval. Three distinct patterns in concealed conduction in the AP were noted. In the first pattern, the ERP_p was always shorter than the ERP_c, whereas the reverse relation was noted in the second pattern. The third pattern showed a combination of the two. In group A, only the first pattern was noted. In group B, the first, second, and third patterns were noted in 4, 2, and 4 patients, respectively. The first pattern was noted only in septal APs and the second and third were seen only in left free-wall APs. The second pattern was seen in patients with retrograde AP conduction, whereas the third one was mainly noted in patients without retrograde AP conduction. These observations indicate that anterograde and retrograde concealed conduction in the AP have different characteristics. Shortening of the ERP_p might be due to the “peeling back” phenomenon, and its lengthening might be caused by the presence of the inhomogeneous refractory periods of the AP. (PACE 1997; 20[Pt. I]:1342-1353)     

Delayed Termination of Re-Entrant Atrioventricular Nodal Tachycardia

Termination of atriovontricular nodal (A VN) re-entrant tachycardia by one or two induced premature beats generally occurs within one tachycardia cycle from the last premature beat. Two cases are described in which programmed stimulation during sustained re-entrant AVN tachycardia caused delayed termination in the second or third tachycardia cycle following the extrastimuli. The site of block was the antegrade pathway in one case and the retrograde pathway in the other. The most likely mechanism was induced second degree block in one limb of the tachycardia circuit. Delayed termination provided evidence for concealed penetration of the tachycardia circuit in one case. We conclude that delayed termination of tachycardia is not an indicator of the underlying mechanism of tachycardia. Delayed termination may reveal concealed penetration of the tachycardia circuit. Lastly, in unusual cases programmed stimulation may fail to cause immediate termination of re-entrant tachycardia but may perturb the tachycardia circuit enough to cause termination in subsequent tachycardia cycles.     

Tachycardia and Apparent Sino-Atrial Block Due to Concealed Sinus Node Re-entry

The role of the middle intercavaJ area ("internodal pathway") in the genesis of atrial re-entry was studied using microelectrode techniques and the extra-stimulus method in the rabbit heart. Following surgical interruption of the anterior and posterior internodal tracts, two patterns of re-entry were observed using the middle internodaJ pathway manifesting alternatively as tachy- and brody-arrhythmias. Re-entry which was produced by critically timed extrastimulation at the septal branch of the crista terminalis (CT) caused tachycardia reciprocating between the sinus node (SN) and intercaval area. Spontaneous re-entrant impulses were also observed, particularly following the addition of cedilanid (0.04 mg/L). In addition, in association with critical prolongation of conduction in the sino-septal area, premature discharge of the dominant pacemaker fibers was observed and resulted in the appearance of bradyarrhythmias. These were commonly manifest as bigeminy and trigeminy on the surface septal electrogram. Hence concealed sinus node re-entry could manifest itself as apparent sino-atrial block or sino-atrial re-entry tachycardia.     

Use of Transient Entrainment During Ventricular Tachycardia to Localize a Critical Area in the Reentry Circuit for Ablation

We have previously shown that demonstration of any of the criteria for transient entrainment is possible only when pacing is performed orthodromically proximal to the area of slow conduction in a reentrant circuit with an excitable gap. Pacing orthodromically distal to the area of slow conduction will not permit demonstration of the transient entrainment criteria (concealed entrainment). Additionally, the demonstration of one form of concealed entrainment, namely pacing during a ventricular tachycardia from a site which increases the tachycardia to the pacing rate but does not change the morphology of the QRS complexes, we suggest also identifies the area of slow conduction is a keystone for maintenance of the reentrant circuit, ablation of this area should be expected to provide effective therapy of the tachycardia. Thus, we propose that using the principles of transient entrainment, one should be able to localize a critical area of slow conduction in the reentrant circuit of Q ventricular tachycardia, ablate it effectively, and thereby successfully treat the ventricular tachycardia.     

Theoretical Evaluation of the Rosenblueth Hypothesis

Rosenblueth's hypothesis states that atrioventricular (AV) nodal conduction delay and Wenckebach periodicity of AV transmission are not due to overall decremental conduction within the AV node but are due to a single step delay which is caused by a special element or layer of the AV nodal tissue. This paper discusses some theoretical considerations which allow detailed evaluation of the original hypothesis. Two artificial conduction structures which incorporate the Rosenblueth phenomenon are presented and tested by theoretical experiments that consider the potential of these structures to produce (a) basic pattern of Wenckebach periods, (b) decremental shortening of RR intervals during Wenckebach periods. These experiments are also employed to test whether or not the Rosenblueth concept can be used to explain (c) appropriate dependence of AV conduction changes on the prematurity of atrial depolarizations, and of (d) alternating cycle lengths such as may be seen with atrioventricular reentrant tachycardia. The results of the theoretical considerations show that the original concept of the Rosenblueth hypothesis is sufficient to explain (a) but it cannot be used for realization of (b), (c) and (d). A modification of the original concept complying with both (a) and (b) is proposed. This modified structure can also reproduce (c), but not simultaneously with (b). The experiments show that anisotropy of intra AV nodal conduction may create an electrophysiological mechanism of single-step delay. Different anisotropic conduction structures have to be considered to reproduce phenomenon (d).     

Adenosine-dependent concealed accessory pathway

Adenosine is routinely used during ventricular pacing to exclude the persistence of retrograde accessory pathways conduction after radiofrequency (RF) ablation procedures by blocking conduction over the atrioventricular node. This is the first report of an adenosine-dependent concealed accessory pathway demonstrating transient conduction only after adenosine administration. Our findings may have potential clinical implications in reducing recurrence after accessory pathway ablation. Furthermore, it may add relevant information regarding the ability of adenosine to elicit dormant conduction after RF ablation, a phenomenon that has acquired considerable interest in the era of pulmonary vein isolation.     

Radiofrequency Catheter Ablation of Accessory Pathways During Entrainment of AV Reentrant Tachycardia

Radiofrequency ablation of accessory pathways must sometimes be done during orthodromic atrioventricular reentrant tachycardia when manifest anterograde accessory pathway conduction is absent or retrograde fusion obscures accessory pathway location during ventricular pacing. Unfortunately, abrupt heart rate slowing upon radiofrequency induced termination of atrioventricular reentrant tachycardia often causes catheter dislodgment. We report our experience in circumventing this problem during radiofrequency ablation by using entrainment of atrioventricular reentrant tachycardia. The latter maintains retrograde activation pattern over the accessory pathway while preventing abrupt ventricular rate change. Eight patients (4 men and 4 women, mean age 37.3 ± 17.9) with eleven left-sided accessory pathways were included. Ablation during entrainment was used as the first approach in three patients with concealed accessory pathways and one patient with a bidirectional accessory pathway. In another four patients, ablation during entrainment was used after technical difficulties in ablating during tachycardia. Only 1–3 radiofrequency applications were required to eliminate the accessory pathway using the entrainment technique. The catheter remained stable when accessory pathway conduction was interrupted by radiofrequency current. In conclusion, entrainment of atrioventricular reentrant tachycardia during radiofrequency application is useful for maintaining catheter position for accessory pathway ablation during atrioventricular reentrant tachycardia.     

Infraatrial supraventricular tachycardias: mechanisms, diagnosis, and management

Tachycardias are traditionally classified as either ventricular tachycardia (VT) or supraventricular tachycardia (SVT). VT can be defined as a tachycardia which requires only ventricular structures for perpetuation. SVT is defined in terms of exclusion of VT and hence is any tachycardia which requires participation of at least one supraventricular structure for perpetuation. Certain SVTs require only participation of the atrioventricular node (AVN) and the His bundle (HB) but not the atrial myocardium or any of the great thoracic veins for perpetuation and hence can be described as "infraatrial." The three main mechanisms of infraatrial SVTs are: (1) intranodal atrioventricular reentrant tachycardia; (2) junctional ectopic tachycardia; and (3) nodoventricular reentrant tachycardia. The clinical significance of infraatrial SVTs is that they are compatible with any A:V ratio and even atrioventricular (AV) dissociation. Infraatrial SVTs are often suspected when a narrow complex tachycardia presents with apparent AV dissociation and a counterintuitive A:V ratio of < 1:1. However, if the same tachycardia is conducted with aberrant conduction or preexcitation, a broad complex tachycardia with an A:V ratio of < 1:1 will arise and that can be easily mistaken for VT. The possible patterns of electrical association and dissociation between different cardiac structures are examined, and how individual types of infraatrial SVT can be diagnosed and managed are reviewed.     

Spontaneous Accelerated Junctional Rhythm: An Unusual but Useful Observation Prior to Radiofrequency Catheter Ablation for Atrioventricular Node Reentrant Tachycardia in Young Patients

Between May 1990 and March 1995, 5 of 29 young patients (ages 4.2–25 years; median 14.1 years) undergoing RF ablation for atrioventricular node reentrant tachycardia (AVNRT) presented with spontaneous accelerated junctional rhythm (AJR) (CL = 500–750 ms), compared to 0 of 58 age matched controls undergoing RF ablation for a concealed AV accessory pathway (P = 0.004). In 3 of the 5 patients with AVNRT and AJR, junctional beats served as a trigger for reentry. During attempted slow pathway modification in the five patients with AVNRT and AJR, AVNRT continued to be inducible until the AJR was entirely eliminated or dramatically slowed. These 5 patients are tachycardia-free in followup (median 15 months; range 6–31 months) with only 1 of the 5 patients continuing to experience episodic AJR at rates slower than observed preablation. Episodic spontaneous AJR is statistically associated with AVNRT in young patients and can serve as a trigger for reentry. Successful modification of slow pathway conduction may be predicted by the elimination of AJR or its modulation to slower rates, suggesting that the rhythm is secondary to enhanced automaticity arising near or within the slow pathway.     

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.     

Conductive Property of the Zone of Slow Conduction of Reentrant Ventricular Tachycardia and Its Relation to Pacing Induced Terminability

In order to assess the functional characteristics of the zone of slow conduction of reentrunt VT, rapid pacing was performed to entrain VT. The orthodromic conduction time was measured as the interval between the stimulus and the orthodromically captured electrogram recorded distal to the zone of slow conduction, hut not precisely at the exit point, and its response to rapid pacing was evaluated. In 32 of 33 consecutive patients, rapid pacing was performed to entrain VT. Of these, rapid pacing was repeated in 28 patients at 3–10 cycle lengths in steps of 10 msec before VT was terminated, or rapid pacing produced an acceleration of the rate. A pacing induced prolongation of the orthodromic conduction time (slowed conduction) was observed in 16 (57.1%) patients and in another 12 (42.9%) patients, the conduction time was constant. The pacing induced termination was observed in 93.8% of VT with slowed conduction and in 50% of VT with constant conduction, and the difference was significant (P < 0.05). There was no difference in the cycle length of VT or the shortest paced cycle length between VT with and without slowed conduction. The zone of slow conduction in human VT showed different conductive properties and VT with slowed conduction was associated with an easier and safer terminability with rapid pacing. The fact might be useful in selecting patients for antitachycardia pacing.     

Recovery Curve and Concealed Conduction in the His-Purkinje System of the Rabbit Heart: Effects of Radiofrequency Modification of the Low AV Junction

The aim of this study was to analyze the recovery curve and concealed conduction in the normal His-Purkinje system and after delivering radiofrequency current in the low AV junction, in the perfused rabbit heart. Twenty-one rabbit hearts were studied. Radiofrequency current (5 W) was delivered in the low AV junction to induce an incomplete His-Purkinje AV block (HV prolongation with 1:1 AV conduction); this was achieved in 9 experiments (Croup I), while 12 experiments developed a complete block (Group II). Atrial stimulation was performed in both Groups at baseline, and in Group Softer radiofrequency delivery, as follows: (1) pacing at increasing rates to determine the His-Purkinje AV block cycle length; (2) atrial extrastimulus test (A₁ A₂)J to calculate the His-Purkinje effective refractory period and the fitting of the recovery curve (H₁H₂ vs H₁V₂) to the exponential equation ΔHV=a.e^-b.(H1H2);(3) concealed conduction protocol (in 15 experiments) consisting of an atrial extrastimulus test with an interposed beat (A₁-A₀-A₂) at a fixed A₁A₂ coupling interval. The baseline recovery curve fitted an exponential equation in 17 experiments (with a 93%± 42% maximum H₂V₂ increase at the shortest H₁H₂), but did not in 4 experiments (the maximum H₂V₂ increase being only 22%± 7%). Radiofrequency application prolonged the HV interval (25 ± 6 ms vs 46 ± 16 ms: P = 0.001) and His-Purkinje effective refractory period (167 ± 28 ms vs 217 ± 57 ms; P = 0.02). The percentage increment was greater for HV than for refractory period (99%± 65% vs 35%± 32%; P = 0.02); however, the increment of the His-Purkinje block cycle length (77%± 74%) only correlated with that of the refractory period (r = 0.95; P = 0.0001). The recovery curve after radiofrequency delivery fitted an exponential equation in all experiments, showing a rightward shift expressed by an increment of the constant In a (2.7 ± 1.9 vs 5.5 ± 5.5; P = 0.02). Concealed conduction appeared in only three experiments at baseline. After radiofrequency, however, it was observed in all experiments, producing a rightward shift of the recovery curve and an In a increase (2.87 ± 1.2 vs 9.9 ± 2.7; P = 0.0001). When H₀ was conducted, the curve rightward shift and In a increase (26 ± 7.5; P = 0.0001) were greater. Conclusions: (1) His-Purkinje physiology, as in A V nodal physiology, can be described by a recovery curve that fits an exponential equation, especially if conduction becomes depressed with radiofrequency current. (2) Radiofrequency application in the low AV junction modifies His-Purkinje conduction more than refractoriness, though the refractoriness increase determines the degree of block at fast atrial rates. (3) Concealed conduction is uncommon in the normal His-Purkinje system during atrial pacing, but very frequent after modifying the low AV junction with radiofrequency current.     

Low Energies and Helifix Electrodes in the Successful Ablation of Atrioventricular Conduction

High energies delivered via standard pacing catheter electrodes produce permanent atrioventricular conduction block and generate high pressures. We investigate the use of lower energies and an active fixation electrode. Ten patients with refractory supraventricular tachycardias (six with paroxysmal atrial fibrillation, three with dual AV nodal pathways, and one with a concealed accessory atrioventricular pathway) were treated. A 6F Vitatron Helifix electrode was positioned to give the maximum His bundle deflection. Four shocks of only 50 joules each were delivered at 1-minute intervals. Long-term follow-up showed that seven patients (70%) had persistent complete heart block and two had atrial fibrillation with slower ventricular rates. Nine patients (90%) were symptom-free without antiarrhythmic therapy. Permanent pacemakers were implanted in eight patients. There were no complications resulting from the procedure. Transvenous ablation of atrioventricular conduction can be safely achieved using a Vitatron Helifix electrode and much lower energy values than have been previously employed.     

Electrophysiologic Study of Tachycardia-Dependent Paroxysmal His Bundle Block in Man

Electrophysiologic sludy was performed in a potienl with tachycardia-dependent paroxysmal atrioventricular block. The site of block was within the His bundle. The effective refractory period of the His bundle was markedly prolonged and it was comparable to the critical atrial cycle length producing type II His bundle block. The most likely mechanism of paroxysmal atrioventricular block was repetitive concealed penetration of the blocking zone by nonconducted impulses that reached the proximal His bundle. Enhancing the blocking ratio at the atrioventricular nodal level resulted in improvement of overall atrioventricular conduction.