Tachycardia cycle length and maximum capacity of anterograde and retrograde atrioventricular conduction in paroxysmal supraventricular tachycardia

Anterograde and retrograde pathways are the two major components of the reentry circuit in patients with paroxysmal supraventricular reentrant tachycardias. Therefore, the capacity of each pathway to maintain 1:1 conduction would be expected to determine the cycle length (CL) of the tachycardia. In this study, the possible relationship between the CL of reentrant tachycardia and the maximum capacities of anterograde and retrograde conduction in the maintenance of a 1:1 response during atrial and ventricular pacing were examined. This relationship was analyzed in 26 patients with orthodromic reentrant tachycardia due to Wolff-Parkinson-White syndrome (group 1) and compared with that in 26 patients with atrioventricular nodal reentrant tachycardia (group 2). There were no statistically significant differences between the two groups in the shortest tachycardia CLs (mean +/- SD, 325 +/- 44 versus 329 +/- 52 ms); in the shortest ventricular pacing CLs with 1:1 response (314 +/- 63 versus 319 +/- 38 ms); nor in the CLs that produced retrograde atrioventricular block (306 +/- 62 versus 301 +/- 37 ms). In contrast, the longest atrial pacing CL that produced Wenckebach's phenomenon and the shortest atrial pacing CL with 1:1 response were significantly shorter for group 1 than for group 2 patients (290 +/- 38 versus 390 +/- 88 ms, P less than 0.001) and (305 +/- 38 versus 406 +/- 90 ms, P less than 0.001), respectively. It was concluded that the CL of orthodromic tachycardia can best be predicted from the shortest atrial pacing CL that maintains 1:1 anterograde conduction via the normal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

Functional Bundle Branch Block as a Delayed Manifestation of Retrograde Concealment in the His-Purkinje System

Delayed Manifestation of Retrograde HPS Concealment. Introduction: The mechanism of functional bundle branch block induced at the onset of supraventricular tachycardia (SVT) is well established. However, no data exist to address the underlying mechanism of functional bundle branch block occurring in the second beat of SVT, when the first beat is conducted with a narrow QRS morphology and preceded by ventricular stimulation. Methods and Results: Two patients showing such a phenomenon form the basis of this report. Patient 1 with AV nodal reentrant tachycardia of the common variety persistently demonstrated functional right bundle branch block in the second SVT complex when a short train of ventricular pacing was introduced during SVT. This occurred without any discernible change in the SVT cycle length. Patient 2 bad a manifest posteroseptal accessory pathway and inducible orthodromic reentrant tachycardia. Functional bundle branch block during propagation of the second SVT complex invariably occurred either in the left bundle when SVT was induced by a bundle branch reentrant complex during premature ventricular stimulation, or in the right bundle when SVT was induced with a short train of ventricular pacing. The development of functional bundle branch block was preceded by minimal or no cycle length variations in the His-bundle inputs. Conclusion: These observations suggest that the type of functional bundle branch block occurring in the second SVT complex as a de novo phenomenon may be related to the relative timing of the retrograde penetration of the right versus left bundle during ventricular pacing or bundle branch reentrant complex. Therefore, due to its longest cycle length of activation and refractoriness, the earliest site of retrograde penetration is the most likely site of functional block during propagation of the second SVT complex. This delayed manifestation of retrograde concealment may provide new information regarding the electrophysiologic behavior of the His-Purkinje system.     

Reliability of retrograde atrial activation patterns during ventricular pacing for localizing accessory pathways

Definitive localization of accessory pathways is based on atrial activation patterns during orthodromic supraventricular tachycardia when retrograde conduction occurs exclusively through the accessory pathway. In some patients, supraventricular tachycardia cannot be induced or is deleterious. To determine whether accessory pathway sites can be identified accurately during ventricular pacing, retrograde atrial activation was assessed during orthodromic supraventricular tachycardia and ventricular pacing at multiple cycle lengths in 41 patients with a single accessory pathway. To obviate retrograde fusion due to concomitant conduction through the normal atrioventricular (AV) conduction system that may obscure the location of the accessory pathway, the difference in conduction time from the site of earliest atrial activation to the His bundle atrial electrogram (delta A-SVT) was measured during orthodromic supraventricular tachycardia and compared with values observed during ventricular pacing (delta A-VP). Characteristic values for the delta A-SVT interval were identified for left lateral (66 +/- 17 ms), left posterior (50 +/- 8 ms), posteroseptal (33 +/- 7 ms), right free wall (22 +/- 15 ms) and anteroseptal (0 +/- 0 ms) accessory pathway sites. During ventricular pacing, the site with the earliest atrial electrogram was used to define the accessory pathway location only if the maximal value of the delta A-VP interval over the range of cycle lengths assessed was comparable with the value of the delta A-SVT interval characteristic of that region. Values of the delta A-SVT interval correlated closely with the maximal values of the delta A-VP interval (r = 0.91). With this approach, 40 (98%) of 41 accessory pathway sites were identified correctly during ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome

Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated. The mechanisms of orthodromic tachycardia induction were studied in 17 patients with Wolff-Parkinson-White syndrome using a specially designed pacing protocol. A beat by beat analysis indicated that the retrograde His-Purkinje system block was the most common initiating mechanism of orthodromic tachycardia in 14 of the 17 cases. In two cases, AV node block preceded the onset of orthodromic tachycardia, whereas the data in the remaining case suggested that both mechanisms were operative but at different pacing cycle lengths. The orthodromic tachycardia induction with His-Purkinje system block occurred within the first two cycles in most cases. When orthodromic tachycardia initiation was delayed beyond the first two cycles of the ventricular train it represented either a 2:1 block in the His-Purkinje system; a linking phenomenon in the His-Purkinje system; or a block in the AV node. These data have methodologic, mechanistic and therapeutic implications for patients with the Wolff-Parkinson-White syndrome.     

Further observations on transient entrainment: importance of pacing site and properties of the components of the reentry circuit

Transient entrainment of circus-movement tachycardia utilizing an atrioventricular (AV) bypass pathway was studied in 13 patients (nine with the orthodromic form, two with the antidromic form, and two with both the orthodromic and antidromic forms). All patients had a left-sided AV bypass pathway. Pacing at selected rates faster than the spontaneous rate was performed during the tachycardia at a site proximal or distal to the AV node, an area of slow conduction within the reentry loop. Rapid pacing from a site proximal to the AV node (from the right atrium during the orthodromic form of the arrhythmia or the right ventricle during the antidromic form of the arrhythmia) always demonstrated at least one of the three entrainment criteria: constant fusion beats except for the last captured beat, which was entrained but not fused (first criterion); progressive fusion (second criterion); localized conduction block to a site(s) for 1 paced beat associated with interruption of the tachycardia followed by activation of that site(s) by the next paced beat from a different direction and with a shorter conduction time (third criterion). In contrast, rapid pacing from a site distal to the AV node (from the right ventricle during the orthodromic form of the arrhythmia, or the right atrium during the antidromic form of the arrhythmia) transiently entrained the tachycardia, but never demonstrated any entrainment criteria because the antidromic wave front from the pacing impulse always blocked in the AV node (concealed entrainment). We conclude that the location of the pacing site relative to the components of a reentry loop is critical to the demonstration of the criteria of transient entrainment; i.e., if it is proximal to an area of slow conduction and/or unidirectional block within a reentry loop, transient entrainment should be demonstrable, but if it is distal, it will not be demonstrable.     

Para-Hisian entrainment: a novel pacing maneuver to differentiate orthodromic atrioventricular reentrant tachycardia from atrioventricular nodal reentrant tachycardia

INTRODUCTION: Para-Hisian pacing during sinus rhythm can help to identify the presence of an accessory pathway (AP). In this maneuver, the retrograde activation time and pattern are compared during capture and loss-of-capture of the His bundle while pacing from a para-Hisian position. However, identification of a retrograde AP does not necessitate that it is operative during the tachycardia of interest; conversely, slowly conducting or "distant" bypass tracts may not be identified. We evaluated the utility of entrainment or resetting of tachycardias from the para-Hisian position to help distinguish atrioventricular nodal reentrant tachycardia (AVNRT) from orthodromic atrioventricular tachycardia (AVRT). METHODS AND RESULTS: Para-Hisian entrainment/resetting was evaluated in 50 patients: 33 with AVNRT and 17 with AVRT. The maneuvers were performed using a standard quadripolar catheter placed at the His position: low output for right ventricular (RV) capture and high output for both RV and His capture. The retrograde atrial activation sequence, SA interval (interval from stimulus to earliest retrograde atrial activation), and "local" VA interval (interval between the ventricular and atrial electrograms at the site of earliest retrograde atrial activation) were compared between His and His/RV capture. The DeltaSA was > 40 ms in patients with AVNRT and was < 40 ms in all but one patient with AVRT. In concert with the DeltaSA interval, the DeltaVA interval was able to fully define the mechanism of the tachycardia in all patients studied. CONCLUSION: Para-Hisian entrainment/resetting can determine the course of retrograde conduction operative during narrow complex tachycardias. It is a useful diagnostic maneuver in differentiating AVNRT and orthodromic AVRT.     

Pseudosimultaneous fast and slow pathway conduction: a common electrophysiologic finding in patients with dual atrioventricular nodal pathways

Two ventricular responses following termination of rapid atrial pacing were noted in 24 of 87 patients with dual atrioventricular (AV) nodal pathways and supraventricular tachycardia. In all 24 patients, the AH intervals of the first and second ventricular responses were comparable with those of the fast and slow pathways, respectively. Careful analysis of the whole pacing sequence revealed that, in 21 patients, this phenomenon resulted from sustained slow pathway conduction with long AH intervals. In these patients, as the AH interval of each paced beat was progressively lengthened during pacing, the corresponding His bundle and ventricular responses were pushed one cycle behind the current atrial paced beat, so that the last paced beat was followed by two His bundle and ventricular responses. In only three patients did double ventricular responses result from simultaneous fast and slow pathway conduction. One of these three patients also showed two ventricular responses resulting from sustained slow pathway conduction. Several factors predispose to the occurrence of this phenomenon in patients with dual AV nodal pathways. These include an ability to sustain slow pathway conduction, a longer slow pathway AH interval, a shorter sinus AH interval (fast pathway) and a shorter atrial paced cycle length that sustains slow pathway conduction. In conclusion, sustained slow pathway conduction with resultant long AH intervals is the mechanism of two ventricular responses following termination of atrial pacing in most patients with dual AV nodal pathways. This phenomenon should be distinguished from the rare occurrence of double ventricular responses to an atrial impulse due to simultaneous fast and slow pathway conduction.     

Demonstration of the presence of slow conduction during sustained ventricular tachycardia in man: use of transient entrainment of the tachycardia

To test the hypothesis that an area of slow conduction is present during reentrant ventricular tachycardia in man, and that the earliest activation site during ventricular tachycardia is within or orthodromically just distal to the area of slow conduction in the reentry loop, we studied 12 episodes of ventricular tachycardia (mean rate 185 +/- 32 beats/min) that were induced in nine patients with ischemic heart disease. Rapid ventricular pacing was performed at selected sites during ventricular tachycardia while recording electrograms from an early activation site relative to the onset of the QRS complex (site A) and from a site close to the pacing site (site B). Rapid pacing from the right ventricular apex during ventricular tachycardia with a right bundle branch block pattern and from selected left ventricular sites during ventricular tachycardia with a left bundle branch block pattern (mean pacing rate 202 +/- 38 beats/min) resulted in constant ventricular fusion beats on the electrocardiogram except for the last captured beat (i.e., the ventricular tachycardia was entrained) in 11 of 12 episodes. During entrainment: sites A and B were activated at the pacing rate, conduction time from the last pacing impulse to the last captured ventricular electrogram at site A (St-A interval) was 359 +/- 69 msec and spanned the diastolic interval, while that at site B (St-B interval) was only 28 +/- 13 msec, site A had the same ventricular electrogram morphology as that during ventricular tachycardia, while site B had a different electrogram morphology, indicating that site A was activated in the same direction during entrainment as during ventricular tachycardia. Eight episodes of ventricular tachycardia were entrained at two or more different pacing rates. The St-A interval increased during pacing at the faster rate(s) in four of eight episodes, while the St-B interval remained unchanged. Rapid ventricular pacing performed from the same site during sinus rhythm (mean pacing rate 201 +/- 37 beats/min) resulted in an St-A interval of 103 +/- 37 msec (p less than .001 vs the value during entrainment) and an St-B interval of 31 +/- 15 msec (p = NS vs the value during entrainment). It is concluded that an area of slow conduction not demonstrable during sinus rhythm exists during ventricular tachycardia, and that the earliest activation site during ventricular tachycardia is at or orthodromically distal to this area of slow conduction.     

Incidence and mechanism of interruption of reentrant ventricular tachycardia with rapid ventricular pacing.

BACKGROUND. Information concerning the electrophysiological characteristics of the reentrant circuit is still limited. To understand the incidence and mechanism of pacing-induced interruption of ventricular tachycardia (VT), rapid pacing was performed to entrain VT, and the local electrogram at the VT origin and the surface electrocardiogram were analyzed. METHODS AND RESULTS. Among 25 patients, evidence of transient entrainment was confirmed in 20 patients, but the critical paced cycle length at which VT was interrupted was obtained in 13 patients when the paced cycle length was decreased in steps of 10 msec. During pacing at the critical cycle length (defined as block cycle length), changes in the local electrogram at VT origin were confirmed in all of the 13 patients; that is, 1) a change in morphology and 2) a change in the timing of activation: a sudden shortening in the stimulus to local electrogram time (third entrainment criterion by Waldo). The two changes mean that the exit is activated from a different direction (retrograde capture) because of an orthodromic block in the slow conduction zone. The QRS complex in the surface electrocardiogram showed a change in configuration from the fusion complex to the fully paced one at the same time when the exit was captured antidromically. CONCLUSIONS. Based on our observations in these patients, ventricular tachycardia interruption is very often associated with orthodromic block in the reentrant circuit at a critical cycle length of rapid pacing.     

Reappraisal of electrical cure of atrioventricular nodal reentrant tachycardia--lessons from a modified catheter ablation technique.

A modified catheter ablation technique was studied prospectively in 29 patients with atrioventricular (AV) nodal reentrant tachycardia. A His bundle electrode catheter was used for mapping and ablation. Cathodic electroshocks (100-250 J) were delivered from the distal two electrodes (connected in common) of the His bundle catheter to the site selected for ablation. The optimal ablation site recorded the earliest retrograde atrial depolarization, simultaneous or earlier than the QRS complex, with absence of a His bundle deflection during AV nodal reentrant tachycardia. One additional electrical shock was delivered if complete abolition of retrograde VA conduction persisted for more than 30 min and AV nodal reentrant tachycardia was not inducible during isoproterenol and/or atropine administration. With a cumulative energy of 323 +/- 27 J and a mean of 2.3 +/- 0.5 shocks interruption or impairment of retrograde nodal conduction was achieved. Antegrade conduction, although modified, was preserved in 27 patients, with persistence of complete AV block in 2 patients. Two of the 27 patients still need antiarrhythmic agents to control tachycardia, the other 25 patients were free of tachycardia within a mean follow-up period of 13 +/- 2 months (range 7 to 20 months). Twenty-three patients received late follow-up electrophysiological studies (3-6 months after the ablation procedures), and the AV nodal function curves were classified into 4 types. The majority of the patients (15/23) had loss of retrograde conduction. Among the 8 patients with prolongation of retrograde conduction, 4 patients still had antegrade dual AV nodal property but all without inducible tachycardia. In conclusion, preferential interruption or impairment of retrograde conduction was the major, but not the sole, mechanism of electrical cure of AV nodal reentrant tachycardia.     

Procainamide and retrograde atrioventricular nodal conduction in man

Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 +/- 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset of retrograde block in the AV node; in seven of 13, VA block occurred at a longer paced CL after PA (344.2 +/- 51.2 msec vs 477.1 +/- 93.2 msec). In one patient, PA did not affect VA conduction. PA invariably produced prolongation in the VA interval at comparable CL of pacing. With ventricular premature stimulation, the retrograde H2A2 intervals during the control period were short (less than 50 msec) in seven of 13, intermediate (60-100 msec) in three of 13 and long (greater than 100 msec) in three of 13 cases. PA either abolished H2A2 conduction (H2 but no A2) or prolonged the H2A2 intervals by 5-20 msec in most cases in this series. The data suggest that i.v. PA almost uniformly depresses retrograde AV nodal conduction in the intact human heart. This depressant response to PA is not indicative of presence of partial or complete AV nodal bypass tracts.     

Usefulness of the delta HA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias

Surface electrocardiographic criteria may be inadequate to distinguish some cases of atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) from those with orthodromic SVT incorporating a posterior septal bypass tract (orthodromic SVT) because of similarities in P-wave morphology and timing during SVT. Invasive electrophysiologic studies may occasionally leave uncertainty in the correct diagnosis, using currently accepted criteria. A new criterion for distinguishing these 2 forms of SVT was therefore devised and tested based on differences in the sequence of activation of the His bundle and atrium during SVT and ventricular pacing. Eighty-four patients underwent invasive electrophysiologic studies (60 with proved AV nodal SVT, 24 with proved orthodromic SVT), during which His to atrial (HA) intervals were measured during SVT as well as ventricular pacing at the same rate. The newly devised criterion, the delta HA interval (HApace-HAsvt) was found to accurately distinguish AV nodal SVT (delta HA greater than 0 ms) from orthodromic SVT (delta HA less than -27 ms). An intermediate value of delta HA = -10 ms was chosen which had a 100% sensitivity, specificity and predictive accuracy in differentiating the 2 forms of SVT. A clear retrograde His potential during ventricular pacing, which is essential for application of this criterion, was present in 78 of 84 (93%) cases. In summary, patients with delta HA intervals greater than -10 ms separate AV nodal reentry from orthodromic SVT incorporating a septal bypass tract, and no overlap exists between the 2 groups. This criterion may be useful in differentiating the mechanism of SVT in cases in which distinction is not possible by other methods.     

Characteristics of entrainment during autodecremental atrial and ventricular stimulation

The entrainment characteristics of orthodromic circus movement tachycardias occurring during autodecremental atrial and ventricular stimulation were studied in 9 patients with manifest Wolff-Parkinson-White syndrome. The phenomenon occurred in 34 of 38 episodes of tachycardia during autodecremental atrial stimulation. It was not seen in 4 episodes because the first impulse penetrating the circuit terminated the arrhythmia. Invariably, the HH and VV intervals were not equal to, but longer than, the stimulus-stimulus intervals, thus not fulfilling the definition of "classic" (constant cycle length) entrainment postulated by Okumura et al. Furthermore, the first 2 of the 3 diagnostic criteria were not demonstrated and the third only could be demonstrated in 7 episodes. Tachycardia termination was achieved in all 38 episodes. Entrainment occurred during autodecremental ventricular stimulation in 79 of 80 episodes, with the AA and H-H- intervals (when visible) being equal to the corresponding paced cycle lengths. Moreover, the intervals between the last paced ventricular beat and the first ventricular beat of the resumed tachycardia were invariably longer than the last stimulus-stimulus intervals. These characteristics were those which Okumura et al attributed to "concealed" entrainment. Tachycardia termination was achieved in 77 of 80 episodes. In summary: (1) autodecremental atrial pacing produced a specific form of entrainment that did not fulfill the "classic" definition of Okumura et al; (2) autodecremental ventricular pacing consistently produced "concealed" entrainment; and (3) autodecremental stimulation was very effective in terminating 115 of 118 (98%) of episodes of circus movement tachycardias.     

Atrioventricular nodal reentrant tachycardia: studies on upper and lower 'common pathways'

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 +/- 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p less than .05). Thus the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.     

Ectopic left atrial rhythm that produces QRS changes in absence of Wolff-Parkinson-White syndrome

In an 18-year-old patient without manifest or concealed Wolff-Parkinson-White syndrome, spontaneous and paced left atrial impulses penetrated a left-sided AV nodal input and thereafter activated the ventricles in a normal fashion exclusively through the His-Purkinje system. On the other hand, sinus and paced right atrial impulses entered a right-sided atrioventricular nodal input that was completely dissociated from the left-sided input to subsequently activate the ventricles partly through Mahaim fibers and partly through the His-Purkinje system. The Mahaim fibers, which acted as "bystanders" during episodes of atrioventricular nodal reciprocating tachycardia, seemed to have extended from a "distal," common (right-sided) intranodal pathway (or "proximal" His bundle) to the right ventricle or, although this is less likely, to the right bundle branch. More studies are necessary to determine whether the association on the surface electrocardiogram of an ectopic slow left atrial rhythm with changes in QRS morphology (but not in QRS duration) always reflects the existence of Mahaim fibers.     

Transient entrainment and interruption of atrioventricular node tachycardia

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.     

QRS complex widening due to loss of left bundle branch capture: pitfall of para-Hisian pacing

During para-Hisian pacing, widening of the paced QRS complex usually indicates loss of His bundle capture. We describe a patient without any accessory pathways in whom widening of the paced QRS complex occurred due to loss of left bundle branch capture during para-Hisian pacing. After initial widening of the QRS complex, further widening was observed due to loss of His bundle capture. With the initial QRS widening, the stimulus-atrial interval and retrograde atrial activation sequence were almost unchanged, so the findings mimicked retrograde conduction over an accessory pathway. This may be a pitfall of the para-Hisian pacing technique.     

Anterograde and retrograde bradycardiac block in the His-Purkinje system. Finding in a patient with acute myocardial infarction

A patient with an acute inferior myocardial infarction developed a complete atrioventricular block and intermitent periods of atrioventricular conduction with QRS complexes showing right bundle branch block associated with left anterior hemiblock. Recordings of the His bundle electrogram showed that the atrioventricular block was infrahisian and that in periods of resumed atrioventricular conduction, the His-ventricle (H-V) interval was long. Ventricular escape beats showed concealed conduction to the atrioventricular node. Anterograde atrioventricular conduction was always resumed through the left posterior division when the preceding division when the preceding intervals between ventricular escape beats and the atrium (V-A intervals) were shorter than 580 msec. The same phenomenon occurred with right ventricular pacing. A retrograde His potential could be observed. Retrograde conduction of ventricular escape beats and ventricular paced beats was blocked if the H-V interval and the interval between the His bundle and the ventricular paced beat (H-V interval) were long (more than 600 msec and 550 msec, respectively). The existence of an intermittent anterograde and retrograde bradycardiac infrahisian block was inferred from the previously mentioned data; a fixed retrograde atrial nodal block was also present.     

Incidence of reentry with an excitable gap in ventricular tachycardia: a prospective evaluation utilizing transient entrainment

The demonstration of transient entrainment has been proposed as evidence of reentry, with an excitable gap as the probable mechanism of tachycardia. A prospective series of 27 consecutive patients with sustained ventricular tachycardia induced by programmed electrical stimulation was studied to determine the frequency with which transient entrainment can be demonstrated and to define the optimal location of pacing and recording electrodes. In all patients, electrodes for pacing and recording were placed in both the left and right ventricles during electrophysiologic study. Among the 19 patients in whom the response to rapid pacing could be evaluated (25 episodes of ventricular tachycardia), transient entrainment was demonstrated in 79% (76% of episodes). Ten of 12 episodes of ventricular tachycardia with a left bundle branch block QRS configuration in lead V1 and 9 of 13 episodes with a right bundle branch block QRS configuration could be transiently entrained (p = NS). Transient entrainment was demonstrated for 8 of 11 episodes of ventricular tachycardia with a left bundle branch block configuration during pacing from the left ventricle, but for only 2 of 10 episodes during pacing from the right ventricular apex (p less than 0.05). Conversely, 9 of 13 episodes of ventricular tachycardia with a right bundle branch block configuration were transiently entrained during pacing from the right ventricular apex, but 0 of 10 episodes were transiently entrained by left ventricular pacing (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)